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Publications of Terrie E. Moffitt    :chronological  alphabetical  combined listing:

%% Journal Articles   
@article{fds376145,
   Author = {Whitman, ET and Ryan, CP and Abraham, WC and Addae, A and Corcoran, DL and Elliott, ML and Hogan, S and Ireland, D and Keenan, R and Knodt, AR and Melzer, TR and Poulton, R and Ramrakha, S and Sugden, K and Williams,
             BS and Zhou, J and Hariri, AR and Belsky, DW and Moffitt, TE and Caspi, A and Alzheimer’s Disease Neuroimaging Initiative},
   Title = {A blood biomarker of the pace of aging is associated with
             brain structure: replication across three
             cohorts.},
   Journal = {Neurobiology of aging},
   Volume = {136},
   Pages = {23-33},
   Year = {2024},
   Month = {April},
   url = {http://dx.doi.org/10.1016/j.neurobiolaging.2024.01.008},
   Abstract = {Biological aging is the correlated decline of multi-organ
             system integrity central to the etiology of many age-related
             diseases. A novel epigenetic measure of biological aging,
             DunedinPACE, is associated with cognitive dysfunction,
             incident dementia, and mortality. Here, we tested for
             associations between DunedinPACE and structural MRI
             phenotypes in three datasets spanning midlife to advanced
             age: the Dunedin Study (age=45 years), the Framingham Heart
             Study Offspring Cohort (mean age=63 years), and the
             Alzheimer's Disease Neuroimaging Initiative (mean age=75
             years). We also tested four additional epigenetic measures
             of aging: the Horvath clock, the Hannum clock, PhenoAge, and
             GrimAge. Across all datasets (total N observations=3380;
             total N individuals=2322), faster DunedinPACE was associated
             with lower total brain volume, lower hippocampal volume,
             greater burden of white matter microlesions, and thinner
             cortex. Across all measures, DunedinPACE and GrimAge had the
             strongest and most consistent associations with brain
             phenotypes. Our findings suggest that single timepoint
             measures of multi-organ decline such as DunedinPACE could be
             useful for gauging nervous system health.},
   Doi = {10.1016/j.neurobiolaging.2024.01.008},
   Key = {fds376145}
}

@article{fds371370,
   Author = {Theadom, A and Barker-Collo, S and Parag, V and Caspi, A and Moffitt,
             TE and Hogan, S and Ramrakha, S and Poulton, R},
   Title = {Mild Traumatic Brain Injury Does Not Significantly Affect
             Midlife Cognitive Functioning Within the General Population:
             Findings From a Prospective Longitudinal Birth Cohort
             Study.},
   Journal = {The Journal of head trauma rehabilitation},
   Volume = {39},
   Number = {2},
   Pages = {E70-E82},
   Year = {2024},
   Month = {March},
   url = {http://dx.doi.org/10.1097/htr.0000000000000875},
   Abstract = {<h4>Objective</h4>To determine whether differences exist in
             mid-adulthood cognitive functioning in people with and
             without history of mild traumatic brain injury
             (mTBI).<h4>Setting</h4>Community-based study.<h4>Participants</h4>People
             born between April 1, 1972, and March 31, 1973, recruited
             into the Dunedin Multidisciplinary Health and Development
             Longitudinal Study, who completed neuropsychological
             assessments in mid-adulthood. Participants who had
             experienced a moderate or severe TBI or mTBI in the past 12
             months were excluded.<h4>Design</h4>Longitudinal,
             prospective, observational study.<h4>Main measures</h4>Data
             were collected on sociodemographic characteristics, medical
             history, childhood cognition (between 7 and 11 years), and
             alcohol and substance dependence (from 21 years of age).
             mTBI history was determined from accident and medical
             records (from birth to 45 years of age). Participants were
             classified as having 1 mTBI and more in their lifetime or no
             mTBI. The Wechsler Adult Intelligence Scale (WAIS-IV) and
             Trail Making Tests A and B (between 38 and 45 years of age)
             were used to assess cognitive functioning. T tests and
             effect sizes were used to identify any differences on
             cognitive functioning domains between the mTBI and no mTBI
             groups. Regression models explored the relative contribution
             of number of mTBIs and age of first mTBI and
             sociodemographic/lifestyle variables on cognitive
             functioning.<h4>Results</h4>Of the 885 participants, 518
             (58.5%) had experienced at least 1 mTBI over their lifetime,
             with a mean number of 2.5 mTBIs. The mTBI group had
             significantly slower processing speed ( P < .01, d = 0.23)
             in mid-adulthood than the no TBI controls, with a medium
             effect size. However, the relationship no longer remained
             significant after controlling for childhood cognition,
             sociodemographic and lifestyle factors. No significant
             differences were observed for overall intelligence, verbal
             comprehension, perceptual reasoning, working memory,
             attention, or cognitive flexibility. Childhood cognition was
             not linked to likelihood of sustaining mTBI later in
             life.<h4>Conclusion</h4>mTBI histories in the general
             population were not associated with lower cognitive
             functioning in mid-adulthood once sociodemographic and
             lifestyle factors were taken into account.},
   Doi = {10.1097/htr.0000000000000875},
   Key = {fds371370}
}

@article{fds368586,
   Author = {Guiney, H and Caspi, A and Ambler, A and Belsky, J and Kokaua, J and Broadbent, J and Cheyne, K and Dickson, N and Hancox, RJ and Harrington,
             H and Hogan, S and Ramrakha, S and Righarts, A and Thomson, WM and Moffitt,
             TE and Poulton, R},
   Title = {Childhood sexual abuse and pervasive problems across
             multiple life domains: Findings from a five-decade
             study.},
   Journal = {Development and psychopathology},
   Volume = {36},
   Number = {1},
   Pages = {219-235},
   Year = {2024},
   Month = {February},
   url = {http://dx.doi.org/10.1017/s0954579422001146},
   Abstract = {The aim of this study was to use longitudinal
             population-based data to examine the associations between
             childhood sexual abuse (CSA) and risk for adverse outcomes
             in multiple life domains across adulthood. In 937
             individuals followed from birth to age 45y, we assessed
             associations between CSA (retrospectively reported at age
             26y) and the experience of 22 adverse outcomes in seven
             domains (physical, mental, sexual, interpersonal, economic,
             antisocial, multi-domain) from young adulthood to midlife
             (26 to 45y). Analyses controlled for sex, socioeconomic
             status, prospectively reported child harm and household
             dysfunction adverse childhood experiences, and adult sexual
             assault, and considered different definitions of CSA. After
             adjusting for confounders, CSA survivors were more likely
             than their peers to experience internalizing, externalizing,
             and thought disorders, suicide attempts, health risk
             behaviors, systemic inflammation, poor oral health, sexually
             transmitted diseases, high-conflict relationships, benefit
             use, financial difficulties, antisocial behavior, and
             cumulative problems across multiple domains in adulthood. In
             sum, CSA was associated with multiple persistent problems
             across adulthood, even after adjusting for confounding life
             stressors, and the risk for particular problems incremented
             with CSA severity. The higher risk for most specific
             problems was small to moderate, but the cumulative long-term
             effects across multiple domains reflect considerable
             individual and societal burden.},
   Doi = {10.1017/s0954579422001146},
   Key = {fds368586}
}

@article{fds375488,
   Author = {Bourassa, KJ and Garrett, ME and Caspi, A and Dennis, M and Hall, KS and Moffitt, TE and Taylor, GA and VA Mid Atlantic MIRECC Workgroup, and Ashley-Koch, AE and Beckham, JC and Kimbrel, NA},
   Title = {Posttraumatic stress disorder, trauma, and accelerated
             biological aging among post-9/11 veterans.},
   Journal = {Transl Psychiatry},
   Volume = {14},
   Number = {1},
   Pages = {4},
   Year = {2024},
   Month = {January},
   url = {http://dx.doi.org/10.1038/s41398-023-02704-y},
   Abstract = {People who experience trauma and develop posttraumatic
             stress disorder (PTSD) are at increased risk for poor
             health. One mechanism that could explain this risk is
             accelerated biological aging, which is associated with the
             accumulation of chronic diseases, disability, and premature
             mortality. Using data from 2309 post-9/11 United States
             military veterans who participated in the VISN 6 MIRECC's
             Post-Deployment Mental Health Study, we tested whether PTSD
             and trauma exposure were associated with accelerated rate of
             biological aging, assessed using a validated DNA methylation
             (DNAm) measure of epigenetic aging-DunedinPACE. Veterans
             with current PTSD were aging faster than those who did not
             have current PTSD, β = 0.18, 95% CI [0.11, 0.27],
             p < .001. This effect represented an additional 0.4
             months of biological aging each year. Veterans were also
             aging faster if they reported more PTSD symptoms,
             β = 0.13, 95% CI [0.09, 0.16], p < 0.001, or higher
             levels of trauma exposure, β = 0.09, 95% CI [0.05,
             0.13], p < 0.001. Notably, veterans with past PTSD were
             aging more slowly than those with current PTSD,
             β = -0.21, 95% CI [-0.35, -0.07], p = .003. All
             reported results accounted for age, gender, self-reported
             race/ethnicity, and education, and remained when controlling
             for smoking. Our findings suggest that an accelerated rate
             of biological aging could help explain how PTSD contributes
             to poor health and highlights the potential benefits of
             providing efficacious treatment to populations at increased
             risk of trauma and PTSD.},
   Doi = {10.1038/s41398-023-02704-y},
   Key = {fds375488}
}

@article{fds370883,
   Author = {Caspi, A and Houts, RM and Fisher, HL and Danese, A and Moffitt,
             TE},
   Title = {The general factor of psychopathology (p): Choosing among
             competing models and interpreting p.},
   Journal = {Clinical psychological science : a journal of the
             Association for Psychological Science},
   Volume = {12},
   Number = {1},
   Pages = {53-82},
   Year = {2024},
   Month = {January},
   url = {http://dx.doi.org/10.1177/21677026221147872},
   Abstract = {Over the past 10 years, the general factor of
             psychopathology, p, has attracted interest and scrutiny. We
             review the history of the idea that all mental disorders
             share something in common, p; how we arrived at this idea;
             and how it became conflated with a statistical
             representation, the Bi-Factor Model. We then leverage the
             Environmental Risk (E-Risk) longitudinal twin study to
             examine the properties and nomological network of different
             statistical representations of p. We find that p performed
             similarly regardless of how it was modelled, suggesting that
             if the sample and content are the same the resulting p
             factor will be similar. We suggest that the meaning of p is
             not to be found by dueling over statistical models but by
             conducting well-specified criterion-validation studies and
             developing new measurement approaches. We outline new
             directions to refresh research efforts to uncover what all
             mental disorders have in common.},
   Doi = {10.1177/21677026221147872},
   Key = {fds370883}
}

@article{fds374321,
   Author = {Matthews, T and Rasmussen, LJH and Ambler, A and Danese, A and Eugen-Olsen, J and Fancourt, D and Fisher, HL and Iversen, KK and Schultz, M and Sugden, K and Williams, B and Caspi, A and Moffitt,
             TE},
   Title = {Social isolation, loneliness, and inflammation: A
             multi-cohort investigation in early and mid-adulthood.},
   Journal = {Brain, behavior, and immunity},
   Volume = {115},
   Pages = {727-736},
   Year = {2024},
   Month = {January},
   url = {http://dx.doi.org/10.1016/j.bbi.2023.11.022},
   Abstract = {Social isolation and loneliness have been associated with
             poor health and increased risk for mortality, and
             inflammation might explain this link. We used data from the
             Danish TRIAGE Study of acutely admitted medical patients
             (N = 6,144, mean age 60 years), and from two
             population-representative birth cohorts: the New Zealand
             Dunedin Longitudinal Study (N = 881, age 45) and the UK
             Environmental Risk (E-Risk) Longitudinal Twin Study
             (N = 1448, age 18), to investigate associations of social
             isolation with three markers of systemic inflammation:
             C-reactive protein (CRP), interleukin-6 (IL-6), and a newer
             inflammation marker, soluble urokinase plasminogen activator
             receptor (suPAR), which is thought to index systemic chronic
             inflammation. In the TRIAGE Study, socially isolated
             patients (those living alone) had significantly higher
             median levels of suPAR (but not CRP or IL-6) compared with
             patients not living by themselves. Social isolation
             prospectively measured in childhood was longitudinally
             associated with higher CRP, IL-6, and suPAR levels in
             adulthood (at age 45 in the Dunedin Study and age 18 in the
             E-Risk Study), but only suPAR remained associated after
             controlling for covariates. Dunedin Study participants who
             reported loneliness at age 38 or age 45 had elevated suPAR
             at age 45. In contrast, E-Risk Study participants reporting
             loneliness at age 18 did not show any elevated markers of
             inflammation. In conclusion, social isolation was robustly
             associated with increased inflammation in adulthood, both in
             medical patients and in the general population. It was
             associated in particular with systemic chronic inflammation,
             evident from the consistently stronger associations with
             suPAR than other inflammation biomarkers.},
   Doi = {10.1016/j.bbi.2023.11.022},
   Key = {fds374321}
}

@article{fds375489,
   Author = {Brennan, GM and Moffitt, TE and Bourassa, KJ and Harrington, HL and Hogan, S and Houts, RM and Poulton, R and Ramrakha, S and Caspi,
             A},
   Title = {The Continuity of Adversity: Negative Emotionality Links
             Early Life Adversity With Adult Stressful Life
             Events},
   Journal = {Clinical Psychological Science},
   Year = {2024},
   Month = {January},
   url = {http://dx.doi.org/10.1177/21677026231220337},
   Abstract = {Adversity that exhibits continuity across the life course
             has long-term detrimental effects on physical and mental
             health. Using 920 participants from the Dunedin Study, we
             tested the following hypotheses: (a) Children (ages 3–15)
             who experienced adversity would also tend to experience
             adversity in adulthood (ages 32–45), and (2) interim
             personality traits in young adulthood (ages 18–26) would
             help account for this longitudinal association. Children who
             experienced more adversity tended to also experience more
             stressful life events as adults, β = 0.11, 95% confidence
             interval [CI] = [0.04, 0.18], p =.002. Negative
             emotionality—particularly its subfacet alienation,
             characterized by mistrust of others—helped explain this
             childhood-to-midlife association (indirect effect: β =
             0.06, 95% CI = [0.04, 0.09], p <.001). Results were robust
             to adjustment for sex, socioeconomic origins, childhood IQ,
             preschool temperament, and other young-adult personality
             traits. Prevention of early life adversity and treatment of
             young-adult negative emotionality may reduce vulnerability
             to later life stress and thereby promote the health of aging
             adults.},
   Doi = {10.1177/21677026231220337},
   Key = {fds375489}
}

@article{fds371008,
   Author = {Brennan, GM and Moffitt, TE and Ambler, A and Harrington, H and Hogan,
             S and Houts, RM and Mani, R and Poulton, R and Ramrakha, S and Caspi,
             A},
   Title = {Tracing the origins of midlife despair: association of
             psychopathology during adolescence with a syndrome of
             despair-related maladies at midlife.},
   Journal = {Psychological medicine},
   Volume = {53},
   Number = {16},
   Pages = {7569-7580},
   Year = {2023},
   Month = {December},
   url = {http://dx.doi.org/10.1017/s0033291723001320},
   Abstract = {<h4>Background</h4>Midlife adults are experiencing a crisis
             of deaths of despair (i.e. deaths from suicide, drug
             overdose, and alcohol-related liver disease). We tested the
             hypothesis that a syndrome of despair-related maladies at
             midlife is preceded by psychopathology during
             adolescence.<h4>Methods</h4>Participants are members of a
             representative cohort of 1037 individuals born in Dunedin,
             New Zealand in 1972-73 and followed to age 45 years, with
             94% retention. Adolescent mental disorders were assessed in
             three diagnostic assessments at ages 11, 13, and 15 years.
             Indicators of despair-related maladies across four domains -
             suicidality, substance misuse, sleep problems, and pain -
             were assessed at age 45 using multi-modal measures including
             self-report, informant-report, and national register
             data.<h4>Results</h4>We identified and validated a syndrome
             of despair-related maladies at midlife involving
             suicidality, substance misuse, sleep problems, and pain.
             Adults who exhibited a more severe syndrome of
             despair-related maladies at midlife tended to have had
             early-onset emotional and behavioral disorders [<i>β</i> =
             0.23, 95% CI (0.16-0.30), <i>p</i> < 0.001], even after
             adjusting for sex, childhood SES, and childhood IQ. A more
             pronounced midlife despair syndrome was observed among
             adults who, as adolescents, were diagnosed with a greater
             number of mental disorders [<i>β</i> = 0.26, 95% CI
             (0.19-0.33), <i>p</i> < 0.001]. Tests of diagnostic
             specificity revealed that associations generalized across
             different adolescent mental disorders.<h4>Conclusions</h4>Midlife
             adults who exhibited a more severe syndrome of
             despair-related maladies tended to have had psychopathology
             as adolescents. Prevention and treatment of adolescent
             psychopathology may mitigate despair-related maladies at
             midlife and ultimately reduce deaths of despair.},
   Doi = {10.1017/s0033291723001320},
   Key = {fds371008}
}

@article{fds373506,
   Author = {Knodt, AR and Elliott, ML and Whitman, ET and Winn, A and Addae, A and Ireland, D and Poulton, R and Ramrakha, S and Caspi, A and Moffitt, TE and Hariri, AR},
   Title = {Test-retest reliability and predictive utility of a
             macroscale principal functional connectivity
             gradient.},
   Journal = {Human brain mapping},
   Volume = {44},
   Number = {18},
   Pages = {6399-6417},
   Year = {2023},
   Month = {December},
   url = {http://dx.doi.org/10.1002/hbm.26517},
   Abstract = {Mapping individual differences in brain function has been
             hampered by poor reliability as well as limited
             interpretability. Leveraging patterns of brain-wide
             functional connectivity (FC) offers some promise in this
             endeavor. In particular, a macroscale principal FC gradient
             that recapitulates a hierarchical organization spanning
             molecular, cellular, and circuit level features along a
             sensory-to-association cortical axis has emerged as both a
             parsimonious and interpretable measure of individual
             differences in behavior. However, the measurement
             reliabilities of this FC gradient have not been fully
             evaluated. Here, we assess the reliabilities of both global
             and regional principal FC gradient measures using
             test-retest data from the young adult Human Connectome
             Project (HCP-YA) and the Dunedin Study. Analyses revealed
             that the reliabilities of principal FC gradient measures
             were (1) consistently higher than those for traditional
             edge-wise FC measures, (2) higher for FC measures derived
             from general FC (GFC) in comparison with resting-state FC,
             and (3) higher for longer scan lengths. We additionally
             examined the relative utility of these principal FC gradient
             measures in predicting cognition and aging in both datasets
             as well as the HCP-aging dataset. These analyses revealed
             that regional FC gradient measures and global gradient range
             were significantly associated with aging in all three
             datasets, and moderately associated with cognition in the
             HCP-YA and Dunedin Study datasets, reflecting contractions
             and expansions of the cortical hierarchy, respectively.
             Collectively, these results demonstrate that measures of the
             principal FC gradient, especially derived using GFC,
             effectively capture a reliable feature of the human brain
             subject to interpretable and biologically meaningful
             individual variation, offering some advantages over
             traditional edge-wise FC measures in the search for
             brain-behavior associations.},
   Doi = {10.1002/hbm.26517},
   Key = {fds373506}
}

@article{fds374319,
   Author = {Synergy for the Influence of the Month of Birth in ADHD
             (SIMBA) study group},
   Title = {Association between relative age at school and persistence
             of ADHD in prospective studies: an individual participant
             data meta-analysis.},
   Journal = {Lancet Psychiatry},
   Volume = {10},
   Number = {12},
   Pages = {922-933},
   Year = {2023},
   Month = {December},
   url = {http://dx.doi.org/10.1016/S2215-0366(23)00272-9},
   Abstract = {BACKGROUND: The youngest children in a school class are more
             likely than the oldest to be diagnosed with ADHD, but this
             relative age effect is less frequent in older than in
             younger school-grade children. However, no study has
             explored the association between relative age and the
             persistence of ADHD diagnosis at older ages. We aimed to
             quantify the association between relative age and
             persistence of ADHD at older ages. METHODS: For this
             meta-analysis, we searched MEDLINE, Embase, CINAHL,
             PsycINFO, and PubPsych up to April 1, 2022, with terms
             related to "cohort" and "ADHD" with no date, publication
             type, or language restrictions. We gathered individual
             participant data from prospective cohorts that included at
             least ten children identified with ADHD before age 10 years.
             ADHD was defined by either a clinical diagnosis or symptoms
             exceeding clinical cutoffs. Relative age was recorded as the
             month of birth in relation to the school-entry cutoff date.
             Study authors were invited to share raw data or to apply a
             script to analyse data locally and generate anonymised
             results. Our outcome was ADHD status at a diagnostic
             reassessment, conducted at least 4 years after the initial
             assessment and after age 10 years. No information on sex,
             gender, or ethnicity was collected. We did a two-stage
             random-effects individual participant data meta-analysis to
             assess the association of relative age with persistence of
             ADHD at follow-up. This study was registered with PROSPERO,
             CRD42020212650. FINDINGS: Of 33 119 studies generated by
             our search, we identified 130 eligible unique studies and
             were able to gather individual participant data from 57
             prospective studies following up 6504 children with ADHD.
             After exclusion of 16 studies in regions with a flexible
             school entry system that did not allow confident linkage of
             birthdate to relative age, the primary analysis included 41
             studies in 15 countries following up 4708 children for a
             period of 4 to 33 years. We found that younger relative age
             was not statistically significantly associated with ADHD
             persistence at follow-up (odds ratio 1·02, 95% CI
             0·99-1·06; p=0·19). We observed statistically significant
             heterogeneity in our model (Q=75·82, p=0·0011, I2=45%).
             Participant-level sensitivity analyses showed similar
             results in cohorts with a robust relative age effect at
             baseline and when restricting to cohorts involving children
             with a clinical diagnosis of ADHD or with a follow-up
             duration of more than 10 years. INTERPRETATION: The
             diagnosis of ADHD in younger children in a class is no more
             likely to be disconfirmed over time than that of older
             children in the class. One interpretation is that the
             relative age effect decreases the likelihood of children of
             older relative age receiving a diagnosis of ADHD, and
             another is that assigning a diagnostic label of ADHD leads
             to unexplored carryover effects of the initial diagnosis
             that persist over time. Future studies should be conducted
             to explore these interpretations further. FUNDING:
             None.},
   Doi = {10.1016/S2215-0366(23)00272-9},
   Key = {fds374319}
}

@article{fds371652,
   Author = {Røysamb, E and Moffitt, TE and Caspi, A and Ystrøm, E and Nes,
             RB},
   Title = {Worldwide Well-Being: Simulated Twins Reveal Genetic and
             (Hidden) Environmental Influences.},
   Journal = {Perspectives on psychological science : a journal of the
             Association for Psychological Science},
   Volume = {18},
   Number = {6},
   Pages = {1562-1574},
   Year = {2023},
   Month = {November},
   url = {http://dx.doi.org/10.1177/17456916231178716},
   Abstract = {What are the major sources of worldwide variability in
             subjective well-being (SWB)? Twin and family studies of SWB
             have found substantial heritability and strong effects from
             unique environments but virtually no effects from shared
             environments. However, extant findings are not necessarily
             valid at the global level. Prior studies have examined
             within-countries variability but did not take into account
             mean differences across nations. In this article, we aim to
             estimate the effects of genetic factors, individual
             environmental exposures, and shared environments for the
             global population. We combine a set of knowns from national
             well-being studies (means and standard deviations) and
             behavioral-genetic studies (heritability) to model a
             scenario of twin studies across 157 countries. For each
             country, we simulate data for a set of twin pairs and pool
             the data into a global sample. We find a worldwide
             heritability of 31% to 32% for SWB. Individual environmental
             factors explain 46% to 52% of the variance (including
             measurement error), and shared environments account for 16%
             to 23% of the global variance in SWB. Worldwide, well-being
             is somewhat less heritable than within nations. In contrast
             to previous within-countries studies, we find a notable
             effect of shared environments. This effect is not limited to
             within families but operates at a national
             level.},
   Doi = {10.1177/17456916231178716},
   Key = {fds371652}
}

@article{fds374320,
   Author = {Caspi, A and Shireby, G and Mill, J and Moffitt, TE and Sugden, K and Hannon, E},
   Title = {Accelerated Pace of Aging in Schizophrenia: Five
             Case-Control Studies.},
   Journal = {Biological psychiatry},
   Pages = {S0006-3223(23)01693-1},
   Year = {2023},
   Month = {November},
   url = {http://dx.doi.org/10.1016/j.biopsych.2023.10.023},
   Abstract = {<h4>Background</h4>Schizophrenia is associated with
             increased risk of developing multiple aging-related
             diseases, including metabolic, respiratory, and
             cardiovascular diseases, and Alzheimer's and related
             dementias, leading to the hypothesis that schizophrenia is
             accompanied by accelerated biological aging. This has been
             difficult to test because there is no widely accepted
             measure of biological aging. Epigenetic clocks are promising
             algorithms that are used to calculate biological age on the
             basis of information from combined cytosine-phosphate-guanine
             sites (CpGs) across the genome, but they have yielded
             inconsistent and often negative results about the
             association between schizophrenia and accelerated aging.
             Here, we tested the schizophrenia-aging hypothesis using a
             DNA methylation measure that is uniquely designed to predict
             an individual's rate of aging.<h4>Methods</h4>We brought
             together 5 case-control datasets to calculate DunedinPACE
             (Pace of Aging Calculated from the Epigenome), a new measure
             trained on longitudinal data to detect differences between
             people in their pace of aging over time. Data were available
             from 1812 psychosis cases (schizophrenia or first-episode
             psychosis) and 1753 controls. Mean chronological age was
             38.9 (SD = 13.6) years.<h4>Results</h4>We observed
             consistent associations across datasets between
             schizophrenia and accelerated aging as measured by
             DunedinPACE. These associations were not attributable to
             tobacco smoking or clozapine medication.<h4>Conclusions</h4>Schizophrenia
             is accompanied by accelerated biological aging by midlife.
             This may explain the wide-ranging risk among people with
             schizophrenia for developing multiple different age-related
             physical diseases, including metabolic, respiratory, and
             cardiovascular diseases, and dementia. Measures of
             biological aging could prove valuable for assessing
             patients' risk for physical and cognitive decline and for
             evaluating intervention effectiveness.},
   Doi = {10.1016/j.biopsych.2023.10.023},
   Key = {fds374320}
}

@article{fds372022,
   Author = {Kessing, LV and Ziersen, SC and Caspi, A and Moffitt, TE and Andersen,
             PK},
   Title = {Lifetime Incidence of Treated Mental Health Disorders and
             Psychotropic Drug Prescriptions and Associated Socioeconomic
             Functioning.},
   Journal = {JAMA psychiatry},
   Volume = {80},
   Number = {10},
   Pages = {1000-1008},
   Year = {2023},
   Month = {October},
   url = {http://dx.doi.org/10.1001/jamapsychiatry.2023.2206},
   Abstract = {<h4>Importance</h4>Few studies have estimated the lifetime
             incidence of mental health disorders and the association
             with socioeconomic functioning.<h4>Objective</h4>To
             investigate whether the lifetime incidence of treated mental
             health disorders is substantially higher than previously
             reported and estimate associations with long-term
             socioeconomic difficulties.<h4>Design, setting, and
             participants</h4>This nationwide population-based register
             linkage study includes a randomly selected sample of 1.5
             million individuals from the population of Denmark from 1995
             to 2018. Data were analyzed from May 2022 to March
             2023.<h4>Main outcomes and measures</h4>Lifetime incidence
             of any treated mental health disorder in the general
             population was estimated from birth to age 100 years taking
             into account the competing risk of all-cause death and
             associations with socioeconomic functioning. Register
             measures were (1) from hospitals, a diagnosis of any mental
             health disorder at an inpatient/outpatient hospital contact;
             (2) from hospitals and prescription statistics, any mental
             health disorder/psychotropic prescription, including a
             hospital-contact diagnosis, or any psychotropic medication
             prescribed by physicians, including general practitioners or
             private psychiatrists; and (3) socioeconomic functioning as
             indicated by highest educational achievement, employment,
             income, residential status, and marital status.<h4>Results</h4>Among
             a sample of 462 864 individuals with any mental health
             disorder, the median (IQR) age was 36.6 years (21.0-53.6
             years), 233 747 (50.5%) were male, and 229 117 (49.5%)
             were female. Of these, 112 641 were registered with a
             hospital-contact mental health disorder diagnosis and
             422 080 with a prescription of psychotropic medication.
             The cumulative incidence of a hospital-contact mental health
             disorder diagnosis was 29.0% (95% CI, 28.8-29.1), 31.8% (95%
             CI, 31.6-32.0) for females, and 26.1% (95% CI, 25.9-26.3)
             for males. When also considering psychotropic prescriptions,
             the cumulative incidence of any mental health
             disorder/psychotropic prescription was 82.6% (95% CI,
             82.4-82.6), 87.5% (95% CI, 87.4-87.7) for females, and 76.7%
             (95% CI, 76.5-76.8) for males. Socioeconomic difficulties
             were associated with mental health disorder/psychotropic
             prescriptions, including lower income (hazard ratio [HR],
             1.55; 95% CI, 1.53-1.56), increased unemployment or
             disability benefit (HR, 2.50; 95% CI, 2.47-2.53), and a
             greater likelihood of living alone (HR, 1.78; 95% CI,
             1.76-1.80) and being unmarried (HR, 2.02; 95% CI, 2.01-2.04)
             during long-term follow-up. These rates were confirmed in 4
             sensitivity analyses with the lowest being 74.8% (95% CI,
             74.7-75.0) (1) by using varying exclusion periods, (2) by
             excluding prescriptions of anxiolytics and quetiapine that
             may be used for off-label indications, (3) by defining any
             mental health disorder/psychotropic prescription as any
             hospital-contact mental health disorder diagnosis or any
             psychotropic medication prescribed at least 2 times, and (4)
             by excluding individuals with somatic diagnoses for which
             psychotropics may be prescribed off-label.<h4>Conclusions
             and relevance</h4>This registry study of data from a large
             representative sample of the Danish population showed that
             the majority of individuals either received a diagnosis of a
             mental health disorder or were prescribed psychotropic
             medication during their lifetime, which was associated with
             subsequent socioeconomic difficulties. These findings may
             help change our understanding of normalcy and mental
             illness, reduce stigmatization, and further prompt
             rethinking the primary prevention of mental illness and
             future mental health clinical resources.},
   Doi = {10.1001/jamapsychiatry.2023.2206},
   Key = {fds372022}
}

@article{fds373683,
   Author = {Whitman, ET and Ryan, CP and Abraham, WC and Addae, A and Corcoran, DL and Elliott, ML and Hogan, S and Ireland, D and Keenan, R and Knodt, AR and Melzer, TR and Poulton, R and Ramrakha, S and Sugden, K and Williams,
             BS and Zhou, J and Hariri, AR and Belsky, DW and Moffitt, TE and Caspi,
             A},
   Title = {A blood biomarker of accelerated aging in the body
             associates with worse structural integrity in the brain:
             replication across three cohorts.},
   Journal = {medRxiv},
   Year = {2023},
   Month = {September},
   url = {http://dx.doi.org/10.1101/2023.09.06.23295140},
   Abstract = {Biological aging is the correlated decline of multi-organ
             system integrity central to the etiology of many age-related
             diseases. A novel epigenetic measure of biological aging,
             DunedinPACE, is associated with cognitive dysfunction,
             incident dementia, and mortality. Here, we tested for
             associations between DunedinPACE and structural MRI
             phenotypes in three datasets spanning midlife to advanced
             age: the Dunedin Study (age=45 years), the Framingham Heart
             Study Offspring Cohort (mean age=63 years), and the
             Alzheimer's Disease Neuroimaging Initiative (mean age=75
             years). We also tested four additional epigenetic measures
             of aging: the Horvath clock, the Hannum clock, PhenoAge, and
             GrimAge. Across all datasets (total N observations=3,380;
             total N individuals=2,322), faster DunedinPACE was
             associated with lower total brain volume, lower hippocampal
             volume, and thinner cortex. In two datasets, faster
             DunedinPACE was associated with greater burden of white
             matter hyperintensities. Across all measures, DunedinPACE
             and GrimAge had the strongest and most consistent
             associations with brain phenotypes. Our findings suggest
             that single timepoint measures of multi-organ decline such
             as DunedinPACE could be useful for gauging nervous system
             health.},
   Doi = {10.1101/2023.09.06.23295140},
   Key = {fds373683}
}

@article{fds367501,
   Author = {Slutske, WS and Richmond-Rakerd, LS and Piasecki, TM and Ramrakha, S and Poulton, R and Moffitt, TE and Caspi, A},
   Title = {Disordered gambling in a longitudinal birth cohort: from
             childhood precursors to adult life outcomes.},
   Journal = {Psychological medicine},
   Volume = {53},
   Number = {12},
   Pages = {5800-5808},
   Year = {2023},
   Month = {September},
   url = {http://dx.doi.org/10.1017/s0033291722003051},
   Abstract = {<h4>Background</h4>Despite its introduction into the
             diagnostic nomenclature over four decades ago, there remain
             large knowledge gaps about disordered gambling. The primary
             aims of the present study were to document the long-term
             course, childhood precursors, and adult life outcomes
             associated with disordered gambling.<h4>Methods</h4>Participants
             enrolled in the population-representative Dunedin Study were
             prospectively followed from birth through age 45. Disordered
             gambling was assessed six times from age 18; composite
             measures of childhood social class, general intelligence,
             and low self-control were based on assessments obtained from
             birth through age 15; adult socioeconomic, financial, and
             legal outcomes were obtained through age 45. Lifetime
             disordered gambling was predicted from the three childhood
             precursors and the adult outcomes were predicted from
             lifetime disordered gambling.<h4>Results</h4>Past-year
             disordered gambling usually occurred at only a single time
             point and recurrence was relatively uncommon. Lower
             childhood social class, general intelligence, and
             self-control significantly predicted lifetime disordered
             gambling in adulthood. In turn, lifetime disordered gambling
             in adulthood significantly predicted occupational,
             educational, and financial problems in adulthood (<i>ds</i>
             = 0.23-0.41). These associations were markedly reduced and
             sometimes rendered nonsignificant after adjusting for
             childhood precursors (<i>ds</i> = 0.04-0.32).<h4>Conclusions</h4>Socioeconomic,
             financial, and legal outcomes in adulthood are not merely
             consequences of disordered gambling, but also are predicted
             from childhood precursors. Deflecting the trajectories of
             young people at risk for developing disordered gambling may
             help to ameliorate not just the development of later
             disordered gambling, but also other associated adverse
             outcomes.},
   Doi = {10.1017/s0033291722003051},
   Key = {fds367501}
}

@article{fds373923,
   Author = {Ruiz, B and Broadbent, JM and Thomson, WM and Ramrakha, S and Moffitt,
             TE and Caspi, A and Poulton, R},
   Title = {Childhood caries is associated with poor health and a faster
             pace of aging by midlife.},
   Journal = {Journal of public health dentistry},
   Volume = {83},
   Number = {4},
   Pages = {381-388},
   Year = {2023},
   Month = {September},
   url = {http://dx.doi.org/10.1111/jphd.12591},
   Abstract = {<h4>Objectives</h4>Childhood caries is associated with
             poorer self-rated general health in adulthood, but it
             remains unclear whether that holds for physical health and
             aging. The aim of this study was to identify whether age-5
             caries is associated with (a) biomarkers for poor physical
             health, and (b) the pace of aging (PoA) by age
             45 years.<h4>Methods</h4>Participants are members of the
             Dunedin Multidisciplinary Health and Development Study birth
             cohort. At age 45, 94.1% (n = 938) of those still alive
             took part. Data on age-5 caries experience and age-45 health
             biomarkers were collected. The PoA captures age-related
             decline across the cardiovascular, metabolic, renal, immune,
             dental and pulmonary systems from age 26 to 45 years. We
             used (a) generalized estimating equations to examine
             associations between age-5 caries and poor physical health
             by age 45 years, and (b) ordinary least squares regression
             to examine whether age-5 caries was associated with the PoA.
             Analyses adjusted for sex, perinatal health, childhood SES
             and childhood IQ.<h4>Results</h4>High caries experience at
             age-5 was associated with higher risk for some metabolic
             abnormalities, including BMI ≥30, high waist
             circumference, and high serum leptin. Those with high caries
             experience at age-5 were aging at a faster rate by age
             45 years than those who had been caries-free.<h4>Conclusions</h4>Oral
             health is essential for wellbeing. Poor oral health can be
             an early signal of a trajectory towards poor health in
             adulthood. Management for both conditions should be
             better-integrated; and integrated population-level
             prevention strategies should be foundational to any health
             system.},
   Doi = {10.1111/jphd.12591},
   Key = {fds373923}
}

@article{fds370497,
   Author = {Sugden, K and Moffitt, TE and Arpawong, TE and Arseneault, L and Belsky,
             DW and Corcoran, DL and Crimmins, EM and Hannon, E and Houts, R and Mill,
             JS and Poulton, R and Ramrakha, S and Wertz, J and Williams, BS and Caspi,
             A},
   Title = {Cross-National and Cross-Generational Evidence That
             Educational Attainment May Slow the Pace of Aging in
             European-Descent Individuals.},
   Journal = {The journals of gerontology. Series B, Psychological
             sciences and social sciences},
   Volume = {78},
   Number = {8},
   Pages = {1375-1385},
   Year = {2023},
   Month = {August},
   url = {http://dx.doi.org/10.1093/geronb/gbad056},
   Abstract = {<h4>Objectives</h4>Individuals with more education are at
             lower risk of developing multiple, different age-related
             diseases than their less-educated peers. A reason for this
             might be that individuals with more education age slower.
             There are 2 complications in testing this hypothesis. First,
             there exists no definitive measure of biological aging.
             Second, shared genetic factors contribute toward both lower
             educational attainment and the development of age-related
             diseases. Here, we tested whether the protective effect of
             educational attainment was associated with the pace of aging
             after accounting for genetic factors.<h4>Methods</h4>We
             examined data from 5 studies together totaling almost 17,000
             individuals with European ancestry born in different
             countries during different historical periods, ranging in
             age from 16 to 98 years old. To assess the pace of aging, we
             used DunedinPACE, a DNA methylation algorithm that reflects
             an individual's rate of aging and predicts age-related
             decline and Alzheimer's disease and related disorders. To
             assess genetic factors related to education, we created a
             polygenic score based on the results of a genome-wide
             association study of educational attainment.<h4>Results</h4>Across
             the 5 studies, and across the life span, higher educational
             attainment was associated with a slower pace of aging even
             after accounting for genetic factors (meta-analysis effect
             size = -0.20; 95% confidence interval [CI]: -0.30 to -0.10;
             p = .006). Further, this effect persisted after taking into
             account tobacco smoking (meta-analysis effect size = -0.13;
             95% CI: -0.21 to -0.05; p = .01).<h4>Discussion</h4>These
             results indicate that higher levels of education have
             positive effects on the pace of aging, and that the benefits
             can be realized irrespective of individuals'
             genetics.},
   Doi = {10.1093/geronb/gbad056},
   Key = {fds370497}
}

@article{fds371651,
   Author = {Wertz, J and Moffitt, TE and Arseneault, L and Barnes, JC and Boivin, M and Corcoran, DL and Danese, A and Hancox, RJ and Harrington, H and Houts,
             RM and Langevin, S and Liu, H and Poulton, R and Sugden, K and Tanksley,
             PT and Williams, BS and Caspi, A},
   Title = {Genetic associations with parental investment from
             conception to wealth inheritance in six cohorts.},
   Journal = {Nature human behaviour},
   Volume = {7},
   Number = {8},
   Pages = {1388-1401},
   Year = {2023},
   Month = {August},
   url = {http://dx.doi.org/10.1038/s41562-023-01618-5},
   Abstract = {Genetic inheritance is not the only way parents' genes may
             affect children. It is also possible that parents' genes are
             associated with investments into children's development. We
             examined evidence for links between parental genetics and
             parental investments, from the prenatal period through to
             adulthood, using data from six population-based cohorts in
             the UK, US and New Zealand, together totalling 36,566
             parents. Our findings revealed associations between parental
             genetics-summarized in a genome-wide polygenic score-and
             parental behaviour across development, from smoking in
             pregnancy, breastfeeding in infancy, parenting in childhood
             and adolescence, to leaving a wealth inheritance to adult
             children. Effect sizes tended to be small at any given time
             point, ranging from RR = 1.12 (95% confidence interval
             (95%CI) 1.09, 1.15) to RR = 0.76 (95%CI 0.72, 0.80)
             during the prenatal period and infancy; β = 0.07 (95%CI
             0.04, 0.11) to β = 0.29 (95%CI 0.27, 0.32) in childhood
             and adolescence, and RR = 1.04 (95%CI 1.01, 1.06) to
             RR = 1.11 (95%CI 1.07, 1.15) in adulthood. There was
             evidence for accumulating effects across development,
             ranging from β = 0.15 (95%CI 0.11, 0.18) to
             β = 0.23 (95%CI 0.16, 0.29) depending on cohort. Our
             findings are consistent with the interpretation that parents
             pass on advantages to offspring not only via direct genetic
             transmission or purely environmental paths, but also via
             genetic associations with parental investment from
             conception to wealth inheritance.},
   Doi = {10.1038/s41562-023-01618-5},
   Key = {fds371651}
}

@article{fds366660,
   Author = {Bourassa, KJ and Moffitt, TE and Harrington, H and Houts, R and Poulton,
             R and Ramrakha, S and Rasmussen, LJH and Wertz, J and Caspi,
             A},
   Title = {Childhood Adversity and Midlife Health: Shining a Light on
             the Black Box of Psychosocial Mechanisms.},
   Journal = {Prevention science : the official journal of the Society for
             Prevention Research},
   Volume = {24},
   Number = {5},
   Pages = {817-828},
   Year = {2023},
   Month = {July},
   url = {http://dx.doi.org/10.1007/s11121-022-01431-y},
   Abstract = {Adverse childhood experiences (ACEs) are associated with
             poorer health, which has spurred public health efforts to
             reduce the number of adverse events children experience.
             Unfortunately, it is unlikely that all ACEs can be
             prevented. For adults who already experienced ACEs in
             childhood, what psychological, social, and behavioral
             intervention targets might reduce risk for negative health
             outcomes? To provide insight into the "black box" of
             psychosocial mechanisms linking ACEs to poor health, our
             study used data from the Dunedin Study, a longitudinal
             cohort assessed from birth to age 45. Mediation models
             (N = 859) were used to examine whether candidate
             psychosocial variables in adulthood explained the
             association between childhood ACEs and health in midlife.
             Potential psychosocial mediators included stressful life
             events, perceived stress, negative emotionality, and health
             behaviors. Children who experienced more ACEs had poorer
             health in midlife. They also had significantly more
             stressful life events, more perceived stress, more negative
             emotionality, and unhealthier behaviors as adults. These
             mediators were each independently associated with poorer
             health in midlife and statistically mediated the association
             between ACEs and midlife health. Health behaviors evidenced
             the strongest indirect effect from ACEs to midlife health.
             Together, these psychosocial mediators accounted for the
             association between ACEs in childhood and health three
             decades later. Public health efforts to mitigate the health
             consequences of ACEs could aim to reduce the stressful life
             events people experience, reduce negative emotionality,
             reduce perceived stress, or improve health behaviors among
             adults who experienced childhood adversity.},
   Doi = {10.1007/s11121-022-01431-y},
   Key = {fds366660}
}

@article{fds369352,
   Author = {Gjerde, LC and Eilertsen, EM and McAdams, TA and Cheesman, R and Moffitt, TE and Caspi, A and Eley, TC and Røysamb, E and Rosenström,
             TH and Ystrom, E},
   Title = {The p factor of psychopathology and personality in
             middle childhood: genetic and gestational risk
             factors.},
   Journal = {Psychological medicine},
   Volume = {53},
   Number = {9},
   Pages = {4275-4285},
   Year = {2023},
   Month = {July},
   url = {http://dx.doi.org/10.1017/s0033291723000077},
   Abstract = {<h4>Background</h4>A joint, hierarchical structure of
             psychopathology and personality has been reported in adults
             but should also be investigated at earlier ages, as
             psychopathology often develops before adulthood. Here, we
             investigate the joint factor structure of psychopathology
             and personality in eight-year-old children, estimate factor
             heritability and explore external validity through
             associations with established developmental risk
             factors.<h4>Methods</h4>Phenotypic and biometric exploratory
             factor analyses with bifactor rotation on genetically
             informative data from the Norwegian Mother, Father, and
             Child Cohort (MoBa) study. The analytic sub-sample comprised
             10 739 children (49% girls). Mothers reported their
             children's symptoms of depression (Short Moods and Feelings
             Questionnaire), anxiety (Screen for Anxiety Related
             Disorders), attention-deficit/hyperactivity disorder
             inattention and hyperactivity, oppositional-defiant
             disorder, conduct disorder (Parent/Teacher Rating Scale for
             Disruptive Behavior Disorders), and Big Five personality
             (short Hierarchical Personality Inventory for Children).
             Developmental risk factors (early gestational age and being
             small for gestational age) were collected from the Medical
             Birth Registry.<h4>Results</h4>Goodness-of-fit indices
             favored a <i>p</i> factor model with three residual latent
             factors interpreted as negative affectivity, positive
             affectivity, and antagonism, whereas psychometric indices
             favored a one-factor model. ADE solutions fitted best, and
             regression analyses indicated a negative association between
             gestational age and the <i>p</i> factor, for both the one-
             and four-factor solutions.<h4>Conclusion</h4>Correlations
             between normative and pathological traits in middle
             childhood mostly reflect one heritable and psychometrically
             interpretable <i>p</i> factor, although optimal fit to data
             required less interpretable residual latent factors. The
             association between the <i>p</i> factor and low gestational
             age warrants further study of early developmental
             mechanisms.},
   Doi = {10.1017/s0033291723000077},
   Key = {fds369352}
}

@article{fds370101,
   Author = {Newbury, JB and Arseneault, L and Moffitt, TE and Odgers, CL and Howe,
             LD and Bakolis, I and Reuben, A and Danese, A and Sugden, K and Williams,
             B and Rasmussen, LJH and Trotta, A and Ambler, AP and Fisher,
             HL},
   Title = {Socioenvironmental Adversity and Adolescent Psychotic
             Experiences: Exploring Potential Mechanisms in a UK
             Longitudinal Cohort.},
   Journal = {Schizophrenia bulletin},
   Volume = {49},
   Number = {4},
   Pages = {1042-1054},
   Year = {2023},
   Month = {July},
   url = {http://dx.doi.org/10.1093/schbul/sbad017},
   Abstract = {<h4>Background and hypothesis</h4>Children exposed to
             socioenvironmental adversities (eg, urbanicity, pollution,
             neighborhood deprivation, crime, and family disadvantage)
             are more likely to subsequently develop subclinical
             psychotic experiences during adolescence (eg, hearing
             voices, paranoia). However, the pathways through which this
             occurs have not been previously investigated. We
             hypothesized that cognitive ability and inflammation would
             partly explain this association.<h4>Study design</h4>Data
             were utilized from the Environmental-Risk Longitudinal Twin
             Study, a cohort of 2232 children born in 1994-1995 in
             England and Wales and followed to age 18. Socioenvironmental
             adversities were measured from birth to age 10 and
             classified into physical risk (defined by high urbanicity
             and air pollution) and socioeconomic risk (defined by high
             neighborhood deprivation, neighborhood disorder, and family
             disadvantage). Cognitive abilities (overall, crystallized,
             fluid, and working memory) were assessed at age 12; and
             inflammatory markers (C-reactive protein, interleukin-6,
             soluble urokinase plasminogen activator receptor) were
             measured at age 18 from blood samples. Participants were
             interviewed at age 18 regarding psychotic
             experiences.<h4>Study results</h4>Higher physical risk and
             socioeconomic risk were associated with increased odds of
             psychotic experiences in adolescence. The largest mediation
             pathways were from socioeconomic risk via overall cognitive
             ability and crystallized ability, which accounted for ~11%
             and ~19% of the association with psychotic experiences,
             respectively. No statistically significant pathways were
             found via inflammatory markers in exploratory (partially
             cross-sectional) analyses.<h4>Conclusions</h4>Cognitive
             ability, especially crystallized ability, may partly explain
             the association between childhood socioenvironmental
             adversity and adolescent psychotic experiences.
             Interventions to support cognitive development among
             children living in disadvantaged settings could buffer them
             against developing subclinical psychotic
             phenomena.},
   Doi = {10.1093/schbul/sbad017},
   Key = {fds370101}
}

@article{fds370499,
   Author = {Gjerde, LC and Eilertsen, EM and McAdams, TA and Cheesman, R and Moffitt, TE and Caspi, A and Eley, TC and Røysamb, E and Rosenström,
             TH and Ystrom, E},
   Title = {The p factor of psychopathology and personality in
             middle childhood: Genetic and gestational risk factors -
             Corrigendum.},
   Journal = {Psychological medicine},
   Volume = {53},
   Number = {9},
   Pages = {4303-4304},
   Year = {2023},
   Month = {July},
   url = {http://dx.doi.org/10.1017/s0033291723000879},
   Doi = {10.1017/s0033291723000879},
   Key = {fds370499}
}

@article{fds373684,
   Author = {Tanksley, PT and Brislin, SJ and Wertz, J and de Vlaming, R and Courchesne-Krak, NS and Mallard, TT and Raffington, LL and Linnér,
             RK and Koellinger, P and Palmer, A and Sanchez-Roige, A and Waldman, I and Dick, D and Moffitt, TE and Caspi, A and Harden, KP},
   Title = {Do polygenic indices capture "direct" effects on child
             externalizing behavior? Within-family analyses in two
             longitudinal birth cohorts.},
   Journal = {medRxiv},
   Year = {2023},
   Month = {June},
   url = {http://dx.doi.org/10.1101/2023.05.31.23290802},
   Abstract = {Behaviors and disorders characterized by difficulties with
             self-regulation, such as problematic substance use,
             antisocial behavior, and symptoms of attention-deficit/hyperactivity
             disorder (ADHD), incur high costs for individuals, families,
             and communities. These externalizing behaviors often appear
             early in the life course and can have far-reaching
             consequences. Researchers have long been interested in
             direct measurements of genetic risk for externalizing
             behaviors, which can be incorporated alongside other known
             risk factors to improve efforts at early identification and
             intervention. In a preregistered analysis drawing on data
             from the Environmental Risk (E-Risk) Longitudinal Twin Study
             (N=862 twins) and the Millennium Cohort Study (MCS; N=2,824
             parent-child trios), two longitudinal cohorts from the UK,
             we leveraged molecular genetic data and within-family
             designs to test for genetic effects on externalizing
             behavior that are unbiased by the common sources of
             environmental confounding. Results are consistent with the
             conclusion that an externalizing polygenic index (PGI)
             captures causal effects of genetic variants on externalizing
             problems in children and adolescents, with an effect size
             that is comparable to those observed for other established
             risk factors in the research literature on externalizing
             behavior. Additionally, we find that polygenic associations
             vary across development (peaking from age 5-10 years), that
             parental genetics (assortment and parent-specific effects)
             and family-level covariates affect prediction little, and
             that sex differences in polygenic prediction are present but
             only detectable using within-family comparisons. Based on
             these findings, we believe that the PGI for externalizing
             behavior is a promising means for studying the development
             of disruptive behaviors across child development.},
   Doi = {10.1101/2023.05.31.23290802},
   Key = {fds373684}
}

@article{fds370496,
   Author = {Bourassa, KJ and Caspi, A and Brennan, GM and Hall, KS and Harrington,
             H and Houts, R and Kimbrel, NA and Poulton, R and Ramrakha, S and Taylor,
             GA and Moffitt, TE},
   Title = {Which Types of Stress Are Associated With Accelerated
             Biological Aging? Comparing Perceived Stress, Stressful Life
             Events, Childhood Adversity, and Posttraumatic Stress
             Disorder.},
   Journal = {Psychosom Med},
   Volume = {85},
   Number = {5},
   Pages = {389-396},
   Year = {2023},
   Month = {June},
   url = {http://dx.doi.org/10.1097/PSY.0000000000001197},
   Abstract = {OBJECTIVE: Stress and stressful events are associated with
             poorer health; however, there are multiple ways to
             conceptualize and measure stress and stress responses. One
             physiological mechanism through which stress could result in
             poorer health is accelerated biological aging. This study
             tested which types of stress were associated with
             accelerated biological aging in adulthood. METHODS: Studying
             955 participants from the Dunedin Longitudinal Study, we
             tested whether four types of stress assessed from ages 32 to
             45 years-perceived stress, number of stressful life events,
             adverse childhood experiences, and posttraumatic stress
             disorder-were associated with accelerated biological aging.
             RESULTS: Higher levels of all four measures of stress were
             significantly associated with accelerated aging in separate
             models. In a combined model, more perceived stress and more
             stressful life events remained associated with faster aging,
             and the stress measures explained 6.9% of the variance in
             aging. The magnitudes of the associations between the four
             measures of stress and biological aging were comparable to
             associations for smoking and low education, two established
             risk factors for accelerated aging. People with high levels
             of perceived stress, numerous adverse childhood experiences
             (4+), high stressful life event counts, or posttraumatic
             stress disorder were aging an additional estimated 2.4
             months, 1.1 additional months, 1.4 months, and 1.4 months
             per year, respectively. CONCLUSIONS: Assessing stress,
             particularly perceived stress, could help identify people at
             risk of accelerated aging. Intervening to treat stress or
             the health-relevant sequelae of stress could potentially
             slow the rate at which people are aging, improving their
             health as they age.},
   Doi = {10.1097/PSY.0000000000001197},
   Key = {fds370496}
}

@article{fds370498,
   Author = {Whitman, ET and Knodt, AR and Elliott, ML and Abraham, WC and Cheyne, K and Hogan, S and Ireland, D and Keenan, R and Leung, JH and Melzer, TR and Poulton, R and Purdy, SC and Ramrakha, S and Thorne, PR and Caspi, A and Moffitt, TE and Hariri, AR},
   Title = {Functional topography of the neocortex predicts covariation
             in complex cognitive and basic motor abilities.},
   Journal = {Cerebral cortex (New York, N.Y. : 1991)},
   Volume = {33},
   Number = {13},
   Pages = {8218-8231},
   Year = {2023},
   Month = {June},
   url = {http://dx.doi.org/10.1093/cercor/bhad109},
   Abstract = {Although higher-order cognitive and lower-order sensorimotor
             abilities are generally regarded as distinct and studied
             separately, there is evidence that they not only covary but
             also that this covariation increases across the lifespan.
             This pattern has been leveraged in clinical settings where a
             simple assessment of sensory or motor ability (e.g. hearing,
             gait speed) can forecast age-related cognitive decline and
             risk for dementia. However, the brain mechanisms underlying
             cognitive, sensory, and motor covariation are largely
             unknown. Here, we examined whether such covariation in
             midlife reflects variability in common versus distinct
             neocortical networks using individualized maps of functional
             topography derived from BOLD fMRI data collected in 769
             45-year-old members of a population-representative cohort.
             Analyses revealed that variability in basic motor but not
             hearing ability reflected individual differences in the
             functional topography of neocortical networks typically
             supporting cognitive ability. These patterns suggest that
             covariation in motor and cognitive abilities in midlife
             reflects convergence of function in higher-order neocortical
             networks and that gait speed may not be simply a measure of
             physical function but rather an integrative index of nervous
             system health.},
   Doi = {10.1093/cercor/bhad109},
   Key = {fds370498}
}

@article{fds370500,
   Author = {Madrid-Valero, JJ and Matthews, T and Barclay, NL and Odgers, CL and Moffitt, TE and Caspi, A and Arseneault, L and Gregory,
             AM},
   Title = {Problematic technology use and sleep quality in young
             adulthood: novel insights from a nationally representative
             twin study.},
   Journal = {Sleep},
   Volume = {46},
   Number = {6},
   Pages = {zsad038},
   Year = {2023},
   Month = {June},
   url = {http://dx.doi.org/10.1093/sleep/zsad038},
   Abstract = {<h4>Study objectives</h4>Digital technology use is
             associated with poor sleep quality in adolescence and young
             adulthood although research findings have been mixed. No
             studies have addressed the association between the two using
             a genetically informative twin design which could extend our
             understanding of the etiology of this relationship. This
             study aimed to test: (1) the association between
             adolescents' perceived problematic use of digital technology
             and poor sleep quality, (2) whether the association between
             problematic use of technology and poor sleep quality remains
             after controlling for familial factors, and (3) genetic and
             environmental influences on the association between
             problematic use of technology and poor sleep
             quality.<h4>Methods</h4>Participants were 2232 study members
             (18-year-old twins) of the Environmental Risk (E-Risk)
             Longitudinal Twin Study. The sample was 48.9% male, 90%
             white, and 55.6% monozygotic. We conducted regression and
             twin difference analyses and fitted twin
             models.<h4>Results</h4>Twin differences for problematic use
             of technology were associated with differences for poor
             sleep quality in the whole sample (p < 0.001; B = 0.15) and
             also when we limited the analyses to identical twins only (p
             < 0.001; B = 0.21). We observed a substantial genetic
             correlation between problematic use of technology and sleep
             quality (rA = 0.31), whereas the environmental correlation
             was lower (rE = 0.16).<h4>Conclusions</h4>Adolescent
             reported problematic use of digital technology is associated
             with poor sleep quality-even after controlling for familial
             factors including genetic confounds. Our results suggest
             that the association between adolescents' sleep and
             problematic digital technology use is not accounted for by
             shared genetic liability or familial factors but could
             reflect a causal association. This robust association needs
             to be examined in future research designed to test causal
             associations.},
   Doi = {10.1093/sleep/zsad038},
   Key = {fds370500}
}

@article{fds362161,
   Author = {Matthews, T and Qualter, P and Bryan, BT and Caspi, A and Danese, A and Moffitt, TE and Odgers, CL and Strange, L and Arseneault,
             L},
   Title = {The developmental course of loneliness in adolescence:
             Implications for mental health, educational attainment, and
             psychosocial functioning.},
   Journal = {Development and psychopathology},
   Volume = {35},
   Number = {2},
   Pages = {537-546},
   Year = {2023},
   Month = {May},
   url = {http://dx.doi.org/10.1017/s0954579421001632},
   Abstract = {The present study examined patterns of stability and change
             in loneliness across adolescence. Data were drawn from the
             Environmental Risk (E-Risk) Longitudinal Twin Study, a UK
             population-representative cohort of 2,232 individuals born
             in 1994 and 1995. Loneliness was assessed when participants
             were aged 12 and 18. Loneliness showed modest stability
             across these ages (<i>r</i> = .25). Behavioral genetic
             modeling indicated that stability in loneliness was
             explained largely by genetic influences (66%), while change
             was explained by nonshared environmental effects (58%).
             Individuals who reported loneliness at both ages were
             broadly similar to individuals who only reported it at age
             18, with both groups at elevated risk of mental health
             problems, physical health risk behaviors, and education and
             employment difficulties. Individuals who were lonely only at
             age 12 generally fared better; however, they were still more
             likely to finish school with lower qualifications. Positive
             family influences in childhood predicted reduced risk of
             loneliness at age 12, while negative peer experiences
             increased the risk. Together, the findings show that while
             early adolescent loneliness does not appear to exert a
             cumulative burden when it persists, it is nonetheless a risk
             for a range of concomitant impairments, some of which can
             endure.},
   Doi = {10.1017/s0954579421001632},
   Key = {fds362161}
}

@article{fds370046,
   Author = {Poulton, R and Caspi, A and Moffitt, TE},
   Title = {Fear and anxiety: Lessons learned from the Dunedin
             longitudinal study.},
   Journal = {Neuroscience and biobehavioral reviews},
   Volume = {148},
   Pages = {105118},
   Year = {2023},
   Month = {May},
   url = {http://dx.doi.org/10.1016/j.neubiorev.2023.105118},
   Abstract = {Four related lines of research on anxiety were reviewed from
             the 'Dunedin Study', an investigation of a representative
             longitudinal birth cohort of 50-years duration, with 94%
             retention at the last follow-up. Findings include: (i)
             Childhood fears deemed evolutionarily-relevant may have
             different pathways and/or mechanisms underlying their
             emergence when compared to evolutionarilyneutral fears. (ii)
             Sequential comorbidity both inside and external to the
             family of disorders is the rule not the exception,
             highlighting the importance of developmental history. (iii)
             The developmental relationship between GAD and MDE is more
             symmetric that previously assumed, with equal numbers of
             persons having GAD preceding MDE and MDE preceding GAD. (iv)
             PTSD in adulthood is influenced by a broad range of
             childhood risk factors, sequential comorbidity is near
             universal, and both high-stress life events and
             mental-disorder history influence the development of PTSD.
             The implications for epidemiology, nosology, the importance
             of developmental history, and prevention/treatment options
             are considered.},
   Doi = {10.1016/j.neubiorev.2023.105118},
   Key = {fds370046}
}

@article{fds370882,
   Author = {Doherty, T and Dempster, E and Hannon, E and Mill, J and Poulton, R and Corcoran, D and Sugden, K and Williams, B and Caspi, A and Moffitt, TE and Delany, SJ and Murphy, TM},
   Title = {A comparison of feature selection methodologies and learning
             algorithms in the development of a DNA methylation-based
             telomere length estimator.},
   Journal = {BMC bioinformatics},
   Volume = {24},
   Number = {1},
   Pages = {178},
   Year = {2023},
   Month = {May},
   url = {http://dx.doi.org/10.1186/s12859-023-05282-4},
   Abstract = {<h4>Background</h4>The field of epigenomics holds great
             promise in understanding and treating disease with advances
             in machine learning (ML) and artificial intelligence being
             vitally important in this pursuit. Increasingly, research
             now utilises DNA methylation measures at cytosine-guanine
             dinucleotides (CpG) to detect disease and estimate
             biological traits such as aging. Given the challenge of high
             dimensionality of DNA methylation data, feature-selection
             techniques are commonly employed to reduce dimensionality
             and identify the most important subset of features. In this
             study, our aim was to test and compare a range of
             feature-selection methods and ML algorithms in the
             development of a novel DNA methylation-based telomere length
             (TL) estimator. We utilised both nested cross-validation and
             two independent test sets for the comparisons.<h4>Results</h4>We
             found that principal component analysis in advance of
             elastic net regression led to the overall best performing
             estimator when evaluated using a nested cross-validation
             analysis and two independent test cohorts. This approach
             achieved a correlation between estimated and actual TL of
             0.295 (83.4% CI [0.201, 0.384]) on the EXTEND test data set.
             Contrastingly, the baseline model of elastic net regression
             with no prior feature reduction stage performed less well in
             general-suggesting a prior feature-selection stage may have
             important utility. A previously developed TL estimator,
             DNAmTL, achieved a correlation of 0.216 (83.4% CI [0.118,
             0.310]) on the EXTEND data. Additionally, we observed that
             different DNA methylation-based TL estimators, which have
             few common CpGs, are associated with many of the same
             biological entities.<h4>Conclusions</h4>The variance in
             performance across tested approaches shows that estimators
             are sensitive to data set heterogeneity and the development
             of an optimal DNA methylation-based estimator should benefit
             from the robust methodological approach used in this study.
             Moreover, our methodology which utilises a range of
             feature-selection approaches and ML algorithms could be
             applied to other biological markers and disease phenotypes,
             to examine their relationship with DNA methylation and
             predictive value.},
   Doi = {10.1186/s12859-023-05282-4},
   Key = {fds370882}
}

@article{fds368070,
   Author = {Lay-Yee, R and Matthews, T and Moffitt, T and Poulton, R and Caspi, A and Milne, B},
   Title = {Are trajectories of social isolation from childhood to
             mid-adulthood associated with adult depression or suicide
             outcomes.},
   Journal = {Social psychiatry and psychiatric epidemiology},
   Volume = {58},
   Number = {3},
   Pages = {373-382},
   Year = {2023},
   Month = {March},
   url = {http://dx.doi.org/10.1007/s00127-022-02389-6},
   Abstract = {<h4>Purpose</h4>Social isolation has been shown to have
             negative effects on mental health outcomes though little is
             known about trajectories across the life course. We examined
             the relationship between trajectory groups and selected
             mental health outcomes in mid-adulthood.<h4>Methods</h4>We
             previously created a typology of social isolation based on
             onset during the life course and persistence into adulthood,
             using group-based trajectory analysis of longitudinal data
             from a New Zealand birth cohort. The typology comprises four
             groups: 'never-isolated', 'adult-only', 'child-only', and
             'persistent (child-adult) isolation'. We undertook logistic
             regression analyses of three mental health outcomes with
             trajectory group as the predictor, adjusting for sex and a
             range of familial and child-behavioural factors.<h4>Results</h4>Lifetime
             suicide attempt, and depression and suicide ideation in
             mid-adulthood were each associated with adult-only but not
             child-only social isolation. Depression in mid-adulthood was
             also associated with persistent child-adult social
             isolation.<h4>Conclusion</h4>Although our findings are
             associational and not causal, they indicate that
             interrupting persistent social isolation may help to prevent
             adult depression whereas halting adult social isolation may
             ameliorate both depression and suicide outcomes.},
   Doi = {10.1007/s00127-022-02389-6},
   Key = {fds368070}
}

@article{fds370501,
   Author = {Whitman, ET and Knodt, AR and Elliott, ML and Abraham, WC and Cheyne, K and Hogan, S and Ireland, D and Keenan, R and Lueng, JH and Melzer, TR and Poulton, R and Purdy, SC and Ramrakha, S and Thorne, PR and Caspi, A and Moffitt, TE and Hariri, AR},
   Title = {Functional Topography of the Neocortex Predicts Covariation
             in Complex Cognitive and Basic Motor Abilities.},
   Journal = {bioRxiv},
   Year = {2023},
   Month = {January},
   url = {http://dx.doi.org/10.1101/2023.01.09.523297},
   Abstract = {Although higher-order cognitive and lower-order sensorimotor
             abilities are generally regarded as distinct and studied
             separately, there is evidence that they not only covary but
             also that this covariation increases across the lifespan.
             This pattern has been leveraged in clinical settings where a
             simple assessment of sensory or motor ability (e.g.,
             hearing, gait speed) can forecast age-related cognitive
             decline and risk for dementia. However, the brain mechanisms
             underlying cognitive, sensory, and motor covariation are
             largely unknown. Here, we examined whether such covariation
             in midlife reflects variability in common versus distinct
             neocortical networks using individualized maps of functional
             topography derived from BOLD fMRI data collected in 769
             45-year old members of a population-representative cohort.
             Analyses revealed that variability in basic motor but not
             hearing ability reflected individual differences in the
             functional topography of neocortical networks typically
             supporting cognitive ability. These patterns suggest that
             covariation in motor and cognitive abilities in midlife
             reflects convergence of function in higher-order neocortical
             networks and that gait speed may not be simply a measure of
             physical function but rather an integrative index of nervous
             system health.},
   Doi = {10.1101/2023.01.09.523297},
   Key = {fds370501}
}

@article{fds361148,
   Author = {Wilson, GA and Cheyne, K and Ramrakha, S and Ambler, A and Tan, GS and Caspi, A and Williams, B and Sugden, K and Houts, R and Niederer, RL and Wong, TY and Moffitt, TE and Poulton, R},
   Title = {Are macular drusen in midlife a marker of accelerated
             biological ageing?},
   Journal = {Clinical & experimental optometry},
   Volume = {106},
   Number = {1},
   Pages = {41-46},
   Year = {2023},
   Month = {January},
   url = {http://dx.doi.org/10.1080/08164622.2021.2012428},
   Abstract = {<h4>Clinical relevance</h4>Macular drusen are associated
             with age-related maculopathy but are not an ocular
             manifestation or biomarker of systemic ageing.<h4>Background</h4>Macular
             drusen are the first sign of age-related maculopathy, an eye
             disease for which age is the strongest risk factor. The aim
             of this cohort study was to investigate whether macular
             drusen in midlife - a sign of the earliest stages of
             age-related macular degeneration (AMD) - are associated with
             accelerated biological ageing more generally.<h4>Methods</h4>Members
             of the long-running Dunedin Multidisciplinary Health and
             Development Study (hereafter the Dunedin Study, n = 1037)
             underwent retinal photography at their most recent
             assessment at the age of 45 years. Images were graded for
             the presence of AMD using a simplified scale from the
             Age-Related Eye Disease Study (AREDS). Accelerated ageing
             was assessed by (i) a measure of Pace of Ageing defined from
             a combination of clinical and serum biomarkers obtained at
             ages 26, 32, 38, and 45 years and (ii) Facial Ageing,
             defined from photographs obtained at age 38 and
             45 years.<h4>Results</h4>Of the 938 participants who
             participated at the age 45 assessments, 834 had gradable
             retinal photographs, and of these 165 (19.8%) had macular
             drusen. There was no significant difference in Pace of
             Ageing (<i>p</i> = .743) or Facial Ageing (<i>p</i>
             = .945) among participants with and without macular
             drusen.<h4>Conclusions</h4>In this representative general
             population sample, macular drusen in midlife were not
             associated with accelerated ageing. Future studies tracking
             longitudinal changes in drusen number and severity at older
             ages may reveal whether drusen are a biomarker of
             accelerated ageing.},
   Doi = {10.1080/08164622.2021.2012428},
   Key = {fds361148}
}

@article{fds366197,
   Author = {Poulton, R and Guiney, H and Ramrakha, S and Moffitt,
             TE},
   Title = {The Dunedin study after half a century: reflections on the
             past, and course for the future},
   Journal = {Journal of the Royal Society of New Zealand},
   Volume = {53},
   Number = {4},
   Pages = {446-465},
   Publisher = {Informa UK Limited},
   Year = {2023},
   Month = {January},
   url = {http://dx.doi.org/10.1080/03036758.2022.2114508},
   Abstract = {Over the last 50 years Dunedin Study researchers have
             published more than 1400 peer-reviewed journal articles,
             books, and reports on many aspects of human health and
             development. In this 50th anniversary piece we reflect on
             (i) our historical roots and necessary re-invention through
             time; (ii) the underpinning principles that have contributed
             to our success; (iii) some selected examples of high-impact
             work from the behavioural, oral health, and respiratory
             domains; (iv) some of the challenges we have encountered
             over time and how to overcome these; and (vi) review where
             we see the Study going in the future. We aim to present some
             of the ‘back story’, which is typically undocumented and
             oft lost to memory, and thus focus on ‘know-how’. Our
             hope is to humanise our research, share insights, and to
             acknowledge the real heroes of the Study–the 1037 Study
             members, their families and their friends, who have
             collectively given so much, for so long, in the hope of
             helping others.},
   Doi = {10.1080/03036758.2022.2114508},
   Key = {fds366197}
}

@article{fds367973,
   Author = {Lorenzo, EC and Kuchel, GA and Kuo, C-L and Moffitt, TE and Diniz,
             BS},
   Title = {Major depression and the biological hallmarks of
             aging.},
   Journal = {Ageing research reviews},
   Volume = {83},
   Pages = {101805},
   Year = {2023},
   Month = {January},
   url = {http://dx.doi.org/10.1016/j.arr.2022.101805},
   Abstract = {Major depressive disorder (MDD) is characterized by
             psychological and physiological manifestations contributing
             to the disease severity and outcome. In recent years,
             several lines of evidence have suggested that individuals
             with MDD have an elevated risk of age-related adverse
             outcomes across the lifespan. This review provided evidence
             of a significant overlap between the biological
             abnormalities in MDD and biological changes commonly
             observed during the aging process (i.e., hallmarks of
             biological aging). Based on such evidence, we formulate a
             mechanistic model showing how abnormalities in the hallmarks
             of biological aging can be a common denominator and mediate
             the elevated risk of age-related health outcomes commonly
             observed in MDD. Finally, we proposed a roadmap for novel
             studies to investigate the intersection between the biology
             of aging and MDD, including the use of geroscience-guided
             interventions, such as senolytics, to delay or improve major
             depression by targeting biological aging.},
   Doi = {10.1016/j.arr.2022.101805},
   Key = {fds367973}
}

@article{fds368322,
   Author = {Guiney, H and Walker, R and Broadbent, J and Caspi, A and Goodin, E and Kokaua, J and Moffitt, TE and Robertson, S and Theodore, R and Poulton,
             R and Endre, Z},
   Title = {Kidney-Function Trajectories From Young Adulthood to
             Midlife: Identifying Risk Strata and Opportunities for
             Intervention.},
   Journal = {Kidney international reports},
   Volume = {8},
   Number = {1},
   Pages = {51-63},
   Year = {2023},
   Month = {January},
   url = {http://dx.doi.org/10.1016/j.ekir.2022.10.005},
   Abstract = {<h4>Introduction</h4>Understanding normative patterns of
             change in kidney function over the life course may allow
             targeting of early interventions to slow or prevent the
             onset of kidney disease, but knowledge about kidney
             functional change before middle age is limited. This study
             used prospective longitudinal data from a representative
             birth cohort to examine common patterns of change from young
             to midadulthood and to identify risk factors and outcomes
             associated with poorer trajectories.<h4>Methods</h4>We used
             group-based trajectory modeling in the Dunedin study birth
             cohort (<i>n</i> = 857) to identify the following: (i)
             common kidney function trajectories between the ages 32 and
             45 years, (ii) early-life factors associated with those
             trajectories, (iii) modifiable physical and psychosocial
             factors across adulthood associated with differences in
             trajectory slope, and (iv) links between trajectories and
             kidney-related outcomes at age 45 years.<h4>Results</h4>Three
             trajectory groups were identified and could be
             differentiated by age 32 years as follows: normal (58% of
             participants), low-normal (36%), and high-risk (6%) groups.
             Those from low socioeconomic backgrounds had higher odds of
             following a high-risk (vs. normal) trajectory. Modifiable
             factors (blood pressure, body mass index, inflammation,
             glycated hemoglobin, smoking, and socioeconomic status)
             across adulthood were associated with steeper age-related
             declines in kidney function, particularly among those in the
             low-normal and high-risk groups. Those in the low-normal and
             high-risk groups also had more adverse kidney-related
             outcomes at age 45 years.<h4>Conclusion</h4>The current
             findings could be used to inform the development of early
             interventions and point to socioeconomic conditions across
             the life course and health-related risk factors and
             behaviors in adulthood as kidney health promotion
             targets.},
   Doi = {10.1016/j.ekir.2022.10.005},
   Key = {fds368322}
}

@article{fds370047,
   Author = {Barrett-Young, A and Abraham, WC and Cheung, CY and Gale, J and Hogan,
             S and Ireland, D and Keenan, R and Knodt, AR and Melzer, TR and Moffitt,
             TE and Ramrakha, S and Tham, YC and Wilson, GA and Wong, TY and Hariri, AR and Poulton, R},
   Title = {Associations Between Thinner Retinal Neuronal Layers and
             Suboptimal Brain Structural Integrity in a Middle-Aged
             Cohort.},
   Journal = {Eye and brain},
   Volume = {15},
   Pages = {25-35},
   Year = {2023},
   Month = {January},
   url = {http://dx.doi.org/10.2147/eb.s402510},
   Abstract = {<h4>Purpose</h4>The retina has potential as a biomarker of
             brain health and Alzheimer's disease (AD) because it is the
             only part of the central nervous system which can be easily
             imaged and has advantages over brain imaging technologies.
             Few studies have compared retinal and brain measurements in
             a middle-aged sample. The objective of our study was to
             investigate whether retinal neuronal measurements were
             associated with structural brain measurements in a
             middle-aged population-based cohort.<h4>Participants and
             methods</h4>Participants were members of the Dunedin
             Multidisciplinary Health and Development Study (n=1037; a
             longitudinal cohort followed from birth and at ages 3, 5, 7,
             9, 11, 13, 15, 18, 21, 26, 32, 38, and most recently at age
             45, when 94% of the living Study members participated).
             Retinal nerve fibre layer (RNFL) and ganglion cell-inner
             plexiform layer (GC-IPL) thickness were measured by optical
             coherence tomography (OCT). Brain age gap estimate
             (brainAGE), cortical surface area, cortical thickness,
             subcortical grey matter volumes, white matter
             hyperintensities, were measured by magnetic resonance
             imaging (MRI).<h4>Results</h4>Participants with both MRI and
             OCT data were included in the analysis (RNFL n=828, female
             n=413 [49.9%], male n=415 [50.1%]; GC-IPL n=825, female
             n=413 [50.1%], male n=412 [49.9%]). Thinner retinal neuronal
             layers were associated with older brain age, smaller
             cortical surface area, thinner average cortex, smaller
             subcortical grey matter volumes, and increased volume of
             white matter hyperintensities.<h4>Conclusion</h4>These
             findings provide evidence that the retinal neuronal layers
             reflect differences in midlife structural brain integrity
             consistent with increased risk for later AD, supporting the
             proposition that the retina may be an early biomarker of
             brain health.},
   Doi = {10.2147/eb.s402510},
   Key = {fds370047}
}

@article{fds370957,
   Author = {Thomas, A and Ryan, C and Caspi, A and Moffitt, T and Sugden, K and Zhou,
             J and Belsky, D and Gu, Y},
   Title = {Diet, pace of biological aging, and risk of dementia in the
             Framingham Heart Study},
   Booktitle = {medRxiv},
   Year = {2023},
   url = {http://dx.doi.org/10.1101/2023.05.24.23290474},
   Abstract = {<h4>Objective</h4>People who eat healthier diets are less
             likely to develop dementia, but the biological mechanism of
             this protection is not well understood. We tested the
             hypothesis that healthy diet protects against dementia
             because it slows the pace of biological aging.<h4>Methods</h4>We
             analyzed Framingham Offspring Cohort data. We included
             participants ≥60 years-old, free of dementia and having
             dietary, epigenetic, and follow-up data. We assessed healthy
             diet as long-term adherence to the Mediterranean-Dash
             Intervention for Neurodegenerative Delay diet (MIND, over 4
             visits spanning 1991-2008). We measured the pace of aging
             from blood DNA methylation data collected in 2005-2008 using
             the DunedinPACE epigenetic clock. Incident dementia and
             mortality were defined using study records compiled from
             2005 to 2008 visit through 2018.<h4>Results</h4>Of
             n = 1,644 included participants (mean age 69.6, 54%
             female), n = 140 developed dementia and n = 471 died
             over 14 years of follow-up. Greater MIND score was
             associated with slower DunedinPACE and reduced risks for
             dementia and mortality. Slower DunedinPACE was associated
             with reduced risks for dementia and mortality. In mediation
             analysis, slower DunedinPACE accounted for 27% of the
             diet-dementia association and 57% of the diet-mortality
             association.<h4>Interpretation</h4>Findings suggest that
             slower pace of aging mediates part of the relationship of
             healthy diet with reduced dementia risk. Monitoring pace of
             aging may inform dementia prevention. However, a large
             fraction of the diet-dementia association remains
             unexplained and may reflect direct connections between diet
             and brain aging that do not overlap other organ systems.
             Investigation of brain-specific mechanisms in well-designed
             mediation studies is warranted. ANN NEUROL
             2024.},
   Doi = {10.1101/2023.05.24.23290474},
   Key = {fds370957}
}

@article{fds365153,
   Author = {Latham, RM and Arseneault, L and Alexandrescu, B and Baldoza, S and Carter, A and Moffitt, TE and Newbury, JB and Fisher,
             HL},
   Title = {Violent experiences and neighbourhoods during adolescence:
             understanding and mitigating the association with mental
             health at the transition to adulthood in a longitudinal
             cohort study.},
   Journal = {Social psychiatry and psychiatric epidemiology},
   Volume = {57},
   Number = {12},
   Pages = {2379-2391},
   Year = {2022},
   Month = {December},
   url = {http://dx.doi.org/10.1007/s00127-022-02343-6},
   Abstract = {<h4>Purpose</h4>Violence occurs at multiple ecological
             levels and can harm mental health. However, studies of
             adolescents' experience of violence have often ignored the
             community context of violence, and vice versa. We examined
             how personal experience of severe physical violence and
             living in areas with high levels of neighbourhood disorder
             during adolescence combine to associate with mental health
             at the transition to adulthood and which factors mitigate
             this.<h4>Method</h4>Data were from the Environmental Risk
             Longitudinal Twin Study, a nationally representative birth
             cohort of 2232 British twins. Participants' experience of
             severe physical violence during adolescence and past-year
             symptoms of psychiatric disorder were assessed via
             interviews at age 18. Neighbourhood disorder was reported by
             residents when participants were aged 13-14. Potential
             protective factors of maternal warmth, sibling warmth, IQ,
             and family socio-economic status were assessed during
             childhood, and perceived social support at age
             18.<h4>Results</h4>Personal experience of severe physical
             violence during adolescence was associated with elevated
             odds of age-18 psychiatric disorder regardless of
             neighbourhood disorder exposure. Cumulative effects of
             exposure to both were evident for internalising and thought
             disorder, but not externalising disorder. For adolescents
             exposed to severe physical violence only, higher levels of
             perceived social support (including from family and friends)
             were associated with lower odds of psychiatric disorder. For
             those who also lived in areas with high neighbourhood
             disorder, only family support mitigated their
             risk.<h4>Conclusion</h4>Increasing support or boosting
             adolescents' perceptions of their existing support network
             may be effective in promoting their mental health following
             violence exposure.},
   Doi = {10.1007/s00127-022-02343-6},
   Key = {fds365153}
}

@article{fds365697,
   Author = {Knodt, AR and Meier, MH and Ambler, A and Gehred, MZ and Harrington, H and Ireland, D and Poulton, R and Ramrakha, S and Caspi, A and Moffitt, TE and Hariri, AR},
   Title = {Diminished Structural Brain Integrity in Long-term Cannabis
             Users Reflects a History of Polysubstance
             Use.},
   Journal = {Biological psychiatry},
   Volume = {92},
   Number = {11},
   Pages = {861-870},
   Year = {2022},
   Month = {December},
   url = {http://dx.doi.org/10.1016/j.biopsych.2022.06.018},
   Abstract = {<h4>Background</h4>Cannabis legalization and use are
             outpacing our understanding of its long-term effects on
             brain and behavior, which is fundamental for effective
             policy and health practices. Existing studies are limited by
             small samples, cross-sectional measures, failure to separate
             long-term from recreational use, and inadequate control for
             other substance use. Here, we address these limitations by
             determining the structural brain integrity of long-term
             cannabis users in the Dunedin Study, a longitudinal
             investigation of a population-representative birth cohort
             followed to midlife.<h4>Methods</h4>We leveraged prospective
             measures of cannabis, alcohol, tobacco, and other illicit
             drug use in addition to structural neuroimaging in 875 study
             members at age 45 to test for differences in both global and
             regional gray and white matter integrity between long-term
             cannabis users and lifelong nonusers. We additionally tested
             for dose-response associations between continuous measures
             of cannabis use and brain structure, including careful
             adjustments for use of other substances.<h4>Results</h4>Long-term
             cannabis users had a thinner cortex, smaller subcortical
             gray matter volumes, and higher machine learning-predicted
             brain age than nonusers. However, these differences in
             structural brain integrity were explained by the propensity
             of long-term cannabis users to engage in polysubstance use,
             especially with alcohol and tobacco.<h4>Conclusions</h4>These
             findings suggest that diminished midlife structural brain
             integrity in long-term cannabis users reflects a broader
             pattern of polysubstance use, underlining the importance of
             understanding comorbid substance use in efforts to curb the
             negative effects of cannabis on brain and behavior as well
             as establish more effective policy and health
             practices.},
   Doi = {10.1016/j.biopsych.2022.06.018},
   Key = {fds365697}
}

@article{fds367502,
   Author = {Moffitt, TE and Phillips, JWR},
   Title = {Preface: Expert Advice to Enhance Aging Research and the
             Health and Retirement Study.},
   Journal = {Forum for health economics & policy},
   Volume = {25},
   Number = {1-2},
   Pages = {1-5},
   Year = {2022},
   Month = {December},
   url = {http://dx.doi.org/10.1515/fhep-2022-0021},
   Doi = {10.1515/fhep-2022-0021},
   Key = {fds367502}
}

@article{fds367812,
   Author = {Langevin, S and Caspi, A and Barnes, JC and Brennan, G and Poulton, R and Purdy, SC and Ramrakha, S and Tanksley, PT and Thorne, PR and Wilson, G and Moffitt, TE},
   Title = {Life-Course Persistent Antisocial Behavior and Accelerated
             Biological Aging in a Longitudinal Birth
             Cohort.},
   Journal = {International journal of environmental research and public
             health},
   Volume = {19},
   Number = {21},
   Pages = {14402},
   Year = {2022},
   Month = {November},
   url = {http://dx.doi.org/10.3390/ijerph192114402},
   Abstract = {Prior research shows that individuals who have exhibited
             antisocial behavior are in poorer health than their
             same-aged peers. A major driver of poor health is aging
             itself, yet research has not investigated relationships
             between offending trajectories and biological aging. We
             tested the hypothesis that individuals following a
             life-course persistent (LCP) antisocial trajectory show
             accelerated aging in midlife. Trajectories of antisocial
             behavior from age 7 to 26 years were studied in the Dunedin
             Multidisciplinary Health and Development Study, a
             population-representative birth cohort (N = 1037). Signs of
             aging were assessed at age 45 years using previously
             validated measures including biomarkers, clinical tests, and
             self-reports. First, we tested whether the association
             between antisocial behavior trajectories and midlife signs
             of faster aging represented a decline from initial childhood
             health. We then tested whether decline was attributable to
             tobacco smoking, antipsychotic medication use, debilitating
             illnesses in adulthood, adverse exposures in childhood
             (maltreatment, socioeconomic disadvantage) and adulthood
             (incarceration), and to childhood self-control difficulties.
             Study members with a history of antisocial behavior had a
             significantly faster pace of biological aging by midlife,
             and this was most evident among individuals following the
             LCP trajectory (β, 0.22, 95%CI, 0.14, 0.28, <i>p</i> ≤
             0.001). This amounted to 4.3 extra years of biological aging
             between ages 25-45 years for Study members following the LCP
             trajectory compared to low-antisocial trajectory
             individuals. LCP offenders also experienced more midlife
             difficulties with hearing (β, -0.14, 95%CI, -0.21, -0.08,
             <i>p</i> ≤ 0.001), balance (β, -0.13, 95%CI, -0.18,
             -0.06, <i>p</i> ≤ 0.001), gait speed (β, -0.18, 95%CI,
             -0.24, -0.10, <i>p</i> ≤ 0.001), and cognitive functioning
             (β, -0.25, 95%CI, -0.31, -0.18, <i>p</i> ≤ 0.001).
             Associations represented a decline from childhood health.
             Associations persisted after controlling individually for
             tobacco smoking, antipsychotic medication use, midlife
             illnesses, maltreatment, socioeconomic status,
             incarceration, and childhood self-control difficulties.
             However, the cumulative effect of these lifestyle
             characteristics together explained why LCP offenders have a
             faster Pace of Aging than their peers. While older adults
             typically age-out of crime, LCP offenders will likely
             age-into the healthcare system earlier than their
             chronologically same-aged peers. Preventing young people
             from offending is likely to have substantial benefits for
             health, and people engaging in a LCP trajectory of
             antisocial behaviors might be the most in need of health
             promotion programs. We offer prevention and intervention
             strategies to reduce the financial burden of offenders on
             healthcare systems and improve their wellbeing.},
   Doi = {10.3390/ijerph192114402},
   Key = {fds367812}
}

@article{fds367974,
   Author = {Tielbeek, JJ and Uffelmann, E and Williams, BS and Colodro-Conde, L and Gagnon, É and Mallard, TT and Levitt, BE and Jansen, PR and Johansson,
             A and Sallis, HM and Pistis, G and Saunders, GRB and Allegrini, AG and Rimfeld, K and Konte, B and Klein, M and Hartmann, AM and Salvatore, JE and Nolte, IM and Demontis, D and Malmberg, ALK and Burt, SA and Savage, JE and Sugden, K and Poulton, R and Harris, KM and Vrieze, S and McGue, M and Iacono, WG and Mota, NR and Mill, J and Viana, JF and Mitchell, BL and Morosoli, JJ and Andlauer, TFM and Ouellet-Morin, I and Tremblay, RE and Côté, SM and Gouin, J-P and Brendgen, MR and Dionne, G and Vitaro, F and Lupton, MK and Martin, NG and COGA Consortium, and Spit for Science
             Working Group, and Castelao, E and Räikkönen, K and Eriksson, JG and Lahti, J and Hartman, CA and Oldehinkel, AJ and Snieder, H and Liu, H and Preisig, M and Whipp, A and Vuoksimaa, E and Lu, Y and Jern, P and Rujescu,
             D and Giegling, I and Palviainen, T and Kaprio, J and Harden, KP and Munafò, MR and Morneau-Vaillancourt, G and Plomin, R and Viding, E and Boutwell, BB and Aliev, F and Dick, DM and Popma, A and Faraone, SV and Børglum, AD and Medland, SE and Franke, B and Boivin, M and Pingault,
             J-B and Glennon, JC and Barnes, JC and Fisher, SE and Moffitt, TE and Caspi, A and Polderman, TJC and Posthuma, D},
   Title = {Uncovering the genetic architecture of broad antisocial
             behavior through a genome-wide association study
             meta-analysis.},
   Journal = {Molecular psychiatry},
   Volume = {27},
   Number = {11},
   Pages = {4453-4463},
   Year = {2022},
   Month = {November},
   url = {http://dx.doi.org/10.1038/s41380-022-01793-3},
   Abstract = {Despite the substantial heritability of antisocial behavior
             (ASB), specific genetic variants robustly associated with
             the trait have not been identified. The present study by the
             Broad Antisocial Behavior Consortium (BroadABC)
             meta-analyzed data from 28 discovery samples
             (N = 85,359) and five independent replication samples
             (N = 8058) with genotypic data and broad measures of
             ASB. We identified the first significant genetic
             associations with broad ASB, involving common intronic
             variants in the forkhead box protein P2 (FOXP2) gene (lead
             SNP rs12536335, p = 6.32 × 10<sup>-10</sup>).
             Furthermore, we observed intronic variation in Foxp2 and one
             of its targets (Cntnap2) distinguishing a mouse model of
             pathological aggression (BALB/cJ strain) from controls
             (BALB/cByJ strain). Polygenic risk score (PRS) analyses in
             independent samples revealed that the genetic risk for ASB
             was associated with several antisocial outcomes across the
             lifespan, including diagnosis of conduct disorder, official
             criminal convictions, and trajectories of antisocial
             development. We found substantial genetic correlations of
             ASB with mental health (depression r<sub>g</sub> = 0.63,
             insomnia r<sub>g</sub> = 0.47), physical health
             (overweight r<sub>g</sub> = 0.19, waist-to-hip ratio
             r<sub>g</sub> = 0.32), smoking (r<sub>g</sub> = 0.54),
             cognitive ability (intelligence r<sub>g</sub> = -0.40),
             educational attainment (years of schooling
             r<sub>g</sub> = -0.46) and reproductive traits (age at
             first birth r<sub>g</sub> = -0.58, father's age at death
             r<sub>g</sub> = -0.54). Our findings provide a starting
             point toward identifying critical biosocial risk mechanisms
             for the development of ASB.},
   Doi = {10.1038/s41380-022-01793-3},
   Key = {fds367974}
}

@article{fds364280,
   Author = {Agnew-Blais, JC and Wertz, J and Arseneault, L and Belsky, DW and Danese, A and Pingault, J-B and Polanczyk, GV and Sugden, K and Williams, B and Moffitt, TE},
   Title = {Mother's and children's ADHD genetic risk, household chaos
             and children's ADHD symptoms: A gene-environment correlation
             study.},
   Journal = {Journal of child psychology and psychiatry, and allied
             disciplines},
   Volume = {63},
   Number = {10},
   Pages = {1153-1163},
   Year = {2022},
   Month = {October},
   url = {http://dx.doi.org/10.1111/jcpp.13659},
   Abstract = {<h4>Background</h4>Chaotic home environments may contribute
             to children's attention-deficit hyperactivity disorder
             (ADHD) symptoms. However, ADHD genetic risk may also
             influence household chaos. This study investigated whether
             children in chaotic households had more ADHD symptoms, if
             mothers and children with higher ADHD genetic risk lived in
             more chaotic households, and the joint association of
             genetic risk and household chaos on the longitudinal course
             of ADHD symptoms across childhood.<h4>Methods</h4>Participants
             were mothers and children from the Environmental Risk
             (E-Risk) Longitudinal Twin Study, a UK population-representative
             birth cohort of 2,232 twins. Children's ADHD symptoms were
             assessed at ages 5, 7, 10 and 12 years. Household chaos
             was rated by research workers at ages 7, 10 and 12, and by
             mother's and twin's self-report at age 12. Genome-wide ADHD
             polygenic risk scores (PRS) were calculated for mothers
             (n = 880) and twins (n = 1,999); of these,
             n = 871 mothers and n = 1,925 children had
             information on children's ADHD and household
             chaos.<h4>Results</h4>Children in more chaotic households
             had higher ADHD symptoms. Mothers and children with higher
             ADHD PRS lived in more chaotic households. Children's ADHD
             PRS was associated with household chaos over and above
             mother's PRS, suggesting evocative gene-environment
             correlation. Children in more chaotic households had higher
             baseline ADHD symptoms and a slower rate of decline in
             symptoms. However, sensitivity analyses estimated that
             gene-environment correlation accounted for a large
             proportion of the association of household chaos on ADHD
             symptoms.<h4>Conclusions</h4>Children's ADHD genetic risk
             was independently associated with higher levels of household
             chaos, emphasising the active role of children in shaping
             their home environment. Our findings suggest that household
             chaos partly reflects children's genetic risk for ADHD,
             calling into question whether household chaos directly
             influences children's core ADHD symptoms. Our findings
             highlight the importance of considering parent and child
             genetic risk in relation to apparent environmental
             exposures.},
   Doi = {10.1111/jcpp.13659},
   Key = {fds364280}
}

@article{fds367349,
   Author = {Meier, MH and Caspi, A and Ambler, A and Hariri, AR and Harrington, H and Hogan, S and Houts, R and Knodt, AR and Ramrakha, S and Richmond-Rakerd,
             LS and Poulton, R and Moffitt, TE},
   Title = {Preparedness for healthy ageing and polysubstance use in
             long-term cannabis users: a population-representative
             longitudinal study.},
   Journal = {The lancet. Healthy longevity},
   Volume = {3},
   Number = {10},
   Pages = {e703-e714},
   Year = {2022},
   Month = {October},
   url = {http://dx.doi.org/10.1016/s2666-7568(22)00201-x},
   Abstract = {<h4>Background</h4>Cannabis is often characterised as a
             young person's drug. However, people who began consuming
             cannabis in the 1970s and 1980s are no longer young and some
             have consumed it for many years. This study tested the
             preregistered hypothesis that long-term cannabis users show
             accelerated biological ageing in midlife and poorer health
             preparedness, financial preparedness, and social
             preparedness for old age.<h4>Methods</h4>In this
             longitudinal study, participants comprised a
             population-representative cohort of 1037 individuals born in
             Dunedin, New Zealand, between April, 1972, and March, 1973,
             and followed to age 45 years. Cannabis, tobacco, and alcohol
             use and dependence were assessed at ages 18 years, 21 years,
             26 years, 32 years, 38 years, and 45 years. Biological
             ageing and health, financial, and social preparedness for
             old age were assessed at age 45 years. Long-term cannabis
             users were compared using independent samples t tests with
             five groups: lifelong cannabis non-users, long-term tobacco
             users, long-term alcohol users, midlife recreational
             cannabis users, and cannabis quitters. In addition,
             regression analyses tested dose-response associations for
             continuously measured persistence of cannabis dependence
             from age 18 years to 45 years, with associations adjusted
             for sex, childhood socioeconomic status, childhood IQ, low
             childhood self-control, family substance dependence history,
             and persistence of alcohol, tobacco, and other illicit drug
             dependence.<h4>Findings</h4>Of 997 cohort members still
             alive at age 45 years, 938 (94%) were assessed at age 45
             years. Long-term cannabis users showed statistically
             significant accelerated biological ageing and were less
             equipped to manage a range of later-life health, financial,
             and social demands than non-users. Standardised mean
             differences between long-term cannabis users and non-users
             were large: 0·70 (95% CI 0·46 to 0·94; p<0·0001) for
             biological ageing, -0·72 (-0·96 to -0·49, p<0·0001) for
             health preparedness, -1·08 (-1·31 to -0·85; p<0·0001)
             for financial preparedness, and -0·59 (-0·84 to -0·34,
             p<0·0001) for social preparedness. Long-term cannabis users
             did not fare better than long-term tobacco or alcohol users.
             Tests of dose-response associations suggested that cannabis
             associations could not be explained by the socioeconomic
             origins, childhood IQ, childhood self-control, and family
             substance-dependence history of long-term cannabis users.
             Statistical adjustment for long-term tobacco, alcohol, and
             other illicit drug dependence suggested that long-term
             cannabis users' tendency toward polysubstance dependence
             accounted for their accelerated biological ageing and poor
             financial and health preparedness, although not for their
             poor social preparedness (β -0·10, 95% CI -0·18 to
             -0·02; p=0·017).<h4>Interpretation</h4>Long-term cannabis
             users are underprepared for the demands of old age. Although
             long-term cannabis use appears detrimental, the greatest
             challenge to healthy ageing is not use of any specific
             substance, but rather the long-term polysubstance use that
             characterises many long-term cannabis users. Substance-use
             interventions should include practical strategies for
             improving health and building financial and social capital
             for healthy longevity.<h4>Funding</h4>The National Institute
             on Aging and the UK Medical Research Council. The Dunedin
             Research Unit is supported by the New Zealand Health
             Research Council and the New Zealand Ministry of Business,
             Innovation and Employment.},
   Doi = {10.1016/s2666-7568(22)00201-x},
   Key = {fds367349}
}

@article{fds364965,
   Author = {Sugden, K and Caspi, A and Elliott, ML and Bourassa, KJ and Chamarti, K and Corcoran, DL and Hariri, AR and Houts, RM and Kothari, M and Kritchevsky, S and Kuchel, GA and Mill, JS and Williams, BS and Belsky,
             DW and Moffitt, TE and Alzheimer's Disease Neuroimaging
             Initiative*},
   Title = {Association of Pace of Aging Measured by Blood-Based DNA
             Methylation With Age-Related Cognitive Impairment and
             Dementia.},
   Journal = {Neurology},
   Volume = {99},
   Number = {13},
   Pages = {e1402-e1413},
   Year = {2022},
   Month = {September},
   url = {http://dx.doi.org/10.1212/wnl.0000000000200898},
   Abstract = {<h4>Background and objectives</h4>DNA methylation algorithms
             are increasingly used to estimate biological aging; however,
             how these proposed measures of whole-organism biological
             aging relate to aging in the brain is not known. We used
             data from the Alzheimer's Disease Neuroimaging Initiative
             (ADNI) and the Framingham Heart Study (FHS) Offspring Cohort
             to test the association between blood-based DNA methylation
             measures of biological aging and cognitive impairment and
             dementia in older adults.<h4>Methods</h4>We tested 3
             "generations" of DNA methylation age algorithms (first
             generation: Horvath and Hannum clocks; second generation:
             PhenoAge and GrimAge; and third generation: DunedinPACE,
             Dunedin Pace of Aging Calculated from the Epigenome) against
             the following measures of cognitive impairment in ADNI:
             clinical diagnosis of dementia and mild cognitive
             impairment, scores on Alzheimer disease (AD) / Alzheimer
             disease and related dementias (ADRD) screening tests
             (Alzheimer's Disease Assessment Scale, Mini-Mental State
             Examination, and Montreal Cognitive Assessment), and scores
             on cognitive tests (Rey Auditory Verbal Learning Test,
             Logical Memory test, and Trail Making Test). In an
             independent replication in the FHS Offspring Cohort, we
             further tested the longitudinal association between the DNA
             methylation algorithms and the risk of developing
             dementia.<h4>Results</h4>In ADNI (<i>N</i> = 649
             individuals), the first-generation (Horvath and Hannum DNA
             methylation age clocks) and the second-generation (PhenoAge
             and GrimAge) DNA methylation measures of aging were not
             consistently associated with measures of cognitive
             impairment in older adults. By contrast, a third-generation
             measure of biological aging, DunedinPACE, was associated
             with clinical diagnosis of Alzheimer disease (beta [95% CI]
             = 0.28 [0.08-0.47]), poorer scores on Alzheimer disease/ADRD
             screening tests (beta [Robust SE] = -0.10 [0.04] to
             0.08[0.04]), and cognitive tests (beta [Robust SE] = -0.12
             [0.04] to 0.10 [0.03]). The association between faster pace
             of aging, as measured by DunedinPACE, and risk of developing
             dementia was confirmed in a longitudinal analysis of the FHS
             Offspring Cohort (<i>N</i> = 2,264 individuals, hazard ratio
             [95% CI] = 1.27 [1.07-1.49]).<h4>Discussion</h4>Third-generation
             blood-based DNA methylation measures of aging could prove
             valuable for measuring differences between individuals in
             the rate at which they age and in their risk for cognitive
             decline, and for evaluating interventions to slow
             aging.},
   Doi = {10.1212/wnl.0000000000200898},
   Key = {fds364965}
}

@article{fds366661,
   Author = {Brayne, C and Moffitt, TE},
   Title = {The limitations of large-scale volunteer databases to
             address inequalities and global challenges in health and
             aging.},
   Journal = {Nature aging},
   Volume = {2},
   Number = {9},
   Pages = {775-783},
   Year = {2022},
   Month = {September},
   url = {http://dx.doi.org/10.1038/s43587-022-00277-x},
   Abstract = {Large-scale volunteer databanks (LSVD) have emerged from the
             recognized value of cohorts, attracting substantial funding
             and promising great scientific value. A major focus is their
             size, with the implicit and sometimes explicit assumption
             that large size (thus power) creates generalizability. We
             contend that this is open to challenge. In the context of
             aging and age-related disease research, LSVD typically have
             limitations such as healthy volunteer, white ethnicity and
             high-education biases, and they omit early and late life
             stages critical for understanding aging. Their outputs are
             heavily focused on biomedical pathways of single chronic
             diseases. LSVD outputs increasingly dominate the funding and
             the publication landscapes. This Perspective discusses LSVD
             limitations and calls for more transparent reporting in LSVD
             research, as well as a greater reflection on the value of
             LSVD in relation to resources consumed. We invite funders
             and researchers to examine whether LSVD do actually
             contribute knowledge needed for our acute global health
             challenges including inequalities.},
   Doi = {10.1038/s43587-022-00277-x},
   Key = {fds366661}
}

@article{fds355030,
   Author = {Murphy, J and Shevlin, M and Arseneault, L and Bentall, R and Caspi, A and Danese, A and Hyland, P and Moffitt, TE and Fisher,
             HL},
   Title = {Externalizing the threat from within: A new direction for
             researching associations between suicide and psychotic
             experiences.},
   Journal = {Development and psychopathology},
   Volume = {34},
   Number = {3},
   Pages = {1034-1044},
   Year = {2022},
   Month = {August},
   url = {http://dx.doi.org/10.1017/s0954579420001728},
   Abstract = {A recent suicidal drive hypothesis posits that psychotic
             experiences (PEs) may serve to externalize internally
             generated and self-directed threat (i.e.,
             self-injurious/suicidal behavior [SIB]) in order to optimize
             survival; however, it must first be demonstrated that such
             internal threat can both precede and inform PEs. The current
             study conducted the first known bidirectional analysis of
             SIB and PEs to test whether SIB could be considered as a
             plausible antecedent for PEs. Prospective data were utilized
             from the Environmental Risk (E-Risk) Longitudinal Twin
             Study, a nationally representative birth cohort of 2232
             twins, that captured SIB (any self-harm or suicidal attempt)
             and PEs at ages 12 and 18 years. Cross-lagged panel models
             demonstrated that the association between SIB at age 12 and
             PEs at age 18 was as strong as the association between PEs
             at age 12 and SIB at age 18. Indeed, the best representation
             of the data was a model where these paths were constrained
             to be equal (<i>OR</i> = 2.48, 95% CI = 1.63-3.79). Clinical
             interview case notes for those who reported both SIB and PEs
             at age 18, revealed that PEs were explicitly characterized
             by SIB/threat/death-related content for 39% of cases. These
             findings justify further investigation of the suicidal drive
             hypothesis.},
   Doi = {10.1017/s0954579420001728},
   Key = {fds355030}
}

@article{fds352502,
   Author = {Newbury, JB and Arseneault, L and Caspi, A and Moffitt, TE and Odgers,
             CL and Belsky, DW and Sugden, K and Williams, B and Ambler, AP and Matthews, T and Fisher, HL},
   Title = {Association between genetic and socioenvironmental risk for
             schizophrenia during upbringing in a UK longitudinal
             cohort.},
   Journal = {Psychological medicine},
   Volume = {52},
   Number = {8},
   Pages = {1527-1537},
   Year = {2022},
   Month = {June},
   url = {http://dx.doi.org/10.1017/s0033291720003347},
   Abstract = {<h4>Background</h4>Associations of socioenvironmental
             features like urbanicity and neighborhood deprivation with
             psychosis are well-established. An enduring question,
             however, is whether these associations are causal. Genetic
             confounding could occur due to downward mobility of
             individuals at high genetic risk for psychiatric problems
             into disadvantaged environments.<h4>Methods</h4>We examined
             correlations of five indices of genetic risk [polygenic risk
             scores (PRS) for schizophrenia and depression, maternal
             psychotic symptoms, family psychiatric history, and
             zygosity-based latent genetic risk] with multiple area-,
             neighborhood-, and family-level risks during upbringing.
             Data were from the Environmental Risk (E-Risk) Longitudinal
             Twin Study, a nationally-representative cohort of 2232
             British twins born in 1994-1995 and followed to age 18 (93%
             retention). Socioenvironmental risks included urbanicity,
             air pollution, neighborhood deprivation, neighborhood crime,
             neighborhood disorder, social cohesion, residential
             mobility, family poverty, and a cumulative environmental
             risk scale. At age 18, participants were privately
             interviewed about psychotic experiences.<h4>Results</h4>Higher
             genetic risk on all indices was associated with riskier
             environments during upbringing. For example, participants
             with higher schizophrenia PRS (OR = 1.19, 95% CI =
             1.06-1.33), depression PRS (OR = 1.20, 95% CI = 1.08-1.34),
             family history (OR = 1.25, 95% CI = 1.11-1.40), and latent
             genetic risk (OR = 1.21, 95% CI = 1.07-1.38) had accumulated
             more socioenvironmental risks for schizophrenia by age 18.
             However, associations between socioenvironmental risks and
             psychotic experiences mostly remained significant after
             covariate adjustment for genetic risk.<h4>Conclusion</h4>Genetic
             risk is correlated with socioenvironmental risk for
             schizophrenia during upbringing, but the associations
             between socioenvironmental risk and adolescent psychotic
             experiences appear, at present, to exist above and beyond
             this gene-environment correlation.},
   Doi = {10.1017/s0033291720003347},
   Key = {fds352502}
}

@article{fds363069,
   Author = {Wootton, RE and Riglin, L and Blakey, R and Agnew-Blais, J and Caye, A and Cadman, T and Havdahl, A and Gonçalves, H and Menezes, AMB and Wehrmeister, FC and Rimfeld, K and Davey Smith and G and Eley, TC and Rohde, LA and Arseneault, L and Moffitt, TE and Stergiakouli, E and Thapar, A and Tilling, K},
   Title = {Decline in attention-deficit hyperactivity disorder traits
             over the life course in the general population: trajectories
             across five population birth cohorts spanning ages 3 to 45
             years.},
   Journal = {International journal of epidemiology},
   Volume = {51},
   Number = {3},
   Pages = {919-930},
   Year = {2022},
   Month = {June},
   url = {http://dx.doi.org/10.1093/ije/dyac049},
   Abstract = {<h4>Background</h4>Trajectories of attention-deficit
             hyperactivity disorder (ADHD) traits spanning early
             childhood to mid-life have not been described in general
             populations across different geographical contexts.
             Population trajectories are crucial to better understanding
             typical developmental patterns.<h4>Methods</h4>We combined
             repeated assessments of ADHD traits from five
             population-based cohorts, spanning ages 3 to 45 years. We
             used two measures: (i) the Strengths and Difficulties
             Questionnaire (SDQ) hyperactive-inattentive subscale
             (175 831 observations, 29 519 individuals); and (ii)
             scores from DSM-referenced scales (118 144 observations,
             28 685 individuals). Multilevel linear spline models
             allowed for non-linear change over time and differences
             between cohorts and raters (parent/teacher/self).<h4>Results</h4>Patterns
             of age-related change differed by measure, cohort and
             country: overall, SDQ scores decreased with age, most
             rapidly declining before age 8 years (-0.157, 95% CI:
             -0.170, -0.144 per year). The pattern was generally
             consistent using DSM scores, although with greater
             between-cohort variation. DSM scores decreased most rapidly
             between ages 14 and 17 years (-1.32%, 95% CI: -1.471,
             -1.170 per year). Average scores were consistently lower for
             females than males (SDQ: -0.818, 95% CI: -0.856, -0.780;
             DSM: -4.934%, 95% CI: -5.378, -4.489). This sex difference
             decreased over age for both measures, due to an overall
             steeper decrease for males.<h4>Conclusions</h4>ADHD trait
             scores declined from childhood to mid-life, with marked
             variation between cohorts. Our results highlight the
             importance of taking a developmental perspective when
             considering typical population traits. When interpreting
             changes in clinical cohorts, it is important to consider the
             pattern of expected change within the general population,
             which is influenced by cultural context and
             measurement.},
   Doi = {10.1093/ije/dyac049},
   Key = {fds363069}
}

@article{fds363993,
   Author = {Moffitt, TE and Caspi, A and Ambler, A and Bourassa, K and Harrington,
             H and Hogan, S and Houts, R and Ramrakha, S and Wood, SL and Poulton,
             R},
   Title = {Deep-seated psychological histories of COVID-19 vaccine
             hesitance and resistance.},
   Journal = {PNAS nexus},
   Volume = {1},
   Number = {2},
   Pages = {pgac034},
   Year = {2022},
   Month = {May},
   url = {http://dx.doi.org/10.1093/pnasnexus/pgac034},
   Abstract = {To design effective pro-vaccination messaging, it is
             important to know "where people are coming from"-the
             personal experiences and long-standing values, motives,
             lifestyles, preferences, emotional tendencies, and
             information-processing capacities of people who end up
             resistant or hesitant toward vaccination. We used
             prospective data from a 5-decade cohort study spanning
             childhood to midlife to construct comprehensive early-life
             psychological histories of groups who differed in their
             vaccine intentions in months just before COVID vaccines
             became available in their country. Vaccine-resistant and
             vaccine-hesitant participants had histories of adverse
             childhood experiences that foster mistrust, longstanding
             mental-health problems that foster misinterpretation of
             messaging, and early-emerging personality traits including
             tendencies toward extreme negative emotions, shutting down
             mentally under stress, nonconformism, and fatalism about
             health. Many vaccine-resistant and -hesitant participants
             had cognitive difficulties in comprehending health
             information. Findings held after control for socioeconomic
             origins. Vaccine intentions are not short-term isolated
             misunderstandings. They are part of a person's style of
             interpreting information and making decisions that is laid
             down before secondary school age. Findings suggest ways to
             tailor vaccine messaging for hesitant and resistant groups.
             To prepare for future pandemics, education about viruses and
             vaccines before or during secondary schooling could reduce
             citizens' level of uncertainty during a pandemic, and
             provide people with pre-existing knowledge frameworks that
             prevent extreme emotional distress reactions and enhance
             receptivity to health messages. Enhanced medical technology
             and economic resilience are important for pandemic
             preparedness, but a prepared public who understands the need
             to mask, social distance, and vaccinate will also be
             important.},
   Doi = {10.1093/pnasnexus/pgac034},
   Key = {fds363993}
}

@article{fds361942,
   Author = {Hancox, RJ and Gray, AR and Zhang, X and Poulton, R and Moffitt, TE and Caspi, A and Sears, MR},
   Title = {Differential Effects of Cannabis and Tobacco on Lung
             Function in Mid-Adult Life.},
   Journal = {American journal of respiratory and critical care
             medicine},
   Volume = {205},
   Number = {10},
   Pages = {1179-1185},
   Year = {2022},
   Month = {May},
   url = {http://dx.doi.org/10.1164/rccm.202109-2058oc},
   Abstract = {<b>Rationale:</b> Evidence suggests that the effects of
             smoking cannabis on lung function are different from
             tobacco. However, long-term follow-up data are scarce and
             mostly based on young adults. <b>Objectives:</b> To assess
             the effects of cannabis and tobacco on lung function in
             mid-adult life. <b>Methods:</b> Cannabis and tobacco use
             were reported at ages 18, 21, 26, 32, 38, and 45 years in a
             population-based cohort study of 1,037 participants.
             Spirometry, plethysmography, and carbon monoxide transfer
             factor were measured at age 45. Associations between lung
             function and cannabis use were adjusted for tobacco use.
             <b>Measurements and Main Results:</b> Data were available
             from 881 (88%) of 997 surviving participants. Cumulative
             cannabis use was associated with lower FEV<sub>1</sub>/FVC
             ratios, owing to a tendency toward higher FVCs. Cannabis use
             was also associated with higher TLC, FRC, residual volume,
             and Va along with lower midexpiratory flows, airway
             conductance, and transfer factor. Quitting regular cannabis
             use between assessments was not associated with changes in
             spirometry. <b>Conclusions:</b> Cannabis use is associated
             with higher lung volumes, suggesting hyperinflation. There
             is evidence of increased large-airway resistance and lower
             midexpiratory airflow, but impairment of FEV<sub>1</sub>/FVC
             ratio is because of higher FVC. This pattern of effects is
             different to those of tobacco. We provide the first evidence
             that lifetime cannabis use may be associated with impairment
             of gas transfer.},
   Doi = {10.1164/rccm.202109-2058oc},
   Key = {fds361942}
}

@article{fds362670,
   Author = {Meier, MH and Caspi, A and R Knodt and A and Hall, W and Ambler, A and Harrington, H and Hogan, S and M Houts and R and Poulton, R and Ramrakha,
             S and Hariri, AR and Moffitt, TE},
   Title = {Long-Term Cannabis Use and Cognitive Reserves and
             Hippocampal Volume in Midlife.},
   Journal = {The American journal of psychiatry},
   Volume = {179},
   Number = {5},
   Pages = {362-374},
   Year = {2022},
   Month = {May},
   url = {http://dx.doi.org/10.1176/appi.ajp.2021.21060664},
   Abstract = {<h4>Objective</h4>Cannabis use is increasing among midlife
             and older adults. This study tested the hypotheses that
             long-term cannabis use is associated with cognitive deficits
             and smaller hippocampal volume in midlife, which is
             important because midlife cognitive deficits and smaller
             hippocampal volume are risk factors for dementia.<h4>Methods</h4>Participants
             are members of a representative cohort of 1,037 individuals
             born in Dunedin, New Zealand, in 1972-1973 and followed to
             age 45, with 94% retention. Cannabis use and dependence were
             assessed at ages 18, 21, 26, 32, 38, and 45. IQ was assessed
             at ages 7, 9, 11, and 45. Specific neuropsychological
             functions and hippocampal volume were assessed at age
             45.<h4>Results</h4>Long-term cannabis users showed IQ
             decline from childhood to midlife (mean=-5.5 IQ points),
             poorer learning and processing speed relative to their
             childhood IQ, and informant-reported memory and attention
             problems. These deficits were specific to long-term cannabis
             users because they were either not present or were smaller
             among long-term tobacco users, long-term alcohol users,
             midlife recreational cannabis users, and cannabis quitters.
             Cognitive deficits among long-term cannabis users could not
             be explained by persistent tobacco, alcohol, or other
             illicit drug use, childhood socioeconomic status, low
             childhood self-control, or family history of substance
             dependence. Long-term cannabis users showed smaller
             hippocampal volume, but smaller hippocampal volume did not
             statistically mediate cannabis-related cognitive
             deficits.<h4>Conclusions</h4>Long-term cannabis users showed
             cognitive deficits and smaller hippocampal volume in
             midlife. Research is needed to ascertain whether long-term
             cannabis users show elevated rates of dementia in later
             life.},
   Doi = {10.1176/appi.ajp.2021.21060664},
   Key = {fds362670}
}

@article{fds362301,
   Author = {Bourassa, KJ and Moffitt, TE and Ambler, A and Hariri, AR and Harrington, H and Houts, RM and Ireland, D and Knodt, A and Poulton, R and Ramrakha, S and Caspi, A},
   Title = {Association of Treatable Health Conditions During
             Adolescence With Accelerated Aging at Midlife.},
   Journal = {JAMA pediatrics},
   Volume = {176},
   Number = {4},
   Pages = {392-399},
   Year = {2022},
   Month = {April},
   url = {http://dx.doi.org/10.1001/jamapediatrics.2021.6417},
   Abstract = {<h4>Importance</h4>Biological aging is a distinct construct
             from health; however, people who age quickly are more likely
             to experience poor health. Identifying pediatric health
             conditions associated with accelerated aging could help
             develop treatment approaches to slow midlife aging and
             prevent poor health in later life.<h4>Objective</h4>To
             examine the association between 4 treatable health
             conditions in adolescence and accelerated aging at
             midlife.<h4>Design, setting, and participants</h4>This
             cohort study analyzed data from participants in the Dunedin
             Study, a longitudinal investigation of health and behavior
             among a birth cohort born between April 1, 1972, and March
             31, 1973, in Dunedin, New Zealand, and followed up until age
             45 years. Participants underwent an assessment at age 45
             years and had data for at least 1 adolescent health
             condition (asthma, smoking, obesity, and psychological
             disorders) and outcome measure (pace of aging, gait speed,
             brain age, and facial age). Data analysis was performed from
             February 11 to September 27, 2021.<h4>Exposures</h4>Asthma,
             cigarette smoking, obesity, and psychological disorders were
             assessed at age 11, 13, and 15 years.<h4>Main outcomes and
             measures</h4>The outcome was a midlife aging factor
             composite score comprising 4 measures of biological aging:
             pace of aging, gait speed, brain age (specifically, BrainAGE
             score), and facial age.<h4>Results</h4>A total of 910
             participants (459 men [50.4%]) met the inclusion criteria,
             including an assessment at age 45 years. Participants who
             had smoked daily (0.61 [95% CI, 0.43-0.79] SD units), had
             obesity (0.82 [95% CI, 0.59-1.06] SD units), or had a
             psychological disorder diagnosis (0.43 [95% CI, 0.29-0.56]
             SD units) during adolescence were biologically older at
             midlife compared with participants without these conditions.
             Participants with asthma were not biologically older at
             midlife (0.02 [95% CI, -0.14 to 0.19] SD units) compared
             with those without asthma. These results remained unchanged
             after adjusting for childhood risk factors such as poor
             health, socioeconomic disadvantage, and adverse
             experiences.<h4>Conclusions and relevance</h4>This study
             found that adolescent smoking, obesity, and psychological
             disorder diagnoses were associated with older biological age
             at midlife. These health conditions could be treated during
             adolescence to reduce the risk of accelerated biological
             aging later in life.},
   Doi = {10.1001/jamapediatrics.2021.6417},
   Key = {fds362301}
}

@article{fds362302,
   Author = {Richmond-Rakerd, LS and D'Souza, S and Milne, BJ and Caspi, A and Moffitt, TE},
   Title = {Longitudinal Associations of Mental Disorders With Dementia:
             30-Year Analysis of 1.7 Million New Zealand
             Citizens.},
   Journal = {JAMA psychiatry},
   Volume = {79},
   Number = {4},
   Pages = {333-340},
   Year = {2022},
   Month = {April},
   url = {http://dx.doi.org/10.1001/jamapsychiatry.2021.4377},
   Abstract = {<h4>Importance</h4>Mental disorders are an underappreciated
             category of modifiable risk factors for dementia. Developing
             an evidence base about the link between mental disorders and
             dementia risk requires studies that use large,
             representative samples, consider the full range of
             psychiatric conditions, ascertain mental disorders from
             early life, use long follow-ups, and distinguish between
             Alzheimer disease and related dementias.<h4>Objective</h4>To
             test whether mental disorders antedate dementia across 3
             decades of observation.<h4>Design, setting, and
             participants</h4>This population-based administrative
             register study of mental disorders and Alzheimer disease and
             related dementias included all individuals born in New
             Zealand between 1928 and 1967 who resided in the country for
             any time during the 30-year observation period between July
             1988 and June 2018. Data were from the New Zealand
             Integrated Data Infrastructure, a collection of
             whole-of-population administrative data sources linked at
             the individual level. Data were analyzed from October 2020
             to November 2021.<h4>Exposures</h4>Diagnoses of mental
             disorders were ascertained from public-hospital
             records.<h4>Main outcomes and measures</h4>Diagnoses of
             dementia were ascertained from public-hospital records,
             mortality records, and pharmaceutical records.<h4>Results</h4>Of
             1 711 386 included individuals, 866 301 (50.6%) were
             male, and individuals were aged 21 to 60 years at baseline.
             Relative to individuals without a mental disorder, those
             with a mental disorder were at increased risk of developing
             subsequent dementia (relative risk [RR], 4.24; 95% CI,
             4.07-4.42; hazard ratio, 6.49; 95% CI, 6.25-6.73). Among
             individuals with dementia, those with a mental disorder
             developed dementia a mean of 5.60 years (95% CI, 5.31-5.90)
             earlier than those without a mental disorder. Associations
             held across sex and age and after accounting for preexisting
             chronic physical diseases and socioeconomic deprivation.
             Associations were present across different types of mental
             disorders and self-harm behavior (RRs ranged from 2.93 [95%
             CI, 2.66-3.21] for neurotic disorders to 6.20 [95% CI,
             5.67-6.78] for psychotic disorders), and were evident for
             Alzheimer disease (RR, 2.76; 95% CI, 2.45-3.11) and all
             other dementias (RR, 5.85; 95% CI, 5.58-6.13).<h4>Conclusions
             and relevance</h4>In this study, mental disorders were
             associated with the onset of dementia in the population.
             Ameliorating mental disorders in early life might also
             ameliorate neurodegenerative conditions and extend quality
             of life in old age.},
   Doi = {10.1001/jamapsychiatry.2021.4377},
   Key = {fds362302}
}

@article{fds361944,
   Author = {Latham, RM and Kieling, C and Arseneault, L and Kohrt, BA and Moffitt,
             TE and Rasmussen, LJH and Rocha, TB-M and Mondelli, V and Fisher,
             HL},
   Title = {Longitudinal associations between adolescents'
             individualised risk for depression and inflammation in a UK
             cohort study.},
   Journal = {Brain Behav Immun},
   Volume = {101},
   Pages = {78-83},
   Year = {2022},
   Month = {March},
   url = {http://dx.doi.org/10.1016/j.bbi.2021.12.027},
   Abstract = {Inflammation is associated with poor physical and mental
             health including major depressive disorder (MDD). Moreover,
             there is evidence that childhood adversity - a risk factor
             for MDD - becomes biologically embedded via elevated
             inflammation. However, the risk of developing MDD arises
             from multiple sources and yet there has been little
             investigation of the links between individuals'
             constellation of MDD risk and subsequent inflammation. We
             therefore examined associations between individual risk for
             MDD calculated in early adolescence and levels of
             inflammation six years later. We use data from the
             Environmental Risk (E-Risk) Longitudinal Twin Study, a
             nationally representative UK birth cohort of 2,232 children
             followed to age 18 with 93% retention. Participants'
             individual risk for developing future MDD was calculated at
             age 12 using a recently developed prediction model
             comprising multiple psychosocial factors. Plasma levels of
             three inflammation biomarkers were measured at age 18:
             C-reactive protein (CRP), interleukin-6 (IL-6), and a newer
             biomarker, soluble urokinase plasminogen activator receptor
             (suPAR), which is thought to reflect the level of systemic
             chronic inflammation. MDD risk scores calculated at age 12
             were positively associated with levels of suPAR (but not CRP
             or IL-6) at age 18 after adjusting for key covariates
             (b = 1.70, 95% CI = 0.46 - 2.95, p = 0.007).
             Adolescents at high risk of MDD (risk scores ≥ 90th
             centile) had significantly higher mean levels of suPAR six
             years later than adolescents who had been identified as low
             risk (risk scores ≤ 10th centile) (b = 0.41, 95%
             CI = 0.18 - 0.64, p < 0.001). Findings support the
             notion that childhood psychosocial risk for MDD leads to
             increased levels of low-grade inflammation. If replicated in
             studies with repeated assessments of inflammation biomarkers
             throughout childhood and adolescence, these findings would
             support targeted interventions to reduce inflammation, as
             measured by suPAR, for adolescents at high risk of MDD to
             potentially prevent development of depression and physical
             health problems related to chronic inflammation.},
   Doi = {10.1016/j.bbi.2021.12.027},
   Key = {fds361944}
}

@article{fds352898,
   Author = {Matthews, T and Caspi, A and Danese, A and Fisher, HL and Moffitt, TE and Arseneault, L},
   Title = {A longitudinal twin study of victimization and loneliness
             from childhood to young adulthood.},
   Journal = {Development and psychopathology},
   Volume = {34},
   Number = {1},
   Pages = {367-377},
   Year = {2022},
   Month = {February},
   url = {http://dx.doi.org/10.1017/s0954579420001005},
   Abstract = {The present study used a longitudinal and discordant twin
             design to explore in depth the developmental associations
             between victimization and loneliness from mid-childhood to
             young adulthood. The data were drawn from the Environmental
             Risk (E-Risk) Longitudinal Twin Study, a birth cohort of
             2,232 individuals born in England and Wales during
             1994-1995. Diverse forms of victimization were considered,
             differing across context, perpetrator, and timing of
             exposure. The results indicated that exposure to different
             forms of victimization was associated with loneliness in a
             dose-response manner. In childhood, bullying victimization
             was uniquely associated with loneliness, over and above
             concurrent psychopathology, social isolation, and genetic
             risk. Moreover, childhood bullying victimization continued
             to predict loneliness in young adulthood, even in the
             absence of ongoing victimization. Within-twin pair analyses
             further indicated that this longitudinal association was
             explained by genetic confounds. In adolescence, varied forms
             of victimization were correlated with young adult
             loneliness, with maltreatment, neglect, and
             cybervictimization remaining robust to controls for genetic
             confounds. These findings indicate that vulnerability to
             loneliness in victimized young people varies according to
             the specific form of victimization in question, and also to
             the developmental period in which it was
             experienced.},
   Doi = {10.1017/s0954579420001005},
   Key = {fds352898}
}

@article{fds361150,
   Author = {Pedersen, W and Moffitt, TE and von Soest, T},
   Title = {Privileged background protects against drug charges: A
             long-term population-based longitudinal study.},
   Journal = {The International journal on drug policy},
   Volume = {100},
   Pages = {103491},
   Year = {2022},
   Month = {February},
   url = {http://dx.doi.org/10.1016/j.drugpo.2021.103491},
   Abstract = {<h4>Background</h4>We investigated the importance of
             indicators of parental socio-economic status (SES) for
             getting an official drug charge, while we controlled for
             self-reported drug law infractions (use of illegal drugs
             and/or drug trafficking) and potential variables confounding
             the association.<h4>Methods</h4>We used data from the
             long-term, population based longitudinal Young in Norway
             Study (N = 2,549). Participants were followed up over four
             survey-based data collections with linkages to crime
             registers from adolescence to adulthood. Data on drug
             charges were assessed based on official registers. The use
             of illegal substances, involvement with drug trafficking and
             potential covariates such as involvement with other types of
             crime, academic resources, and risk factors in the family,
             were assessed by means of self-reports.<h4>Results</h4>Two
             per cent had been charged for drug-related offences, and 37%
             reported drug offending. Use of cannabis was the primary
             infraction statistically related to a criminal charge.
             Having parents with 4+ years university education (14% of
             the sample) was associated with lower risk for being charged
             than having parents with no higher education (OR 4.87; 95%
             CI: 1.16-20.52) or with a short university education (OR
             4.76; 1.05-21.48). The association between parental
             education and drug charges remained stable when controlling
             for self-reported drug law infractions and other potential
             covariates.<h4>Conclusion</h4>In Norway, adolescents who
             have parents with higher university education, may be
             protected from getting a drug charge, even though they
             report similar levels of drug law infractions as other
             adolescents.},
   Doi = {10.1016/j.drugpo.2021.103491},
   Key = {fds361150}
}

@article{fds355032,
   Author = {Matthews, T and Fisher, HL and Bryan, BT and Danese, A and Moffitt, TE and Qualter, P and Verity, L and Arseneault, L},
   Title = {This is what loneliness looks like: A mixed-methods study of
             loneliness in adolescence and young adulthood.},
   Journal = {International journal of behavioral development},
   Volume = {46},
   Number = {1},
   Pages = {18-27},
   Year = {2022},
   Month = {January},
   url = {http://dx.doi.org/10.1177/0165025420979357},
   Abstract = {The present study used quantitative and qualitative methods
             to explore how lonely young people are seen from others'
             perspectives, in terms of their personality, behaviour and
             life circumstances. Data were drawn from the Environmental
             Risk Longitudinal Twin Study, a cohort of 2,232 individuals
             born in the United Kingdom in the mid-1990s. When
             participants were aged 18, they provided self-reports of
             loneliness, and informant ratings of loneliness were
             provided by interviewers, as well as participants' parents
             and siblings. Interviewers further provided Big Five
             personality ratings, and detailed written notes in which
             they documented their perceptions of the participants and
             their reflections on the content of the interview. In the
             quantitative section of the paper, regression analyses were
             used to examine the perceptibility of loneliness, and how
             participants' loneliness related to their perceived
             personality traits. The informant ratings of participants'
             loneliness showed good agreement with self-reports.
             Furthermore, loneliness was associated with lower perceived
             conscientiousness, agreeableness and extraversion, and
             higher perceived neuroticism. Within-twin pair analyses
             indicated that these associations were partly explained by
             common underlying genetic influences. In the qualitative
             section of the study, the loneliest 5% of study participants
             (N=108) were selected, and thematic analysis was applied to
             the study' interviewers' notes about those participants.
             Three themes were identified and named: 'uncomfortable in
             own skin', 'clustering of risk', and 'difficulties accessing
             social resources'. These results add depth to the current
             conceptualisation of loneliness, and emphasise the
             complexity and intersectional nature of the circumstances
             severely lonely young adults live in.},
   Doi = {10.1177/0165025420979357},
   Key = {fds355032}
}

@article{fds361943,
   Author = {Belsky, DW and Caspi, A and Corcoran, DL and Sugden, K and Poulton, R and Arseneault, L and Baccarelli, A and Chamarti, K and Gao, X and Hannon,
             E and Harrington, HL and Houts, R and Kothari, M and Kwon, D and Mill, J and Schwartz, J and Vokonas, P and Wang, C and Williams, BS and Moffitt,
             TE},
   Title = {DunedinPACE, a DNA methylation biomarker of the pace of
             aging.},
   Journal = {eLife},
   Volume = {11},
   Pages = {e73420},
   Year = {2022},
   Month = {January},
   url = {http://dx.doi.org/10.7554/elife.73420},
   Abstract = {<h4>Background</h4>Measures to quantify changes in the pace
             of biological aging in response to intervention are needed
             to evaluate geroprotective interventions for humans.
             Previously, we showed that quantification of the pace of
             biological aging from a DNA-methylation blood test was
             possible (Belsky et al., 2020). Here, we report a
             next-generation DNA-methylation biomarker of Pace of Aging,
             DunedinPACE (for Pace of Aging Calculated from the
             Epigenome).<h4>Methods</h4>We used data from the Dunedin
             Study 1972-1973 birth cohort tracking within-individual
             decline in 19 indicators of organ-system integrity across
             four time points spanning two decades to model Pace of
             Aging. We distilled this two-decade Pace of Aging into a
             single-time-point DNA-methylation blood-test using
             elastic-net regression and a DNA-methylation dataset
             restricted to exclude probes with low test-retest
             reliability. We evaluated the resulting measure, named
             DunedinPACE, in five additional datasets.<h4>Results</h4>DunedinPACE
             showed high test-retest reliability, was associated with
             morbidity, disability, and mortality, and indicated faster
             aging in young adults with childhood adversity. DunedinPACE
             effect-sizes were similar to GrimAge Clock effect-sizes. In
             analysis of incident morbidity, disability, and mortality,
             DunedinPACE and added incremental prediction beyond
             GrimAge.<h4>Conclusions</h4>DunedinPACE is a novel blood
             biomarker of the pace of aging for gerontology and
             geroscience.<h4>Funding</h4>This research was supported by
             US-National Institute on Aging grants AG032282, AG061378,
             AG066887, and UK Medical Research Council grant
             MR/P005918/1.},
   Doi = {10.7554/elife.73420},
   Key = {fds361943}
}

@article{fds367503,
   Author = {Reuben, A and Moffitt, TE and Abraham, WC and Ambler, A and Elliott, ML and Hariri, AR and Harrington, H and Hogan, S and Houts, RM and Ireland, D and Knodt, AR and Leung, J and Pearson, A and Poulton, R and Purdy, SC and Ramrakha, S and Rasmussen, LJH and Sugden, K and Thorne, PR and Williams, B and Wilson, G and Caspi, A},
   Title = {Improving risk indexes for Alzheimer's disease and related
             dementias for use in midlife.},
   Journal = {Brain communications},
   Volume = {4},
   Number = {5},
   Pages = {fcac223},
   Year = {2022},
   Month = {January},
   url = {http://dx.doi.org/10.1093/braincomms/fcac223},
   Abstract = {Knowledge of a person's risk for Alzheimer's disease and
             related dementias (ADRDs) is required to triage candidates
             for preventive interventions, surveillance, and treatment
             trials. ADRD risk indexes exist for this purpose, but each
             includes only a subset of known risk factors. Information
             missing from published indexes could improve risk
             prediction. In the Dunedin Study of a population-representative
             New Zealand-based birth cohort followed to midlife
             (<i>N</i> = 938, 49.5% female), we compared associations
             of four leading risk indexes with midlife antecedents of
             ADRD against a novel benchmark index comprised of nearly all
             known ADRD risk factors, the Dunedin ADRD Risk Benchmark
             (DunedinARB). Existing indexes included the Cardiovascular
             Risk Factors, Aging, and Dementia index (CAIDE), LIfestyle
             for BRAin health index (LIBRA), Australian National
             University Alzheimer's Disease Risk Index (ANU-ADRI), and
             risks selected by the Lancet Commission on Dementia. The
             Dunedin benchmark was comprised of 48 separate indicators of
             risk organized into 10 conceptually distinct risk domains.
             Midlife antecedents of ADRD treated as outcome measures
             included age-45 measures of brain structural integrity
             [magnetic resonance imaging-assessed: (i)
             machine-learning-algorithm-estimated brain age, (ii)
             log-transformed volume of white matter hyperintensities, and
             (iii) mean grey matter volume of the hippocampus] and
             measures of brain functional integrity [(i) objective
             cognitive function assessed via the Wechsler Adult
             Intelligence Scale-IV, (ii) subjective problems in everyday
             cognitive function, and (iii) objective cognitive decline
             measured as residualized change in cognitive scores from
             childhood to midlife on matched Weschler Intelligence
             scales]. All indexes were quantitatively distributed and
             proved informative about midlife antecedents of ADRD,
             including algorithm-estimated brain age (<i>β</i>'s from
             0.16 to 0.22), white matter hyperintensities volume
             (<i>β</i>'s from 0.16 to 0.19), hippocampal volume
             (<i>β</i>'s from -0.08 to -0.11), tested cognitive deficits
             (<i>β</i>'s from -0.36 to -0.49), everyday cognitive
             problems (<i>β</i>'s from 0.14 to 0.38), and longitudinal
             cognitive decline (<i>β</i>'s from -0.18 to -0.26).
             Existing indexes compared favourably to the comprehensive
             benchmark in their association with the brain structural
             integrity measures but were outperformed in their
             association with the functional integrity measures,
             particularly subjective cognitive problems and tested
             cognitive decline. Results indicated that existing indexes
             could be improved with targeted additions, particularly of
             measures assessing socioeconomic status, physical and
             sensory function, epigenetic aging, and subjective overall
             health. Existing premorbid ADRD risk indexes perform well in
             identifying linear gradients of risk among members of the
             general population at midlife, even when they include only a
             small subset of potential risk factors. They could be
             improved, however, with targeted additions to more
             holistically capture the different facets of risk for this
             multiply determined, age-related disease.},
   Doi = {10.1093/braincomms/fcac223},
   Key = {fds367503}
}

@article{fds359350,
   Author = {Lay-Yee, R and Matthews, T and Moffitt, T and Poulton, R and Caspi, A and Milne, B},
   Title = {Do socially isolated children become socially isolated
             adults?},
   Journal = {Advances in life course research},
   Volume = {50},
   Pages = {100419},
   Year = {2021},
   Month = {December},
   url = {http://dx.doi.org/10.1016/j.alcr.2021.100419},
   Abstract = {Social isolation - the lack of social contacts in number and
             frequency - has been shown to have a negative impact on
             health and well-being. Using group-based trajectory analysis
             of longitudinal data from a New Zealand birth cohort, we
             created a typology of social isolation based on onset during
             the life course and persistence into adulthood. We then
             characterized each type according to risk factors related to
             family environment and child behavior that have been shown
             previously to be associated with social isolation. Based on
             fit statistics and distinctness of trajectories we
             considered the four-class model to be the most appropriate:
             (1) 'never isolated' (71.6 % of the cohort), (2) 'adult
             only' (10.1 %), (3) 'child only' (14.3 %), and (4)
             'persistent isolation' (4.0 %). Family-environmental factors
             - i.e. having a teen-aged mother, having a single parent,
             frequent changes in residence, or maltreatment - tended to
             be associated with both child and adult onset and
             persistence of social isolation, whereas child-behavioral
             factors - i.e. self-control or internalizing symptoms -
             applied more to the child onset of social isolation.
             Sensitivity analyses using empirically defined groups -
             based on 15 % 'cut-offs' for isolation in childhood and
             adulthood - produced similar life-course groupings and
             similar associations. Our findings provide insights into the
             development of social isolation and demonstrate the
             changeability of social isolation across almost four decades
             of the life span. They also suggest family-based and
             child-based interventions could address child onset and the
             persistence of social isolation into adulthood.},
   Doi = {10.1016/j.alcr.2021.100419},
   Key = {fds359350}
}

@article{fds357259,
   Author = {Becker, J and Burik, CAP and Goldman, G and Wang, N and Jayashankar, H and Bennett, M and Belsky, DW and Karlsson Linnér and R and Ahlskog, R and Kleinman, A and Hinds, DA and 23andMe Research Group, and Caspi, A and Corcoran, DL and Moffitt, TE and Poulton, R and Sugden, K and Williams,
             BS and Harris, KM and Steptoe, A and Ajnakina, O and Milani, L and Esko, T and Iacono, WG and McGue, M and Magnusson, PKE and Mallard, TT and Harden,
             KP and Tucker-Drob, EM and Herd, P and Freese, J and Young, A and Beauchamp, JP and Koellinger, PD and Oskarsson, S and Johannesson, M and Visscher, PM and Meyer, MN and Laibson, D and Cesarini, D and Benjamin,
             DJ and Turley, P and Okbay, A},
   Title = {Resource profile and user guide of the Polygenic Index
             Repository.},
   Journal = {Nature human behaviour},
   Volume = {5},
   Number = {12},
   Pages = {1744-1758},
   Year = {2021},
   Month = {December},
   url = {http://dx.doi.org/10.1038/s41562-021-01119-3},
   Abstract = {Polygenic indexes (PGIs) are DNA-based predictors. Their
             value for research in many scientific disciplines is growing
             rapidly. As a resource for researchers, we used a consistent
             methodology to construct PGIs for 47 phenotypes in 11
             datasets. To maximize the PGIs' prediction accuracies, we
             constructed them using genome-wide association studies-some
             not previously published-from multiple data sources,
             including 23andMe and UK Biobank. We present a theoretical
             framework to help interpret analyses involving PGIs. A key
             insight is that a PGI can be understood as an unbiased but
             noisy measure of a latent variable we call the 'additive SNP
             factor'. Regressions in which the true regressor is this
             factor but the PGI is used as its proxy therefore suffer
             from errors-in-variables bias. We derive an estimator that
             corrects for the bias, illustrate the correction, and make a
             Python tool for implementing it publicly
             available.},
   Doi = {10.1038/s41562-021-01119-3},
   Key = {fds357259}
}

@article{fds358109,
   Author = {Bourassa, KJ and Rasmussen, LJH and Danese, A and Eugen-Olsen, J and Harrington, H and Houts, R and Poulton, R and Ramrakha, S and Sugden, K and Williams, B and Moffitt, TE and Caspi, A},
   Title = {Linking stressful life events and chronic inflammation using
             suPAR (soluble urokinase plasminogen activator
             receptor).},
   Journal = {Brain, behavior, and immunity},
   Volume = {97},
   Pages = {79-88},
   Year = {2021},
   Month = {October},
   url = {http://dx.doi.org/10.1016/j.bbi.2021.06.018},
   Abstract = {Stressful life events have been linked to declining health,
             and inflammation has been proposed as a physiological
             mechanism that might explain this association. Using 828
             participants from the Dunedin Longitudinal Study, we tested
             whether people who experienced more stressful life events
             during adulthood would show elevated systemic inflammation
             when followed up in midlife, at age 45. We studied three
             inflammatory biomarkers: C-reactive protein (CRP),
             interleukin-6 (IL-6), and a newer biomarker, soluble
             urokinase plasminogen activator receptor (suPAR), which is
             thought to index systemic chronic inflammation. Stressful
             life events were not associated with CRP or IL-6. However,
             people who experienced more stressful life events from age
             38 to 44 had elevated suPAR at age 45, and had significantly
             greater increases in suPAR from baseline to follow-up across
             the same period. When examining stressful life events across
             the lifespan, both adverse childhood experiences (ACEs) and
             adult stressful life events were independently associated
             with suPAR at age 45. ACEs moderated the association of
             adult stressful life events and suPAR at age 45-children
             with more ACEs showed higher suPAR levels after experiencing
             stressful life events as adults. The results suggest
             systemic chronic inflammation is one physiological mechanism
             that could link stressful life events and health, and
             support the use of suPAR as a useful biomarker for such
             research.},
   Doi = {10.1016/j.bbi.2021.06.018},
   Key = {fds358109}
}

@article{fds359678,
   Author = {Carlisi, CO and Moffitt, TE and Knodt, AR and Harrington, H and Langevin, S and Ireland, D and Melzer, TR and Poulton, R and Ramrakha,
             S and Caspi, A and Hariri, AR and Viding, E},
   Title = {Association of subcortical gray-matter volumes with
             life-course-persistent antisocial behavior in a
             population-representative longitudinal birth
             cohort.},
   Journal = {Development and psychopathology},
   Pages = {1-11},
   Year = {2021},
   Month = {October},
   url = {http://dx.doi.org/10.1017/s0954579421000377},
   Abstract = {Neuropsychological evidence supports the developmental
             taxonomy theory of antisocial behavior, suggesting that
             abnormal brain development distinguishes
             life-course-persistent from adolescence-limited antisocial
             behavior. Recent neuroimaging work confirmed that
             prospectively-measured life-course-persistent antisocial
             behavior is associated with differences in cortical brain
             structure. Whether this extends to subcortical brain
             structures remains uninvestigated. This study compared
             subcortical gray-matter volumes between 672 members of the
             Dunedin Study previously defined as exhibiting
             life-course-persistent, adolescence-limited or low-level
             antisocial behavior based on repeated assessments at ages
             7-26 years. Gray-matter volumes of 10 subcortical structures
             were compared across groups. The life-course-persistent
             group had lower volumes of amygdala, brain stem, cerebellum,
             hippocampus, pallidum, thalamus, and ventral diencephalon
             compared to the low-antisocial group. Differences between
             life-course-persistent and adolescence-limited individuals
             were comparable in effect size to differences between
             life-course-persistent and low-antisocial individuals, but
             were not statistically significant due to less statistical
             power. Gray-matter volumes in adolescence-limited
             individuals were near the norm in this population-representative
             cohort and similar to volumes in low-antisocial individuals.
             Although this study could not establish causal links between
             brain volume and antisocial behavior, it constitutes new
             biological evidence that all people with antisocial behavior
             are not the same, supporting a need for greater
             developmental and diagnostic precision in clinical,
             forensic, and policy-based interventions.},
   Doi = {10.1017/s0954579421000377},
   Key = {fds359678}
}

@article{fds359679,
   Author = {van Dongen, J and Gordon, SD and McRae, AF and Odintsova, VV and Mbarek,
             H and Breeze, CE and Sugden, K and Lundgren, S and Castillo-Fernandez,
             JE and Hannon, E and Moffitt, TE and Hagenbeek, FA and van
             Beijsterveldt, CEM and Jan Hottenga and J and Tsai, P-C and BIOS
             Consortium, and Genetics of DNA Methylation Consortium, and Min,
             JL and Hemani, G and Ehli, EA and Paul, F and Stern, CD and Heijmans, BT and Slagboom, PE and Daxinger, L and van der Maarel, SM and de Geus, EJC and Willemsen, G and Montgomery, GW and Reversade, B and Ollikainen, M and Kaprio, J and Spector, TD and Bell, JT and Mill, J and Caspi, A and Martin,
             NG and Boomsma, DI},
   Title = {Identical twins carry a persistent epigenetic signature of
             early genome programming.},
   Journal = {Nature communications},
   Volume = {12},
   Number = {1},
   Pages = {5618},
   Year = {2021},
   Month = {September},
   url = {http://dx.doi.org/10.1038/s41467-021-25583-7},
   Abstract = {Monozygotic (MZ) twins and higher-order multiples arise when
             a zygote splits during pre-implantation stages of
             development. The mechanisms underpinning this event have
             remained a mystery. Because MZ twinning rarely runs in
             families, the leading hypothesis is that it occurs at
             random. Here, we show that MZ twinning is strongly
             associated with a stable DNA methylation signature in adult
             somatic tissues. This signature spans regions near telomeres
             and centromeres, Polycomb-repressed regions and
             heterochromatin, genes involved in cell-adhesion, WNT
             signaling, cell fate, and putative human metastable
             epialleles. Our study also demonstrates a never-anticipated
             corollary: because identical twins keep a lifelong molecular
             signature, we can retrospectively diagnose if a person was
             conceived as monozygotic twin.},
   Doi = {10.1038/s41467-021-25583-7},
   Key = {fds359679}
}

@article{fds359348,
   Author = {Min, JL and Hemani, G and Hannon, E and Dekkers, KF and Castillo-Fernandez, J and Luijk, R and Carnero-Montoro, E and Lawson,
             DJ and Burrows, K and Suderman, M and Bretherick, AD and Richardson, TG and Klughammer, J and Iotchkova, V and Sharp, G and Al Khleifat and A and Shatunov, A and Iacoangeli, A and McArdle, WL and Ho, KM and Kumar, A and Söderhäll, C and Soriano-Tárraga, C and Giralt-Steinhauer, E and Kazmi, N and Mason, D and McRae, AF and Corcoran, DL and Sugden, K and Kasela, S and Cardona, A and Day, FR and Cugliari, G and Viberti, C and Guarrera, S and Lerro, M and Gupta, R and Bollepalli, S and Mandaviya,
             P and Zeng, Y and Clarke, T-K and Walker, RM and Schmoll, V and Czamara, D and Ruiz-Arenas, C and Rezwan, FI and Marioni, RE and Lin, T and Awaloff, Y and Germain, M and Aïssi, D and Zwamborn, R and van Eijk, K and Dekker, A and van Dongen, J and Hottenga, J-J and Willemsen, G and Xu, C-J and Barturen, G and Català-Moll, F and Kerick, M and Wang, C and Melton, P and Elliott, HR and Shin, J and Bernard, M and Yet, I and Smart, M and Gorrie-Stone, T and BIOS Consortium, and Shaw, C and Al Chalabi and A and Ring, SM and Pershagen, G and Melén, E and Jiménez-Conde, J and Roquer, J and Lawlor, DA and Wright, J and Martin, NG and Montgomery,
             GW and Moffitt, TE and Poulton, R and Esko, T and Milani, L and Metspalu,
             A and Perry, JRB and Ong, KK and Wareham, NJ and Matullo, G and Sacerdote,
             C and Panico, S and Caspi, A and Arseneault, L and Gagnon, F and Ollikainen, M and Kaprio, J and Felix, JF and Rivadeneira, F and Tiemeier, H and van IJzendoorn, MH and Uitterlinden, AG and Jaddoe,
             VWV and Haley, C and McIntosh, AM and Evans, KL and Murray, A and Räikkönen, K and Lahti, J and Nohr, EA and Sørensen, TIA and Hansen,
             T and Morgen, CS and Binder, EB and Lucae, S and Gonzalez, JR and Bustamante, M and Sunyer, J and Holloway, JW and Karmaus, W and Zhang,
             H and Deary, IJ and Wray, NR and Starr, JM and Beekman, M and van Heemst,
             D and Slagboom, PE and Morange, P-E and Trégouët, D-A and Veldink, JH and Davies, GE and de Geus, EJC and Boomsma, DI and Vonk, JM and Brunekreef,
             B and Koppelman, GH and Alarcón-Riquelme, ME and Huang, R-C and Pennell, CE and van Meurs, J and Ikram, MA and Hughes, AD and Tillin, T and Chaturvedi, N and Pausova, Z and Paus, T and Spector, TD and Kumari, M and Schalkwyk, LC and Visscher, PM and Davey Smith and G and Bock, C and Gaunt,
             TR and Bell, JT and Heijmans, BT and Mill, J and Relton,
             CL},
   Title = {Genomic and phenotypic insights from an atlas of genetic
             effects on DNA methylation.},
   Journal = {Nature genetics},
   Volume = {53},
   Number = {9},
   Pages = {1311-1321},
   Year = {2021},
   Month = {September},
   url = {http://dx.doi.org/10.1038/s41588-021-00923-x},
   Abstract = {Characterizing genetic influences on DNA methylation (DNAm)
             provides an opportunity to understand mechanisms
             underpinning gene regulation and disease. In the present
             study, we describe results of DNAm quantitative trait locus
             (mQTL) analyses on 32,851 participants, identifying genetic
             variants associated with DNAm at 420,509 DNAm sites in
             blood. We present a database of >270,000 independent mQTLs,
             of which 8.5% comprise long-range (trans) associations.
             Identified mQTL associations explain 15-17% of the additive
             genetic variance of DNAm. We show that the genetic
             architecture of DNAm levels is highly polygenic. Using
             shared genetic control between distal DNAm sites, we
             constructed networks, identifying 405 discrete genomic
             communities enriched for genomic annotations and complex
             traits. Shared genetic variants are associated with both
             DNAm levels and complex diseases, but only in a minority of
             cases do these associations reflect causal relationships
             from DNAm to trait or vice versa, indicating a more complex
             genotype-phenotype map than previously anticipated.},
   Doi = {10.1038/s41588-021-00923-x},
   Key = {fds359348}
}

@article{fds358969,
   Author = {Wertz, J and Israel, S and Arseneault, L and Belsky, DW and Bourassa,
             KJ and Harrington, H and Houts, R and Poulton, R and Richmond-Rakerd,
             LS and Røysamb, E and Moffitt, TE and Caspi, A},
   Title = {Vital personality scores and healthy aging: Life-course
             associations and familial transmission.},
   Journal = {Social science & medicine (1982)},
   Volume = {285},
   Pages = {114283},
   Year = {2021},
   Month = {September},
   url = {http://dx.doi.org/10.1016/j.socscimed.2021.114283},
   Abstract = {<h4>Objectives</h4>Personality traits are linked with
             healthy aging, but it is not clear how these associations
             come to manifest across the life-course and across
             generations. To study this question, we tested a series of
             hypotheses about (a) personality-trait prediction of markers
             of healthy aging across the life-course, (b) developmental
             origins, stability and change of links between personality
             and healthy aging across time, and (c) intergenerational
             transmission of links between personality and healthy aging.
             For our analyses we used a measure that aggregates the
             contributions of Big 5 personality traits to healthy aging:
             a "vital personality" score.<h4>Methods</h4>Data came from
             two population-based longitudinal cohort studies, one based
             in New Zealand and the other in the UK, comprising over 6000
             study members across two generations, and spanning an age
             range from birth to late life.<h4>Results</h4>Our analyses
             revealed three main findings: first, individuals with higher
             vital personality scores engaged in fewer health-risk
             behaviors, aged slower, and lived longer. Second,
             individuals' vital personality scores were preceded by
             differences in early-life temperament and were relatively
             stable across adulthood, but also increased from young
             adulthood to midlife. Third, individuals with higher vital
             personality scores had children with similarly vital
             partners, promoted healthier behaviors in their children,
             and had children who grew up to have more vital personality
             scores themselves, for genetic and environmental
             reasons.<h4>Conclusion</h4>Our study shows how the health
             benefits associated with personality accrue throughout the
             life-course and across generations.},
   Doi = {10.1016/j.socscimed.2021.114283},
   Key = {fds358969}
}

@article{fds355028,
   Author = {Agnew-Blais, JC and Belsky, DW and Caspi, A and Danese, A and Moffitt,
             TE and Polanczyk, GV and Sugden, K and Wertz, J and Williams, BS and Lewis,
             CM and Arseneault, L},
   Title = {Polygenic Risk and the Course of Attention-Deficit/Hyperactivity
             Disorder From Childhood to Young Adulthood: Findings From a
             Nationally Representative Cohort.},
   Journal = {Journal of the American Academy of Child and Adolescent
             Psychiatry},
   Volume = {60},
   Number = {9},
   Pages = {1147-1156},
   Year = {2021},
   Month = {September},
   url = {http://dx.doi.org/10.1016/j.jaac.2020.12.033},
   Abstract = {<h4>Objective</h4>To understand whether genetic risk for
             attention-deficit/hyperactivity disorder (ADHD) is
             associated with the course of the disorder across childhood
             and into young adulthood.<h4>Method</h4>Participants were
             from the Environmental Risk (E-Risk) Longitudinal Twin
             Study, a population-based birth cohort of 2,232 twins. ADHD
             was assessed at ages 5, 7, 10, and 12 with mother- and
             teacher-reports and at age 18 with self-report. Polygenic
             risk scores (PRSs) were created using a genome-wide
             association study of ADHD case status. Associations with PRS
             were examined at multiple points in childhood and
             longitudinally from early childhood to adolescence. We
             investigated ADHD PRS and course to young adulthood, as
             reflected by ADHD remission, persistence, and late
             onset.<h4>Results</h4>Participants with higher ADHD PRSs had
             increased risk for meeting ADHD diagnostic criteria (odds
             ratios ranging from 1.17 at age 10 to 1.54 at age 12) and
             for elevated symptoms at ages 5, 7, 10, and 12. Higher PRS
             was longitudinally associated with more hyperactivity/impulsivity
             (incidence rate ratio = 1.18) and inattention (incidence
             rate ratio = 1.14) from age 5 to age 12. In young
             adulthood, participants with persistent ADHD exhibited the
             highest PRS (mean PRS = 0.37), followed by participants
             with remission (mean PRS = 0.21); both groups had higher
             PRS than controls (mean PRS = -0.03), but did not
             significantly differ from one another. Participants with
             late-onset ADHD did not show elevated PRS for ADHD,
             depression, alcohol dependence, or marijuana use
             disorder.<h4>Conclusion</h4>Genetic risk scores derived from
             case-control genome-wide association studies may have
             relevance not only for incidence of mental health disorders,
             but also for understanding the longitudinal course of mental
             health disorders.},
   Doi = {10.1016/j.jaac.2020.12.033},
   Key = {fds355028}
}

@article{fds356797,
   Author = {Bourassa, KJ and Moffitt, TE and Harrington, H and Houts, R and Poulton,
             R and Ramrakha, S and Caspi, A},
   Title = {Lower Cardiovascular Reactivity is Associated with More
             Childhood Adversity and Poorer Midlife Health: Replicated
             Findings from the Dunedin and MIDUS Cohorts.},
   Journal = {Clinical psychological science : a journal of the
             Association for Psychological Science},
   Volume = {9},
   Number = {5},
   Pages = {961-978},
   Year = {2021},
   Month = {September},
   url = {http://dx.doi.org/10.1177/2167702621993900},
   Abstract = {Cardiovascular reactivity has been proposed as a biomarker
             linking childhood adversity and poorer health. The current
             study examined the association of childhood adversity,
             cardiovascular reactivity, and health in the Dunedin
             (<i>n</i>=922) and MIDUS studies (<i>n</i>=1,015). In both
             studies, participants who experienced more childhood
             adversity had lower cardiovascular reactivity. In addition,
             people with lower cardiovascular reactivity had poorer
             self-reported health and greater inflammation. Dunedin
             participants with lower cardiovascular reactivity were aging
             biologically faster, and MIDUS participants with lower heart
             rate reactivity had increased risk of early mortality.
             Cardiovascular reactivity was not associated with
             hypertension in either study. Results were partially
             accounted for by greater reactivity among more
             conscientious, less depressed, and higher-functioning
             participants. These results suggest that people who
             experienced childhood adversity have a blunted physiological
             response, which is associated with poorer health. The
             findings highlight the importance of accounting for
             individual differences when assessing cardiovascular
             reactivity using cognitive stressor tasks.},
   Doi = {10.1177/2167702621993900},
   Key = {fds356797}
}

@article{fds357403,
   Author = {Sierra, F and Caspi, A and Fortinsky, RH and Haynes, L and Lithgow, GJ and Moffitt, TE and Olshansky, SJ and Perry, D and Verdin, E and Kuchel,
             GA},
   Title = {Moving geroscience from the bench to clinical care and
             health policy.},
   Journal = {Journal of the American Geriatrics Society},
   Volume = {69},
   Number = {9},
   Pages = {2455-2463},
   Year = {2021},
   Month = {September},
   url = {http://dx.doi.org/10.1111/jgs.17301},
   Abstract = {Geriatricians and others must embrace the emerging field of
             geroscience. Until recently geroscience research was pursued
             in laboratory animals, but now this field requires
             specialized expertise in the care of vulnerable older
             patients with multiple chronic diseases and geriatric
             syndromes, the population likely to benefit the most from
             emerging therapies. While chronological aging measures the
             inevitable passage of clock time that occurs equally for
             everyone, biological aging varies among individuals, and
             importantly, it is modifiable. Advances in our understanding
             of biological aging, the discovery of strategies for
             modifying its rate, and an appreciation of aging as a shared
             risk factor for chronic diseases have jointly led to the
             Geroscience Hypothesis. This hypothesis states that
             interventions modifying aging biology can slow its
             progression-resulting in the delay or prevention of the
             onset of multiple diseases and disorders. Here we wish to
             report on the Third Geroscience Summit held at National
             Institutes of Health on November 4-5, 2019, which
             highlighted the importance of engaging other disciplines
             including clinicians. Involvement by scientists with
             expertise in clinical trials, health outcomes research,
             behavioral and social sciences, health policy, and economics
             is urgently needed to translate geroscience discoveries from
             the bench to clinical care and health policy. Adding to the
             urgency of broadening this geroscience coalition is the
             emergence of biological aging as one the most important
             modifiable factors of COVID-19, combined with the inability
             of our society to once again recognize and confront aging as
             a priority and opportunity when facing these types of public
             health emergencies.},
   Doi = {10.1111/jgs.17301},
   Key = {fds357403}
}

@article{fds362303,
   Author = {van der Laan, CM and Morosoli-García, JJ and van de Weijer, SGA and Colodro-Conde, L and ACTION Consortium, and Lupton, MK and Mitchell,
             BL and McAloney, K and Parker, R and Burns, JM and Hickie, IB and Pool, R and Hottenga, J-J and Martin, NG and Medland, SE and Nivard, MG and Boomsma,
             DI},
   Title = {Continuity of Genetic Risk for Aggressive Behavior Across
             the Life-Course.},
   Journal = {Behav Genet},
   Volume = {51},
   Number = {5},
   Pages = {592-606},
   Year = {2021},
   Month = {September},
   url = {http://dx.doi.org/10.1007/s10519-021-10076-6},
   Abstract = {We test whether genetic influences that explain individual
             differences in aggression in early life also explain
             individual differences across the life-course. In two
             cohorts from The Netherlands (N = 13,471) and Australia
             (N = 5628), polygenic scores (PGSs) were computed based
             on a genome-wide meta-analysis of childhood/adolescence
             aggression. In a novel analytic approach, we ran a mixed
             effects model for each age (Netherlands: 12-70 years,
             Australia: 16-73 years), with observations at the focus age
             weighted as 1, and decaying weights for ages further away.
             We call this approach a 'rolling weights' model. In The
             Netherlands, the estimated effect of the PGS was relatively
             similar from age 12 to age 41, and decreased from age 41-70.
             In Australia, there was a peak in the effect of the PGS
             around age 40 years. These results are a first indication
             from a molecular genetics perspective that genetic
             influences on aggressive behavior that are expressed in
             childhood continue to play a role later in
             life.},
   Doi = {10.1007/s10519-021-10076-6},
   Key = {fds362303}
}

@article{fds358967,
   Author = {Lewis, SJ and Koenen, KC and Ambler, A and Arseneault, L and Caspi, A and Fisher, HL and Moffitt, TE and Danese, A},
   Title = {Unravelling the contribution of complex trauma to
             psychopathology and cognitive deficits: a cohort
             study.},
   Journal = {The British journal of psychiatry : the journal of mental
             science},
   Volume = {219},
   Number = {2},
   Pages = {448-455},
   Year = {2021},
   Month = {August},
   url = {http://dx.doi.org/10.1192/bjp.2021.57},
   Abstract = {<h4>Background</h4>Complex traumas are traumatic experiences
             that involve multiple interpersonal threats during childhood
             or adolescence, such as repeated abuse. Complex traumas are
             hypothesized to lead to more severe psychopathology and
             poorer cognitive function than other non-complex traumas.
             However, empirical testing of this hypothesis has been
             limited to clinical/convenience samples and cross-sectional
             designs.<h4>Aims</h4>To investigate psychopathology and
             cognitive function in young people exposed to complex,
             non-complex, or no trauma from a population-representative
             longitudinal cohort, and to consider the role of
             pre-existing vulnerabilities.<h4>Method</h4>Participants
             were from the Environmental Risk (E-Risk) Longitudinal Twin
             Study, a population-representative birth-cohort of 2,232
             British children. At age 18 years (93% participation), we
             assessed lifetime exposure to complex and non-complex
             trauma, past-year psychopathology, and current cognitive
             function. We also prospectively assessed early childhood
             vulnerabilities: internalizing and externalizing symptoms at
             age 5, IQ at age 5, family history of mental illness, family
             socioeconomic status, and sex.<h4>Results</h4>Participants
             exposed to complex trauma had more severe psychopathology
             and poorer cognitive function at age 18 compared to both
             trauma-unexposed participants and those exposed to
             non-complex trauma. Early childhood vulnerabilities
             predicted risk of later complex trauma exposure, and largely
             explained associations of complex trauma with cognitive
             deficits, but not with psychopathology.<h4>Conclusions</h4>By
             conflating complex and non-complex traumas, current research
             and clinical practice under-estimate the severity of
             psychopathology, cognitive deficits, and pre-existing
             vulnerabilities linked with complex trauma. A better
             understanding of the mental health needs of people exposed
             to complex trauma could inform the development of new
             effective interventions.},
   Doi = {10.1192/bjp.2021.57},
   Key = {fds358967}
}

@article{fds357995,
   Author = {Andersen, SH and Richmond-Rakerd, LS and Moffitt, TE and Caspi,
             A},
   Title = {Nationwide evidence that education disrupts the
             intergenerational transmission of disadvantage.},
   Journal = {Proceedings of the National Academy of Sciences of the
             United States of America},
   Volume = {118},
   Number = {31},
   Pages = {e2103896118},
   Year = {2021},
   Month = {August},
   url = {http://dx.doi.org/10.1073/pnas.2103896118},
   Abstract = {Despite overall improvements in health and living standards
             in the Western world, health and social disadvantages
             persist across generations. Using nationwide administrative
             databases linked for 2.1 million Danish citizens, we
             leveraged a three-generation approach to test whether
             multiple, different health and social disadvantages-poor
             physical health, poor mental health, social welfare
             dependency, criminal offending, and Child Protective
             Services involvement-were transmitted within families and
             whether education disrupted these statistical associations.
             Health and social disadvantages concentrated, aggregated,
             and accumulated within a small, high-need segment of
             families: Adults who relied disproportionately on multiple,
             different health and social services tended to have parents
             who relied disproportionately on multiple, different health
             and social services and tended to have children who
             evidenced risk for disadvantage at an early age, through
             appearance in protective services records. Intra- and
             intergenerational comparisons were consistent with the
             possibility that education disrupted this transmission.
             Within families, siblings who obtained more education were
             at a reduced risk for later-life disadvantage compared with
             their cosiblings who obtained less education, despite shared
             family background. Supporting the education potential of the
             most vulnerable citizens might mitigate the
             multigenerational transmission of multiple disadvantages and
             reduce health and social disparities.},
   Doi = {10.1073/pnas.2103896118},
   Key = {fds357995}
}

@article{fds347346,
   Author = {Romer, AL and Knodt, AR and Sison, ML and Ireland, D and Houts, R and Ramrakha, S and Poulton, R and Keenan, R and Melzer, TR and Moffitt, TE and Caspi, A and Hariri, AR},
   Title = {Replicability of structural brain alterations associated
             with general psychopathology: evidence from a
             population-representative birth cohort.},
   Journal = {Molecular psychiatry},
   Volume = {26},
   Number = {8},
   Pages = {3839-3846},
   Year = {2021},
   Month = {August},
   url = {http://dx.doi.org/10.1038/s41380-019-0621-z},
   Abstract = {Transdiagnostic research has identified a general
             psychopathology factor-often called the 'p' factor-that
             accounts for shared variation across internalizing,
             externalizing, and thought disorders in diverse samples. It
             has been argued that the p factor may reflect dysfunctional
             thinking present in serious mental illness. In support of
             this, we previously used a theory-free, data-driven
             multimodal neuroimaging approach to find that higher p
             factor scores are associated with structural alterations
             within a cerebello-thalamo-cortical circuit (CTCC) and
             visual association cortex, both of which are important for
             monitoring and coordinating information processing in the
             service of executive control. Here we attempt to replicate
             these associations by conducting region-of-interest analyses
             using data from 875 members of the Dunedin Longitudinal
             Study, a five-decade study of a population-representative
             birth cohort, collected when they were 45 years old. We
             further sought to replicate a more recent report that p
             factor scores can be predicted by patterns of distributed
             cerebellar morphology as estimated through independent
             component analysis. We successfully replicated associations
             between higher p factor scores and both reduced gray matter
             volume of the visual association cortex and fractional
             anisotropy of pontine white matter pathways within the CTCC.
             In contrast, we failed to replicate prior associations
             between cerebellar structure and p factor scores.
             Collectively, our findings encourage further focus on the
             CTCC and visual association cortex as core neural substrates
             and potential biomarkers of general psychopathology.},
   Doi = {10.1038/s41380-019-0621-z},
   Key = {fds347346}
}

@article{fds347650,
   Author = {Elliott, ML and Belsky, DW and Knodt, AR and Ireland, D and Melzer, TR and Poulton, R and Ramrakha, S and Caspi, A and Moffitt, TE and Hariri,
             AR},
   Title = {Brain-age in midlife is associated with accelerated
             biological aging and cognitive decline in a longitudinal
             birth cohort.},
   Journal = {Molecular psychiatry},
   Volume = {26},
   Number = {8},
   Pages = {3829-3838},
   Year = {2021},
   Month = {August},
   url = {http://dx.doi.org/10.1038/s41380-019-0626-7},
   Abstract = {An individual's brainAGE is the difference between
             chronological age and age predicted from machine-learning
             models of brain-imaging data. BrainAGE has been proposed as
             a biomarker of age-related deterioration of the brain.
             Having an older brainAGE has been linked to Alzheimer's,
             dementia, and mortality. However, these findings are largely
             based on cross-sectional associations which can confuse age
             differences with cohort differences. To illuminate the
             validity of brainAGE as a biomarker of accelerated brain
             aging, a study is needed of a large cohort all born in the
             same year who nevertheless vary on brainAGE. In the Dunedin
             Study, a population-representative 1972-73 birth cohort, we
             measured brainAGE at age 45 years, as well as the pace of
             biological aging and cognitive decline in longitudinal data
             from childhood to midlife (N = 869). In this cohort, all
             chronological age 45 years, brainAGE was measured reliably
             (ICC = 0.81) and ranged from 24 to 72 years. Those with
             older midlife brainAGEs tended to have poorer cognitive
             function in both adulthood and childhood, as well as
             impaired brain health at age 3. Furthermore, those with
             older brainAGEs had an accelerated pace of biological aging,
             older facial appearance, and early signs of cognitive
             decline from childhood to midlife. These findings help to
             validate brainAGE as a potential surrogate biomarker for
             midlife intervention studies that seek to measure
             dementia-prevention efforts in midlife. However, the
             findings also caution against the assumption that brainAGE
             scores represent only age-related deterioration of the brain
             as they may also index central nervous system variation
             present since childhood.},
   Doi = {10.1038/s41380-019-0626-7},
   Key = {fds347650}
}

@article{fds356107,
   Author = {Gehred, MZ and Knodt, AR and Ambler, A and Bourassa, KJ and Danese, A and Elliott, ML and Hogan, S and Ireland, D and Poulton, R and Ramrakha, S and Reuben, A and Sison, ML and Moffitt, TE and Hariri, AR and Caspi,
             A},
   Title = {Long-term Neural Embedding of Childhood Adversity in a
             Population-Representative Birth Cohort Followed for 5
             Decades.},
   Journal = {Biological psychiatry},
   Volume = {90},
   Number = {3},
   Pages = {182-193},
   Year = {2021},
   Month = {August},
   url = {http://dx.doi.org/10.1016/j.biopsych.2021.02.971},
   Abstract = {<h4>Background</h4>Childhood adversity has been previously
             associated with alterations in brain structure, but
             heterogeneous designs, methods, and measures have
             contributed to mixed results and have impeded progress in
             mapping the biological embedding of childhood adversity. We
             sought to identify long-term differences in structural brain
             integrity associated with childhood adversity.<h4>Methods</h4>Multiple
             regression was used to test associations between
             prospectively ascertained adversity during childhood and
             adversity retrospectively reported in adulthood with
             structural magnetic resonance imaging measures of midlife
             global and regional cortical thickness, cortical surface
             area, and subcortical gray matter volume in 861 (425 female)
             members of the Dunedin Study, a longitudinal investigation
             of a population-representative birth cohort.<h4>Results</h4>Both
             prospectively ascertained childhood adversity and
             retrospectively reported adversity were associated with
             alterations in midlife structural brain integrity, but
             associations with prospectively ascertained childhood
             adversity were consistently stronger and more widely
             distributed than associations with retrospectively reported
             childhood adversity. Sensitivity analyses revealed that
             these associations were not driven by any particular
             adversity or category of adversity (i.e., threat or
             deprivation) or by childhood socioeconomic disadvantage.
             Network enrichment analyses revealed that these associations
             were not localized but were broadly distributed along a
             hierarchical cortical gradient of information
             processing.<h4>Conclusions</h4>Exposure to childhood
             adversity broadly is associated with widespread differences
             in midlife gray matter across cortical and subcortical
             structures, suggesting that biological embedding of
             childhood adversity in the brain is long lasting, but not
             localized. Research using retrospectively reported adversity
             likely underestimates the magnitude of these associations.
             These findings may inform future research investigating
             mechanisms through which adversity becomes embedded in the
             brain and influences mental health and cognition.},
   Doi = {10.1016/j.biopsych.2021.02.971},
   Key = {fds356107}
}

@article{fds356796,
   Author = {Mason, D and Ronald, A and Ambler, A and Caspi, A and Houts, R and Poulton,
             R and Ramrakha, S and Wertz, J and Moffitt, TE and Happé,
             F},
   Title = {Autistic traits are associated with faster pace of aging:
             Evidence from the Dunedin study at age 45.},
   Journal = {Autism research : official journal of the International
             Society for Autism Research},
   Volume = {14},
   Number = {8},
   Pages = {1684-1694},
   Year = {2021},
   Month = {August},
   url = {http://dx.doi.org/10.1002/aur.2534},
   Abstract = {Growing evidence indicates that the defining characteristics
             of autism spectrum disorder (ASD) are distributed throughout
             the general population; hence, understanding the correlates
             of aging in people with high autistic traits could shed
             light on ASD and aging. 915 members of the Dunedin
             longitudinal birth cohort completed a measure of autistic
             traits at age 45. A composite measure of the "pace of aging"
             was derived by tracking the decline in 19 biomarkers across
             ages 26, 32, 38, and 45 years. Facial age was also
             assessed. Reports of perceived health were collected from
             participants themselves, informants, and interviewers.
             Higher self-reported autistic traits significantly
             correlated with a faster pace of aging, older facial age,
             and poorer self-, informant-, and interviewer-rated health.
             After control for sex, SES and IQ, autistic traits were
             significantly associated with each variable: pace of aging
             (β = 0.09), facial age (β = 0.08), self-
             (β = -0.15), informant (β = -0.12), and
             interviewer-rated (β = -0.17) health. Autistic traits
             measured at age 45 are associated with faster aging.
             Participants with high autistic traits appear to be more
             vulnerable to poor health outcomes, as previously reported
             for those clinically diagnosed with ASD. Therefore, autistic
             traits may have important health implications. Replicating
             these findings in samples of autistic people is needed to
             identify the mechanism of their effect on aging and physical
             health to improve outcomes for those with ASD diagnoses or
             high autistic traits. LAY SUMMARY: The role that autistic
             traits have in relation to health outcomes has not been
             investigated. We looked at how physical health and aging
             (measured with self-reported questions and decline in
             multiple biological measures) were related to autistic
             traits (measured with a questionnaire, at age 45). We found
             that higher autistic traits were associated with poorer
             reports of physical health, and a faster pace of aging. This
             suggests that both those with autism and those with higher
             autistic traits may be more likely to experience poorer
             health outcomes.},
   Doi = {10.1002/aur.2534},
   Key = {fds356796}
}

@article{fds361945,
   Author = {Lewis, SJ and Koenen, KC and Ambler, A and Arseneault, L and Caspi, A and Fisher, HL and Moffitt, TE and Danese, A},
   Title = {Unravelling the contribution of complex trauma to
             psychopathology and cognitive deficits: a cohort
             study.},
   Journal = {The British journal of psychiatry : the journal of mental
             science},
   Volume = {219},
   Number = {2},
   Pages = {448-455},
   Year = {2021},
   Month = {August},
   url = {http://dx.doi.org/10.1192/bjp.2021.57},
   Abstract = {<h4>Background</h4>Complex traumas are traumatic experiences
             that involve multiple interpersonal threats during childhood
             or adolescence, such as repeated abuse. These traumas are
             hypothesised to cause more severe psychopathology and poorer
             cognitive function than other non-complex traumas. However,
             empirical testing has been limited to clinical/convenience
             samples and cross-sectional designs.<h4>Aims</h4>To
             investigate psychopathology and cognitive function in young
             people exposed to complex, non-complex or no trauma, from a
             population-representative longitudinal cohort, and to
             consider the role of pre-existing vulnerabilities.<h4>Method</h4>Participants
             were from the Environmental Risk Longitudinal Twin Study, a
             population-representative birth cohort of 2232 British
             children. At age 18 years (93% participation), we assessed
             lifetime exposure to complex and non-complex trauma,
             past-year psychopathology and current cognitive function. We
             also prospectively assessed early childhood vulnerabilities:
             internalising and externalising symptoms at 5 years of age,
             IQ at 5 years of age, family history of mental illness,
             family socioeconomic status and sex.<h4>Results</h4>Participants
             exposed to complex trauma had more severe psychopathology
             and poorer cognitive function at 18 years of age, compared
             with both trauma-unexposed participants and those exposed to
             non-complex trauma. Early childhood vulnerabilities
             predicted risk of later complex trauma exposure, and largely
             explained associations of complex trauma with cognitive
             deficits, but not with psychopathology.<h4>Conclusions</h4>By
             conflating complex and non-complex traumas, current research
             and clinical practice underestimate the severity of
             psychopathology, cognitive deficits and pre-existing
             vulnerabilities linked with complex trauma. A better
             understanding of the mental health needs of people exposed
             to complex trauma could inform the development of new, more
             effective interventions.},
   Doi = {10.1192/bjp.2021.57},
   Key = {fds361945}
}

@article{fds358968,
   Author = {Ip, HF and van der Laan, CM and Krapohl, EML and Brikell, I and Sánchez-Mora, C and Nolte, IM and St Pourcain and B and Bolhuis, K and Palviainen, T and Zafarmand, H and Colodro-Conde, L and Gordon, S and Zayats, T and Aliev, F and Jiang, C and Wang, CA and Saunders, G and Karhunen, V and Hammerschlag, AR and Adkins, DE and Border, R and Peterson, RE and Prinz, JA and Thiering, E and Seppälä, I and Vilor-Tejedor, N and Ahluwalia, TS and Day, FR and Hottenga, J-J and Allegrini, AG and Rimfeld, K and Chen, Q and Lu, Y and Martin, J and Soler
             Artigas, M and Rovira, P and Bosch, R and Español, G and Ramos Quiroga,
             JA and Neumann, A and Ensink, J and Grasby, K and Morosoli, JJ and Tong, X and Marrington, S and Middeldorp, C and Scott, JG and Vinkhuyzen, A and Shabalin, AA and Corley, R and Evans, LM and Sugden, K and Alemany, S and Sass, L and Vinding, R and Ruth, K and Tyrrell, J and Davies, GE and Ehli,
             EA and Hagenbeek, FA and De Zeeuw and E and Van Beijsterveldt and TCEM and Larsson, H and Snieder, H and Verhulst, FC and Amin, N and Whipp, AM and Korhonen, T and Vuoksimaa, E and Rose, RJ and Uitterlinden, AG and Heath, AC and Madden, P and Haavik, J and Harris, JR and Helgeland, Ø and Johansson, S and Knudsen, GPS and Njolstad, PR and Lu, Q and Rodriguez,
             A and Henders, AK and Mamun, A and Najman, JM and Brown, S and Hopfer, C and Krauter, K and Reynolds, C and Smolen, A and Stallings, M and Wadsworth,
             S and Wall, TL and Silberg, JL and Miller, A and Keltikangas-Järvinen,
             L and Hakulinen, C and Pulkki-Råback, L and Havdahl, A and Magnus, P and Raitakari, OT and Perry, JRB and Llop, S and Lopez-Espinosa, M-J and Bønnelykke, K and Bisgaard, H and Sunyer, J and Lehtimäki, T and Arseneault, L and Standl, M and Heinrich, J and Boden, J and Pearson, J and Horwood, LJ and Kennedy, M and Poulton, R and Eaves, LJ and Maes, HH and Hewitt, J and Copeland, WE and Costello, EJ and Williams, GM and Wray,
             N and Järvelin, M-R and McGue, M and Iacono, W and Caspi, A and Moffitt,
             TE and Whitehouse, A and Pennell, CE and Klump, KL and Burt, SA and Dick,
             DM and Reichborn-Kjennerud, T and Martin, NG and Medland, SE and Vrijkotte, T and Kaprio, J and Tiemeier, H and Davey Smith and G and Hartman, CA and Oldehinkel, AJ and Casas, M and Ribasés, M and Lichtenstein, P and Lundström, S and Plomin, R and Bartels, M and Nivard, MG and Boomsma, DI},
   Title = {Genetic association study of childhood aggression across
             raters, instruments, and age.},
   Journal = {Transl Psychiatry},
   Volume = {11},
   Number = {1},
   Pages = {413},
   Year = {2021},
   Month = {July},
   url = {http://dx.doi.org/10.1038/s41398-021-01480-x},
   Abstract = {Childhood aggressive behavior (AGG) has a substantial
             heritability of around 50%. Here we present a genome-wide
             association meta-analysis (GWAMA) of childhood AGG, in which
             all phenotype measures across childhood ages from multiple
             assessors were included. We analyzed phenotype assessments
             for a total of 328 935 observations from 87 485 children
             aged between 1.5 and 18 years, while accounting for sample
             overlap. We also meta-analyzed within subsets of the data,
             i.e., within rater, instrument and age. SNP-heritability for
             the overall meta-analysis (AGGoverall) was 3.31%
             (SE = 0.0038). We found no genome-wide significant SNPs
             for AGGoverall. The gene-based analysis returned three
             significant genes: ST3GAL3 (P = 1.6E-06), PCDH7
             (P = 2.0E-06), and IPO13 (P = 2.5E-06). All three
             genes have previously been associated with educational
             traits. Polygenic scores based on our GWAMA significantly
             predicted aggression in a holdout sample of children
             (variance explained = 0.44%) and in retrospectively assessed
             childhood aggression (variance explained = 0.20%). Genetic
             correlations (rg) among rater-specific assessment of AGG
             ranged from rg = 0.46 between self- and
             teacher-assessment to rg = 0.81 between mother- and
             teacher-assessment. We obtained moderate-to-strong rgs with
             selected phenotypes from multiple domains, but hardly with
             any of the classical biomarkers thought to be associated
             with AGG. Significant genetic correlations were observed
             with most psychiatric and psychological traits (range
             [Formula: see text]: 0.19-1.00), except for
             obsessive-compulsive disorder. Aggression had a negative
             genetic correlation (rg = ~-0.5) with cognitive traits
             and age at first birth. Aggression was strongly genetically
             correlated with smoking phenotypes (range [Formula: see
             text]: 0.46-0.60). The genetic correlations between
             aggression and psychiatric disorders were weaker for
             teacher-reported AGG than for mother- and self-reported AGG.
             The current GWAMA of childhood aggression provides a
             powerful tool to interrogate the rater-specific genetic
             etiology of AGG.},
   Doi = {10.1038/s41398-021-01480-x},
   Key = {fds358968}
}

@article{fds352446,
   Author = {Latham, RM and Quilter, E and Arseneault, L and Danese, A and Moffitt,
             TE and Newbury, JB and Fisher, HL},
   Title = {Childhood maltreatment and poor functional outcomes at the
             transition to adulthood: a comparison of prospective
             informant- and retrospective self-reports of
             maltreatment.},
   Journal = {Social psychiatry and psychiatric epidemiology},
   Volume = {56},
   Number = {7},
   Pages = {1161-1173},
   Year = {2021},
   Month = {July},
   url = {http://dx.doi.org/10.1007/s00127-020-01926-5},
   Abstract = {<h4>Purpose</h4>Growing evidence suggests that prospective
             informant-reports and retrospective self-reports of
             childhood maltreatment may be differentially associated with
             adult psychopathology. However, it remains unknown how
             associations for these two maltreatment reporting types
             compare when considering functional outcomes. The present
             study compared associations between childhood maltreatment
             and functional outcomes at age 18 years using these two
             methods.<h4>Methods</h4>We used data from the Environmental
             Risk (E-Risk) Longitudinal Twin Study, a nationally
             representative birth cohort of 2232 children born in England
             and Wales in 1994-1995. Maltreatment prior to age 12 years
             was assessed prospectively (during multiple home visits
             between birth and age of 12 years based on interviews with
             caregivers, researcher observations, and information from
             practitioners where child protection referrals were made)
             and retrospectively (at age 18 via self-report on the
             Childhood Trauma Questionnaire). Nine functional outcomes
             were measured at age 18, forming two variables capturing:
             (i) psychosocial and (ii) vocational disadvantage.<h4>Results</h4>Among
             the 2054 participants with available data, childhood
             maltreatment was associated with poorer functional outcomes
             regardless of whether this was reported only prospectively,
             only retrospectively, or both. Stronger associations with
             psychosocial disadvantage arose in the context of
             retrospective recall by participants (OR = 8.25, 95% CI
             4.93-13.82) than prospective reports by informants
             (OR = 2.03, 95% CI 1.36-3.04) of maltreatment.
             Conversely, associations with vocational disadvantage were
             comparable for both prospective informant-reports
             (OR = 2.19, 95% CI 1.42-3.38) and retrospective
             self-reports (OR = 1.93, 95% CI 1.33-2.81) of
             maltreatment.<h4>Conclusion</h4>Results highlight the
             importance of considering the maltreatment report type used
             when interpreting the functional consequences of childhood
             maltreatment.},
   Doi = {10.1007/s00127-020-01926-5},
   Key = {fds352446}
}

@article{fds352899,
   Author = {Cheung, CY and Xu, D and Cheng, C-Y and Sabanayagam, C and Tham, Y-C and Yu, M and Rim, TH and Chai, CY and Gopinath, B and Mitchell, P and Poulton,
             R and Moffitt, TE and Caspi, A and Yam, JC and Tham, CC and Jonas, JB and Wang, YX and Song, SJ and Burrell, LM and Farouque, O and Li, LJ and Tan,
             G and Ting, DSW and Hsu, W and Lee, ML and Wong, TY},
   Title = {A deep-learning system for the assessment of cardiovascular
             disease risk via the measurement of retinal-vessel
             calibre.},
   Journal = {Nature biomedical engineering},
   Volume = {5},
   Number = {6},
   Pages = {498-508},
   Year = {2021},
   Month = {June},
   url = {http://dx.doi.org/10.1038/s41551-020-00626-4},
   Abstract = {Retinal blood vessels provide information on the risk of
             cardiovascular disease (CVD). Here, we report the
             development and validation of deep-learning models for the
             automated measurement of retinal-vessel calibre in retinal
             photographs, using diverse multiethnic multicountry datasets
             that comprise more than 70,000 images. Retinal-vessel
             calibre measured by the models and by expert human graders
             showed high agreement, with overall intraclass correlation
             coefficients of between 0.82 and 0.95. The models performed
             comparably to or better than expert graders in associations
             between measurements of retinal-vessel calibre and CVD risk
             factors, including blood pressure, body-mass index, total
             cholesterol and glycated-haemoglobin levels. In
             retrospectively measured prospective datasets from a
             population-based study, baseline measurements performed by
             the deep-learning system were associated with incident CVD.
             Our findings motivate the development of clinically
             applicable explainable end-to-end deep-learning systems for
             the prediction of CVD on the basis of the features of
             retinal vessels in retinal photographs.},
   Doi = {10.1038/s41551-020-00626-4},
   Key = {fds352899}
}

@article{fds355027,
   Author = {van Dongen, J and Hagenbeek, FA and Suderman, M and Roetman, PJ and Sugden, K and Chiocchetti, AG and Ismail, K and Mulder, RH and Hafferty,
             JD and Adams, MJ and Walker, RM and Morris, SW and Lahti, J and Küpers,
             LK and Escaramis, G and Alemany, S and Jan Bonder and M and Meijer, M and Ip,
             HF and Jansen, R and Baselmans, BML and Parmar, P and Lowry, E and Streit,
             F and Sirignano, L and Send, TS and Frank, J and Jylhävä, J and Wang, Y and Mishra, PP and Colins, OF and Corcoran, DL and Poulton, R and Mill, J and Hannon, E and Arseneault, L and Korhonen, T and Vuoksimaa, E and Felix,
             JF and Bakermans-Kranenburg, MJ and Campbell, A and Czamara, D and Binder, E and Corpeleijn, E and Gonzalez, JR and Grazuleviciene, R and Gutzkow, KB and Evandt, J and Vafeiadi, M and Klein, M and van der Meer,
             D and Ligthart, L and BIOS Consortium, and Kluft, C and Davies, GE and Hakulinen, C and Keltikangas-Järvinen, L and Franke, B and Freitag,
             CM and Konrad, K and Hervas, A and Fernández-Rivas, A and Vetro, A and Raitakari, O and Lehtimäki, T and Vermeiren, R and Strandberg, T and Räikkönen, K and Snieder, H and Witt, SH and Deuschle, M and Pedersen,
             NL and Hägg, S and Sunyer, J and Franke, L and Kaprio, J and Ollikainen,
             M and Moffitt, TE and Tiemeier, H and van IJzendoorn, MH and Relton, C and Vrijheid, M and Sebert, S and Jarvelin, M-R and Caspi, A and Evans, KL and McIntosh, AM and Bartels, M and Boomsma, DI},
   Title = {DNA methylation signatures of aggression and closely related
             constructs: A meta-analysis of epigenome-wide studies across
             the lifespan.},
   Journal = {Molecular psychiatry},
   Volume = {26},
   Number = {6},
   Pages = {2148-2162},
   Year = {2021},
   Month = {June},
   url = {http://dx.doi.org/10.1038/s41380-020-00987-x},
   Abstract = {DNA methylation profiles of aggressive behavior may capture
             lifetime cumulative effects of genetic, stochastic, and
             environmental influences associated with aggression. Here,
             we report the first large meta-analysis of epigenome-wide
             association studies (EWAS) of aggressive behavior
             (N = 15,324 participants). In peripheral blood samples
             of 14,434 participants from 18 cohorts with mean ages
             ranging from 7 to 68 years, 13 methylation sites were
             significantly associated with aggression
             (alpha = 1.2 × 10<sup>-7</sup>; Bonferroni
             correction). In cord blood samples of 2425 children from
             five cohorts with aggression assessed at mean ages ranging
             from 4 to 7 years, 83% of these sites showed the same
             direction of association with childhood aggression
             (r = 0.74, p = 0.006) but no epigenome-wide
             significant sites were found. Top-sites (48 at a false
             discovery rate of 5% in the peripheral blood meta-analysis
             or in a combined meta-analysis of peripheral blood and cord
             blood) have been associated with chemical exposures,
             smoking, cognition, metabolic traits, and genetic variation
             (mQTLs). Three genes whose expression levels were associated
             with top-sites were previously linked to schizophrenia and
             general risk tolerance. At six CpGs, DNA methylation
             variation in blood mirrors variation in the brain. On
             average 44% (range = 3-82%) of the aggression-methylation
             association was explained by current and former smoking and
             BMI. These findings point at loci that are sensitive to
             chemical exposures with potential implications for neuronal
             functions. We hope these results to be a starting point for
             studies leading to applications as peripheral biomarkers and
             to reveal causal relationships with aggression and related
             traits.},
   Doi = {10.1038/s41380-020-00987-x},
   Key = {fds355027}
}

@article{fds356032,
   Author = {Latham, RM and Kieling, C and Arseneault, L and Botter-Maio Rocha and T and Beddows, A and Beevers, SD and Danese, A and De Oliveira and K and Kohrt,
             BA and Moffitt, TE and Mondelli, V and Newbury, JB and Reuben, A and Fisher, HL},
   Title = {Childhood exposure to ambient air pollution and predicting
             individual risk of depression onset in UK
             adolescents.},
   Journal = {J Psychiatr Res},
   Volume = {138},
   Pages = {60-67},
   Year = {2021},
   Month = {June},
   url = {http://dx.doi.org/10.1016/j.jpsychires.2021.03.042},
   Abstract = {Knowledge about early risk factors for major depressive
             disorder (MDD) is critical to identify those who are at high
             risk. A multivariable model to predict adolescents'
             individual risk of future MDD has recently been developed
             however its performance in a UK sample was far from perfect.
             Given the potential role of air pollution in the aetiology
             of depression, we investigate whether including childhood
             exposure to air pollution as an additional predictor in the
             risk prediction model improves the identification of UK
             adolescents who are at greatest risk for developing MDD. We
             used data from the Environmental Risk (E-Risk) Longitudinal
             Twin Study, a nationally representative UK birth cohort of
             2232 children followed to age 18 with 93% retention. Annual
             exposure to four pollutants - nitrogen dioxide (NO2),
             nitrogen oxides (NOX), particulate matter <2.5 μm (PM2.5)
             and <10 μm (PM10) - were estimated at address-level when
             children were aged 10. MDD was assessed via interviews at
             age 18. The risk of developing MDD was elevated most for
             participants with the highest (top quartile) level of annual
             exposure to NOX (adjusted OR = 1.43, 95% CI = 0.96-2.13)
             and PM2.5 (adjusted OR = 1.35, 95% CI = 0.95-1.92). The
             separate inclusion of these ambient pollution estimates into
             the risk prediction model improved model specificity but
             reduced model sensitivity - resulting in minimal net
             improvement in model performance. Findings indicate a
             potential role for childhood ambient air pollution exposure
             in the development of adolescent MDD but suggest that
             inclusion of risk factors other than this may be important
             for improving the performance of the risk prediction
             model.},
   Doi = {10.1016/j.jpsychires.2021.03.042},
   Key = {fds356032}
}

@article{fds357404,
   Author = {Dowsett, J and Ferkingstad, E and Rasmussen, LJH and Thørner, LW and Magnússon, MK and Sugden, K and Thorleifsson, G and Frigge, M and Burgdorf, KS and Ostrowski, SR and Sørensen, E and Erikstrup, C and Pedersen, OB and Hansen, TF and Banasik, K and Brunak, S and DBDS
             Genomic Consortium, and Tragante, V and Lund, SH and Stefansdottir,
             L and Gunnarson, B and Poulton, R and Arseneault, L and Caspi, A and Moffitt, TE and Gudbjartsson, D and Eugen-Olsen, J and Stefánsson,
             H and Stefánsson, K and Ullum, H},
   Title = {Eleven genomic loci affect plasma levels of chronic
             inflammation marker soluble urokinase-type plasminogen
             activator receptor.},
   Journal = {Communications biology},
   Volume = {4},
   Number = {1},
   Pages = {655},
   Year = {2021},
   Month = {June},
   url = {http://dx.doi.org/10.1038/s42003-021-02144-8},
   Abstract = {Soluble urokinase-type plasminogen activator receptor
             (suPAR) is a chronic inflammation marker associated with the
             development of a range of diseases, including cancer and
             cardiovascular disease. The genetics of suPAR remain
             unexplored but may shed light on the biology of the marker
             and its connection to outcomes. We report a heritability
             estimate of 60% for the variation in suPAR and performed a
             genome-wide association meta-analysis on suPAR levels
             measured in Iceland (N = 35,559) and in Denmark
             (N = 12,177). We identified 13 independently genome-wide
             significant sequence variants associated with suPAR across
             11 distinct loci. Associated variants were found in and
             around genes encoding uPAR (PLAUR), its ligand uPA (PLAU),
             the kidney-disease-associated gene PLA2R1 as well as genes
             with relations to glycosylation, glycoprotein biosynthesis,
             and the immune response. These findings provide new insight
             into the causes of variation in suPAR plasma levels, which
             may clarify suPAR's potential role in associated diseases,
             as well as the underlying mechanisms that give suPAR its
             prognostic value as a unique marker of chronic
             inflammation.},
   Doi = {10.1038/s42003-021-02144-8},
   Key = {fds357404}
}

@article{fds355370,
   Author = {Wertz, J and Caspi, A and Ambler, A and Broadbent, J and Hancox, RJ and Harrington, H and Hogan, S and Houts, RM and Leung, JH and Poulton, R and Purdy, SC and Ramrakha, S and Rasmussen, LJH and Richmond-Rakerd, LS and Thorne, PR and Wilson, GA and Moffitt, TE},
   Title = {Association of History of Psychopathology With Accelerated
             Aging at Midlife.},
   Journal = {JAMA psychiatry},
   Volume = {78},
   Number = {5},
   Pages = {530-539},
   Year = {2021},
   Month = {May},
   url = {http://dx.doi.org/10.1001/jamapsychiatry.2020.4626},
   Abstract = {<h4>Importance</h4>Individuals with mental disorders are at
             an elevated risk of developing chronic age-related physical
             diseases. However, it is not clear whether psychopathology
             is also associated with processes of accelerated aging that
             precede the onset of age-related disease.<h4>Objective</h4>To
             test the hypothesis that a history of psychopathology is
             associated with indicators of accelerated aging at
             midlife.<h4>Design, setting, and participants</h4>This
             prospective cohort study was based on the Dunedin
             Multidisciplinary Health and Development Study, a
             population-representative birth cohort of 1037 individuals
             born between April 1, 1972, and March 31, 1973, in Dunedin,
             New Zealand. Members were followed up to age 45 years (until
             April 2019). Data were analyzed from January 6 to December
             7, 2020.<h4>Exposures</h4>Mental disorders were assessed in
             6 diagnostic assessments from ages 18 to 45 years and
             transformed through confirmatory factor analysis into
             continuous measures of general psychopathology (p-factor)
             and dimensions of internalizing, externalizing, and thought
             disorders (all standardized to a mean [SD] of 100
             [15]).<h4>Main outcomes and measures</h4>Signs of aging
             (biological pace of aging; declines in sensory, motor, and
             cognitive functioning; and facial age) were assessed up to
             age 45 years using previously validated measures including
             biomarkers, clinical tests, and self-reports.<h4>Results</h4>Of
             the original 1037 cohort participants, 997 were still alive
             at age 45 years, of whom 938 (94%) were assessed (474 men
             [50.5%]). Participants who had experienced more
             psychopathology exhibited a faster pace of biological aging
             (β, 0.27; 95% CI, 0.21-0.33; P < .01); experienced more
             difficulties with hearing (β, 0.18; 95% CI, 0.12-0.24;
             P < .01), vision (β, 0.08; 95% CI, 0.01-0.14;
             P < .05), balance (β, 0.20; 95% CI, 0.14-0.26;
             P < .01), and motor functioning (β, 0.19; 95% CI,
             0.12-0.25; P < .01); experienced more cognitive
             difficulties (β, 0.24; 95% CI, 0.18-0.31; P < .01); and
             were rated as looking older (β, 0.20; 95% CI, 0.14-0.26;
             P < .01). Associations persisted after controlling for
             sex, childhood health indicators, maltreatment, and
             socioeconomic status and after taking into account being
             overweight, smoking, use of antipsychotic medication, and
             the presence of physical disease. Tests of diagnostic
             specificity revealed that associations were generalizable
             across externalizing, internalizing, and thought
             disorders.<h4>Conclusions and relevance</h4>In this cohort
             study, a history of psychopathology was associated with
             accelerated aging at midlife, years before the typical onset
             of age-related diseases. This link is not specific to any
             particular disorder family but generalizes across disorders.
             Prevention of psychopathology and monitoring of individuals
             with mental disorders for signs of accelerated aging may
             have the potential to reduce health inequalities and extend
             healthy lives.},
   Doi = {10.1001/jamapsychiatry.2020.4626},
   Key = {fds355370}
}

@article{fds355026,
   Author = {Baldwin, JR and Caspi, A and Meehan, AJ and Ambler, A and Arseneault, L and Fisher, HL and Harrington, H and Matthews, T and Odgers, CL and Poulton,
             R and Ramrakha, S and Moffitt, TE and Danese, A},
   Title = {Population vs Individual Prediction of Poor Health From
             Results of Adverse Childhood Experiences
             Screening.},
   Journal = {JAMA pediatrics},
   Volume = {175},
   Number = {4},
   Pages = {385-393},
   Year = {2021},
   Month = {April},
   url = {http://dx.doi.org/10.1001/jamapediatrics.2020.5602},
   Abstract = {<h4>Importance</h4>Adverse childhood experiences (ACEs) are
             well-established risk factors for health problems in a
             population. However, it is not known whether screening for
             ACEs can accurately identify individuals who develop later
             health problems.<h4>Objective</h4>To test the predictive
             accuracy of ACE screening for later health
             problems.<h4>Design, setting, and participants</h4>This
             study comprised 2 birth cohorts: the Environmental Risk
             (E-Risk) Longitudinal Twin Study observed 2232 participants
             born during the period from 1994 to 1995 until they were
             aged 18 years (2012-2014); the Dunedin Multidisciplinary
             Health and Development Study observed 1037 participants born
             during the period from 1972 to 1973 until they were aged 45
             years (2017-2019). Statistical analysis was performed from
             May 28, 2018, to July 29, 2020.<h4>Exposures</h4>ACEs were
             measured prospectively in childhood through repeated
             interviews and observations in both cohorts. ACEs were also
             measured retrospectively in the Dunedin cohort through
             interviews at 38 years.<h4>Main outcomes and
             measures</h4>Health outcomes were assessed at 18 years in
             E-Risk and at 45 years in the Dunedin cohort. Mental health
             problems were assessed through clinical interviews using the
             Diagnostic Interview Schedule. Physical health problems were
             assessed through interviews, anthropometric measurements,
             and blood collection.<h4>Results</h4>Of 2232 E-Risk
             participants, 2009 (1051 girls [52%]) were included in the
             analysis. Of 1037 Dunedin cohort participants, 918 (460 boys
             [50%]) were included in the analysis. In E-Risk, children
             with higher ACE scores had greater risk of later health
             problems (any mental health problem: relative risk, 1.14
             [95% CI, 1.10-1.18] per each additional ACE; any physical
             health problem: relative risk, 1.09 [95% CI, 1.07-1.12] per
             each additional ACE). ACE scores were associated with health
             problems independent of other information typically
             available to clinicians (ie, sex, socioeconomic
             disadvantage, and history of health problems). However, ACE
             scores had poor accuracy in predicting an individual's risk
             of later health problems (any mental health problem: area
             under the receiver operating characteristic curve, 0.58 [95%
             CI, 0.56-0.61]; any physical health problem: area under the
             receiver operating characteristic curve, 0.60 [95% CI,
             0.58-0.63]; chance prediction: area under the receiver
             operating characteristic curve, 0.50). Findings were
             consistent in the Dunedin cohort using both prospective and
             retrospective ACE measures.<h4>Conclusions and
             relevance</h4>This study suggests that, although ACE scores
             can forecast mean group differences in health, they have
             poor accuracy in predicting an individual's risk of later
             health problems. Therefore, targeting interventions based on
             ACE screening is likely to be ineffective in preventing poor
             health outcomes.},
   Doi = {10.1001/jamapediatrics.2020.5602},
   Key = {fds355026}
}

@article{fds355722,
   Author = {Elliott, ML and Knodt, AR and Caspi, A and Moffitt, TE and Hariri,
             AR},
   Title = {Need for Psychometric Theory in Neuroscience Research and
             Training: Reply to Kragel et al. (2021).},
   Journal = {Psychological science},
   Volume = {32},
   Number = {4},
   Pages = {627-629},
   Year = {2021},
   Month = {April},
   url = {http://dx.doi.org/10.1177/0956797621996665},
   Doi = {10.1177/0956797621996665},
   Key = {fds355722}
}

@article{fds356031,
   Author = {Reuben, A and Arseneault, L and Beddows, A and Beevers, SD and Moffitt,
             TE and Ambler, A and Latham, RM and Newbury, JB and Odgers, CL and Schaefer, JD and Fisher, HL},
   Title = {Association of Air Pollution Exposure in Childhood and
             Adolescence With Psychopathology at the Transition to
             Adulthood.},
   Journal = {JAMA network open},
   Volume = {4},
   Number = {4},
   Pages = {e217508},
   Year = {2021},
   Month = {April},
   url = {http://dx.doi.org/10.1001/jamanetworkopen.2021.7508},
   Abstract = {<h4>Importance</h4>Air pollution exposure damages the brain,
             but its associations with the development of psychopathology
             are not fully characterized.<h4>Objective</h4>To assess
             whether air pollution exposure in childhood and adolescence
             is associated with greater psychopathology at 18 years of
             age.<h4>Design, setting, and participants</h4>The
             Environmental-Risk Longitudinal Twin Study is a
             population-based cohort study of 2232 children born from
             January 1, 1994, to December 4, 1995, across England and
             Wales and followed up to 18 years of age. Pollution data
             generation was completed on April 22, 2020; data were
             analyzed from April 27 to July 31, 2020.<h4>Exposures</h4>High-resolution
             annualized estimates of outdoor nitrogen oxides (NOx) and
             particulate matter with aerodynamic diameter less than 2.5
             μm (PM2.5) linked to home addresses at the ages of 10 and
             18 years and then averaged.<h4>Main outcomes and
             measures</h4>Mental health disorder symptoms assessed
             through structured interview at 18 years of age and
             transformed through confirmatory factor analysis into
             continuous measures of general psychopathology (primary
             outcome) and internalizing, externalizing, and thought
             disorder symptoms (secondary outcomes) standardized to a
             mean (SD) of 100 (15). Hypotheses were formulated after
             data collection, and analyses were preregistered.<h4>Results</h4>A
             total of 2039 participants (1070 [52.5%] female) had full
             data available. After adjustment for family and individual
             factors, each interquartile range increment increase in NOx
             exposure was associated with a 1.40-point increase (95%
             CI, 0.41-2.38; P = .005) in general psychopathology.
             There was no association between continuously measured PM2.5
             and general psychopathology (b = 0.45; 95% CI, -0.26 to
             1.11; P = .22); however, those in the highest quartile
             of PM2.5 exposure scored 2.04 points higher (95%
             CI, 0.36-3.72; P = .02) than those in the bottom 3
             quartiles. Copollutant models, including both NOx and PM2.5,
             implicated NOx alone in these significant findings. NOx
             exposure was associated with all secondary outcomes,
             although associations were weakest for internalizing
             (adjusted b = 1.07; 95% CI, 0.10-2.04; P = .03),
             medium for externalizing (adjusted b = 1.42; 95%
             CI, 0.53-2.31; P = .002), and strongest for thought
             disorder symptoms (adjusted b = 1.54; 95%
             CI, 0.50-2.57; P = .004). Despite NOx concentrations
             being highest in neighborhoods with worse physical, social,
             and economic conditions, adjusting estimates for
             neighborhood characteristics did not change the
             results.<h4>Conclusions and relevance</h4>Youths exposed to
             higher levels of outdoor NOx experienced greater
             psychopathology at the transition to adulthood. Air
             pollution may be a nonspecific risk factor for the
             development of psychopathology.},
   Doi = {10.1001/jamanetworkopen.2021.7508},
   Key = {fds356031}
}

@article{fds362094,
   Author = {Buffarini, R and Coll, CVN and Moffitt, T and Freias da Silveira and M and Barros, F and Murray, J},
   Title = {Intimate partner violence against women and child
             maltreatment in a Brazilian birth cohort study:
             co-occurrence and shared risk factors.},
   Journal = {BMJ global health},
   Volume = {6},
   Number = {4},
   Pages = {e004306},
   Year = {2021},
   Month = {April},
   url = {http://dx.doi.org/10.1136/bmjgh-2020-004306},
   Abstract = {<h4>Background</h4>Intimate partner violence (IPV) against
             women and child maltreatment (CM) are major public health
             problems and human rights issues and may have shared causes.
             However, their overlap is understudied. We investigated the
             prevalence of IPV and CM, their co-occurrence in households
             and possible shared risk factors, in the general population
             of a Brazilian urban setting.<h4>Methods</h4>Prospective
             population-based birth cohort, including over 3500
             mother-child dyads with maternal reports on both IPV and CM
             when children were 4 years old. Eleven neighbourhood, family
             and parental risk factors were measured between birth and
             age 4 years. Bivariate and multivariate Poisson regression
             models with robust variance were used to test which
             potential risk factors were associated with IPV, CM and
             their co-occurrence.<h4>Results</h4>The prevalence of any
             IPV and CM were 22.8% and 10.9%, respectively; the
             co-occurrence of both types of violence was 5%. Multivariate
             analyses showed that the overlap of IPV and CM was strongly
             associated with neighbourhood violence, absence of the
             child's biological father, paternal antisocial behaviour in
             general and a mother-partner relationship characterised by
             high levels of criticism, maternal depression and younger
             maternal age. A concentration of many risk factors among 10%
             of the population was associated with a sixfold increase in
             risk for overlapping IPV and CM compared with households
             with no risk factors.<h4>Conclusion</h4>IPV and CM share
             important risk factors in the family and neighbourhood
             environments and are particularly common in households with
             multiple social disadvantages and family difficulties.
             Integrated preventive interventions are needed.},
   Doi = {10.1136/bmjgh-2020-004306},
   Key = {fds362094}
}

@article{fds355721,
   Author = {Hannon, E and Mansell, G and Walker, E and Nabais, MF and Burrage, J and Kepa, A and Best-Lane, J and Rose, A and Heck, S and Moffitt, TE and Caspi,
             A and Arseneault, L and Mill, J},
   Title = {Assessing the co-variability of DNA methylation across
             peripheral cells and tissues: Implications for the
             interpretation of findings in epigenetic
             epidemiology.},
   Journal = {PLoS genetics},
   Volume = {17},
   Number = {3},
   Pages = {e1009443},
   Year = {2021},
   Month = {March},
   url = {http://dx.doi.org/10.1371/journal.pgen.1009443},
   Abstract = {Most epigenome-wide association studies (EWAS) quantify DNA
             methylation (DNAm) in peripheral tissues such as whole blood
             to identify positions in the genome where variation is
             statistically associated with a trait or exposure. As whole
             blood comprises a mix of cell types, it is unclear whether
             trait-associated DNAm variation is specific to an individual
             cellular population. We collected three peripheral tissues
             (whole blood, buccal epithelial and nasal epithelial cells)
             from thirty individuals. Whole blood samples were
             subsequently processed using fluorescence-activated cell
             sorting (FACS) to purify five constituent cell-types
             (monocytes, granulocytes, CD4+ T cells, CD8+ T cells, and B
             cells). DNAm was profiled in all eight sample-types from
             each individual using the Illumina EPIC array. We identified
             significant differences in both the level and variability of
             DNAm between different sample types, and DNAm data-derived
             estimates of age and smoking were found to differ
             dramatically across sample types from the same individual.
             We found that for the majority of loci variation in DNAm in
             individual blood cell types was only weakly predictive of
             variance in DNAm measured in whole blood, although the
             proportion of variance explained was greater than that
             explained by either buccal or nasal epithelial samples.
             Covariation across sample types was much higher for DNAm
             sites influenced by genetic factors. Overall, we observe
             that DNAm variation in whole blood is additively influenced
             by a combination of the major blood cell types. For a subset
             of sites, however, variable DNAm detected in whole blood can
             be attributed to variation in a single blood cell type
             providing potential mechanistic insight about EWAS findings.
             Our results suggest that associations between whole blood
             DNAm and traits or exposures reflect differences in multiple
             cell types and our data will facilitate the interpretation
             of findings in epigenetic epidemiology.},
   Doi = {10.1371/journal.pgen.1009443},
   Key = {fds355721}
}

@article{fds356033,
   Author = {Elliott, ML and Caspi, A and Houts, RM and Ambler, A and Broadbent, JM and Hancox, RJ and Harrington, H and Hogan, S and Keenan, R and Knodt, A and Leung, JH and Melzer, TR and Purdy, SC and Ramrakha, S and Richmond-Rakerd, LS and Righarts, A and Sugden, K and Thomson, WM and Thorne, PR and Williams, BS and Wilson, G and Hariri, AR and Poulton, R and Moffitt, TE},
   Title = {Disparities in the pace of biological aging among midlife
             adults of the same chronological age have implications for
             future frailty risk and policy.},
   Journal = {Nature aging},
   Volume = {1},
   Number = {3},
   Pages = {295-308},
   Year = {2021},
   Month = {March},
   url = {http://dx.doi.org/10.1038/s43587-021-00044-4},
   Abstract = {Some humans age faster than others. Variation in biological
             aging can be measured in midlife, but the implications of
             this variation are poorly understood. We tested associations
             between midlife biological aging and indicators of future
             frailty-risk in the Dunedin cohort of 1037 infants born the
             same year and followed to age 45. Participants' Pace of
             Aging was quantified by tracking declining function in 19
             biomarkers indexing the cardiovascular, metabolic, renal,
             immune, dental, and pulmonary systems across ages 26, 32,
             38, and 45 years. At age 45 in 2019, participants with
             faster Pace of Aging had more cognitive difficulties, signs
             of advanced brain aging, diminished sensory-motor functions,
             older appearance, and more pessimistic perceptions of aging.
             People who are aging more rapidly than same-age peers in
             midlife may prematurely need supports to sustain
             independence that are usually reserved for older adults.
             Chronological age does not adequately identify need for such
             supports.},
   Doi = {10.1038/s43587-021-00044-4},
   Key = {fds356033}
}

@article{fds348495,
   Author = {Rocha, TB-M and Fisher, HL and Caye, A and Anselmi, L and Arseneault, L and Barros, FC and Caspi, A and Danese, A and Gonçalves, H and Harrington,
             HL and Houts, R and Menezes, AMB and Moffitt, TE and Mondelli, V and Poulton, R and Rohde, LA and Wehrmeister, F and Kieling,
             C},
   Title = {Identifying Adolescents at Risk for Depression:
             A Prediction Score Performance in Cohorts Based
             in 3 Different Continents.},
   Journal = {Journal of the American Academy of Child and Adolescent
             Psychiatry},
   Volume = {60},
   Number = {2},
   Pages = {262-273},
   Year = {2021},
   Month = {February},
   url = {http://dx.doi.org/10.1016/j.jaac.2019.12.004},
   Abstract = {<h4>Objective</h4>Prediction models have become frequent in
             the medical literature, but most published studies are
             conducted in a single setting. Heterogeneity between
             development and validation samples has been posited as a
             major obstacle for the generalization of models. We aimed to
             develop a multivariable prognostic model using
             sociodemographic variables easily obtainable from
             adolescents at age 15 to predict a depressive disorder
             diagnosis at age 18 and to evaluate its generalizability in
             2 samples from diverse socioeconomic and cultural
             settings.<h4>Method</h4>Data from the 1993 Pelotas Birth
             Cohort were used to develop the prediction model, and its
             generalizability was evaluated in 2 representative cohort
             studies: the Environmental Risk (E-Risk) Longitudinal Twin
             Study and the Dunedin Multidisciplinary Health and
             Development Study.<h4>Results</h4>At age 15, 2,192
             adolescents with no evidence of current or previous
             depression were included (44.6% male). The apparent
             C-statistic of the models derived in Pelotas ranged from
             0.76 to 0.79, and the model obtained from a penalized
             logistic regression was selected for subsequent external
             evaluation. Major discrepancies between the samples were
             identified, impacting the external prognostic performance of
             the model (Dunedin and E-Risk C-statistics of 0.63 and 0.59,
             respectively). The implementation of recommended strategies
             to account for this heterogeneity among samples improved the
             model's calibration in both samples.<h4>Conclusion</h4>An
             adolescent depression risk score comprising easily
             obtainable predictors was developed with good prognostic
             performance in a Brazilian sample. Heterogeneity among
             settings was not trivial, but strategies to deal with sample
             diversity were identified as pivotal for providing better
             risk stratification across samples. Future efforts should
             focus on developing better methodological approaches for
             incorporating heterogeneity in prognostic
             research.},
   Doi = {10.1016/j.jaac.2019.12.004},
   Key = {fds348495}
}

@article{fds351008,
   Author = {Romer, AL and Elliott, ML and Knodt, AR and Sison, ML and Ireland, D and Houts, R and Ramrakha, S and Poulton, R and Keenan, R and Melzer, TR and Moffitt, TE and Caspi, A and Hariri, AR},
   Title = {Pervasively Thinner Neocortex as a Transdiagnostic Feature
             of General Psychopathology.},
   Journal = {The American journal of psychiatry},
   Volume = {178},
   Number = {2},
   Pages = {174-182},
   Year = {2021},
   Month = {February},
   url = {http://dx.doi.org/10.1176/appi.ajp.2020.19090934},
   Abstract = {<h4>Objective</h4>Neuroimaging research has revealed that
             structural brain alterations are common across broad
             diagnostic families of disorders rather than specific to a
             single psychiatric disorder. Such overlap in the structural
             brain correlates of mental disorders mirrors already
             well-documented phenotypic comorbidity of psychiatric
             symptoms and diagnoses, which can be indexed by a general
             psychopathology or <i>p</i> factor. The authors hypothesized
             that if general psychopathology drives the convergence of
             structural alterations common across disorders, then 1)
             there should be few associations unique to any one
             diagnostic family of disorders, and 2) associations with the
             <i>p</i> factor should overlap with those for the broader
             diagnostic families.<h4>Methods</h4>Analyses were conducted
             on structural MRI and psychopathology data collected from
             861 members of the population-representative Dunedin
             Multidisciplinary Health and Development Study at age
             45.<h4>Results</h4>Study members with high scores across
             three broad diagnostic families of disorders (externalizing,
             internalizing, thought disorder) exhibited highly
             overlapping patterns of reduced global and widely
             distributed parcel-wise neocortical thickness. Study members
             with high <i>p</i> factor scores exhibited patterns of
             reduced global and parcel-wise neocortical thickness nearly
             identical to those associated with the three broad
             diagnostic families.<h4>Conclusions</h4>A pattern of
             pervasively reduced neocortical thickness appears to be
             common across all forms of mental disorders and may
             represent a transdiagnostic feature of general
             psychopathology. As has been documented with regard to
             symptoms and diagnoses, the underlying brain structural
             correlates of mental disorders may not exhibit specificity,
             and the continued pursuit of such specific correlates may
             limit progress toward more effective strategies for
             etiological understanding, prevention, and
             intervention.},
   Doi = {10.1176/appi.ajp.2020.19090934},
   Key = {fds351008}
}

@article{fds351564,
   Author = {Rasmussen, LJH and Caspi, A and Ambler, A and Danese, A and Elliott, M and Eugen-Olsen, J and Hariri, AR and Harrington, H and Houts, R and Poulton, R and Ramrakha, S and Sugden, K and Williams, B and Moffitt,
             TE},
   Title = {Association Between Elevated suPAR, a New Biomarker of
             Inflammation, and Accelerated Aging.},
   Journal = {The journals of gerontology. Series A, Biological sciences
             and medical sciences},
   Volume = {76},
   Number = {2},
   Pages = {318-327},
   Year = {2021},
   Month = {January},
   url = {http://dx.doi.org/10.1093/gerona/glaa178},
   Abstract = {<h4>Background</h4>To understand and measure the association
             between chronic inflammation, aging, and age-related
             diseases, broadly applicable standard biomarkers of systemic
             chronic inflammation are needed. We tested whether elevated
             blood levels of the emerging chronic inflammation marker
             soluble urokinase plasminogen activator receptor (suPAR)
             were associated with accelerated aging, lower functional
             capacity, and cognitive decline.<h4>Methods</h4>We used data
             from the Dunedin Study, a population-representative
             1972-1973 New Zealand birth cohort (n = 1037) that has
             observed participants to age 45 years. Plasma suPAR levels
             were analyzed at ages 38 and 45 years. We performed
             regression analyses adjusted for sex, smoking, C-reactive
             protein, and current health conditions.<h4>Results</h4>Of
             997 still-living participants, 875 (88%) had plasma suPAR
             measured at age 45. Elevated suPAR was associated with
             accelerated pace of biological aging across multiple organ
             systems, older facial appearance, and with structural signs
             of older brain age. Moreover, participants with higher suPAR
             levels had greater decline in physical function and
             cognitive function from childhood to adulthood compared to
             those with lower suPAR levels. Finally, improvements in
             health habits between ages 38 and 45 (smoking cessation or
             increased physical activity) were associated with less steep
             increases in suPAR levels over those years.<h4>Conclusions</h4>Our
             findings provide initial support for the utility of suPAR in
             studying the role of chronic inflammation in accelerated
             aging and functional decline.},
   Doi = {10.1093/gerona/glaa178},
   Key = {fds351564}
}

@article{fds354589,
   Author = {Richmond-Rakerd, LS and Caspi, A and Ambler, A and d'Arbeloff, T and de
             Bruine, M and Elliott, M and Harrington, H and Hogan, S and Houts, RM and Ireland, D and Keenan, R and Knodt, AR and Melzer, TR and Park, S and Poulton, R and Ramrakha, S and Rasmussen, LJH and Sack, E and Schmidt,
             AT and Sison, ML and Wertz, J and Hariri, AR and Moffitt,
             TE},
   Title = {Childhood self-control forecasts the pace of midlife aging
             and preparedness for old age.},
   Journal = {Proceedings of the National Academy of Sciences of the
             United States of America},
   Volume = {118},
   Number = {3},
   Pages = {e2010211118},
   Year = {2021},
   Month = {January},
   url = {http://dx.doi.org/10.1073/pnas.2010211118},
   Abstract = {The ability to control one's own emotions, thoughts, and
             behaviors in early life predicts a range of positive
             outcomes in later life, including longevity. Does it also
             predict how well people age? We studied the association
             between self-control and midlife aging in a
             population-representative cohort of children followed from
             birth to age 45 y, the Dunedin Study. We measured children's
             self-control across their first decade of life using a
             multi-occasion/multi-informant strategy. We measured their
             pace of aging and aging preparedness in midlife using
             measures derived from biological and physiological
             assessments, structural brain-imaging scans, observer
             ratings, self-reports, informant reports, and administrative
             records. As adults, children with better self-control aged
             more slowly in their bodies and showed fewer signs of aging
             in their brains. By midlife, these children were also better
             equipped to manage a range of later-life health, financial,
             and social demands. Associations with children's
             self-control could be separated from their social class
             origins and intelligence, indicating that self-control might
             be an active ingredient in healthy aging. Children also
             shifted naturally in their level of self-control across
             adult life, suggesting the possibility that self-control may
             be a malleable target for intervention. Furthermore,
             individuals' self-control in adulthood was associated with
             their aging outcomes after accounting for their self-control
             in childhood, indicating that midlife might offer another
             window of opportunity to promote healthy
             aging.},
   Doi = {10.1073/pnas.2010211118},
   Key = {fds354589}
}

@article{fds355029,
   Author = {Demange, PA and Malanchini, M and Mallard, TT and Biroli, P and Cox, SR and Grotzinger, AD and Tucker-Drob, EM and Abdellaoui, A and Arseneault,
             L and van Bergen, E and Boomsma, DI and Caspi, A and Corcoran, DL and Domingue, BW and Harris, KM and Ip, HF and Mitchell, C and Moffitt, TE and Poulton, R and Prinz, JA and Sugden, K and Wertz, J and Williams, BS and de
             Zeeuw, EL and Belsky, DW and Harden, KP and Nivard,
             MG},
   Title = {Investigating the genetic architecture of noncognitive
             skills using GWAS-by-subtraction.},
   Journal = {Nature genetics},
   Volume = {53},
   Number = {1},
   Pages = {35-44},
   Year = {2021},
   Month = {January},
   url = {http://dx.doi.org/10.1038/s41588-020-00754-2},
   Abstract = {Little is known about the genetic architecture of traits
             affecting educational attainment other than cognitive
             ability. We used genomic structural equation modeling and
             prior genome-wide association studies (GWASs) of educational
             attainment (n = 1,131,881) and cognitive test
             performance (n = 257,841) to estimate SNP associations
             with educational attainment variation that is independent of
             cognitive ability. We identified 157 genome-wide-significant
             loci and a polygenic architecture accounting for 57% of
             genetic variance in educational attainment. Noncognitive
             genetics were enriched in the same brain tissues and cell
             types as cognitive performance, but showed different
             associations with gray-matter brain volumes. Noncognitive
             genetics were further distinguished by associations with
             personality traits, less risky behavior and increased risk
             for certain psychiatric disorders. For socioeconomic success
             and longevity, noncognitive and cognitive-performance
             genetics demonstrated associations of similar magnitude. By
             conducting a GWAS of a phenotype that was not directly
             measured, we offer a view of genetic architecture of
             noncognitive skills influencing educational
             success.},
   Doi = {10.1038/s41588-020-00754-2},
   Key = {fds355029}
}

@article{fds355031,
   Author = {Richmond-Rakerd, LS and D'Souza, S and Milne, BJ and Caspi, A and Moffitt, TE},
   Title = {Longitudinal Associations of Mental Disorders With Physical
             Diseases and Mortality Among 2.3 Million New Zealand
             Citizens.},
   Journal = {JAMA network open},
   Volume = {4},
   Number = {1},
   Pages = {e2033448},
   Year = {2021},
   Month = {January},
   url = {http://dx.doi.org/10.1001/jamanetworkopen.2020.33448},
   Abstract = {<h4>Importance</h4>Excess risk of physical disease and
             mortality has been observed among individuals with
             psychiatric conditions, suggesting that ameliorating mental
             disorders might also be associated with ameliorating the
             later onset of physical disability and early mortality.
             However, the temporal association between mental disorders
             and physical diseases remains unclear, as many studies have
             relied on retrospective recall, used cross-sectional designs
             or prospective designs with limited follow-up periods, or
             given inadequate consideration to preexisting physical
             illnesses.<h4>Objective</h4>To examine whether mental
             disorders are associated with subsequent physical diseases
             and mortality across 3 decades of observation.<h4>Design,
             setting, and participants</h4>This population-based cohort
             study used data from the New Zealand Integrated Data
             Infrastructure, a collection of nationwide administrative
             data sources linked at the individual level, to identify
             mental disorders, physical diseases, and deaths recorded
             between July 1, 1988, and June 30, 2018, in the population
             of New Zealand. All individuals born in New Zealand between
             January 1, 1928, and December 31, 1978, who resided in the
             country at any time during the 30-year observation period
             were included in the analysis. Data were analyzed from July
             2019 to November 2020.<h4>Exposures</h4>Nationwide
             administrative records of mental disorder diagnoses made in
             public hospitals.<h4>Main outcomes and measures</h4>Chronic
             physical disease diagnoses made in public hospitals, deaths,
             and health care use.<h4>Results</h4>The study population
             comprised 2 349 897 individuals (1 191 981 men
             [50.7%]; age range at baseline, 10-60 years). Individuals
             with a mental disorder developed subsequent physical
             diseases at younger ages (hazard ratio [HR], 2.33; 95% CI,
             2.30-2.36) and died at younger ages (HR, 3.80; 95% CI,
             3.72-3.89) than those without a mental disorder. These
             associations remained across sex and age and after
             accounting for preexisting physical diseases. Associations
             were observed across different types of mental disorders and
             self-harm behavior (relative risks, 1.78-2.43;
             P < .001 for all comparisons). Mental disorders were
             associated with the onset of physical diseases and the
             accumulation of physical disease diagnoses (incidence rate
             ratio [IRR], 2.00; 95% CI, 1.98-2.03), a higher number of
             hospitalizations (IRR, 2.43; 95% CI, 2.39-2.48), longer
             hospital stays for treatment (IRR, 2.70; 95% CI,
             2.62-2.79), and higher associated health care costs
             (b = 0.115; 95% CI, 0.112-0.118).<h4>Conclusions and
             relevance</h4>In this study, mental disorders were likely to
             begin and peak in young adulthood, and they antedated
             physical diseases and early mortality in the population.
             These findings suggest that ameliorating mental disorders
             may have implications for improving the length and quality
             of life and for reducing the health care costs associated
             with physical diseases.},
   Doi = {10.1001/jamanetworkopen.2020.33448},
   Key = {fds355031}
}

@article{fds356034,
   Author = {d'Arbeloff, T and Elliott, ML and Knodt, AR and Sison, M and Melzer, TR and Ireland, D and Ramrakha, S and Poulton, R and Caspi, A and Moffitt, TE and Hariri, AR},
   Title = {Midlife Cardiovascular Fitness Is Reflected in the Brain's
             White Matter.},
   Journal = {Frontiers in aging neuroscience},
   Volume = {13},
   Pages = {652575},
   Year = {2021},
   Month = {January},
   url = {http://dx.doi.org/10.3389/fnagi.2021.652575},
   Abstract = {Disappointing results from clinical trials designed to delay
             structural brain decline and the accompanying increase in
             risk for dementia in older adults have precipitated a shift
             in testing promising interventions from late in life toward
             midlife before irreversible damage has accumulated. This
             shift, however, requires targeting midlife biomarkers that
             are associated with clinical changes manifesting only in
             late life. Here we explored possible links between one
             putative biomarker, distributed integrity of brain white
             matter, and two intervention targets, cardiovascular fitness
             and healthy lifestyle behaviors, in midlife. At age 45,
             fractional anisotropy (FA) derived from diffusion weighted
             MRI was used to estimate the microstructural integrity of
             distributed white matter tracts in a population-representative
             birth cohort. Age-45 cardiovascular fitness
             (VO<sub>2</sub>Max; <i>N</i> = 801) was estimated from heart
             rates obtained during submaximal exercise tests; age-45
             healthy lifestyle behaviors were estimated using the Nyberg
             Health Index (<i>N</i> = 854). Ten-fold cross-validated
             elastic net predictive modeling revealed that estimated
             VO<sub>2</sub>Max was modestly associated with distributed
             FA. In contrast, there was no significant association
             between Nyberg Health Index scores and FA. Our findings
             suggest that cardiovascular fitness levels, but not healthy
             lifestyle behaviors, are associated with the distributed
             integrity of white matter in the brain in midlife. These
             patterns could help inform future clinical intervention
             research targeting ADRDs.},
   Doi = {10.3389/fnagi.2021.652575},
   Key = {fds356034}
}

@article{fds365996,
   Author = {Belsky, DW and Caspi, A and Corcoran, DL and Sugden, K and Poulton, R and Arseneault, L and Baccarelli, A and Chamarti, K and Gao, X and Hannon,
             E and Harrington, HL and Houts, R and Kothari, M and Kwon, D and Mill, J and Schwartz, J and Vokonas, P and Wang, C and Williams, B and Moffitt,
             TE},
   Title = {DunedinPACE: A DNA methylation biomarker of the Pace of
             Aging},
   Year = {2021},
   url = {http://dx.doi.org/10.1101/2021.08.30.21262858},
   Abstract = {<h4>ABSTRACT</h4> Measures to quantify changes in the pace
             of biological aging in response to intervention are needed
             to evaluate geroprotective interventions for humans. We used
             data from the Dunedin Study 1972-3 birth cohort tracking
             within-individual decline in 19 indicators of organ-system
             integrity across four time points spanning two decades to
             model Pace of Aging. We distilled this two-decade Pace of
             Aging into a single-time-point DNA-methylation blood-test
             using elastic-net regression and a DNA-methylation dataset
             restricted to exclude probes with low test-retest
             reliability. We evaluated the resulting measure, named
             DunedinPACE, in five additional datasets. DunedinPACE showed
             high test-retest reliability, was associated with morbidity,
             disability, and mortality, and indicated faster aging in
             young adults with childhood adversity. DunedinPACE
             effect-sizes were similar to GrimAge Clock effect-sizes. In
             analysis of morbidity, disability, and mortality,
             DunedinPACE and added incremental prediction beyond GrimAge.
             DunedinPACE is a novel blood biomarker of the pace of aging
             for gerontology and geroscience.},
   Doi = {10.1101/2021.08.30.21262858},
   Key = {fds365996}
}

@article{fds348496,
   Author = {Agnew-Blais, JC and Polanczyk, GV and Danese, A and Wertz, J and Moffitt, TE and Arseneault, L},
   Title = {Are changes in ADHD course reflected in differences in IQ
             and executive functioning from childhood to young
             adulthood?},
   Journal = {Psychological medicine},
   Volume = {50},
   Number = {16},
   Pages = {2799-2808},
   Year = {2020},
   Month = {December},
   url = {http://dx.doi.org/10.1017/s0033291719003015},
   Abstract = {<h4>Background</h4>Attention-deficit hyperactivity disorder
             (ADHD) is associated with poorer cognitive functioning. We
             used a developmental, genetically-sensitive approach to
             examine intelligence quotient (IQ) from early childhood to
             young adulthood among those with different ADHD courses to
             investigate whether changes in ADHD were reflected in
             differences in IQ. We also examined executive functioning in
             childhood and young adulthood among different ADHD
             courses.<h4>Methods</h4>Study participants were part of the
             Environmental Risk (E-Risk) Longitudinal Twin Study, a
             population-based birth cohort of 2232 twins. We assessed
             ADHD in childhood (ages 5, 7, 10 and 12) and young adulthood
             (age 18). We examined ADHD course as reflected by remission,
             persistence and late-onset. IQ was evaluated at ages 5, 12
             and 18, and executive functioning at ages 5 and
             18.<h4>Results</h4>ADHD groups showed deficits in IQ across
             development compared to controls; those with persistent ADHD
             showed the greatest deficit, followed by remitted and
             late-onset. ADHD groups did not differ from controls in
             developmental trajectory of IQ, suggesting changes in ADHD
             were not reflected in IQ. All ADHD groups performed more
             poorly on executive functioning tasks at ages 5 and 18;
             persisters and remitters differed only on an inhibitory
             control task at age 18.<h4>Conclusions</h4>Differences in
             ADHD course - persistence, remission and late-onset - were
             not directly reflected in changes in IQ. Instead, having
             ADHD at any point across development was associated with
             lower average IQ and poorer executive functioning. Our
             finding that individuals with persistent ADHD have poorer
             response inhibition than those who remitted requires
             replication.},
   Doi = {10.1017/s0033291719003015},
   Key = {fds348496}
}

@article{fds348994,
   Author = {Richmond-Rakerd, LS and Moffitt, TE and Arseneault, L and Belsky, DW and Connor, J and Corcoran, DL and Harrington, H and Houts, RM and Poulton,
             R and Prinz, JA and Ramrakha, S and Sugden, K and Wertz, J and Williams,
             BS and Caspi, A},
   Title = {A polygenic score for age-at-first-birth predicts
             disinhibition.},
   Journal = {Journal of child psychology and psychiatry, and allied
             disciplines},
   Volume = {61},
   Number = {12},
   Pages = {1349-1359},
   Year = {2020},
   Month = {December},
   url = {http://dx.doi.org/10.1111/jcpp.13224},
   Abstract = {<h4>Background</h4>A recent genome-wide association study
             identified molecular-genetic associations with
             age-at-first-birth. However, the meaning of these genetic
             discoveries is unclear. Drawing on evidence linking early
             pregnancy with disinhibitory behavior, we tested the
             hypothesis that genetic discoveries for age-at-first-birth
             predict disinhibition.<h4>Methods</h4>We included
             participants with genotype data from the two-decade-long
             Environmental Risk (E-Risk) Study (N = 1,999) and the
             four-decade-long Dunedin Study (N = 918). We calculated a
             genome-wide polygenic score for age-at-first-birth and
             tested whether it was associated with a range of
             disinhibitory outcomes across the life course, including low
             childhood self-control; risk for externalizing
             psychopathology; officially recorded criminal offending;
             substance dependence; informant reports of disinhibitory
             problems; and number of lifetime sexual partners. We further
             tested whether associations were attributable to accelerated
             pubertal maturation.<h4>Results</h4>In both cohorts, the
             age-at-first-birth polygenic score predicted low childhood
             self-control, externalizing psychopathology, officially
             recorded criminal offending, substance dependence, and
             number of sexual partners. Associations were modest, but
             robust across replication. Childhood disinhibition partly
             mediated associations between the polygenic score and
             reproductive behaviors. In contrast, associations were not
             attributable to accelerated pubertal timing.<h4>Conclusions</h4>Genomic
             discoveries for age-at-first-birth are about more than
             reproductive biology: They provide insight into the
             disinhibitory traits and behaviors that accompany early
             parenthood. Age-at-first-birth is a useful proxy phenotype
             for researchers interested in disinhibition. Further,
             interventions that improve self-regulation abilities may
             benefit young parents and their children.},
   Doi = {10.1111/jcpp.13224},
   Key = {fds348994}
}

@article{fds351563,
   Author = {Moffitt, TE},
   Title = {Behavioral and Social Research to Accelerate the Geroscience
             Translation Agenda.},
   Journal = {Ageing research reviews},
   Volume = {63},
   Pages = {101146},
   Year = {2020},
   Month = {November},
   url = {http://dx.doi.org/10.1016/j.arr.2020.101146},
   Abstract = {Geroscience is the study of how to slow biological aging to
             extend healthspan and longevity. Geroscience has not
             heretofore incorporated behavioral or social-science methods
             or findings into its agenda, but the current expansion of
             the agenda to human trials of anti-aging therapies will be
             greatly aided by behavioral and social science. This article
             recommends some ways in which geroscience can be augmented
             through collaboration with behavioral and social science to:
             accomplish translation from animal models to humans; inform
             the design of clinical trials of anti-aging therapies;
             develop outcome measures for evaluating efficacy of
             anti-aging therapies, and reduce and not exacerbate health
             disparities.},
   Doi = {10.1016/j.arr.2020.101146},
   Key = {fds351563}
}

@article{fds352501,
   Author = {Pedersen, W and Hart, RK and Moffitt, TE and von Soest,
             T},
   Title = {Delinquency abstainers in adolescence and educational and
             labor market outcomes in midlife: A population-based 25-year
             longitudinal study.},
   Journal = {Developmental psychology},
   Volume = {56},
   Number = {11},
   Pages = {2167-2176},
   Year = {2020},
   Month = {November},
   url = {http://dx.doi.org/10.1037/dev0001117},
   Abstract = {Research has suggested that adolescent delinquency
             abstainers might have unfavorable characteristics, impeding
             their access to peer networks. However, recent studies have
             emphasized the possible heterogeneity of abstainers. We know
             little about the long-term adaption of delinquency
             abstainers. We identify subtypes of delinquency abstainers
             and investigate subsequent adult academic careers, income
             levels, and possible marginalization in the labor market. We
             use the population-based Young in Norway Longitudinal study,
             where participants (<i>N</i> = 2,494) are followed up by
             surveys and registers from their teens until their mid-30s.
             By means of latent class analysis, abstainers were divided
             in three groups according to degree of social integration.
             Results showed that delinquency abstainers performed as well
             or better in adulthood than those with moderate delinquency
             involvement and markedly better than the highly delinquent.
             Lonely abstainers performed just as well as all other groups
             when it comes to higher education and earnings. However,
             they had a higher probability of marginalization in the
             labor market than the social abstainers. We conclude that no
             group fared better than delinquency abstainers with strong
             social ties. The outcomes of the lonely abstainers were
             close to those of the majority. Thus, in this cohort who
             came of age in the 1990s, delinquency abstainers are not
             particularly vulnerable, and theory about abstainers needs
             to be modernized. (PsycInfo Database Record (c) 2020 APA,
             all rights reserved).},
   Doi = {10.1037/dev0001117},
   Key = {fds352501}
}

@article{fds353269,
   Author = {Reuben, A and Elliott, ML and Abraham, WC and Broadbent, J and Houts,
             RM and Ireland, D and Knodt, AR and Poulton, R and Ramrakha, S and Hariri,
             AR and Caspi, A and Moffitt, TE},
   Title = {Association of Childhood Lead Exposure With MRI Measurements
             of Structural Brain Integrity in Midlife.},
   Journal = {JAMA},
   Volume = {324},
   Number = {19},
   Pages = {1970-1979},
   Year = {2020},
   Month = {November},
   url = {http://dx.doi.org/10.1001/jama.2020.19998},
   Abstract = {<h4>Importance</h4>Childhood lead exposure has been linked
             to disrupted brain development, but long-term consequences
             for structural brain integrity are unknown.<h4>Objective</h4>To
             test the hypothesis that childhood lead exposure is
             associated with magnetic resonance imaging (MRI)
             measurements of lower structural integrity of the brain in
             midlife.<h4>Design, setting, and participants</h4>The
             Dunedin Study followed a population-representative 1972-1973
             birth cohort in New Zealand (N = 564 analytic sample) to
             age 45 years (until April 2019).<h4>Exposures</h4>Childhood
             blood lead levels measured at age 11 years.<h4>Main outcomes
             and measures</h4>Structural brain integrity at age 45 years
             assessed via MRI (primary outcomes): gray matter (cortical
             thickness, surface area, hippocampal volume), white matter
             (white matter hyperintensities, fractional anisotropy
             [theoretical range, 0 {diffusion is perfectly isotropic} to
             100 {diffusion is perfectly anisotropic}]), and the Brain
             Age Gap Estimation (BrainAGE), a composite index of the gap
             between chronological age and a machine learning
             algorithm-estimated brain age (0 indicates a brain age
             equivalent to chronological age; positive and negative
             values represent an older and younger brain age,
             respectively). Cognitive function at age 45 years was
             assessed objectively via the Wechsler Adult Intelligence
             Scale IV (IQ range, 40-160, standardized to a mean of 100
             [SD, 15]) and subjectively via informant and self-reports
             (z-score units; scale mean, 0 [SD, 1]).<h4>Results</h4>Of
             1037 original participants, 997 were alive at age 45 years,
             of whom 564 (57%) had received lead testing at age 11 years
             (302 [54%] male) (median follow-up, 34 [interquartile range,
             33.7-34.7] years). Mean blood lead level at age 11 years was
             10.99 (SD, 4.63) μg/dL. After adjusting for covariates,
             each 5-μg/dL higher childhood blood lead level was
             significantly associated with 1.19-cm2 smaller cortical
             surface area (95% CI, -2.35 to -0.02 cm2; P = .05),
             0.10-cm3 smaller hippocampal volume (95% CI, -0.17 to -0.03
             cm3; P = .006), lower global fractional anisotropy
             (b = -0.12; 95% CI, -0.24 to -0.01; P = .04), and a
             BrainAGE index 0.77 years older (95% CI, 0.02-1.51 years;
             P = .05) at age 45 years. There were no statistically
             significant associations between blood lead level and
             log-transformed white matter hyperintensity volume
             (b = 0.05 log mm3; 95% CI, -0.02 to 0.13 log mm3;
             P = .17) or mean cortical thickness (b = -0.004 mm;
             95% CI, -0.012 to 0.004 mm; P = .39). Each 5-μg/dL
             higher childhood blood lead level was significantly
             associated with a 2.07-point lower IQ score at age 45 years
             (95% CI, -3.39 to -0.74; P = .002) and a 0.12-point
             higher score on informant-rated cognitive problems (95% CI,
             0.01-0.23; P = .03). There was no statistically
             significant association between childhood blood lead levels
             and self-reported cognitive problems (b = -0.02 points;
             95% CI, -0.10 to 0.07; P = .68).<h4>Conclusions and
             relevance</h4>In this longitudinal cohort study with a
             median 34-year follow-up, higher childhood blood lead level
             was associated with differences in some MRI measures of
             brain structure that suggested lower structural brain
             integrity in midlife. Because of the large number of
             statistical comparisons, some findings may represent type I
             error.},
   Doi = {10.1001/jama.2020.19998},
   Key = {fds353269}
}

@article{fds345814,
   Author = {Wertz, J and Caspi, A and Ambler, A and Arseneault, L and Belsky, DW and Danese, A and Fisher, HL and Matthews, T and Richmond-Rakerd, LS and Moffitt, TE},
   Title = {Borderline Symptoms at Age 12 Signal Risk for Poor Outcomes
             During the Transition to Adulthood: Findings From a
             Genetically Sensitive Longitudinal Cohort
             Study.},
   Journal = {Journal of the American Academy of Child and Adolescent
             Psychiatry},
   Volume = {59},
   Number = {10},
   Pages = {1165-1177.e2},
   Year = {2020},
   Month = {October},
   url = {http://dx.doi.org/10.1016/j.jaac.2019.07.005},
   Abstract = {<h4>Objective</h4>Borderline personality disorder in
             adolescence remains a controversial construct. We addressed
             concerns about the prognostic significance of adolescent
             borderline pathology by testing whether borderline symptoms
             at age 12 years predict functioning during the transition to
             adulthood, at age 18 years, in areas critical to life-course
             development.<h4>Method</h4>We studied members of the
             Environmental Risk (E-Risk) Longitudinal Twin Study, which
             tracks the development of a birth cohort of 2,232 British
             twin children. At age 12, study members' borderline symptoms
             were measured using mothers' reports. At age 18, study
             members' personality, psychopathology, functional outcomes,
             and experiences of victimization were measured using
             self-reports, coinformant reports, and official
             records.<h4>Results</h4>At age 18, study members who had
             more borderline symptoms at age 12 were more likely to have
             difficult personalities, to struggle with poor mental
             health, to experience poor functional outcomes, and to have
             become victims of violence. Reports of poor outcomes were
             corroborated by coinformants and official records.
             Borderline symptoms in study members at 12 years old
             predicted poor outcomes over and above other behavioral and
             emotional problems during adolescence. Twin analyses showed
             that borderline symptoms in 12-year-olds were influenced by
             familial risk, particularly genetic risk, which accounted
             for associations with most poor outcomes at
             age 18.<h4>Conclusion</h4>Borderline symptoms in
             12-year-olds signal risk for pervasive poor functioning
             during the transition to adulthood. This association is
             driven by genetic influences, suggesting that borderline
             symptoms and poor outcomes are manifestations of shared
             genetic risk.},
   Doi = {10.1016/j.jaac.2019.07.005},
   Key = {fds345814}
}

@article{fds352897,
   Author = {d'Arbeloff, T and Cooke, M and Knodt, AR and Sison, M and Melzer, TR and Ireland, D and Poulton, R and Ramrakha, S and Moffitt, TE and Caspi, A and Hariri, AR},
   Title = {Is cardiovascular fitness associated with structural brain
             integrity in midlife? Evidence from a population-representative
             birth cohort study.},
   Journal = {Aging},
   Volume = {12},
   Number = {20},
   Pages = {20888-20914},
   Year = {2020},
   Month = {October},
   url = {http://dx.doi.org/10.18632/aging.104112},
   Abstract = {Improving cardiovascular fitness may buffer against
             age-related cognitive decline and mitigate dementia risk by
             staving off brain atrophy. However, it is unclear if such
             effects reflect factors operating in childhood
             (neuroselection) or adulthood (neuroprotection). Using data
             from 807 members of the Dunedin Study, a
             population-representative birth cohort, we investigated
             associations between cardiovascular fitness and structural
             brain integrity at age 45, and the extent to which
             associations reflected possible neuroselection or
             neuroprotection by controlling for childhood IQ. Higher
             fitness, as indexed by VO<sub>2</sub>Max, was not associated
             with average cortical thickness, total surface area, or
             subcortical gray matter volume including the hippocampus.
             However, higher fitness was associated with thicker cortex
             in prefrontal and temporal regions as well as greater
             cerebellar gray matter volume. Higher fitness was also
             associated with decreased hippocampal fissure volume. These
             associations were unaffected by the inclusion of childhood
             IQ in analyses. In contrast, a higher rate of decline in
             cardiovascular fitness from 26 to 45 years was not robustly
             associated with structural brain integrity. Our findings are
             consistent with a neuroprotective account of adult
             cardiovascular fitness but suggest that effects are not
             uniformly observed across the brain and reflect
             contemporaneous fitness more so than decline over
             time.},
   Doi = {10.18632/aging.104112},
   Key = {fds352897}
}

@article{fds347030,
   Author = {Wertz, J and Moffitt, TE and Agnew-Blais, J and Arseneault, L and Belsky, DW and Corcoran, DL and Houts, R and Matthews, T and Prinz, JA and Richmond-Rakerd, LS and Sugden, K and Williams, B and Caspi,
             A},
   Title = {Using DNA From Mothers and Children to Study Parental
             Investment in Children's Educational Attainment.},
   Journal = {Child development},
   Volume = {91},
   Number = {5},
   Pages = {1745-1761},
   Year = {2020},
   Month = {September},
   url = {http://dx.doi.org/10.1111/cdev.13329},
   Abstract = {This study tested implications of new genetic discoveries
             for understanding the association between parental
             investment and children's educational attainment. A novel
             design matched genetic data from 860 British mothers and
             their children with home-visit measures of parenting: the
             E-Risk Study. Three findings emerged. First, both mothers'
             and children's education-associated genetics, summarized in
             a genome-wide polygenic score, were associated with
             parenting-a gene-environment correlation. Second, accounting
             for genetic influences slightly reduced associations between
             parenting and children's attainment-indicating some genetic
             confounding. Third, mothers' genetics were associated with
             children's attainment over and above children's own
             genetics, via cognitively stimulating parenting-an
             environmentally mediated effect. Findings imply that, when
             interpreting parents' effects on children, environmentalists
             must consider genetic transmission, but geneticists must
             also consider environmental transmission.},
   Doi = {10.1111/cdev.13329},
   Key = {fds347030}
}

@article{fds348030,
   Author = {Rivenbark, J and Arseneault, L and Caspi, A and Danese, A and Fisher,
             HL and Moffitt, TE and Rasmussen, LJH and Russell, MA and Odgers,
             CL},
   Title = {Adolescents' perceptions of family social status correlate
             with health and life chances: A twin difference longitudinal
             cohort study.},
   Journal = {Proceedings of the National Academy of Sciences of the
             United States of America},
   Volume = {117},
   Number = {38},
   Pages = {23323-23328},
   Year = {2020},
   Month = {September},
   url = {http://dx.doi.org/10.1073/pnas.1820845116},
   Abstract = {Children from lower-income households are at increased risk
             for poor health, educational failure, and behavioral
             problems. This social gradient is one of the most reproduced
             findings in health and social science. How people view their
             position in social hierarchies also signals poor health.
             However, when adolescents' views of their social position
             begin to independently relate to well-being is currently
             unknown. A cotwin design was leveraged to test whether
             adolescents with identical family backgrounds, but who
             viewed their family's social status as higher than their
             same-aged and sex sibling, experienced better well-being in
             early and late adolescence. Participants were members of the
             Environmental Risk Longitudinal Twin Study, a representative
             cohort of British twins (<i>n</i> = 2,232) followed across
             the first 2 decades of life. By late adolescence,
             perceptions of subjective family social status (SFSS)
             robustly correlated with multiple indicators of health and
             well-being, including depression; anxiety; conduct problems;
             marijuana use; optimism; not in education, employment, or
             training (NEET) status; and crime. Findings held controlling
             for objective socioeconomic status both statistically and by
             cotwin design after accounting for measures of childhood
             intelligence (IQ), negative affect, and prior mental health
             risk and when self-report, informant report, and
             administrative data were used. Little support was found for
             the biological embedding of adolescents' perceptions of
             familial social status as indexed by inflammatory biomarkers
             or cognitive tests in late adolescence or for SFSS in early
             adolescence as a robust correlate of well-being or predictor
             of future problems. Future experimental studies are required
             to test whether altering adolescents' subjective social
             status will lead to improved well-being and social
             mobility.},
   Doi = {10.1073/pnas.1820845116},
   Key = {fds348030}
}

@article{fds349084,
   Author = {Tanksley, PT and Barnes, JC and Boutwell, BB and Arseneault, L and Caspi, A and Danese, A and Fisher, HL and Moffitt,
             TE},
   Title = {Identifying Psychological Pathways to Polyvictimization:
             Evidence from a Longitudinal Cohort Study of Twins from the
             United Kingdom.},
   Journal = {Journal of experimental criminology},
   Volume = {16},
   Number = {3},
   Pages = {431-461},
   Year = {2020},
   Month = {September},
   url = {http://dx.doi.org/10.1007/s11292-020-09422-1},
   Abstract = {<h4>Objectives</h4>Examine the extent to which
             cognitive/psychological characteristics predict later
             polyvictimization. We employ a twin-based design that allows
             us to test the social neurocriminology hypothesis that
             environmental factors influence brain-based characteristics
             and influence behaviors like victimization.<h4>Methods</h4>Using
             data from the Environmental Risk Longitudinal Twin Study
             (<i>N</i> = 1986), we capitalize on the natural experiment
             embedded in a discordant-twin design that allows for the
             adjustment of family environments and genetic
             factors.<h4>Results</h4>The findings indicate that
             self-control, as well as symptoms of conduct disorder and
             anxiety, are related to polyvictimization even after
             adjusting for family environments and partially adjusting
             for genetic influences. After fully adjusting for genetic
             factors, only self-control was a statistically significant
             predictor of polyvictimization.<h4>Conclusion</h4>The
             findings suggest polyvictimization is influenced by
             cognitive/psychological characteristics that individuals
             carry with them across contexts. Policies aimed at reducing
             victimization risks should consider interventions that
             address cognitive functioning and mental
             health.},
   Doi = {10.1007/s11292-020-09422-1},
   Key = {fds349084}
}

@article{fds352227,
   Author = {Moffitt, TE},
   Title = {Innovations in Life-Course Crime Research—ASC Division of
             Developmental and Life-Course Criminology David P.
             Farrington Lecture, 2018},
   Journal = {Journal of Developmental and Life-Course
             Criminology},
   Volume = {6},
   Number = {3},
   Pages = {251-255},
   Year = {2020},
   Month = {September},
   url = {http://dx.doi.org/10.1007/s40865-020-00153-5},
   Doi = {10.1007/s40865-020-00153-5},
   Key = {fds352227}
}

@article{fds351007,
   Author = {Bourassa, KJ and Sbarra, DA and Caspi, A and Moffitt,
             TE},
   Title = {Social Distancing as a Health Behavior: County-Level
             Movement in the United States During the COVID-19 Pandemic
             Is Associated with Conventional Health Behaviors.},
   Journal = {Annals of behavioral medicine : a publication of the Society
             of Behavioral Medicine},
   Volume = {54},
   Number = {8},
   Pages = {548-556},
   Year = {2020},
   Month = {August},
   url = {http://dx.doi.org/10.1093/abm/kaaa049},
   Abstract = {<h4>Background</h4>Social distancing-when people limit close
             contact with others outside their household-is a primary
             intervention available to combat the COVID-19 pandemic. The
             importance of social distancing is unlikely to change until
             effective treatments or vaccines become widely available.
             However, relatively little is known about how best to
             promote social distancing. Applying knowledge from social
             and behavioral research on conventional health behaviors
             (e.g., smoking, physical activity) to support public health
             efforts and research on social distancing is promising, but
             empirical evidence supporting this approach is
             needed.<h4>Purpose</h4>We examined whether one type of
             social distancing behavior-reduced movement outside the
             home-was associated with conventional health
             behaviors.<h4>Method</h4>We examined the association between
             GPS-derived movement behavior in 2,858 counties in USA from
             March 1 to April 7, 2020 and the prevalence of county-level
             indicators influenced by residents' conventional health
             behaviors.<h4>Results</h4>Changes in movement were
             associated with conventional health behaviors, and the
             magnitude of these associations were similar to the
             associations among the conventional health behaviors.
             Counties with healthier behaviors-particularly less obesity
             and greater physical activity-evidenced greater reduction in
             movement outside the home during the initial phases of the
             pandemic in the USA.<h4>Conclusions</h4>Social distancing,
             in the form of reduced movement outside the home, is
             associated with conventional health behaviors. Existing
             scientific literature on health behavior and health behavior
             change can be more confidently used to promote social
             distancing behaviors during the COVID-19
             pandemic.},
   Doi = {10.1093/abm/kaaa049},
   Key = {fds351007}
}

@article{fds350137,
   Author = {Elliott, ML and Knodt, AR and Ireland, D and Morris, ML and Poulton, R and Ramrakha, S and Sison, ML and Moffitt, TE and Caspi, A and Hariri,
             AR},
   Title = {What Is the Test-Retest Reliability of Common
             Task-Functional MRI Measures? New Empirical Evidence and a
             Meta-Analysis.},
   Journal = {Psychological science},
   Volume = {31},
   Number = {7},
   Pages = {792-806},
   Year = {2020},
   Month = {July},
   url = {http://dx.doi.org/10.1177/0956797620916786},
   Abstract = {Identifying brain biomarkers of disease risk is a growing
             priority in neuroscience. The ability to identify meaningful
             biomarkers is limited by measurement reliability; unreliable
             measures are unsuitable for predicting clinical outcomes.
             Measuring brain activity using task functional MRI (fMRI) is
             a major focus of biomarker development; however, the
             reliability of task fMRI has not been systematically
             evaluated. We present converging evidence demonstrating poor
             reliability of task-fMRI measures. First, a meta-analysis of
             90 experiments (<i>N</i> = 1,008) revealed poor overall
             reliability-mean intraclass correlation coefficient (ICC) =
             .397. Second, the test-retest reliabilities of activity in a
             priori regions of interest across 11 common fMRI tasks
             collected by the Human Connectome Project (<i>N</i> = 45)
             and the Dunedin Study (<i>N</i> = 20) were poor (ICCs =
             .067-.485). Collectively, these findings demonstrate that
             common task-fMRI measures are not currently suitable for
             brain biomarker discovery or for individual-differences
             research. We review how this state of affairs came to be and
             highlight avenues for improving task-fMRI
             reliability.},
   Doi = {10.1177/0956797620916786},
   Key = {fds350137}
}

@article{fds349475,
   Author = {Rasmussen, LJH and Moffitt, TE and Caspi, A},
   Title = {Major Concerns Over Improving Measurement of Inflammation
             Remain-Reply.},
   Journal = {JAMA pediatrics},
   Volume = {174},
   Number = {6},
   Pages = {624-625},
   Year = {2020},
   Month = {June},
   url = {http://dx.doi.org/10.1001/jamapediatrics.2020.0291},
   Doi = {10.1001/jamapediatrics.2020.0291},
   Key = {fds349475}
}

@article{fds349929,
   Author = {Reuben, A and Sugden, K and Arseneault, L and Corcoran, DL and Danese,
             A and Fisher, HL and Moffitt, TE and Newbury, JB and Odgers, C and Prinz,
             J and Rasmussen, LJH and Williams, B and Mill, J and Caspi,
             A},
   Title = {Association of Neighborhood Disadvantage in Childhood With
             DNA Methylation in Young Adulthood.},
   Journal = {JAMA network open},
   Volume = {3},
   Number = {6},
   Pages = {e206095},
   Year = {2020},
   Month = {June},
   url = {http://dx.doi.org/10.1001/jamanetworkopen.2020.6095},
   Abstract = {<h4>Importance</h4>DNA methylation has been proposed as an
             epigenetic mechanism by which the childhood neighborhood
             environment may have implications for the genome that
             compromise adult health.<h4>Objective</h4>To ascertain
             whether childhood neighborhood socioeconomic disadvantage is
             associated with differences in DNA methylation by age 18
             years.<h4>Design, setting, and participants</h4>This
             longitudinal cohort study analyzed data from the
             Environmental Risk (E-Risk) Longitudinal Twin Study, a
             nationally representative birth cohort of children born
             between 1994 and 1995 in England and Wales and followed up
             from age 5 to 18 years. Data analysis was performed from
             March 15, 2019, to June 30, 2019.<h4>Exposures</h4>High-resolution
             neighborhood data (indexing deprivation, dilapidation,
             disconnection, and dangerousness) collected across
             childhood.<h4>Main outcomes and measures</h4>DNA methylation
             in whole blood was drawn at age 18 years. Associations
             between neighborhood socioeconomic disadvantage and
             methylation were tested using 3 prespecified approaches: (1)
             testing probes annotated to candidate genes involved in
             biological responses to growing up in socioeconomically
             disadvantaged neighborhoods and investigated in previous
             epigenetic research (stress reactivity-related and
             inflammation-related genes), (2) polyepigenetic scores
             indexing differential methylation in phenotypes associated
             with growing up in disadvantaged neighborhoods (obesity,
             inflammation, and smoking), and (3) a theory-free
             epigenome-wide association study.<h4>Results</h4>A total of
             1619 participants (806 female individuals [50%]) had
             complete neighborhood and DNA methylation data. Children
             raised in socioeconomically disadvantaged neighborhoods
             exhibited differential DNA methylation in genes involved in
             inflammation (β = 0.12; 95% CI, 0.06-0.19;
             P < .001) and smoking (β = 0.18; 95% CI, 0.11-0.25;
             P < .001) but not obesity (β = 0.05; 95% CI, -0.01
             to 0.11; P = .12). An epigenome-wide association study
             identified multiple CpG sites at an arraywide significance
             level of P < 1.16 × 10-7 in genes involved in the
             metabolism of hydrocarbons. Associations between
             neighborhood disadvantage and methylation were small but
             robust to family-level socioeconomic factors and to
             individual-level tobacco smoking.<h4>Conclusions and
             relevance</h4>Children raised in more socioeconomically
             disadvantaged neighborhoods appeared to enter young
             adulthood epigenetically distinct from their less
             disadvantaged peers. This finding suggests that epigenetic
             regulation may be a mechanism by which the childhood
             neighborhood environment alters adult health.},
   Doi = {10.1001/jamanetworkopen.2020.6095},
   Key = {fds349929}
}

@article{fds349777,
   Author = {Belsky, DW and Caspi, A and Arseneault, L and Baccarelli, A and Corcoran, DL and Gao, X and Hannon, E and Harrington, HL and Rasmussen,
             LJ and Houts, R and Huffman, K and Kraus, WE and Kwon, D and Mill, J and Pieper, CF and Prinz, JA and Poulton, R and Schwartz, J and Sugden, K and Vokonas, P and Williams, BS and Moffitt, TE},
   Title = {Quantification of the pace of biological aging in humans
             through a blood test, the DunedinPoAm DNA methylation
             algorithm.},
   Journal = {Elife},
   Volume = {9},
   Year = {2020},
   Month = {May},
   url = {http://dx.doi.org/10.7554/eLife.54870},
   Abstract = {Biological aging is the gradual, progressive decline in
             system integrity that occurs with advancing chronological
             age, causing morbidity and disability. Measurements of the
             pace of aging are needed as surrogate endpoints in trials of
             therapies designed to prevent disease by slowing biological
             aging. We report a blood-DNA-methylation measure that is
             sensitive to variation in pace of biological aging among
             individuals born the same year. We first modeled
             change-over-time in 18 biomarkers tracking organ-system
             integrity across 12 years of follow-up in n = 954 members of
             the Dunedin Study born in 1972-1973. Rates of change in each
             biomarker over ages 26-38 years were composited to form a
             measure of aging-related decline, termed Pace-of-Aging.
             Elastic-net regression was used to develop a DNA-methylation
             predictor of Pace-of-Aging, called DunedinPoAm for
             Dunedin(P)ace(o)f(A)ging(m)ethylation. Validation analysis
             in cohort studies and the CALERIE trial provide
             proof-of-principle for DunedinPoAm as a single-time-point
             measure of a person's pace of biological
             aging.},
   Doi = {10.7554/eLife.54870},
   Key = {fds349777}
}

@article{fds348417,
   Author = {Motz, RT and Barnes, JC and Caspi, A and Arseneault, L and Cullen, FT and Houts, R and Wertz, J and Moffitt, TE},
   Title = {Does contact with the justice system deter or promote future
             delinquency? Results from a longitudinal study of British
             adolescent twins.},
   Journal = {Criminology : an interdisciplinary journal},
   Volume = {58},
   Number = {2},
   Pages = {307-335},
   Year = {2020},
   Month = {May},
   url = {http://dx.doi.org/10.1111/1745-9125.12236},
   Abstract = {What impact does formal punishment have on antisocial
             conduct-does it deter or promote it? The findings from a
             long line of research on the labeling tradition indicate
             formal punishments have the opposite-of-intended consequence
             of promoting future misbehavior. In another body of work,
             the results show support for deterrence-based hypotheses
             that punishment deters future misbehavior. So, which is it?
             We draw on a nationally representative sample of British
             adolescent twins from the Environmental Risk (E-Risk)
             Longitudinal Twin Study to perform a robust test of the
             deterrence versus labeling question. We leverage a powerful
             research design in which twins can serve as the
             counterfactual for their co-twin, thereby ruling out many
             sources of confounding that have likely impacted prior
             studies. The pattern of findings provides support for
             labeling theory, showing that contact with the justice
             system-through spending a night in jail/prison, being issued
             an anti-social behaviour order (ASBO), or having an official
             record-promotes delinquency. We conclude by discussing the
             impact these findings may have on criminologists' and
             practitioners' perspective on the role of the juvenile
             justice system in society.},
   Doi = {10.1111/1745-9125.12236},
   Key = {fds348417}
}

@article{fds352503,
   Author = {Sugden, K and Hannon, EJ and Arseneault, L and Belsky, DW and Corcoran,
             DL and Fisher, HL and Houts, RM and Kandaswamy, R and Moffitt, TE and Poulton, R and Prinz, JA and Rasmussen, LJH and Williams, BS and Wong,
             CCY and Mill, J and Caspi, A},
   Title = {Patterns of Reliability: Assessing the Reproducibility and
             Integrity of DNA Methylation Measurement.},
   Journal = {Patterns (New York, N.Y.)},
   Volume = {1},
   Number = {2},
   Pages = {100014},
   Year = {2020},
   Month = {May},
   url = {http://dx.doi.org/10.1016/j.patter.2020.100014},
   Abstract = {DNA methylation plays an important role in both normal human
             development and risk of disease. The most utilized method of
             assessing DNA methylation uses BeadChips, generating an
             epigenome-wide "snapshot" of >450,000 observations (probe
             measurements) per assay. However, the reliability of each of
             these measurements is not equal, and little consideration is
             paid to consequences for research. We correlated repeat
             measurements of the same DNA samples using the Illumina
             HumanMethylation450K and the Infinium MethylationEPIC
             BeadChips in 350 blood DNA samples. Probes that were
             reliably measured were more heritable and showed consistent
             associations with environmental exposures, gene expression,
             and greater cross-tissue concordance. Unreliable probes were
             less replicable and generated an unknown volume of false
             negatives. This serves as a lesson for working with DNA
             methylation data, but the lessons are equally applicable to
             working with other data: as we advance toward generating
             increasingly greater volumes of data, failure to document
             reliability risks harming reproducibility.},
   Doi = {10.1016/j.patter.2020.100014},
   Key = {fds352503}
}

@article{fds349443,
   Author = {Caspi, A and Houts, RM and Ambler, A and Danese, A and Elliott, ML and Hariri, A and Harrington, H and Hogan, S and Poulton, R and Ramrakha, S and Rasmussen, LJH and Reuben, A and Richmond-Rakerd, L and Sugden, K and Wertz, J and Williams, BS and Moffitt, TE},
   Title = {Longitudinal Assessment of Mental Health Disorders and
             Comorbidities Across 4 Decades Among Participants in the
             Dunedin Birth Cohort Study.},
   Journal = {JAMA network open},
   Volume = {3},
   Number = {4},
   Pages = {e203221},
   Year = {2020},
   Month = {April},
   url = {http://dx.doi.org/10.1001/jamanetworkopen.2020.3221},
   Abstract = {<h4>Importance</h4>Mental health professionals typically
             encounter patients at 1 point in patients' lives. This
             cross-sectional window understandably fosters focus on the
             current presenting diagnosis. Research programs, treatment
             protocols, specialist clinics, and specialist journals are
             oriented to presenting diagnoses, on the assumption that
             diagnosis informs about causes and prognosis. This study
             tests an alternative hypothesis: people with mental
             disorders experience many different kinds of disorders
             across diagnostic families, when followed for 4
             decades.<h4>Objective</h4>To describe mental disorder life
             histories across the first half of the life
             course.<h4>Design, setting, and participants</h4>This cohort
             study involved participants born in New Zealand from 1972 to
             1973 who were enrolled in the population-representative
             Dunedin Study. Participants were observed from birth to age
             45 years (until April 2019). Data were analyzed from May
             2019 to January 2020.<h4>Main outcomes and
             measures</h4>Diagnosed impairing disorders were assessed 9
             times from ages 11 to 45 years. Brain function was assessed
             through neurocognitive examinations conducted at age 3
             years, neuropsychological testing during childhood and
             adulthood, and midlife neuroimaging-based brain
             age.<h4>Results</h4>Of 1037 original participants (535 male
             [51.6%]), 1013 had mental health data available. The
             proportions of participants meeting the criteria for a
             mental disorder were as follows: 35% (346 of 975) at ages 11
             to 15 years, 50% (473 of 941) at age 18 years, 51% (489 of
             961) at age 21 years, 48% (472 of 977) at age 26 years, 46%
             (444 of 969) at age 32 years, 45% (429 of 955) at age 38
             years, and 44% (407 of 927) at age 45 years. The onset of
             the disorder occurred by adolescence for 59% of participants
             (600 of 1013), eventually affecting 86% of the cohort (869
             of 1013) by midlife. By age 45 years, 85% of participants
             (737 of 869) with a disorder had accumulated comorbid
             diagnoses. Participants with adolescent-onset disorders
             subsequently presented with disorders at more past-year
             assessments (r = 0.71; 95% CI, 0.68 to 0.74;
             P < .001) and met the criteria for more diverse
             disorders (r = 0.64; 95% CI, 0.60 to 0.67;
             P < .001). Confirmatory factor analysis summarizing
             mental disorder life histories across 4 decades identified a
             general factor of psychopathology, the p-factor.
             Longitudinal analyses showed that high p-factor scores
             (indicating extensive mental disorder life histories) were
             antedated by poor neurocognitive functioning at age 3 years
             (r = -0.18; 95% CI, -0.24 to -0.12; P < .001), were
             accompanied by childhood-to-adulthood cognitive decline
             (r = -0.11; 95% CI, -0.17 to -0.04; P < .001), and
             were associated with older brain age at midlife
             (r = 0.14; 95% CI, 0.07 to 0.20; P < .001).<h4>Conclusions
             and relevance</h4>These findings suggest that mental
             disorder life histories shift among different successive
             disorders. Data from the present study, alongside nationwide
             data from Danish health registers, inform a life-course
             perspective on mental disorders. This perspective cautions
             against overreliance on diagnosis-specific research and
             clinical protocols.},
   Doi = {10.1001/jamanetworkopen.2020.3221},
   Key = {fds349443}
}

@article{fds348416,
   Author = {Richmond-Rakerd, LS and D'Souza, S and Andersen, SH and Hogan, S and Houts, RM and Poulton, R and Ramrakha, S and Caspi, A and Milne, BJ and Moffitt, TE},
   Title = {Clustering of health, crime and social-welfare inequality in
             4 million citizens from two nations.},
   Journal = {Nature human behaviour},
   Volume = {4},
   Number = {3},
   Pages = {255-264},
   Year = {2020},
   Month = {March},
   url = {http://dx.doi.org/10.1038/s41562-019-0810-4},
   Abstract = {Health and social scientists have documented the hospital
             revolving-door problem, the concentration of crime, and
             long-term welfare dependence. Have these distinct fields
             identified the same citizens? Using administrative databases
             linked to 1.7 million New Zealanders, we quantified and
             monetized inequality in distributions of health and social
             problems and tested whether they aggregate within
             individuals. Marked inequality was observed: Gini
             coefficients equalled 0.96 for criminal convictions, 0.91
             for public-hospital nights, 0.86 for welfare benefits, 0.74
             for prescription-drug fills and 0.54 for injury-insurance
             claims. Marked aggregation was uncovered: a small population
             segment accounted for a disproportionate share of use-events
             and costs across multiple sectors. These findings were
             replicated in 2.3 million Danes. We then integrated the New
             Zealand databases with the four-decade-long Dunedin Study.
             The high-need/high-cost population segment experienced
             early-life factors that reduce workforce readiness,
             including low education and poor mental health. In midlife
             they reported low life satisfaction. Investing in young
             people's education and training potential could reduce
             health and social inequalities and enhance population
             wellbeing.},
   Doi = {10.1038/s41562-019-0810-4},
   Key = {fds348416}
}

@article{fds366295,
   Author = {Carlisi, CO and Moffitt, TE and Knodt, AR and Harrington, H and Ireland,
             D and Melzer, TR and Poulton, R and Ramrakha, S and Caspi, A and Hariri,
             AR and Viding, E},
   Title = {Associations between life-course-persistent antisocial
             behaviour and brain structure in a population-representative
             longitudinal birth cohort.},
   Journal = {The lancet. Psychiatry},
   Volume = {7},
   Number = {3},
   Pages = {245-253},
   Year = {2020},
   Month = {March},
   url = {http://dx.doi.org/10.1016/s2215-0366(20)30002-x},
   Abstract = {<h4>Background</h4>Studies with behavioural and
             neuropsychological tests have supported the developmental
             taxonomy theory of antisocial behaviour, which specifies
             abnormal brain development as a fundamental aspect of
             life-course-persistent antisocial behaviour, but no study
             has characterised features of brain structure associated
             with life-course-persistent versus adolescence-limited
             trajectories, as defined by prospective data. We aimed to
             determine whether life-course-persistent antisocial
             behaviour is associated with neurocognitive abnormalities by
             testing the hypothesis that it is also associated with brain
             structure abnormalities.<h4>Methods</h4>We used structural
             MRI data collected at 45 years of age from participants in
             the Dunedin Study, a population-representative longitudinal
             birth cohort of 1037 individuals born between April 1, 1972,
             and March 31, 1973, in Dunedin, New Zealand, who were
             resident in the province and who participated in the first
             assessment at 3 years of age. Participants underwent MRI,
             and mean global cortical surface area and cortical thickness
             were extracted for each participant. Participants had been
             previously subtyped as exhibiting life-course-persistent,
             adolescence-limited, or no history of persistent antisocial
             behaviour (ie, a low trajectory group) based on
             informant-reported and self-reported conduct problems from
             the ages of 7 years to 26 years. Study personnel who
             processed the MRI images were masked to antisocial group
             membership. We used linear estimated ordinary least squares
             regressions to compare each antisocial trajectory group
             (life-course persistent and adolescence limited) with the
             low trajectory group to examine whether antisocial behaviour
             was related to abnormalities in mean global surface area and
             mean cortical thickness. Next, we used parcel-wise linear
             regressions to identify antisocial trajectory group
             differences in surface area and cortical thickness. All
             results were controlled for sex and false discovery rate
             corrected.<h4>Findings</h4>Data from 672 participants were
             analysed, and 80 (12%) were classified as having
             life-course-persistent antisocial behaviour, 151 (23%) as
             having adolescence-limited antisocial behaviour, and 441
             (66%) as having low antisocial behaviour. Individuals on the
             life-course-persistent trajectory had a smaller mean surface
             area (standardised β=-0·18 [95% CI -0·24 to -0·11];
             p<0·0001) and lower mean cortical thickness (standardised
             β=-0·10 [95% CI -0·19 to -0·02]; p=0·020) than did
             those in the low group. Compared with the low group, the
             life-course-persistent group had reduced surface area in 282
             of 360 anatomically defined parcels and thinner cortex in 11
             of 360 parcels encompassing circumscribed frontal and
             temporal regions associated with executive function, affect
             regulation, and motivation. Widespread differences in brain
             surface morphometry were not observed for the
             adolescence-limited group compared with either
             non-antisocial behaviour or life-course-persistent
             groups.<h4>Interpretation</h4>These analyses provide initial
             evidence that differences in brain surface morphometry are
             associated with life-course-persistent, but not
             adolescence-limited, antisocial behaviour. As such, the
             analyses are consistent with the developmental taxonomy
             theory of antisocial behaviour and highlight the importance
             of using prospective longitudinal data to define different
             patterns of antisocial behaviour development.<h4>Funding</h4>US
             National Institute on Aging, Health Research Council of New
             Zealand, New Zealand Ministry of Business, Innovation and
             Employment, UK Medical Research Council, Avielle Foundation,
             and Wellcome Trust.},
   Doi = {10.1016/s2215-0366(20)30002-x},
   Key = {fds366295}
}

@article{fds345813,
   Author = {Trotta, A and Arseneault, L and Caspi, A and Moffitt, TE and Danese, A and Pariante, C and Fisher, HL},
   Title = {Mental Health and Functional Outcomes in Young Adulthood of
             Children With Psychotic Symptoms: A Longitudinal Cohort
             Study.},
   Journal = {Schizophrenia bulletin},
   Volume = {46},
   Number = {2},
   Pages = {261-271},
   Year = {2020},
   Month = {February},
   url = {http://dx.doi.org/10.1093/schbul/sbz069},
   Abstract = {<h4>Background</h4>Childhood psychotic symptoms have been
             associated with various psychiatric disorders in adulthood
             but their role as early markers of poor outcomes during the
             crucial transition to adulthood is largely unknown.
             Therefore, we investigated associations between age-12
             psychotic symptoms and a range of mental health problems and
             functional outcomes at age 18.<h4>Methods</h4>Data were used
             from the Environmental Risk Longitudinal Twin Study, a
             nationally representative birth cohort of 2232 twins born in
             1994-1995 in England and Wales, followed to age 18 with 93%
             retention. Childhood psychotic symptoms were assessed in
             structured interviews at age 12. At age 18, study members'
             mental health problems, functional outcomes, risky
             behaviors, and offending were measured using self-reports
             and official records.<h4>Results</h4>Children with psychotic
             symptoms (N = 125, 5.9%) were more likely to experience a
             range of mental health problems in young adulthood than
             children without such symptoms. They were also more likely
             to be obese, smoke cigarettes, be lonely, be parents, and
             report a lower quality of life, but not more likely to
             commit crimes. Childhood psychotic symptoms predicted these
             poor outcomes over and above other emotional and behavioral
             problems during childhood. Nevertheless, twin analyses
             indicated that these associations were largely accounted for
             by shared family factors.<h4>Conclusions</h4>Psychotic
             symptoms in childhood signal risk for pervasive mental
             health and functional difficulties in young adulthood and
             thus may provide a useful screen for an array of later
             problems. However, early psychotic symptoms and poor
             outcomes may be manifestations of shared environmental and
             genetic risks.},
   Doi = {10.1093/schbul/sbz069},
   Key = {fds345813}
}

@article{fds347029,
   Author = {Rasmussen, LJH and Moffitt, TE and Arseneault, L and Danese, A and Eugen-Olsen, J and Fisher, HL and Harrington, H and Houts, R and Matthews, T and Sugden, K and Williams, B and Caspi,
             A},
   Title = {Association of Adverse Experiences and Exposure to Violence
             in Childhood and Adolescence With Inflammatory Burden in
             Young People.},
   Journal = {JAMA pediatrics},
   Volume = {174},
   Number = {1},
   Pages = {38-47},
   Year = {2020},
   Month = {January},
   url = {http://dx.doi.org/10.1001/jamapediatrics.2019.3875},
   Abstract = {<h4>Importance</h4>Childhood stress exposure is associated
             with inflammation as measured by C-reactive protein (CRP)
             and interleukin 6 (IL-6). However, findings are inconsistent
             and effect sizes are small. The addition of soluble
             urokinase plasminogen activator receptor (suPAR), a new
             biomarker of chronic inflammation, may improve measurement
             of stress-related inflammatory burden.<h4>Objectives</h4>To
             assess whether exposure to adverse experiences, stress, and
             violence is associated with an increase in suPAR levels in
             young people and to test the hypothesis that measuring suPAR
             in addition to CRP or IL-6 levels improves the assessment of
             the inflammatory burden associated with early-life
             stress.<h4>Design, setting, and participants</h4>This cohort
             study included 1391 participants from a 1994 to 1995 birth
             cohort of twins from the nationally representative
             Environmental Risk Longitudinal Twin Study in the United
             Kingdom. Participants were followed up until 18 years of age
             (93% retention). Plasma samples were analyzed in July 2018,
             and statistical analysis was performed from October 1, 2018,
             to May 31, 2019.<h4>Exposures</h4>Adverse childhood
             experiences and childhood and adolescent experience of
             stress and violence exposure.<h4>Main outcomes and
             measures</h4>Plasma CRP, IL-6, and suPAR levels at 18 years
             of age.<h4>Results</h4>Among 1391 young people (mean [SD]
             age, 18.4 [0.36] years; 733 [52.7%] female), those who had
             been exposed to stressful experiences had elevated suPAR
             levels by 18 years of age after controlling for sex, body
             mass index, and smoking: 0.03-ng/mL (95% CI, 0.01-0.05
             ng/mL) increase in suPAR per each additional adverse
             childhood experience, 0.09-ng/mL (95% CI, 0.01-0.17 ng/mL)
             increase in suPAR per each additional severe childhood
             experience of stress or violence, and 0.04-ng/mL (95% CI,
             -0.02 to 0.10 ng/mL) increase in suPAR per each additional
             severe adolescent experience of stress or violence.
             Individuals exposed to multiple types of violence in both
             childhood and adolescence had 0.26-ng/mL (95% CI, 0.07-0.45
             ng/mL) higher suPAR levels compared with children who did
             not experience stress or violence. These stress-exposed
             young people were significantly more likely to have elevated
             suPAR levels at 18 years of age even if they did not have
             elevated CRP or IL-6 levels. Measuring suPAR in addition to
             CRP or IL-6 increased the association between stress
             exposure and inflammatory burden. For example, after
             adjusting for CRP and IL-6 levels, each additional adverse
             childhood experience was associated with a 0.05-mL (95% CI,
             0.03-0.07 ng/mL) increase in suPAR, each additional severe
             childhood experience of stress or violence was associated
             with a 0.14-ng/mL (95% CI, 0.06-0.22 ng/mL) increase in
             suPAR, and each additional severe adolescent experience of
             stress or violence was associated with a 0.10-ng/mL (95% CI,
             0.04-0.16 ng/mL) increase in suPAR.<h4>Conclusions and
             relevance</h4>The results suggest that adult inflammation is
             associated with childhood exposure to stress. Adding
             information about suPAR to traditional biomarkers of
             inflammation may improve the measurement of inflammatory
             burden associated with exposure to stress and
             violence.},
   Doi = {10.1001/jamapediatrics.2019.3875},
   Key = {fds347029}
}

@article{fds347192,
   Author = {Barnes, JC and Liu, H and Motz, RT and Tanksley, PT and Kail, R and Beckley, AL and Belsky, DW and Domingue, BW and Moffitt, TE and Pratt,
             TC and Wertz, J},
   Title = {The propensity for aggressive behavior and lifetime
             incarceration risk: A test for gene-environment interaction
             (G × E) using whole-genome data},
   Journal = {Aggression and Violent Behavior},
   Volume = {49},
   Year = {2019},
   Month = {November},
   url = {http://dx.doi.org/10.1016/j.avb.2019.07.002},
   Abstract = {Incarceration is a disruptive event that is experienced by a
             considerable proportion of the United States population.
             Research has identified social factors that predict
             incarceration risk, but scholars have called for a focus on
             the ways that individual differences combine with social
             factors to affect incarceration risk. Our study is an
             initial attempt to heed this call using whole-genome data.
             We use data from the Health and Retirement Study (HRS) (N =
             6716) to construct a genome-wide measure of genetic
             propensity for aggressive behavior and use it to predict
             lifetime incarceration risk. We find that participants with
             a higher genetic propensity for aggression are more likely
             to experience incarceration, but the effect is stronger for
             males than females. Importantly, we identify a
             gene-environment interaction (G × E)—genetic propensity
             is reduced, substantively and statistically, to a
             non-significant predictor for males raised in homes where at
             least one parent graduated high school. We close by placing
             these findings in the broader context of concerns that have
             been raised about genetics research in criminology.},
   Doi = {10.1016/j.avb.2019.07.002},
   Key = {fds347192}
}

@article{fds346708,
   Author = {Rasmussen, LJH and Caspi, A and Ambler, A and Broadbent, JM and Cohen,
             HJ and d'Arbeloff, T and Elliott, M and Hancox, RJ and Harrington, H and Hogan, S and Houts, R and Ireland, D and Knodt, AR and Meredith-Jones,
             K and Morey, MC and Morrison, L and Poulton, R and Ramrakha, S and Richmond-Rakerd, L and Sison, ML and Sneddon, K and Thomson, WM and Hariri, AR and Moffitt, TE},
   Title = {Association of Neurocognitive and Physical Function With
             Gait Speed in Midlife.},
   Journal = {JAMA Netw Open},
   Volume = {2},
   Number = {10},
   Pages = {e1913123},
   Year = {2019},
   Month = {October},
   url = {http://dx.doi.org/10.1001/jamanetworkopen.2019.13123},
   Abstract = {IMPORTANCE: Gait speed is a well-known indicator of risk of
             functional decline and mortality in older adults, but little
             is known about the factors associated with gait speed
             earlier in life. OBJECTIVES: To test the hypothesis that
             slow gait speed reflects accelerated biological aging at
             midlife, as well as poor neurocognitive functioning in
             childhood and cognitive decline from childhood to midlife.
             DESIGN, SETTING, AND PARTICIPANTS: This cohort study uses
             data from the Dunedin Multidisciplinary Health and
             Development Study, a population-based study of a
             representative 1972 to 1973 birth cohort in New Zealand that
             observed participants to age 45 years (until April 2019).
             Data analysis was performed from April to June 2019.
             EXPOSURES: Childhood neurocognitive functions and
             accelerated aging, brain structure, and concurrent physical
             and cognitive functions in adulthood. MAIN OUTCOMES AND
             MEASURES: Gait speed at age 45 years, measured under 3
             walking conditions: usual, dual task, and maximum gait
             speeds. RESULTS: Of the 1037 original participants (91% of
             eligible births; 535 [51.6%] male), 997 were alive at age 45
             years, of whom 904 (90.7%) had gait speed measured (455
             [50.3%] male; 93% white). The mean (SD) gait speeds were
             1.30 (0.17) m/s for usual gait, 1.16 (0.23) m/s for dual
             task gait, and 1.99 (0.29) m/s for maximum gait. Adults with
             more physical limitations (standardized regression
             coefficient [β], -0.27; 95% CI, -0.34 to -0.21;
             P < .001), poorer physical functions (ie, weak grip
             strength [β, 0.36; 95% CI, 0.25 to 0.46], poor balance [β,
             0.28; 95% CI, 0.21 to 0.34], poor visual-motor coordination
             [β, 0.24; 95% CI, 0.17 to 0.30], and poor performance on
             the chair-stand [β, 0.34; 95% CI, 0.27 to 0.40] or 2-minute
             step tests [β, 0.33; 95% CI, 0.27 to 0.39]; all
             P < .001), accelerated biological aging across multiple
             organ systems (β, -0.33; 95% CI, -0.40 to -0.27;
             P < .001), older facial appearance (β, -0.25; 95% CI,
             -0.31 to -0.18; P < .001), smaller brain volume (β,
             0.15; 95% CI, 0.06 to 0.23; P < .001), more cortical
             thinning (β, 0.09; 95% CI, 0.02 to 0.16; P = .01),
             smaller cortical surface area (β, 0.13; 95% CI, 0.04 to
             0.21; P = .003), and more white matter hyperintensities
             (β, -0.09; 95% CI, -0.15 to -0.02; P = .01) had slower
             gait speed. Participants with lower IQ in midlife (β, 0.38;
             95% CI, 0.32 to 0.44; P < .001) and participants who
             exhibited cognitive decline from childhood to adulthood (β,
             0.10; 95% CI, 0.04 to 0.17; P < .001) had slower gait at
             age 45 years. Those with poor neurocognitive functioning as
             early as age 3 years had slower gait in midlife (β, 0.26;
             95% CI, 0.20 to 0.32; P < .001). CONCLUSIONS AND
             RELEVANCE: Adults' gait speed is associated with more than
             geriatric functional status; it is also associated with
             midlife aging and lifelong brain health.},
   Doi = {10.1001/jamanetworkopen.2019.13123},
   Key = {fds346708}
}

@article{fds342485,
   Author = {van Dongen, J and Zilhão, NR and Sugden, K and BIOS Consortium, and Hannon, EJ and Mill, J and Caspi, A and Agnew-Blais, J and Arseneault,
             L and Corcoran, DL and Moffitt, TE and Poulton, R and Franke, B and Boomsma, DI},
   Title = {Epigenome-wide Association Study of Attention-Deficit/Hyperactivity
             Disorder Symptoms in Adults.},
   Journal = {Biological psychiatry},
   Volume = {86},
   Number = {8},
   Pages = {599-607},
   Year = {2019},
   Month = {October},
   url = {http://dx.doi.org/10.1016/j.biopsych.2019.02.016},
   Abstract = {<h4>Background</h4>Previous studies have reported
             associations between attention-deficit/hyperactivity
             disorder symptoms and DNA methylation in children. We report
             the first epigenome-wide association study meta-analysis of
             adult attention-deficit/hyperactivity disorder symptoms,
             based on peripheral blood DNA methylation (Infinium
             HumanMethylation450K array) in three population-based adult
             cohorts.<h4>Methods</h4>An epigenome-wide association study
             was performed in the Netherlands Twin Register (N = 2258,
             mean age 37 years), Dunedin Multidisciplinary Health and
             Development Study (N = 800, age 38 years), and
             Environmental Risk Longitudinal Twin Study (N = 1631, age
             18 years), and results were combined through meta-analysis
             (total sample size N = 4689). Region-based analyses
             accounting for the correlation between nearby methylation
             sites were also performed.<h4>Results</h4>One epigenome-wide
             significant differentially methylated position was detected
             in the Dunedin study, but meta-analysis did not detect
             differentially methylated positions that were robustly
             associated across cohorts. In region-based analyses, six
             significant differentially methylation regions (DMRs) were
             identified in the Netherlands Twin Register, 19 in the
             Dunedin study, and none in the Environmental Risk
             Longitudinal Twin Study. Of these DMRs, 92% were associated
             with methylation quantitative trait loci, and 68% showed
             moderate to large blood-brain correlations for DNA
             methylation levels. DMRs included six nonoverlapping DMRs
             (three in the Netherlands Twin Register, three in the
             Dunedin study) in the major histocompatibility complex,
             which were associated with expression of genes in the major
             histocompatibility complex, including C4A and C4B,
             previously implicated in schizophrenia.<h4>Conclusions</h4>Our
             findings point at new candidate loci involved in immune and
             neuronal functions that await further replication. Our work
             also illustrates the need for further research to examine to
             what extent epigenetic associations with psychiatric traits
             depend on characteristics such as age, comorbidities,
             exposures, and genetic background.},
   Doi = {10.1016/j.biopsych.2019.02.016},
   Key = {fds342485}
}

@article{fds342367,
   Author = {Wertz, J and Belsky, J and Moffitt, TE and Belsky, DW and Harrington, H and Avinun, R and Poulton, R and Ramrakha, S and Caspi,
             A},
   Title = {Genetics of nurture: A test of the hypothesis that parents'
             genetics predict their observed caregiving.},
   Journal = {Developmental psychology},
   Volume = {55},
   Number = {7},
   Pages = {1461-1472},
   Year = {2019},
   Month = {July},
   url = {http://dx.doi.org/10.1037/dev0000709},
   Abstract = {Twin studies have documented that parenting behavior is
             partly heritable, but it is unclear how parents' genetics
             shape their caregiving. Using tools of molecular genetics,
             the present study investigated this process by testing
             hypotheses about associations between a genome-wide
             polygenic score for educational attainment and parental
             caregiving in 702 members of the Dunedin Study, a
             population-representative birth cohort. Data have been
             prospectively collected from when Study members were born
             through to midlife, and include assessments of the
             caregiving they provided once they became parents. Results
             showed that parents' polygenic scores predicted warm,
             sensitive, and stimulating caregiving, both in personal
             interactions with their young children (as captured on
             video) and through the home environments they created for
             their families (as observed by home visitors). The magnitude
             of this effect was small. Polygenic-score associations were
             independent of well-established predictors of parenting,
             such as parents' own childhood experiences of parenting and
             the age at which they became parents. Polygenic-score
             associations were mediated by parents' early-emerging
             cognitive abilities and self-control skills. Findings have
             implications for theory and research about genetic
             influences on caregiving and child development. (PsycINFO
             Database Record (c) 2019 APA, all rights
             reserved).},
   Doi = {10.1037/dev0000709},
   Key = {fds342367}
}

@article{fds340542,
   Author = {Elliott, ML and Belsky, DW and Anderson, K and Corcoran, DL and Ge, T and Knodt, A and Prinz, JA and Sugden, K and Williams, B and Ireland, D and Poulton, R and Caspi, A and Holmes, A and Moffitt, T and Hariri,
             AR},
   Title = {A Polygenic Score for Higher Educational Attainment is
             Associated with Larger Brains.},
   Journal = {Cerebral cortex (New York, N.Y. : 1991)},
   Volume = {29},
   Number = {8},
   Pages = {3496-3504},
   Year = {2019},
   Month = {July},
   url = {http://dx.doi.org/10.1093/cercor/bhy219},
   Abstract = {People who score higher on intelligence tests tend to have
             larger brains. Twin studies suggest the same genetic factors
             influence both brain size and intelligence. This has led to
             the hypothesis that genetics influence intelligence partly
             by contributing to the development of larger brains. We
             tested this hypothesis using four large imaging genetics
             studies (combined N = 7965) with polygenic scores derived
             from a genome-wide association study (GWAS) of educational
             attainment, a correlate of intelligence. We conducted
             meta-analysis to test associations among participants'
             genetics, total brain volume (i.e., brain size), and
             cognitive test performance. Consistent with previous
             findings, participants with higher polygenic scores achieved
             higher scores on cognitive tests, as did participants with
             larger brains. Participants with higher polygenic scores
             also had larger brains. We found some evidence that brain
             size partly mediated associations between participants'
             education polygenic scores and their cognitive test
             performance. Effect sizes were larger in the
             population-based samples than in the convenience-based
             samples. Recruitment and retention of population-representative
             samples should be a priority for neuroscience research.
             Findings suggest promise for studies integrating GWAS
             discoveries with brain imaging to understand neurobiology
             linking genetics with cognitive performance.},
   Doi = {10.1093/cercor/bhy219},
   Key = {fds340542}
}

@article{fds344829,
   Author = {Caye, A and Agnew-Blais, J and Arseneault, L and Gonçalves, H and Kieling, C and Langley, K and Menezes, AMB and Moffitt, TE and Passos,
             IC and Rocha, TB and Sibley, MH and Swanson, JM and Thapar, A and Wehrmeister, F and Rohde, LA},
   Title = {A risk calculator to predict adult attention-deficit/hyperactivity
             disorder: generation and external validation in three birth
             cohorts and one clinical sample - ERRATUM.},
   Journal = {Epidemiology and psychiatric sciences},
   Volume = {29},
   Pages = {e41},
   Year = {2019},
   Month = {July},
   url = {http://dx.doi.org/10.1017/s2045796019000337},
   Doi = {10.1017/s2045796019000337},
   Key = {fds344829}
}

@article{fds342775,
   Author = {Reuben, A and Arseneault, L and Belsky, DW and Caspi, A and Fisher, HL and Houts, RM and Moffitt, TE and Odgers, C},
   Title = {Residential neighborhood greenery and children's cognitive
             development.},
   Journal = {Social science & medicine (1982)},
   Volume = {230},
   Pages = {271-279},
   Year = {2019},
   Month = {June},
   url = {http://dx.doi.org/10.1016/j.socscimed.2019.04.029},
   Abstract = {Children who grow up in neighborhoods with more green
             vegetation show enhanced cognitive development in specific
             domains over short timespans. However, it is unknown if
             neighborhood greenery per se is uniquely predictive of
             children's overall cognitive development measured across
             many years. The E-Risk Longitudinal Study, a nationally
             representative 1994-5 birth-cohort of children in Britain
             (n = 1658 urban and suburban-dwelling participants), was
             used to test whether residential neighborhood greenery
             uniquely predicts children's cognitive development across
             childhood and adolescence. Greenery exposure was assessed
             from ages 5 to 18 using the satellite imagery-based
             normalized difference vegetation index (NDVI) in 1-mile
             buffers around the home. Fluid and crystalized intellectual
             performance was assessed in the home at ages 5, 12, and 18
             using the Wechsler Intelligence Scale, and executive
             function, working memory, and attention ability were
             assessed in the home at age 18 using the Cambridge
             Neuropsychological Test Automated Battery. Children living
             in residences surrounded by more neighborhood greenery
             scored significantly higher, on average, on IQ measures at
             all ages. However, the association between greenery and
             cognitive measures did not hold after accounting for family
             or neighborhood socioeconomic status. After adjustment for
             study covariates, child greenery exposure was not a
             significant predictor of longitudinal increases in IQ across
             childhood and adolescence or of executive function, working
             memory, or attention ability at age 18. Children raised in
             greener neighborhoods exhibit better overall cognitive
             ability, but the association is likely accounted for by
             family and neighborhood socioeconomic factors.},
   Doi = {10.1016/j.socscimed.2019.04.029},
   Key = {fds342775}
}

@article{fds342366,
   Author = {Belsky, DW and Caspi, A and Arseneault, L and Corcoran, DL and Domingue,
             BW and Harris, KM and Houts, RM and Mill, JS and Moffitt, TE and Prinz, J and Sugden, K and Wertz, J and Williams, B and Odgers,
             CL},
   Title = {Genetics and the geography of health, behaviour and
             attainment.},
   Journal = {Nature human behaviour},
   Volume = {3},
   Number = {6},
   Pages = {576-586},
   Year = {2019},
   Month = {June},
   url = {http://dx.doi.org/10.1038/s41562-019-0562-1},
   Abstract = {Young people's life chances can be predicted by
             characteristics of their neighbourhood<sup>1</sup>. Children
             growing up in disadvantaged neighbourhoods exhibit worse
             physical and mental health and suffer poorer educational and
             economic outcomes than children growing up in advantaged
             neighbourhoods. Increasing recognition that aspects of
             social inequalities tend, in fact, to be geographical
             inequalities<sup>2-5</sup> is stimulating research and
             focusing policy interest on the role of place in shaping
             health, behaviour and social outcomes. Where neighbourhood
             effects are causal, neighbourhood-level interventions can be
             effective. Where neighbourhood effects reflect selection of
             families with different characteristics into different
             neighbourhoods, interventions should instead target families
             or individuals directly. To test how selection may affect
             different neighbourhood-linked problems, we linked
             neighbourhood data with genetic, health and social outcome
             data for >7,000 European-descent UK and US young people in
             the E-Risk and Add Health studies. We tested
             selection/concentration of genetic risks for obesity,
             schizophrenia, teen pregnancy and poor educational outcomes
             in high-risk neighbourhoods, including genetic analysis of
             neighbourhood mobility. Findings argue against genetic
             selection/concentration as an explanation for neighbourhood
             gradients in obesity and mental health problems. By
             contrast, modest genetic selection/concentration was evident
             for teen pregnancy and poor educational outcomes, suggesting
             that neighbourhood effects for these outcomes should be
             interpreted with care.},
   Doi = {10.1038/s41562-019-0562-1},
   Key = {fds342366}
}

@article{fds341891,
   Author = {Thomson, WM and Broadbent, JM and Caspi, A and Poulton, R and Moffitt,
             TE},
   Title = {Childhood IQ predicts age-38 oral disease experience and
             service-use.},
   Journal = {Community dentistry and oral epidemiology},
   Volume = {47},
   Number = {3},
   Pages = {252-258},
   Year = {2019},
   Month = {June},
   url = {http://dx.doi.org/10.1111/cdoe.12451},
   Abstract = {<h4>Objectives</h4>Given that people with higher
             intelligence have been shown to live longer, enjoy better
             health and have more favourable health behaviours, we
             investigated the association between childhood IQ and a
             range of important dental health and service-use indicators
             at age 38.<h4>Methods</h4>Long-standing prospective study of
             a complete birth cohort, with childhood IQ (assessed at ages
             7, 9, 11 and 13 years) used to allocate participants
             (N = 818) to one of four ordinal categories of childhood
             IQ.<h4>Results</h4>There were distinct and consistent
             gradients by childhood IQ in almost all of the dental caries
             experience measures (with the exception of filled teeth)
             whereby each was most severe in the lowest child IQ category
             and least severe in the highest; the exception was the mean
             FT score, for which there was no discernible gradient.
             Indicators of self-care and periodontal disease experience
             showed similar gradients, and multivariate modelling using
             the continuous IQ score confirmed the observed
             patterns.<h4>Conclusions</h4>Childhood cognitive function is
             a key determinant of oral health and dental service-use by
             midlife, with those of lower cognitive capacity as children
             likely to have poorer oral health, less favourable oral
             health-related beliefs, and more detrimental self-care and
             dental visiting practices by age 38. There is a need to
             shape dental clinical services and public health
             interventions so that people with the poorest cognitive
             function do not continue to be disadvantaged.},
   Doi = {10.1111/cdoe.12451},
   Key = {fds341891}
}

@article{fds343356,
   Author = {Caye, A and Agnew-Blais, J and Arseneault, L and Gonçalves, H and Kieling, C and Langley, K and Menezes, AMB and Moffitt, TE and Passos,
             IC and Rocha, TB and Sibley, MH and Swanson, JM and Thapar, A and Wehrmeister, F and Rohde, LA},
   Title = {A risk calculator to predict adult attention-deficit/hyperactivity
             disorder: generation and external validation in three birth
             cohorts and one clinical sample.},
   Journal = {Epidemiology and psychiatric sciences},
   Volume = {29},
   Pages = {e37},
   Year = {2019},
   Month = {May},
   url = {http://dx.doi.org/10.1017/s2045796019000283},
   Abstract = {<h4>Aim</h4>Few personalised medicine investigations have
             been conducted for mental health. We aimed to generate and
             validate a risk tool that predicts adult
             attention-deficit/hyperactivity disorder
             (ADHD).<h4>Methods</h4>Using logistic regression models, we
             generated a risk tool in a representative population cohort
             (ALSPAC - UK, 5113 participants, followed from birth to age
             17) using childhood clinical and sociodemographic data with
             internal validation. Predictors included sex, socioeconomic
             status, single-parent family, ADHD symptoms, comorbid
             disruptive disorders, childhood maltreatment, ADHD symptoms,
             depressive symptoms, mother's depression and intelligence
             quotient. The outcome was defined as a categorical diagnosis
             of ADHD in young adulthood without requiring age at onset
             criteria. We also tested Machine Learning approaches for
             developing the risk models: Random Forest, Stochastic
             Gradient Boosting and Artificial Neural Network. The risk
             tool was externally validated in the E-Risk cohort (UK, 2040
             participants, birth to age 18), the 1993 Pelotas Birth
             Cohort (Brazil, 3911 participants, birth to age 18) and the
             MTA clinical sample (USA, 476 children with ADHD and 241
             controls followed for 16 years from a minimum of 8 and a
             maximum of 26 years old).<h4>Results</h4>The overall
             prevalence of adult ADHD ranged from 8.1 to 12% in the
             population-based samples, and was 28.6% in the clinical
             sample. The internal performance of the model in the
             generating sample was good, with an area under the curve
             (AUC) for predicting adult ADHD of 0.82 (95% confidence
             interval (CI) 0.79-0.83). Calibration plots showed good
             agreement between predicted and observed event frequencies
             from 0 to 60% probability. In the UK birth cohort test
             sample, the AUC was 0.75 (95% CI 0.71-0.78). In the
             Brazilian birth cohort test sample, the AUC was
             significantly lower -0.57 (95% CI 0.54-0.60). In the
             clinical trial test sample, the AUC was 0.76 (95% CI
             0.73-0.80). The risk model did not predict adult anxiety or
             major depressive disorder. Machine Learning approaches did
             not outperform logistic regression models. An open-source
             and free risk calculator was generated for clinical use and
             is available online at https://ufrgs.br/prodah/adhd-calculator/.<h4>Conclusions</h4>The
             risk tool based on childhood characteristics specifically
             predicts adult ADHD in European and North-American
             population-based and clinical samples with comparable
             discrimination to commonly used clinical tools in internal
             medicine and higher than most previous attempts for mental
             and neurological disorders. However, its use in
             middle-income settings requires caution.},
   Doi = {10.1017/s2045796019000283},
   Key = {fds343356}
}

@article{fds341830,
   Author = {Baldwin, JR and Arseneault, L and Caspi, A and Moffitt, TE and Fisher,
             HL and Odgers, CL and Ambler, A and Houts, RM and Matthews, T and Ougrin,
             D and Richmond-Rakerd, LS and Takizawa, R and Danese,
             A},
   Title = {Adolescent Victimization and Self-Injurious Thoughts and
             Behaviors: A Genetically Sensitive Cohort
             Study.},
   Journal = {Journal of the American Academy of Child and Adolescent
             Psychiatry},
   Volume = {58},
   Number = {5},
   Pages = {506-513},
   Year = {2019},
   Month = {May},
   url = {http://dx.doi.org/10.1016/j.jaac.2018.07.903},
   Abstract = {<h4>Objective</h4>Victimized adolescents have an increased
             risk of self-injurious thoughts and behaviors. However, poor
             understanding of causal and non-causal mechanisms underlying
             this observed risk limits the development of interventions
             to prevent premature death in adolescents. This study tested
             whether pre-existing family-wide and individual
             vulnerabilities account for victimized adolescents'
             increased risk of self-injurious thoughts and
             behaviors.<h4>Method</h4>Participants were 2,232 British
             children followed from birth to 18 years of age as part of
             the Environmental Risk Longitudinal Twin Study. Adolescent
             victimization (maltreatment, neglect, sexual victimization,
             family violence, peer/sibling victimization, cyber
             victimization, and crime victimization) was assessed through
             interviews with participants and co-informant questionnaires
             at the 18-year assessment. Suicidal ideation, self-harm, and
             suicide attempt in adolescence were assessed through
             interviews with participants at 18 years.<h4>Results</h4>Victimized
             adolescents had an increased risk of suicidal ideation (odds
             ratio [OR] 2.40, 95% CI 2.11-2.74), self-harm (OR 2.38, 95%
             CI 2.10-2.69), and suicide attempt (OR 3.14, 95% CI
             2.54-3.88). Co-twin control and propensity score matching
             analyses showed that these associations were largely
             accounted for by pre-existing familial and individual
             vulnerabilities, respectively. Over and above their prior
             vulnerabilities, victimized adolescents still showed a
             modest increase in risk for suicidal ideation (OR 1.45,
             95%CI 1.10-1.91) and self-harm (OR 1.50, 95% CI 1.18-1.91)
             but not for suicide attempt (OR 1.28, 95% CI
             0.83-1.98).<h4>Conclusion</h4>Risk for self-injurious
             thoughts and behaviors in victimized adolescents is
             explained only in part by the experience of victimization.
             Pre-existing vulnerabilities account for a large proportion
             of the risk. Therefore, effective interventions to prevent
             premature death in victimized adolescents should not only
             target the experience of victimization but also address
             pre-existing vulnerabilities.},
   Doi = {10.1016/j.jaac.2018.07.903},
   Key = {fds341830}
}

@article{fds342368,
   Author = {Moffitt, TE and Caspi, A},
   Title = {Psychiatry's Opportunity to Prevent the Rising Burden of
             Age-Related Disease.},
   Journal = {JAMA psychiatry},
   Volume = {76},
   Number = {5},
   Pages = {461-462},
   Year = {2019},
   Month = {May},
   url = {http://dx.doi.org/10.1001/jamapsychiatry.2019.0037},
   Doi = {10.1001/jamapsychiatry.2019.0037},
   Key = {fds342368}
}

@article{fds342484,
   Author = {Matthews, T and Odgers, CL and Danese, A and Fisher, HL and Newbury, JB and Caspi, A and Moffitt, TE and Arseneault, L},
   Title = {Loneliness and Neighborhood Characteristics: A
             Multi-Informant, Nationally Representative Study of Young
             Adults.},
   Journal = {Psychological science},
   Volume = {30},
   Number = {5},
   Pages = {765-775},
   Year = {2019},
   Month = {May},
   url = {http://dx.doi.org/10.1177/0956797619836102},
   Abstract = {In this study, we investigated associations between the
             characteristics of the neighborhoods in which young adults
             live and their feelings of loneliness, using data from
             different sources. Participants were drawn from the
             Environmental Risk Longitudinal Twin Study. Loneliness was
             measured via self-reports at ages 12 and 18 years and also
             by interviewer ratings at age 18. Neighborhood
             characteristics were assessed between the ages of 12 and 18
             via government data, systematic social observations, a
             resident survey, and participants' self-reports. Greater
             loneliness was associated with perceptions of lower
             collective efficacy and greater neighborhood disorder but
             not with more objective measures of neighborhood
             characteristics. Lonelier individuals perceived the
             collective efficacy of their neighborhoods to be lower than
             did their less lonely siblings who lived at the same
             address. These findings suggest that feelings of loneliness
             are associated with negatively biased perceptions of
             neighborhood characteristics, which may have implications
             for lonely individuals' likelihood of escaping
             loneliness.},
   Doi = {10.1177/0956797619836102},
   Key = {fds342484}
}

@article{fds341052,
   Author = {Reuben, A and Schaefer, JD and Moffitt, TE and Broadbent, J and Harrington, H and Houts, RM and Ramrakha, S and Poulton, R and Caspi,
             A},
   Title = {Association of Childhood Lead Exposure With Adult
             Personality Traits and Lifelong Mental Health.},
   Journal = {JAMA psychiatry},
   Volume = {76},
   Number = {4},
   Pages = {418-425},
   Year = {2019},
   Month = {April},
   url = {http://dx.doi.org/10.1001/jamapsychiatry.2018.4192},
   Abstract = {<h4>Importance</h4>Millions of adults now entering middle
             age were exposed to high levels of lead, a developmental
             neurotoxin, as children. Although childhood lead exposure
             has been linked to disrupted behavioral development, the
             long-term consequences for adult mental and behavioral
             health have not been fully characterized.<h4>Objective</h4>To
             examine whether childhood lead exposure is associated with
             greater psychopathology across the life course and difficult
             adult personality traits.<h4>Design, setting, and
             participants</h4>This prospective cohort study was based on
             a population-representative birth cohort of individuals born
             between April 1, 1972, and March 31, 1973, in Dunedin, New
             Zealand, the Dunedin Multidisciplinary Health and
             Development Study. Members were followed up in December 2012
             when they were 38 years of age. Data analysis was performed
             from March 14, 2018, to October 24, 2018.<h4>Exposures</h4>Childhood
             lead exposure ascertained as blood lead levels measured at
             11 years of age. Blood lead levels were unrelated to family
             socioeconomic status.<h4>Main outcomes and
             measures</h4>Primary outcomes were adult mental health
             disorder symptoms assessed through clinical interview at 18,
             21, 26, 32, and 38 years of age and transformed through
             confirmatory factor analysis into continuous measures of
             general psychopathology and internalizing, externalizing,
             and thought disorder symptoms (all standardized to a mean
             [SD] of 100 [15]) and adult personality assessed through
             informant report using the Big Five Personality Inventory
             (assessing neuroticism, extraversion, openness to
             experience, agreeableness, and conscientiousness) at 26, 32,
             and 38 years of age (all scores standardized to a mean [SD]
             of 0 [1]). Hypotheses were formulated after data collection;
             an analysis plan was posted in advance.<h4>Results</h4>Of
             1037 original study members, 579 (55.8%) were tested for
             lead exposure at 11 years of age (311 [53.7%] male). The
             mean (SD) blood lead level was 11.08 (4.96) μg/dL. After
             adjusting for study covariates, each 5-μg/dL increase in
             childhood blood lead level was associated with a 1.34-point
             increase (95% CI, 0.11-2.57; P = .03) in general
             psychopathology, driven by internalizing (b = 1.41; 95%
             CI, 0.19-2.62; P = .02) and thought disorder
             (b = 1.30; 95% CI, 0.06-2.54; P = .04) symptoms.
             Each 5-μg/dL increase in childhood blood lead level was
             also associated with a 0.10-SD increase in neuroticism (95%
             CI, 0.02-0.08; P = .02), a 0.09-SD decrease in
             agreeableness (95% CI, -0.18 to -0.01; P = .03), and a
             0.14-SD decrease in conscientiousness (95% CI, -0.25 to
             -0.03; P = .01). There were no statistically significant
             associations with informant-rated extraversion
             (b = -0.09; 95% CI, -0.17 to 0.004; P = .06) and
             openness to experience (b = -0.07; 95% CI, -0.17 to
             0.03; P = .15).<h4>Conclusions and relevance</h4>In this
             multidecade, longitudinal study of lead-exposed children,
             higher childhood blood lead level was associated with
             greater psychopathology across the life course and difficult
             adult personality traits. Childhood lead exposure may have
             long-term consequences for adult mental health and
             personality.},
   Doi = {10.1001/jamapsychiatry.2018.4192},
   Key = {fds341052}
}

@article{fds336532,
   Author = {Elliott, ML and Knodt, AR and Cooke, M and Kim, MJ and Melzer, TR and Keenan, R and Ireland, D and Ramrakha, S and Poulton, R and Caspi, A and Moffitt, TE and Hariri, AR},
   Title = {General functional connectivity: Shared features of
             resting-state and task fMRI drive reliable and heritable
             individual differences in functional brain
             networks.},
   Journal = {NeuroImage},
   Volume = {189},
   Pages = {516-532},
   Year = {2019},
   Month = {April},
   url = {http://dx.doi.org/10.1016/j.neuroimage.2019.01.068},
   Abstract = {Intrinsic connectivity, measured using resting-state fMRI,
             has emerged as a fundamental tool in the study of the human
             brain. However, due to practical limitations, many studies
             do not collect enough resting-state data to generate
             reliable measures of intrinsic connectivity necessary for
             studying individual differences. Here we present general
             functional connectivity (GFC) as a method for leveraging
             shared features across resting-state and task fMRI and
             demonstrate in the Human Connectome Project and the Dunedin
             Study that GFC offers better test-retest reliability than
             intrinsic connectivity estimated from the same amount of
             resting-state data alone. Furthermore, at equivalent scan
             lengths, GFC displayed higher estimates of heritability than
             resting-state functional connectivity. We also found that
             predictions of cognitive ability from GFC generalized across
             datasets, performing as well or better than resting-state or
             task data alone. Collectively, our work suggests that GFC
             can improve the reliability of intrinsic connectivity
             estimates in existing datasets and, subsequently, the
             opportunity to identify meaningful correlates of individual
             differences in behavior. Given that task and resting-state
             data are often collected together, many researchers can
             immediately derive more reliable measures of intrinsic
             connectivity through the adoption of GFC rather than solely
             using resting-state data. Moreover, by better capturing
             heritable variation in intrinsic connectivity, GFC
             represents a novel endophenotype with broad applications in
             clinical neuroscience and biomarker discovery.},
   Doi = {10.1016/j.neuroimage.2019.01.068},
   Key = {fds336532}
}

@article{fds341053,
   Author = {Richmond-Rakerd, LS and Caspi, A and Arseneault, L and Baldwin, JR and Danese, A and Houts, RM and Matthews, T and Wertz, J and Moffitt,
             TE},
   Title = {Adolescents Who Self-Harm and Commit Violent Crime: Testing
             Early-Life Predictors of Dual Harm in a Longitudinal Cohort
             Study.},
   Journal = {The American journal of psychiatry},
   Volume = {176},
   Number = {3},
   Pages = {186-195},
   Year = {2019},
   Month = {March},
   url = {http://dx.doi.org/10.1176/appi.ajp.2018.18060740},
   Abstract = {<h4>Objective</h4>Self-harm is associated with violent
             offending. However, little is known about young people who
             engage in "dual-harm" behavior. The authors investigated
             antecedents, clinical features, and life characteristics
             distinguishing dual-harming adolescents from those who
             self-harm only.<h4>Methods</h4>Participants were from the
             Environmental Risk (E-Risk) Longitudinal Twin Study, a
             nationally representative U.K. cohort of 2,232 twins born in
             1994 and 1995. Self-harm in adolescence was assessed through
             interviews at age 18. Violent offending was assessed using a
             computer questionnaire at age 18 and police records through
             age 22. Risk factors were assessed between ages 5 and 12.
             Adolescent mental health, victimization, personality
             functioning, and use of support services were measured at
             age 18.<h4>Results</h4>Self-harm was associated with violent
             crime (odds ratio=3.50, 95% CI=2.61-4.70), even after
             accounting for familial risk factors. Dual harmers had been
             victims of violence from childhood and exhibited lower
             childhood self-control and lower childhood IQ than self-only
             harmers. Dual harmers experienced higher rates of concurrent
             psychotic symptoms and substance dependence. They also
             exhibited distinct personality styles characterized by
             resistance to change and by emotional and interpersonal
             lability. However, dual harmers were not more likely than
             self-only harmers to have contact with mental health
             services.<h4>Conclusions</h4>Dual harmers have self-control
             difficulties and are immersed in violence from a young age.
             A treatment- rather than punishment-oriented approach is
             indicated to meet these individuals' needs. Connecting
             self-harming adolescents with delinquency-reduction programs
             and transdiagnostic approaches that target self-regulation
             may reduce harmful behaviors. Preventing childhood
             maltreatment and implementing strategies to reduce
             victimization exposure could mitigate risk for both
             internalized and externalized violence.},
   Doi = {10.1176/appi.ajp.2018.18060740},
   Key = {fds341053}
}

@article{fds341514,
   Author = {Lewis, SJ and Arseneault, L and Caspi, A and Fisher, HL and Matthews, T and Moffitt, TE and Odgers, CL and Stahl, D and Teng, JY and Danese,
             A},
   Title = {The epidemiology of trauma and post-traumatic stress
             disorder in a representative cohort of young people in
             England and Wales.},
   Journal = {The lancet. Psychiatry},
   Volume = {6},
   Number = {3},
   Pages = {247-256},
   Year = {2019},
   Month = {March},
   url = {http://dx.doi.org/10.1016/s2215-0366(19)30031-8},
   Abstract = {<h4>Background</h4>Despite the emphasis placed on childhood
             trauma in psychiatry, comparatively little is known about
             the epidemiology of trauma and trauma-related
             psychopathology in young people. We therefore aimed to
             evaluate the prevalence, clinical features, and risk factors
             associated with trauma exposure and post-traumatic stress
             disorder (PTSD) in young people.<h4>Methods</h4>We carried
             out a comprehensive epidemiological study based on
             participants from the Environmental Risk Longitudinal Twin
             Study, a population-representative birth-cohort of 2232
             children born in England and Wales in 1994-95. At the
             follow-up home visit at age 18 years, participants were
             assessed with structured interviews for trauma exposure,
             PTSD, other psychopathology, risk events, functional
             impairment, and service use. Risk factors for PTSD were
             measured prospectively over four previous assessments
             between age 5 and 12 years. The key outcomes were the
             prevalence, clinical features, and risk factors associated
             with trauma exposure and PTSD. We also derived and tested
             the internal validity of a PTSD risk calculator.<h4>Findings</h4>We
             found that 642 (31·1%) of 2064 participants reported trauma
             exposure and 160 (7·8%) of 2063 experienced PTSD by age 18
             years. Trauma-exposed participants had high rates of
             psychopathology (187 [29·2%] of 641 for major depressive
             episode, 146 [22·9%] of 638 for conduct disorder, and 102
             [15·9%] of 641 for alcohol dependence), risk events (160
             [25·0%] of 641 for self-harm, 53 [8·3%] of 640 for suicide
             attempt, and 42 [6·6%] of 640 for violent offence), and
             functional impairment. Participants with lifetime PTSD had
             even higher rates of psychopathology (87 [54·7%] of 159 for
             major depressive episode, 43 [27·0%] of 159 for conduct
             disorder, and 41 [25·6%] of 160 for alcohol dependence),
             risk events (78 [48·8%] of 160 for self-harm, 32 [20·1%]
             of 159 for suicide attempt, and 19 [11·9%] of 159 for
             violent offence), and functional impairment. However, only
             33 (20·6%) of 160 participants with PTSD received help from
             mental health professionals. The PTSD risk calculator had an
             internally validated area under the receiver operating
             characteristic curve of 0·74, indicating adequate
             discrimination of trauma-exposed participants with and
             without PTSD, and internally validated calibration-in-the-large
             of -0·10 and calibration slope of 0·90, indicating
             adequate calibration.<h4>Interpretation</h4>Trauma exposure
             and PTSD are associated with complex psychiatric
             presentations, high risk, and significant impairment in
             young people. Improved screening, reduced barriers to care
             provision, and comprehensive clinical assessment are needed
             to ensure that trauma-exposed young people and those with
             PTSD receive appropriate treatment.<h4>Funding</h4>The
             Medical Research Council, the National Institute of Child
             Health and Development, the Jacobs Foundation, the Nuffield
             Foundation, the National Society for Prevention of Cruelty
             to Children, the Economic and Social Research Council, the
             National Institute for Health Research, MQ, and Canadian
             Institutes for Advanced Research.},
   Doi = {10.1016/s2215-0366(19)30031-8},
   Key = {fds341514}
}

@article{fds341515,
   Author = {Sugden, K and Hannon, EJ and Arseneault, L and Belsky, DW and Broadbent,
             JM and Corcoran, DL and Hancox, RJ and Houts, RM and Moffitt, TE and Poulton, R and Prinz, JA and Thomson, WM and Williams, BS and Wong, CCY and Mill, J and Caspi, A},
   Title = {Establishing a generalized polyepigenetic biomarker for
             tobacco smoking.},
   Journal = {Translational psychiatry},
   Volume = {9},
   Number = {1},
   Pages = {92},
   Year = {2019},
   Month = {February},
   url = {http://dx.doi.org/10.1038/s41398-019-0430-9},
   Abstract = {Large-scale epigenome-wide association meta-analyses have
             identified multiple 'signatures'' of smoking. Drawing on
             these findings, we describe the construction of a
             polyepigenetic DNA methylation score that indexes smoking
             behavior and that can be utilized for multiple purposes in
             population health research. To validate the score, we use
             data from two birth cohort studies: The Dunedin Longitudinal
             Study, followed to age-38 years, and the Environmental Risk
             Study, followed to age-18 years. Longitudinal data show that
             changes in DNA methylation accumulate with increased
             exposure to tobacco smoking and attenuate with quitting.
             Data from twins discordant for smoking behavior show that
             smoking influences DNA methylation independently of genetic
             and environmental risk factors. Physiological data show that
             changes in DNA methylation track smoking-related changes in
             lung function and gum health over time. Moreover, DNA
             methylation changes predict corresponding changes in gene
             expression in pathways related to inflammation, immune
             response, and cellular trafficking. Finally, we present
             prospective data about the link between adverse childhood
             experiences (ACEs) and epigenetic modifications; these
             findings document the importance of controlling for
             smoking-related DNA methylation changes when studying
             biological embedding of stress in life-course research. We
             introduce the polyepigenetic DNA methylation score as a tool
             both for discovery and theory-guided research in epigenetic
             epidemiology.},
   Doi = {10.1038/s41398-019-0430-9},
   Key = {fds341515}
}

@article{fds336528,
   Author = {Rasmussen, LJH and Moffitt, TE and Eugen-Olsen, J and Belsky, DW and Danese, A and Harrington, H and Houts, RM and Poulton, R and Sugden, K and Williams, B and Caspi, A},
   Title = {Cumulative childhood risk is associated with a new measure
             of chronic inflammation in adulthood.},
   Journal = {Journal of child psychology and psychiatry, and allied
             disciplines},
   Volume = {60},
   Number = {2},
   Pages = {199-208},
   Year = {2019},
   Month = {February},
   url = {http://dx.doi.org/10.1111/jcpp.12928},
   Abstract = {<h4>Background</h4>Childhood risk factors are associated
             with elevated inflammatory biomarkers in adulthood, but it
             is unknown whether these risk factors are associated with
             increased adult levels of the chronic inflammation marker
             soluble urokinase plasminogen activator receptor (suPAR). We
             aimed to test the hypothesis that childhood exposure to risk
             factors for adult disease is associated with elevated suPAR
             in adulthood and to compare suPAR with the oft-reported
             inflammatory biomarker C-reactive protein
             (CRP).<h4>Methods</h4>Prospective study of a
             population-representative 1972-1973 birth cohort; the
             Dunedin Multidisciplinary Health and Development Study
             observed participants to age 38 years. Main childhood
             predictors were poor health, socioeconomic disadvantage,
             adverse childhood experiences (ACEs), low IQ, and poor
             self-control. Main adult outcomes were adulthood
             inflammation measured as suPAR and high-sensitivity CRP
             (hsCRP).<h4>Results</h4>Participants with available plasma
             samples at age 38 were included (N = 837, 50.5% male).
             suPAR (mean 2.40 ng/ml; SD 0.91) was positively correlated
             with hsCRP (r 0.15, p < .001). After controlling for sex,
             body mass index (BMI), and smoking, children who experienced
             more ACEs, lower IQ, or had poorer self-control showed
             elevated adult suPAR. When the five childhood risks were
             aggregated into a Cumulative Childhood Risk index, and
             controlling for sex, BMI, and smoking, Cumulative Childhood
             Risk was associated with higher suPAR (b 0.10; SE 0.03;
             p = .002). Cumulative Childhood Risk predicted elevated
             suPAR, after controlling for hsCRP (b 0.18; SE 0.03;
             p < .001).<h4>Conclusions</h4>Exposure to more childhood
             risk factors was associated with higher suPAR levels,
             independent of CRP. suPAR is a useful addition to studies
             connecting childhood risk to adult inflammatory
             burden.},
   Doi = {10.1111/jcpp.12928},
   Key = {fds336528}
}

@article{fds333592,
   Author = {Choi, KW and Houts, R and Arseneault, L and Pariante, C and Sikkema, KJ and Moffitt, TE},
   Title = {Maternal depression in the intergenerational transmission of
             childhood maltreatment and its sequelae: Testing postpartum
             effects in a longitudinal birth cohort.},
   Journal = {Development and psychopathology},
   Volume = {31},
   Number = {1},
   Pages = {143-156},
   Year = {2019},
   Month = {February},
   url = {http://dx.doi.org/10.1017/s0954579418000032},
   Abstract = {Mothers who have experienced childhood maltreatment are more
             likely to have children also exposed to maltreatment, a
             phenomenon known as intergenerational transmission. Factors
             in the perinatal period may contribute uniquely to this
             transmission, but timing effects have not been ascertained.
             Using structural equation modeling with 1,016 mothers and
             their 2,032 children in the Environmental Risk Longitudinal
             Twin Study, we tested the mediating role of postpartum
             depression between maternal childhood maltreatment and a
             cascade of negative child outcomes, specifically child
             exposure to maltreatment, internalizing symptoms, and
             externalizing symptoms: (a) adjusting for later maternal
             depression, (b) comparing across sex differences, and (c)
             examining the relative role of maltreatment subtypes.
             Mothers who had been maltreated as children, especially
             those who had experienced emotional or sexual abuse, were at
             increased risk for postpartum depression. In turn,
             postpartum depression predicted children's exposure to
             maltreatment, followed by emotional and behavioral problems.
             Indirect effects from maternal childhood maltreatment to
             child outcomes were robust across child sex and supported
             significant mediation through postpartum depression;
             however, this appeared to be carried by mothers' depression
             beyond the postpartum period. Identifying and treating
             postpartum depression, and preventing its recurrence, may
             help interrupt the intergenerational transmission of
             maltreatment and its sequelae.},
   Doi = {10.1017/s0954579418000032},
   Key = {fds333592}
}

@article{fds340540,
   Author = {Hartwig, FP and Davies, NM and Horta, BL and Ahluwalia, TS and Bisgaard,
             H and Bønnelykke, K and Caspi, A and Moffitt, TE and Poulton, R and Sajjad, A and Tiemeier, HW and Dalmau-Bueno, A and Guxens, M and Bustamante, M and Santa-Marina, L and Parker, N and Paus, T and Pausova,
             Z and Lauritzen, L and Schnurr, TM and Michaelsen, KF and Hansen, T and Oddy, W and Pennell, CE and Warrington, NM and Davey Smith and G and Victora, CG},
   Title = {Effect modification of FADS2 polymorphisms on the
             association between breastfeeding and intelligence: results
             from a collaborative meta-analysis.},
   Journal = {International journal of epidemiology},
   Volume = {48},
   Number = {1},
   Pages = {45-57},
   Year = {2019},
   Month = {February},
   url = {http://dx.doi.org/10.1093/ije/dyy273},
   Abstract = {<h4>Background</h4>Accumulating evidence suggests that
             breastfeeding benefits children's intelligence, possibly due
             to long-chain polyunsaturated fatty acids (LC-PUFAs) present
             in breast milk. Under a nutritional adequacy hypothesis, an
             interaction between breastfeeding and genetic variants
             associated with endogenous LC-PUFAs synthesis might be
             expected. However, the literature on this topic is
             controversial.<h4>Methods</h4>We investigated this gene ×
             environment interaction through a collaborative effort. The
             primary analysis involved >12 000 individuals and used ever
             breastfeeding, FADS2 polymorphisms rs174575 and rs1535 coded
             assuming a recessive effect of the G allele, and
             intelligence quotient (IQ) in Z scores.<h4>Results</h4>There
             was no strong evidence of interaction, with pooled
             covariate-adjusted interaction coefficients (i.e. difference
             between genetic groups of the difference in IQ Z scores
             comparing ever with never breastfed individuals) of
             0.12[(95% confidence interval (CI): -0.19; 0.43] and 0.06
             (95% CI: -0.16; 0.27) for the rs174575 and rs1535 variants,
             respectively. Secondary analyses corroborated these results.
             In studies with ≥5.85 and <5.85 months of breastfeeding
             duration, pooled estimates for the rs174575 variant were
             0.50 (95% CI: -0.06; 1.06) and 0.14 (95% CI: -0.10; 0.38),
             respectively, and 0.27 (95% CI: -0.28; 0.82) and -0.01 (95%
             CI: -0.19; 0.16) for the rs1535 variant.<h4>Conclusions</h4>Our
             findings did not support an interaction between ever
             breastfeeding and FADS2 polymorphisms. However, subgroup
             analysis suggested that breastfeeding may supply LC-PUFAs
             requirements for cognitive development if breastfeeding
             lasts for some (currently unknown) time. Future studies in
             large individual-level datasets would allow properly powered
             subgroup analyses and further improve our understanding on
             the breastfeeding × FADS2 interaction.},
   Doi = {10.1093/ije/dyy273},
   Key = {fds340540}
}

@article{fds340541,
   Author = {Roberts, S and Arseneault, L and Barratt, B and Beevers, S and Danese,
             A and Odgers, CL and Moffitt, TE and Reuben, A and Kelly, FJ and Fisher,
             HL},
   Title = {Exploration of NO2 and PM2.5 air
             pollution and mental health problems using high-resolution
             data in London-based children from a UK longitudinal cohort
             study.},
   Journal = {Psychiatry research},
   Volume = {272},
   Pages = {8-17},
   Year = {2019},
   Month = {February},
   url = {http://dx.doi.org/10.1016/j.psychres.2018.12.050},
   Abstract = {Air pollution is a worldwide environmental health issue.
             Increasingly, reports suggest that poor air quality may be
             associated with mental health problems, but these studies
             often use global measures and rarely focus on early
             development when psychopathology commonly emerges. To
             address this, we combined high-resolution air pollution
             exposure estimates and prospectively-collected phenotypic
             data to explore concurrent and longitudinal associations
             between air pollutants of major concern in urban areas and
             mental health problems in childhood and adolescence.
             Exploratory analyses were conducted on 284 London-based
             children from the Environmental Risk (E-Risk) Longitudinal
             Twin Study. Exposure to annualized PM<sub>2.5</sub> and
             NO<sub>2</sub> concentrations was estimated at address-level
             when children were aged 12. Symptoms of anxiety, depression,
             conduct disorder, and attention-deficit hyperactivity
             disorder were assessed at ages 12 and 18. Psychiatric
             diagnoses were ascertained from interviews with the
             participants at age 18. We found no associations between
             age-12 pollution exposure and concurrent mental health
             problems. However, age-12 pollution estimates were
             significantly associated with increased odds of major
             depressive disorder at age 18, even after controlling for
             common risk factors. This study demonstrates the potential
             utility of incorporating high-resolution pollution estimates
             into large epidemiological cohorts to robustly investigate
             associations between air pollution and youth mental
             health.},
   Doi = {10.1016/j.psychres.2018.12.050},
   Key = {fds340541}
}

@article{fds336530,
   Author = {Matthews, T and Danese, A and Caspi, A and Fisher, HL and Goldman-Mellor, S and Kepa, A and Moffitt, TE and Odgers, CL and Arseneault, L},
   Title = {Lonely young adults in modern Britain: findings from an
             epidemiological cohort study.},
   Journal = {Psychological medicine},
   Volume = {49},
   Number = {2},
   Pages = {268-277},
   Year = {2019},
   Month = {January},
   url = {http://dx.doi.org/10.1017/s0033291718000788},
   Abstract = {<h4>Background</h4>The aim of this study was to build a
             detailed, integrative profile of the correlates of young
             adults' feelings of loneliness, in terms of their current
             health and functioning and their childhood experiences and
             circumstances.<h4>Methods</h4>Data were drawn from the
             Environmental Risk Longitudinal Twin Study, a birth cohort
             of 2232 individuals born in England and Wales in 1994 and
             1995. Loneliness was measured when participants were aged
             18. Regression analyses were used to test concurrent
             associations between loneliness and health and functioning
             in young adulthood. Longitudinal analyses were conducted to
             examine childhood factors associated with young adult
             loneliness.<h4>Results</h4>Lonelier young adults were more
             likely to experience mental health problems, to engage in
             physical health risk behaviours, and to use more negative
             strategies to cope with stress. They were less confident in
             their employment prospects and were more likely to be out of
             work. Lonelier young adults were, as children, more likely
             to have had mental health difficulties and to have
             experienced bullying and social isolation. Loneliness was
             evenly distributed across genders and socioeconomic
             backgrounds.<h4>Conclusions</h4>Young adults' experience of
             loneliness co-occurs with a diverse range of problems, with
             potential implications for health in later life. The
             findings underscore the importance of early intervention to
             prevent lonely young adults from being trapped in loneliness
             as they age.},
   Doi = {10.1017/s0033291718000788},
   Key = {fds336530}
}

@article{fds348497,
   Author = {d'Arbeloff, T and Elliott, ML and Knodt, AR and Melzer, TR and Keenan,
             R and Ireland, D and Ramrakha, S and Poulton, R and Anderson, T and Caspi,
             A and Moffitt, TE and Hariri, AR},
   Title = {White matter hyperintensities are common in midlife and
             already associated with cognitive decline.},
   Journal = {Brain communications},
   Volume = {1},
   Number = {1},
   Pages = {fcz041},
   Year = {2019},
   Month = {January},
   url = {http://dx.doi.org/10.1093/braincomms/fcz041},
   Abstract = {White matter hyperintensities proliferate as the brain ages
             and are associated with increased risk for cognitive decline
             as well as Alzheimer's disease and related dementias. As
             such, white matter hyperintensities have been targeted as a
             surrogate biomarker in intervention trials with older
             adults. However, it is unclear at what stage of aging white
             matter hyperintensities begin to relate to cognition and if
             they may be a viable target for early prevention. In the
             Dunedin Study, a population-representative cohort followed
             since birth, we measured white matter hyperintensities in
             843 45-year-old participants using T<sub>2</sub>-weighted
             magnetic resonance imaging and we assessed cognitive decline
             from childhood to midlife. We found that white matter
             hyperintensities were common at age 45 and that white matter
             hyperintensity volume was modestly associated with both
             lower childhood (<i>ß</i> = -0.08, <i>P </i>=<i> </i>0.013)
             and adult IQ (<i>ß</i>=-0.15, <i>P </i><<i> </i>0.001).
             Moreover, white matter hyperintensity volume was associated
             with greater cognitive decline from childhood to midlife
             (<i>ß</i>=-0.09, <i>P </i><<i> </i>0.001). Our results
             demonstrate that a link between white matter
             hyperintensities and early signs of cognitive decline is
             detectable decades before clinical symptoms of dementia
             emerge. Thus, white matter hyperintensities may be a useful
             surrogate biomarker for identifying individuals in midlife
             at risk for future accelerated cognitive decline and
             selecting participants for dementia prevention
             trials.},
   Doi = {10.1093/braincomms/fcz041},
   Key = {fds348497}
}

@article{fds351567,
   Author = {Elliott, M and Knodt, A and Ireland, D and Morris, M and Poulton, R and Ramrakha, S and Sison, M and Moffitt, T and Caspi, A and Hariri,
             A},
   Title = {What is the test-retest reliability of common task-fMRI
             measures? New empirical evidence and a meta-analysis},
   Year = {2019},
   url = {http://dx.doi.org/10.1101/681700},
   Abstract = {Identifying brain biomarkers of disease risk is a growing
             priority in neuroscience. The ability to identify meaningful
             biomarkers is limited by measurement reliability; unreliable
             measures are unsuitable for predicting clinical outcomes.
             Measuring brain activity using task-fMRI is a major focus of
             biomarker development; however, the reliability of task-fMRI
             has not been systematically evaluated. We present converging
             evidence demonstrating poor reliability of task-fMRI
             measures. First, a meta-analysis of 90 experiments (N=1,008)
             revealed poor overall reliability (mean ICC=.397). Second,
             the test-retest reliabilities of activity in a priori
             regions of interest across 11 common fMRI tasks collected in
             the context of the Human Connectome Project (N=45) and the
             Dunedin Study (N=20) were poor (ICCs=.067-.485).
             Collectively, these findings demonstrate that common
             task-fMRI measures are not currently suitable for brain
             biomarker discovery or individual differences research. We
             review how this state of affairs came to be and highlight
             avenues for improving task-fMRI reliability.},
   Doi = {10.1101/681700},
   Key = {fds351567}
}

@article{fds342402,
   Title = {Correction for Belsky et al., Genetic analysis of
             social-class mobility in five longitudinal
             studies.},
   Journal = {Proceedings of the National Academy of Sciences of the
             United States of America},
   Volume = {115},
   Number = {46},
   Pages = {E10998},
   Publisher = {Proceedings of the National Academy of Sciences},
   Year = {2018},
   Month = {November},
   url = {http://dx.doi.org/10.1073/pnas.1817958115},
   Doi = {10.1073/pnas.1817958115},
   Key = {fds342402}
}

@article{fds339247,
   Author = {Selzam, S and Coleman, JRI and Caspi, A and Moffitt, TE and Plomin,
             R},
   Title = {A polygenic p factor for major psychiatric
             disorders.},
   Journal = {Translational psychiatry},
   Volume = {8},
   Number = {1},
   Pages = {205},
   Year = {2018},
   Month = {October},
   url = {http://dx.doi.org/10.1038/s41398-018-0217-4},
   Abstract = {It has recently been proposed that a single dimension,
             called the p factor, can capture a person's liability to
             mental disorder. Relevant to the p hypothesis, recent
             genetic research has found surprisingly high genetic
             correlations between pairs of psychiatric disorders. Here,
             for the first time, we compare genetic correlations from
             different methods and examine their support for a genetic p
             factor. We tested the hypothesis of a genetic p factor by
             applying principal component analysis to matrices of genetic
             correlations between major psychiatric disorders estimated
             by three methods-family study, genome-wide complex trait
             analysis, and linkage-disequilibrium score regression-and on
             a matrix of polygenic score correlations constructed for
             each individual in a UK-representative sample of 7 026
             unrelated individuals. All disorders loaded positively on a
             first unrotated principal component, which accounted for 57,
             43, 35, and 22% of the variance respectively for the four
             methods. Our results showed that all four methods provided
             strong support for a genetic p factor that represents the
             pinnacle of the hierarchical genetic architecture of
             psychopathology.},
   Doi = {10.1038/s41398-018-0217-4},
   Key = {fds339247}
}

@article{fds336531,
   Author = {Caspi, A and Moffitt, TE},
   Title = {All for One and One for All: Mental Disorders in One
             Dimension.},
   Journal = {The American journal of psychiatry},
   Volume = {175},
   Number = {9},
   Pages = {831-844},
   Year = {2018},
   Month = {September},
   url = {http://dx.doi.org/10.1176/appi.ajp.2018.17121383},
   Abstract = {In both child and adult psychiatry, empirical evidence has
             now accrued to suggest that a single dimension is able to
             measure a person's liability to mental disorder, comorbidity
             among disorders, persistence of disorders over time, and
             severity of symptoms. This single dimension of general
             psychopathology has been termed "p," because it conceptually
             parallels a dimension already familiar to behavioral
             scientists and clinicians: the "g" factor of general
             intelligence. As the g dimension reflects low to high mental
             ability, the p dimension represents low to high
             psychopathology severity, with thought disorder at the
             extreme. The dimension of p unites all disorders. It
             influences present/absent status on hundreds of psychiatric
             symptoms, which modern nosological systems typically
             aggregate into dozens of distinct diagnoses, which in turn
             aggregate into three overarching domains, namely, the
             externalizing, internalizing, and psychotic experience
             domains, which finally aggregate into one dimension of
             psychopathology from low to high: p. Studies show that the
             higher a person scores on p, the worse that person fares on
             measures of family history of psychiatric illness, brain
             function, childhood developmental history, and adult life
             impairment. A dimension of p may help account for ubiquitous
             nonspecificity in psychiatry: multiple disorders share the
             same risk factors and biomarkers and often respond to the
             same therapies. Here, the authors summarize the history of
             the unidimensional idea, review modern research into p,
             demystify statistical models, articulate some implications
             of p for prevention and clinical practice, and outline a
             transdiagnostic research agenda. [AJP AT 175: Remembering
             Our Past As We Envision Our Future October 1910: A Study of
             Association in Insanity Grace Helen Kent and A.J. Rosanoff:
             "No sharp distinction can be drawn between mental health and
             mental disease; a large collection of material shows a
             gradual and not an abrupt transition from the normal state
             to pathological states."(Am J Psychiatry 1910; 67(2):317-390
             )].},
   Doi = {10.1176/appi.ajp.2018.17121383},
   Key = {fds336531}
}

@article{fds336525,
   Author = {Agnew-Blais, JC and Polanczyk, GV and Danese, A and Wertz, J and Moffitt, TE and Arseneault, L},
   Title = {Young adult mental health and functional outcomes among
             individuals with remitted, persistent and late-onset
             ADHD.},
   Journal = {The British journal of psychiatry : the journal of mental
             science},
   Volume = {213},
   Number = {3},
   Pages = {526-534},
   Year = {2018},
   Month = {September},
   url = {http://dx.doi.org/10.1192/bjp.2018.97},
   Abstract = {<h4>Background</h4>Attention-deficit hyperactivity disorder
             (ADHD) is associated with mental health problems and
             functional impairment across many domains. However, how the
             longitudinal course of ADHD affects later functioning
             remains unclear.AimsWe aimed to disentangle how ADHD
             developmental patterns are associated with young adult
             functioning.<h4>Method</h4>The Environmental Risk (E-Risk)
             Longitudinal Twin Study is a population-based cohort of 2232
             twins born in England and Wales in 1994-1995. We assessed
             ADHD in childhood at ages 5, 7, 10 and 12 years and in young
             adulthood at age 18 years. We examined three developmental
             patterns of ADHD from childhood to young adulthood -
             remitted, persistent and late-onset ADHD - and compared
             these groups with one another and with non-ADHD controls on
             functioning at age 18 years. We additionally tested whether
             group differences were attributable to childhood IQ,
             childhood conduct disorder or familial factors shared
             between twins.<h4>Results</h4>Compared with individuals
             without ADHD, those with remitted ADHD showed poorer
             physical health and socioeconomic outcomes in young
             adulthood. Individuals with persistent or late-onset ADHD
             showed poorer functioning across all domains, including
             mental health, substance misuse, psychosocial, physical
             health and socioeconomic outcomes. Overall, these
             associations were not explained by childhood IQ, childhood
             conduct disorder or shared familial factors.<h4>Conclusions</h4>Long-term
             associations of childhood ADHD with adverse physical health
             and socioeconomic outcomes underscore the need for early
             intervention. Young adult ADHD showed stronger associations
             with poorer mental health, substance misuse and psychosocial
             outcomes, emphasising the importance of identifying and
             treating adults with ADHD.Declaration of
             interestNone.},
   Doi = {10.1192/bjp.2018.97},
   Key = {fds336525}
}

@article{fds336526,
   Author = {Crush, E and Arseneault, L and Moffitt, TE and Danese, A and Caspi, A and Jaffee, SR and Matthews, T and Fisher, HL},
   Title = {Protective factors for psychotic experiences amongst
             adolescents exposed to multiple forms of
             victimization.},
   Journal = {Journal of psychiatric research},
   Volume = {104},
   Pages = {32-38},
   Year = {2018},
   Month = {September},
   url = {http://dx.doi.org/10.1016/j.jpsychires.2018.06.011},
   Abstract = {Experiencing multiple types of victimization
             (poly-victimization) during adolescence is associated with
             the onset of psychotic experiences (such as hearing voices,
             having visions, or being extremely paranoid). However, many
             poly-victimized adolescents will not develop such
             subclinical phenomena and the factors that protect them are
             unknown. This study investigated whether individual, family,
             or community-level characteristics were associated with an
             absence of psychotic experiences amongst poly-victimized
             adolescents. Participants were from the Environmental Risk
             (E-Risk) Longitudinal Twin Study, a nationally-representative
             cohort of 2232 UK-born twins. Exposure to seven different
             types of victimization between ages 12-18 was ascertained
             using a modified version of the Juvenile Victimization
             Questionnaire at age 18. Adolescents were also interviewed
             about psychotic experiences at age 18. Protective factors
             were measured at ages 12 and 18. We found that exposure to
             poly-victimization during adolescence was associated with
             age-18 psychotic experiences (OR = 4.62, 95% CI
             3.59-5.94, P < 0.001), but more than a third of the
             poly-victimized adolescents reported having no psychotic
             experiences (40.1%). Greater social support was found to be
             protective against adolescent psychotic experiences even
             amongst those exposed to poly-victimization. Engaging in
             physical activity and greater neighborhood social cohesion
             were also associated with a reduced likelihood of age-18
             psychotic experiences in the whole sample, with
             non-significant trends in the poly-victimized group.
             Increasing social support and promoting physical activity
             appear to be important areas for future research into the
             development of preventive interventions targeting adolescent
             psychotic experiences. This adds further weight to calls to
             increase the promotion of these factors on a public health
             scale.},
   Doi = {10.1016/j.jpsychires.2018.06.011},
   Key = {fds336526}
}

@article{fds340986,
   Author = {Hannon, E and Knox, O and Sugden, K and Burrage, J and Wong, CCY and Belsky, DW and Corcoran, DL and Arseneault, L and Moffitt, TE and Caspi,
             A and Mill, J},
   Title = {Characterizing genetic and environmental influences on
             variable DNA methylation using monozygotic and dizygotic
             twins.},
   Journal = {PLoS genetics},
   Volume = {14},
   Number = {8},
   Pages = {e1007544},
   Year = {2018},
   Month = {August},
   url = {http://dx.doi.org/10.1371/journal.pgen.1007544},
   Abstract = {Variation in DNA methylation is being increasingly
             associated with health and disease outcomes. Although DNA
             methylation is hypothesized to be a mechanism by which both
             genetic and non-genetic factors can influence the regulation
             of gene expression, little is known about the extent to
             which DNA methylation at specific sites is influenced by
             heritable as well as environmental factors. We quantified
             DNA methylation in whole blood at age 18 in a birth cohort
             of 1,464 individuals comprising 426 monozygotic (MZ) and 306
             same-sex dizygotic (DZ) twin pairs. Site-specific levels of
             DNA methylation were more strongly correlated across the
             genome between MZ than DZ twins. Structural equation models
             revealed that although the average contribution of additive
             genetic influences on DNA methylation across the genome was
             relatively low, it was notably elevated at the highly
             variable sites characterized by intermediate levels of DNAm
             that are most relevant for epigenetic epidemiology. Sites at
             which variable DNA methylation was most influenced by
             genetic factors were significantly enriched for DNA
             methylation quantitative trait loci (mQTL) effects, and
             overlapped with sites where inter-individual variation
             correlates across tissues. Finally, we show that DNA
             methylation at sites robustly associated with environmental
             exposures such as tobacco smoking and obesity is also
             influenced by additive genetic effects, highlighting the
             need to control for genetic background in analyses of
             exposure-associated DNA methylation differences. Estimates
             of the contribution of genetic and environmental influences
             to DNA methylation at all sites profiled in this study are
             available as a resource for the research community
             (http://www.epigenomicslab.com/online-data-resources).},
   Doi = {10.1371/journal.pgen.1007544},
   Key = {fds340986}
}

@article{fds336524,
   Author = {Belsky, DW and Domingue, BW and Wedow, R and Arseneault, L and Boardman,
             JD and Caspi, A and Conley, D and Fletcher, JM and Freese, J and Herd, P and Moffitt, TE and Poulton, R and Sicinski, K and Wertz, J and Harris,
             KM},
   Title = {Genetic analysis of social-class mobility in five
             longitudinal studies.},
   Journal = {Proceedings of the National Academy of Sciences of the
             United States of America},
   Volume = {115},
   Number = {31},
   Pages = {E7275-E7284},
   Year = {2018},
   Month = {July},
   url = {http://dx.doi.org/10.1073/pnas.1801238115},
   Abstract = {A summary genetic measure, called a "polygenic score,"
             derived from a genome-wide association study (GWAS) of
             education can modestly predict a person's educational and
             economic success. This prediction could signal a biological
             mechanism: Education-linked genetics could encode
             characteristics that help people get ahead in life.
             Alternatively, prediction could reflect social history:
             People from well-off families might stay well-off for social
             reasons, and these families might also look alike
             genetically. A key test to distinguish biological mechanism
             from social history is if people with higher education
             polygenic scores tend to climb the social ladder beyond
             their parents' position. Upward mobility would indicate
             education-linked genetics encodes characteristics that
             foster success. We tested if education-linked polygenic
             scores predicted social mobility in >20,000 individuals in
             five longitudinal studies in the United States, Britain, and
             New Zealand. Participants with higher polygenic scores
             achieved more education and career success and accumulated
             more wealth. However, they also tended to come from
             better-off families. In the key test, participants with
             higher polygenic scores tended to be upwardly mobile
             compared with their parents. Moreover, in sibling-difference
             analysis, the sibling with the higher polygenic score was
             more upwardly mobile. Thus, education GWAS discoveries are
             not mere correlates of privilege; they influence social
             mobility within a life. Additional analyses revealed that a
             mother's polygenic score predicted her child's attainment
             over and above the child's own polygenic score, suggesting
             parents' genetics can also affect their children's
             attainment through environmental pathways. Education GWAS
             discoveries affect socioeconomic attainment through
             influence on individuals' family-of-origin environments and
             their social mobility.},
   Doi = {10.1073/pnas.1801238115},
   Key = {fds336524}
}

@article{fds340543,
   Author = {Freedman, R and Brown, AS and Cannon, TD and Druss, BG and Earls, FJ and Escobar, J and Hurd, YL and Lewis, DA and López-Jaramillo, C and Luby,
             J and Mayberg, HS and Moffitt, TE and Oquendo, M and Perlis, RH and Pine,
             DS and Rush, AJ and Tamminga, CA and Tohen, M and Vieta, E and Wisner, KL and Xin, Y},
   Title = {Can a Framework Be Established for the Safe Use of
             Ketamine?},
   Journal = {Am J Psychiatry},
   Volume = {175},
   Number = {7},
   Pages = {587-589},
   Year = {2018},
   Month = {July},
   url = {http://dx.doi.org/10.1176/appi.ajp.2018.18030290},
   Doi = {10.1176/appi.ajp.2018.18030290},
   Key = {fds340543}
}

@article{fds332178,
   Author = {Marzi, SJ and Sugden, K and Arseneault, L and Belsky, DW and Burrage, J and Corcoran, DL and Danese, A and Fisher, HL and Hannon, E and Moffitt, TE and Odgers, CL and Pariante, C and Poulton, R and Williams, BS and Wong,
             CCY and Mill, J and Caspi, A},
   Title = {Analysis of DNA Methylation in Young People: Limited
             Evidence for an Association Between Victimization Stress and
             Epigenetic Variation in Blood.},
   Journal = {The American journal of psychiatry},
   Volume = {175},
   Number = {6},
   Pages = {517-529},
   Year = {2018},
   Month = {June},
   url = {http://dx.doi.org/10.1176/appi.ajp.2017.17060693},
   Abstract = {<h4>Objective</h4>DNA methylation has been proposed as an
             epigenetic mechanism by which early-life experiences become
             "embedded" in the genome and alter transcriptional processes
             to compromise health. The authors sought to investigate
             whether early-life victimization stress is associated with
             genome-wide DNA methylation.<h4>Method</h4>The authors
             tested the hypothesis that victimization is associated with
             DNA methylation in the Environmental Risk (E-Risk)
             Longitudinal Study, a nationally representative 1994-1995
             birth cohort of 2,232 twins born in England and Wales and
             assessed at ages 5, 7, 10, 12, and 18 years. Multiple forms
             of victimization were ascertained in childhood and
             adolescence (including physical, sexual, and emotional
             abuse; neglect; exposure to intimate-partner violence;
             bullying; cyber-victimization; and crime).<h4>Results</h4>Epigenome-wide
             analyses of polyvictimization across childhood and
             adolescence revealed few significant associations with DNA
             methylation in peripheral blood at age 18, but these
             analyses were confounded by tobacco smoking and/or did not
             survive co-twin control tests. Secondary analyses of
             specific forms of victimization revealed sparse associations
             with DNA methylation that did not replicate across different
             operationalizations of the same putative victimization
             experience. Hypothesis-driven analyses of six candidate
             genes in the stress response (NR3C1, FKBP5, BDNF, AVP,
             CRHR1, SLC6A4) did not reveal predicted associations with
             DNA methylation in probes annotated to these
             genes.<h4>Conclusions</h4>Findings from this epidemiological
             analysis of the epigenetic effects of early-life stress do
             not support the hypothesis of robust changes in DNA
             methylation in victimized young people. We need to come to
             terms with the possibility that epigenetic epidemiology is
             not yet well matched to experimental, nonhuman models in
             uncovering the biological embedding of stress.},
   Doi = {10.1176/appi.ajp.2017.17060693},
   Key = {fds332178}
}

@article{fds336527,
   Author = {Belsky, DW and Moffitt, TE and Cohen, AA and Corcoran, DL and Levine,
             ME and Prinz, JA and Schaefer, J and Sugden, K and Williams, B and Poulton,
             R and Caspi, A},
   Title = {Eleven Telomere, Epigenetic Clock, and Biomarker-Composite
             Quantifications of Biological Aging: Do They Measure the
             Same Thing?},
   Journal = {American journal of epidemiology},
   Volume = {187},
   Number = {6},
   Pages = {1220-1230},
   Year = {2018},
   Month = {June},
   url = {http://dx.doi.org/10.1093/aje/kwx346},
   Abstract = {The geroscience hypothesis posits that therapies to slow
             biological processes of aging can prevent disease and extend
             healthy years of life. To test such "geroprotective"
             therapies in humans, outcome measures are needed that can
             assess extension of disease-free life span. This need has
             spurred development of different methods to quantify
             biological aging. But different methods have not been
             systematically compared in the same humans. We implemented 7
             methods to quantify biological aging using repeated-measures
             physiological and genomic data in 964 middle-aged humans in
             the Dunedin Study (New Zealand; persons born 1972-1973). We
             studied 11 measures in total: telomere-length and erosion, 3
             epigenetic-clocks and their ticking rates, and 3
             biomarker-composites. Contrary to expectation, we found low
             agreement between different measures of biological aging. We
             next compared associations between biological aging measures
             and outcomes that geroprotective therapies seek to modify:
             physical functioning, cognitive decline, and subjective
             signs of aging, including aged facial appearance. The
             71-cytosine-phosphate-guanine epigenetic clock and biomarker
             composites were consistently related to these aging-related
             outcomes. However, effect sizes were modest. Results
             suggested that various proposed approaches to quantifying
             biological aging may not measure the same aspects of the
             aging process. Further systematic evaluation and refinement
             of measures of biological aging is needed to furnish
             outcomes for geroprotector trials.},
   Doi = {10.1093/aje/kwx346},
   Key = {fds336527}
}

@article{fds331412,
   Author = {Rivenbark, JG and Odgers, CL and Caspi, A and Harrington, H and Hogan,
             S and Houts, RM and Poulton, R and Moffitt, TE},
   Title = {The high societal costs of childhood conduct problems:
             evidence from administrative records up to age 38 in a
             longitudinal birth cohort.},
   Journal = {Journal of child psychology and psychiatry, and allied
             disciplines},
   Volume = {59},
   Number = {6},
   Pages = {703-710},
   Year = {2018},
   Month = {June},
   url = {http://dx.doi.org/10.1111/jcpp.12850},
   Abstract = {<h4>Background</h4>Children with conduct problems that
             persist into adulthood are at increased risk for future
             behavioral, health, and social problems. However, the longer
             term public service usage among these children has not been
             fully documented. To aid public health and intervention
             planning, adult service usage across criminal justice,
             health care, and social welfare domains is compared among
             all individuals from a representative cohort who followed
             different conduct problem trajectories from childhood into
             adulthood.<h4>Methods</h4>Participants are from the Dunedin
             Multidisciplinary Health and Development Study, a
             prospective, representative cohort of consecutive births
             (N = 1,037) from April 1972 to March 1973 in Dunedin, New
             Zealand. Regression analyses were used to compare levels of
             public service usage up to age 38, gathered via
             administrative and electronic medical records, between
             participants who displayed distinct subtypes of childhood
             conduct problems (low, childhood-limited, adolescent-onset,
             and life-course persistent).<h4>Results</h4>Children
             exhibiting life-course persistent conduct problems used
             significantly more services as adults than those with low
             levels of childhood conduct problems. Although this group
             comprised only 9.0% of the population, they accounted for
             53.3% of all convictions, 15.7% of emergency department
             visits, 20.5% of prescription fills, 13.1% of injury claims,
             and 24.7% of welfare benefit months. Half of this group
             (50.0%) also accrued high service use across all three
             domains of criminal justice, health, and social welfare
             services, as compared to only 11.3% of those with low
             conduct problems (OR = 7.27, 95% CI = 4.42-12.0).<h4>Conclusions</h4>Conduct
             problems in childhood signal high future costs in terms of
             service utilization across multiple sectors. Future
             evaluations of interventions aimed at conduct problems
             should also track potential reductions in health burden and
             service usage that stretch into midlife.},
   Doi = {10.1111/jcpp.12850},
   Key = {fds331412}
}

@article{fds336529,
   Author = {Schaefer, JD and Moffitt, TE and Arseneault, L and Danese, A and Fisher,
             HL and Houts, R and Sheridan, MA and Wertz, J and Caspi,
             A},
   Title = {Adolescent Victimization and Early-Adult Psychopathology:
             Approaching Causal Inference Using a Longitudinal Twin Study
             to Rule Out Noncausal Explanations.},
   Journal = {Clinical psychological science : a journal of the
             Association for Psychological Science},
   Volume = {6},
   Number = {3},
   Pages = {352-371},
   Year = {2018},
   Month = {May},
   url = {http://dx.doi.org/10.1177/2167702617741381},
   Abstract = {Adolescence is the peak age for both victimization and
             mental disorder onset. Previous research has reported
             associations between victimization exposure and many
             psychiatric conditions. However, causality remains
             controversial. Within the Environmental Risk Longitudinal
             Twin Study, we tested whether seven types of adolescent
             victimization increased risk of multiple psychiatric
             conditions and approached causal inference by systematically
             ruling out noncausal explanations. Longitudinal
             within-individual analyses showed that victimization was
             followed by increased mental health problems over a
             childhood baseline of emotional/behavioral problems.
             Discordant-twin analyses showed that victimization increased
             risk of mental health problems independent of family
             background and genetic risk. Both childhood and adolescent
             victimization made unique contributions to risk.
             Victimization predicted heightened generalized liability
             (the "p factor") to multiple psychiatric spectra, including
             internalizing, externalizing, and thought disorders. Results
             recommend violence reduction and identification and
             treatment of adolescent victims to reduce psychiatric
             burden.},
   Doi = {10.1177/2167702617741381},
   Key = {fds336529}
}

@article{fds333593,
   Author = {Wertz, J and Caspi, A and Belsky, DW and Beckley, AL and Arseneault, L and Barnes, JC and Corcoran, DL and Hogan, S and Houts, RM and Morgan, N and Odgers, CL and Prinz, JA and Sugden, K and Williams, BS and Poulton, R and Moffitt, TE},
   Title = {Genetics and Crime: Integrating New Genomic Discoveries Into
             Psychological Research About Antisocial Behavior.},
   Journal = {Psychological science},
   Volume = {29},
   Number = {5},
   Pages = {791-803},
   Year = {2018},
   Month = {May},
   url = {http://dx.doi.org/10.1177/0956797617744542},
   Abstract = {Drawing on psychological and sociological theories of crime
             causation, we tested the hypothesis that genetic risk for
             low educational attainment (assessed via a genome-wide
             polygenic score) is associated with criminal offending. We
             further tested hypotheses of how polygenic risk relates to
             the development of antisocial behavior from childhood
             through adulthood. Across the Dunedin and Environmental Risk
             (E-Risk) birth cohorts of individuals growing up 20 years
             and 20,000 kilometers apart, education polygenic scores
             predicted risk of a criminal record with modest effects.
             Polygenic risk manifested during primary schooling in lower
             cognitive abilities, lower self-control, academic
             difficulties, and truancy, and it was associated with a
             life-course-persistent pattern of antisocial behavior that
             onsets in childhood and persists into adulthood. Crime is
             central in the nature-nurture debate, and findings reported
             here demonstrate how molecular-genetic discoveries can be
             incorporated into established theories of antisocial
             behavior. They also suggest that improving school
             experiences might prevent genetic influences on crime from
             unfolding.},
   Doi = {10.1177/0956797617744542},
   Key = {fds333593}
}

@article{fds326211,
   Author = {Romer, AL and Knodt, AR and Houts, R and Brigidi, BD and Moffitt, TE and Caspi, A and Hariri, AR},
   Title = {Structural alterations within cerebellar circuitry are
             associated with general liability for common mental
             disorders.},
   Journal = {Molecular psychiatry},
   Volume = {23},
   Number = {4},
   Pages = {1084-1090},
   Year = {2018},
   Month = {April},
   url = {http://dx.doi.org/10.1038/mp.2017.57},
   Abstract = {Accumulating mental-health research encourages a shift in
             focus toward transdiagnostic dimensional features that are
             shared across categorical disorders. In support of this
             shift, recent studies have identified a general liability
             factor for psychopathology-sometimes called the 'p factor'-
             that underlies shared risk for a wide range of mental
             disorders. Identifying neural correlates of this general
             liability would substantiate its importance in
             characterizing the shared origins of mental disorders and
             help us begin to understand the mechanisms through which the
             'p factor' contributes to risk. Here we believe we first
             replicate the 'p factor' using cross-sectional data from a
             volunteer sample of 1246 university students, and then using
             high-resolution multimodal structural neuroimaging, we
             demonstrate that individuals with higher 'p factor' scores
             show reduced structural integrity of white matter pathways,
             as indexed by lower fractional anisotropy values, uniquely
             within the pons. Whole-brain analyses further revealed that
             higher 'p factor' scores are associated with reduced gray
             matter volume in the occipital lobe and left cerebellar
             lobule VIIb, which is functionally connected with prefrontal
             regions supporting cognitive control. Consistent with the
             preponderance of cerebellar afferents within the pons, we
             observed a significant positive correlation between the
             white matter integrity of the pons and cerebellar gray
             matter volume associated with higher 'p factor' scores. The
             results of our analyses provide initial evidence that
             structural alterations in corticocerebellar circuitry
             supporting core functions related to the basic integration,
             coordination and monitoring of information may contribute to
             a general liability for common mental disorders.},
   Doi = {10.1038/mp.2017.57},
   Key = {fds326211}
}

@article{fds333594,
   Author = {Beckley, AL and Caspi, A and Arseneault, L and Barnes, JC and Fisher,
             HL and Harrington, H and Houts, R and Morgan, N and Odgers, CL and Wertz,
             J and Moffitt, TE},
   Title = {The Developmental Nature of the Victim-Offender
             Overlap.},
   Journal = {Journal of developmental and life-course
             criminology},
   Volume = {4},
   Number = {1},
   Pages = {24-49},
   Year = {2018},
   Month = {March},
   url = {http://dx.doi.org/10.1007/s40865-017-0068-3},
   Abstract = {<h4>Purpose</h4>It is well-established that victims and
             offenders are often the same people, a phenomenon known as
             the victim-offender overlap, but the developmental nature of
             this overlap remains uncertain. In this study, we drew from
             a developmental theoretical framework to test effects of
             genetics, individual characteristics, and
             routine-activity-based risks. Drawing from developmental
             literature, we additionally tested the effect of an
             accumulation of adverse childhood experiences
             (ACEs).<h4>Methods</h4>Data came from the Environmental Risk
             (E-Risk) Study, a representative UK birth cohort of 2232
             twins born in 1994-1995 and followed to age 18 (with 93%
             retention). Crime victimization and offending were assessed
             through self-reports at age 18 (but findings replicated
             using crime records). We used the classical twin study
             method to decompose variance in the victim-offender overlap
             into genetic and environmental components. We used logistic
             regression to test the effects of childhood risk
             factors.<h4>Results</h4>In contrast to past twin studies, we
             found that environment (as well as genes) contributed to the
             victim-offender overlap. Our logistic regression results
             showed that childhood low self-control and childhood
             antisocial behavior nearly doubled the odds of becoming a
             victim-offender, compared to a victim-only or an
             offender-only. Each additional ACE increased the odds of
             becoming a victim-offender, compared to a victim-only or an
             offender-only, by approximately 12%, pointing to the
             importance of cumulative childhood adversity.<h4>Conclusions</h4>This
             study showed that the victim-offender overlap is, at least
             partially, developmental in nature and predictable from
             personal childhood characteristics and an accumulation of
             many adverse childhood experiences.},
   Doi = {10.1007/s40865-017-0068-3},
   Key = {fds333594}
}

@article{fds329193,
   Author = {Newbury, J and Arseneault, L and Caspi, A and Moffitt, TE and Odgers,
             CL and Fisher, HL},
   Title = {Cumulative Effects of Neighborhood Social Adversity and
             Personal Crime Victimization on Adolescent Psychotic
             Experiences.},
   Journal = {Schizophrenia bulletin},
   Volume = {44},
   Number = {2},
   Pages = {348-358},
   Year = {2018},
   Month = {February},
   url = {http://dx.doi.org/10.1093/schbul/sbx060},
   Abstract = {<h4>Background</h4>Little is known about the impact of
             urbanicity, adverse neighborhood conditions and violent
             crime victimization on the emergence of adolescent psychotic
             experiences.<h4>Methods</h4>Participants were from the
             Environmental Risk (E-Risk) Longitudinal Twin Study, a
             nationally-representative cohort of 2232 British twins who
             were interviewed about adolescent psychotic experiences at
             age 18. Urbanicity, neighborhood characteristics, and
             personal victimization by violent crime were measured during
             childhood and adolescence via geocoded census data, surveys
             of over 5000 immediate neighbors of the E-Risk participants,
             and interviews with participants themselves.<h4>Results</h4>Adolescents
             raised in urban vs rural neighborhoods were significantly
             more likely to have psychotic experiences (OR = 1.67, 95% CI
             = 1.21-2.30, P = .002). This association remained
             significant after considering potential confounders
             including family socioeconomic status, family psychiatric
             history, and adolescent substance problems (OR = 1.43, 95%
             CI = 1.01-2.03, P = .042), but became nonsignificant after
             considering adverse social conditions in urban neighborhoods
             such as low social cohesion and high neighborhood disorder
             (OR = 1.35, 95% CI = 0.94-1.92, P = .102). The combined
             association of adverse neighborhood social conditions and
             personal crime victimization with adolescent psychotic
             experiences (adjusted OR = 4.86, 95% CI = 3.28-7.20, P <
             .001) was substantially greater than for either exposure
             alone, highlighting a potential interaction between
             neighborhood conditions and crime victimization (interaction
             contrast ratio = 1.81, 95% CI = -0.03 to 3.65) that was
             significant at the P = .054 level.<h4>Conclusions</h4>Cumulative
             effects of adverse neighborhood social conditions and
             personal victimization by violent crime during upbringing
             partly explain why adolescents in urban settings are more
             likely to report psychotic experiences. Early intervention
             efforts for psychosis could be targeted towards victimized
             youth living in urban and socially adverse
             neighborhoods.},
   Doi = {10.1093/schbul/sbx060},
   Key = {fds329193}
}

@article{fds328906,
   Author = {Meier, MH and Caspi, A and Danese, A and Fisher, HL and Houts, R and Arseneault, L and Moffitt, TE},
   Title = {Associations between adolescent cannabis use and
             neuropsychological decline: a longitudinal co-twin control
             study.},
   Journal = {Addiction (Abingdon, England)},
   Volume = {113},
   Number = {2},
   Pages = {257-265},
   Year = {2018},
   Month = {February},
   url = {http://dx.doi.org/10.1111/add.13946},
   Abstract = {<h4>Aims</h4>This study tested whether adolescents who used
             cannabis or met criteria for cannabis dependence showed
             neuropsychological impairment prior to cannabis initiation
             and neuropsychological decline from before to after cannabis
             initiation.<h4>Design</h4>A longitudinal co-twin control
             study.<h4>Setting and participants</h4>Participants were
             1989 twins from the Environmental Risk (E-Risk) Longitudinal
             Twin Study, a nationally representative birth cohort of
             twins born in England and Wales from 1994 to
             1995.<h4>Measurements</h4>Frequency of cannabis use and
             cannabis dependence were assessed at age 18. Intelligence
             quotient (IQ) was obtained at ages 5, 12 and 18. Executive
             functions were assessed at age 18.<h4>Findings</h4>Compared
             with adolescents who did not use cannabis, adolescents who
             used cannabis had lower IQ in childhood prior to cannabis
             initiation and lower IQ at age 18, but there was little
             evidence that cannabis use was associated with IQ decline
             from ages 12-18. For example, adolescents with cannabis
             dependence had age 12 and age 18 IQ scores that were 5.61
             (t = -3.11, P = 0.002) and 7.34 IQ points (t = -5.27,
             P < 0.001) lower than adolescents without cannabis
             dependence, but adolescents with cannabis dependence did not
             show greater IQ decline from age 12-18 (t = -1.27,
             P = 0.20). Moreover, adolescents who used cannabis had
             poorer executive functions at age 18 than adolescents who
             did not use cannabis, but these associations were generally
             not apparent within twin pairs. For example, twins who used
             cannabis more frequently than their co-twin performed
             similarly to their co-twin on five of six executive function
             tests (Ps > 0.10). The one exception was that twins who
             used cannabis more frequently than their co-twin performed
             worse on one working memory test (Spatial Span reversed;
             β = -0.07, P = 0.036).<h4>Conclusions</h4>Short-term
             cannabis use in adolescence does not appear to cause IQ
             decline or impair executive functions, even when cannabis
             use reaches the level of dependence. Family background
             factors explain why adolescent cannabis users perform worse
             on IQ and executive function tests.},
   Doi = {10.1111/add.13946},
   Key = {fds328906}
}

@article{fds332179,
   Author = {Beckley, AL and Caspi, A and Broadbent, J and Harrington, H and Houts,
             RM and Poulton, R and Ramrakha, S and Reuben, A and Moffitt,
             TE},
   Title = {Association of Childhood Blood Lead Levels With Criminal
             Offending.},
   Journal = {JAMA pediatrics},
   Volume = {172},
   Number = {2},
   Pages = {166-173},
   Year = {2018},
   Month = {February},
   url = {http://dx.doi.org/10.1001/jamapediatrics.2017.4005},
   Abstract = {<h4>Importance</h4>Lead is a neurotoxin with well-documented
             effects on health. Research suggests that lead may be
             associated with criminal behavior. This association is
             difficult to disentangle from low socioeconomic status, a
             factor in both lead exposure and criminal
             offending.<h4>Objective</h4>To test the hypothesis that a
             higher childhood blood lead level (BLL) is associated with
             greater risk of criminal conviction, recidivism (repeat
             conviction), conviction for violent offenses, and variety of
             self-reported criminal offending in a setting where BLL was
             not associated with low socioeconomic status.<h4>Design,
             setting, and participants</h4>A total of 553 individuals
             participated in a prospective study based on a
             population-representative cohort born between April 1, 1972,
             and March 31, 1973, from New Zealand; the Dunedin
             Multidisciplinary Health and Development Study observed
             participants to age 38 years (December 2012). Statistical
             analysis was performed from November 10, 2016, to September
             5, 2017.<h4>Exposures</h4>Blood lead level measured at age
             11 years.<h4>Main outcomes and measures</h4>Official
             criminal conviction cumulative to age 38 years (data
             collected in 2013), single conviction or recidivism,
             conviction for nonviolent or violent crime, and
             self-reported variety of crime types at ages 15, 18, 21, 26,
             32, and 38 years.<h4>Results</h4>Participants included 553
             individuals (255 female and 298 male participants) who had
             their blood tested for lead at age 11 years. The mean (SD)
             BLL at age 11 years was 11.01 (4.62) μg/dL. A total of 154
             participants (27.8%) had a criminal conviction, 86 (15.6%)
             had recidivated, and 53 (9.6%) had a violent offense
             conviction. Variety scores for self-reported offending
             ranged from 0 to 10 offense types at each assessment; higher
             numbers indicated greater crime involvement. Self-reported
             offending followed the well-established age-crime curve (ie,
             the mean [SD] variety of self-reported offending increased
             from 1.99 [2.82] at age 15 years to its peak of 4.24 [3.15]
             at age 18 years and 4.22 [3.02] at age 21 years and declined
             thereafter to 1.10 [1.59] at age 38 years). Blood lead level
             was a poor discriminator between no conviction and
             conviction (area under the curve, 0.58). Overall,
             associations between BLL and conviction outcomes were weak.
             The estimated effect of BLL was lower for recidivism than
             for single convictions and lower for violent offending than
             for nonviolent offending. Sex-adjusted associations between
             BLL reached statistical significance for only 1 of the 6
             self-reported offending outcomes at age 15 years
             (r = 0.10; 95% CI, 0.01-0.18; P = .02).<h4>Conclusions
             and relevance</h4>This study overcomes past limitations of
             studies of BLL and crime by studying the association in a
             place and time where the correlation was not confounded by
             childhood socioeconomic status. Findings failed to support a
             dose-response association between BLL and consequential
             criminal offending.},
   Doi = {10.1001/jamapediatrics.2017.4005},
   Key = {fds332179}
}

@article{fds329770,
   Author = {Newbury, JB and Arseneault, L and Moffitt, TE and Caspi, A and Danese,
             A and Baldwin, JR and Fisher, HL},
   Title = {Measuring childhood maltreatment to predict early-adult
             psychopathology: Comparison of prospective informant-reports
             and retrospective self-reports.},
   Journal = {Journal of psychiatric research},
   Volume = {96},
   Pages = {57-64},
   Year = {2018},
   Month = {January},
   url = {http://dx.doi.org/10.1016/j.jpsychires.2017.09.020},
   Abstract = {Both prospective informant-reports and retrospective
             self-reports may be used to measure childhood maltreatment,
             though both methods entail potential limitations such as
             underestimation and memory biases. The validity and utility
             of standard measures of childhood maltreatment requires
             clarification in order to inform the design of future
             studies investigating the mental health consequences of
             maltreatment. The present study assessed agreement between
             prospective informant-reports and retrospective self-reports
             of childhood maltreatment, as well as the comparative
             utility of both reports for predicting a range of
             psychiatric problems at age 18. Data were obtained from the
             Environmental Risk (E-Risk) Longitudinal Twin Study, a
             nationally-representative birth cohort of 2232 children
             followed to 18 years of age (with 93% retention). Childhood
             maltreatment was assessed in two ways: (i) prospective
             informant-reports from caregivers, researchers, and
             clinicians when children were aged 5, 7, 10 and 12; and (ii)
             retrospective self-reports of maltreatment experiences
             occurring up to age 12, obtained at age 18 using the
             Childhood Trauma Questionnaire. Participants were privately
             interviewed at age 18 concerning several psychiatric
             problems including depression, anxiety, self-injury,
             alcohol/cannabis dependence, and conduct disorder. There was
             only slight to fair agreement between prospective and
             retrospective reports of childhood maltreatment (all
             Kappa's ≤ 0.31). Both prospective and retrospective
             reports of maltreatment were associated with age-18
             psychiatric problems, though the strongest associations were
             found when maltreatment was retrospectively self-reported.
             These findings indicate that prospective and retrospective
             reports of childhood maltreatment capture largely
             non-overlapping groups of individuals. Young adults who
             recall being maltreated have a particularly elevated risk
             for psychopathology.},
   Doi = {10.1016/j.jpsychires.2017.09.020},
   Key = {fds329770}
}

@article{fds329192,
   Author = {Baldwin, JR and Arseneault, L and Caspi, A and Fisher, HL and Moffitt,
             TE and Odgers, CL and Pariante, C and Ambler, A and Dove, R and Kepa, A and Matthews, T and Menard, A and Sugden, K and Williams, B and Danese,
             A},
   Title = {Childhood victimization and inflammation in young adulthood:
             A genetically sensitive cohort study.},
   Journal = {Brain, behavior, and immunity},
   Volume = {67},
   Pages = {211-217},
   Year = {2018},
   Month = {January},
   url = {http://dx.doi.org/10.1016/j.bbi.2017.08.025},
   Abstract = {<h4>Objective</h4>Childhood victimization is an important
             risk factor for later immune-related disorders. Previous
             evidence has demonstrated that childhood victimization is
             associated with elevated levels of inflammation biomarkers
             measured decades after exposure. However, it is unclear
             whether this association is (1) already detectable in young
             people, (2) different in males and females, and (3)
             confounded by genetic liability to inflammation. Here we
             sought to address these questions.<h4>Method</h4>Participants
             were 2232 children followed from birth to age 18years as
             part of the Environmental Risk (E-Risk) Longitudinal Twin
             Study. Childhood victimization was measured prospectively
             from birth to age 12years. Inflammation was measured through
             C-reactive protein (CRP) levels in dried blood spots at age
             18years. Latent genetic liability for high inflammation
             levels was assessed through a twin-based
             method.<h4>Results</h4>Greater exposure to childhood
             victimization was associated with higher CRP levels at age
             18 (serum-equivalent means were 0.65 in non-victimized Study
             members, 0.74 in those exposed to one victimization type,
             and 0.81 in those exposed to poly-victimization; p=0.018).
             However, this association was driven by a significant
             association in females (serum-equivalent means were 0.75 in
             non-victimized females, 0.87 in those exposed to one type of
             victimization, and 1.19 in those exposed to
             poly-victimization; p=0.010), while no significant
             association was observed in males (p=0.19). Victimized
             females showed elevated CRP levels independent of latent
             genetic influence, as well as childhood socioeconomic
             status, and waist-hip ratio and body temperature at the time
             of CRP assessment.<h4>Conclusion</h4>Childhood victimization
             is associated with elevated CRP levels in young women,
             independent of latent genetic influences and other key risk
             factors. These results strengthen causal inference about the
             effects of childhood victimization on inflammation levels in
             females by accounting for potential genetic
             confounding.},
   Doi = {10.1016/j.bbi.2017.08.025},
   Key = {fds329192}
}

@article{fds333009,
   Author = {Moffitt, TE},
   Title = {Male antisocial behaviour in adolescence and
             beyond.},
   Journal = {Nature human behaviour},
   Volume = {2},
   Number = {3},
   Pages = {177-186},
   Year = {2018},
   Month = {January},
   url = {http://dx.doi.org/10.1038/s41562-018-0309-4},
   Abstract = {Male antisocial behavior is concentrated in the adolescent
             period of the life course, as documented by the curve of
             crime over age. This article reviews recent evidence
             regarding the hypothesis that the age-crime curve conceals
             two groups with different causes. Life-course persistent
             males show extreme, pervasive, persistent antisocial
             behavior from early childhood to adulthood. They are
             hypothesized to be rare, with pathological risk factors and
             poor life outcomes. In contrast, adolescence-limited males
             show similar levels of antisocial behavior but primarily
             during the adolescent stage of development. They are
             hypothesized to be common and normative, whereas abstainers
             from offending are rare. This article recaps the taxonomy's
             25-year history, concluding that it is standing the test of
             time in research, and making an impact on policy in
             early-years prevention and juvenile justice. Research is
             needed into how the taxonomy relates to neuroscience,
             health, genetics, and changes in modern crime, including
             digital crime.},
   Doi = {10.1038/s41562-018-0309-4},
   Key = {fds333009}
}

@article{fds332046,
   Author = {Wertz, J and Agnew-Blais, J and Caspi, A and Danese, A and Fisher, HL and Goldman-Mellor, S and Moffitt, TE and Arseneault,
             L},
   Title = {From Childhood Conduct Problems to Poor Functioning at Age
             18 Years: Examining Explanations in a Longitudinal Cohort
             Study.},
   Journal = {Journal of the American Academy of Child and Adolescent
             Psychiatry},
   Volume = {57},
   Number = {1},
   Pages = {54-60.e4},
   Year = {2018},
   Month = {January},
   url = {http://dx.doi.org/10.1016/j.jaac.2017.09.437},
   Abstract = {<h4>Objective</h4>Childhood conduct problems are associated
             with poor functioning in early adulthood. We tested a series
             of hypotheses to understand the mechanisms underlying this
             association.<h4>Method</h4>We used data from the
             Environmental Risk (E-Risk) Longitudinal Twin Study, a birth
             cohort of 2,232 twins born in England and Wales in 1994 and
             1995, followed up to age 18 years with 93% retention. Severe
             conduct problems in childhood were assessed at ages 5, 7,
             and 10 years using parent and teacher reports. Poor
             functioning at age 18 years, including cautions and
             convictions, daily cigarette smoking, heavy drinking, and
             psychosocial difficulties, was measured through interviews
             with participants and official crime record
             searches.<h4>Results</h4>Participants 18 years old with
             versus without a childhood history of severe conduct
             problems had greater rates of each poor functional outcome,
             and they were more likely to experience multiple poor
             outcomes. This association was partly accounted for by
             concurrent psychopathology in early adulthood, as well as by
             early familial risk factors, both genetic and environmental.
             Childhood conduct problems, however, continued to predict
             poor outcomes at age 18 years after accounting for these
             explanations.<h4>Conclusion</h4>Children with severe conduct
             problems display poor functioning at age 18 years because of
             concurrent problems in early adulthood and familial risk
             factors originating in childhood. However, conduct problems
             also exert a lasting effect on young people's lives
             independent of these factors, pointing to early conduct
             problems as a target for early interventions aimed at
             preventing poor functional outcomes.},
   Doi = {10.1016/j.jaac.2017.09.437},
   Key = {fds332046}
}

@article{fds330410,
   Author = {Newbury, JB and Arseneault, L and Caspi, A and Moffitt, TE and Odgers,
             CL and Baldwin, JR and Zavos, HMS and Fisher, HL},
   Title = {In the eye of the beholder: Perceptions of neighborhood
             adversity and psychotic experiences in adolescence.},
   Journal = {Development and psychopathology},
   Volume = {29},
   Number = {5},
   Pages = {1823-1837},
   Year = {2017},
   Month = {December},
   url = {http://dx.doi.org/10.1017/s0954579417001420},
   Abstract = {Adolescent psychotic experiences increase risk for
             schizophrenia and other severe psychopathology in adulthood.
             Converging evidence implicates urban and adverse
             neighborhood conditions in the etiology of adolescent
             psychotic experiences, but the role of young people's
             personal perceptions of disorder (i.e., physical and social
             signs of threat) in their neighborhood is unknown. This was
             examined using data from the Environmental Risk Longitudinal
             Twin Study, a nationally representative birth cohort of
             2,232 British twins. Participants were interviewed at age 18
             about psychotic phenomena and perceptions of disorder in the
             neighborhood. Multilevel, longitudinal, and genetically
             sensitive analyses investigated the association between
             perceptions of neighborhood disorder and adolescent
             psychotic experiences. Adolescents who perceived higher
             levels of neighborhood disorder were significantly more
             likely to have psychotic experiences, even after accounting
             for objectively/independently measured levels of crime and
             disorder, neighborhood- and family-level socioeconomic
             status, family psychiatric history, adolescent substance and
             mood problems, and childhood psychotic symptoms: odds ratio
             = 1.62, 95% confidence interval [1.27, 2.05], p < .001. The
             phenotypic overlap between adolescent psychotic experiences
             and perceptions of neighborhood disorder was explained by
             overlapping common environmental influences, rC = .88, 95%
             confidence interval [0.26, 1.00]. Findings suggest that
             early psychological interventions to prevent adolescent
             psychotic experiences should explore the role of young
             people's (potentially modifiable) perceptions of threatening
             neighborhood conditions.},
   Doi = {10.1017/s0954579417001420},
   Key = {fds330410}
}

@article{fds330411,
   Author = {Schaefer, JD and Scult, MA and Caspi, A and Arseneault, L and Belsky,
             DW and Hariri, AR and Harrington, H and Houts, R and Ramrakha, S and Poulton, R and Moffitt, TE},
   Title = {Is low cognitive functioning a predictor or consequence of
             major depressive disorder? A test in two longitudinal birth
             cohorts.},
   Journal = {Development and psychopathology},
   Pages = {1-15},
   Year = {2017},
   Month = {November},
   url = {http://dx.doi.org/10.1017/s095457941700164x},
   Abstract = {Cognitive impairment has been identified as an important
             aspect of major depressive disorder (MDD). We tested two
             theories regarding the association between MDD and cognitive
             functioning using data from longitudinal cohort studies. One
             theory, the cognitive reserve hypothesis, suggests that
             higher cognitive ability in childhood decreases risk of
             later MDD. The second, the scarring hypothesis, instead
             suggests that MDD leads to persistent cognitive deficits
             following disorder onset. We tested both theories in the
             Dunedin Study, a population-representative cohort followed
             from birth to midlife and assessed repeatedly for both
             cognitive functioning and psychopathology. We also used data
             from the Environmental Risk Longitudinal Twin Study to test
             whether childhood cognitive functioning predicts future MDD
             risk independent of family-wide and genetic risk using a
             discordant twin design. Contrary to both hypotheses, we
             found that childhood cognitive functioning did not predict
             future risk of MDD, nor did study members with a past
             history of MDD show evidence of greater cognitive decline
             unless MDD was accompanied by other comorbid psychiatric
             conditions. Our results thus suggest that low cognitive
             functioning is related to comorbidity, but is neither an
             antecedent nor an enduring consequence of MDD. Future
             research may benefit from considering cognitive deficits
             that occur during depressive episodes from a transdiagnostic
             perspective.},
   Doi = {10.1017/s095457941700164x},
   Key = {fds330411}
}

@article{fds328626,
   Author = {Matthews, T and Danese, A and Gregory, AM and Caspi, A and Moffitt, TE and Arseneault, L},
   Title = {Sleeping with one eye open: loneliness and sleep quality in
             young adults.},
   Journal = {Psychological medicine},
   Volume = {47},
   Number = {12},
   Pages = {2177-2186},
   Year = {2017},
   Month = {September},
   url = {http://dx.doi.org/10.1017/s0033291717000629},
   Abstract = {<h4>Background</h4>Feelings of loneliness are common among
             young adults, and are hypothesized to impair the quality of
             sleep. In the present study, we tested associations between
             loneliness and sleep quality in a nationally representative
             sample of young adults. Further, based on the hypothesis
             that sleep problems in lonely individuals are driven by
             increased vigilance for threat, we tested whether past
             exposure to violence exacerbated this association.<h4>Method</h4>Data
             were drawn from the Environmental Risk (E-Risk) Longitudinal
             Twin Study, a birth cohort of 2232 twins born in England and
             Wales in 1994 and 1995. We measured loneliness using items
             from the UCLA Loneliness Scale, and sleep quality using the
             Pittsburgh Sleep Quality Index. We controlled for covariates
             including social isolation, psychopathology, employment
             status and being a parent of an infant. We examined twin
             differences to control for unmeasured genetic and family
             environment factors.<h4>Results</h4>Feelings of loneliness
             were associated with worse overall sleep quality. Loneliness
             was associated specifically with subjective sleep quality
             and daytime dysfunction. These associations were robust to
             controls for covariates. Among monozygotic twins,
             within-twin pair differences in loneliness were
             significantly associated with within-pair differences in
             sleep quality, indicating an association independent of
             unmeasured familial influences. The association between
             loneliness and sleep quality was exacerbated among
             individuals exposed to violence victimization in adolescence
             or maltreatment in childhood.<h4>Conclusions</h4>Loneliness
             is robustly associated with poorer sleep quality in young
             people, underscoring the importance of early interventions
             to mitigate the long-term outcomes of loneliness. Special
             care should be directed towards individuals who have
             experienced victimization.},
   Doi = {10.1017/s0033291717000629},
   Key = {fds328626}
}

@article{fds328905,
   Author = {Williams, MJA and Milne, BJ and Ambler, A and Theodore, R and Ramrakha,
             S and Caspi, A and Moffitt, TE and Poulton, R},
   Title = {Childhood body mass index and endothelial dysfunction
             evaluated by peripheral arterial tonometry in early
             midlife.},
   Journal = {International journal of obesity (2005)},
   Volume = {41},
   Number = {9},
   Pages = {1355-1360},
   Year = {2017},
   Month = {September},
   url = {http://dx.doi.org/10.1038/ijo.2017.108},
   Abstract = {<h4>Background/objectives</h4>Endothelial dysfunction
             predicts mortality but it is unknown whether childhood
             obesity predicts adult endothelial dysfunction. The aim of
             this study was to determine whether anthropometric indices
             of body fat in childhood, adolescence and early midlife are
             associated with endothelial dysfunction in early
             midlife.<h4>Subjects/methods</h4>Participants belonged to a
             representative birth cohort of 1037 individuals born in
             Dunedin, New Zealand in 1972 and 1973 and followed to age 38
             years, with 95% retention (the Dunedin Multidisciplinary
             Health and Development Study). We assessed anthropometric
             indices of obesity at ages 3, 5, 7, 9, 11, 13, 15, 18, 21,
             26, 32 and 38 years. We tested associations between
             endothelial function assessed by peripheral arterial
             tonometry (PAT) at age 38 and; age 38 cardiovascular risk
             factors; age 3 body mass index (BMI); and four BMI
             trajectory groups from childhood to early
             midlife.<h4>Results</h4>Early midlife endothelial
             dysfunction was associated with BMI, large waist
             circumference, low high-density lipoprotein cholesterol, low
             cardiorespiratory fitness and increased high-sensitivity
             C-reactive protein. After adjustment for sex and childhood
             socioeconomic status, 3-year-olds with BMI 1 s.d. above the
             mean had Framingham-reactive hyperemia index (F-RHI) ratios
             that were 0.10 below those with normal BMI (β=-0.10, 95%
             confidence interval (CI) -0.17 to -0.03, P=0.007) at age 38.
             Cohort members in the 'overweight', 'obese' and 'morbidly
             obese' trajectories had F-RHI ratios that were 0.08
             (β=-0.08, 95% CI -0.14 to -0.03, P=0.003), 0.13 (β=-0.13,
             95% CI -0.21 to -0.06, P<0.001) and 0.17 (β=-0.17, 95% CI
             -0.33 to -0.01, P=0.033), respectively, below age-peers in
             the 'normal' trajectory.<h4>Conclusions</h4>Childhood BMI
             and the trajectories of BMI from childhood to early midlife
             predict endothelial dysfunction evaluated by PAT in early
             midlife.},
   Doi = {10.1038/ijo.2017.108},
   Key = {fds328905}
}

@article{fds327018,
   Author = {Suppli, NP and Bukh, JD and Moffitt, TE and Caspi, A and Johansen, C and Tjønneland, A and Kessing, LV and Dalton, SO},
   Title = {Genetic variants in 5-HTTLPR, BDNF, HTR1A, COMT, and FKBP5
             and risk for treated depression after cancer
             diagnosis.},
   Journal = {Depression and anxiety},
   Volume = {34},
   Number = {9},
   Pages = {845-855},
   Year = {2017},
   Month = {September},
   url = {http://dx.doi.org/10.1002/da.22660},
   Abstract = {<h4>Background</h4>The role of gene-environment interactions
             in the pathogenesis of depression is unclear. Previous
             studies addressed vulnerability for depression after
             childhood adversity and stressful life events among carriers
             of numerous specific genetic variants; however, the
             importance of individual genetic variants, the environmental
             exposures with which they interact, and the magnitude of the
             risk conveyed by these interactions remain
             elusive.<h4>Methods</h4>We included 7,320 people with a
             first primary cancer identified in the prospective Diet,
             Cancer and Health study in an exposed-only cohort study. The
             mean age of the individuals was 68 years (5th, 95th
             percentiles: 58, 78) at cancer diagnosis. Using Cox
             regression models and cumulative incidence plots, we
             analyzed the associations between genetic variants in
             5-HTTLPR, BDNF, HTR1A, COMT, and FKBP5 and use of
             antidepressants as well as hospital contact for depression
             after diagnosis of cancer.<h4>Results</h4>Overall, we
             observed no statistically significant associations, with
             nonsignificant hazard ratio estimates for use of
             antidepressants of 0.95-1.07.<h4>Conclusions</h4>This study
             of elderly people indicates that it is unlikely that the
             investigated genetic variants are clinically relevantly
             associated with depression after diagnosis of cancer. The
             mechanisms for gene-environment interactions in younger
             individuals are probably different, and we advise caution in
             extrapolating our results to early life stress. However,
             conclusion from the present study might be generalizable to
             elderly persons exposed to other stressful life
             events.},
   Doi = {10.1002/da.22660},
   Key = {fds327018}
}

@article{fds321669,
   Author = {Erskine, HE and Baxter, AJ and Patton, G and Moffitt, TE and Patel, V and Whiteford, HA and Scott, JG},
   Title = {The global coverage of prevalence data for mental disorders
             in children and adolescents.},
   Journal = {Epidemiology and psychiatric sciences},
   Volume = {26},
   Number = {4},
   Pages = {395-402},
   Year = {2017},
   Month = {August},
   url = {http://dx.doi.org/10.1017/s2045796015001158},
   Abstract = {<h4>Aims</h4>Children and adolescents make up almost a
             quarter of the world's population with 85% living in low-
             and middle-income countries (LMICs). Globally, mental (and
             substance use) disorders are the leading cause of disability
             in young people; however, the representativeness or
             'coverage' of the prevalence data is unknown. Coverage
             refers to the proportion of the target population (ages 5-17
             years) represented by the available data.<h4>Methods</h4>Prevalence
             data for conduct disorder (CD), attention-deficit/hyperactivity
             disorder (ADHD), autism spectrum disorders (ASDs), eating
             disorders (EDs), depression, and anxiety disorders were
             sourced from systematic reviews conducted for the Global
             Burden of Disease Study 2010 (GBD 2010) and 2013 (GBD 2013).
             For each study, the location proportion was multiplied by
             the age proportion to give study coverage. Location
             proportion was calculated by dividing the total study
             location population by the total study location population.
             Age proportion was calculated by dividing the population of
             the country aged within the age range of the study sample by
             the population of the country aged within the age range of
             the study sample. If a study only sampled one sex, study
             coverage was halved. Coverage across studies was then summed
             for each country to give coverage by country. This method
             was repeated at the region and global level, and separately
             for GBD 2013 and GBD 2010.<h4>Results</h4>Mean global
             coverage of prevalence data for mental disorders in ages
             5-17 years was 6.7% (CD: 5.0%, ADHD: 5.5%, ASDs: 16.1%, EDs:
             4.4%, depression: 6.2%, anxiety: 3.2%). Of 187 countries,
             124 had no data for any disorder. Many LMICs were poorly
             represented in the available prevalence data, for example,
             no region in sub-Saharan Africa had more than 2% coverage
             for any disorder. While coverage increased between GBD 2010
             and GBD 2013, this differed greatly between disorders and
             few new countries provided data.<h4>Conclusions</h4>The
             global coverage of prevalence data for mental disorders in
             children and adolescents is limited. Practical methodology
             must be developed and epidemiological surveys funded to
             provide representative prevalence estimates so as to inform
             appropriate resource allocation and support policies that
             address mental health needs of children and
             adolescents.},
   Doi = {10.1017/s2045796015001158},
   Key = {fds321669}
}

@article{fds326210,
   Author = {Belsky, DW and Caspi, A and Cohen, HJ and Kraus, WE and Ramrakha, S and Poulton, R and Moffitt, TE},
   Title = {Impact of early personal-history characteristics on the Pace
             of Aging: implications for clinical trials of therapies to
             slow aging and extend healthspan.},
   Journal = {Aging Cell},
   Volume = {16},
   Number = {4},
   Pages = {644-651},
   Year = {2017},
   Month = {August},
   url = {http://dx.doi.org/10.1111/acel.12591},
   Abstract = {Therapies to extend healthspan are poised to move from
             laboratory animal models to human clinical trials.
             Translation from mouse to human will entail challenges,
             among them the multifactorial heterogeneity of human aging.
             To inform clinical trials about this heterogeneity, we
             report how humans' pace of biological aging relates to
             personal-history characteristics. Because geroprotective
             therapies must be delivered by midlife to prevent
             age-related disease onset, we studied young-adult members of
             the Dunedin Study 1972-73 birth cohort (n = 954). Cohort
             members' Pace of Aging was measured as coordinated decline
             in the integrity of multiple organ systems, by quantifying
             rate of decline across repeated measurements of 18
             biomarkers assayed when cohort members were ages 26, 32, and
             38 years. The childhood personal-history characteristics
             studied were known predictors of age-related disease and
             mortality, and were measured prospectively during childhood.
             Personal-history characteristics of familial longevity,
             childhood social class, adverse childhood experiences, and
             childhood health, intelligence, and self-control all
             predicted differences in cohort members' adulthood Pace of
             Aging. Accumulation of more personal-history risks predicted
             faster Pace of Aging. Because trials of anti-aging therapies
             will need to ascertain personal histories retrospectively,
             we replicated results using cohort members' retrospective
             personal-history reports made in adulthood. Because many
             trials recruit participants from clinical settings, we
             replicated results in the cohort subset who had recent
             health system contact according to electronic medical
             records. Quick, inexpensive measures of trial participants'
             early personal histories can enable clinical trials to study
             who volunteers for trials, who adheres to treatment, and who
             responds to anti-aging therapies.},
   Doi = {10.1111/acel.12591},
   Key = {fds326210}
}

@article{fds325850,
   Author = {Kotov, R and Krueger, RF and Watson, D and Achenbach, TM and Althoff,
             RR and Bagby, RM and Brown, TA and Carpenter, WT and Caspi, A and Clark,
             LA and Eaton, NR and Forbes, MK and Forbush, KT and Goldberg, D and Hasin,
             D and Hyman, SE and Ivanova, MY and Lynam, DR and Markon, K and Miller, JD and Moffitt, TE and Morey, LC and Mullins-Sweatt, SN and Ormel, J and Patrick, CJ and Regier, DA and Rescorla, L and Ruggero, CJ and Samuel,
             DB and Sellbom, M and Simms, LJ and Skodol, AE and Slade, T and South, SC and Tackett, JL and Waldman, ID and Waszczuk, MA and Widiger, TA and Wright,
             AGC and Zimmerman, M},
   Title = {The Hierarchical Taxonomy of Psychopathology (HiTOP): A
             dimensional alternative to traditional nosologies.},
   Journal = {Journal of abnormal psychology},
   Volume = {126},
   Number = {4},
   Pages = {454-477},
   Year = {2017},
   Month = {May},
   url = {http://dx.doi.org/10.1037/abn0000258},
   Abstract = {The reliability and validity of traditional taxonomies are
             limited by arbitrary boundaries between psychopathology and
             normality, often unclear boundaries between disorders,
             frequent disorder co-occurrence, heterogeneity within
             disorders, and diagnostic instability. These taxonomies went
             beyond evidence available on the structure of
             psychopathology and were shaped by a variety of other
             considerations, which may explain the aforementioned
             shortcomings. The Hierarchical Taxonomy Of Psychopathology
             (HiTOP) model has emerged as a research effort to address
             these problems. It constructs psychopathological syndromes
             and their components/subtypes based on the observed
             covariation of symptoms, grouping related symptoms together
             and thus reducing heterogeneity. It also combines
             co-occurring syndromes into spectra, thereby mapping out
             comorbidity. Moreover, it characterizes these phenomena
             dimensionally, which addresses boundary problems and
             diagnostic instability. Here, we review the development of
             the HiTOP and the relevant evidence. The new classification
             already covers most forms of psychopathology. Dimensional
             measures have been developed to assess many of the
             identified components, syndromes, and spectra. Several
             domains of this model are ready for clinical and research
             applications. The HiTOP promises to improve research and
             clinical practice by addressing the aforementioned
             shortcomings of traditional nosologies. It also provides an
             effective way to summarize and convey information on risk
             factors, etiology, pathophysiology, phenomenology, illness
             course, and treatment response. This can greatly improve the
             utility of the diagnosis of mental disorders. The new
             classification remains a work in progress. However, it is
             developing rapidly and is poised to advance mental health
             research and care significantly as the relevant science
             matures. (PsycINFO Database Record},
   Doi = {10.1037/abn0000258},
   Key = {fds325850}
}

@article{fds325487,
   Author = {Arseneault, L and Agnew-Blais, J and Moffitt, TE},
   Title = {Child vs Adult Onset of Attention-Deficit/Hyperactivity
             Disorder-Reply.},
   Journal = {JAMA psychiatry},
   Volume = {74},
   Number = {4},
   Pages = {422-423},
   Year = {2017},
   Month = {April},
   url = {http://dx.doi.org/10.1001/jamapsychiatry.2016.2781},
   Doi = {10.1001/jamapsychiatry.2016.2781},
   Key = {fds325487}
}

@article{fds324440,
   Author = {Danese, A and Moffitt, TE and Arseneault, L and Bleiberg, BA and Dinardo, PB and Gandelman, SB and Houts, R and Ambler, A and Fisher, HL and Poulton, R and Caspi, A},
   Title = {The Origins of Cognitive Deficits in Victimized Children:
             Implications for Neuroscientists and Clinicians.},
   Journal = {The American journal of psychiatry},
   Volume = {174},
   Number = {4},
   Pages = {349-361},
   Year = {2017},
   Month = {April},
   url = {http://dx.doi.org/10.1176/appi.ajp.2016.16030333},
   Abstract = {<h4>Objective</h4>Individuals reporting a history of
             childhood violence victimization have impaired brain
             function. However, the clinical significance,
             reproducibility, and causality of these findings are
             disputed. The authors used data from two large cohort
             studies to address these research questions
             directly.<h4>Method</h4>The authors tested the association
             between prospectively collected measures of childhood
             violence victimization and cognitive functions in childhood,
             adolescence, and adulthood among 2,232 members of the U.K.
             E-Risk Study and 1,037 members of the New Zealand Dunedin
             Study who were followed up from birth until ages 18 and 38
             years, respectively. Multiple measures of victimization and
             cognition were used, and comparisons were made of cognitive
             scores for twins discordant for victimization.<h4>Results</h4>Individuals
             exposed to childhood victimization had pervasive impairments
             in clinically relevant cognitive functions, including
             general intelligence, executive function, processing speed,
             memory, perceptual reasoning, and verbal comprehension in
             adolescence and adulthood. However, the observed cognitive
             deficits in victimized individuals were largely explained by
             cognitive deficits that predated childhood victimization and
             by confounding genetic and environmental
             risks.<h4>Conclusions</h4>Findings from two
             population-representative birth cohorts totaling more than
             3,000 individuals and born 20 years and 20,000 km apart
             suggest that the association between childhood violence
             victimization and later cognition is largely noncausal, in
             contrast to conventional interpretations. These findings
             support the adoption of a more circumspect approach to
             causal inference in the neuroscience of stress. Clinically,
             cognitive deficits should be conceptualized as individual
             risk factors for victimization as well as potential
             complicating features during treatment.},
   Doi = {10.1176/appi.ajp.2016.16030333},
   Key = {fds324440}
}

@article{fds325849,
   Author = {Reuben, A and Caspi, A and Belsky, DW and Broadbent, J and Harrington,
             H and Sugden, K and Houts, RM and Ramrakha, S and Poulton, R and Moffitt,
             TE},
   Title = {Association of Childhood Blood Lead Levels With Cognitive
             Function and Socioeconomic Status at Age 38 Years and With
             IQ Change and Socioeconomic Mobility Between Childhood and
             Adulthood.},
   Journal = {JAMA},
   Volume = {317},
   Number = {12},
   Pages = {1244-1251},
   Year = {2017},
   Month = {March},
   url = {http://dx.doi.org/10.1001/jama.2017.1712},
   Abstract = {<h4>Importance</h4>Many children in the United States and
             around the world are exposed to lead, a developmental
             neurotoxin. The long-term cognitive and socioeconomic
             consequences of lead exposure are uncertain.<h4>Objective</h4>To
             test the hypothesis that childhood lead exposure is
             associated with cognitive function and socioeconomic status
             in adulthood and with changes in IQ and socioeconomic
             mobility between childhood and midlife.<h4>Design, setting,
             and participants</h4>A prospective cohort study based on a
             population-representative 1972-1973 birth cohort from New
             Zealand; the Dunedin Multidisciplinary Health and
             Development Study observed participants to age 38 years
             (until December 2012).<h4>Exposures</h4>Childhood lead
             exposure ascertained as blood lead levels measured at age 11
             years. High blood lead levels were observed among children
             from all socioeconomic status levels in this cohort.<h4>Main
             outcomes and measures</h4>The IQ (primary outcome) and
             indexes of Verbal Comprehension, Perceptual Reasoning,
             Working Memory, and Processing Speed (secondary outcomes)
             were assessed at age 38 years using the Wechsler Adult
             Intelligence Scale-IV (WAIS-IV; IQ range, 40-160).
             Socioeconomic status (primary outcome) was assessed at age
             38 years using the New Zealand Socioeconomic Index-2006
             (NZSEI-06; range, 10 [lowest]-90 [highest]).<h4>Results</h4>Of
             1037 original participants, 1007 were alive at age 38 years,
             of whom 565 (56%) had been lead tested at age 11 years (54%
             male; 93% white). Mean (SD) blood lead level at age 11 years
             was 10.99 (4.63) µg/dL. Among blood-tested participants
             included at age 38 years, mean WAIS-IV score was 101.16
             (14.82) and mean NZSEI-06 score was 49.75 (17.12). After
             adjusting for maternal IQ, childhood IQ, and childhood
             socioeconomic status, each 5-µg/dL higher level of blood
             lead in childhood was associated with a 1.61-point lower
             score (95% CI, -2.48 to -0.74) in adult IQ, a 2.07-point
             lower score (95% CI, -3.14 to -1.01) in perceptual
             reasoning, and a 1.26-point lower score (95% CI, -2.38 to
             -0.14) in working memory. Associations of childhood blood
             lead level with deficits in verbal comprehension and
             processing speed were not statistically significant. After
             adjusting for confounders, each 5-µg/dL higher level of
             blood lead in childhood was associated with a 1.79-unit
             lower score (95% CI, -3.17 to -0.40) in socioeconomic
             status. An association between greater blood lead levels and
             a decline in IQ and socioeconomic status from childhood to
             adulthood was observed with 40% of the association with
             downward mobility mediated by cognitive decline from
             childhood.<h4>Conclusions and relevance</h4>In this cohort
             born in New Zealand in 1972-1973, childhood lead exposure
             was associated with lower cognitive function and
             socioeconomic status at age 38 years and with declines in IQ
             and with downward social mobility. Childhood lead exposure
             may have long-term ramifications.},
   Doi = {10.1001/jama.2017.1712},
   Key = {fds325849}
}

@article{fds321664,
   Author = {Gregory, AM and Agnew-Blais, JC and Matthews, T and Moffitt, TE and Arseneault, L},
   Title = {ADHD and Sleep Quality: Longitudinal Analyses From Childhood
             to Early Adulthood in a Twin Cohort.},
   Journal = {Journal of clinical child and adolescent psychology : the
             official journal for the Society of Clinical Child and
             Adolescent Psychology, American Psychological Association,
             Division 53},
   Volume = {46},
   Number = {2},
   Pages = {284-294},
   Year = {2017},
   Month = {March},
   url = {http://dx.doi.org/10.1080/15374416.2016.1183499},
   Abstract = {Attention-deficit/hyperactivity disorder (ADHD) is
             associated with poor sleep quality, but there is more to
             learn about the longitudinal association and aetiology of
             this association. We investigated the following: (a) Is
             there an association between childhood ADHD and poor sleep
             quality in young adulthood? (b) Is this driven by the
             long-term effects of childhood ADHD or concurrent
             associations with ADHD in young adulthood? (c) To what
             extent do genetic and environmental influences explain the
             overlap between symptoms of ADHD and poor sleep quality?
             Participants were from the Environmental Risk Longitudinal
             Twin Study of 2,232 twin children born in the United Kingdom
             in 1994-1995. We ascertained ADHD diagnoses at ages 5, 7,
             10, 12, and 18. We assessed sleep quality using the
             Pittsburgh Sleep Quality Index at age 18. We used regression
             models to examine longitudinal associations and bivariate
             twin modelling to test genetic and environmental influences.
             Children with ADHD had poorer sleep quality in young
             adulthood, but only if their ADHD persisted. Adults with
             ADHD had more sleep problems than those without ADHD, over
             and above psychiatric comorbidity and maternal insomnia.
             ADHD and sleep problems in young adulthood were associated
             because of genetic (55%) and nonshared environmental
             influences (45%). Should ADHD remit, children with ADHD do
             not appear to have an increased risk of later sleep
             problems. Good quality sleep is important for multiple areas
             of functioning, and a better understanding of why adults
             with ADHD have poorer sleep quality will further the goal of
             improving treatments.},
   Doi = {10.1080/15374416.2016.1183499},
   Key = {fds321664}
}

@article{fds324773,
   Author = {Moffitt, TE and Belsky, DW and Danese, A and Poulton, R and Caspi,
             A},
   Title = {The Longitudinal Study of Aging in Human Young Adults:
             Knowledge Gaps and Research Agenda.},
   Journal = {The journals of gerontology. Series A, Biological sciences
             and medical sciences},
   Volume = {72},
   Number = {2},
   Pages = {210-215},
   Year = {2017},
   Month = {February},
   url = {http://dx.doi.org/10.1093/gerona/glw191},
   Abstract = {<h4>Background</h4>To prevent onset of age-related diseases
             and physical and cognitive decline, interventions to slow
             human aging and extend health span must eventually be
             applied to people while they are still young and healthy.
             Yet most human aging research examines older adults, many
             with chronic disease, and little is known about aging in
             healthy young humans.<h4>Method</h4>This article explains
             how this knowledge gap is a barrier to extending health span
             and puts forward the case that geroscience should invest in
             researching the pace of aging in young adults. As one
             illustrative example, we describe an initial effort to study
             the pace of aging in a young-adult birth cohort by using
             repeated waves of biomarkers collected across the third and
             fourth decades to quantify the pace of coordinated
             physiological deterioration across multiple organ systems
             (eg, pulmonary, periodontal, cardiovascular, renal, hepatic,
             metabolic, and immune function).<h4>Results</h4>Findings
             provided proof of principle that it is possible to quantify
             individual variation in the pace of aging in young adults
             still free of age-related diseases.<h4>Conclusions</h4>This
             article articulates research needs to improve longitudinal
             measurement of the pace of aging in young people, to
             pinpoint factors that slow or speed the pace of aging, to
             compare pace of aging against genomic clocks, to explain
             slow-aging young adults, and to apply pace of aging in
             preventive clinical trials of antiaging therapies. This
             article puts forward a research agenda to fill the knowledge
             gap concerning lifelong causes of aging.},
   Doi = {10.1093/gerona/glw191},
   Key = {fds324773}
}

@article{fds321672,
   Author = {Schaefer, JD and Caspi, A and Belsky, DW and Harrington, H and Houts, R and Horwood, LJ and Hussong, A and Ramrakha, S and Poulton, R and Moffitt,
             TE},
   Title = {Enduring mental health: Prevalence and prediction.},
   Journal = {Journal of abnormal psychology},
   Volume = {126},
   Number = {2},
   Pages = {212-224},
   Year = {2017},
   Month = {February},
   url = {http://dx.doi.org/10.1037/abn0000232},
   Abstract = {We review epidemiological evidence indicating that most
             people will develop a diagnosable mental disorder,
             suggesting that only a minority experience enduring mental
             health. This minority has received little empirical study,
             leaving the prevalence and predictors of enduring mental
             health unknown. We turn to the population-representative
             Dunedin cohort, followed from birth to midlife, to compare
             people never-diagnosed with mental disorder (N = 171; 17%
             prevalence) to those diagnosed at 1-2 study waves, the
             cohort mode (N = 409). Surprisingly, compared to this modal
             group, never-diagnosed Study members were not born into
             unusually well-to-do families, nor did their enduring mental
             health follow markedly sound physical health, or unusually
             high intelligence. Instead, they tended to have an
             advantageous temperament/personality style, and negligible
             family history of mental disorder. As adults, they report
             superior educational and occupational attainment, greater
             life satisfaction, and higher-quality relationships. Our
             findings draw attention to "enduring mental health" as a
             revealing psychological phenotype and suggest it deserves
             further study. (PsycINFO Database Record},
   Doi = {10.1037/abn0000232},
   Key = {fds321672}
}

@article{fds320829,
   Author = {Scult, MA and Paulli, AR and Mazure, ES and Moffitt, TE and Hariri, AR and Strauman, TJ},
   Title = {The association between cognitive function and subsequent
             depression: a systematic review and meta-analysis.},
   Journal = {Psychol Med},
   Volume = {47},
   Number = {1},
   Pages = {1-17},
   Year = {2017},
   Month = {January},
   url = {http://dx.doi.org/10.1017/S0033291716002075},
   Abstract = {Despite a growing interest in understanding the cognitive
             deficits associated with major depressive disorder (MDD), it
             is largely unknown whether such deficits exist before
             disorder onset or how they might influence the severity of
             subsequent illness. The purpose of the present study was to
             conduct a systematic review and meta-analysis of
             longitudinal datasets to determine whether cognitive
             function acts as a predictor of later MDD diagnosis or
             change in depression symptoms. Eligible studies included
             longitudinal designs with baseline measures of cognitive
             functioning, and later unipolar MDD diagnosis or symptom
             assessment. The systematic review identified 29
             publications, representing 34 unique samples, and 121 749
             participants, that met the inclusion/exclusion criteria.
             Quantitative meta-analysis demonstrated that higher
             cognitive function was associated with decreased levels of
             subsequent depression (r = -0.088, 95% confidence interval.
             -0.121 to -0.054, p < 0.001). However, sensitivity analyses
             revealed that this association is likely driven by
             concurrent depression symptoms at the time of cognitive
             assessment. Our review and meta-analysis indicate that the
             association between lower cognitive function and later
             depression is confounded by the presence of contemporaneous
             depression symptoms at the time of cognitive assessment.
             Thus, cognitive deficits predicting MDD likely represent
             deleterious effects of subclinical depression symptoms on
             performance rather than premorbid risk factors for
             disorder.},
   Doi = {10.1017/S0033291716002075},
   Key = {fds320829}
}

@article{fds321662,
   Author = {Neumann, A and Pappa, I and Lahey, BB and Verhulst, FC and Medina-Gomez,
             C and Jaddoe, VW and Bakermans-Kranenburg, MJ and Moffitt, TE and van
             IJzendoorn, MH and Tiemeier, H},
   Title = {Single Nucleotide Polymorphism Heritability of a General
             Psychopathology Factor in Children.},
   Journal = {Journal of the American Academy of Child and Adolescent
             Psychiatry},
   Volume = {55},
   Number = {12},
   Pages = {1038-1045.e4},
   Year = {2016},
   Month = {December},
   url = {http://dx.doi.org/10.1016/j.jaac.2016.09.498},
   Abstract = {<h4>Objective</h4>Co-occurrence of mental disorders is
             commonly observed, but the etiology underlying this
             observation is poorly understood. Studies in adolescents
             and adults have identified a general psychopathology factor
             associated with a high risk for different psychiatric
             disorders. We defined a multi-informant general
             psychopathology factor in school-aged children and estimated
             its single nucleotide polymorphism (SNP) heritability. The
             goal was to test the hypothesis that child behavioral and
             emotional problems are under the influence of highly
             pleiotropic common autosomal genetic variants that
             nonspecifically increase the risk for different dimensions
             of psychopathology.<h4>Method</h4>Children from the
             Generation R cohort were repeatedly assessed between ages 6
             to 8 years. Child behavior problems were reported by
             parents, teachers, and children. Confirmatory factor
             analysis estimated a general psychopathology factor across
             informants using various psychiatric problem scales.
             Validation of the general psychopathology factor was based
             on IQ and temperamental measures. Genome-wide complex trait
             analysis (GCTA) was used to estimate the SNP heritability
             (N = 2,115).<h4>Results</h4>The general psychopathology
             factor was associated with lower IQ, higher negative
             affectivity, and lower effortful control, but not with
             surgency. Importantly, the general psychopathology factor
             showed a significant SNP heritability of 38% (SE = 0.16,
             p = .008).<h4>Conclusion</h4>Common autosomal SNPs are
             pleiotropically associated with internalizing,
             externalizing, and other child behavior problems, and
             underlie a general psychopathology factor in
             childhood.},
   Doi = {10.1016/j.jaac.2016.09.498},
   Key = {fds321662}
}

@article{fds321663,
   Author = {Caye, A and Swanson, J and Thapar, A and Sibley, M and Arseneault, L and Hechtman, L and Arnold, LE and Niclasen, J and Moffitt, T and Rohde,
             LA},
   Title = {Life Span Studies of ADHD-Conceptual Challenges and
             Predictors of Persistence and Outcome.},
   Journal = {Current psychiatry reports},
   Volume = {18},
   Number = {12},
   Pages = {111},
   Year = {2016},
   Month = {December},
   url = {http://dx.doi.org/10.1007/s11920-016-0750-x},
   Abstract = {There is a renewed interest in better conceptualizing
             trajectories of attention-deficit/hyperactivity disorder
             (ADHD) from childhood to adulthood, driven by an increased
             recognition of long-term impairment and potential
             persistence beyond childhood and adolescence. This review
             addresses the following major issues relevant to the course
             of ADHD in light of current evidence from longitudinal
             studies: (1) conceptual and methodological issues related to
             measurement of persistence of ADHD, (2) estimates of
             persistence rate from childhood to adulthood and its
             predictors, (3) long-term negative outcomes of childhood
             ADHD and their early predictors, and (4) the recently
             proposed new adult-onset ADHD. Estimates of persistence vary
             widely in the literature, and diagnostic criteria, sample
             characteristics, and information source are the most
             important factors explaining variability among studies.
             Evidence indicates that ADHD severity, comorbid conduct
             disorder and major depressive disorder, and treatment for
             ADHD are the main predictors of ADHD persistence from
             childhood to adulthood. Comorbid conduct disorder and ADHD
             severity in childhood are the most important predictors of
             adverse outcomes in adulthood among children with ADHD.
             Three recent population studies suggested the existence of a
             significant proportion of individuals who report onset of
             ADHD symptoms and impairments after childhood. Finally, we
             highlight areas for improvement to increase our
             understanding of ADHD across the life span.},
   Doi = {10.1007/s11920-016-0750-x},
   Key = {fds321663}
}

@article{fds323692,
   Author = {Cerdá, M and Moffitt, TE and Meier, MH and Harrington, H and Houts, R and Ramrakha, S and Hogan, S and Poulton, R and Caspi,
             A},
   Title = {Persistent cannabis dependence and alcohol dependence
             represent risks for midlife economic and social problems: A
             longitudinal cohort study.},
   Journal = {Clinical psychological science : a journal of the
             Association for Psychological Science},
   Volume = {4},
   Number = {6},
   Pages = {1028-1046},
   Year = {2016},
   Month = {November},
   url = {http://dx.doi.org/10.1177/2167702616630958},
   Abstract = {With the increasing legalization of cannabis, understanding
             the consequences of cannabis use is particularly timely. We
             examined the association between cannabis use and
             dependence, prospectively assessed between ages 18-38, and
             economic and social problems at age 38. We studied
             participants in the Dunedin Longitudinal Study, a cohort
             (n=1,037) followed from birth to age 38. Study members with
             regular cannabis use and persistent dependence experienced
             downward socioeconomic mobility, more financial
             difficulties, workplace problems, and relationship conflict
             in early midlife. Cannabis dependence was not linked to
             traffic-related convictions. Associations were not explained
             by socioeconomic adversity, childhood psychopathology,
             achievement orientation, or family structure;
             cannabis-related criminal convictions; early onset of
             cannabis dependence; or comorbid substance dependence.
             Cannabis dependence was associated with more financial
             difficulties than alcohol dependence; no difference was
             found in risks for other economic or social problems.
             Cannabis dependence is not associated with fewer harmful
             economic and social problems than alcohol
             dependence.},
   Doi = {10.1177/2167702616630958},
   Key = {fds323692}
}

@article{fds320827,
   Author = {Baldwin, JR and Arseneault, L and Odgers, C and Belsky, DW and Matthews,
             T and Ambler, A and Caspi, A and Moffitt, TE and Danese,
             A},
   Title = {Childhood Bullying Victimization and Overweight in Young
             Adulthood: A Cohort Study.},
   Journal = {Psychosomatic medicine},
   Volume = {78},
   Number = {9},
   Pages = {1094-1103},
   Year = {2016},
   Month = {November},
   url = {http://dx.doi.org/10.1097/psy.0000000000000388},
   Abstract = {<h4>Objective</h4>To test whether bullied children have an
             elevated risk of being overweight in young adulthood and
             whether this association is: (1) consistent with a
             dose-response relationship, namely, its strength increases
             with the chronicity of victimization; (2) consistent across
             different measures of overweight; (3) specific to bullying
             and not explained by co-occurring maltreatment; (4)
             independent of key potential confounders; and (5) consistent
             with the temporal sequence of bullying preceding
             overweight.<h4>Method</h4>A representative birth cohort of
             2,232 children was followed to age 18 years as part of the
             Environmental Risk Longitudinal Twin Study. Childhood
             bullying victimization was reported by mothers and children
             during primary school and early secondary school. At the
             age-18 follow-up, we assessed a categorical measure of
             overweight, body mass index, and waist-hip ratio. Indicators
             of overweight were also collected at ages 10 and 12. Co-twin
             body mass and birth weight were used to index genetic and
             fetal liability to overweight, respectively.<h4>Results</h4>Bullied
             children were more likely to be overweight than non-bullied
             children at age 18, and this association was (1) strongest
             in chronically bullied children (odds ratio = 1.69; 95%
             confidence interval [CI] = 1.21-2.35); (2) consistent across
             measures of overweight (body mass index: b = 1.12; 95% CI =
             0.37-1.87; waist-hip ratio: b = 1.76; 95% CI = 0.84-2.69);
             (3) specific to bullying and not explained by co-occurring
             maltreatment; (4) independent of child socioeconomic status,
             food insecurity, mental health, and cognition, and pubertal
             development; and (5) not present at the time of bullying
             victimization, and independent of childhood weight and
             genetic and fetal liability.<h4>Conclusion</h4>Childhood
             bullying victimization predicts overweight in young
             adulthood.},
   Doi = {10.1097/psy.0000000000000388},
   Key = {fds320827}
}

@article{fds320833,
   Author = {Newbury, J and Arseneault, L and Caspi, A and Moffitt, TE and Odgers,
             CL and Fisher, HL},
   Title = {Why Are Children in Urban Neighborhoods at Increased Risk
             for Psychotic Symptoms? Findings From a UK Longitudinal
             Cohort Study.},
   Journal = {Schizophrenia bulletin},
   Volume = {42},
   Number = {6},
   Pages = {1372-1383},
   Year = {2016},
   Month = {November},
   url = {http://dx.doi.org/10.1093/schbul/sbw052},
   Abstract = {<h4>Background</h4>Urban upbringing is associated with a
             2-fold adulthood psychosis risk, and this association
             replicates for childhood psychotic symptoms. No study has
             investigated whether specific features of urban
             neighborhoods increase children's risk for psychotic
             symptoms, despite these early psychotic phenomena elevating
             risk for schizophrenia and other psychiatric disorders in
             adulthood.<h4>Methods</h4>Analyses were conducted on over
             2000 children from the Environmental Risk (E-Risk)
             Longitudinal Twin Study, a nationally-representative cohort
             of UK-born twins. Neighborhood-level characteristics were
             assessed for each family via: a geodemographic discriminator
             indexing neighborhood-level deprivation, postal surveys of
             over 5000 residents living alongside the children, and
             in-home interviews with the children's mothers. Children
             were interviewed about psychotic symptoms at age 12.
             Analyses were adjusted for important family-level
             confounders including socioeconomic status (SES),
             psychiatric history, and maternal psychosis.<h4>Results</h4>Urban
             residency at age-5 (OR = 1.80, 95% CI = 1.16-2.77) and
             age-12 (OR = 1.76, 95% CI = 1.15-2.69) were both
             significantly associated with childhood psychotic symptoms,
             but not with age-12 anxiety, depression, or antisocial
             behavior. The association was not attributable to family
             SES, family psychiatric history, or maternal psychosis, each
             implicated in childhood mental health. Low social cohesion,
             together with crime victimization in the neighborhood
             explained nearly a quarter of the association between
             urbanicity and childhood psychotic symptoms after
             considering family-level confounders.<h4>Conclusions</h4>Low
             social cohesion and crime victimization in the neighborhood
             partly explain why children in cities have an elevated risk
             of developing psychotic symptoms. Greater understanding of
             the mechanisms leading from neighborhood-level exposures to
             psychotic symptoms could help target interventions for
             emerging childhood psychotic symptoms.},
   Doi = {10.1093/schbul/sbw052},
   Key = {fds320833}
}

@article{fds320826,
   Author = {Schaefer, JD and Caspi, A and Belsky, DW and Harrington, H and Houts, R and Israel, S and Levine, ME and Sugden, K and Williams, B and Poulton, R and Moffitt, TE},
   Title = {Early-Life Intelligence Predicts Midlife Biological
             Age.},
   Journal = {The journals of gerontology. Series B, Psychological
             sciences and social sciences},
   Volume = {71},
   Number = {6},
   Pages = {968-977},
   Year = {2016},
   Month = {November},
   url = {http://dx.doi.org/10.1093/geronb/gbv035},
   Abstract = {<h4>Objectives</h4>Early-life intelligence has been shown to
             predict multiple causes of death in populations around the
             world. This finding suggests that intelligence might
             influence mortality through its effects on a general process
             of physiological deterioration (i.e., individual variation
             in "biological age"). We examined whether intelligence could
             predict measures of aging at midlife before the onset of
             most age-related disease.<h4>Methods</h4>We tested whether
             intelligence assessed in early childhood, middle childhood,
             and midlife predicted midlife biological age in members of
             the Dunedin Study, a population-representative birth
             cohort.<h4>Results</h4>Lower intelligence predicted more
             advanced biological age at midlife as captured by perceived
             facial age, a 10-biomarker algorithm based on data from the
             National Health and Nutrition Examination Survey (NHANES),
             and Framingham heart age (r = 0.1-0.2). Correlations between
             intelligence and telomere length were less consistent. The
             associations between intelligence and biological age were
             not explained by differences in childhood health or parental
             socioeconomic status, and intelligence remained a
             significant predictor of biological age even when
             intelligence was assessed before Study members began their
             formal schooling.<h4>Discussion</h4>These results suggest
             that accelerated aging may serve as one of the factors
             linking low early-life intelligence to increased rates of
             morbidity and mortality.},
   Doi = {10.1093/geronb/gbv035},
   Key = {fds320826}
}

@article{fds320828,
   Author = {Reuben, A and Moffitt, TE and Caspi, A and Belsky, DW and Harrington, H and Schroeder, F and Hogan, S and Ramrakha, S and Poulton, R and Danese,
             A},
   Title = {Lest we forget: comparing retrospective and prospective
             assessments of adverse childhood experiences in the
             prediction of adult health.},
   Journal = {Journal of child psychology and psychiatry, and allied
             disciplines},
   Volume = {57},
   Number = {10},
   Pages = {1103-1112},
   Year = {2016},
   Month = {October},
   url = {http://dx.doi.org/10.1111/jcpp.12621},
   Abstract = {<h4>Background</h4>Adverse childhood experiences (ACEs; e.g.
             abuse, neglect, and parental loss) have been associated with
             increased risk for later-life disease and dysfunction using
             adults' retrospective self-reports of ACEs. Research should
             test whether associations between ACEs and health outcomes
             are the same for prospective and retrospective ACE
             measures.<h4>Methods</h4>We estimated agreement between ACEs
             prospectively recorded throughout childhood (by Study staff
             at Study member ages 3, 5, 7, 9, 11, 13, and 15) and
             retrospectively recalled in adulthood (by Study members when
             they reached age 38), in the population-representative
             Dunedin cohort (N = 1,037). We related both retrospective
             and prospective ACE measures to physical, mental, cognitive,
             and social health at midlife measured through both objective
             (e.g. biomarkers and neuropsychological tests) and
             subjective (e.g. self-reported) means.<h4>Results</h4>Dunedin
             and U.S. Centers for Disease Control ACE distributions were
             similar. Retrospective and prospective measures of adversity
             showed moderate agreement (r = .47, p < .001; weighted
             Kappa = .31, 95% CI: .27-.35). Both associated with all
             midlife outcomes. As compared to prospective ACEs,
             retrospective ACEs showed stronger associations with life
             outcomes that were subjectively assessed, and weaker
             associations with life outcomes that were objectively
             assessed. Recalled ACEs and poor subjective outcomes were
             correlated regardless of whether prospectively recorded ACEs
             were evident. Individuals who recalled more ACEs than had
             been prospectively recorded were more neurotic than average,
             and individuals who recalled fewer ACEs than recorded were
             more agreeable.<h4>Conclusions</h4>Prospective ACE records
             confirm associations between childhood adversity and
             negative life outcomes found previously using retrospective
             ACE reports. However, more agreeable and neurotic
             dispositions may, respectively, bias retrospective ACE
             measures toward underestimating the impact of adversity on
             objectively measured life outcomes and overestimating the
             impact of adversity on self-reported outcomes. Associations
             between personality factors and the propensity to recall
             adversity were extremely modest and warrant further
             investigation. Risk predictions based on retrospective ACE
             reports should utilize objective outcome measures. Where
             objective outcome measurements are difficult to obtain,
             correction factors may be warranted.},
   Doi = {10.1111/jcpp.12621},
   Key = {fds320828}
}

@article{fds253113,
   Author = {Franken, A and Moffitt, TE and Steglich, CEG and Dijkstra, JK and Harakeh, Z and Vollebergh, WAM},
   Title = {The Role of Self-Control and Early Adolescents' Friendships
             in the Development of Externalizing Behavior: The SNARE
             Study.},
   Journal = {Journal of youth and adolescence},
   Volume = {45},
   Number = {9},
   Pages = {1800-1811},
   Year = {2016},
   Month = {September},
   ISSN = {0047-2891},
   url = {http://dx.doi.org/10.1007/s10964-015-0287-z},
   Abstract = {This social network study investigated the moderating role
             of self-control in the association between friendship and
             the development of externalizing behavior: Antisocial
             behavior, alcohol use, tobacco use. Previous studies have
             shown inconsistent findings, and did not control for
             possible friendship network or selection effects. We tested
             two complementary hypotheses: (1) That early-adolescents
             with low self-control develop externalizing behavior
             regardless of their friends' behavior, or (2) as a result of
             being influenced by their friends' externalizing behavior to
             a greater extent. Hypotheses were investigated using data
             from the SNARE (Social Network Analysis of Risk behavior in
             Early adolescence) study (N = 1144, 50 % boys, M age
             12.7, SD = 0.47). We controlled for selection effects and
             the network structure, using a data-analysis package called
             SIENA. The main findings indicate that personal low
             self-control and friends' externalizing behaviors both
             predict early adolescents' increasing externalizing
             behaviors, but they do so independently. Therefore,
             interventions should focus on all early adolescents' with a
             lower self-control, rather than focus on those adolescents
             with a lower self-control who also have friends who engage
             in externalizing behavior.},
   Doi = {10.1007/s10964-015-0287-z},
   Key = {fds253113}
}

@article{fds320830,
   Author = {Beckley, AL and Caspi, A and Harrington, H and Houts, RM and Mcgee, TR and Morgan, N and Schroeder, F and Ramrakha, S and Poulton, R and Moffitt,
             TE},
   Title = {Adult-onset offenders: Is a tailored theory
             warranted?},
   Journal = {Journal of criminal justice},
   Volume = {46},
   Pages = {64-81},
   Year = {2016},
   Month = {September},
   url = {http://dx.doi.org/10.1016/j.jcrimjus.2016.03.001},
   Abstract = {<h4>Purpose</h4>To describe official adult-onset offenders,
             investigate their antisocial histories and test hypotheses
             about their origins.<h4>Methods</h4>We defined adult-onset
             offenders among 931 Dunedin Study members followed to age
             38, using criminal-court conviction records.<h4>Results</h4>Official
             adult-onset offenders were 14% of men, and 32% of convicted
             men, but accounted for only 15% of convictions. As
             anticipated by developmental theories emphasizing early-life
             influences on crime, adult-onset offenders' histories of
             antisocial behavior spanned back to childhood. Relative to
             juvenile-offenders, during adolescence they had fewer
             delinquent peers and were more socially inhibited, which may
             have protected them from conviction. As anticipated by
             theories emphasizing the importance of situational
             influences on offending, adult-onset offenders, relative to
             non-offenders, during adulthood more often had
             schizophrenia, bipolar disorder, and alcohol-dependence, had
             weaker social bonds, anticipated fewer informal sanctions,
             and self-reported more offenses. Contrary to some
             expectations, adult-onset offenders did not have high IQ or
             high socioeconomic-status families protecting them from
             juvenile conviction.<h4>Conclusions</h4>A tailored theory
             for adult-onset offenders is unwarranted because few people
             begin crime <i>de novo</i> as adults. Official adult-onset
             offenders fall on a continuum of crime and its correlates,
             between official non-offenders and official juvenile-onset
             offenders. Existing theories can accommodate adult-onset
             offenders.},
   Doi = {10.1016/j.jcrimjus.2016.03.001},
   Key = {fds320830}
}

@article{fds340547,
   Author = {Belsky, DW and Moffitt, TE and Cohen, AA and Corcoran, D and Levine, ME and Prinz, J and Schaefer, J and Sugden, K and Williams, B and Poulton, R and Caspi, A},
   Title = {Telomere, epigenetic clock, and biomarker-composite
             quantifications of biological aging: Do they measure the
             same thing?},
   Year = {2016},
   Month = {August},
   url = {http://dx.doi.org/10.1101/071373},
   Abstract = {ABSTRACT The geroscience hypothesis posits that therapies to
             retard biological processes of aging can prevent disease. To
             test such “geroprotective” therapies in humans,
             surrogate endpoints are needed for extension of disease-free
             lifespan. Methods to quantify biological aging could provide
             such surrogate endpoints, but different methods have not
             been systematically evaluated in the same humans. We studied
             seven measures of biological aging in 964 middle-aged humans
             in the Dunedin Study: telomere-length, three
             epigenetic-clocks, and three biomarker-composites. Agreement
             between these different measures of biological aging was
             low. We also compared associations between biological aging
             measures and outcomes that geroprotective therapies will
             seek to modify: physical functioning, cognitive decline, and
             subjective signs of aging. The 71-CpG epigenetic clock and
             the biomarker composites were consistently related to these
             outcomes. Effect-sizes were modest. Quantification of
             biological aging is a young field. Next steps are to move
             toward systematic evaluation and refinement of
             methods.},
   Doi = {10.1101/071373},
   Key = {fds340547}
}

@article{fds321665,
   Author = {Wertz, J and Nottingham, K and Agnew-Blais, J and Matthews, T and Pariante, CM and Moffitt, TE and Arseneault, L},
   Title = {Parental monitoring and knowledge: Testing bidirectional
             associations with youths' antisocial behavior.},
   Journal = {Development and psychopathology},
   Volume = {28},
   Number = {3},
   Pages = {623-638},
   Year = {2016},
   Month = {August},
   url = {http://dx.doi.org/10.1017/s0954579416000213},
   Abstract = {In the present study, we used separate measures of parental
             monitoring and parental knowledge and compared their
             associations with youths' antisocial behavior during
             preadolescence, between the ages of 10 and 12. Parental
             monitoring and knowledge were reported by mothers, fathers,
             and youths taking part in the Environmental Risk (E-Risk)
             Longitudinal Twin Study that follows 1,116 families with
             twins. Information on youths' antisocial behavior was
             obtained from mothers as well as teachers. We report two
             main findings. First, longitudinal cross-lagged models
             revealed that greater parental monitoring did not predict
             less antisocial behavior later, once family characteristics
             were taken into account. Second, greater youth antisocial
             behavior predicted less parental knowledge later. This
             effect of youths' behavior on parents' knowledge was
             consistent across mothers', fathers', youths', and teachers'
             reports, and robust to controls for family confounders. The
             association was partially genetically mediated according to
             a Cholesky decomposition twin model; youths' genetically
             influenced antisocial behavior led to a decrease in parents'
             knowledge of youths' activities. These two findings question
             the assumption that greater parental monitoring can reduce
             preadolescents' antisocial behavior. They also indicate that
             parents' knowledge of their children's activities is
             influenced by youths' behavior.},
   Doi = {10.1017/s0954579416000213},
   Key = {fds321665}
}

@article{fds321666,
   Author = {Agnew-Blais, JC and Polanczyk, GV and Danese, A and Wertz, J and Moffitt, TE and Arseneault, L},
   Title = {Evaluation of the Persistence, Remission, and Emergence of
             Attention-Deficit/Hyperactivity Disorder in Young
             Adulthood.},
   Journal = {JAMA psychiatry},
   Volume = {73},
   Number = {7},
   Pages = {713-720},
   Year = {2016},
   Month = {July},
   url = {http://dx.doi.org/10.1001/jamapsychiatry.2016.0465},
   Abstract = {<h4>Importance</h4>Attention-deficit/hyperactivity disorder
             (ADHD) is now recognized to occur in adulthood and is
             associated with a range of negative outcomes. However, less
             is known about the prospective course of ADHD into
             adulthood, the risk factors for its persistence, and the
             possibility of its emergence in young adulthood in
             nonclinical populations.<h4>Objective</h4>To investigate
             childhood risk factors and young adult functioning of
             individuals with persistent, remitted, and late-onset young
             adult ADHD.<h4>Design, setting, and participants</h4>The
             study sample was the Environmental Risk (E-Risk)
             Longitudinal Twin Study, a nationally representative birth
             cohort of 2232 twins born in England and Wales from January
             1, 1994, to December 4, 1995. Evaluation of childhood ADHD
             (ages 5, 7, 10, and 12 years) included prenatal and
             perinatal factors, clinical characteristics, and aspects of
             the family environment. Among participants aged 18 years,
             ADHD symptoms and associated impairment, overall
             functioning, and other mental health disorders were
             examined. Data analysis was conducted from February 19 to
             September 10, 2015.<h4>Main outcomes and
             measures</h4>Attention-deficit/hyperactivity disorder
             according to DSM-IV diagnostic criteria in childhood and
             DSM-5 diagnostic criteria in young adulthood.<h4>Results</h4>Of
             2232 participants in the E-Risk Study, 2040 were included in
             the present analysis. In total, 247 individuals met
             diagnostic criteria for childhood ADHD; of these, 54 (21.9%)
             also met diagnostic criteria for the disorder at age 18
             years. Persistence was associated with more symptoms (odds
             ratio [OR], 1.11 [95% CI, 1.04-1.19]) and lower IQ (OR, 0.98
             [95% CI, 0.95-1.00]). At age 18 years, individuals with
             persistent ADHD had more functional impairment (school/work:
             OR, 3.30 [95% CI, 2.18-5.00], home/with friends: OR, 6.26
             [95% CI, 3.07-12.76]), generalized anxiety disorder (OR,
             5.19 [95% CI, 2.01-13.38]), conduct disorder (OR, 2.03 [95%
             CI, 1.03-3.99]), and marijuana dependence (OR, 2.88 [95% CI,
             1.07-7.71]) compared with those whose ADHD remitted. Among
             166 individuals with adult ADHD, 112 (67.5%) did not meet
             criteria for ADHD at any assessment in childhood. Results
             from logistic regressions indicated that individuals with
             late-onset ADHD showed fewer externalizing problems (OR,
             0.93 [95% CI, 0.91-0.96]) and higher IQ (OR, 1.04 [95% CI,
             1.02-1.07]) in childhood compared with the persistent group.
             However, at age 18 years, those with late-onset ADHD
             demonstrated comparable ADHD symptoms and impairment as well
             as similarly elevated rates of mental health
             disorders.<h4>Conclusions and relevance</h4>We identified
             heterogeneity in the DSM-5 young adult ADHD population such
             that this group consisted of a large, late-onset ADHD group
             with no childhood diagnosis, and a smaller group with
             persistent ADHD. The extent to which childhood-onset and
             late-onset adult ADHD may reflect different causes has
             implications for genetic studies and treatment of
             ADHD.},
   Doi = {10.1001/jamapsychiatry.2016.0465},
   Key = {fds321666}
}

@article{fds320831,
   Author = {Belsky, DW and Moffitt, TE and Corcoran, DL and Domingue, B and Harrington, H and Hogan, S and Houts, R and Ramrakha, S and Sugden, K and Williams, BS and Poulton, R and Caspi, A},
   Title = {The Genetics of Success: How Single-Nucleotide Polymorphisms
             Associated With Educational Attainment Relate to Life-Course
             Development.},
   Journal = {Psychological science},
   Volume = {27},
   Number = {7},
   Pages = {957-972},
   Year = {2016},
   Month = {July},
   url = {http://dx.doi.org/10.1177/0956797616643070},
   Abstract = {A previous genome-wide association study (GWAS) of more than
             100,000 individuals identified molecular-genetic predictors
             of educational attainment. We undertook in-depth life-course
             investigation of the polygenic score derived from this GWAS
             using the four-decade Dunedin Study (N = 918). There were
             five main findings. First, polygenic scores predicted adult
             economic outcomes even after accounting for educational
             attainments. Second, genes and environments were correlated:
             Children with higher polygenic scores were born into
             better-off homes. Third, children's polygenic scores
             predicted their adult outcomes even when analyses accounted
             for their social-class origins; social-mobility analysis
             showed that children with higher polygenic scores were more
             upwardly mobile than children with lower scores. Fourth,
             polygenic scores predicted behavior across the life course,
             from early acquisition of speech and reading skills through
             geographic mobility and mate choice and on to financial
             planning for retirement. Fifth, polygenic-score associations
             were mediated by psychological characteristics, including
             intelligence, self-control, and interpersonal skill. Effect
             sizes were small. Factors connecting DNA sequence with life
             outcomes may provide targets for interventions to promote
             population-wide positive development.},
   Doi = {10.1177/0956797616643070},
   Key = {fds320831}
}

@article{fds320832,
   Author = {Meier, MH and Caspi, A and Cerdá, M and Hancox, RJ and Harrington, H and Houts, R and Poulton, R and Ramrakha, S and Thomson, WM and Moffitt,
             TE},
   Title = {Associations Between Cannabis Use and Physical Health
             Problems in Early Midlife: A Longitudinal Comparison of
             Persistent Cannabis vs Tobacco Users.},
   Journal = {JAMA psychiatry},
   Volume = {73},
   Number = {7},
   Pages = {731-740},
   Year = {2016},
   Month = {July},
   url = {http://dx.doi.org/10.1001/jamapsychiatry.2016.0637},
   Abstract = {<h4>Importance</h4>After major policy changes in the United
             States, policymakers, health care professionals, and the
             general public seek information about whether recreational
             cannabis use is associated with physical health problems
             later in life.<h4>Objective</h4>To test associations between
             cannabis use over 20 years and a variety of physical health
             indexes at early midlife.<h4>Design, setting, and
             participants</h4>Participants belonged to a representative
             birth cohort of 1037 individuals born in Dunedin, New
             Zealand, in 1972 and 1973 and followed to age 38 years, with
             95% retention (the Dunedin Multidisciplinary Health and
             Development Study). We tested whether cannabis use from ages
             18 to 38 years was associated with physical health at age
             38, even after controlling for tobacco use, childhood
             health, and childhood socioeconomic status. We also tested
             whether cannabis use from ages 26 to 38 years was associated
             with within-individual health decline using the same
             measures of health at both ages.<h4>Exposures</h4>We
             assessed frequency of cannabis use and cannabis dependence
             at ages 18, 21, 26, 32, and 38 years.<h4>Main outcomes and
             measures</h4>We obtained laboratory measures of physical
             health (periodontal health, lung function, systemic
             inflammation, and metabolic health), as well as
             self-reported physical health, at ages 26 and 38
             years.<h4>Results</h4>The 1037 study participants were 51.6%
             male (n = 535). Of these, 484 had ever used tobacco daily
             and 675 had ever used cannabis. Cannabis use was associated
             with poorer periodontal health at age 38 years and
             within-individual decline in periodontal health from ages 26
             to 38 years. For example, cannabis joint-years from ages 18
             to 38 years was associated with poorer periodontal health at
             age 38 years, even after controlling for tobacco pack-years
             (β = 0.12; 95% CI, 0.05-0.18; P <.001). Additionally,
             cannabis joint-years from ages 26 to 38 years was associated
             with poorer periodontal health at age 38 years, even after
             accounting for periodontal health at age 26 years and
             tobacco pack-years (β = 0.10; 95% CI, 0.05-0.16; P <.001)
             However, cannabis use was unrelated to other physical health
             problems. Unlike cannabis use, tobacco use was associated
             with worse lung function, systemic inflammation, and
             metabolic health at age 38 years, as well as
             within-individual decline in health from ages 26 to 38
             years.<h4>Conclusions and relevance</h4>Cannabis use for up
             to 20 years is associated with periodontal disease but is
             not associated with other physical health problems in early
             midlife.},
   Doi = {10.1001/jamapsychiatry.2016.0637},
   Key = {fds320832}
}

@article{fds320834,
   Author = {Meier, MH and Hall, W and Caspi, A and Belsky, DW and Cerdá, M and Harrington, HL and Houts, R and Poulton, R and Moffitt,
             TE},
   Title = {Which adolescents develop persistent substance dependence in
             adulthood? Using population-representative longitudinal data
             to inform universal risk assessment.},
   Journal = {Psychological medicine},
   Volume = {46},
   Number = {4},
   Pages = {877-889},
   Year = {2016},
   Month = {March},
   url = {http://dx.doi.org/10.1017/s0033291715002482},
   Abstract = {<h4>Background</h4>To our knowledge, there are no universal
             screening tools for substance dependence that (1) were
             developed using a population-based sample, (2) estimate
             total risk briefly and inexpensively by incorporating a
             relatively small number of well-established risk factors,
             and (3) aggregate risk factors using a simple algorithm. We
             created a universal screening tool that incorporates these
             features to identify adolescents at risk for persistent
             substance dependence in adulthood.<h4>Method</h4>Participants
             were members of a representative cohort of 1037 individuals
             born in Dunedin, New Zealand in 1972-1973 and followed
             prospectively to age 38 years, with 95% retention. We
             assessed a small set of childhood and adolescent risk
             factors: family history of substance dependence, childhood
             psychopathology (conduct disorder, depression), early
             exposure to substances, frequent substance use in
             adolescence, sex, and childhood socioeconomic status. We
             defined the outcome (persistent substance dependence in
             adulthood) as dependence on one or more of alcohol, tobacco,
             cannabis, or hard drugs at ⩾3 assessment ages: 21, 26, 32,
             and 38 years.<h4>Results</h4>A cumulative risk index, a
             simple sum of nine childhood and adolescent risk factors,
             predicted persistent substance dependence in adulthood with
             considerable accuracy (AUC = 0.80).<h4>Conclusions</h4>A
             cumulative risk score can accurately predict which
             adolescents in the general population will develop
             persistent substance dependence in adulthood.},
   Doi = {10.1017/s0033291715002482},
   Key = {fds320834}
}

@article{fds320835,
   Author = {Matthews, T and Danese, A and Wertz, J and Odgers, CL and Ambler, A and Moffitt, TE and Arseneault, L},
   Title = {Social isolation, loneliness and depression in young
             adulthood: a behavioural genetic analysis.},
   Journal = {Social psychiatry and psychiatric epidemiology},
   Volume = {51},
   Number = {3},
   Pages = {339-348},
   Year = {2016},
   Month = {March},
   url = {http://dx.doi.org/10.1007/s00127-016-1178-7},
   Abstract = {<h4>Purpose</h4>To investigate the association between
             social isolation and loneliness, how they relate to
             depression, and whether these associations are explained by
             genetic influences.<h4>Methods</h4>We used data from the
             age-18 wave of the Environmental Risk Longitudinal Twin
             Study, a birth cohort of 1116 same-sex twin pairs born in
             England and Wales in 1994 and 1995. Participants reported on
             their levels of social isolation, loneliness and depressive
             symptoms. We conducted regression analyses to test the
             differential associations of isolation and loneliness with
             depression. Using the twin study design, we estimated the
             proportion of variance in each construct and their
             covariance that was accounted for by genetic and
             environmental factors.<h4>Results</h4>Social isolation and
             loneliness were moderately correlated (r = 0.39), reflecting
             the separateness of these constructs, and both were
             associated with depression. When entered simultaneously in a
             regression analysis, loneliness was more robustly associated
             with depression. We observed similar degrees of genetic
             influence on social isolation (40 %) and loneliness (38 %),
             and a smaller genetic influence on depressive symptoms (29
             %), with the remaining variance accounted for by the
             non-shared environment. Genetic correlations of 0.65 between
             isolation and loneliness and 0.63 between loneliness and
             depression indicated a strong role of genetic influences in
             the co-occurrence of these phenotypes.<h4>Conclusions</h4>Socially
             isolated young adults do not necessarily experience
             loneliness. However, those who are lonely are often
             depressed, partly because the same genes influence
             loneliness and depression. Interventions should not only aim
             at increasing social connections but also focus on
             subjective feelings of loneliness.},
   Doi = {10.1007/s00127-016-1178-7},
   Key = {fds320835}
}

@article{fds253111,
   Author = {Goldman-Mellor, S and Caspi, A and Arseneault, L and Ajala, N and Ambler, A and Danese, A and Fisher, H and Hucker, A and Odgers, C and Williams, T and Wong, C and Moffitt, TE},
   Title = {Committed to work but vulnerable: self-perceptions and
             mental health in NEET 18-year olds from a contemporary
             British cohort.},
   Journal = {Journal of child psychology and psychiatry, and allied
             disciplines},
   Volume = {57},
   Number = {2},
   Pages = {196-203},
   Year = {2016},
   Month = {February},
   ISSN = {0021-9630},
   url = {http://dx.doi.org/10.1111/jcpp.12459},
   Abstract = {<h4>Background</h4>Labour market disengagement among youths
             has lasting negative economic and social consequences, yet
             is poorly understood. We compared four types of work-related
             self-perceptions, as well as vulnerability to mental health
             and substance abuse problems, among youths not in education,
             employment or training (NEET) and among their
             peers.<h4>Methods</h4>Participants were from the
             Environmental Risk (E-Risk) longitudinal study, a nationally
             representative UK cohort of 2,232 twins born in 1994-1995.
             We measured commitment to work, job-search effort,
             professional/technical skills, 'soft' skills (e.g. teamwork,
             decision-making, communication), optimism about getting
             ahead, and mental health and substance use disorders at age
             18. We also examined childhood mental health.<h4>Results</h4>At
             age 18, 11.6% of participants were NEET. NEET participants
             reported themselves as committed to work and searching for
             jobs with greater diligence than their non-NEET peers.
             However, they reported fewer 'soft' skills (B = -0.98,
             p < .001) and felt less optimistic about their likelihood
             of getting ahead in life (B = -2.41, p < .001). NEET
             youths also had higher rates of concurrent mental health and
             substance abuse problems, but these did not explain the
             relationship with work-related self-perceptions. Nearly 60%
             of NEET (vs. 35% of non-NEET) youths had already experienced
             ≥1 mental health problem in childhood/adolescence.
             Associations of NEET status with concurrent mental health
             problems were independent of pre-existing mental health
             vulnerability.<h4>Conclusions</h4>Our findings indicate that
             while NEET is clearly an economic and mental health issue,
             it does not appear to be a motivation issue. Alongside
             skills, work-related self-perceptions and mental health
             problems may be targets for intervention and service
             provision among this high-risk population.},
   Doi = {10.1111/jcpp.12459},
   Key = {fds253111}
}

@article{fds321667,
   Author = {Thomson, WM and Zeng, J and Broadbent, JM and Foster Page and LA and Shalev, I and Moffitt, TE and Caspi, A and Williams, SM and Braithwaite,
             AW and Robertson, SP and Poulton, R},
   Title = {Telomere length and periodontal attachment loss: a
             prospective cohort study.},
   Journal = {Journal of clinical periodontology},
   Volume = {43},
   Number = {2},
   Pages = {121-127},
   Year = {2016},
   Month = {February},
   url = {http://dx.doi.org/10.1111/jcpe.12499},
   Abstract = {<h4>Aim</h4>The aim of the study was to examine the
             association between telomere erosion and periodontitis in a
             long-standing prospective cohort study of New Zealand
             adults. Specific hypotheses tested were as follows: (i) that
             exposure to periodontitis at ages 26 and 38 was associated
             with accelerated leucocyte telomere erosion and (ii) that
             accelerated leucocyte telomere erosion was associated with
             higher rates of periodontitis by ages 26 and
             38.<h4>Materials and methods</h4>Periodontal attachment loss
             data were collected at ages 26 and 38. Blood samples taken
             at the same ages were analysed to obtain estimates of
             leucocyte telomere length and erosion over a 12-year
             period.<h4>Results</h4>Overall, the mean telomere length was
             reduced by 0.15 T/S ratio (adjusted) from age 26 to 38 among
             the 661 participants reported on here. During the same
             period, the mean attachment loss increased by 10%, after
             adjusting for sex, socio-economic status and smoking.
             Regression models showed that attachment loss did not
             predict telomere length, and that telomere erosion did not
             predict attachment loss.<h4>Conclusions</h4>Although both
             periodontitis and telomere length are age-dependent, they do
             not appear to be linked, suggesting that determination of
             leucocyte telomere length may not be a promising clinical
             approach at this age for identifying people who are at risk
             for periodontitis.},
   Doi = {10.1111/jcpe.12499},
   Key = {fds321667}
}

@article{fds321668,
   Author = {Broadbent, JM and Thomson, WM and Moffitt, TE and Poulton,
             R},
   Title = {Broadbent et al. Respond.},
   Journal = {American journal of public health},
   Volume = {106},
   Number = {2},
   Pages = {213-214},
   Year = {2016},
   Month = {February},
   url = {http://dx.doi.org/10.2105/ajph.2015.303013},
   Doi = {10.2105/ajph.2015.303013},
   Key = {fds321668}
}

@article{fds327554,
   Author = {Cannon, T and Moffitt, T and Brennan, P and Raine, A and Baker,
             L},
   Title = {Sarnoff A. Mednick (1928-2015).},
   Journal = {The American psychologist},
   Volume = {71},
   Number = {2},
   Pages = {148},
   Year = {2016},
   Month = {February},
   url = {http://dx.doi.org/10.1037/a0039815},
   Abstract = {Presents the obituary of Sarnoff A. Mednick (1928 -2015).
             Sarnoff A. Mednick was considered among the most important
             figures in psychopathology research in his generation. He
             pioneered the high-risk research design and made numerous
             contributions to our understanding of creativity and of the
             origins of schizophrenia and criminality. The son of Jewish
             immigrants, Mednick was born on January 27, 1928, and was
             raised in the Bronx in New York City, New York. He earned a
             bachelor's degree from the City College of New York in 1948
             and a master's degree from Columbia University. In 1954, he
             earned his doctorate in psychology from Northwestern
             University. Following a postdoctoral fellowship at the
             University of Chicago, he was appointed an instructor at
             Harvard University and then became a visiting assistant
             research professor at the University of California, Berkeley
             (1958 -1959). In 1968, he became a professor at the New
             School for Social Research in New York, where he taught
             until 1977, when he joined the faculty at the University of
             Southern California until his retirement in August 2008.
             Mednick, professor emeritus of psychology at the University
             of Southern California, died of natural causes on April 10,
             2015, in Toledo, Ohio. He was 87.},
   Doi = {10.1037/a0039815},
   Key = {fds327554}
}

@article{fds328947,
   Author = {Caspi, A and Houts, RM and Belsky, DW and Harrington, H and Hogan, S and Ramrakha, S and Poulton, R and Moffitt, TE},
   Title = {Childhood forecasting of a small segment of the population
             with large economic burden.},
   Journal = {Nature human behaviour},
   Volume = {1},
   Pages = {0005},
   Year = {2016},
   Month = {January},
   url = {http://dx.doi.org/10.1038/s41562-016-0005},
   Abstract = {Policy-makers are interested in early-years interventions to
             ameliorate childhood risks. They hope for improved adult
             outcomes in the long run, bringing return on investment. How
             much return can be expected depends, partly, on how strongly
             childhood risks forecast adult outcomes. But there is
             disagreement about whether childhood determines adulthood.
             We integrated multiple nationwide administrative databases
             and electronic medical records with the four-decade Dunedin
             birth-cohort study to test child-to-adult prediction in a
             different way, by using a population-segmentation approach.
             A segment comprising one-fifth of the cohort accounted for
             36% of the cohort's injury insurance-claims; 40% of excess
             obese-kilograms; 54% of cigarettes smoked; 57% of hospital
             nights; 66% of welfare benefits; 77% of fatherless
             childrearing; 78% of prescription fills; and 81% of criminal
             convictions. Childhood risks, including poor age-three brain
             health, predicted this segment with large effect sizes.
             Early-years interventions effective with this population
             segment could yield very large returns on
             investment.},
   Doi = {10.1038/s41562-016-0005},
   Key = {fds328947}
}

@article{fds321670,
   Author = {Wertz, J and Zavos, HMS and Matthews, T and Gray, R and Best-Lane, J and Pariante, CM and Moffitt, TE and Arseneault, L},
   Title = {Etiology of Pervasive Versus Situational Antisocial
             Behaviors: A Multi-Informant Longitudinal Cohort
             Study.},
   Journal = {Child development},
   Volume = {87},
   Number = {1},
   Pages = {312-325},
   Year = {2016},
   Month = {January},
   url = {http://dx.doi.org/10.1111/cdev.12456},
   Abstract = {The aim of this study was to disentangle pervasive from
             situational antisocial behaviors using multiple informants,
             and to investigate their genetic and environmental
             etiologies in preadolescence and across time. Antisocial
             behaviors were assessed in 2,232 twins from the
             Environmental Risk (E-Risk) Longitudinal Twin Study at ages
             5 and 12. Pervasive antisocial behaviors were defined as
             behaviors that mothers, teachers, interviewers, and twins
             themselves agreed on. Results from a psychometric model
             indicated that the variation in children's pervasive
             antisocial behaviors was mostly accounted for by familial
             influences that originated in childhood, whereas situational
             behaviors were explained by newly emerging nonshared
             environmental and genetic influences. This study shows that
             children's pervasive and situational antisocial behaviors
             have distinct etiologies that could guide research and
             treatment.},
   Doi = {10.1111/cdev.12456},
   Key = {fds321670}
}

@article{fds321671,
   Author = {Sugden, K and Moffitt, TE and Pinto, L and Poulton, R and Williams, BS and Caspi, A},
   Title = {Is Toxoplasma Gondii Infection Related to Brain and Behavior
             Impairments in Humans? Evidence from a Population-Representative
             Birth Cohort.},
   Journal = {PloS one},
   Volume = {11},
   Number = {2},
   Pages = {e0148435},
   Year = {2016},
   Month = {January},
   url = {http://dx.doi.org/10.1371/journal.pone.0148435},
   Abstract = {<h4>Background</h4>Toxoplasma gondii (T. gondii) is a
             protozoan parasite present in around a third of the human
             population. Infected individuals are commonly asymptomatic,
             though recent reports have suggested that infection might
             influence aspects of the host's behavior. In particular,
             Toxoplasma infection has been linked to schizophrenia,
             suicide attempt, differences in aspects of personality and
             poorer neurocognitive performance. However, these studies
             are often conducted in clinical samples or convenience
             samples.<h4>Methods/results</h4>In a population-representative
             birth-cohort of individuals tested for presence of
             antibodies to T. gondii (N = 837) we investigated the
             association between infection and four facets of human
             behavior: neuropsychiatric disorder (schizophrenia and major
             depression), poor impulse control (suicidal behavior and
             criminality), personality, and neurocognitive performance.
             Suicide attempt was marginally more frequent among
             individuals with T. gondii seropositivity (p = .06).
             Seropositive individuals also performed worse on one out of
             14 measures of neuropsychological function.<h4>Conclusion</h4>On
             the whole, there was little evidence that T. gondii was
             related to increased risk of psychiatric disorder, poor
             impulse control, personality aberrations or neurocognitive
             impairment.},
   Doi = {10.1371/journal.pone.0148435},
   Key = {fds321671}
}

@article{fds291136,
   Author = {Theodore, RF and Broadbent, J and Nagin, D and Ambler, A and Hogan, S and Ramrakha, S and Cutfield, W and Williams, MJA and Harrington, H and Moffitt, TE and Caspi, A and Milne, B and Poulton,
             R},
   Title = {Childhood to Early-Midlife Systolic Blood Pressure
             Trajectories: Early-Life Predictors, Effect Modifiers, and
             Adult Cardiovascular Outcomes.},
   Journal = {Hypertension (Dallas, Tex. : 1979)},
   Volume = {66},
   Number = {6},
   Pages = {1108-1115},
   Year = {2015},
   Month = {December},
   ISSN = {0194-911X},
   url = {http://dx.doi.org/10.1161/hypertensionaha.115.05831},
   Abstract = {Previous studies examining blood pressure change over time
             have modeled an average population trajectory. Recent
             research among older adults suggests there may be subgroups
             with different blood pressure trajectories. Identifying
             subgroups at risk of developing adult hypertension early in
             life can inform effective risk reduction efforts. We sought
             to identify different systolic blood pressure trajectories
             from childhood, their correlated risk factors, and
             early-midlife cardiovascular outcomes. Blood pressure data
             at ages 7, 11, 18, 26, 32, and 38 years from a longitudinal,
             representative birth cohort study (n=975) were used to
             identify 4 distinct trajectory groups via group-based
             trajectory modeling: normal (21.8%), high-normal (43.3%),
             prehypertensive (31.6%), and hypertensive (4.2%). The
             categories refer to blood pressure beginning at the age of 7
             years and most recently measured at the age of 38 years.
             Family history of high blood pressure (odds ratio [OR],
             43.23; 95% confidence interval [CI], 5.27-354.65), male sex
             (OR, 109.48; 95% CI, 26.82-446.96), being first born (OR,
             2.5; 95% CI, 1.00-8.69) and low birth weight (OR, 2.79; 95%
             CI, 2.49-3.09) were associated with hypertensive group
             membership (compared with the normal group). Higher body
             mass index and cigarette smoking resulted in increasing
             blood pressure across trajectories, particularly for the
             higher blood pressure groups. Prehypertensive and
             hypertensive trajectory groups had worse cardiovascular
             outcomes by early midlife. Harmful blood pressure
             trajectories are identifiable in childhood, associated with
             both antecedent and modifiable risk factors over time, and
             predict adult cardiovascular disease risk. Early detection
             and subsequent targeted prevention and intervention may
             reduce the lifecourse burden associated with higher blood
             pressure.},
   Doi = {10.1161/hypertensionaha.115.05831},
   Key = {fds291136}
}

@article{fds291137,
   Author = {Kimonis, ER and Fanti, KA and Frick, PJ and Moffitt, TE and Essau, C and Bijttebier, P and Marsee, MA},
   Title = {Using self-reported callous-unemotional traits to
             cross-nationally assess the DSM-5 'With Limited Prosocial
             Emotions' specifier.},
   Journal = {Journal of child psychology and psychiatry, and allied
             disciplines},
   Volume = {56},
   Number = {11},
   Pages = {1249-1261},
   Year = {2015},
   Month = {November},
   ISSN = {0021-9630},
   url = {http://dx.doi.org/10.1111/jcpp.12357},
   Abstract = {<h4>Background</h4>The presence of callous-unemotional (CU)
             traits designates an important subgroup of antisocial youth
             at risk for severe, persistent, and impairing conduct
             problems. As a result, the fifth revision of the Diagnostic
             and Statistical Manual includes a specifier for youth
             meeting diagnostic criteria for Conduct Disorder who show
             elevated CU traits. The current study evaluated the DSM-5
             criteria using Item Response Theory (IRT) analyses and
             evaluated two methods for using a self-report measure of CU
             traits to make this diagnosis.<h4>Methods</h4>The sample
             included 2257 adolescent (M age = 15.64, SD = 1.69 years)
             boys (53%) and girls (47%) from community and incarcerated
             settings in the United States and the European countries of
             Belgium, Germany, and Cyprus.<h4>Results</h4>IRT analyses
             suggested that four- or eight-item sets from the self-report
             measure (comparable to the symptoms used by the DSM-5
             specifier) provided good model fit, suggesting that they
             assess a single underlying CU construct. Further, the most
             stringent method of scoring the self-report scale (i.e.
             taking only the most extreme responses) to approximate
             symptom presence provided the best discrimination in IRT
             analyses, showed reasonable prevalence rates of the
             specifier, and designated community adolescents who were
             highly antisocial, whereas the less stringent method best
             discriminated detained youth.<h4>Conclusions</h4>Refined
             self-report scales developed on the basis of IRT findings
             provided good assessments of most of the symptoms used in
             the DSM-5 criteria. These scales may be used as one
             component of a multimethod assessment of the 'With Limited
             Prosocial Emotions' specifier for Conduct
             Disorder.},
   Doi = {10.1111/jcpp.12357},
   Key = {fds291137}
}

@article{fds320836,
   Author = {Fisher, HL and Caspi, A and Moffitt, TE and Wertz, J and Gray, R and Newbury, J and Ambler, A and Zavos, H and Danese, A and Mill, J and Odgers,
             CL and Pariante, C and Wong, CCY and Arseneault, L},
   Title = {Measuring adolescents' exposure to victimization: The
             Environmental Risk (E-Risk) Longitudinal Twin
             Study.},
   Journal = {Development and psychopathology},
   Volume = {27},
   Number = {4 Pt 2},
   Pages = {1399-1416},
   Year = {2015},
   Month = {November},
   url = {http://dx.doi.org/10.1017/s0954579415000838},
   Abstract = {This paper presents multilevel findings on adolescents'
             victimization exposure from a large longitudinal cohort of
             twins. Data were obtained from the Environmental Risk
             (E-Risk) Longitudinal Twin Study, an epidemiological study
             of 2,232 children (1,116 twin pairs) followed to 18 years of
             age (with 93% retention). To assess adolescent
             victimization, we combined best practices in survey research
             on victimization with optimal approaches to measuring life
             stress and traumatic experiences, and introduce a reliable
             system for coding severity of victimization. One in three
             children experienced at least one type of severe
             victimization during adolescence (crime victimization,
             peer/sibling victimization, Internet/mobile phone
             victimization, sexual victimization, family violence,
             maltreatment, or neglect), and most types of victimization
             were more prevalent among children from low socioeconomic
             backgrounds. Exposure to multiple victimization types was
             common, as was revictimization; over half of those
             physically maltreated in childhood were also exposed to
             severe physical violence in adolescence. Biometric twin
             analyses revealed that environmental factors had the
             greatest influence on most types of victimization, while
             severe physical maltreatment from caregivers during
             adolescence was predominantly influenced by heritable
             factors. The findings from this study showcase how distinct
             levels of victimization measurement can be harmonized in
             large-scale studies of health and development.},
   Doi = {10.1017/s0954579415000838},
   Key = {fds320836}
}

@article{fds253115,
   Author = {Moffitt, TE and Houts, R and Asherson, P and Belsky, DW and Corcoran,
             DL and Hammerle, M and Harrington, H and Hogan, S and Meier, MH and Polanczyk, GV and Poulton, R and Ramrakha, S and Sugden, K and Williams,
             B and Rohde, LA and Caspi, A},
   Title = {Is Adult ADHD a Childhood-Onset Neurodevelopmental Disorder?
             Evidence From a Four-Decade Longitudinal Cohort
             Study.},
   Journal = {The American journal of psychiatry},
   Volume = {172},
   Number = {10},
   Pages = {967-977},
   Year = {2015},
   Month = {October},
   ISSN = {0002-953X},
   url = {http://dx.doi.org/10.1176/appi.ajp.2015.14101266},
   Abstract = {<h4>Objective</h4>Despite a prevailing assumption that adult
             ADHD is a childhood-onset neurodevelopmental disorder, no
             prospective longitudinal study has described the childhoods
             of the adult ADHD population. The authors report follow-back
             analyses of ADHD cases diagnosed in adulthood, alongside
             follow-forward analyses of ADHD cases diagnosed in
             childhood, in one cohort.<h4>Method</h4>Participants
             belonged to a representative birth cohort of 1,037
             individuals born in Dunedin, New Zealand, in 1972 and 1973
             and followed to age 38, with 95% retention. Symptoms of
             ADHD, associated clinical features, comorbid disorders,
             neuropsychological deficits, genome-wide association
             study-derived polygenic risk, and life impairment indicators
             were assessed. Data sources were participants, parents,
             teachers, informants, neuropsychological test results, and
             administrative records. Adult ADHD diagnoses used DSM-5
             criteria, apart from onset age and cross-setting
             corroboration, which were study outcome measures.<h4>Results</h4>As
             expected, childhood ADHD had a prevalence of 6%
             (predominantly male) and was associated with childhood
             comorbid disorders, neurocognitive deficits, polygenic risk,
             and residual adult life impairment. Also as expected, adult
             ADHD had a prevalence of 3% (gender balanced) and was
             associated with adult substance dependence, adult life
             impairment, and treatment contact. Unexpectedly, the
             childhood ADHD and adult ADHD groups comprised virtually
             nonoverlapping sets; 90% of adult ADHD cases lacked a
             history of childhood ADHD. Also unexpectedly, the adult ADHD
             group did not show tested neuropsychological deficits in
             childhood or adulthood, nor did they show polygenic risk for
             childhood ADHD.<h4>Conclusions</h4>The findings raise the
             possibility that adults presenting with the ADHD symptom
             picture may not have a childhood-onset neurodevelopmental
             disorder. If this finding is replicated, then the disorder's
             place in the classification system must be reconsidered, and
             research must investigate the etiology of adult
             ADHD.},
   Doi = {10.1176/appi.ajp.2015.14101266},
   Key = {fds253115}
}

@article{fds253125,
   Author = {Odgers, CL and Donley, S and Caspi, A and Bates, CJ and Moffitt,
             TE},
   Title = {Living alongside more affluent neighbors predicts greater
             involvement in antisocial behavior among low-income
             boys.},
   Journal = {Journal of child psychology and psychiatry, and allied
             disciplines},
   Volume = {56},
   Number = {10},
   Pages = {1055-1064},
   Year = {2015},
   Month = {October},
   ISSN = {0021-9630},
   url = {http://dx.doi.org/10.1111/jcpp.12380},
   Abstract = {<h4>Background</h4>The creation of economically mixed
             communities has been proposed as one way to improve the life
             outcomes of children growing up in poverty. However, whether
             low-income children benefit from living alongside more
             affluent neighbors is unknown.<h4>Method</h4>Prospectively
             gathered data on over 1,600 children from the Environmental
             Risk (E-Risk) Longitudinal Twin Study living in urban
             environments is used to test whether living alongside more
             affluent neighbors (measured via high-resolution geo-spatial
             indices) predicts low-income children's antisocial behavior
             (reported by mothers and teachers at the ages of 5, 7, 10,
             and 12).<h4>Results</h4>Results indicated that low-income
             boys (but not girls) surrounded by more affluent neighbors
             had higher levels of antisocial behavior than their peers
             embedded in concentrated poverty. The negative effect of
             growing up alongside more affluent neighbors on low-income
             boys' antisocial behavior held across childhood and after
             controlling for key neighborhood and family-level
             factors.<h4>Conclusions</h4>Findings suggest that efforts to
             create more economically mixed communities for children, if
             not properly supported, may have iatrogenic effects on boys'
             antisocial behavior.},
   Doi = {10.1111/jcpp.12380},
   Key = {fds253125}
}

@article{fds320837,
   Author = {Suppli, NP and Bukh, JD and Moffitt, TE and Caspi, A and Johansen, C and Albieri, V and Tjønneland, A and Kessing, LV and Dalton,
             SO},
   Title = {5-HTTLPR and use of antidepressants after colorectal cancer
             including a meta-analysis of 5-HTTLPR and depression after
             cancer.},
   Journal = {Translational psychiatry},
   Volume = {5},
   Pages = {e631},
   Year = {2015},
   Month = {September},
   url = {http://dx.doi.org/10.1038/tp.2015.121},
   Abstract = {The serotonin-transporter-linked polymorphic region
             (5-HTTLPR) is one of the most extensively investigated
             candidates to be involved in gene-environment interaction
             associated with depression. Nevertheless, the interaction
             remains controversial. In an original study, we tested the
             hypothesis that risk for use of antidepressants following a
             diagnosis of colorectal cancer is associated with bi- and
             triallelic genotypes of 5-HTTLPR. In addition, in an
             inclusive meta-analysis, we tested the hypothesis that
             depression following a diagnosis of cancer is associated
             with biallelic 5-HTTLPR genotype. We created an exposed-only
             cohort of 849 colorectal cancer patients from the Danish
             Diet, Cancer and Health cohort study. The hypothesized
             association was investigated with Cox regression models and
             competing risk analyses. Five studies comprising a total of
             1484 cancer patients were included in the meta-analysis.
             Nationwide registries provided information on dates of
             diagnosis of colorectal cancer and use of antidepressants.
             Unadjusted odds ratios of depression according to the
             biallelic 5-HTTLPR genotype were included in the
             meta-analysis. 5-HTTLPR genotypes were not associated with
             use of antidepressants after colorectal cancer. Estimated
             hazard ratios ranged 0.92-1.08, and we observed no
             statistically significant associations across biallelic and
             triallelic genotypes in crude as well as adjusted models.
             The meta-analysis showed no statistically significant
             associations of 5-HTTLPR biallelic genotype with depression
             after cancer. Our findings in an original study and a
             meta-analysis do not support the hypothesis of an
             association between the 5-HTTLPR genotype and depression
             after cancer.},
   Doi = {10.1038/tp.2015.121},
   Key = {fds320837}
}

@article{fds253112,
   Author = {Global Burden of Disease Study 2013 Collaborators},
   Title = {Global, regional, and national incidence, prevalence, and
             years lived with disability for 301 acute and chronic
             diseases and injuries in 188 countries, 1990-2013: a
             systematic analysis for the Global Burden of Disease Study
             2013.},
   Journal = {Lancet},
   Volume = {386},
   Number = {9995},
   Pages = {743-800},
   Year = {2015},
   Month = {August},
   ISSN = {0140-6736},
   url = {http://dx.doi.org/10.1016/S0140-6736(15)60692-4},
   Abstract = {BACKGROUND: Up-to-date evidence about levels and trends in
             disease and injury incidence, prevalence, and years lived
             with disability (YLDs) is an essential input into global,
             regional, and national health policies. In the Global Burden
             of Disease Study 2013 (GBD 2013), we estimated these
             quantities for acute and chronic diseases and injuries for
             188 countries between 1990 and 2013. METHODS: Estimates were
             calculated for disease and injury incidence, prevalence, and
             YLDs using GBD 2010 methods with some important refinements.
             Results for incidence of acute disorders and prevalence of
             chronic disorders are new additions to the analysis. Key
             improvements include expansion to the cause and sequelae
             list, updated systematic reviews, use of detailed injury
             codes, improvements to the Bayesian meta-regression method
             (DisMod-MR), and use of severity splits for various causes.
             An index of data representativeness, showing data
             availability, was calculated for each cause and impairment
             during three periods globally and at the country level for
             2013. In total, 35 620 distinct sources of data were used
             and documented to calculated estimates for 301 diseases and
             injuries and 2337 sequelae. The comorbidity simulation
             provides estimates for the number of sequelae, concurrently,
             by individuals by country, year, age, and sex. Disability
             weights were updated with the addition of new
             population-based survey data from four countries. FINDINGS:
             Disease and injury were highly prevalent; only a small
             fraction of individuals had no sequelae. Comorbidity rose
             substantially with age and in absolute terms from 1990 to
             2013. Incidence of acute sequelae were predominantly
             infectious diseases and short-term injuries, with over 2
             billion cases of upper respiratory infections and diarrhoeal
             disease episodes in 2013, with the notable exception of
             tooth pain due to permanent caries with more than 200
             million incident cases in 2013. Conversely, leading chronic
             sequelae were largely attributable to non-communicable
             diseases, with prevalence estimates for asymptomatic
             permanent caries and tension-type headache of 2·4 billion
             and 1·6 billion, respectively. The distribution of the
             number of sequelae in populations varied widely across
             regions, with an expected relation between age and disease
             prevalence. YLDs for both sexes increased from 537·6
             million in 1990 to 764·8 million in 2013 due to population
             growth and ageing, whereas the age-standardised rate
             decreased little from 114·87 per 1000 people to 110·31 per
             1000 people between 1990 and 2013. Leading causes of YLDs
             included low back pain and major depressive disorder among
             the top ten causes of YLDs in every country. YLD rates per
             person, by major cause groups, indicated the main drivers of
             increases were due to musculoskeletal, mental, and substance
             use disorders, neurological disorders, and chronic
             respiratory diseases; however HIV/AIDS was a notable driver
             of increasing YLDs in sub-Saharan Africa. Also, the
             proportion of disability-adjusted life years due to YLDs
             increased globally from 21·1% in 1990 to 31·2% in 2013.
             INTERPRETATION: Ageing of the world's population is leading
             to a substantial increase in the numbers of individuals with
             sequelae of diseases and injuries. Rates of YLDs are
             declining much more slowly than mortality rates. The
             non-fatal dimensions of disease and injury will require more
             and more attention from health systems. The transition to
             non-fatal outcomes as the dominant source of burden of
             disease is occurring rapidly outside of sub-Saharan Africa.
             Our results can guide future health initiatives through
             examination of epidemiological trends and a better
             understanding of variation across countries. FUNDING: Bill &
             Melinda Gates Foundation.},
   Doi = {10.1016/S0140-6736(15)60692-4},
   Key = {fds253112}
}

@article{fds253114,
   Author = {Belsky, DW and Caspi, A and Houts, R and Cohen, HJ and Corcoran, DL and Danese, A and Harrington, H and Israel, S and Levine, ME and Schaefer,
             JD and Sugden, K and Williams, B and Yashin, AI and Poulton, R and Moffitt,
             TE},
   Title = {Quantification of biological aging in young
             adults.},
   Journal = {Proc Natl Acad Sci U S A},
   Volume = {112},
   Number = {30},
   Pages = {E4104-E4110},
   Year = {2015},
   Month = {July},
   ISSN = {0027-8424},
   url = {http://hdl.handle.net/10161/10319 Duke open
             access},
   Abstract = {Antiaging therapies show promise in model organism research.
             Translation to humans is needed to address the challenges of
             an aging global population. Interventions to slow human
             aging will need to be applied to still-young individuals.
             However, most human aging research examines older adults,
             many with chronic disease. As a result, little is known
             about aging in young humans. We studied aging in 954 young
             humans, the Dunedin Study birth cohort, tracking multiple
             biomarkers across three time points spanning their third and
             fourth decades of life. We developed and validated two
             methods by which aging can be measured in young adults, one
             cross-sectional and one longitudinal. Our longitudinal
             measure allows quantification of the pace of coordinated
             physiological deterioration across multiple organ systems
             (e.g., pulmonary, periodontal, cardiovascular, renal,
             hepatic, and immune function). We applied these methods to
             assess biological aging in young humans who had not yet
             developed age-related diseases. Young individuals of the
             same chronological age varied in their "biological aging"
             (declining integrity of multiple organ systems). Already,
             before midlife, individuals who were aging more rapidly were
             less physically able, showed cognitive decline and brain
             aging, self-reported worse health, and looked older.
             Measured biological aging in young adults can be used to
             identify causes of aging and evaluate rejuvenation
             therapies.},
   Doi = {10.1073/pnas.1506264112},
   Key = {fds253114}
}

@article{fds253116,
   Author = {Poulton, R and Moffitt, TE and Silva, PA},
   Title = {The Dunedin Multidisciplinary Health and Development Study:
             overview of the first 40 years, with an eye to the
             future.},
   Journal = {Social psychiatry and psychiatric epidemiology},
   Volume = {50},
   Number = {5},
   Pages = {679-693},
   Year = {2015},
   Month = {May},
   ISSN = {0933-7954},
   url = {http://dx.doi.org/10.1007/s00127-015-1048-8},
   Abstract = {The Dunedin Multidisciplinary Health and Development Study
             began more than four decades ago. Unusual at the time, it
             was founded as a multidisciplinary research enterprise, and
             was strongly supported by the Dunedin community, both
             professional and lay, in its early years. Seven research
             themes have evolved over the past 40 years focusing on
             mental health and neuro-cognition, cardiovascular risk,
             respiratory health, oral health, sexual and reproductive
             health, and psychosocial functioning. A seventh, more
             applied theme, seeks to maximise the value of the Study
             findings for New Zealand's indigenous people-Māori (or
             tangata whenua transl people of the land). The study has
             published over 1200 papers and reports to date, with almost
             2/3 of these being in peer-reviewed journals. Here we
             provide an overview of the study, its history, leadership
             structure, scientific approach, operational foci, and some
             recent examples of work that illustrate the following: (a)
             the value of multidisciplinary data; (b) how the study is
             well positioned to address contemporary issues; and (c) how
             research can simultaneously address multiple audiences-from
             researchers and theoreticians to policy makers and
             practitioners. Near-future research plans are described, and
             we end by reflecting upon the core aspects of the study that
             portend future useful contributions.},
   Doi = {10.1007/s00127-015-1048-8},
   Key = {fds253116}
}

@article{fds253121,
   Author = {Ouellet-Morin, I and Fisher, HL and York-Smith, M and Fincham-Campbell, S and Moffitt, TE and Arseneault,
             L},
   Title = {Intimate partner violence and new-onset depression: a
             longitudinal study of women's childhood and adult histories
             of abuse.},
   Journal = {Depression and anxiety},
   Volume = {32},
   Number = {5},
   Pages = {316-324},
   Year = {2015},
   Month = {May},
   ISSN = {1091-4269},
   url = {http://dx.doi.org/10.1002/da.22347},
   Abstract = {<h4>Background</h4>Studies indicate that women victims of
             intimate partner violence are at increased risk for poor
             mental health. This research disentangled the effect of
             partner violence on new-onset depression and psychosis
             spectrum symptoms from effects of child maltreatment and
             other confounding factors, including substance abuse and
             antisocial personality.<h4>Methods</h4>Participants were
             1,052 mothers involved in the Environmental Risk (E-Risk)
             Longitudinal Twin Study, a nationally representative cohort
             of families followed prospectively. To test the
             directionality of associations between partner violence and
             depression, only women without a history of depression at
             the beginning of the study were considered (n = 978).
             Partner violence and mental health were assessed during
             face-to-face interviews with women across three time
             points.<h4>Results</h4>Four of 10 women reported being the
             victim of violence from their partner in a 10-year period.
             They represent 33% of our cohort and they account for 51% of
             new-onset depression. These women had a twofold increase in
             their risk of suffering from new-onset depression once the
             effect of childhood maltreatment, socioeconomic deprivation,
             antisocial personality, and young motherhood were
             controlled. Women who were abused both in childhood and
             adulthood were four to seven times more likely to suffer
             from depression than never-abused women. We observed similar
             associations with psychosis spectrum symptoms.<h4>Conclusions</h4>Women
             victims of partner violence account for more than their
             share of depression. Findings strengthen existing evidence
             that partner violence independently contributes to women's
             poor mental health. Psychological difficulties among a
             considerable number of women could be reduced by stopping
             partner violence.},
   Doi = {10.1002/da.22347},
   Key = {fds253121}
}

@article{fds253123,
   Author = {Parsons, MJ and Moffitt, TE and Gregory, AM and Goldman-Mellor, S and Nolan, PM and Poulton, R and Caspi, A},
   Title = {Social jetlag, obesity and metabolic disorder: investigation
             in a cohort study.},
   Journal = {International journal of obesity (2005)},
   Volume = {39},
   Number = {5},
   Pages = {842-848},
   Year = {2015},
   Month = {May},
   ISSN = {0307-0565},
   url = {http://dx.doi.org/10.1038/ijo.2014.201},
   Abstract = {<h4>Background</h4>Obesity is one of the leading causes of
             preventable death worldwide. Circadian rhythms are known to
             control both sleep timing and energy homeostasis, and
             disruptions in circadian rhythms have been linked with
             metabolic dysfunction and obesity-associated disease. In
             previous research, social jetlag, a measure of chronic
             circadian disruption caused by the discrepancy between our
             internal versus social clocks, was associated with elevated
             self-reported body mass index, possibly indicative of a more
             generalized association with obesity and metabolic
             dysfunction.<h4>Methods</h4>We studied participants from the
             population-representative Dunedin Longitudinal Study
             (N=1037) to determine whether social jetlag was associated
             with clinically assessed measurements of metabolic
             phenotypes and disease indicators for obesity-related
             disease, specifically, indicators of inflammation and
             diabetes.<h4>Results</h4>Our analysis was restricted to
             N=815 non-shift workers in our cohort. Among these
             participants, we found that social jetlag was associated
             with numerous clinically assessed measures of metabolic
             dysfunction and obesity. We distinguished between obese
             individuals who were metabolically healthy versus unhealthy,
             and found higher social jetlag levels in metabolically
             unhealthy obese individuals. Among metabolically unhealthy
             obese individuals, social jetlag was additionally associated
             with elevated glycated hemoglobin and an indicator of
             inflammation.<h4>Conclusions</h4>The findings are consistent
             with the possibility that 'living against our internal
             clock' may contribute to metabolic dysfunction and its
             consequences. Further research aimed at understanding that
             the physiology and social features of social jetlag may
             inform obesity prevention and have ramifications for
             policies and practices that contribute to increased social
             jetlag, such as work schedules and daylight savings
             time.},
   Doi = {10.1038/ijo.2014.201},
   Key = {fds253123}
}

@article{fds253127,
   Author = {Erskine, HE and Moffitt, TE and Copeland, WE and Costello, EJ and Ferrari, AJ and Patton, G and Degenhardt, L and Vos, T and Whiteford,
             HA and Scott, JG},
   Title = {A heavy burden on young minds: the global burden of mental
             and substance use disorders in children and
             youth.},
   Journal = {Psychol Med},
   Volume = {45},
   Number = {7},
   Pages = {1551-1563},
   Year = {2015},
   Month = {May},
   ISSN = {0033-2917},
   url = {http://dx.doi.org/10.1017/S0033291714002888},
   Abstract = {BACKGROUND: Mental and substance use disorders are common
             and often persistent, with many emerging in early life.
             Compared to adult mental and substance use disorders, the
             global burden attributable to these disorders in children
             and youth has received relatively little attention. METHOD:
             Data from the Global Burden of Disease Study 2010 was used
             to investigate the burden of mental and substance disorders
             in children and youth aged 0-24 years. Burden was estimated
             in terms of disability-adjusted life years (DALYs), derived
             from the sum of years lived with disability (YLDs) and years
             of life lost (YLLs). RESULTS: Globally, mental and substance
             use disorders are the leading cause of disability in
             children and youth, accounting for a quarter of all YLDs
             (54.2 million). In terms of DALYs, they ranked 6th with 55.5
             million DALYs (5.7%) and rose to 5th when mortality burden
             of suicide was reattributed. While mental and substance use
             disorders were the leading cause of DALYs in high-income
             countries (HICs), they ranked 7th in low- and middle-income
             countries (LMICs) due to mortality attributable to
             infectious diseases. CONCLUSIONS: Mental and substance use
             disorders are significant contributors to disease burden in
             children and youth across the globe. As reproductive health
             and the management of infectious diseases improves in LMICs,
             the proportion of disease burden in children and youth
             attributable to mental and substance use disorders will
             increase, necessitating a realignment of health services in
             these countries.},
   Doi = {10.1017/S0033291714002888},
   Key = {fds253127}
}

@article{fds253117,
   Author = {Goldman-Mellor, S and Caspi, A and Gregory, AM and Harrington, H and Poulton, R and Moffitt, TE},
   Title = {Is insomnia associated with deficits in neuropsychological
             functioning? Evidence from a population-based
             study.},
   Journal = {Sleep},
   Volume = {38},
   Number = {4},
   Pages = {623-631},
   Year = {2015},
   Month = {April},
   ISSN = {0161-8105},
   url = {http://dx.doi.org/10.5665/sleep.4584},
   Abstract = {<h4>Study objectives</h4>People with insomnia complain of
             cognitive deficits in daily life. Results from empirical
             studies examining associations between insomnia and
             cognitive impairment, however, are mixed. Research is needed
             that compares treatment-seeking and community-based insomnia
             study samples, measures subjective as well as objective
             cognitive functioning, and considers participants'
             pre-insomnia cognitive function.<h4>Design and
             participants</h4>We used data from the Dunedin Study, a
             representative birth cohort of 1,037 individuals, to examine
             whether insomnia in early midlife was associated with
             subjective and objective cognitive functioning. We also
             tested whether individuals with insomnia who reported
             seeking treatment for their sleep problems
             (treatment-seekers) showed greater impairment than other
             individuals with insomnia (non-treatment-seekers). The role
             of key confounders, including childhood cognitive ability
             and comorbid health conditions, was evaluated.<h4>Measurements</h4>Insomnia
             was diagnosed at age 38 according to DSM-IV criteria.
             Objective neuropsychological assessments at age 38 included
             the WAIS-IV IQ test, the Wechsler Memory Scale, and the
             Trail-Making Test. Childhood cognitive functioning was
             assessed using the Wechsler Intelligence Scale for
             Children-Revised (WISC-R).<h4>Results</h4>A total of 949
             cohort members were assessed for insomnia symptoms and other
             study measures at age 38. Although cohort members with
             insomnia (n = 186, 19.6%) had greater subjective cognitive
             impairment than their peers at age 38, they did not exhibit
             greater objective impairment on formal testing.
             Treatment-seekers, however, exhibited significant objective
             impairment compared to non-treatment-seekers. Controlling
             for comorbidity, daytime impairment, and medications
             slightly decreased this association. Childhood cognitive
             deficits antedated the adult cognitive deficits of
             treatment-seekers.<h4>Conclusions</h4>Links between insomnia
             and cognitive impairment may be strongest among individuals
             who seek clinical treatment. Clinicians should take into
             account the presence of complex health problems and lower
             premorbid cognitive function when planning treatment for
             insomnia patients.},
   Doi = {10.5665/sleep.4584},
   Key = {fds253117}
}

@article{fds253119,
   Author = {Broadbent, JM and Thomson, WM and Moffitt, TE and Poulton,
             R},
   Title = {Broadbent et al. respond.},
   Journal = {American journal of public health},
   Volume = {105},
   Number = {4},
   Pages = {e3-e4},
   Year = {2015},
   Month = {April},
   ISSN = {0090-0036},
   url = {http://dx.doi.org/10.2105/ajph.2015.302647},
   Doi = {10.2105/ajph.2015.302647},
   Key = {fds253119}
}

@article{fds253124,
   Author = {Belsky, DW and Caspi, A and Israel, S and Blumenthal, JA and Poulton, R and Moffitt, TE},
   Title = {Cardiorespiratory fitness and cognitive function in midlife:
             neuroprotection or neuroselection?},
   Journal = {Ann Neurol},
   Volume = {77},
   Number = {4},
   Pages = {607-617},
   Year = {2015},
   Month = {April},
   ISSN = {0364-5134},
   url = {http://hdl.handle.net/10161/9709 Duke open
             access},
   Abstract = {OBJECTIVE: A study was undertaken to determine whether
             better cognitive functioning at midlife among more
             physically fit individuals reflects neuroprotection, by
             which fitness protects against age-related cognitive
             decline, or neuroselection, by which children with higher
             cognitive functioning select more active lifestyles.
             METHODS: Children in the Dunedin Longitudinal Study
             (N = 1,037) completed the Wechsler Intelligence Scales
             and the Trail Making, Rey Delayed Recall, and Grooved
             Pegboard tasks as children and again at midlife
             (age = 38 years). Adult cardiorespiratory fitness was
             assessed using a submaximal exercise test to estimate
             maximum oxygen consumption adjusted for body weight in
             milliliters/minute/kilogram. We tested whether more fit
             individuals had better cognitive functioning than their less
             fit counterparts (which could be consistent with
             neuroprotection), and whether better childhood cognitive
             functioning predisposed to better adult cardiorespiratory
             fitness (neuroselection). Finally, we examined possible
             mechanisms of neuroselection. RESULTS: Participants with
             better cardiorespiratory fitness had higher cognitive test
             scores at midlife. However, fitness-associated advantages in
             cognitive functioning were already present in childhood.
             After accounting for childhood baseline performance on the
             same cognitive tests, there was no association between
             cardiorespiratory fitness and midlife cognitive functioning.
             Socioeconomic and health advantages in childhood and
             healthier lifestyles during young adulthood explained most
             of the association between childhood cognitive functioning
             and adult cardiorespiratory fitness. INTERPRETATION: We
             found no evidence for a neuroprotective effect of
             cardiorespiratory fitness as of midlife. Instead, children
             with better cognitive functioning are selecting healthier
             lives. Fitness interventions may enhance cognitive
             functioning. However, observational and experimental studies
             testing neuroprotective effects of physical fitness should
             consider confounding by neuroselection.},
   Doi = {10.1002/ana.24356},
   Key = {fds253124}
}

@article{fds253106,
   Author = {Broadbent, JM and Thomson, WM and Moffitt, TE and Poulton,
             R},
   Title = {Health effects of water fluoridation: a response to the
             letter by Menkes et al.},
   Journal = {The New Zealand medical journal},
   Volume = {128},
   Number = {1410},
   Pages = {73-74},
   Year = {2015},
   Month = {March},
   ISSN = {0028-8446},
   Key = {fds253106}
}

@article{fds253122,
   Author = {Matthews, T and Danese, A and Wertz, J and Ambler, A and Kelly, M and Diver, A and Caspi, A and Moffitt, TE and Arseneault,
             L},
   Title = {Social isolation and mental health at primary and secondary
             school entry: a longitudinal cohort study.},
   Journal = {Journal of the American Academy of Child and Adolescent
             Psychiatry},
   Volume = {54},
   Number = {3},
   Pages = {225-232},
   Year = {2015},
   Month = {March},
   ISSN = {0890-8567},
   url = {http://dx.doi.org/10.1016/j.jaac.2014.12.008},
   Abstract = {<h4>Objective</h4>We tested whether children who are
             socially isolated early in their schooling develop mental
             health problems in early adolescence, taking into account
             their mental health and family risk at school
             entry.<h4>Method</h4>We used data from the Environmental
             Risk (E-Risk) Longitudinal Twin Study, a birth cohort of
             2,232 children born in England and Wales in 1994 and 1995.
             We measured social isolation using mothers' and teachers'
             reports at ages 5 and 12 years. We assessed mental health
             symptoms via mothers' and teachers' ratings at age 5
             and self-report measures at age 12. We collected
             mother-reported information about the family environment
             when children were 5 years old. We conducted regression
             analyses to test concurrent and longitudinal associations
             between early family factors, social isolation, and mental
             health difficulties.<h4>Results</h4>At both primary and
             secondary school, children who were socially isolated
             experienced greater mental health difficulties. Children
             with behavioral problems or attention-deficit/hyperactivity
             disorder (ADHD) symptoms at age 5 years had an elevated risk
             of becoming more socially isolated at age 12. However,
             children who were isolated at age 5 did not have greater
             mental health symptoms at age 12, over and above
             pre-existing difficulties.<h4>Conclusion</h4>Although social
             isolation and mental health problems co-occur in childhood,
             early isolation does not predict worse mental health
             problems later on. However, children who exhibit problematic
             behaviors may struggle to cope with the social challenges
             that accompany their progression through the early school
             years.},
   Doi = {10.1016/j.jaac.2014.12.008},
   Key = {fds253122}
}

@article{fds253120,
   Author = {Moffitt, TE and Beckley, A},
   Title = {Abandon twin research? Embrace epigenetic research?
             Premature advice for criminologists},
   Journal = {Criminology},
   Volume = {53},
   Number = {1},
   Pages = {121-126},
   Publisher = {WILEY},
   Year = {2015},
   Month = {February},
   ISSN = {0011-1384},
   url = {http://dx.doi.org/10.1111/1745-9125.12061},
   Doi = {10.1111/1745-9125.12061},
   Key = {fds253120}
}

@article{fds253118,
   Author = {GBD 2013 Mortality and Causes of Death Collaborators},
   Title = {Global, regional, and national age-sex specific all-cause
             and cause-specific mortality for 240 causes of death,
             1990-2013: a systematic analysis for the Global Burden of
             Disease Study 2013.},
   Journal = {Lancet},
   Volume = {385},
   Number = {9963},
   Pages = {117-171},
   Year = {2015},
   Month = {January},
   ISSN = {0140-6736},
   url = {http://dx.doi.org/10.1016/S0140-6736(14)61682-2},
   Abstract = {BACKGROUND: Up-to-date evidence on levels and trends for
             age-sex-specific all-cause and cause-specific mortality is
             essential for the formation of global, regional, and
             national health policies. In the Global Burden of Disease
             Study 2013 (GBD 2013) we estimated yearly deaths for 188
             countries between 1990, and 2013. We used the results to
             assess whether there is epidemiological convergence across
             countries. METHODS: We estimated age-sex-specific all-cause
             mortality using the GBD 2010 methods with some refinements
             to improve accuracy applied to an updated database of vital
             registration, survey, and census data. We generally
             estimated cause of death as in the GBD 2010. Key
             improvements included the addition of more recent vital
             registration data for 72 countries, an updated verbal
             autopsy literature review, two new and detailed data systems
             for China, and more detail for Mexico, UK, Turkey, and
             Russia. We improved statistical models for garbage code
             redistribution. We used six different modelling strategies
             across the 240 causes; cause of death ensemble modelling
             (CODEm) was the dominant strategy for causes with sufficient
             information. Trends for Alzheimer's disease and other
             dementias were informed by meta-regression of prevalence
             studies. For pathogen-specific causes of diarrhoea and lower
             respiratory infections we used a counterfactual approach. We
             computed two measures of convergence (inequality) across
             countries: the average relative difference across all pairs
             of countries (Gini coefficient) and the average absolute
             difference across countries. To summarise broad findings, we
             used multiple decrement life-tables to decompose
             probabilities of death from birth to exact age 15 years,
             from exact age 15 years to exact age 50 years, and from
             exact age 50 years to exact age 75 years, and life
             expectancy at birth into major causes. For all quantities
             reported, we computed 95% uncertainty intervals (UIs). We
             constrained cause-specific fractions within each
             age-sex-country-year group to sum to all-cause mortality
             based on draws from the uncertainty distributions. FINDINGS:
             Global life expectancy for both sexes increased from 65.3
             years (UI 65.0-65.6) in 1990, to 71.5 years (UI 71.0-71.9)
             in 2013, while the number of deaths increased from 47.5
             million (UI 46.8-48.2) to 54.9 million (UI 53.6-56.3) over
             the same interval. Global progress masked variation by age
             and sex: for children, average absolute differences between
             countries decreased but relative differences increased. For
             women aged 25-39 years and older than 75 years and for men
             aged 20-49 years and 65 years and older, both absolute and
             relative differences increased. Decomposition of global and
             regional life expectancy showed the prominent role of
             reductions in age-standardised death rates for
             cardiovascular diseases and cancers in high-income regions,
             and reductions in child deaths from diarrhoea, lower
             respiratory infections, and neonatal causes in low-income
             regions. HIV/AIDS reduced life expectancy in southern
             sub-Saharan Africa. For most communicable causes of death
             both numbers of deaths and age-standardised death rates fell
             whereas for most non-communicable causes, demographic shifts
             have increased numbers of deaths but decreased
             age-standardised death rates. Global deaths from injury
             increased by 10.7%, from 4.3 million deaths in 1990 to 4.8
             million in 2013; but age-standardised rates declined over
             the same period by 21%. For some causes of more than 100,000
             deaths per year in 2013, age-standardised death rates
             increased between 1990 and 2013, including HIV/AIDS,
             pancreatic cancer, atrial fibrillation and flutter, drug use
             disorders, diabetes, chronic kidney disease, and sickle-cell
             anaemias. Diarrhoeal diseases, lower respiratory infections,
             neonatal causes, and malaria are still in the top five
             causes of death in children younger than 5 years. The most
             important pathogens are rotavirus for diarrhoea and
             pneumococcus for lower respiratory infections.
             Country-specific probabilities of death over three phases of
             life were substantially varied between and within regions.
             INTERPRETATION: For most countries, the general pattern of
             reductions in age-sex specific mortality has been associated
             with a progressive shift towards a larger share of the
             remaining deaths caused by non-communicable disease and
             injuries. Assessing epidemiological convergence across
             countries depends on whether an absolute or relative measure
             of inequality is used. Nevertheless, age-standardised death
             rates for seven substantial causes are increasing,
             suggesting the potential for reversals in some countries.
             Important gaps exist in the empirical data for cause of
             death estimates for some countries; for example, no national
             data for India are available for the past decade. FUNDING:
             Bill & Melinda Gates Foundation.},
   Doi = {10.1016/S0140-6736(14)61682-2},
   Key = {fds253118}
}

@article{fds253139,
   Author = {Broadbent, JM and Thomson, WM and Ramrakha, S and Moffitt, TE and Zeng,
             J and Foster Page and LA and Poulton, R},
   Title = {Community Water Fluoridation and Intelligence: Prospective
             Study in New Zealand.},
   Journal = {American journal of public health},
   Volume = {105},
   Number = {1},
   Pages = {72-76},
   Year = {2015},
   Month = {January},
   ISSN = {0090-0036},
   url = {http://dx.doi.org/10.2105/ajph.2013.301857},
   Abstract = {Objectives. This study aimed to clarify the relationship
             between community water fluoridation (CWF) and IQ. Methods.
             We conducted a prospective study of a general population
             sample of those born in Dunedin, New Zealand, between April
             1, 1972, and March 30, 1973 (95.4% retention of cohort after
             38 years of prospective follow-up). Residence in a CWF area,
             use of fluoride dentifrice and intake of 0.5-milligram
             fluoride tablets were assessed in early life (prior to age 5
             years); we assessed IQ repeatedly between ages 7 to 13 years
             and at age 38 years. Results. No clear differences in IQ
             because of fluoride exposure were noted. These findings held
             after adjusting for potential confounding variables,
             including sex, socioeconomic status, breastfeeding, and
             birth weight (as well as educational attainment for adult IQ
             outcomes). Conclusions. These findings do not support the
             assertion that fluoride in the context of CWF programs is
             neurotoxic. Associations between very high fluoride exposure
             and low IQ reported in previous studies may have been
             affected by confounding, particularly by urban or rural
             status.},
   Doi = {10.2105/ajph.2013.301857},
   Key = {fds253139}
}

@article{fds320838,
   Author = {Fisher, HL and Murphy, TM and Arseneault, L and Caspi, A and Moffitt,
             TE and Viana, J and Hannon, E and Pidsley, R and Burrage, J and Dempster,
             EL and Wong, CCY and Pariante, CM and Mill, J},
   Title = {Methylomic analysis of monozygotic twins discordant for
             childhood psychotic symptoms.},
   Journal = {Epigenetics},
   Volume = {10},
   Number = {11},
   Pages = {1014-1023},
   Year = {2015},
   Month = {January},
   url = {http://dx.doi.org/10.1080/15592294.2015.1099797},
   Abstract = {Childhood psychotic symptoms are associated with increased
             rates of schizophrenia, other psychiatric disorders, and
             suicide attempts in adulthood; thus, elucidating early risk
             indicators is crucial to target prevention efforts. There is
             considerable discordance for psychotic symptoms between
             monozygotic twins, indicating that child-specific
             non-genetic factors must be involved. Epigenetic processes
             may constitute one of these factors and have not yet been
             investigated in relation to childhood psychotic symptoms.
             Therefore, this study explored whether differences in DNA
             methylation at age 10 were associated with monozygotic twin
             discordance for psychotic symptoms at age 12. The
             Environmental Risk (E-Risk) Longitudinal Twin Study cohort
             of 2,232 children (1,116 twin pairs) was assessed for age-12
             psychotic symptoms and 24 monozygotic twin pairs discordant
             for symptoms were identified for methylomic comparison.
             Children provided buccal samples at ages 5 and 10. DNA was
             bisulfite modified and DNA methylation was quantified using
             the Infinium HumanMethylation450 array. Differentially
             methylated positions (DMPs) associated with psychotic
             symptoms were subsequently tested in post-mortem prefrontal
             cortex tissue from adult schizophrenia patients and
             age-matched controls. Site-specific DNA methylation
             differences were observed at age 10 between monozygotic
             twins discordant for age-12 psychotic symptoms. Similar DMPs
             were not found at age 5. The top-ranked psychosis-associated
             DMP (cg23933044), located in the promoter of the C5ORF42
             gene, was also hypomethylated in post-mortem prefrontal
             cortex brain tissue from schizophrenia patients compared to
             unaffected controls. These data tentatively suggest that
             epigenetic variation in peripheral tissue is associated with
             childhood psychotic symptoms and may indicate susceptibility
             to schizophrenia and other mental health
             problems.},
   Doi = {10.1080/15592294.2015.1099797},
   Key = {fds320838}
}

@article{fds320839,
   Author = {Murphy, TM and Wong, CCY and Arseneault, L and Burrage, J and Macdonald,
             R and Hannon, E and Fisher, HL and Ambler, A and Moffitt, TE and Caspi, A and Mill, J},
   Title = {Methylomic markers of persistent childhood asthma: a
             longitudinal study of asthma-discordant monozygotic
             twins.},
   Journal = {Clinical epigenetics},
   Volume = {7},
   Pages = {130},
   Year = {2015},
   Month = {January},
   url = {http://dx.doi.org/10.1186/s13148-015-0163-4},
   Abstract = {<h4>Background</h4>Asthma is the most common chronic
             inflammatory disorder in children. The aetiology of asthma
             pathology is complex and highly heterogeneous, involving the
             interplay between genetic and environmental risk factors
             that is hypothesized to involve epigenetic processes. Our
             aim was to explore whether methylomic variation in early
             childhood is associated with discordance for asthma symptoms
             within monozygotic (MZ) twin pairs recruited from the
             Environmental Risk (E-Risk) longitudinal twin study. We also
             aimed to identify differences in DNA methylation that are
             associated with asthma that develops in childhood and
             persists into early adulthood as these may represent useful
             prognostic biomarkers.<h4>Results</h4>We examined
             genome-wide patterns of DNA methylation in buccal cell
             samples collected from 37 MZ twin pairs discordant for
             asthma at age 10. DNA methylation at individual CpG sites
             demonstrated significant variability within discordant MZ
             twin pairs with the top-ranked nominally significant
             differentially methylated position (DMP) located in the
             HGSNAT gene. We stratified our analysis by assessing DNA
             methylation differences in a sub-group of MZ twin pairs who
             remained persistently discordant for asthma at age 18. The
             top-ranked nominally significant DMP associated with
             persisting asthma is located in the vicinity of the HLX
             gene, which has been previously implicated in childhood
             asthma.<h4>Conclusions</h4>We identified DNA methylation
             differences associated with childhood asthma in peripheral
             DNA samples from discordant MZ twin pairs. Our data suggest
             that differences in DNA methylation associated with
             childhood asthma which persists into early adulthood are
             distinct from those associated with asthma which
             remits.},
   Doi = {10.1186/s13148-015-0163-4},
   Key = {fds320839}
}

@article{fds253129,
   Author = {Israel, S and Caspi, A and Belsky, DW and Harrington, H and Hogan, S and Houts, R and Ramrakha, S and Sanders, S and Poulton, R and Moffitt,
             TE},
   Title = {Credit scores, cardiovascular disease risk, and human
             capital},
   Journal = {Proceedings of the National Academy of Sciences},
   Volume = {111},
   Number = {48},
   Pages = {201409794-201409794},
   Year = {2014},
   Month = {November},
   ISSN = {0027-8424},
   url = {http://hdl.handle.net/10161/9270 Duke open
             access},
   Abstract = {Credit scores are the most widely used instruments to assess
             whether or not a person is a financial risk. Credit scoring
             has been so successful that it has expanded beyond lending
             and into our everyday lives, even to inform how insurers
             evaluate our health. The pervasive application of credit
             scoring has outpaced knowledge about why credit scores are
             such useful indicators of individual behavior. Here we test
             if the same factors that lead to poor credit scores also
             lead to poor health. Following the Dunedin (New Zealand)
             Longitudinal Study cohort of 1,037 study members, we
             examined the association between credit scores and
             cardiovascular disease risk and the underlying factors that
             account for this association. We find that credit scores are
             negatively correlated with cardiovascular disease risk.
             Variation in household income was not sufficient to account
             for this association. Rather, individual differences in
             human capital factors—educational attainment, cognitive
             ability, and self-control—predicted both credit scores and
             cardiovascular disease risk and accounted for ∼45% of the
             correlation between credit scores and cardiovascular disease
             risk. Tracing human capital factors back to their childhood
             antecedents revealed that the characteristic attitudes,
             behaviors, and competencies children develop in their first
             decade of life account for a significant portion (∼22%) of
             the link between credit scores and cardiovascular disease
             risk at midlife. We discuss the implications of these
             findings for policy debates about data privacy, financial
             literacy, and early childhood interventions.},
   Doi = {10.1073/pnas.1409794111},
   Key = {fds253129}
}

@article{fds253130,
   Author = {Shalev, I and Moffitt, TE and Braithwaite, AW and Danese, A and Fleming,
             NI and Goldman-Mellor, S and Harrington, HL and Houts, RM and Israel, S and Poulton, R and Robertson, SP and Sugden, K and Williams, B and Caspi,
             A},
   Title = {Internalizing disorders and leukocyte telomere erosion: a
             prospective study of depression, generalized anxiety
             disorder and post-traumatic stress disorder.},
   Journal = {Molecular psychiatry},
   Volume = {19},
   Number = {11},
   Pages = {1163-1170},
   Year = {2014},
   Month = {November},
   ISSN = {1359-4184},
   url = {http://dx.doi.org/10.1038/mp.2013.183},
   Abstract = {There is evidence that persistent psychiatric disorders lead
             to age-related disease and premature mortality. Telomere
             length has emerged as a promising biomarker in studies that
             test the hypothesis that internalizing psychiatric disorders
             are associated with accumulating cellular damage. We tested
             the association between the persistence of internalizing
             disorders (depression, generalized anxiety disorder and
             post-traumatic stress disorder) and leukocyte telomere
             length (LTL) in the prospective longitudinal Dunedin Study
             (n=1037). Analyses showed that the persistence of
             internalizing disorders across repeated assessments from
             ages 11 to 38 years predicted shorter LTL at age 38 years in
             a dose-response manner, specifically in men (β=-0.137, 95%
             confidence interval (CI): -0.232, -0.042, P=0.005). This
             association was not accounted for by alternative explanatory
             factors, including childhood maltreatment, tobacco smoking,
             substance dependence, psychiatric medication use, poor
             physical health or low socioeconomic status. Additional
             analyses using DNA from blood collected at two time points
             (ages 26 and 38 years) showed that LTL erosion was
             accelerated among men who were diagnosed with internalizing
             disorder in the interim (β=-0.111, 95% CI: -0.184, -0.037,
             P=0.003). No significant associations were found among women
             in any analysis, highlighting potential sex differences in
             internalizing-related telomere biology. These findings point
             to a potential mechanism linking internalizing disorders to
             accelerated biological aging in the first half of the life
             course, particularly in men. Because internalizing disorders
             are treatable, the findings suggest the hypothesis that
             treating psychiatric disorders in the first half of the life
             course may reduce the population burden of age-related
             disease and extend health expectancy.},
   Doi = {10.1038/mp.2013.183},
   Key = {fds253130}
}

@article{fds253131,
   Author = {Shalev, I and Caspi, A and Ambler, A and Belsky, DW and Chapple, S and Cohen, HJ and Israel, S and Poulton, R and Ramrakha, S and Rivera, CD and Sugden, K and Williams, B and Wolke, D and Moffitt,
             TE},
   Title = {Perinatal complications and aging indicators by
             midlife.},
   Journal = {Pediatrics},
   Volume = {134},
   Number = {5},
   Pages = {e1315-e1323},
   Year = {2014},
   Month = {November},
   ISSN = {0031-4005},
   url = {http://dx.doi.org/10.1542/peds.2014-1669},
   Abstract = {BACKGROUND: Perinatal complications predict increased risk
             for morbidity and early mortality. Evidence of perinatal
             programming of adult mortality raises the question of what
             mechanisms embed this long-term effect. We tested a
             hypothesis related to the theory of developmental origins of
             health and disease: that perinatal complications assessed at
             birth predict indicators of accelerated aging by midlife.
             METHODS: Perinatal complications, including both maternal
             and neonatal complications, were assessed in the Dunedin
             Multidisciplinary Health and Development Study cohort (N =
             1037), a 38-year, prospective longitudinal study of a
             representative birth cohort. Two aging indicators were
             assessed at age 38 years, objectively by leukocyte telomere
             length (TL) and subjectively by perceived facial age.
             RESULTS: Perinatal complications predicted both leukocyte TL
             (β = -0.101; 95% confidence interval, -0.169 to -0.033; P =
             .004) and perceived age (β = 0.097; 95% confidence
             interval, 0.029 to 0.165; P = .005) by midlife. We repeated
             analyses with controls for measures of family history and
             social risk that could predispose to perinatal complications
             and accelerated aging, and for measures of poor health taken
             in between birth and the age-38 follow-up. These covariates
             attenuated, but did not fully explain the associations
             observed between perinatal complications and aging
             indicators. CONCLUSIONS: Our findings provide support for
             early-life developmental programming by linking newborns'
             perinatal complications to accelerated aging at midlife. We
             observed indications of accelerated aging "inside," as
             measured by leukocyte TL, an indicator of cellular aging,
             and "outside," as measured by perceived age, an indicator of
             declining tissue integrity. A better understanding of
             mechanisms underlying perinatal programming of adult aging
             is needed.},
   Doi = {10.1542/peds.2014-1669},
   Key = {fds253131}
}

@article{fds336534,
   Author = {Goldman-Mellor, S and Gregory, AM and Caspi, A and Harrington, H and Parsons, M and Poulton, R and Moffitt, TE},
   Title = {Mental health antecedents of early midlife insomnia:
             evidence from a four-decade longitudinal
             study.},
   Journal = {Sleep},
   Volume = {37},
   Number = {11},
   Pages = {1767-1775},
   Year = {2014},
   Month = {November},
   url = {http://dx.doi.org/10.5665/sleep.4168},
   Abstract = {<h4>Study objectives</h4>Insomnia is a highly prevalent
             condition that constitutes a major public health and
             economic burden. However, little is known about the
             developmental etiology of adulthood insomnia.<h4>Design</h4>We
             examined whether indicators of psychological vulnerability
             across multiple developmental periods (psychiatric diagnoses
             in young adulthood and adolescence, childhood behavioral
             problems, and familial psychiatric history) predicted
             subsequent insomnia in adulthood.<h4>Setting and
             participants</h4>We used data from the ongoing Dunedin
             Multidisciplinary Health and Development Study, a
             population-representative birth cohort study of 1,037
             children in New Zealand who were followed prospectively from
             birth (1972-1973) through their fourth decade of life with a
             95% retention rate.<h4>Measurements</h4>Insomnia was
             diagnosed at age 38 according to DSM-IV criteria.
             Psychiatric diagnoses, behavioral problems, and family
             psychiatric histories were assessed between ages 5 and
             38.<h4>Results</h4>In cross-sectional analyses, insomnia was
             highly comorbid with multiple psychiatric disorders. After
             controlling for this concurrent comorbidity, our results
             showed that individuals who have family histories of
             depression or anxiety, and who manifest lifelong depression
             and anxiety beginning in childhood, are at uniquely high
             risk for age-38 insomnia. Other disorders did not predict
             adulthood insomnia.<h4>Conclusions</h4>The link between
             lifelong depression and anxiety symptoms and adulthood
             insomnia calls for further studies to clarify the
             neurophysiological systems or behavioral conditioning
             processes that may underlie this association.},
   Doi = {10.5665/sleep.4168},
   Key = {fds336534}
}

@article{fds253132,
   Author = {Goldman-Mellor, S and Gregory, AM and Caspi, A and Harrington, H and Parsons, M and Poulton, R and Moffitt, TE},
   Title = {Mental Health Antecedents of Early Midlife Insomnia:
             Evidence from a Four-Decade Longitudinal
             Study.},
   Journal = {Sleep},
   Year = {2014},
   Month = {October},
   ISSN = {0161-8105},
   Abstract = {Study Objectives: Insomnia is a highly prevalent condition
             that constitutes a major public health and economic burden.
             However, little is known about the developmental etiology of
             adulthood insomnia. Design: We examined whether indicators
             of psychological vulnerability across multiple developmental
             periods (psychiatric diagnoses in young adulthood and
             adolescence, childhood behavioral problems, and familial
             psychiatric history) predicted subsequent insomnia in
             adulthood. Setting and Participants: We used data from the
             ongoing Dunedin Multidisciplinary Health and Development
             Study, a population-representative birth cohort study of
             1,037 children in New Zealand who were followed
             prospectively from birth (1972-1973) through their fourth
             decade of life with a 95% retention rate. Measurements:
             Insomnia was diagnosed at age 38 according to DSM-IV
             criteria. Psychiatric diagnoses, behavioral problems, and
             family psychiatric histories were assessed between ages 5
             and 38. Results: In cross-sectional analyses, insomnia was
             highly comorbid with multiple psychiatric disorders. After
             controlling for this concurrent comorbidity, our results
             showed that individuals who have family histories of
             depression or anxiety, and who manifest lifelong depression
             and anxiety beginning in childhood, are at uniquely high
             risk for age-38 insomnia. Other disorders did not predict
             adulthood insomnia. Conclusions: The link between lifelong
             depression and anxiety symptoms and adulthood insomnia calls
             for further studies to clarify the neurophysiological
             systems or behavioral conditioning processes that may
             underlie this association.},
   Key = {fds253132}
}

@article{fds253135,
   Author = {Belsky, DW and Shalev, I and Sears, MR and Hancox, RJ and Lee
             Harrington, H and Houts, R and Moffitt, TE and Sugden, K and Williams,
             B and Poulton, R and Caspi, A},
   Title = {Is chronic asthma associated with shorter leukocyte telomere
             length at midlife?},
   Journal = {American Journal of Respiratory and Critical Care
             Medicine},
   Volume = {190},
   Number = {4},
   Pages = {384-391},
   Year = {2014},
   Month = {August},
   ISSN = {1073-449X},
   url = {http://hdl.handle.net/10161/9380 Duke open
             access},
   Abstract = {RATIONALE: Asthma is prospectively associated with
             age-related chronic diseases and mortality, suggesting the
             hypothesis that asthma may relate to a general, multisystem
             phenotype of accelerated aging. OBJECTIVES: To test whether
             chronic asthma is associated with a proposed biomarker of
             accelerated aging, leukocyte telomere length. METHODS:
             Asthma was ascertained prospectively in the Dunedin
             Multidisciplinary Health and Development Study cohort (n =
             1,037) at nine in-person assessments spanning ages 9-38
             years. Leukocyte telomere length was measured at ages 26 and
             38 years. Asthma was classified as life-course-persistent,
             childhood-onset not meeting criteria for persistence, and
             adolescent/adult-onset. We tested associations between
             asthma and leukocyte telomere length using regression
             models. We tested for confounding of asthma-leukocyte
             telomere length associations using covariate adjustment. We
             tested serum C-reactive protein and white blood cell counts
             as potential mediators of asthma-leukocyte telomere length
             associations. MEASUREMENTS AND MAIN RESULTS: Study members
             with life-course-persistent asthma had shorter leukocyte
             telomere length as compared with sex- and age-matched peers
             with no reported asthma. In contrast, leukocyte telomere
             length in study members with childhood-onset and
             adolescent/adult-onset asthma was not different from
             leukocyte telomere length in peers with no reported asthma.
             Adjustment for life histories of obesity and smoking did not
             change results. Study members with life-course-persistent
             asthma had elevated blood eosinophil counts. Blood
             eosinophil count mediated 29% of the life-course-persistent
             asthma-leukocyte telomere length association. CONCLUSIONS:
             Life-course-persistent asthma is related to a proposed
             biomarker of accelerated aging, possibly via systemic
             eosinophilic inflammation. Life histories of asthma can
             inform studies of aging.},
   Doi = {10.1164/rccm.201402-0370OC},
   Key = {fds253135}
}

@article{fds253134,
   Author = {Polanczyk, GV and Moffitt, TE},
   Title = {How evidence on the developmental nature of
             attention-deficit/hyperactivity disorder can increase the
             validity and utility of diagnostic criteria.},
   Journal = {Journal of the American Academy of Child and Adolescent
             Psychiatry},
   Volume = {53},
   Number = {7},
   Pages = {723-725},
   Year = {2014},
   Month = {July},
   ISSN = {0890-8567},
   url = {http://dx.doi.org/10.1016/j.jaac.2014.04.012},
   Doi = {10.1016/j.jaac.2014.04.012},
   Key = {fds253134}
}

@article{fds253137,
   Author = {Breslau, N and Koenen, KC and Luo, Z and Agnew-Blais, J and Swanson, S and Houts, RM and Poulton, R and Moffitt, TE},
   Title = {Childhood maltreatment, juvenile disorders and adult
             post-traumatic stress disorder: a prospective
             investigation.},
   Journal = {Psychological medicine},
   Volume = {44},
   Number = {9},
   Pages = {1937-1945},
   Year = {2014},
   Month = {July},
   ISSN = {0033-2917},
   url = {http://dx.doi.org/10.1017/s0033291713002651},
   Abstract = {<h4>Background</h4>We examine prospectively the influence of
             two separate but potentially inter-related factors in the
             etiology of post-traumatic stress disorder (PTSD): childhood
             maltreatment as conferring a susceptibility to the PTSD
             response to adult trauma and juvenile disorders as
             precursors of adult PTSD.<h4>Method</h4>The Dunedin
             Multidisciplinary Health and Development Study (DMHDS) is a
             birth cohort (n = 1037) from the general population of New
             Zealand's South Island, with multiple assessments up to age
             38 years. DSM-IV PTSD was assessed among participants
             exposed to trauma at ages 26-38. Complete data were
             available on 928 participants.<h4>Results</h4>Severe
             maltreatment in the first decade of life, experienced by
             8.5% of the sample, was associated significantly with the
             risk of PTSD among those exposed to adult trauma [odds ratio
             (OR) 2.64, 95% confidence interval (CI) 1.16-6.01], compared
             to no maltreatment. Moderate maltreatment, experienced by
             27.2%, was not associated significantly with that risk (OR
             1.55, 95% CI 0.85-2.85). However, the two estimates did not
             differ significantly from one another. Juvenile disorders
             (ages 11-15), experienced by 35% of the sample, independent
             of childhood maltreatment, were associated significantly
             with the risk of PTSD response to adult trauma (OR 2.35, 95%
             CI 1.32-4.18).<h4>Conclusions</h4>Severe maltreatment is
             associated with risk of PTSD response to adult trauma,
             compared to no maltreatment, and juvenile disorders,
             independent of earlier maltreatment, are associated with
             that risk. The role of moderate maltreatment remains
             unresolved. Larger longitudinal studies are needed to assess
             the impact of moderate maltreatment, experienced by the
             majority of adult trauma victims with a history of
             maltreatment.},
   Doi = {10.1017/s0033291713002651},
   Key = {fds253137}
}

@article{fds253133,
   Author = {Moffitt, TE and Caspi, A},
   Title = {Bias in a protocol for a meta-analysis of 5-HTTLPR, stress,
             and depression.},
   Journal = {BMC psychiatry},
   Volume = {14},
   Pages = {179},
   Year = {2014},
   Month = {June},
   url = {http://dx.doi.org/10.1186/1471-244x-14-179},
   Doi = {10.1186/1471-244x-14-179},
   Key = {fds253133}
}

@article{fds253141,
   Author = {Israel, S and Moffitt, TE},
   Title = {Assessing conscientious personality in primary care: an
             opportunity for prevention and health promotion.},
   Journal = {Developmental psychology},
   Volume = {50},
   Number = {5},
   Pages = {1475-1477},
   Year = {2014},
   Month = {May},
   ISSN = {0012-1649},
   url = {http://dx.doi.org/10.1037/a0036113},
   Abstract = {The articles in this special section bolster the already
             strong evidence base that personality differences in the
             trait of conscientiousness predict health. What is now
             needed is a research agenda for translating documented risk
             associations between low conscientiousness and poor health
             into policies and interventions that improve health outcomes
             for individuals and populations. In this commentary, we
             highlight 1 such avenue: introducing brief personality
             assessment into primary care practice. We provide examples
             of how conscientiousness assessment may help health care
             professionals get to know their patients better and
             potentially serve as a guide for more personalized care. We
             also raise key considerations for implementation research
             aimed at examining the feasibility and utility of
             integrating conscientiousness assessment into primary care
             settings.},
   Doi = {10.1037/a0036113},
   Key = {fds253141}
}

@article{fds336535,
   Author = {Erskine, HE and Ferrari, AJ and Polanczyk, GV and Moffitt, TE and Murray, CJL and Vos, T and Whiteford, HA and Scott,
             JG},
   Title = {The global burden of conduct disorder and
             attention-deficit/hyperactivity disorder in
             2010.},
   Journal = {Journal of child psychology and psychiatry, and allied
             disciplines},
   Volume = {55},
   Number = {4},
   Pages = {328-336},
   Year = {2014},
   Month = {April},
   url = {http://dx.doi.org/10.1111/jcpp.12186},
   Abstract = {<h4>Objective</h4>The Global Burden of Disease Study 2010
             (GBD 2010) is the first to include conduct disorder (CD) and
             attention-deficit/hyperactivity disorder (ADHD) for burden
             quantification.<h4>Method</h4>A previous systematic review
             pooled the available epidemiological data for CD and ADHD,
             and predicted prevalence by country, region, age and sex for
             each disorder. Prevalence was then multiplied by a
             disability weight to calculate years lived with disability
             (YLDs). As no evidence of deaths resulting directly from
             either CD or ADHD was found, no years of life lost (YLLs)
             were calculated. Therefore, the number of
             disability-adjusted life years (DALYs) was equal to that of
             YLDs.<h4>Results</h4>Globally, CD was responsible for 5.75
             million YLDs/DALYs with ADHD responsible for a further
             491,500. Collectively, CD and ADHD accounted for 0.80% of
             total global YLDs and 0.25% of total global DALYs. In terms
             of global DALYs, CD was the 72nd leading contributor and
             among the 15 leading causes in children aged 5-19 years.
             Between 1990 and 2010, global DALYs attributable to CD and
             ADHD remained stable after accounting for population growth
             and ageing.<h4>Conclusions</h4>The global burden of CD and
             ADHD is significant, particularly in male children.
             Appropriate allocation of resources to address the high
             morbidity associated with CD and ADHD is necessary to reduce
             global burden. However, burden estimation was limited by
             data lacking for all four epidemiological parameters and by
             methodological challenges in quantifying disability. Future
             studies need to address these limitations in order to
             increase the accuracy of burden quantification.},
   Doi = {10.1111/jcpp.12186},
   Key = {fds336535}
}

@article{fds253136,
   Author = {McEwen, FS and Moffitt, TE and Arseneault, L},
   Title = {Is childhood cruelty to animals a marker for physical
             maltreatment in a prospective cohort study of
             children?},
   Journal = {Child abuse & neglect},
   Volume = {38},
   Number = {3},
   Pages = {533-543},
   Year = {2014},
   Month = {March},
   ISSN = {0145-2134},
   url = {http://dx.doi.org/10.1016/j.chiabu.2013.10.016},
   Abstract = {Childhood cruelty to animals is thought to indicate that a
             child may have been maltreated. This study examined: (a)
             prevalence of cruelty to animals among 5- to 12-year-old
             children; (b) the association between cruelty to animals,
             child physical maltreatment, and adult domestic violence;
             and (c) whether cruelty to animals is a marker of
             maltreatment taking into account age, persistence of
             cruelty, and socioeconomic disadvantage. Data were from the
             Environmental Risk (E-Risk) Longitudinal Twin Study, an
             epidemiological representative cohort of 2,232 children
             living in the United Kingdom. Mothers reported on cruelty to
             animals when children were 5, 7, 10, and 12 years, on child
             maltreatment up to age 12, and adult domestic violence. Nine
             percent of children were cruel to animals during the study
             and 2.6% persistently (≥2 time-points). Children cruel to
             animals were more likely to have been maltreated than other
             children (OR=3.32) although the majority (56.4%) had not
             been maltreated. Animal cruelty was not associated with
             domestic violence when maltreatment was controlled for. In
             disadvantaged families, 6 in 10 children cruel to animals
             had been maltreated. In other families, the likelihood of
             maltreatment increased with age (from 3 in 10 5-year-olds to
             4.5 in 10 12-year-olds) and persistence (4.5 in 10 of those
             persistently cruel). Although childhood cruelty to animals
             is associated with maltreatment, not every child showing
             cruelty had been maltreated. The usefulness of cruelty to
             animals as a marker for maltreatment increases with the
             child's age, persistence of behavior, and poorer social
             background.},
   Doi = {10.1016/j.chiabu.2013.10.016},
   Key = {fds253136}
}

@article{fds253138,
   Author = {Caspi, A and Houts, RM and Belsky, DW and Goldman-Mellor, SJ and Harrington, H and Israel, S and Meier, MH and Ramrakha, S and Shalev, I and Poulton, R and Moffitt, TE},
   Title = {The p Factor: One General Psychopathology Factor in the
             Structure of Psychiatric Disorders?},
   Journal = {Clinical Psychological Science: A Journal of the Association
             for Psychological Science},
   Volume = {2},
   Number = {2},
   Pages = {119-137},
   Year = {2014},
   Month = {March},
   ISSN = {2167-7026},
   url = {http://dx.doi.org/10.1177/2167702613497473},
   Abstract = {Mental disorders traditionally have been viewed as distinct,
             episodic, and categorical conditions. This view has been
             challenged by evidence that many disorders are sequentially
             comorbid, recurrent/chronic, and exist on a continuum. Using
             the Dunedin Multidisciplinary Health and Development Study,
             we examined the structure of psychopathology, taking into
             account dimensionality, persistence, co-occurrence, and
             sequential comorbidity of mental disorders across 20 years,
             from adolescence to midlife. Psychiatric disorders were
             initially explained by three higher-order factors
             (Internalizing, Externalizing, and Thought Disorder) but
             explained even better with one General Psychopathology
             dimension. We have called this dimension the p factor
             because it conceptually parallels a familiar dimension in
             psychological science: the g factor of general intelligence.
             Higher p scores are associated with more life impairment,
             greater familiality, worse developmental histories, and more
             compromised early-life brain function. The p factor explains
             why it is challenging to find causes, consequences,
             biomarkers, and treatments with specificity to individual
             mental disorders. Transdiagnostic approaches may improve
             research.},
   Doi = {10.1177/2167702613497473},
   Key = {fds253138}
}

@article{fds253144,
   Author = {Meier, MH and Moffitt, TE and Caspi, A and Poulton,
             R},
   Title = {Response to Bora.},
   Journal = {The American journal of psychiatry},
   Volume = {171},
   Number = {3},
   Pages = {369-370},
   Year = {2014},
   Month = {March},
   ISSN = {0002-953X},
   url = {http://dx.doi.org/10.1176/appi.ajp.2013.13091283r},
   Doi = {10.1176/appi.ajp.2013.13091283r},
   Key = {fds253144}
}

@article{fds253150,
   Author = {Goldman-Mellor, SJ and Caspi, A and Harrington, H and Hogan, S and Nada-Raja, S and Poulton, R and Moffitt, TE},
   Title = {Suicide attempt in young people: a signal for long-term
             health care and social needs.},
   Journal = {JAMA psychiatry},
   Volume = {71},
   Number = {2},
   Pages = {119-127},
   Year = {2014},
   Month = {February},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/24306041},
   Abstract = {<h4>Importance</h4>Suicidal behavior has increased since the
             onset of the global recession, a trend that may have
             long-term health and social implications.<h4>Objective</h4>To
             test whether suicide attempts among young people signal
             increased risk for later poor health and social functioning
             above and beyond a preexisting psychiatric
             disorder.<h4>Design</h4>We followed up a cohort of young
             people and assessed multiple aspects of their health and
             social functioning as they approached midlife. Outcomes
             among individuals who had self-reported a suicide attempt up
             through age 24 years (young suicide attempters) were
             compared with those who reported no attempt through age 24
             years (nonattempters). Psychiatric history and social class
             were controlled for.<h4>Setting and participants</h4>The
             population-representative Dunedin Multidisciplinary Health
             and Development Study, which involved 1037 birth cohort
             members comprising 91 young suicide attempters and 946
             nonattempters, 95% of whom were followed up to age 38
             years.<h4>Main outcomes and measures</h4>Outcomes were
             selected to represent significant individual and societal
             costs: mental health, physical health, harm toward others,
             and need for support.<h4>Results</h4>As adults approaching
             midlife, young suicide attempters were significantly more
             likely to have persistent mental health problems (eg,
             depression, substance dependence, and additional suicide
             attempts) compared with nonattempters. They were also more
             likely to have physical health problems (eg, metabolic
             syndrome and elevated inflammation). They engaged in more
             violence (eg, violent crime and intimate partner abuse) and
             needed more social support (eg, long-term welfare receipt
             and unemployment). Furthermore, they reported being lonelier
             and less satisfied with their lives. These associations
             remained after adjustment for youth psychiatric diagnoses
             and social class.<h4>Conclusions and relevance</h4>Many
             young suicide attempters remain vulnerable to costly health
             and social problems into midlife. As rates of suicidal
             behavior rise with the continuing global recession,
             additional suicide prevention efforts and long-term
             monitoring and after-care services are needed.},
   Doi = {10.1001/jamapsychiatry.2013.2803},
   Key = {fds253150}
}

@article{fds253147,
   Author = {Meier, MH and Caspi, A and Reichenberg, A and Keefe, RSE and Fisher, HL and Harrington, H and Houts, R and Poulton, R and Moffitt,
             TE},
   Title = {Neuropsychological decline in schizophrenia from the
             premorbid to the postonset period: evidence from a
             population-representative longitudinal study.},
   Journal = {Am J Psychiatry},
   Volume = {171},
   Number = {1},
   Pages = {91-101},
   Year = {2014},
   Month = {January},
   ISSN = {0002-953X},
   url = {http://dx.doi.org/10.1176/appi.ajp.2013.12111438},
   Abstract = {OBJECTIVE: Despite the widespread belief that
             neuropsychological decline is a cardinal feature of the
             progression from the premorbid stage to the chronic form of
             schizophrenia, few longitudinal studies have examined change
             in neuropsychological functioning from before to after
             illness onset. The authors examined whether
             neuropsychological decline is unique to schizophrenia,
             whether it is generalized or confined to particular mental
             functions, and whether individuals with schizophrenia also
             have cognitive problems in everyday life. METHOD:
             Participants were members of a representative cohort of
             1,037 individuals born in Dunedin, New Zealand, in 1972 and
             1973 and followed prospectively to age 38, with 95%
             retention. Assessment of IQ and specific neuropsychological
             functions was conducted at ages 7, 9, 11, and 13, and again
             at age 38. Informants also reported on any cognitive
             problems at age 38. RESULTS: Individuals with schizophrenia
             exhibited declines in IQ and in a range of mental functions,
             particularly those tapping processing speed, learning,
             executive function, and motor function. There was little
             evidence of decline in verbal abilities or delayed memory,
             however, and the developmental progression of deficits in
             schizophrenia differed across mental functions. Processing
             speed deficits increased gradually from childhood to beyond
             the early teen years, whereas verbal deficits emerged early
             but remained static thereafter. Neuropsychological decline
             was specific to schizophrenia, as no evidence of decline was
             apparent among individuals with persistent depression,
             children with mild cognitive impairment, individuals matched
             on childhood risk factors for schizophrenia, and
             psychiatrically healthy individuals. Informants also noticed
             more cognitive problems in individuals with schizophrenia.
             CONCLUSIONS: There is substantial neuropsychological decline
             in schizophrenia from the premorbid to the postonset period,
             but the extent and developmental progression of decline
             varies across mental functions. Findings suggest that
             different pathophysiological mechanisms may underlie
             deficits in different mental functions.},
   Doi = {10.1176/appi.ajp.2013.12111438},
   Key = {fds253147}
}

@article{fds253145,
   Author = {Israel, S and Moffitt, TE and Belsky, DW and Hancox, RJ and Poulton, R and Roberts, B and Murray, W and Caspi, A},
   Title = {Translating personality psychology to help personalize
             preventive medicine for young adult patients},
   Journal = {Journal of Personality and Social Psychology},
   Volume = {106},
   Number = {3},
   Pages = {484-498},
   Year = {2014},
   ISSN = {0022-3514},
   url = {http://dx.doi.org/10.1037/a0035687},
   Abstract = {The rising number of newly insured young adults brought on
             by health care reform will soon increase demands on primary
             care physicians. Physicians will face more young adult
             patients, which presents an opportunity for more
             prevention-oriented care. In the present study, we evaluated
             whether brief observer reports of young adults’
             personality traits could predict which individuals would be
             at greater risk for poor health as they entered midlife.
             Following the cohort of 1,000 individuals from the Dunedin
             Multidisciplinary Health and Development Study (Moffitt,
             Caspi, Rutter, & Silva, 2001), we show that very brief
             measures of young adults’ personalities predicted their
             midlife physical health across multiple domains (metabolic
             abnormalities, cardiorespiratory fitness, pulmonary
             function, periodontal disease, and systemic inflammation).
             Individuals scoring low on the traits of Conscientiousness
             and Openness to Experience went on to develop poorer health
             even after accounting for preexisting differences in
             education, socioeconomic status, smoking, obesity,
             self-reported health, medical conditions, and family medical
             history. Moreover, personality ratings from peer informants
             who knew participants well, and from a nurse and
             receptionist who had just met participants for the first
             time, predicted health decline from young adulthood to
             midlife despite striking differences in level of
             acquaintance. Personality effect sizes were on par with
             other well-established health risk factors such as
             socioeconomic status, smoking, and self-reported health. We
             discuss the potential utility of personality measurement to
             function as an inexpensive and accessible tool for health
             care professionals to personalize preventive medicine.
             Adding personality information to existing health care
             electronic infrastructures could also advance personality
             theory by generating opportunities to examine how
             personality processes influence doctor–patient
             communication, health service use, and patient
             outcomes.},
   Doi = {10.1037/a0035687},
   Key = {fds253145}
}

@article{fds253149,
   Author = {Meier, MH and Shalev, I and Moffitt, TE and Kapur, S and Keefe, RSE and Wong, TY and Belsky, DW and Harrington, H and Hogan, S and Houts, R and Caspi, A and Poulton, R},
   Title = {Microvascular abnormality in schizophrenia as shown by
             retinal imaging.},
   Journal = {Am J Psychiatry},
   Volume = {170},
   Number = {12},
   Pages = {1451-1459},
   Year = {2013},
   Month = {December},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/24030514},
   Abstract = {OBJECTIVE: Retinal and cerebral microvessels are
             structurally and functionally homologous, but unlike
             cerebral microvessels, retinal microvessels can be
             noninvasively measured in vivo by retinal imaging. The
             authors tested the hypothesis that individuals with
             schizophrenia exhibit microvascular abnormality and
             evaluated the utility of retinal imaging as a tool for
             schizophrenia research. METHOD: Participants were members of
             the Dunedin Study, a population-representative cohort
             followed from birth with 95% retention. Study members
             underwent retinal imaging at age 38. The authors assessed
             retinal arteriolar and venular caliber for all members of
             the cohort, including individuals who developed
             schizophrenia. RESULTS: Study members who developed
             schizophrenia were distinguished by wider retinal venules,
             suggesting microvascular abnormality reflective of
             insufficient brain oxygen supply. Analyses that controlled
             for confounding health conditions suggested that wider
             retinal venules are not simply an artifact of co-occurring
             health problems in schizophrenia patients. Wider venules
             were also associated with a dimensional measure of adult
             psychosis symptoms and with psychosis symptoms reported in
             childhood. CONCLUSIONS: The findings provide initial support
             for the hypothesis that individuals with schizophrenia show
             microvascular abnormality. Moreover, the results suggest
             that the same vascular mechanisms underlie subthreshold
             symptoms and clinical disorder and that these associations
             may begin early in life. These findings highlight the
             promise of retinal imaging as a tool for understanding the
             pathogenesis of schizophrenia.},
   Doi = {10.1176/appi.ajp.2013.13020234},
   Key = {fds253149}
}

@article{fds253151,
   Author = {Belsky, DW and Caspi, A and Goldman-Mellor, S and Meier, MH and Ramrakha, S and Poulton, R and Moffitt, TE},
   Title = {Is obesity associated with a decline in intelligence
             quotient during the first half of the life
             course?},
   Journal = {American Journal of Epidemiology},
   Volume = {178},
   Number = {9},
   Pages = {1461-1468},
   Year = {2013},
   Month = {November},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/24029684},
   Abstract = {Cross-sectional studies have found that obesity is
             associated with low intellectual ability and neuroimaging
             abnormalities in adolescence and adulthood. Some have
             interpreted these associations to suggest that obesity
             causes intellectual decline in the first half of the life
             course. We analyzed data from a prospective longitudinal
             study to test whether becoming obese was associated with
             intellectual decline from childhood to midlife. We used data
             from the ongoing Dunedin Multidisciplinary Health and
             Development Study, a population-representative birth cohort
             study of 1,037 children in New Zealand who were followed
             prospectively from birth (1972–1973) through their fourth
             decade of life with a 95% retention rate. Intelligence
             quotient (IQ) was measured in childhood and adulthood.
             Anthropometric measurements were taken at birth and at 12
             subsequent in-person assessments. As expected, cohort
             members who became obese had lower adulthood IQ scores.
             However, obese cohort members exhibited no excess decline in
             IQ. Instead, these cohort members had lower IQ scores since
             childhood. This pattern remained consistent when we
             accounted for children’s birth weights and growth during
             the first years of life, as well as for childhood-onset
             obesity. Lower IQ scores among children who later developed
             obesity were present as early as 3 years of age. We observed
             no evidence that obesity contributed to a decline in IQ,
             even among obese individuals who displayed evidence of the
             metabolic syndrome and/or elevated systemic
             inflammation.},
   Doi = {10.1093/aje/kwt135},
   Key = {fds253151}
}

@article{fds253152,
   Author = {Jaffee, SR and Bowes, L and Ouellet-Morin, I and Fisher, HL and Moffitt,
             TE and Merrick, MT and Arseneault, L},
   Title = {Safe, stable, nurturing relationships break the
             intergenerational cycle of abuse: a prospective nationally
             representative cohort of children in the United
             Kingdom.},
   Journal = {The Journal of adolescent health : official publication of
             the Society for Adolescent Medicine},
   Volume = {53},
   Number = {4 Suppl},
   Pages = {S4-10},
   Year = {2013},
   Month = {October},
   ISSN = {1054-139X},
   url = {http://dx.doi.org/10.1016/j.jadohealth.2013.04.007},
   Abstract = {<h4>Purpose</h4>To identify contextual and interpersonal
             factors that distinguish families in which the
             intergenerational transmission of maltreatment is maintained
             from families in which the cycle is broken.<h4>Methods</h4>The
             sample was composed of 1,116 families in the United Kingdom
             who participated in the Environmental Risk (E-Risk)
             Longitudinal Twin Study. We assessed mother's childhood
             history of maltreatment retrospectively with a validated and
             reliable interview. Prospective reports of children's
             physical maltreatment were collected repeatedly up to 12
             years. We compared families in which mothers but not
             children had experienced maltreatment with families in which
             both mothers and children had experienced maltreatment, and
             with families without maltreatment, on a range of contextual
             and interpersonal factors known to affect child
             development.<h4>Results</h4>In multivariate analyses,
             supportive and trusting relationships with intimate
             partners, high levels of maternal warmth toward children,
             and low levels of partner violence between adults
             distinguished families in which mothers but not children
             experienced maltreatment from families in which mothers and
             children experienced maltreatment. Families in which only
             mothers experienced maltreatment were largely similar to
             families in which neither generation experienced
             maltreatment, except that mothers belonging to the former
             group were more likely to have a lifetime history of
             depression and low levels of social support.<h4>Conclusions</h4>Safe,
             stable, nurturing relationships between intimate partners
             and between mothers and children are associated with
             breaking the cycle of abuse in families. Additional research
             is needed to determine whether these factors have a causal
             role in preventing the transmission of maltreatment from one
             generation to the next.},
   Doi = {10.1016/j.jadohealth.2013.04.007},
   Key = {fds253152}
}

@article{fds253153,
   Author = {Fisher, HL and Caspi, A and Poulton, R and Meier, MH and Houts, R and Harrington, H and Arseneault, L and Moffitt, TE},
   Title = {Specificity of childhood psychotic symptoms for predicting
             schizophrenia by 38 years of age: a birth cohort
             study.},
   Journal = {Psychological medicine},
   Volume = {43},
   Number = {10},
   Pages = {2077-2086},
   Year = {2013},
   Month = {October},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/23302254},
   Abstract = {<h4>Background</h4>Childhood psychotic symptoms have been
             used as a subclinical phenotype of schizophrenia in
             etiological research and as a target for preventative
             interventions. However, recent studies have cast doubt on
             the specificity of these symptoms for schizophrenia,
             suggesting alternative outcomes such as anxiety and
             depression. Using a prospective longitudinal birth cohort we
             investigated whether childhood psychotic symptoms predicted
             a diagnosis of schizophrenia or other psychiatric disorders
             by 38 years of age.<h4>Method</h4>Participants were drawn
             from a birth cohort of 1037 children from Dunedin, New
             Zealand, who were followed prospectively to 38 years of age
             (96% retention rate). Structured clinical interviews were
             administered at age 11 to assess psychotic symptoms and
             study members underwent psychiatric assessments at ages 18,
             21, 26, 32 and 38 to obtain past-year DSM-III-R/IV diagnoses
             and self-reports of attempted suicides since
             adolescence.<h4>Results</h4>Psychotic symptoms at age 11
             predicted elevated rates of research diagnoses of
             schizophrenia and posttraumatic stress disorder (PTSD) and
             also suicide attempts by age 38, even when controlling for
             gender, social class and childhood psychopathology. No
             significant associations were found for persistent anxiety,
             persistent depression, mania or persistent substance
             dependence. Very few of the children presenting with age-11
             psychotic symptoms were free from disorder by age
             38.<h4>Conclusions</h4>Childhood psychotic symptoms were not
             specific to a diagnosis of schizophrenia in adulthood and
             thus future studies of early symptoms should be cautious in
             extrapolating findings only to this clinical disorder.
             However, these symptoms may be useful as a marker of adult
             mental health problems more broadly.},
   Doi = {10.1017/s0033291712003091},
   Key = {fds253153}
}

@article{fds253231,
   Author = {Belsky, DW and Moffitt, TE and Caspi, A},
   Title = {Genetics in population health science: strategies and
             opportunities},
   Journal = {American journal of public health},
   Volume = {103 Suppl 1},
   Number = {S1},
   Pages = {S73-83},
   Year = {2013},
   Month = {October},
   ISSN = {1541-0048},
   url = {http://ajph.aphapublications.org/doi/abs/10.2105/AJPH.2012.301139},
   Abstract = {Translational research is needed to leverage discoveries
             from the frontiers of genome science to improve public
             health. So far, public health researchers have largely
             ignored genetic discoveries, and geneticists have ignored
             important aspects of population health science. This mutual
             neglect should end. In this article, we discuss 3 areas
             where public health researchers can help to advance
             translation: (1) risk assessment: investigate genetic
             profiles as components in composite risk assessments; (2)
             targeted intervention: conduct life-course longitudinal
             studies to understand when genetic risks manifest in
             development and whether intervention during sensitive
             periods can have lasting effects; and (3) improved
             understanding of environmental causation: collaborate with
             geneticists on gene-environment interaction research. We
             illustrate with examples from our own research on obesity
             and smoking.},
   Doi = {10.2105/AJPH.2012.301139},
   Key = {fds253231}
}

@article{fds253154,
   Author = {Murray, CJL and Atkinson, C and Bhalla, K and Birbeck, G and Burstein,
             R and Chou, D and Dellavalle, R and Danaei, G and Ezzati, M and Fahimi, A and Flaxman, D and Foreman, and Gabriel, S and Gakidou, E and Kassebaum, N and Khatibzadeh, S and Lim, S and Lipshultz, SE and London, S and Lopez, and MacIntyre, MF and Mokdad, AH and Moran, A and Moran, AE and Mozaffarian,
             D and Murphy, T and Naghavi, M and Pope, C and Roberts, T and Salomon, J and Schwebel, DC and Shahraz, S and Sleet, DA and Murray, and Abraham, J and Ali, MK and Bartels, DH and Chen, H and Criqui, MH and Dahodwala, and Jarlais, and Ding, EL and Dorsey, ER and Ebel, BE and Fahami, and Flaxman, S and Flaxman, AD and Gonzalez-Medina, D and Grant, B and Hagan, H and Hoffman, H and Leasher, JL and Lin, J and Lozano, R and Lu, Y and Mallinger, L and McDermott, MM and Micha, R and Miller, TR and Mokdad,
             AA and Naghavi, M and Narayan, KMV and Omer, SB and Pelizzari, PM and Phillips, D and Ranganathan, D and Rivara, FP and Sampson, U and Sanman,
             E and Sapkota, A and Sharaz, S and Shivakoti, R and Singh, GM and Singh, D and Tavakkoli, M and Towbin, JA and Wilkinson, JD and Zabetian, A and Murray, and Ali, MK and Alvardo, M and Baddour, LM and Benjamin, EJ and Bolliger, I and Carnahan, E and Chugh, SS and Cohen, A and Colson, KE and Cooper, LT and Couser, W and Dabhadkar, KC and Dellavalle, RP and Jarlais, and Dicker, D and Duber, H and Engell, RE and Felson, DT and Finucane, MM and Flaxman, S and Fleming, T and Foreman, and Forouzanfar, MH and Freedman, G and Freeman, MK and Gillum, RF and Gosselin, R and Gutierrez, HR and Havmoeller, R and Jacobsen, KH and James, SL and Jasrasaria, R and Jayarman, S and Johns, N and Lan, Q and Meltzer, M and Mensah, GA and Michaud, C and Mock, C and Moffitt, TE and Nelson, RG and Olives, C and Ortblad, K and Ostro, B and Raju, M and Razavi, H and Ritz, B and Sacco, RL and Shibuya, K and Silberberg, D and Singh, JA and Steenland, K and Taylor, JA and Thurston, GD and Vavilala,
             MS and Vos, T and Wagner, GR and Weinstock, MA and Weisskopf, MG and Wulf,
             S and Murray, and U.S. Burden of Disease Collaborators},
   Title = {The state of US health, 1990-2010: burden of diseases,
             injuries, and risk factors.},
   Journal = {JAMA},
   Volume = {310},
   Number = {6},
   Pages = {591-608},
   Year = {2013},
   Month = {August},
   ISSN = {0098-7484},
   url = {http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000323058400015&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=47d3190e77e5a3a53558812f597b0b92},
   Abstract = {<h4>Importance</h4>Understanding the major health problems
             in the United States and how they are changing over time is
             critical for informing national health policy.<h4>Objectives</h4>To
             measure the burden of diseases, injuries, and leading risk
             factors in the United States from 1990 to 2010 and to
             compare these measurements with those of the 34 countries in
             the Organisation for Economic Co-operation and Development
             (OECD) countries.<h4>Design</h4>We used the systematic
             analysis of descriptive epidemiology of 291 diseases and
             injuries, 1160 sequelae of these diseases and injuries, and
             67 risk factors or clusters of risk factors from 1990 to
             2010 for 187 countries developed for the Global Burden of
             Disease 2010 Study to describe the health status of the
             United States and to compare US health outcomes with those
             of 34 OECD countries. Years of life lost due to premature
             mortality (YLLs) were computed by multiplying the number of
             deaths at each age by a reference life expectancy at that
             age. Years lived with disability (YLDs) were calculated by
             multiplying prevalence (based on systematic reviews) by the
             disability weight (based on population-based surveys) for
             each sequela; disability in this study refers to any short-
             or long-term loss of health. Disability-adjusted life-years
             (DALYs) were estimated as the sum of YLDs and YLLs. Deaths
             and DALYs related to risk factors were based on systematic
             reviews and meta-analyses of exposure data and relative
             risks for risk-outcome pairs. Healthy life expectancy (HALE)
             was used to summarize overall population health, accounting
             for both length of life and levels of ill health experienced
             at different ages.<h4>Results</h4>US life expectancy for
             both sexes combined increased from 75.2 years in 1990 to
             78.2 years in 2010; during the same period, HALE increased
             from 65.8 years to 68.1 years. The diseases and injuries
             with the largest number of YLLs in 2010 were ischemic heart
             disease, lung cancer, stroke, chronic obstructive pulmonary
             disease, and road injury. Age-standardized YLL rates
             increased for Alzheimer disease, drug use disorders, chronic
             kidney disease, kidney cancer, and falls. The diseases with
             the largest number of YLDs in 2010 were low back pain, major
             depressive disorder, other musculoskeletal disorders, neck
             pain, and anxiety disorders. As the US population has aged,
             YLDs have comprised a larger share of DALYs than have YLLs.
             The leading risk factors related to DALYs were dietary
             risks, tobacco smoking, high body mass index, high blood
             pressure, high fasting plasma glucose, physical inactivity,
             and alcohol use. Among 34 OECD countries between 1990 and
             2010, the US rank for the age-standardized death rate
             changed from 18th to 27th, for the age-standardized YLL rate
             from 23rd to 28th, for the age-standardized YLD rate from
             5th to 6th, for life expectancy at birth from 20th to 27th,
             and for HALE from 14th to 26th.<h4>Conclusions and
             relevance</h4>From 1990 to 2010, the United States made
             substantial progress in improving health. Life expectancy at
             birth and HALE increased, all-cause death rates at all ages
             decreased, and age-specific rates of years lived with
             disability remained stable. However, morbidity and chronic
             disability now account for nearly half of the US health
             burden, and improvements in population health in the United
             States have not kept pace with advances in population health
             in other wealthy nations.},
   Doi = {10.1001/jama.2013.13805},
   Key = {fds253154}
}

@article{fds253155,
   Author = {Meier, MH and Caspi, A and Houts, R and Slutske, WS and Harrington, H and Jackson, KM and Belsky, DW and Poulton, R and Moffitt,
             TE},
   Title = {Prospective developmental subtypes of alcohol dependence
             from age 18 to 32 years: implications for nosology,
             etiology, and intervention.},
   Journal = {Development and psychopathology},
   Volume = {25},
   Number = {3},
   Pages = {785-800},
   Year = {2013},
   Month = {August},
   ISSN = {0954-5794},
   url = {http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000322120600016&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=47d3190e77e5a3a53558812f597b0b92},
   Abstract = {The purpose of the present study is to identify child and
             adult correlates that differentiate (a) individuals with
             persistent alcohol dependence from individuals with
             developmentally limited alcohol dependence and (b)
             individuals with adult-onset alcohol dependence from
             individuals who never diagnose. There are 1,037 members of
             the Dunedin Longitudinal Study, which is a birth cohort
             followed prospectively from birth until age 32. Past-year
             DSM-IV alcohol dependence diagnoses are ascertained with
             structured diagnostic interviews at ages 18, 21, 26, and 32.
             Individuals are classified as developmentally limited,
             persistent, or adult-onset subtypes based on their
             time-ordered pattern of diagnoses. The persistent subtype
             generally exhibits the worst scores on all correlates,
             including family psychiatric history, adolescent and adult
             externalizing and internalizing problems, adolescent and
             adult substance use, adult quality of life, and coping
             strategies. The prospective predictors that distinguished
             them from the developmentally limited subtype involved
             family liability, adolescent negative affectivity, daily
             alcohol use, and frequent marijuana use. Furthermore, young
             people who develop the persistent subtype of alcohol
             dependence are distinguished from the developmentally
             limited subtype by an inability to reduce drinking and by
             continued use despite problems by age 18. The adult-onset
             group members are virtually indistinguishable from ordinary
             cohort members as children or adolescents; however, in
             adulthood, adult-onset cases are distinguished by problems
             with depression, substance use, stress, and strategies for
             coping with stress. Information about age of onset and
             developmental course is fundamental for identifying subtypes
             of alcohol dependence. Subtype-specific etiologies point to
             targeted prevention and intervention efforts based on the
             characteristics of each subtype.},
   Doi = {10.1017/s0954579413000175},
   Key = {fds253155}
}

@article{fds253226,
   Author = {Ramrakha, S and Paul, C and Bell, ML and Dickson, N and Moffitt, TE and Caspi, A},
   Title = {The relationship between multiple sex partners and anxiety,
             depression, and substance dependence disorders: a cohort
             study.},
   Journal = {Archives of sexual behavior},
   Volume = {42},
   Number = {5},
   Pages = {863-872},
   Year = {2013},
   Month = {July},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/23400516},
   Keywords = {sex • depression • substance dependence},
   Abstract = {Changes in sexual behavior have resulted in longer periods
             of multiple serial or concurrent relationships. This study
             investigated the effects of multiple heterosexual partners
             on mental health, specifically, whether higher numbers of
             partners were linked to later anxiety, depression, and
             substance dependency. Data from the Dunedin
             Multidisciplinary Health and Development Study, a
             prospective, longitudinal study of a birth cohort born in
             1972-1973 in Dunedin, New Zealand were used. The
             relationship between numbers of sex partners over three age
             periods (18-20, 21-25, and 26-32 years) and diagnoses of
             anxiety, depression, and substance dependence disorder at
             21, 26, and 32 years were examined, using logistic
             regression. Interaction by gender was examined. Adjustment
             was made for prior mental health status. There was no
             significant association between number of sex partners and
             later anxiety and depression. Increasing numbers of sex
             partners were associated with increasing risk of substance
             dependence disorder at all three ages. The association was
             stronger for women and remained after adjusting for prior
             disorder. For women reporting 2.5 or more partners per year,
             compared to 0-1 partners, the adjusted odd ratios (and 95 %
             CIs) were 9.6 (4.4-20.9), 7.3 (2.5-21.3), and 17.5
             (3.5-88.1) at 21, 26, and 32 years, respectively. Analyses
             using new cases of these disorders showed similar patterns.
             This study established a strong association between number
             of sex partners and later substance disorder, especially for
             women, which persisted beyond prior substance use and mental
             health problems more generally. The reasons for this
             association deserve investigation.},
   Doi = {10.1007/s10508-012-0053-1},
   Key = {fds253226}
}

@article{fds253229,
   Author = {Shalev, I and Moffitt, TE and Wong, TY and Meier, MH and Houts, RM and Ding, J and Cheung, CY and Ikram, MK and Caspi, A and Poulton,
             R},
   Title = {Retinal vessel caliber and lifelong neuropsychological
             functioning: retinal imaging as an investigative tool for
             cognitive epidemiology.},
   Journal = {Psychol Sci},
   Volume = {24},
   Number = {7},
   Pages = {1198-1207},
   Year = {2013},
   Month = {July},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/23678508},
   Keywords = {brain • cognitive ability • cognitive neuroscience
             • intelligence • retinal imaging • venular
             caliber},
   Abstract = {Why do more intelligent people live healthier and longer
             lives? One possibility is that intelligence tests assess
             health of the brain, but psychological science has lacked
             technology to evaluate this hypothesis. Digital retinal
             imaging, a new, noninvasive method to visualize
             microcirculation in the eye, may reflect vascular conditions
             in the brain. We studied the association between retinal
             vessel caliber and neuropsychological functioning in the
             representative Dunedin birth cohort. Wider venular caliber
             was associated with poorer neuropsychological functioning at
             midlife, independently of potentially confounding factors.
             This association was not limited to any specific test domain
             and extended to informants' reports of cohort members'
             cognitive difficulties in everyday life. Moreover, wider
             venular caliber was associated with lower childhood IQ
             tested 25 years earlier. The findings indicate that retinal
             venular caliber may be an indicator of neuropsychological
             health years before the onset of dementing diseases and
             suggest that digital retinal imaging may be a useful
             investigative tool for psychological science.},
   Doi = {10.1177/0956797612470959},
   Key = {fds253229}
}

@article{fds199232,
   Author = {Bowes, L. and Maughan, B. and Ball, H. and Shakoor, S. and Ouellet-Morin, I. and Caspi, A. and Moffitt, T.E. and Arseneault,
             L.},
   Title = {Chronic bullying victimization across school transitions:
             The role of genetic and environmental influences},
   Journal = {Development and Psychopathology},
   Volume = {25},
   Number = {2},
   Pages = {333-346},
   Year = {2013},
   Month = {May},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/23627948},
   Abstract = {We investigated the antecedents and consequences of chronic
             victimization by bullies across a school transition using a
             genetically sensitive longitudinal design. Data were from
             the Environmental Risk Longitudinal Twin Study (E-Risk), an
             epidemiological cohort of 2,232 children. We used mothers'
             and children's reports of bullying victimization during
             primary school and early secondary school. Children who
             experienced frequent victimization at both time points were
             classed as "chronic victims" and were found to have an
             increased risk for mental health problems and academic
             difficulties compared to children who were bullied only in
             primary school, children bullied for the first time in
             secondary school, and never-bullied children. Biometric
             analyses revealed that stability in victimization over this
             period was influenced primarily by genetic and shared
             environmental factors. Regression analyses showed that
             children's early characteristics such as preexistent
             adjustment difficulties and IQ predicted chronic versus
             transitory victimization. Family risk factors for chronic
             victimization included socioeconomic disadvantage, low
             maternal warmth, and maltreatment. Our results suggest that
             bullying intervention programs should consider the role of
             the victims' behaviors and family background in increasing
             vulnerability to chronic victimization. Our study highlights
             the importance of widening antibullying interventions to
             include families to reduce the likelihood of children
             entering a pathway toward chronic victimization.},
   Doi = {10.1017/S0954579412001095},
   Key = {fds199232}
}

@article{fds253232,
   Author = {Belsky, DW and Moffitt, TE and Baker, TB and Biddle, AK and Evans, JP and Harrington, H and Houts, R and Meier, M and Sugden, K and Williams, B and Poulton, R and Caspi, A},
   Title = {Polygenic risk and the developmental progression to heavy,
             persistent smoking and nicotine dependence: evidence from a
             4-decade longitudinal study.},
   Journal = {JAMA psychiatry},
   Volume = {70},
   Number = {5},
   Pages = {534-542},
   Year = {2013},
   Month = {May},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/23536134},
   Keywords = {smoking • genetics},
   Abstract = {<h4>Importance</h4>Genome-wide hypothesis-free discovery
             methods have identified loci that are associated with heavy
             smoking in adulthood. Research is needed to understand
             developmental processes that link newly discovered genetic
             risks with adult heavy smoking.<h4>Objective</h4>To test how
             genetic risks discovered in genome-wide association studies
             of adult smoking influence the developmental progression of
             smoking behavior from initiation through conversion to daily
             smoking, progression to heavy smoking, nicotine dependence,
             and struggles with cessation.<h4>Design</h4>A 38-year,
             prospective, longitudinal study of a representative birth
             cohort.<h4>Setting</h4>The Dunedin Multidisciplinary Health
             and Development Study of New Zealand.<h4>Participants</h4>The
             study included 1037 male and female participants.<h4>Exposure</h4>We
             assessed genetic risk with a multilocus genetic risk score.
             The genetic risk score was composed of single-nucleotide
             polymorphisms identified in 3 meta-analyses of genome-wide
             association studies of smoking quantity phenotypes.<h4>Main
             outcomes and measures</h4>Smoking initiation, conversion to
             daily smoking, progression to heavy smoking, nicotine
             dependence (Fagerström Test of Nicotine Dependence), and
             cessation difficulties were evaluated at 8 assessments
             spanning the ages of 11 to 38 years.<h4>Results</h4>Genetic
             risk score was unrelated to smoking initiation. However,
             individuals at higher genetic risk were more likely to
             convert to daily smoking as teenagers, progressed more
             rapidly from smoking initiation to heavy smoking, persisted
             longer in smoking heavily, developed nicotine dependence
             more frequently, were more reliant on smoking to cope with
             stress, and were more likely to fail in their cessation
             attempts. Further analysis revealed that 2 adolescent
             developmental phenotypes-early conversion to daily smoking
             and rapid progression to heavy smoking-mediated associations
             between the genetic risk score and mature phenotypes of
             persistent heavy smoking, nicotine dependence, and cessation
             failure. The genetic risk score predicted smoking risk over
             and above family history.<h4>Conclusions and
             relevance</h4>Initiatives that disrupt the developmental
             progression of smoking behavior among adolescents may
             mitigate genetic risks for developing adult smoking
             problems. Future genetic research may maximize discovery
             potential by focusing on smoking behavior soon after smoking
             initiation and by studying young smokers.},
   Doi = {10.1001/jamapsychiatry.2013.736},
   Key = {fds253232}
}

@article{fds253241,
   Author = {Shalev, I and Moffitt, TE and Sugden, K and Williams, B and Houts, RM and Danese, A and Mill, J and Arseneault, L and Caspi,
             A},
   Title = {Exposure to violence during childhood is associated with
             telomere erosion from 5 to 10 years of age: a longitudinal
             study.},
   Journal = {Molecular psychiatry},
   Volume = {18},
   Number = {5},
   Pages = {576-581},
   Year = {2013},
   Month = {May},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/22525489},
   Keywords = {childhood stress • cumulative violence exposure •
             telomere length},
   Abstract = {There is increasing interest in discovering mechanisms that
             mediate the effects of childhood stress on late-life disease
             morbidity and mortality. Previous studies have suggested one
             potential mechanism linking stress to cellular aging,
             disease and mortality in humans: telomere erosion. We
             examined telomere erosion in relation to children's exposure
             to violence, a salient early-life stressor, which has known
             long-term consequences for well-being and is a major
             public-health and social-welfare problem. In the first
             prospective-longitudinal study with repeated telomere
             measurements in children while they experienced stress, we
             tested the hypothesis that childhood violence exposure would
             accelerate telomere erosion from age 5 to age 10 years.
             Violence was assessed as exposure to maternal domestic
             violence, frequent bullying victimization and physical
             maltreatment by an adult. Participants were 236 children
             (49% females; 42% with one or more violence exposures)
             recruited from the Environmental-Risk Longitudinal Twin
             Study, a nationally representative 1994-1995 birth cohort.
             Each child's mean relative telomere length was measured
             simultaneously in baseline and follow-up DNA samples, using
             the quantitative PCR method for T/S ratio (the ratio of
             telomere repeat copy numbers to single-copy gene numbers).
             Compared with their counterparts, the children who
             experienced two or more kinds of violence exposure showed
             significantly more telomere erosion between age-5 baseline
             and age-10 follow-up measurements, even after adjusting for
             sex, socioeconomic status and body mass index (B=-0.052,
             s.e.=0.021, P=0.015). This finding provides support for a
             mechanism linking cumulative childhood stress to telomere
             maintenance, observed already at a young age, with potential
             impact for life-long health.},
   Doi = {10.1038/mp.2012.32},
   Key = {fds253241}
}

@article{fds336536,
   Author = {Moffitt, TE and Meier, MH and Caspi, A and Poulton,
             R},
   Title = {Reply to Rogeberg and Daly: No evidence that socioeconomic
             status or personality differences confound the association
             between cannabis use and IQ decline.},
   Journal = {Proceedings of the National Academy of Sciences of the
             United States of America},
   Volume = {110},
   Number = {11},
   Pages = {E980-E982},
   Year = {2013},
   Month = {March},
   url = {http://dx.doi.org/10.1073/pnas.1300618110},
   Doi = {10.1073/pnas.1300618110},
   Key = {fds336536}
}

@article{fds253105,
   Author = {Piquero, AR and Moffitt, TE},
   Title = {Life-course persistent offending},
   Pages = {177-196},
   Publisher = {Willan},
   Year = {2013},
   Month = {January},
   url = {http://dx.doi.org/10.4324/9781843924494},
   Doi = {10.4324/9781843924494},
   Key = {fds253105}
}

@article{fds253146,
   Author = {Moffitt, TE and Poulton, R and Caspi, A},
   Title = {Lifelong Impact of Early Self-Control Childhood
             self-discipline predicts adult quality of
             life},
   Journal = {AMERICAN SCIENTIST},
   Volume = {101},
   Number = {5},
   Pages = {352-359},
   Publisher = {SIGMA XI-SCI RES SOC},
   Year = {2013},
   ISSN = {0003-0996},
   url = {http://dx.doi.org/10.1511/2013.104.352},
   Abstract = {An individual's preschool self-control predicts their life
             satisfaction, crime record, income level, physical health,
             and parenting skill in adolescence and even adulthood. The
             Dunedin Multidisciplinary Health and Development Study is a
             40 year investigation of health and behavior in just over
             1000 individuals born between April 1972 and March 1973 in
             Dunedin, New Zealand. The study began with babies as an
             obstetric survey of newborn health but evolved into a
             powerful long term study, including behavior and psychology.
             This study lends itself to analyzing correlations to
             understand behavioral patterns over the participants' with
             low self-control and poor outcomes have not dropped out of
             the study, enabling to explore a full range of life
             experiences. A study of 1000 children using Dunedin approach
             revealed that the children who showed early difficulty with
             self-control grew up to have poorer health, greater
             substance abuse, more financial difficulties , higher crime
             conviction rates, and lower parenting skill.},
   Doi = {10.1511/2013.104.352},
   Key = {fds253146}
}

@article{fds253156,
   Author = {Belsky, DW and Sears, MR and Hancox, RJ and Harrington, H and Houts, R and Moffitt, TE and Sugden, K and Williams, B and Poulton, R and Caspi,
             A},
   Title = {Polygenic risk and the development and course of asthma: an
             analysis of data from a four-decade longitudinal
             study},
   Journal = {The Lancet Respiratory Medicine},
   Volume = {1},
   Number = {6},
   Pages = {453-361},
   Year = {2013},
   ISSN = {2213-2600},
   url = {http://dx.doi.org/10.1016/S2213-2600(13)70101-2},
   Abstract = {Background Genome-wide association studies (GWAS) have
             discovered genetic variants that predispose individuals to
             asthma. To integrate these new discoveries with emerging
             models of asthma pathobiology, we aimed to test how genetic
             discoveries relate to developmental and biological
             characteristics of asthma. Methods In this prospective
             longitudinal study, we investigated a multilocus profile of
             genetic risk derived from published GWAS of asthma case
             status. We then tested associations between this genetic
             risk score and developmental and biological characteristics
             of asthma in participants enrolled in a population-based
             long-running birth cohort, the Dunedin Multidisciplinary
             Health and Development Study (n=1037). We used data on
             asthma onset, asthma persistence, atopy, airway
             hyper-responsiveness, incompletely reversible airflow
             obstruction, and asthma-related school and work absenteeism
             and hospital admissions obtained during nine prospective
             assessments spanning the ages of 9 to 38 years. Analyses
             included cohort members of European descent from whom
             genetic data had been obtained. Findings Of the 880 cohort
             members included in our analysis, those at higher genetic
             risk developed asthma earlier in life than did those with
             lower genetic risk (hazard ratio [HR] 1·12, 95% CI
             1·01–1·26). Of cohort members with childhood-onset
             asthma, those with higher genetic risk were more likely to
             develop life-course-persistent asthma than were those with a
             lower genetic risk (relative risk [RR] 1·36, 95% CI
             1·14–1·63). Participants with asthma at higher genetic
             risk more often had atopy (RR 1·07, 1·01–1·14), airway
             hyper-responsiveness (RR 1·16, 1·03–1·32), and
             incompletely reversible airflow obstruction (RR 1·28,
             1·04–1·57) than did those with a lower genetic risk.
             They were also more likely to miss school or work (incident
             rate ratio 1·38, 1·02–1·86) and be admitted to hospital
             (HR 1·38, 1·07–1·79) because of asthma. Genotypic
             information about asthma risk was independent of and
             additive to information derived from cohort members’
             family histories of asthma. Interpretation Our findings
             confirm that GWAS discoveries for asthma are associated with
             a childhood-onset phenotype. Genetic risk assessments might
             be able to predict which childhood-onset asthma cases remit
             and which become life-course-persistent, who might develop
             impaired lung function, and the burden of asthma in terms of
             missed school and work and hospital admissions, although
             these predictions are not sufficiently sensitive or specific
             to support immediate clinical translation.},
   Doi = {10.1016/S2213-2600(13)70101-2},
   Key = {fds253156}
}

@article{fds253228,
   Author = {Belsky, DW and Moffitt, TE and Sugden, K and Williams, B and Houts, R and McCarthy, J and Caspi, A},
   Title = {Development and evaluation of a genetic risk score for
             obesity.},
   Journal = {Biodemography Soc Biol},
   Volume = {59},
   Number = {1},
   Pages = {85-100},
   Year = {2013},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/23701538},
   Abstract = {Multi-locus profiles of genetic risk, so-called "genetic
             risk scores," can be used to translate discoveries from
             genome-wide association studies into tools for population
             health research. We developed a genetic risk score for
             obesity from results of 16 published genome-wide association
             studies of obesity phenotypes in European-descent samples.
             We then evaluated this genetic risk score using data from
             the Atherosclerosis Risk in Communities (ARIC) cohort GWAS
             sample (N = 10,745, 55% female, 77% white, 23% African
             American). Our 32-locus GRS was a statistically significant
             predictor of body mass index (BMI) and obesity among ARIC
             whites [for BMI, r = 0.13, p<1 × 10(-30); for obesity,
             area under the receiver operating characteristic curve (AUC)
             = 0.57 (95% CI 0.55-0.58)]. The GRS predicted differences in
             obesity risk net of demographic, geographic, and
             socioeconomic information. The GRS performed less well among
             African Americans. The genetic risk score we derived from
             GWAS provides a molecular measurement of genetic
             predisposition to elevated BMI and obesity.[Supplemental
             materials are available for this article. Go to the
             publisher's online edition of Biodemography and Social
             Biology for the following resource: Supplement to
             Development & Evaluation of a Genetic Risk Score for
             Obesity.].},
   Doi = {10.1080/19485565.2013.774628},
   Key = {fds253228}
}

@article{fds253160,
   Author = {Murray, CJL and Vos, T and Lozano, R and Naghavi, M and Flaxman, AD and Michaud, C and Ezzati, M and Shibuya, K and Salomon, JA and Abdalla, S and Aboyans, V and Abraham, J and Ackerman, I and Aggarwal, R and Ahn, SY and Ali, MK and Alvarado, M and Anderson, HR and Anderson, LM and Andrews,
             KG and Atkinson, C and Baddour, LM and Bahalim, AN and Barker-Collo, S and Barrero, LH and Bartels, DH and Basáñez, M-G and Baxter, A and Bell,
             ML and Benjamin, EJ and Bennett, D and Bernabé, E and Bhalla, K and Bhandari, B and Bikbov, B and Bin Abdulhak and A and Birbeck, G and Black,
             JA and Blencowe, H and Blore, JD and Blyth, F and Bolliger, I and Bonaventure, A and Boufous, S and Bourne, R and Boussinesq, M and Braithwaite, T and Brayne, C and Bridgett, L and Brooker, S and Brooks,
             P and Brugha, TS and Bryan-Hancock, C and Bucello, C and Buchbinder, R and Buckle, G and Budke, CM and Burch, M and Burney, P and Burstein, R and Calabria, B and Campbell, B and Canter, CE and Carabin, H and Carapetis,
             J and Carmona, L and Cella, C and Charlson, F and Chen, H and Cheng, AT-A and Chou, D and Chugh, SS and Coffeng, LE and Colan, SD and Colquhoun, S and Colson, KE and Condon, J and Connor, MD and Cooper, LT and Corriere, M and Cortinovis, M and de Vaccaro, KC and Couser, W and Cowie, BC and Criqui,
             MH and Cross, M and Dabhadkar, KC and Dahiya, M and Dahodwala, N and Damsere-Derry, J and Danaei, G and Davis, A and De Leo and D and Degenhardt, L and Dellavalle, R and Delossantos, A and Denenberg, J and Derrett, S and Des Jarlais and DC and Dharmaratne, SD and Dherani, M and Diaz-Torne, C and Dolk, H and Dorsey, ER and Driscoll, T and Duber, H and Ebel, B and Edmond, K and Elbaz, A and Ali, SE and Erskine, H and Erwin,
             PJ and Espindola, P and Ewoigbokhan, SE and Farzadfar, F and Feigin, V and Felson, DT and Ferrari, A and Ferri, CP and Fèvre, EM and Finucane, MM and Flaxman, S and Flood, L and Foreman, K and Forouzanfar, MH and Fowkes,
             FGR and Fransen, M and Freeman, MK and Gabbe, BJ and Gabriel, SE and Gakidou, E and Ganatra, HA and Garcia, B and Gaspari, F and Gillum, RF and Gmel, G and Gonzalez-Medina, D and Gosselin, R and Grainger, R and Grant, B and Groeger, J and Guillemin, F and Gunnell, D and Gupta, R and Haagsma, J and Hagan, H and Halasa, YA and Hall, W and Haring, D and Haro,
             JM and Harrison, JE and Havmoeller, R and Hay, RJ and Higashi, H and Hill,
             C and Hoen, B and Hoffman, H and Hotez, PJ and Hoy, D and Huang, JJ and Ibeanusi, SE and Jacobsen, KH and James, SL and Jarvis, D and Jasrasaria, R and Jayaraman, S and Johns, N and Jonas, JB and Karthikeyan, G and Kassebaum, N and Kawakami, N and Keren, A and Khoo,
             J-P and King, CH and Knowlton, LM and Kobusingye, O and Koranteng, A and Krishnamurthi, R and Laden, F and Lalloo, R and Laslett, LL and Lathlean, T and Leasher, JL and Lee, YY and Leigh, J and Levinson, D and Lim, SS and Limb, E and Lin, JK and Lipnick, M and Lipshultz, SE and Liu,
             W and Loane, M and Ohno, SL and Lyons, R and Mabweijano, J and MacIntyre,
             MF and Malekzadeh, R and Mallinger, L and Manivannan, S and Marcenes, W and March, L and Margolis, DJ and Marks, GB and Marks, R and Matsumori, A and Matzopoulos, R and Mayosi, BM and McAnulty, JH and McDermott, MM and McGill, N and McGrath, J and Medina-Mora, ME and Meltzer, M and Mensah,
             GA and Merriman, TR and Meyer, A-C and Miglioli, V and Miller, M and Miller, TR and Mitchell, PB and Mock, C and Mocumbi, AO and Moffitt, TE and Mokdad, AA and Monasta, L and Montico, M and Moradi-Lakeh, M and Moran,
             A and Morawska, L and Mori, R and Murdoch, ME and Mwaniki, MK and Naidoo,
             K and Nair, MN and Naldi, L and Narayan, KMV and Nelson, PK and Nelson, RG and Nevitt, MC and Newton, CR and Nolte, S and Norman, P and Norman, R and O'Donnell, M and O'Hanlon, S and Olives, C and Omer, SB and Ortblad, K and Osborne, R and Ozgediz, D and Page, A and Pahari, B and Pandian, JD and Rivero, AP and Patten, SB and Pearce, N and Padilla, RP and Perez-Ruiz,
             F and Perico, N and Pesudovs, K and Phillips, D and Phillips, MR and Pierce, K and Pion, S and Polanczyk, GV and Polinder, S and Pope, CA and Popova, S and Porrini, E and Pourmalek, F and Prince, M and Pullan, RL and Ramaiah, KD and Ranganathan, D and Razavi, H and Regan, M and Rehm, JT and Rein, DB and Remuzzi, G and Richardson, K and Rivara, FP and Roberts, T and Robinson, C and De Leòn and FR and Ronfani, L and Room, R and Rosenfeld,
             LC and Rushton, L and Sacco, RL and Saha, S and Sampson, U and Sanchez-Riera, L and Sanman, E and Schwebel, DC and Scott, JG and Segui-Gomez, M and Shahraz, S and Shepard, DS and Shin, H and Shivakoti,
             R and Singh, D and Singh, GM and Singh, JA and Singleton, J and Sleet, DA and Sliwa, K and Smith, E and Smith, JL and Stapelberg, NJC and Steer, A and Steiner, T and Stolk, WA and Stovner, LJ and Sudfeld, C and Syed, S and Tamburlini, G and Tavakkoli, M and Taylor, HR and Taylor, JA and Taylor,
             WJ and Thomas, B and Thomson, WM and Thurston, GD and Tleyjeh, IM and Tonelli, M and Towbin, JA and Truelsen, T and Tsilimbaris, MK and Ubeda,
             C and Undurraga, EA and van der Werf, MJ and van Os, J and Vavilala, MS and Venketasubramanian, N and Wang, M and Wang, W and Watt, K and Weatherall, DJ and Weinstock, MA and Weintraub, R and Weisskopf, MG and Weissman, MM and White, RA and Whiteford, H and Wiebe, N and Wiersma,
             ST and Wilkinson, JD and Williams, HC and Williams, SRM and Witt, E and Wolfe, F and Woolf, AD and Wulf, S and Yeh, P-H and Zaidi, AKM and Zheng,
             Z-J and Zonies, D and Lopez, AD and AlMazroa, MA and Memish,
             ZA},
   Title = {Disability-adjusted life years (DALYs) for 291 diseases and
             injuries in 21 regions, 1990-2010: a systematic analysis for
             the Global Burden of Disease Study 2010.},
   Journal = {Lancet (London, England)},
   Volume = {380},
   Number = {9859},
   Pages = {2197-2223},
   Year = {2012},
   Month = {December},
   ISSN = {0140-6736},
   url = {http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000312387000016&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=47d3190e77e5a3a53558812f597b0b92},
   Abstract = {<h4>Background</h4>Measuring disease and injury burden in
             populations requires a composite metric that captures both
             premature mortality and the prevalence and severity of
             ill-health. The 1990 Global Burden of Disease study proposed
             disability-adjusted life years (DALYs) to measure disease
             burden. No comprehensive update of disease burden worldwide
             incorporating a systematic reassessment of disease and
             injury-specific epidemiology has been done since the 1990
             study. We aimed to calculate disease burden worldwide and
             for 21 regions for 1990, 2005, and 2010 with methods to
             enable meaningful comparisons over time.<h4>Methods</h4>We
             calculated DALYs as the sum of years of life lost (YLLs) and
             years lived with disability (YLDs). DALYs were calculated
             for 291 causes, 20 age groups, both sexes, and for 187
             countries, and aggregated to regional and global estimates
             of disease burden for three points in time with strictly
             comparable definitions and methods. YLLs were calculated
             from age-sex-country-time-specific estimates of mortality by
             cause, with death by standardised lost life expectancy at
             each age. YLDs were calculated as prevalence of 1160
             disabling sequelae, by age, sex, and cause, and weighted by
             new disability weights for each health state. Neither YLLs
             nor YLDs were age-weighted or discounted. Uncertainty around
             cause-specific DALYs was calculated incorporating
             uncertainty in levels of all-cause mortality, cause-specific
             mortality, prevalence, and disability weights.<h4>Findings</h4>Global
             DALYs remained stable from 1990 (2·503 billion) to 2010
             (2·490 billion). Crude DALYs per 1000 decreased by 23% (472
             per 1000 to 361 per 1000). An important shift has occurred
             in DALY composition with the contribution of deaths and
             disability among children (younger than 5 years of age)
             declining from 41% of global DALYs in 1990 to 25% in 2010.
             YLLs typically account for about half of disease burden in
             more developed regions (high-income Asia Pacific, western
             Europe, high-income North America, and Australasia), rising
             to over 80% of DALYs in sub-Saharan Africa. In 1990, 47% of
             DALYs worldwide were from communicable, maternal, neonatal,
             and nutritional disorders, 43% from non-communicable
             diseases, and 10% from injuries. By 2010, this had shifted
             to 35%, 54%, and 11%, respectively. Ischaemic heart disease
             was the leading cause of DALYs worldwide in 2010 (up from
             fourth rank in 1990, increasing by 29%), followed by lower
             respiratory infections (top rank in 1990; 44% decline in
             DALYs), stroke (fifth in 1990; 19% increase), diarrhoeal
             diseases (second in 1990; 51% decrease), and HIV/AIDS (33rd
             in 1990; 351% increase). Major depressive disorder increased
             from 15th to 11th rank (37% increase) and road injury from
             12th to 10th rank (34% increase). Substantial heterogeneity
             exists in rankings of leading causes of disease burden among
             regions.<h4>Interpretation</h4>Global disease burden has
             continued to shift away from communicable to
             non-communicable diseases and from premature death to years
             lived with disability. In sub-Saharan Africa, however, many
             communicable, maternal, neonatal, and nutritional disorders
             remain the dominant causes of disease burden. The rising
             burden from mental and behavioural disorders,
             musculoskeletal disorders, and diabetes will impose new
             challenges on health systems. Regional heterogeneity
             highlights the importance of understanding local burden of
             disease and setting goals and targets for the post-2015
             agenda taking such patterns into account. Because of
             improved definitions, methods, and data, these results for
             1990 and 2010 supersede all previously published Global
             Burden of Disease results.<h4>Funding</h4>Bill & Melinda
             Gates Foundation.},
   Doi = {10.1016/s0140-6736(12)61689-4},
   Key = {fds253160}
}

@article{fds253161,
   Author = {Vos, T and Flaxman, AD and Naghavi, M and Lozano, R and Michaud, C and Ezzati, M and Shibuya, K and Salomon, JA and Abdalla, S and Aboyans, V and Abraham, J and Ackerman, I and Aggarwal, R and Ahn, SY and Ali, MK and Alvarado, M and Anderson, HR and Anderson, LM and Andrews, KG and Atkinson, C and Baddour, LM and Bahalim, AN and Barker-Collo, S and Barrero, LH and Bartels, DH and Basáñez, M-G and Baxter, A and Bell,
             ML and Benjamin, EJ and Bennett, D and Bernabé, E and Bhalla, K and Bhandari, B and Bikbov, B and Bin Abdulhak and A and Birbeck, G and Black,
             JA and Blencowe, H and Blore, JD and Blyth, F and Bolliger, I and Bonaventure, A and Boufous, S and Bourne, R and Boussinesq, M and Braithwaite, T and Brayne, C and Bridgett, L and Brooker, S and Brooks,
             P and Brugha, TS and Bryan-Hancock, C and Bucello, C and Buchbinder, R and Buckle, G and Budke, CM and Burch, M and Burney, P and Burstein, R and Calabria, B and Campbell, B and Canter, CE and Carabin, H and Carapetis,
             J and Carmona, L and Cella, C and Charlson, F and Chen, H and Cheng, AT-A and Chou, D and Chugh, SS and Coffeng, LE and Colan, SD and Colquhoun, S and Colson, KE and Condon, J and Connor, MD and Cooper, LT and Corriere, M and Cortinovis, M and de Vaccaro, KC and Couser, W and Cowie, BC and Criqui,
             MH and Cross, M and Dabhadkar, KC and Dahiya, M and Dahodwala, N and Damsere-Derry, J and Danaei, G and Davis, A and De Leo and D and Degenhardt, L and Dellavalle, R and Delossantos, A and Denenberg, J and Derrett, S and Des Jarlais and DC and Dharmaratne, SD and Dherani, M and Diaz-Torne, C and Dolk, H and Dorsey, ER and Driscoll, T and Duber, H and Ebel, B and Edmond, K and Elbaz, A and Ali, SE and Erskine, H and Erwin,
             PJ and Espindola, P and Ewoigbokhan, SE and Farzadfar, F and Feigin, V and Felson, DT and Ferrari, A and Ferri, CP and Fèvre, EM and Finucane, MM and Flaxman, S and Flood, L and Foreman, K and Forouzanfar, MH and Fowkes,
             FGR and Franklin, R and Fransen, M and Freeman, MK and Gabbe, BJ and Gabriel, SE and Gakidou, E and Ganatra, HA and Garcia, B and Gaspari, F and Gillum, RF and Gmel, G and Gosselin, R and Grainger, R and Groeger, J and Guillemin, F and Gunnell, D and Gupta, R and Haagsma, J and Hagan, H and Halasa, YA and Hall, W and Haring, D and Haro, JM and Harrison, JE and Havmoeller, R and Hay, RJ and Higashi, H and Hill, C and Hoen, B and Hoffman, H and Hotez, PJ and Hoy, D and Huang, JJ and Ibeanusi, SE and Jacobsen, KH and James, SL and Jarvis, D and Jasrasaria, R and Jayaraman, S and Johns, N and Jonas, JB and Karthikeyan, G and Kassebaum, N and Kawakami, N and Keren, A and Khoo, J-P and King, CH and Knowlton, LM and Kobusingye, O and Koranteng, A and Krishnamurthi, R and Lalloo, R and Laslett, LL and Lathlean, T and Leasher, JL and Lee, YY and Leigh, J and Lim, SS and Limb, E and Lin, JK and Lipnick, M and Lipshultz,
             SE and Liu, W and Loane, M and Ohno, SL and Lyons, R and Ma, J and Mabweijano,
             J and MacIntyre, MF and Malekzadeh, R and Mallinger, L and Manivannan,
             S and Marcenes, W and March, L and Margolis, DJ and Marks, GB and Marks, R and Matsumori, A and Matzopoulos, R and Mayosi, BM and McAnulty, JH and McDermott, MM and McGill, N and McGrath, J and Medina-Mora, ME and Meltzer, M and Mensah, GA and Merriman, TR and Meyer, A-C and Miglioli,
             V and Miller, M and Miller, TR and Mitchell, PB and Mocumbi, AO and Moffitt, TE and Mokdad, AA and Monasta, L and Montico, M and Moradi-Lakeh, M and Moran, A and Morawska, L and Mori, R and Murdoch,
             ME and Mwaniki, MK and Naidoo, K and Nair, MN and Naldi, L and Narayan,
             KMV and Nelson, PK and Nelson, RG and Nevitt, MC and Newton, CR and Nolte,
             S and Norman, P and Norman, R and O'Donnell, M and O'Hanlon, S and Olives,
             C and Omer, SB and Ortblad, K and Osborne, R and Ozgediz, D and Page, A and Pahari, B and Pandian, JD and Rivero, AP and Patten, SB and Pearce, N and Padilla, RP and Perez-Ruiz, F and Perico, N and Pesudovs, K and Phillips, D and Phillips, MR and Pierce, K and Pion, S and Polanczyk,
             GV and Polinder, S and Pope, CA and Popova, S and Porrini, E and Pourmalek,
             F and Prince, M and Pullan, RL and Ramaiah, KD and Ranganathan, D and Razavi, H and Regan, M and Rehm, JT and Rein, DB and Remuzzi, G and Richardson, K and Rivara, FP and Roberts, T and Robinson, C and De
             Leòn, FR and Ronfani, L and Room, R and Rosenfeld, LC and Rushton, L and Sacco, RL and Saha, S and Sampson, U and Sanchez-Riera, L and Sanman, E and Schwebel, DC and Scott, JG and Segui-Gomez, M and Shahraz, S and Shepard, DS and Shin, H and Shivakoti, R and Singh, D and Singh, GM and Singh, JA and Singleton, J and Sleet, DA and Sliwa, K and Smith, E and Smith, JL and Stapelberg, NJC and Steer, A and Steiner, T and Stolk, WA and Stovner, LJ and Sudfeld, C and Syed, S and Tamburlini, G and Tavakkoli,
             M and Taylor, HR and Taylor, JA and Taylor, WJ and Thomas, B and Thomson,
             WM and Thurston, GD and Tleyjeh, IM and Tonelli, M and Towbin, JA and Truelsen, T and Tsilimbaris, MK and Ubeda, C and Undurraga, EA and van
             der Werf, MJ and van Os, J and Vavilala, MS and Venketasubramanian,
             N and Wang, M and Wang, W and Watt, K and Weatherall, DJ and Weinstock, MA and Weintraub, R and Weisskopf, MG and Weissman, MM and White, RA and Whiteford, H and Wiersma, ST and Wilkinson, JD and Williams, HC and Williams, SRM and Witt, E and Wolfe, F and Woolf, AD and Wulf, S and Yeh,
             P-H and Zaidi, AKM and Zheng, Z-J and Zonies, D and Lopez, AD and Murray,
             CJL and AlMazroa, MA and Memish, ZA},
   Title = {Years lived with disability (YLDs) for 1160 sequelae of 289
             diseases and injuries 1990-2010: a systematic analysis for
             the Global Burden of Disease Study 2010.},
   Journal = {Lancet (London, England)},
   Volume = {380},
   Number = {9859},
   Pages = {2163-2196},
   Year = {2012},
   Month = {December},
   ISSN = {0140-6736},
   url = {http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000312387000015&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=47d3190e77e5a3a53558812f597b0b92},
   Abstract = {<h4>Background</h4>Non-fatal health outcomes from diseases
             and injuries are a crucial consideration in the promotion
             and monitoring of individual and population health. The
             Global Burden of Disease (GBD) studies done in 1990 and 2000
             have been the only studies to quantify non-fatal health
             outcomes across an exhaustive set of disorders at the global
             and regional level. Neither effort quantified uncertainty in
             prevalence or years lived with disability
             (YLDs).<h4>Methods</h4>Of the 291 diseases and injuries in
             the GBD cause list, 289 cause disability. For 1160 sequelae
             of the 289 diseases and injuries, we undertook a systematic
             analysis of prevalence, incidence, remission, duration, and
             excess mortality. Sources included published studies, case
             notification, population-based cancer registries, other
             disease registries, antenatal clinic serosurveillance,
             hospital discharge data, ambulatory care data, household
             surveys, other surveys, and cohort studies. For most
             sequelae, we used a Bayesian meta-regression method,
             DisMod-MR, designed to address key limitations in
             descriptive epidemiological data, including missing data,
             inconsistency, and large methodological variation between
             data sources. For some disorders, we used natural history
             models, geospatial models, back-calculation models (models
             calculating incidence from population mortality rates and
             case fatality), or registration completeness models (models
             adjusting for incomplete registration with health-system
             access and other covariates). Disability weights for 220
             unique health states were used to capture the severity of
             health loss. YLDs by cause at age, sex, country, and year
             levels were adjusted for comorbidity with simulation
             methods. We included uncertainty estimates at all stages of
             the analysis.<h4>Findings</h4>Global prevalence for all ages
             combined in 2010 across the 1160 sequelae ranged from fewer
             than one case per 1 million people to 350,000 cases per 1
             million people. Prevalence and severity of health loss were
             weakly correlated (correlation coefficient -0·37). In 2010,
             there were 777 million YLDs from all causes, up from 583
             million in 1990. The main contributors to global YLDs were
             mental and behavioural disorders, musculoskeletal disorders,
             and diabetes or endocrine diseases. The leading specific
             causes of YLDs were much the same in 2010 as they were in
             1990: low back pain, major depressive disorder,
             iron-deficiency anaemia, neck pain, chronic obstructive
             pulmonary disease, anxiety disorders, migraine, diabetes,
             and falls. Age-specific prevalence of YLDs increased with
             age in all regions and has decreased slightly from 1990 to
             2010. Regional patterns of the leading causes of YLDs were
             more similar compared with years of life lost due to
             premature mortality. Neglected tropical diseases, HIV/AIDS,
             tuberculosis, malaria, and anaemia were important causes of
             YLDs in sub-Saharan Africa.<h4>Interpretation</h4>Rates of
             YLDs per 100,000 people have remained largely constant over
             time but rise steadily with age. Population growth and
             ageing have increased YLD numbers and crude rates over the
             past two decades. Prevalences of the most common causes of
             YLDs, such as mental and behavioural disorders and
             musculoskeletal disorders, have not decreased. Health
             systems will need to address the needs of the rising numbers
             of individuals with a range of disorders that largely cause
             disability but not mortality. Quantification of the burden
             of non-fatal health outcomes will be crucial to understand
             how well health systems are responding to these challenges.
             Effective and affordable strategies to deal with this rising
             burden are an urgent priority for health systems in most
             parts of the world.<h4>Funding</h4>Bill & Melinda Gates
             Foundation.},
   Doi = {10.1016/s0140-6736(12)61729-2},
   Key = {fds253161}
}

@article{fds253237,
   Author = {Loeber, R and Menting, B and Lynam, DR and Moffitt, TE and Stouthamer-Loeber, M and Stallings, R and Farrington, DP and Pardini,
             D},
   Title = {Findings from the Pittsburgh Youth Study: cognitive
             impulsivity and intelligence as predictors of the age-crime
             curve.},
   Journal = {Journal of the American Academy of Child and Adolescent
             Psychiatry},
   Volume = {51},
   Number = {11},
   Pages = {1136-1149},
   Year = {2012},
   Month = {November},
   ISSN = {0890-8567},
   url = {http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000310939300006&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=47d3190e77e5a3a53558812f597b0b92},
   Abstract = {<h4>Objective</h4>This article first summarizes key research
             findings from the Pittsburgh Youth Study from 1987 to the
             present, and focuses on delinquency in 1,517 young men who
             have been followed up from late childhood into their 20s.
             Second, the article addresses how indicators of self-control
             prospectively predict later offending, and whether the
             prediction shows individual difference in the age-crime
             curve, particularly the up-slope, peak, and down-slope of
             that curve.<h4>Method</h4>Longitudinal analyses were
             conducted on a sample of boys in the middle sample of the
             Pittsburgh Youth Study (n = 422), whose cognitive
             impulsivity and intelligence were assessed at about age 12
             years. Criminal records on the sample were until age
             28.<h4>Results</h4>The results show that cognitive
             impulsivity and intelligence, measured between ages 12 and
             13 by means of psychometric tests, predicted the age-crime
             curve. The age-arrest curve was substantially higher in boys
             with high cognitive impulsivity and in boys with low IQ.
             However, there was a significant interaction between
             cognitive impulsivity and intelligence. For boys with high
             IQ, cognitive impulsivity was associated with a greater
             escalation in the prevalence of offending during early
             adolescence, followed by a more rapid decline in offending
             as boys entered early adulthood with a slight subsequent
             increase in criminal offending then occurring late 20. In
             contrast, there was no evidence that cognitive impulsivity
             independently influenced criminal offending at any
             developmental period for boys with low IQ.<h4>Conclusions</h4>The
             results are discussed in terms of interventions to reduce
             individuals' delinquency from childhood through early
             adulthood and lower the age-crime curve for populations.
             However, the association was complex because it was
             moderated by both age and intelligence.},
   Doi = {10.1016/j.jaac.2012.08.019},
   Key = {fds253237}
}

@misc{fds253236,
   Author = {Meier, MH and Caspi, A and Ambler, A and Harrington, H and Houts, R and Keefe, RSE and McDonald, K and Ward, A and Poulton, R and Moffitt,
             TE},
   Title = {Persistent cannabis users show neuropsychological decline
             from childhood to midlife.},
   Journal = {Proc Natl Acad Sci U S A},
   Volume = {109},
   Number = {40},
   Pages = {E2657-E2664},
   Year = {2012},
   Month = {October},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/22927402},
   Abstract = {Recent reports show that fewer adolescents believe that
             regular cannabis use is harmful to health. Concomitantly,
             adolescents are initiating cannabis use at younger ages, and
             more adolescents are using cannabis on a daily basis. The
             purpose of the present study was to test the association
             between persistent cannabis use and neuropsychological
             decline and determine whether decline is concentrated among
             adolescent-onset cannabis users. Participants were members
             of the Dunedin Study, a prospective study of a birth cohort
             of 1,037 individuals followed from birth (1972/1973) to age
             38 y. Cannabis use was ascertained in interviews at ages 18,
             21, 26, 32, and 38 y. Neuropsychological testing was
             conducted at age 13 y, before initiation of cannabis use,
             and again at age 38 y, after a pattern of persistent
             cannabis use had developed. Persistent cannabis use was
             associated with neuropsychological decline broadly across
             domains of functioning, even after controlling for years of
             education. Informants also reported noticing more cognitive
             problems for persistent cannabis users. Impairment was
             concentrated among adolescent-onset cannabis users, with
             more persistent use associated with greater decline.
             Further, cessation of cannabis use did not fully restore
             neuropsychological functioning among adolescent-onset
             cannabis users. Findings are suggestive of a neurotoxic
             effect of cannabis on the adolescent brain and highlight the
             importance of prevention and policy efforts targeting
             adolescents.},
   Doi = {10.1073/pnas.1206820109},
   Key = {fds253236}
}

@article{fds253222,
   Author = {Thomson, WM and Caspi, A and Moffitt, T and Broadbent,
             J},
   Title = {'Contamination' by personality},
   Journal = {European Journal of Oral Sciences},
   Volume = {120},
   Number = {5},
   Pages = {473},
   Publisher = {WILEY},
   Year = {2012},
   Month = {October},
   ISSN = {0909-8836},
   url = {http://dx.doi.org/10.1111/j.1600-0722.2012.00996.x},
   Doi = {10.1111/j.1600-0722.2012.00996.x},
   Key = {fds253222}
}

@article{fds253233,
   Author = {Odgers, CL and Caspi, A and Bates, CJ and Sampson, RJ and Moffitt,
             TE},
   Title = {Systematic social observation of children's neighborhoods
             using Google Street View: a reliable and cost-effective
             method.},
   Journal = {Journal of child psychology and psychiatry, and allied
             disciplines},
   Volume = {53},
   Number = {10},
   Pages = {1009-1017},
   Year = {2012},
   Month = {October},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/22676812},
   Abstract = {<h4>Background</h4>Children growing up in poor versus
             affluent neighborhoods are more likely to spend time in
             prison, develop health problems and die at an early age. The
             question of how neighborhood conditions influence our
             behavior and health has attracted the attention of public
             health officials and scholars for generations. Online tools
             are now providing new opportunities to measure neighborhood
             features and may provide a cost effective way to advance our
             understanding of neighborhood effects on child
             health.<h4>Method</h4>A virtual systematic social
             observation (SSO) study was conducted to test whether Google
             Street View could be used to reliably capture the
             neighborhood conditions of families participating in the
             Environmental-Risk (E-Risk) Longitudinal Twin Study.
             Multiple raters coded a subsample of 120 neighborhoods and
             convergent and discriminant validity was evaluated on the
             full sample of over 1,000 neighborhoods by linking virtual
             SSO measures to: (a) consumer based geo-demographic
             classifications of deprivation and health, (b) local
             resident surveys of disorder and safety, and (c) parent and
             teacher assessments of children's antisocial behavior,
             prosocial behavior, and body mass index.<h4>Results</h4>High
             levels of observed agreement were documented for signs of
             physical disorder, physical decay, dangerousness and street
             safety. Inter-rater agreement estimates fell within the
             moderate to substantial range for all of the scales (ICCs
             ranged from .48 to .91). Negative neighborhood features,
             including SSO-rated disorder and decay and dangerousness
             corresponded with local resident reports, demonstrated a
             graded relationship with census-defined indices of
             socioeconomic status, and predicted higher levels of
             antisocial behavior among local children. In addition,
             positive neighborhood features, including SSO-rated street
             safety and the percentage of green space, were associated
             with higher prosocial behavior and healthy weight status
             among children.<h4>Conclusions</h4>Our results support the
             use of Google Street View as a reliable and cost effective
             tool for measuring both negative and positive features of
             local neighborhoods.},
   Doi = {10.1111/j.1469-7610.2012.02565.x},
   Key = {fds253233}
}

@article{fds253143,
   Author = {Shalev, I and Moffitt, TE and Caspi, A},
   Title = {Childhood trauma and telomere maintenance},
   Journal = {European Journal of Psychotraumatology},
   Volume = {3},
   Publisher = {Informa UK Limited},
   Year = {2012},
   Month = {September},
   ISSN = {2000-8198},
   url = {http://dx.doi.org/10.3402/ejpt.v3i0.19505},
   Doi = {10.3402/ejpt.v3i0.19505},
   Key = {fds253143}
}

@misc{fds253238,
   Author = {Odgers, CL and Caspi, A and Russell, MA and Sampson, RJ and Arseneault,
             L and Moffitt, TE},
   Title = {Supportive parenting mediates neighborhood socioeconomic
             disparities in children's antisocial behavior from ages 5 to
             12.},
   Journal = {Development and psychopathology},
   Volume = {24},
   Number = {3},
   Pages = {705-721},
   Year = {2012},
   Month = {August},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/22781850},
   Abstract = {We report a graded relationship between neighborhood
             socioeconomic status (SES) and children's antisocial
             behavior that (a) can be observed at school entry, (b)
             widens across childhood, (c) remains after controlling for
             family-level SES and risk, and (d) is completely mediated by
             maternal warmth and parental monitoring (defined throughout
             as supportive parenting). The children were participants in
             the Environmental Risk Longitudinal Twin Study (N = 2,232),
             which prospectively tracked the development of children and
             their neighborhoods across childhood. Direct and independent
             effects of neighborhood-level SES on children's antisocial
             behavior were observed as early as age 5, and the gap
             between children living in deprived versus more affluent
             neighborhoods widened as children approached adolescence. By
             age 12, the effect of neighborhood SES on children's
             antisocial behavior was as large as the effect observed for
             our most robust predictor of antisocial behavior: sex (Cohen
             d = 0.51 when comparing children growing up in deprived vs.
             more affluent neighborhoods in comparison to Cohen d = 0.53
             when comparing antisocial behavior among boys vs. girls).
             However, these relatively large differences in children's
             levels and rate of change in antisocial behavior across
             deprived versus more affluent neighborhoods were completely
             mediated by supportive parenting practices. The implications
             of our findings for studying and reducing socioeconomic
             disparities in antisocial behavior among children are
             discussed.},
   Doi = {10.1017/s0954579412000326},
   Key = {fds253238}
}

@article{fds253223,
   Author = {Belsky, DW and Moffitt, TE and Houts, R and Bennett, GG and Biddle, AK and Blumenthal, JA and Evans, JP and Harrington, H and Sugden, K and Williams, B and Poulton, R and Caspi, A},
   Title = {Polygenic risk, rapid childhood growth, and the development
             of obesity: evidence from a 4-decade longitudinal
             study.},
   Journal = {Arch Pediatr Adolesc Med},
   Volume = {166},
   Number = {6},
   Pages = {515-521},
   Year = {2012},
   Month = {June},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/22665028},
   Abstract = {OBJECTIVE: To test how genomic loci identified in
             genome-wide association studies influence the development of
             obesity. DESIGN: A 38-year prospective longitudinal study of
             a representative birth cohort. SETTING: The Dunedin
             Multidisciplinary Health and Development Study, Dunedin, New
             Zealand. PARTICIPANTS: One thousand thirty-seven male and
             female study members. MAIN EXPOSURES: We assessed genetic
             risk with a multilocus genetic risk score. The genetic risk
             score was composed of single-nucleotide polymorphisms
             identified in genome-wide association studies of
             obesity-related phenotypes. We assessed family history from
             parent body mass index data collected when study members
             were 11 years of age. MAIN OUTCOME MEASURES: Body mass index
             growth curves, developmental phenotypes of obesity, and
             adult obesity outcomes were defined from anthropometric
             assessments at birth and at 12 subsequent in-person
             interviews through 38 years of age. RESULTS: Individuals
             with higher genetic risk scores were more likely to be
             chronically obese in adulthood. Genetic risk first
             manifested as rapid growth during early childhood. Genetic
             risk was unrelated to birth weight. After birth, children at
             higher genetic risk gained weight more rapidly and reached
             adiposity rebound earlier and at a higher body mass index.
             In turn, these developmental phenotypes predicted adult
             obesity, mediating about half the genetic effect on adult
             obesity risk. Genetic associations with growth and obesity
             risk were independent of family history, indicating that the
             genetic risk score could provide novel information to
             clinicians. CONCLUSIONS: Genetic variation linked with
             obesity risk operates, in part, through accelerating growth
             in the early childhood years after birth. Etiological
             research and prevention strategies should target early
             childhood to address the obesity epidemic.},
   Doi = {10.1001/archpediatrics.2012.131},
   Key = {fds253223}
}

@article{fds304725,
   Author = {Slutske, WS and Moffitt, TE and Poulton, R and Caspi,
             A},
   Title = {Undercontrolled temperament at age 3 predicts disordered
             gambling at age 32: a longitudinal study of a complete birth
             cohort.},
   Journal = {Psychological science},
   Volume = {23},
   Number = {5},
   Pages = {510-516},
   Year = {2012},
   Month = {May},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/22457426},
   Abstract = {Using data from the large, 30-year prospective Dunedin
             cohort study, we examined whether preexisting individual
             differences in childhood temperament predicted adulthood
             disordered gambling (a diagnosis covering the full continuum
             of gambling-related problems). A 90-min observational
             assessment at age 3 was used to categorize children into
             five temperament groups, including one primarily
             characterized by behavioral and emotional undercontrol. The
             children with undercontrolled temperament at 3 years of age
             were more than twice as likely to evidence disordered
             gambling at ages 21 and 32 than were children who were
             well-adjusted at age 3. These associations could not be
             explained by differences in childhood IQ or family
             socioeconomic status. Cleanly demonstrating the temporal
             relation between behavioral undercontrol and adult
             disordered gambling is an important step toward building
             more developmentally sensitive theories of disordered
             gambling and may put researchers in a better position to
             begin considering potential routes to disordered-gambling
             prevention through enhancing self-control and emotional
             regulation.},
   Doi = {10.1177/0956797611429708},
   Key = {fds304725}
}

@article{fds253219,
   Author = {Shearer, DM and Thomson, WM and Caspi, A and Moffitt, TE and Broadbent,
             JM and Poulton, R},
   Title = {Family history and oral health: findings from the Dunedin
             Study.},
   Journal = {Community dentistry and oral epidemiology},
   Volume = {40},
   Number = {2},
   Pages = {105-115},
   Year = {2012},
   Month = {April},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/22022823},
   Abstract = {<h4>Context</h4>The effects of the oral health status of one
             generation on that of the next within families are
             unclear.<h4>Objectives</h4>  To determine whether parental
             oral health history is a risk factor for oral
             disease.<h4>Methods</h4>Oral examination and interview data
             were collected during the age-32 assessments in the Dunedin
             Study. Parental data were also collected on this occasion.
             The sample was divided into two familial-risk groups for
             caries/tooth loss (high risk and low risk) based on parents'
             self-reported history of tooth loss at the age-32 assessment
             interview.<h4>Main outcome measures</h4>Probands' dental
             caries and tooth loss status at age 32, together with
             lifelong dental caries trajectory (age 5-32).<h4>Results</h4>Caries/tooth
             loss risk analysis was conducted for 640 proband-parent
             groups. Reference groups were the low-familial-risk groups.
             After controlling for confounding factors (sex, episodic use
             of dental services, socio-economic status and plaque
             trajectory), the prevalence ratio (PR) for having lost 1+
             teeth by age 32 for the high-familial-risk group was 1.41
             [95% confidence interval (CI) 1.05, 1.88] and the rate ratio
             for DMFS at age 32 was 1.41 (95% CI 1.24, 1.60). In the
             high-familial-risk group, the PR of following a high caries
             trajectory was 2.05 (95% CI 1.37, 3.06). Associations were
             strongest when information was available about both parents'
             oral health. Nonetheless, when information was available for
             one parent only, associations were significant for some
             outcomes.<h4>Conclusions</h4>People with poor oral health
             tend to have parents with poor oral health. Family/parental
             history of oral health is a valid representation of the
             intricacies of the shared genetic and environmental factors
             that contribute to an individual's oral health status.
             Associations are strongest when data from both parents can
             be obtained.},
   Doi = {10.1111/j.1600-0528.2011.00641.x},
   Key = {fds253219}
}

@article{fds253240,
   Author = {Gregory, AM and Moffitt, TE and Ambler, A and Arseneault, L and Houts,
             RM and Caspi, A},
   Title = {Maternal insomnia and children's family socialization
             environments.},
   Journal = {Sleep},
   Volume = {35},
   Number = {4},
   Pages = {579-582},
   Year = {2012},
   Month = {April},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/22467996},
   Abstract = {<h4>Study objectives</h4>To examine concurrent associations
             between maternal insomnia and different aspects of the
             family socialization environment.<h4>Design</h4>Mothers
             reported on their symptoms of insomnia in a private
             standardized interview and interviewers evaluated the family
             socialization environment using the Coder's
             Inventory.<h4>Setting</h4>Assessments were conducted in
             participants' homes within the U.K.<h4>Patients or
             participants</h4>One thousand one hundred sixteen mothers of
             British children enrolled in the Environmental Risk (E-Risk)
             study were invited to participate when their children were
             aged 12 years.<h4>Interventions</h4>N/A.<h4>Measurements and
             results</h4>After controlling for family socioeconomic
             status (SES), mothers' relationship status, and maternal
             depression, maternal insomnia was associated with a poorer
             family socialization environment (β = -0.10, [95%
             confidence intervals (CI) = -0.16, -0.04], P < 0.001). When
             family socialization environment subscales were examined,
             after controlling for family SES, mothers' relationship
             status, and maternal depression, maternal insomnia was
             associated with greater chaos (β = 0.09, [95% CI = 0.03,
             0.15], P = 0.002), greater child neglect (β = 0.13, [95% CI
             = 0.07, 0.18], P < 0.001), less happiness (β = -0.13, [95%
             CI = -0.18, -0.07], P < 0.001), less child stimulation (β =
             -0.06, [95% CI = -0.11, 0.00], P = 0.043), but not poorer
             state of the home, such as orderliness (β = -0.04, [95% CI
             = -0.10, 0.02], P = 0.182).<h4>Conclusions</h4>Maternal
             insomnia is associated with the family socialization
             environment. This finding emphasizes the need to consider
             insomnia in the family context.},
   Doi = {10.5665/sleep.1750},
   Key = {fds253240}
}

@article{fds253104,
   Author = {Keltner, D and Moffitt, TE and Stouthamer-Loeber,
             M},
   Title = {Facial Expressions of Emotion and Psychopathology in
             Adolescent Boys},
   Pages = {532-548},
   Publisher = {Oxford University Press},
   Year = {2012},
   Month = {March},
   url = {http://dx.doi.org/10.1093/acprof:oso/9780195179644.003.0026},
   Abstract = {This chapter tests the three hypotheses concerning the
             relations between facial expressions of emotion and
             adolescent psychopathology. First, it is expected that
             externalizing adolescents, who are prone to aggressive and
             delinquent behavior, show more anger. Second, it is expected
             that internalizing adolescents, who are prone to anxiety,
             depression, withdrawn behavior, and somatic complaints, show
             more fear and sadness. The last hypothesis referred to
             embarrassment, which is believed to contribute to
             psychological adjustment by motivating people to avoid
             social-moral transgressions and to apologize for
             transgressions that have occurred. The results provide the
             first evidence for the claim that different adolescent
             disorders are manifest in distinct facial expressions of
             emotion. Furthermore, it documented links between adolescent
             psychopathology and emotional expression even though the
             measures of emotion and psychopathology came from two
             sources (the child's teacher and the child) rather than one,
             and emotional responses were assessed in one brief
             situation.},
   Doi = {10.1093/acprof:oso/9780195179644.003.0026},
   Key = {fds253104}
}

@article{fds253243,
   Author = {Shakoor, S and Jaffee, SR and Bowes, L and Ouellet-Morin, I and Andreou,
             P and Happé, F and Moffitt, TE and Arseneault, L},
   Title = {A prospective longitudinal study of children's theory of
             mind and adolescent involvement in bullying.},
   Journal = {Journal of child psychology and psychiatry, and allied
             disciplines},
   Volume = {53},
   Number = {3},
   Pages = {254-261},
   Year = {2012},
   Month = {March},
   ISSN = {0021-9630},
   url = {http://dx.doi.org/10.1111/j.1469-7610.2011.02488.x},
   Abstract = {<h4>Background</h4>Theory of mind (ToM) allows the
             understanding and prediction of other people's behaviours
             based on their mental states (e.g. beliefs). It is important
             for healthy social relationships and thus may contribute
             towards children's involvement in bullying. The present
             study investigated whether children involved in bullying
             during early adolescence had poor ToM in
             childhood.<h4>Method</h4>Participants were members of the
             Environmental Risk (E-Risk) Longitudinal Twin Study, a
             nationally representative sample of 2,232 children and their
             families. We visited families when children were 5, 7, 10
             and 12 years. ToM was assessed when the children were 5
             years using eight standardized tasks. Identification of
             those children who were involved in bullying as victims,
             bullies and bully-victims using mothers', teachers' and
             children's reports was carried out when they were 12 years'
             old.<h4>Results</h4>Poor ToM predicted becoming a victim
             (effect size, d = 0.26), bully (d = 0.25) or bully-victim (d
             = 0.44) in early adolescence. These associations remained
             for victims and bully-victims when child-specific (e.g. IQ)
             and family factors (e.g. child maltreatment) were controlled
             for. Emotional and behavioural problems during middle
             childhood did not modify the association between poor ToM
             and adolescent bullying experiences.<h4>Conclusion</h4>Identifying
             and supporting children with poor ToM early in life could
             help reduce their vulnerability for involvement in bullying
             and thus limit its adverse effects on mental
             health.},
   Doi = {10.1111/j.1469-7610.2011.02488.x},
   Key = {fds253243}
}

@article{fds253250,
   Author = {Belsky, DW and Caspi, A and Arseneault, L and Bleidorn, W and Fonagy, P and Goodman, M and Houts, R and Moffitt, TE},
   Title = {Etiological features of borderline personality related
             characteristics in a birth cohort of 12-year-old
             children.},
   Journal = {Development and psychopathology},
   Volume = {24},
   Number = {1},
   Pages = {251-265},
   Year = {2012},
   Month = {February},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/22293008},
   Abstract = {It has been reported that borderline personality related
             characteristics can be observed in children, and that these
             characteristics are associated with increased risk for the
             development of borderline personality disorder. It is not
             clear whether borderline personality related characteristics
             in children share etiological features with adult borderline
             personality disorder. We investigated the etiology of
             borderline personality related characteristics in a
             longitudinal cohort study of 1,116 pairs of same-sex twins
             followed from birth through age 12 years. Borderline
             personality related characteristics measured at age 12 years
             were highly heritable, were more common in children who had
             exhibited poor cognitive function, impulsivity, and more
             behavioral and emotional problems at age 5 years, and
             co-occurred with symptoms of conduct disorder, depression,
             anxiety, and psychosis. Exposure to harsh treatment in the
             family environment through age 10 years predicted borderline
             personality related characteristics at age 12 years. This
             association showed evidence of environmental mediation and
             was stronger among children with a family history of
             psychiatric illness, consistent with diathesis-stress models
             of borderline etiology. Results indicate that borderline
             personality related characteristics in children share
             etiological features with borderline personality disorder in
             adults and suggest that inherited and environmental risk
             factors make independent and interactive contributions to
             borderline etiology.},
   Doi = {10.1017/s0954579411000812},
   Key = {fds253250}
}

@article{fds253110,
   Author = {Hussong, AM and Curran, PJ and Moffit, TE and Caspi,
             A},
   Title = {Testing turning points using latest growth curve models:
             Competing models of substance abuse and desistance in young
             adulthood},
   Pages = {90-113},
   Publisher = {Routledge},
   Year = {2012},
   Month = {January},
   url = {http://dx.doi.org/10.4324/9780203843147},
   Doi = {10.4324/9780203843147},
   Key = {fds253110}
}

@article{fds213395,
   Author = {Global Burden of Disease Study Diseases and Injuries
             Group},
   Title = {Global burden of diseases and injuries for 291 causes, 21
             regions, 1990-2010: A systematic analysis},
   Journal = {The Lancet},
   Year = {2012},
   Key = {fds213395}
}

@article{fds213396,
   Author = {Global Burden of Disease Study Diseases and Injuries
             Group},
   Title = {The global burden of non-fatal health outcomes for 1,160
             sequelae of 291 diseases and injuries, for 1990-2010: A
             systematic analysis},
   Journal = {The Lancet},
   Year = {2012},
   Key = {fds213396}
}

@misc{fds213392,
   Author = {Odgers, CL and Caspi, A and Bates, CJ and Sampson, RJ and Moffitt, TE},
   Title = {Systematic social observations of local neighborhoods using
             Google Street View: A reliable and cost-effective
             tool.},
   Journal = {Journal of Child Psychology and Psychiatry},
   Volume = {53},
   Number = {10},
   Pages = {1009-1017},
   Year = {2012},
   url = {http://dx.doi.org/10.1111/j.1469-7610.2012.02565.x},
   Doi = {10.1111/j.1469-7610.2012.02565.x},
   Key = {fds213392}
}

@article{fds253157,
   Author = {Gunduz Cinar and O and Macpherson, KP and Cinar, R and Gamble George and J and Sugden, K and Williams, B and Godlewski, G and Ramikie, TS and Gorka,
             AX and Alapafuja, SO and Nikas, SP and Makriyannis, A and Poulton, R and Patel, S and Hariri, AR and Caspi, A and Moffitt, TE and Kunos, G and Holmes, A},
   Title = {Convergent translational evidence of a role for anandamide
             in amygdala-mediated fear extinction, threat processing and
             stress-reactivity},
   Journal = {Molecular psychiatry},
   Volume = {18},
   Number = {7},
   Pages = {813-823},
   Year = {2012},
   ISSN = {1359-4184},
   url = {http://dx.doi.org/10.1038/mp.2012.72},
   Abstract = {Endocannabinoids are released 'on-demand' on the basis of
             physiological need, and can be pharmacologically augmented
             by inhibiting their catabolic degradation. The
             endocannabinoid anandamide is degraded by the catabolic
             enzyme fatty acid amide hydrolase (FAAH). Anandamide is
             implicated in the mediation of fear behaviors, including
             fear extinction, suggesting that selectively elevating brain
             anandamide could modulate plastic changes in fear. Here we
             first tested this hypothesis with preclinical experiments
             employing a novel, potent and selective FAAH inhibitor,
             AM3506 (5-(4-hydroxyphenyl)pentanesulfonyl fluoride).
             Systemic AM3506 administration before extinction decreased
             fear during a retrieval test in a mouse model of impaired
             extinction. AM3506 had no effects on fear in the absence of
             extinction training, or on various non-fear-related
             measures. Anandamide levels in the basolateral amygdala were
             increased by extinction training and augmented by systemic
             AM3506, whereas application of AM3506 to amygdala slices
             promoted long-term depression of inhibitory transmission, a
             form of synaptic plasticity linked to extinction. Further
             supporting the amygdala as effect-locus, the fear-reducing
             effects of systemic AM3506 were blocked by intra-amygdala
             infusion of a CB1 receptor antagonist and were fully
             recapitulated by intra-amygdala infusion of AM3506. On the
             basis of these preclinical findings, we hypothesized that
             variation in the human FAAH gene would predict individual
             differences in amygdala threat-processing and stress-coping
             traits. Consistent with this, carriers of a low-expressing
             FAAH variant (385A allele; rs324420) exhibited quicker
             habituation of amygdala reactivity to threat, and had lower
             scores on the personality trait of stress-reactivity. Our
             findings show that augmenting amygdala anandamide enables
             extinction-driven reductions in fear in mouse and may
             promote stress-coping in humans.Molecular Psychiatry advance
             online publication, 12 June 2012; doi:10.1038/mp.2012.72.},
   Doi = {10.1038/mp.2012.72},
   Key = {fds253157}
}

@article{fds336537,
   Author = {Fisher, H and Moffitt, TE and Belsky, D and Houts, R and Arseneault, L and Caspi, A},
   Title = {Bullying victimisation increases risk of self-harm in early
             adolescence},
   Journal = {British Medical Journal E-pub.},
   Volume = {344},
   Pages = {e2683},
   Year = {2012},
   url = {http://dx.doi.org/10.1136/bmj.e2683},
   Doi = {10.1136/bmj.e2683},
   Key = {fds336537}
}

@article{fds253221,
   Author = {Fisher, HL and Moffitt, TE and Houts, RM and Belsky, DW and Arseneault,
             L and Caspi, A},
   Title = {Bullying victimisation and risk of self harm in early
             adolescence: longitudinal cohort study},
   Journal = {BMJ},
   Volume = {344},
   Pages = {e2683-e2683},
   Year = {2012},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/22539176},
   Abstract = {OBJECTIVES: To test whether frequent bullying victimisation
             in childhood increases the likelihood of self harming in
             early adolescence, and to identify which bullied children
             are at highest risk of self harm. DESIGN: The Environmental
             Risk (E-Risk) longitudinal study of a nationally
             representative UK cohort of 1116 twin pairs born in 1994-95
             (2232 children). SETTING: England and Wales, United Kingdom.
             PARTICIPANTS: Children assessed at 5, 7, 10, and 12 years of
             age. MAIN OUTCOME MEASURES: Relative risks of children’s
             self harming behaviour in the six months before their 12th
             birthday. RESULTS: Self harm data were available for 2141
             children. Among children aged 12 who had self harmed (2.9%;
             n=62), more than half were victims of frequent bullying
             (56%; n=35). Exposure to frequent bullying predicted higher
             rates of self harm even after children’s pre-morbid
             emotional and behavioural problems, low IQ, and family
             environmental risks were taken into account (bullying
             victimisation reported by mother: adjusted relative risk
             1.92, 95% confidence interval 1.18 to 3.12; bullying
             victimisation reported by child: 2.44, 1.36 to 4.40).
             Victimised twins were more likely to self harm than were
             their non-victimised twin sibling (bullying victimisation
             reported by mother: 13/162 v 3/162, ratio=4.3, 95%
             confidence interval 1.3 to 14.0; bullying victimisation
             reported by child: 12/144 v 7/144, ratio=1.7, 0.71 to 4.1).
             Compared with bullied children who did not self harm,
             bullied children who self harmed were distinguished by a
             family history of attempted/completed suicide, concurrent
             mental health problems, and a history of physical
             maltreatment by an adult. CONCLUSIONS: Prevention of
             non-suicidal self injury in young adolescents should focus
             on helping bullied children to cope more appropriately with
             their distress. Programmes should target children who have
             additional mental health problems, have a family history of
             attempted/completed suicide, or have been maltreated by an
             adult.},
   Doi = {10.1136/bmj.e2683},
   Key = {fds253221}
}

@article{fds253230,
   Author = {Moffitt, and TE, and Tank, TK-GT},
   Title = {Childhood exposure to violence and lifelong health: Clinical
             intervention science and stress biology research join
             forces.},
   Journal = {Development and Psychopathology, 25th Anniversary Special
             issue},
   Volume = {25},
   Number = {4 Pt 2},
   Pages = {1619-1634},
   Year = {2012},
   url = {http://dx.doi.org/10.1017/s0954579413000801},
   Abstract = {Many young people who are mistreated by an adult, victimized
             by bullies, criminally assaulted, or who witness domestic
             violence react to this violence exposure by developing
             behavioral, emotional, or learning problems. What is less
             well known is that adverse experiences like violence
             exposure can lead to hidden physical alterations inside a
             child's body, alterations that may have adverse effects on
             life-long health. We discuss why this is important for the
             field of developmental psychopathology and for society, and
             we recommend that stress-biology research and intervention
             science join forces to tackle the problem. We examine the
             evidence base in relation to stress-sensitive measures for
             the body (inflammatory reactions, telomere erosion,
             epigenetic methylation, and gene expression) and brain
             (mental disorders, neuroimaging, and neuropsychological
             testing). We also review promising interventions for
             families, couples, and children that have been designed to
             reduce the effects of childhood violence exposure. We invite
             intervention scientists and stress-biology researchers to
             collaborate in adding stress-biology measures to randomized
             clinical trials of interventions intended to reduce effects
             of violence exposure and other traumas on young
             people.},
   Doi = {10.1017/s0954579413000801},
   Key = {fds253230}
}

@article{fds253234,
   Author = {Gunduz-Cinar, O and MacPherson, KP and Cinar, R and Gamble-George, J and Sugden, K and Williams, B and Ramikie, TS and Gorka, AX and Makriyannis,
             A and Poulton, R and Patel, S and Hariri, AR and Caspi, A and Moffitt, TE and Kunos, G and Holmes, A},
   Title = {Enhanced endocannabinoids promote fear plasticity},
   Journal = {Molecular Psychiatry},
   Year = {2012},
   Key = {fds253234}
}

@misc{fds253235,
   Author = {Belsky, DW and Moffitt, TE and Houts, RM and Bennett, GG and Biddle, AK and Blumethal, JA and Evans, JP and Harrington, HL and Sugden, K and Williams, B and Poulton, R and Caspi, A},
   Title = {Polygenic risk for adult obesity is mediated by rapid
             childhood growth: Evidence from a 4-decade longitudinal
             study},
   Journal = {Archives of Pediatric and Adolescent Medicine},
   Volume = {166},
   Number = {6},
   Pages = {515-521},
   Year = {2012},
   Key = {fds253235}
}

@article{fds253239,
   Author = {Slutske, W and Moffitt, TE and Poulton, R and Caspi,
             A},
   Title = {Under-controlled child temperament predicts adult problem
             gambling},
   Journal = {Psychological Science},
   Volume = {23},
   Number = {5},
   Pages = {510-516},
   Year = {2012},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/22457426},
   Abstract = {Using data from the large, 30-year prospective Dunedin
             cohort study, we examined whether preexisting individual
             differences in childhood temperament predicted adulthood
             disordered gambling (a diagnosis covering the full continuum
             of gambling-related problems). A 90-min observational
             assessment at age 3 was used to categorize children into
             five temperament groups, including one primarily
             characterized by behavioral and emotional undercontrol. The
             children with undercontrolled temperament at 3 years of age
             were more than twice as likely to evidence disordered
             gambling at ages 21 and 32 than were children who were
             well-adjusted at age 3. These associations could not be
             explained by differences in childhood IQ or family
             socioeconomic status. Cleanly demonstrating the temporal
             relation between behavioral undercontrol and adult
             disordered gambling is an important step toward building
             more developmentally sensitive theories of disordered
             gambling and may put researchers in a better position to
             begin considering potential routes to disordered-gambling
             prevention through enhancing self-control and emotional
             regulation.},
   Doi = {10.1177/0956797611429708},
   Key = {fds253239}
}

@article{fds253242,
   Author = {Piquero, NL and Moffitt, TE},
   Title = {Can childhood factors predict workplace deviance?},
   Journal = {Justice Quarterly},
   Volume = {31},
   Number = {4},
   Pages = {664-692},
   Year = {2012},
   url = {http://dx.doi.org/10.1080/07418825.2012.661446},
   Abstract = {Compared to the more common focus on street crime, empirical
             research on workplace deviance has been hampered by highly
             select samples, cross-sectional research designs, and
             limited inclusion of relevant predictor variables that bear
             on important theoretical debates. A key debate concerns the
             extent to which childhood conduct-problem trajectories
             influence crime over the life-course, including adults'
             workplace crime, whether childhood low self-control is a
             more important determinant than trajectories, and/or whether
             each or both of these childhood factors relate to later
             criminal activity. This paper provides evidence on this
             debate by examining two types of workplace deviance:
             production and property deviance separately for males and
             females. We use data from the Dunedin Multidisciplinary
             Health and Development Study, a birth cohort followed into
             adulthood, to examine how childhood factors (conduct-problem
             trajectories and low self-control) and then adult job
             characteristics predict workplace deviance at age 32.
             Analyses revealed that none of the childhood factors matter
             for predicting female deviance in the workplace but that
             conduct-problem trajectories did account for male workplace
             deviance.},
   Doi = {10.1080/07418825.2012.661446},
   Key = {fds253242}
}

@article{fds253217,
   Author = {Uher, R and Caspi, A and Houts, R and Sugden, K and Williams, B and Poulton, R and Moffitt, TE},
   Title = {Serotonin transporter gene moderates childhood
             maltreatment's effects on persistent but not single-episode
             depression: replications and implications for resolving
             inconsistent results.},
   Journal = {Journal of affective disorders},
   Volume = {135},
   Number = {1-3},
   Pages = {56-65},
   Year = {2011},
   Month = {December},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/21439648},
   Abstract = {<h4>Background</h4>Genetic and environmental factors shape
             life-long vulnerability to depression, but most
             gene-environment interaction (G×E) research has focused on
             cross-sectional assessments rather than life-course
             phenotypes. This study tests the hypothesis that the G×E
             involving the length polymorphism in the
             serotonin-transporter-gene-linked-promoter-region (5-HTTLPR)
             and childhood maltreatment is specific to depression that
             runs a persistent course in adulthood.<h4>Methods</h4>The
             hypothesis is tested in two cohorts. Men and women in the
             Dunedin Study (N=847), New Zealand, followed to age 32 years
             with 96% retention and women in the E-Risk Study (N=930),
             England, followed to age 40 years with 96% retention.
             Diagnoses of past-year major depressive episode were
             established at four separate assessments. Depression
             diagnosed on two or more occasions was considered
             persistent.<h4>Results</h4>In both cohorts, statistical
             tests of gene-environment interactions showed positive
             results for persistent depression but not single-episode
             depression. Individuals with two short 5-HTTLPR alleles and
             childhood maltreatment had elevated risk of persistent but
             not single-episode depression.<h4>Limitations</h4>Some cases
             of recurrent depression may have been misclassified as
             single-episode due to non-contiguous assessment windows, but
             this would have a conservative effect on the findings.
             Chronic and recurrent depression could not be reliably
             distinguished due to non-contiguous periods of assessment.
             Therefore, the term persistent depression is used to
             describe either chronic or recurrent course.<h4>Conclusions</h4>The
             specific effect on persistent depression increases the
             significance of this G×E for public health. Research that
             does not distinguish persistent course may underestimate
             G×E effects and account for some replication failures in
             G×E research.},
   Doi = {10.1016/j.jad.2011.03.010},
   Key = {fds253217}
}

@article{fds253218,
   Author = {Grisham, JR and Fullana, MA and Mataix-Cols, D and Moffitt, TE and Caspi, A and Poulton, R},
   Title = {Risk factors prospectively associated with adult
             obsessive-compulsive symptom dimensions and
             obsessive-compulsive disorder.},
   Journal = {Psychological medicine},
   Volume = {41},
   Number = {12},
   Pages = {2495-2506},
   Year = {2011},
   Month = {December},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/21672296},
   Abstract = {<h4>Background</h4>Very few longitudinal studies have
             evaluated prospective neurodevelopmental and psychosocial
             risk factors for obsessive-compulsive disorder (OCD).
             Furthermore, despite the heterogeneous nature of OCD, no
             research has examined risk factors for its primary symptom
             dimensions, such as contamination/washing.<h4>Method</h4>Potential
             risk factors for symptoms or diagnosis of OCD in adulthood
             and for specific adult obsessive-compulsive (OC) symptom
             dimensions were examined in the Dunedin Study birth cohort.
             The presence of obsessions and compulsions and psychological
             disorders was assessed using the Diagnostic Interview
             Schedule (DIS) at ages 26 and 32 years. Individuals with a
             diagnosis of OCD at either age (n=36) were compared to both
             a healthy control group (n=613) and an anxious control group
             (n=310) to determine whether associations between a risk
             factor and an OCD diagnosis were specific.<h4>Results</h4>Childhood
             neurodevelopmental, behavioral, personality and
             environmental risk factors were associated with a diagnosis
             of OCD and with OC symptoms at ages 26 and 32. Social
             isolation, retrospectively reported physical abuse and
             negative emotionality were specific predictors of an adult
             OCD diagnosis. Of note, most risk factors were associated
             with OC symptoms in adulthood and several risk factors
             predicted specific OCD dimensions. Perinatal insults were
             linked to increased risk for symmetry/ordering and shameful
             thoughts dimensions, whereas poor childhood motor skills
             predicted the harm/checking dimension. Difficult
             temperament, internalizing symptoms and conduct problems in
             childhood also predicted specific symptom dimensions and
             lower IQ non-specifically predicted increased risk for most
             dimensions.<h4>Conclusions</h4>The current findings
             underscore the need for a dimensional approach in evaluating
             childhood risk factors for obsessions and
             compulsions.},
   Doi = {10.1017/s0033291711000894},
   Key = {fds253218}
}

@misc{fds253264,
   Author = {Ouellet-Morin, I and Odgers, CL and Danese, A and Bowes, L and Shakoor,
             S and Papadopoulos, AS and Caspi, A and Moffitt, TE and Arseneault,
             L},
   Title = {Blunted cortisol responses to stress signal social and
             behavioral problems among maltreated/bullied 12-year-old
             children.},
   Journal = {Biological psychiatry},
   Volume = {70},
   Number = {11},
   Pages = {1016-1023},
   Year = {2011},
   Month = {December},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/21839988},
   Abstract = {<h4>Background</h4>Evidence from animal and human studies
             suggests that early-life stress such as physical
             maltreatment has long-lasting effects on the
             hypothalamic-pituitary-adrenal (HPA) axis and is associated
             with blunted HPA axis reactivity in adulthood. Few studies
             have investigated whether blunted HPA axis reactivity
             observed in children exposed to early-life stress signals
             social, emotional, and behavioral problems.<h4>Methods</h4>Participants
             were 190 12-year-old children (50.5% males) recruited from
             the Environmental Risk Longitudinal Twin Study, a nationally
             representative 1994 to 1995 cohort of families with twins.
             Cortisol responses to psychosocial stress were measured in
             maltreated/bullied (n = 64) and comparison children (n =
             126). We ascertained maltreatment and bullying victimization
             using mothers' reports and assessed children's social,
             emotional, and behavioral problems at ages 5 and 12 using
             mothers' and teachers' reports.<h4>Results</h4>Piecewise
             multilevel growth curve analyses indicated that
             maltreated/bullied and comparison children showed distinct
             cortisol responses to stress. Specifically,
             maltreated/bullied children had lower cortisol responses
             than comparison children who exhibited a significant
             increase. Lower cortisol responses were, in turn, associated
             with more social and behavioral problems among
             maltreated/bullied children.<h4>Conclusions</h4>These
             findings provide support for the influence of childhood harm
             on blunted HPA axis reactivity and its potential impact on
             children's functioning. Our findings emphasize the need to
             integrate stress biomarkers in guiding prevention efforts
             for young victims.},
   Doi = {10.1016/j.biopsych.2011.06.017},
   Key = {fds253264}
}

@article{fds253249,
   Author = {Thomson, WM and Caspi, A and Poulton, R and Moffitt, TE and Broadbent,
             JM},
   Title = {Personality and oral health.},
   Journal = {European journal of oral sciences},
   Volume = {119},
   Number = {5},
   Pages = {366-372},
   Year = {2011},
   Month = {October},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/21896053},
   Abstract = {We investigated age-26 personality characteristics and
             age-32 oral health in a prospective study of a complete
             birth cohort born in Dunedin, New Zealand. Personality was
             measured using the Multidimensional Personality
             Questionnaire (MPQ). Oral health was measured using the
             short-form Oral Health Impact Profile (OHIP-14), a global
             measure, and dental examinations. Personality profiles were
             constructed for 916 individuals (50.8% men) using
             standardized MPQ scores, and multivariate analyses examined
             their association with oral health. Those reporting 1+
             OHIP-14 impacts had higher Negative Emotionality scores (and
             lower Constraint and Positive Emotionality MPQ superfactor
             scores) than those who did not. After controlling for
             gender, clinical status, and the other two MPQ superfactors,
             those scoring higher on Negative Emotionality had a greater
             risk of reporting 1+ OHIP-14 impacts, as well as 3+ OHIP-14
             impacts and worse-than-average oral health. They also had a
             greater risk of having lost at least one tooth from caries
             and of having 3+ decayed surfaces. Personality
             characteristics appear to shape self-reports of oral health.
             Personality is also a risk factor for clinical disease
             status, at least with respect to dental caries and its
             sequelae. Because the attitudes and values tapped into by
             personality tests can be altered by brief cognitive
             interventions, those might be useful in preventive
             dentistry.},
   Doi = {10.1111/j.1600-0722.2011.00840.x},
   Key = {fds253249}
}

@article{fds253263,
   Author = {Zimmermann, P and Brückl, T and Nocon, A and Pfister, H and Binder, EB and Uhr, M and Lieb, R and Moffitt, TE and Caspi, A and Holsboer, F and Ising,
             M},
   Title = {Interaction of FKBP5 gene variants and adverse life events
             in predicting depression onset: results from a 10-year
             prospective community study.},
   Journal = {The American journal of psychiatry},
   Volume = {168},
   Number = {10},
   Pages = {1107-1116},
   Year = {2011},
   Month = {October},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/21865530},
   Abstract = {<h4>Objective</h4>The binding protein FKBP5 is an important
             modulator of the function of the glucocorticoid receptor,
             the main receptor of the stress hormone system. This turns
             the FKBP5 gene into a key candidate for gene-environment
             interactions, which are considered critical for pathogenesis
             of stress-related disorders. The authors explored
             gene-environment interactions between FKBP5 gene variants
             and adverse life events in predicting the first occurrence
             of a major depressive episode.<h4>Method</h4>The analyses
             were based on 884 Caucasians in a 10-year prospective
             community study. At baseline, they were 14-24 years old and
             did not fulfill criteria for a major depressive episode. The
             DSM-IV-based Munich Composite International Diagnostic
             Interview was used to assess adverse life events preceding
             baseline and major depressive episodes during follow-up. On
             the basis of previous findings, five single-nucleotide
             polymorphisms (SNPs) within the FKBP5 gene were selected for
             genotyping.<h4>Results</h4>While the authors did not observe
             genetic main effects, they found interactions between the
             five SNPs and traumatic (but not separation) events, with
             the strongest effect for severe trauma. The effect of trauma
             on incident major depressive episodes was evident among
             subjects homozygous for the minor alleles but not subjects
             with other genotypes. The findings were replicated in the
             U.K. Environmental Risk Longitudinal Twin
             Study.<h4>Conclusions</h4>These hypothesis-driven results
             suggest that an interaction between FKBP5 genotype and
             trauma is involved in the onset of depression. Subjects
             homozygous for the minor alleles of the investigated FKBP5
             SNPs seem to be particularly sensitive to effects of trauma
             exposure in terms of triggering depression
             onset.},
   Doi = {10.1176/appi.ajp.2011.10111577},
   Key = {fds253263}
}

@article{fds253247,
   Author = {Fontaine, NMG and McCrory, EJP and Boivin, M and Moffitt, TE and Viding,
             E},
   Title = {Predictors and outcomes of joint trajectories of
             callous-unemotional traits and conduct problems in
             childhood.},
   Journal = {Journal of abnormal psychology},
   Volume = {120},
   Number = {3},
   Pages = {730-742},
   Year = {2011},
   Month = {August},
   ISSN = {0021-843X},
   url = {http://dx.doi.org/10.1037/a0022620},
   Abstract = {Callous-unemotional (CU) traits are associated with
             antisocial and delinquent behaviors in children and
             represent a potential risk factor for adult psychopathy.
             However, there is a paucity of longitudinal research that
             explores the development of these traits, their longitudinal
             association with conduct problems (CP), and their
             psychosocial predictors and outcomes. Using a large sample
             of children followed longitudinally from the Twins Early
             Development Study (N=9,578), we described the joint
             developmental trajectories of CU traits and CP during
             childhood (between ages 7 and 12) and examined the child-
             and family-level predictors (4 years old) and concomitant
             outcomes (12 years old) associated with the trajectories.
             The developmental trajectories were characterized with
             teachers' ratings of CU traits and CP from ages 7 to 12.
             Using general growth mixture modeling, we identified four
             trajectories of CU traits (stable high, increasing,
             decreasing, and stable low) and two trajectories of CP (high
             and low). Compared with the children who followed a low
             trajectory of CU traits and CP, those who followed a high
             trajectory of CU traits and CP had more negative child- and
             family-level predictors at 4 years (including CP,
             hyperactivity, negative parental discipline, and chaos in
             the home). Children with high or increasing levels of CU
             traits and concomitant high levels of CP presented the most
             negative outcomes at 12 years (including hyperactivity, peer
             problems, emotional problems, and negative parental
             feelings). Children with high CU traits and concomitant high
             levels of CP in childhood should be prioritized for targeted
             intervention.},
   Doi = {10.1037/a0022620},
   Key = {fds253247}
}

@article{fds253248,
   Author = {Ouellet-Morin, I and Danese, A and Bowes, L and Shakoor, S and Ambler,
             A and Pariante, CM and Papadopoulos, AS and Caspi, A and Moffitt, TE and Arseneault, L},
   Title = {A discordant monozygotic twin design shows blunted cortisol
             reactivity among bullied children.},
   Journal = {Journal of the American Academy of Child and Adolescent
             Psychiatry},
   Volume = {50},
   Number = {6},
   Pages = {574-582.e3},
   Year = {2011},
   Month = {June},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/21621141},
   Abstract = {<h4>Objective</h4>Childhood adverse experiences are known to
             engender persistent changes in stress-related systems and
             brain structures involved in mood, cognition, and behavior
             in animal models. Uncertainty remains about the causal
             effect of early stressful experiences on physiological
             response to stress in human beings, as the impact of these
             experiences has rarely been investigated while controlling
             for both genetic and shared environmental
             influences.<h4>Method</h4>We tested whether bullying
             victimization, a repeated adverse experience in childhood,
             influences cortisol responses to a psychosocial stress test
             (PST) using a discordant monozygotic (MZ) twin design.
             Thirty pairs (43.3% males) of 12-year-old MZ twins
             discordant for bullying victimization were identified in the
             Environmental Risk (E-Risk) Longitudinal Twin Study, a
             nationally representative 1994-1995 cohort of families with
             twins.<h4>Results</h4>Bullied and nonbullied MZ twins showed
             distinct patterns of cortisol secretion after the PST.
             Specifically, bullied twins exhibited a blunted cortisol
             response compared with their nonbullied MZ co-twins, who
             showed the expected increase. This difference in cortisol
             response to stress could not be attributed to children's
             genetic makeup, their familial environments, pre-existing
             and concomitant individual factors, or the perception of
             stress and emotional response to the PST.<h4>Conclusion</h4>Results
             from this natural experiment provide support for a causal
             effect of adverse childhood experiences on the
             neuroendocrine response to stress.},
   Doi = {10.1016/j.jaac.2011.02.015},
   Key = {fds253248}
}

@article{fds253245,
   Author = {Shearer, DM and Thomson, WM and Caspi, A and Moffitt, TE and Broadbent,
             JM and Poulton, R},
   Title = {Inter-generational continuity in periodontal health:
             findings from the Dunedin family history
             study.},
   Journal = {Journal of clinical periodontology},
   Volume = {38},
   Number = {4},
   Pages = {301-309},
   Year = {2011},
   Month = {April},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/21281332},
   Abstract = {<h4>Objective</h4>To determine whether parental periodontal
             disease history is a risk factor for periodontal disease in
             adult offspring.<h4>Methods</h4>Proband periodontal
             examination [combined attachment loss (CAL) at age 32, and
             incidence of CAL from ages 26 to 32] and interview data were
             collected during the age-32 assessments in the Dunedin
             Study. Parental data were also collected. The sample was
             divided into two familial-risk groups for periodontal
             disease (high- and low-risk) based on parents' self-reported
             periodontal disease.<h4>Results</h4>Periodontal risk
             analysis involved 625 proband-parent(s) groups. After
             controlling for confounding factors, the high-familial-risk
             periodontal group was more likely to have 1+ sites with 4+mm
             CAL [relative risk (RR) 1.45; 95% confidence interval (CI)
             1.11-1.88], 2+ sites with 4+mm CAL (RR 1.45; 95% CI
             1.03-2.05), 1+ sites with 5+mm CAL (RR 1.60; 95% CI
             1.02-2.50), and 1+ sites with 3+mm incident CAL (RR 1.64;
             95% CI 1.01-2.66) than the low-familial-risk group.
             Predictive validity was enhanced when information was
             available from both parents.<h4>Conclusions</h4>Parents with
             poor periodontal health tend to have offspring with poor
             periodontal health. Family/parental history of oral health
             is a valid representation of the shared genetic and
             environmental factors that contribute to an individual's
             periodontal status, and may help to predict patient
             prognosis and preventive treatment need.},
   Doi = {10.1111/j.1600-051x.2011.01704.x},
   Key = {fds253245}
}

@article{fds253246,
   Author = {Shakoor, S and Jaffee, SR and Andreou, P and Bowes, L and Ambler, AP and Caspi, A and Moffitt, TE and Arseneault, L},
   Title = {Mothers and children as informants of bullying
             victimization: results from an epidemiological cohort of
             children.},
   Journal = {Journal of abnormal child psychology},
   Volume = {39},
   Number = {3},
   Pages = {379-387},
   Year = {2011},
   Month = {April},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/20938734},
   Abstract = {Stressful events early in life can affect children's mental
             health problems. Collecting valid and reliable information
             about children's bad experiences is important for research
             and clinical purposes. This study aimed to (1) investigate
             whether mothers and children provide valid reports of
             bullying victimization, (2) examine the inter-rater
             reliability between the two informants, (3) test the
             predictive validity of their reports with children's
             emotional and behavioral problems and (4) compare the
             genetic and environmental etiology of bullying victimization
             as reported by mothers and children. We assessed bullying
             victimization in the Environmental-Risk (E-Risk)
             Longitudinal Twin Study, a nationally-representative sample
             of 1,116 families with twins. We collected reports from
             mothers and children during private interviews, including
             detailed narratives. Findings showed that we can rely on
             mothers and children as informants of bullying
             victimization: both informants provided information which
             adhered to the definition of bullying as involving repeated
             hurtful actions between peers in the presence of a power
             imbalance. Although mothers and children modestly agreed
             with each other about who was bullied during primary and
             secondary school, reports of bullying victimization from
             both informants were similarly associated with children's
             emotional and behavioral problems and provided similar
             estimates of genetic and environmental influences. Findings
             from this study suggest that collecting information from
             multiple informants is ideal to capture all instances of
             bullying victimization. However, in the absence of child
             self-reports, mothers can be considered as a viable
             alternative, and vice versa.},
   Doi = {10.1007/s10802-010-9463-5},
   Key = {fds253246}
}

@article{fds253261,
   Author = {Danese, A and Caspi, A and Williams, B and Ambler, A and Sugden, K and Mika, J and Werts, H and Freeman, J and Pariante, CM and Moffitt, TE and Arseneault, L},
   Title = {Biological embedding of stress through inflammation
             processes in childhood.},
   Journal = {Molecular psychiatry},
   Volume = {16},
   Number = {3},
   Pages = {244-246},
   Year = {2011},
   Month = {March},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/20157309},
   Doi = {10.1038/mp.2010.5},
   Key = {fds253261}
}

@article{fds253244,
   Author = {Moffitt, TE and Arseneault, L and Belsky, D and Dickson, N and Hancox,
             RJ and Harrington, H and Houts, R and Poulton, R and Roberts, BW and Ross,
             S and Sears, MR and Thomson, WM and Caspi, A},
   Title = {A gradient of childhood self-control predicts health,
             wealth, and public safety.},
   Journal = {Proceedings of the National Academy of Sciences of the
             United States of America},
   Volume = {108},
   Number = {7},
   Pages = {2693-2698},
   Year = {2011},
   Month = {February},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/21262822},
   Abstract = {Policy-makers are considering large-scale programs aimed at
             self-control to improve citizens' health and wealth and
             reduce crime. Experimental and economic studies suggest such
             programs could reap benefits. Yet, is self-control important
             for the health, wealth, and public safety of the population?
             Following a cohort of 1,000 children from birth to the age
             of 32 y, we show that childhood self-control predicts
             physical health, substance dependence, personal finances,
             and criminal offending outcomes, following a gradient of
             self-control. Effects of children's self-control could be
             disentangled from their intelligence and social class as
             well as from mistakes they made as adolescents. In another
             cohort of 500 sibling-pairs, the sibling with lower
             self-control had poorer outcomes, despite shared family
             background. Interventions addressing self-control might
             reduce a panoply of societal costs, save taxpayers money,
             and promote prosperity.},
   Doi = {10.1073/pnas.1010076108},
   Key = {fds253244}
}

@article{fds253262,
   Author = {Arseneault, L and Cannon, M and Fisher, HL and Polanczyk, G and Moffitt,
             TE and Caspi, A},
   Title = {Childhood trauma and children's emerging psychotic symptoms:
             A genetically sensitive longitudinal cohort
             study.},
   Journal = {The American journal of psychiatry},
   Volume = {168},
   Number = {1},
   Pages = {65-72},
   Year = {2011},
   Month = {January},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/20952460},
   Abstract = {<h4>Objective</h4>Using longitudinal and prospective
             measures of trauma during childhood, the authors assessed
             the risk of developing psychotic symptoms associated with
             maltreatment, bullying, and accidents in a nationally
             representative U.K. cohort of young twins.<h4>Method</h4>Data
             were from the Environmental Risk Longitudinal Twin Study,
             which follows 2,232 twin children and their families.
             Mothers were interviewed during home visits when children
             were ages 5, 7, 10, and 12 on whether the children had
             experienced maltreatment by an adult, bullying by peers, or
             involvement in an accident. At age 12, children were asked
             about bullying experiences and psychotic symptoms.
             Children's reports of psychotic symptoms were verified by
             clinicians.<h4>Results</h4>Children who experienced
             mal-treatment by an adult (relative risk=3.16, 95%
             CI=1.92-5.19) or bullying by peers (relative risk=2.47, 95%
             CI=1.74-3.52) were more likely to report psychotic symptoms
             at age 12 than were children who did not experience such
             traumatic events. The higher risk for psychotic symptoms was
             observed whether these events occurred early in life or
             later in childhood. The risk associated with childhood
             trauma remained significant in analyses controlling for
             children's gender, socioeconomic deprivation, and IQ; for
             children's early symptoms of internalizing or externalizing
             problems; and for children's genetic liability to developing
             psychosis. In contrast, the risk associated with accidents
             was small (relative risk=1.47, 95% CI=1.02-2.13) and
             inconsistent across ages.<h4>Conclusions</h4>Trauma
             characterized by intention to harm is associated with
             children's reports of psychotic symptoms. Clinicians working
             with children who report early symptoms of psychosis should
             inquire about traumatic events such as maltreatment and
             bullying.},
   Doi = {10.1176/appi.ajp.2010.10040567},
   Key = {fds253262}
}

@misc{fds198722,
   Author = {Ouellet-Morin, I. and Danese, A. and Bowes, L. and Shakoor, S. and Ambler, A. and Pariante, C. and Papadopoulos, A. and Caspi, A
             Moffitt and T.E. and Arseneault, L.},
   Title = {A discordant MZ twin design shows blunted cortisol
             reactivity among bullied children},
   Journal = {Journal of the American Academy of Child and Adolescent
             Psychiatry},
   Volume = {50},
   Pages = {574-582},
   Year = {2011},
   Key = {fds198722}
}

@article{fds336538,
   Author = {Shearer, DM and Thomson, WM and Caspi, A and Moffitt, TE and Poulton,
             R},
   Title = {Family history and oral health: findings from the Dunedin
             Family History Study},
   Journal = {Community Dentistry and Oral Epidemiology},
   Year = {2011},
   Key = {fds336538}
}

@article{fds253227,
   Author = {Bowes, L and Maughan, B and Ball, H and Shakoor, S and Ouellet Morin and I and Caspi, A and Moffitt, TE and Arseneault, L},
   Title = {Chronic bullying victimization across school transition: The
             role of genetic and environmental influences},
   Journal = {Development and Psychopathology},
   Volume = {25},
   Number = {2},
   Pages = {333-346},
   Year = {2011},
   url = {http://dx.doi.org/10.1017/s0954579412001095},
   Abstract = {We investigated the antecedents and consequences of chronic
             victimization by bullies across a school transition using a
             genetically sensitive longitudinal design. Data were from
             the Environmental Risk Longitudinal Twin Study (E-Risk), an
             epidemiological cohort of 2,232 children. We used mothers'
             and children's reports of bullying victimization during
             primary school and early secondary school. Children who
             experienced frequent victimization at both time points were
             classed as "chronic victims" and were found to have an
             increased risk for mental health problems and academic
             difficulties compared to children who were bullied only in
             primary school, children bullied for the first time in
             secondary school, and never-bullied children. Biometric
             analyses revealed that stability in victimization over this
             period was influenced primarily by genetic and shared
             environmental factors. Regression analyses showed that
             children's early characteristics such as preexistent
             adjustment difficulties and IQ predicted chronic versus
             transitory victimization. Family risk factors for chronic
             victimization included socioeconomic disadvantage, low
             maternal warmth, and maltreatment. Our results suggest that
             bullying intervention programs should consider the role of
             the victims' behaviors and family background in increasing
             vulnerability to chronic victimization. Our study highlights
             the importance of widening antibullying interventions to
             include families to reduce the likelihood of children
             entering a pathway toward chronic victimization.},
   Doi = {10.1017/s0954579412001095},
   Key = {fds253227}
}

@article{fds253258,
   Author = {Grisham, JR and Fullana, MA and Mataix Cols and D and Moffitt, TE and Caspi, A and Poulton, R},
   Title = {Childhood risk factors associated with adult
             obsessive-compulsive symptoms and obsessive-compulsive
             disorder},
   Journal = {Psychological Medicine},
   Year = {2011},
   Key = {fds253258}
}

@article{fds336539,
   Author = {Uher, R and Caspi, A and Houts, R and Sugden, K and Williams, B and Poulton, R and Moffitt, TE},
   Title = {Serotonin transporter gene moderates childhood
             maltreatment’s effects on persistent but not
             single-episode depression: Replications and implications for
             resolving inconsistent results},
   Journal = {J of Affective Disorders},
   Pages = {On-line publication},
   Year = {2011},
   Key = {fds336539}
}

@article{fds253216,
   Author = {Houts, RM and Caspi, A and Pianta, RC and Arseneault, L and Moffitt,
             TE},
   Title = {The challenging pupil in the classroom: the effect of the
             child on the teacher.},
   Journal = {Psychological science},
   Volume = {21},
   Number = {12},
   Pages = {1802-1810},
   Year = {2010},
   Month = {December},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/21078897},
   Abstract = {Teaching children requires effort, and some children
             naturally require more effort than others. In this study, we
             tested whether teacher effort devoted to individual children
             varies as a function of each child's personal
             characteristics. In a nationwide longitudinal study of 1,102
             pairs of twins followed for 7 years, between the ages of 5
             and 12 years, we asked teachers about the effort they
             invested in each child in our study. We found that teacher
             effort was a function of heritable child characteristics,
             that a child's challenging behavior assessed at 5 years of
             age predicted teacher effort toward the same child at 12
             years of age, and that challenging child behavior and
             teacher effort share a common etiology with respect to
             children's genes. We found that child effects accounted for
             a significant proportion of variance in teacher effort, but
             also observed variation in effort exerted by teachers that
             could not be attributed to children's behavior. Treating
             children who exhibit challenging behavior and enhancing
             teachers' skills in managing such behavior could increase
             the time and energy teachers have to deliver their
             curriculum in class.},
   Doi = {10.1177/0956797610388047},
   Key = {fds253216}
}

@article{fds287927,
   Author = {Pardini, DA and Frick, PJ and Moffitt, TE},
   Title = {Building an evidence base for DSM-5 conceptualizations of
             oppositional defiant disorder and conduct disorder:
             introduction to the special section.},
   Journal = {Journal of abnormal psychology},
   Volume = {119},
   Number = {4},
   Pages = {683-688},
   Year = {2010},
   Month = {November},
   ISSN = {0021-843X},
   url = {http://dx.doi.org/10.1037/a0021441},
   Abstract = {The DSM-5 ADHD and Disruptive Behavior Disorders Work Group
             recently outlined a research agenda designed to support
             possible revisions to the diagnostic criteria for
             oppositional defiant disorder (ODD) and conduct disorder
             (CD). Some of the areas in need of further investigation
             include (a) examining the clinical utility of the current
             diagnostic system in girls, (b) further clarifying the
             developmental progression from ODD to CD, (c) determining
             whether facets of ODD symptoms can help explain heterotypic
             continuity and enhance predictive validity, (d) evaluating
             the clinical utility of a new subtyping scheme for CD on the
             basis of the presence of callous-unemotional traits, and (e)
             comparing the clinical utility of dimensional versus
             categorical conceptualizations of ODD and CD. This special
             section was organized in an attempt to provide data on these
             issues using a diverse array of longitudinal data sets
             consisting of both epidemiological and clinic-based samples
             that collectively cover a large developmental span ranging
             from childhood through early adulthood.},
   Doi = {10.1037/a0021441},
   Key = {fds287927}
}

@article{fds253266,
   Author = {Belsky, DW and Moffitt, TE and Arseneault, L and Melchior, M and Caspi,
             A},
   Title = {Context and sequelae of food insecurity in children's
             development.},
   Journal = {American journal of epidemiology},
   Volume = {172},
   Number = {7},
   Pages = {809-818},
   Year = {2010},
   Month = {October},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/20716700},
   Abstract = {The authors examined the role of food insecurity in the
             etiology of children's cognitive and mental health problems.
             Data from a prospective longitudinal study of 1,116 United
             Kingdom families with twins (sample constructed in
             1999-2000) were used to test associations among household
             food insecurity; income; maternal personality; household
             sensitivity to children's needs; and children's cognitive,
             behavioral, and emotional development. Food-insecure
             children had lower IQs and higher levels of behavioral and
             emotional problems relative to their peers. After
             differences in household income, the personalities of
             children's mothers, and the sensitivity of household
             organization to children's needs were accounted for,
             food-insecure children had moderately higher levels of
             emotional problems relative to food-secure children (β =
             0.22, P = 0.02). Differences in children's cognitive
             development were accounted for by household income, and
             differences in their behavioral development were accounted
             for by their mothers' personalities and their households'
             sensitivity to children's needs. Results suggest that food
             insecurity was associated with school-aged children's
             emotional problems but not with their cognitive or
             behavioral problems after accounting for differences in the
             home environments in which children were reared. Mothers'
             personality and household sensitivity to children's needs
             may present challenges to improving outcomes of children
             with food insecurity.},
   Doi = {10.1093/aje/kwq201},
   Key = {fds253266}
}

@article{fds253265,
   Author = {Wong, CCY and Caspi, A and Williams, B and Craig, IW and Houts, R and Ambler, A and Moffitt, TE and Mill, J},
   Title = {A longitudinal study of epigenetic variation in
             twins.},
   Journal = {Epigenetics},
   Volume = {5},
   Number = {6},
   Pages = {516-526},
   Year = {2010},
   Month = {August},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/20505345},
   Abstract = {DNA methylation is a key epigenetic mechanism involved in
             the developmental regulation of gene expression. Alterations
             in DNA methylation are established contributors to
             inter-individual phenotypic variation and have been
             associated with disease susceptibility. The degree to which
             changes in loci-specific DNA methylation are under the
             influence of heritable and environmental factors is largely
             unknown. In this study, we quantitatively measured DNA
             methylation across the promoter regions of the dopamine
             receptor 4 gene (DRD4), the serotonin transporter gene
             (SLC6A4/SERT) and the X-linked monoamine oxidase A gene
             (MAOA) using DNA sampled at both ages 5 and 10 years in 46
             MZ twin-pairs and 45 DZ twin-pairs (total n=182). Our data
             suggest that DNA methylation differences are apparent
             already in early childhood, even between genetically
             identical individuals, and that individual differences in
             methylation are not stable over time. Our
             longitudinal-developmental study suggests that environmental
             influences are important factors accounting for
             interindividual DNA methylation differences, and that these
             influences differ across the genome. The observation of
             dynamic changes in DNA methylation over time highlights the
             importance of longitudinal research designs for epigenetic
             research.},
   Doi = {10.4161/epi.5.6.12226},
   Key = {fds253265}
}

@article{fds253268,
   Author = {Sugden, K and Arseneault, L and Harrington, H and Moffitt, TE and Williams, B and Caspi, A},
   Title = {Serotonin transporter gene moderates the development of
             emotional problems among children following bullying
             victimization.},
   Journal = {Journal of the American Academy of Child and Adolescent
             Psychiatry},
   Volume = {49},
   Number = {8},
   Pages = {830-840},
   Year = {2010},
   Month = {August},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/20643316},
   Abstract = {<h4>Objective</h4>Bullying is the act of intentionally and
             repeatedly causing harm to someone who has difficulty
             defending him- or herself, and is a relatively widespread
             school-age phenomenon. Being the victim of bullying is
             associated with a broad spectrum of emotional problems;
             however, not all children who are bullied go on to develop
             such problems.<h4>Method</h4>We tested the hypothesis that
             the relationship between bullying victimization and
             emotional problems was moderated by variation in the
             serotonin transporter (5-HTT) gene in 2,232 British children
             comprising the Environmental Risk (E-Risk) study
             cohort.<h4>Results</h4>Our data supported the hypothesis
             that children's bullying victimization leads to their
             developing emotional problems, and that genetic variation in
             the 5-HTTLPR moderates this relationship. Specifically,
             frequently bullied children with the SS genotype were at
             greater risk for developing emotional problems at age 12
             than were children with the SL or LL genotype. Furthermore,
             we demonstrated that this genetic moderation persisted (a)
             after controlling for children's previctimization emotional
             problems by assessing intraindividual change in problems
             between ages 5 and 12 years, and (b) after controlling for
             other risk factors shared by children growing up in the same
             family by comparing emotional problems in twins discordant
             for bullying victimization.<h4>Conclusions</h4>These
             findings are further evidence that the 5-HTTLPR moderates
             the risk of emotional disturbance after exposure to
             stressful events.},
   Doi = {10.1016/j.jaac.2010.01.024},
   Key = {fds253268}
}

@article{fds253267,
   Author = {Poulton, R and Moffitt, TE},
   Title = {The Dunedin Multidisciplinary Health and Development Study:
             tips and traps from a 40-year longitudinal
             study},
   Journal = {The ISSBD Newsletter},
   Year = {2010},
   Month = {July},
   Key = {fds253267}
}

@article{fds253269,
   Author = {Bowes, L and Maughan, B and Caspi, A and Moffitt, TE and Arseneault,
             L},
   Title = {Families promote emotional and behavioural resilience to
             bullying: evidence of an environmental effect.},
   Journal = {Journal of child psychology and psychiatry, and allied
             disciplines},
   Volume = {51},
   Number = {7},
   Pages = {809-817},
   Year = {2010},
   Month = {July},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/20132419},
   Abstract = {<h4>Background</h4>Bullied children are at risk for later
             emotional and behavioural problems. 'Resilient' children
             function better than would be expected given their
             experience of bullying victimisation. This study examined
             the role of families in promoting resilience following
             bullying victimisation in primary school.<h4>Method</h4>Data
             were from the Environmental Risk (E-Risk) Study which
             describes a nationally representative sample of 1,116 twin
             pairs and their families. We used mothers' and children's
             reports to examine bullying victimisation during primary
             school and mothers' and teachers' reports to measure
             children's emotional and behavioural adjustment at ages 10
             and 12. We used mothers' and interviewers' reports to derive
             measures of protective factors in the home including
             maternal warmth, sibling warmth and positive atmosphere at
             home.<h4>Results</h4>Results from linear regression models
             showed that family factors were associated with children's
             resilience to bullying victimisation. Maternal warmth,
             sibling warmth and a positive atmosphere at home were
             particularly important in bullied children compared to
             non-bullied children in promoting emotional and behavioural
             adjustment. We used a twin differences design to separate
             out environmental protective factors in twins who are
             genetically identical. Differences in maternal warmth
             between twins from genetically identical monozygotic pairs
             concordant for bullying victimisation were correlated with
             twin differences in behavioural problems (r = -.23) such
             that the twin who received the most warmth had fewer
             behavioural problems. This shows that maternal warmth has an
             environmental effect in protecting children from the
             negative outcomes associated with being bullied.<h4>Conclusions</h4>Warm
             family relationships and positive home environments help to
             buffer children from the negative outcomes associated with
             bullying victimisation. Warm parent-child relationships can
             exert an environmentally mediated effect on children's
             behavioural adjustment following bullying victimisation.
             Identifying protective factors that promote resilience to
             bullying victimisation could lead to improved intervention
             strategies targeting the home environment.},
   Doi = {10.1111/j.1469-7610.2010.02216.x},
   Key = {fds253269}
}

@article{fds253253,
   Author = {Moffitt, TE and Caspi, A and Taylor, A and Kokaua, J and Milne, BJ and Polanczyk, G and Poulton, R},
   Title = {How common are common mental disorders? Evidence that
             lifetime prevalence rates are doubled by prospective versus
             retrospective ascertainment.},
   Journal = {Psychological medicine},
   Volume = {40},
   Number = {6},
   Pages = {899-909},
   Year = {2010},
   Month = {June},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/19719899},
   Abstract = {<h4>Background</h4>Most information about the lifetime
             prevalence of mental disorders comes from retrospective
             surveys, but how much these surveys have undercounted due to
             recall failure is unknown. We compared results from a
             prospective study with those from retrospective
             studies.<h4>Method</h4>The representative 1972-1973 Dunedin
             New Zealand birth cohort (n=1037) was followed to age 32
             years with 96% retention, and compared to the national New
             Zealand Mental Health Survey (NZMHS) and two US National
             Comorbidity Surveys (NCS and NCS-R). Measures were research
             diagnoses of anxiety, depression, alcohol dependence and
             cannabis dependence from ages 18 to 32 years.<h4>Results</h4>The
             prevalence of lifetime disorder to age 32 was approximately
             doubled in prospective as compared to retrospective data for
             all four disorder types. Moreover, across disorders,
             prospective measurement yielded a mean past-year-to-lifetime
             ratio of 38% whereas retrospective measurement yielded
             higher mean past-year-to-lifetime ratios of 57% (NZMHS,
             NCS-R) and 65% (NCS).<h4>Conclusions</h4>Prospective
             longitudinal studies complement retrospective surveys by
             providing unique information about lifetime prevalence. The
             experience of at least one episode of DSM-defined disorder
             during a lifetime may be far more common in the population
             than previously thought. Research should ask what this means
             for etiological theory, construct validity of the DSM
             approach, public perception of stigma, estimates of the
             burden of disease and public health policy.},
   Doi = {10.1017/s0033291709991036},
   Key = {fds253253}
}

@article{fds253215,
   Author = {Melchior, M and Caspi, A and Belsky, D and Moffitt,
             TE},
   Title = {In reply},
   Journal = {Pediatrics},
   Volume = {125},
   Number = {5},
   Pages = {e1267-e1268},
   Publisher = {American Academy of Pediatrics (AAP)},
   Year = {2010},
   Month = {May},
   ISSN = {0031-4005},
   url = {http://dx.doi.org/10.1542/peds.2010-0808a},
   Doi = {10.1542/peds.2010-0808a},
   Key = {fds253215}
}

@misc{fds253273,
   Author = {Caspi, A and Hariri, AR and Holmes, A and Uher, R and Moffitt,
             TE},
   Title = {Genetic sensitivity to the environment: the case of the
             serotonin transporter gene and its implications for studying
             complex diseases and traits.},
   Journal = {The American journal of psychiatry},
   Volume = {167},
   Number = {5},
   Pages = {509-527},
   Year = {2010},
   Month = {May},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/20231323},
   Abstract = {Evidence of marked variability in response among people
             exposed to the same environmental risk implies that
             individual differences in genetic susceptibility might be at
             work. The study of such Gene-by-Environment (GxE)
             interactions has gained momentum. In this article, the
             authors review research about one of the most extensive
             areas of inquiry: variation in the promoter region of the
             serotonin transporter gene (SLC6A4; also known as 5-HTT) and
             its contribution to stress sensitivity. Research in this
             area has both advanced basic science and generated broader
             lessons for studying complex diseases and traits. The
             authors evaluate four lines of evidence about the 5-HTT
             stress-sensitivity hypothesis: 1) observational studies
             about the serotonin transporter linked polymorphic region
             (5-HTTLPR), stress sensitivity, and depression in humans; 2)
             experimental neuroscience studies about the 5-HTTLPR and
             biological phenotypes relevant to the human stress response;
             3) studies of 5-HTT variation and stress sensitivity in
             nonhuman primates; and 4) studies of stress sensitivity and
             genetically engineered 5-HTT mutations in rodents. The
             authors then dispel some misconceptions and offer
             recommendations for GxE research. The authors discuss how
             GxE interaction hypotheses can be tested with large and
             small samples, how GxE research can be carried out before as
             well as after replicated gene discovery, the uses of GxE
             research as a tool for gene discovery, the importance of
             construct validation in evaluating GxE research, and the
             contribution of GxE research to the public understanding of
             genetic science.},
   Doi = {10.1176/appi.ajp.2010.09101452},
   Key = {fds253273}
}

@article{fds253275,
   Author = {Piquero, AR and Farrington, DP and Nagin, DS and Moffitt,
             TE},
   Title = {Trajectories of offending and their relation to life failure
             in late middle age: Findings from the Cambridge study in
             Delinquent Development},
   Journal = {Journal of Research in Crime and Delinquency},
   Volume = {47},
   Number = {2},
   Pages = {151-173},
   Publisher = {SAGE Publications},
   Year = {2010},
   Month = {May},
   ISSN = {0022-4278},
   url = {http://dx.doi.org/10.1177/0022427809357713},
   Abstract = {Researchers have hypothesized that over the life course,
             criminal offending varies with problems in other domains,
             including life failure and physical and mental health.To
             examine this issue, the authors use data from the Cambridge
             Study in Delinquent Development, a prospective longitudinal
             survey of 411 South London males first studied at age 8 in
             1961. Developmental trajectories of criminal activity were
             defined on the basis of conviction records through age 40,
             and these were used to predict self-report measures of life
             failure at age 48 obtained during personal interviews.
             Results indicate that offending in the first 40 years of
             life relates to life failure, that childhood risk factors
             are also implicated in adult life outcomes, and that
             differences emerge in how offender trajectories predict life
             failure after controlling for individual and environmental
             risk factors. This is the first longitudinal investigation
             to show that chronic offending is associated with life
             failure into the late 40s, an age period not previously
             reported, and it also shows that different offending
             trajectories have different outcomes in late middle age. ©
             The Author(s) 2010.},
   Doi = {10.1177/0022427809357713},
   Key = {fds253275}
}

@article{fds304724,
   Author = {Polanczyk, G and Moffitt, TE and Arseneault, L and Cannon, M and Ambler,
             A and Keefe, RSE and Houts, R and Odgers, CL and Caspi,
             A},
   Title = {Etiological and clinical features of childhood psychotic
             symptoms: results from a birth cohort.},
   Journal = {Arch Gen Psychiatry},
   Volume = {67},
   Number = {4},
   Pages = {328-338},
   Year = {2010},
   Month = {April},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/20368509},
   Abstract = {CONTEXT: It has been reported that childhood psychotic
             symptoms are common in the general population and may signal
             neurodevelopmental processes that lead to schizophrenia.
             However, it is not clear whether these symptoms are
             associated with the same extensive risk factors established
             for adult schizophrenia. OBJECTIVE: To examine the construct
             validity of children's self-reported psychotic symptoms by
             testing whether these symptoms share the risk factors and
             clinical features of adult schizophrenia. DESIGN:
             Prospective, longitudinal cohort study of a nationally
             representative birth cohort in Great Britain. PARTICIPANTS:
             A total of 2232 twelve-year-old children followed up since
             age 5 years (retention, 96%). Main Outcome Measure
             Children's self-reported hallucinations and delusions.
             RESULTS: Children's psychotic symptoms are familial and
             heritable and are associated with social risk factors (eg,
             urbanicity); cognitive impairments at age 5; home-rearing
             risk factors (eg, maternal expressed emotion); behavioral,
             emotional, and educational problems at age 5; and comorbid
             conditions, including self-harm. CONCLUSIONS: The results
             provide a comprehensive picture of the construct validity of
             children's self-reported psychotic symptoms. For
             researchers, the findings indicate that children who have
             psychotic symptoms can be recruited for neuroscience
             research to determine the pathogenesis of schizophrenia. For
             clinicians, the findings indicate that psychotic symptoms in
             childhood are often a marker of an impaired developmental
             process and should be actively assessed.},
   Doi = {10.1001/archgenpsychiatry.2010.14},
   Key = {fds304724}
}

@article{fds304723,
   Author = {Polanczyk, G and Caspi, A and Houts, R and Kollins, SH and Rohde, LA and Moffitt, TE},
   Title = {Implications of extending the ADHD age-of-onset criterion to
             age 12: results from a prospectively studied birth
             cohort.},
   Journal = {J Am Acad Child Adolesc Psychiatry},
   Volume = {49},
   Number = {3},
   Pages = {210-216},
   Year = {2010},
   Month = {March},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/20410710},
   Abstract = {OBJECTIVE: To evaluate whether including children with onset
             of symptoms between ages 7 and 12 years in the ADHD
             diagnostic category would: (a) increase the prevalence of
             the disorder at age 12, and (b) change the clinical and
             cognitive features, impairment profile, and risk factors for
             ADHD compared with findings in the literature based on the
             DSM-IV definition of the disorder. METHOD: A birth cohort of
             2,232 British children was prospectively evaluated at ages 7
             and 12 years for ADHD using information from mothers and
             teachers. The prevalence of diagnosed ADHD at age 12 was
             evaluated with and without the inclusion of individuals who
             met DSM-IV age-of-onset criterion through mothers' or
             teachers' reports of symptoms at age 7. Children with onset
             of ADHD symptoms before versus after age 7 were compared on
             their clinical and cognitive features, impairment profile,
             and risk factors for ADHD. RESULTS: Extending the
             age-of-onset criterion to age 12 resulted in a negligible
             increase in ADHD prevalence by age 12 years of 0.1%.
             Children who first manifested ADHD symptoms between ages 7
             and 12 did not present correlates or risk factors that were
             significantly different from children who manifested
             symptoms before age 7. CONCLUSIONS: Results from this
             prospective birth cohort might suggest that adults who are
             able to report symptom onset by age 12 also had symptoms by
             age 7, even if they are not able to report them. The data
             suggest that the prevalence estimate, correlates and risk
             factors of ADHD will not be affected if the new diagnostic
             scheme extends the age-of-onset criterion to age
             12.},
   Doi = {10.1016/j.jaac.2009.12.014},
   Key = {fds304723}
}

@article{fds253276,
   Author = {Reichenberg, A and Caspi, A and Harrington, H and Houts, R and Keefe,
             RSE and Murray, RM and Poulton, R and Moffitt, TE},
   Title = {Static and dynamic cognitive deficits in childhood preceding
             adult schizophrenia: a 30-year study.},
   Journal = {Am J Psychiatry},
   Volume = {167},
   Number = {2},
   Pages = {160-169},
   Year = {2010},
   Month = {February},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/20048021},
   Abstract = {OBJECTIVE: Premorbid cognitive deficits in schizophrenia are
             well documented and have been interpreted as supporting a
             neurodevelopmental etiological model. The authors
             investigated the following three unresolved questions about
             premorbid cognitive deficits: What is their developmental
             course? Do all premorbid cognitive deficits follow the same
             course? Are premorbid cognitive deficits specific to
             schizophrenia or shared by other psychiatric disorders?
             METHOD: Participants were members of a representative cohort
             of 1,037 males and females born between 1972 and 1973 in
             Dunedin, New Zealand. Cohort members underwent follow-up
             evaluations at specific intervals from age 3 to 32 years,
             with a 96% retention rate. Cognitive development was
             analyzed and compared in children who later developed
             schizophrenia or recurrent depression as well as in healthy
             comparison subjects. RESULTS: Children who developed adult
             schizophrenia exhibited developmental deficits (i.e., static
             cognitive impairments that emerge early and remain stable)
             on tests indexing verbal and visual knowledge acquisition,
             reasoning, and conceptualization. In addition, these
             children exhibited developmental lags (i.e., growth that is
             slower relative to healthy comparison subjects) on tests
             indexing processing speed, attention, visual-spatial problem
             solving ability, and working memory. These two premorbid
             cognitive patterns were not observed in children who later
             developed recurrent depression. CONCLUSIONS: These findings
             suggest that the origins of schizophrenia include two
             interrelated developmental processes evident from childhood
             to early adolescence (ages 7-13 years). Children who will
             grow up to develop adult schizophrenia enter primary school
             struggling with verbal reasoning and lag further behind
             their peers in working memory, attention, and processing
             speed as they get older.},
   Doi = {10.1176/appi.ajp.2009.09040574},
   Key = {fds253276}
}

@article{fds304722,
   Author = {Kaufman, J and Gelernter, J and Kaffman, A and Caspi, A and Moffitt,
             T},
   Title = {Arguable assumptions, debatable conclusions.},
   Journal = {Biological psychiatry},
   Volume = {67},
   Number = {4},
   Pages = {e19-e20},
   Year = {2010},
   Month = {February},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/20006323},
   Doi = {10.1016/j.biopsych.2009.07.041},
   Key = {fds304722}
}

@article{fds253171,
   Author = {Kieling, C and Kieling, RR and Rohde, LA and Frick, PJ and Moffitt, T and Nigg, JT and Tannock, R and Castellanos, FX},
   Title = {The age at onset of attention deficit hyperactivity
             disorder.},
   Journal = {The American journal of psychiatry},
   Volume = {167},
   Number = {1},
   Pages = {14-16},
   Year = {2010},
   Month = {January},
   ISSN = {0002-953X},
   url = {http://dx.doi.org/10.1176/appi.ajp.2009.09060796},
   Doi = {10.1176/appi.ajp.2009.09060796},
   Key = {fds253171}
}

@article{fds304721,
   Author = {Hancox, RJ and Poulton, R and Ely, M and Welch, D and Taylor, DR and McLachlan, CR and Greene, JM and Moffitt, TE and Caspi, A and Sears,
             MR},
   Title = {Effects of cannabis on lung function: a population-based
             cohort study.},
   Journal = {The European respiratory journal},
   Volume = {35},
   Number = {1},
   Pages = {42-47},
   Year = {2010},
   Month = {January},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/19679602},
   Abstract = {The effects of cannabis on lung function remain unclear and
             may be different from those of tobacco. We compared the
             associations between use of these substances and lung
             function in a population-based cohort (n = 1,037). Cannabis
             and tobacco use were reported at ages 18, 21, 26 and 32 yrs.
             Spirometry, plethysmography and carbon monoxide transfer
             factor were measured at 32 yrs. Associations between lung
             function and exposure to each substance were adjusted for
             exposure to the other substance. Cumulative cannabis use was
             associated with higher forced vital capacity, total lung
             capacity, functional residual capacity and residual volume.
             Cannabis was also associated with higher airway resistance
             but not with forced expiratory volume in 1 s, forced
             expiratory ratio or transfer factor. These findings were
             similar among those who did not smoke tobacco. In contrast,
             tobacco use was associated with lower forced expiratory
             volume in 1 s, lower forced expiratory ratio, lower transfer
             factor and higher static lung volumes, but not with airway
             resistance. Cannabis appears to have different effects on
             lung function from those of tobacco. Cannabis use was
             associated with higher lung volumes, suggesting
             hyperinflation and increased large-airways resistance, but
             there was little evidence for airflow obstruction or
             impairment of gas transfer.},
   Doi = {10.1183/09031936.00065009},
   Key = {fds304721}
}

@article{fds168662,
   Author = {Moffitt, T.E. and Caspi, A. and Taylor, A. and Kokaua, J. and Milne, B.J. and Polanczyk, G. and Poulton, R.},
   Title = {How common are common mental disorders? Evidence that
             lifetime rates are doubled by prospective versus
             retrospective ascertainment},
   Journal = {Psychological Medicine},
   Volume = {39},
   Year = {2010},
   Key = {fds168662}
}

@article{fds336540,
   Author = {Kieling, C and Kieling, RR and Rhode, LA and Canino, G and Klien, R and Leibenluft, E and Pine, D and Frick, PJ and Moffitt, TE and Nigg, JT and Taylor, E and Rannock, R and Shaffer, D and Castellanos,
             X},
   Title = {The age-of onset of attention-deficit hyperactivity
             disorder.},
   Journal = {American Journal of Psychiatry},
   Volume = {167},
   Pages = {718-719},
   Year = {2010},
   Key = {fds336540}
}

@article{fds253251,
   Author = {Pardidn, D and Moffitt, TE},
   Title = {special section},
   Journal = {J or Abnormal Psychology},
   Volume = {119},
   Pages = {683-688},
   Year = {2010},
   url = {http://dx.doi.org/10.1037/a0021441},
   Doi = {10.1037/a0021441},
   Key = {fds253251}
}

@misc{fds253270,
   Author = {Polanczyk, G and Moffitt, TE and Arseneault, L and Cannon, M and Ambler,
             A and Keefe, RSE and Houts, R and Odgers, CL and Caspi,
             A},
   Title = {Childhood psychotic symptoms share etiological and clinical
             features with adult schizophrenia: Results from a
             representative borth cohort.},
   Journal = {Archives of General Psychiatry},
   Volume = {67},
   Number = {4},
   Pages = {328-338},
   Year = {2010},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/20368509},
   Abstract = {CONTEXT: It has been reported that childhood psychotic
             symptoms are common in the general population and may signal
             neurodevelopmental processes that lead to schizophrenia.
             However, it is not clear whether these symptoms are
             associated with the same extensive risk factors established
             for adult schizophrenia. OBJECTIVE: To examine the construct
             validity of children's self-reported psychotic symptoms by
             testing whether these symptoms share the risk factors and
             clinical features of adult schizophrenia. DESIGN:
             Prospective, longitudinal cohort study of a nationally
             representative birth cohort in Great Britain. PARTICIPANTS:
             A total of 2232 twelve-year-old children followed up since
             age 5 years (retention, 96%). Main Outcome Measure
             Children's self-reported hallucinations and delusions.
             RESULTS: Children's psychotic symptoms are familial and
             heritable and are associated with social risk factors (eg,
             urbanicity); cognitive impairments at age 5; home-rearing
             risk factors (eg, maternal expressed emotion); behavioral,
             emotional, and educational problems at age 5; and comorbid
             conditions, including self-harm. CONCLUSIONS: The results
             provide a comprehensive picture of the construct validity of
             children's self-reported psychotic symptoms. For
             researchers, the findings indicate that children who have
             psychotic symptoms can be recruited for neuroscience
             research to determine the pathogenesis of schizophrenia. For
             clinicians, the findings indicate that psychotic symptoms in
             childhood are often a marker of an impaired developmental
             process and should be actively assessed.},
   Doi = {10.1001/archgenpsychiatry.2010.14},
   Key = {fds253270}
}

@article{fds253271,
   Author = {Grisham, J and Poulton, R and Moffitt, TE},
   Title = {Reply to Mushtaq et al.},
   Journal = {British Journal of Psychiatry},
   Volume = {195},
   Pages = {55},
   Year = {2010},
   Key = {fds253271}
}

@article{fds253272,
   Author = {Kaufman, J and Gelernter, J and Kaffman, A and Caspi, A and Moffitt,
             TE},
   Title = {Arguable assumptions, Questionable conclusions (reply to
             Munafo)},
   Journal = {Biological Psychiatry},
   Volume = {67},
   Number = {4},
   Pages = {e19-e20},
   Year = {2010},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/20006323},
   Doi = {10.1016/j.biopsych.2009.07.041},
   Key = {fds253272}
}

@article{fds253274,
   Author = {Polanczyk, G and Caspi, A and Houts, R and Kollins, S and Rhode, LA and Moffitt, TE},
   Title = {Extending the ADHD age of onset criterion to 12 years of
             age: Impact on prevalence and correlates evaluated in a
             prospectively studied birth cohort},
   Journal = {JAACAP},
   Volume = {49},
   Number = {3},
   Pages = {210-216},
   Year = {2010},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/20410710},
   Abstract = {OBJECTIVE: To evaluate whether including children with onset
             of symptoms between ages 7 and 12 years in the ADHD
             diagnostic category would: (a) increase the prevalence of
             the disorder at age 12, and (b) change the clinical and
             cognitive features, impairment profile, and risk factors for
             ADHD compared with findings in the literature based on the
             DSM-IV definition of the disorder. METHOD: A birth cohort of
             2,232 British children was prospectively evaluated at ages 7
             and 12 years for ADHD using information from mothers and
             teachers. The prevalence of diagnosed ADHD at age 12 was
             evaluated with and without the inclusion of individuals who
             met DSM-IV age-of-onset criterion through mothers' or
             teachers' reports of symptoms at age 7. Children with onset
             of ADHD symptoms before versus after age 7 were compared on
             their clinical and cognitive features, impairment profile,
             and risk factors for ADHD. RESULTS: Extending the
             age-of-onset criterion to age 12 resulted in a negligible
             increase in ADHD prevalence by age 12 years of 0.1%.
             Children who first manifested ADHD symptoms between ages 7
             and 12 did not present correlates or risk factors that were
             significantly different from children who manifested
             symptoms before age 7. CONCLUSIONS: Results from this
             prospective birth cohort might suggest that adults who are
             able to report symptom onset by age 12 also had symptoms by
             age 7, even if they are not able to report them. The data
             suggest that the prevalence estimate, correlates and risk
             factors of ADHD will not be affected if the new diagnostic
             scheme extends the age-of-onset criterion to age
             12.},
   Key = {fds253274}
}

@article{fds253277,
   Author = {Hancox, RJ and Poulton, R and Ely, M and Welch, D and Taylor, DR and McLachlan, CR and Greene, J and Moffitt, TE and Caspi, A and Sears,
             MR},
   Title = {Differential effects of cannabis and tobacco smoking on lung
             function: A population-based study.},
   Journal = {European Respiratory Journal},
   Volume = {35},
   Number = {1},
   Pages = {42-47},
   Year = {2010},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/19679602},
   Abstract = {The effects of cannabis on lung function remain unclear and
             may be different from those of tobacco. We compared the
             associations between use of these substances and lung
             function in a population-based cohort (n = 1,037). Cannabis
             and tobacco use were reported at ages 18, 21, 26 and 32 yrs.
             Spirometry, plethysmography and carbon monoxide transfer
             factor were measured at 32 yrs. Associations between lung
             function and exposure to each substance were adjusted for
             exposure to the other substance. Cumulative cannabis use was
             associated with higher forced vital capacity, total lung
             capacity, functional residual capacity and residual volume.
             Cannabis was also associated with higher airway resistance
             but not with forced expiratory volume in 1 s, forced
             expiratory ratio or transfer factor. These findings were
             similar among those who did not smoke tobacco. In contrast,
             tobacco use was associated with lower forced expiratory
             volume in 1 s, lower forced expiratory ratio, lower transfer
             factor and higher static lung volumes, but not with airway
             resistance. Cannabis appears to have different effects on
             lung function from those of tobacco. Cannabis use was
             associated with higher lung volumes, suggesting
             hyperinflation and increased large-airways resistance, but
             there was little evidence for airflow obstruction or
             impairment of gas transfer.},
   Doi = {10.1183/09031936.00065009},
   Key = {fds253277}
}

@article{fds336541,
   Author = {Houts, RM and Caspi, A and Pianta, RC and Arseneault, L and Moffitt,
             TE},
   Title = {The challenging pupil in the classroom: Child effects on
             teachers},
   Journal = {Psychological Science},
   Year = {2010},
   Key = {fds336541}
}

@article{fds253169,
   Author = {Grisham, JR and Moffitt, TE and Poulton, R},
   Title = {Authors' reply},
   Journal = {British Journal of Psychiatry},
   Volume = {195},
   Number = {6},
   Pages = {555},
   Publisher = {Royal College of Psychiatrists},
   Year = {2009},
   Month = {December},
   ISSN = {0007-1250},
   url = {http://dx.doi.org/10.1192/bjp.195.6.555},
   Doi = {10.1192/bjp.195.6.555},
   Key = {fds253169}
}

@article{fds253282,
   Author = {Danese, A and Moffitt, TE and Harrington, H and Milne, BJ and Polanczyk,
             G and Pariante, CM and Poulton, R and Caspi, A},
   Title = {Adverse childhood experiences and adult risk factors for
             age-related disease: depression, inflammation, and
             clustering of metabolic risk markers.},
   Journal = {Archives of pediatrics & adolescent medicine},
   Volume = {163},
   Number = {12},
   Pages = {1135-1143},
   Year = {2009},
   Month = {December},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/19996051},
   Abstract = {<h4>Objective</h4>To understand why children exposed to
             adverse psychosocial experiences are at elevated risk for
             age-related disease, such as cardiovascular disease, by
             testing whether adverse childhood experiences predict
             enduring abnormalities in stress-sensitive biological
             systems, namely, the nervous, immune, and
             endocrine/metabolic systems.<h4>Design</h4>A 32-year
             prospective longitudinal study of a representative birth
             cohort.<h4>Setting</h4>New Zealand.<h4>Participants</h4>A
             total of 1037 members of the Dunedin Multidisciplinary
             Health and Development Study. Main Exposures During their
             first decade of life, study members were assessed for
             exposure to 3 adverse psychosocial experiences:
             socioeconomic disadvantage, maltreatment, and social
             isolation.<h4>Main outcome measures</h4>At age 32 years,
             study members were assessed for the presence of 3
             age-related-disease risks: major depression, high
             inflammation levels (high-sensitivity C-reactive protein
             level >3 mg/L), and the clustering of metabolic risk
             biomarkers (overweight, high blood pressure, high total
             cholesterol, low high-density lipoprotein cholesterol, high
             glycated hemoglobin, and low maximum oxygen consumption
             levels.<h4>Results</h4>Children exposed to adverse
             psychosocial experiences were at elevated risk of
             depression, high inflammation levels, and clustering of
             metabolic risk markers. Children who had experienced
             socioeconomic disadvantage (incidence rate ratio, 1.89; 95%
             confidence interval, 1.36-2.62), maltreatment (1.81;
             1.38-2.38), or social isolation (1.87; 1.38-2.51) had
             elevated age-related-disease risks in adulthood. The effects
             of adverse childhood experiences on age-related-disease
             risks in adulthood were nonredundant, cumulative, and
             independent of the influence of established developmental
             and concurrent risk factors.<h4>Conclusions</h4>Children
             exposed to adverse psychosocial experiences have enduring
             emotional, immune, and metabolic abnormalities that
             contribute to explaining their elevated risk for age-related
             disease. The promotion of healthy psychosocial experiences
             for children is a necessary and potentially cost-effective
             target for the prevention of age-related
             disease.},
   Doi = {10.1001/archpediatrics.2009.214},
   Key = {fds253282}
}

@article{fds253209,
   Author = {Melchior, M and Caspi, A and Howard, LM and Ambler, AP and Bolton, H and Mountain, N and Moffitt, TE},
   Title = {Mental health context of food insecurity: a representative
             cohort of families with young children.},
   Journal = {Pediatrics},
   Volume = {124},
   Number = {4},
   Pages = {e564-e572},
   Year = {2009},
   Month = {October},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/19786424},
   Abstract = {<h4>Objective</h4>Children from food-insecure families (ie,
             families that lack access to sufficient, safe, and
             nutritious food) are at risk for developmental problems.
             Food insecurity disproportionately occurs among
             low-socioeconomic status (SES) and low-income families;
             however, interventions that supplement families' income or
             diet have not eradicated food insecurity. This may be
             because food insecurity is also related to nonfinancial
             factors such as the presence of maternal mental health
             problems. To clarify whether addressing mothers' mental
             health problems may be a promising strategy for reducing the
             burden of food insecurity, we tested the hypothesis that
             low-SES families are especially vulnerable to food
             insecurity when the mother experiences depression, alcohol
             or drug abuse, psychosis spectrum disorder, or domestic
             violence.<h4>Methods</h4>We used data from a nationally
             representative cohort of 1116 British families (the
             Environmental Risk Longitudinal Study). Food insecurity,
             family SES, maternal mental health and exposure to domestic
             violence, and children's behavioral outcomes were measured
             by using validated methods.<h4>Results</h4>Overall, 9.7% of
             study families were food-insecure. Among low-SES families,
             controlling for income variation, food insecurity
             co-occurred with maternal depression (odds ratio [OR]: 2.82
             [95% confidence interval (CI): 1.62-4.93]), psychosis
             spectrum disorder (OR: 4.01 [95% CI: 2.03-7.94]), and
             domestic violence (OR: 2.36 [95% CI: 1.18-4.73]). In
             addition, food insecurity predicted elevated rates of
             children's behavior problems.<h4>Conclusions</h4>Among
             families with young children, food insecurity is frequent,
             particularly when the mother experiences mental health
             problems. This suggests that interventions that improve
             women's mental health may also contribute to decreasing the
             burden of food insecurity and its impact on the next
             generation.},
   Doi = {10.1542/peds.2009-0583},
   Key = {fds253209}
}

@article{fds253284,
   Author = {Polanczyk, G and Caspi, A and Williams, B and Price, TS and Danese, A and Sugden, K and Uher, R and Poulton, R and Moffitt,
             TE},
   Title = {Protective effect of CRHR1 gene variants on the development
             of adult depression following childhood maltreatment:
             replication and extension.},
   Journal = {Archives of general psychiatry},
   Volume = {66},
   Number = {9},
   Pages = {978-985},
   Year = {2009},
   Month = {September},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/19736354},
   Abstract = {<h4>Context</h4>A previous study reported a gene x
             environment interaction in which a haplotype in the
             corticotropin-releasing hormone receptor 1 gene (CRHR1) was
             associated with protection against adult depressive symptoms
             in individuals who were maltreated as children (as assessed
             by the Childhood Trauma Questionnaire [CTQ]).<h4>Objective</h4>To
             replicate the interaction between childhood maltreatment and
             a TAT haplotype formed by rs7209436, rs110402, and rs242924
             in CRHR1, predicting adult depression.<h4>Design</h4>Two
             prospective longitudinal cohort studies.<h4>Setting</h4>England
             and New Zealand.<h4>Participants</h4>Participants in the
             first sample were women in the E-Risk Study (N = 1116),
             followed up to age 40 years with 96% retention. Participants
             in the second sample were men and women in the Dunedin Study
             (N = 1037), followed up to age 32 years with 96% retention.
             Main Outcome Measure Research diagnoses of past-year and
             recurrent major depressive disorder.<h4>Results</h4>In the
             E-Risk Study, the TAT haplotype was associated with a
             significant protective effect. In this effect, women who
             reported childhood maltreatment on the CTQ were protected
             against depression. In the Dunedin Study, which used a
             different type of measure of maltreatment, this finding was
             not replicated.<h4>Conclusions</h4>A haplotype in CRHR1 has
             been suggested to exert a protective effect against adult
             depression among research participants who reported
             maltreatment on the CTQ, a measure that elicits emotional
             memories. This suggests the hypothesis that CRHR1's
             protective effect may relate to its function in the
             consolidation of memories of emotionally arousing
             experiences.},
   Doi = {10.1001/archgenpsychiatry.2009.114},
   Key = {fds253284}
}

@article{fds253283,
   Author = {Grisham, JR and Anderson, TM and Poulton, R and Moffitt, TE and Andrews,
             G},
   Title = {Childhood neuropsychological deficits associated with adult
             obsessive-compulsive disorder.},
   Journal = {The British journal of psychiatry : the journal of mental
             science},
   Volume = {195},
   Number = {2},
   Pages = {138-141},
   Year = {2009},
   Month = {August},
   ISSN = {0007-1250},
   url = {http://dx.doi.org/10.1192/bjp.bp.108.056812},
   Abstract = {<h4>Background</h4>Existing neuropsychological studies of
             obsessive-compulsive disorder (OCD) are cross-sectional and
             do not provide evidence of whether deficits are
             trait-related (antecedent and independent of symptomatology)
             or state-related (a consequence, dependent on
             symptomatology).<h4>Aims</h4>To investigate whether there
             are premorbid neuropsychological deficits associated with
             adult OCD.<h4>Method</h4>Longitudinal data were collected
             from participants of the Dunedin Multidisciplinary Health
             and Developmental study. Neuropsychological data collected
             at age 13 were linked with age 32 diagnosis of
             OCD.<h4>Results</h4>The group who had OCD at age 32 differed
             significantly from the control group with no OCD on their
             performance at age 13 on neuropsychological tests of
             visuospatial, visuoconstructive and visuomotor skills,
             controlling for gender and socioeconomic status, but did not
             differ on tests of general IQ or verbal ability. Performance
             of the group with OCD on tests of executive functioning was
             mixed.<h4>Conclusions</h4>Individuals with OCD have
             premorbid impairment in visuospatial abilities and some
             forms of executive functioning, consistent with biological
             models of OCD.},
   Doi = {10.1192/bjp.bp.108.056812},
   Key = {fds253283}
}

@article{fds253210,
   Author = {Milne, BJ and Caspi, A and Harrington, H and Poulton, R and Rutter, M and Moffitt, TE},
   Title = {Predictive value of family history on severity of illness:
             the case for depression, anxiety, alcohol dependence, and
             drug dependence.},
   Journal = {Archives of general psychiatry},
   Volume = {66},
   Number = {7},
   Pages = {738-747},
   Year = {2009},
   Month = {July},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/19581565},
   Abstract = {<h4>Context</h4>If family history is associated with
             clinical features that are thought to index seriousness of
             disorder, this could inform clinicians predicting patients'
             prognosis and researchers selecting cases for genetic
             studies. Although tests of associations between family
             history and clinical features are numerous for depression,
             such tests are relatively lacking for other
             disorders.<h4>Objective</h4>To test the hypothesis that
             family history is associated with 4 clinical indexes of
             disorder (recurrence, impairment, service use, and age at
             onset) in relation to 4 psychiatric disorders (major
             depressive episode, anxiety disorder, alcohol dependence,
             and drug dependence).<h4>Design</h4>Prospective longitudinal
             cohort study.<h4>Setting</h4>New Zealand.<h4>Participants</h4>A
             total of 981 members of the 1972 to 1973 Dunedin Study birth
             cohort (96% retention).<h4>Main outcome measures</h4>For
             each disorder, family history scores were calculated as the
             proportion of affected family members from data on 3
             generations of the participants' families. Data collected
             prospectively at the study's repeated assessments (ages
             11-32 years) were used to assess recurrence, impairment, and
             age at onset; data collected by means of a life history
             calendar at age 32 years were used to assess service
             use.<h4>Results</h4>Family history was associated with the
             presence of all 4 disorder types. In addition, family
             history was associated with a more recurrent course for all
             4 disorders (but not significantly for women with
             depression), worse impairment, and greater service use.
             Family history was not associated with younger age at onset
             for any disorder.<h4>Conclusions</h4>Associations between
             family history of a disorder and clinical features of that
             disorder in probands showed consistent direction of effects
             across depression, anxiety disorder, alcohol dependence, and
             drug dependence. For these disorder types, family history is
             useful for determining patients' clinical prognosis and for
             selecting cases for genetic studies.},
   Doi = {10.1001/archgenpsychiatry.2009.55},
   Key = {fds253210}
}

@article{fds253287,
   Author = {Odgers, CL and Moffitt, TE and Tach, LM and Sampson, A and Taylor, RJ and Matthews, CL and Caspi, A},
   Title = {The protective effects of neighborhood collective efficacy
             on British children growing up in deprivation: a
             developmental analysis.},
   Journal = {Developmental psychology},
   Volume = {45},
   Number = {4},
   Pages = {942-957},
   Year = {2009},
   Month = {July},
   ISSN = {0012-1649},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/19586172},
   Abstract = {This article reports on the influence of neighborhood-level
             deprivation and collective efficacy on children's antisocial
             behavior between the ages of 5 and 10 years. Latent growth
             curve modeling was applied to characterize the developmental
             course of antisocial behavior among children in the E-Risk
             Longitudinal Twin Study, an epidemiological cohort of 2,232
             children. Children in deprived versus affluent neighborhoods
             had higher levels of antisocial behavior at school entry
             (24.1 vs. 20.5, p < .001) and a slower rate of decline from
             involvement in antisocial behavior between the ages of 5 and
             10 (-0.54 vs. -0.78, p < .01). Neighborhood collective
             efficacy was negatively associated with levels of antisocial
             behavior at school entry (r = -.10, p < .01) but only in
             deprived neighborhoods; this relationship held after
             controlling for neighborhood problems and family-level
             factors. Collective efficacy did not predict the rate of
             change in antisocial behavior between the ages of 5 and 10.
             Findings suggest that neighborhood collective efficacy may
             have a protective effect on children living in deprived
             contexts.},
   Doi = {10.1037/a0016162},
   Key = {fds253287}
}

@article{fds253285,
   Author = {Kim-Cohen, J and Arseneault, L and Newcombe, R and Adams, F and Bolton,
             H and Cant, L and Delgado, K and Freeman, J and Golaszewski, A and Kelesidi, K and Matthews, C and Mountain, N and Oxley, D and Watson, S and Werts, H and Caspi, A and Moffitt, TE},
   Title = {Five-year predictive validity of DSM-IV conduct disorder
             research diagnosis in 4(1/2)-5-year-old children.},
   Journal = {European child & adolescent psychiatry},
   Volume = {18},
   Number = {5},
   Pages = {284-291},
   Year = {2009},
   Month = {May},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/19165535},
   Abstract = {<h4>Objective</h4>This longitudinal study of a non-referred,
             population-based sample tested the 5-year predictive
             validity of the DSM-IV conduct disorder (CD) research
             diagnosis in children 4(1/2)-5 years of age.<h4>Method</h4>In
             the E-Risk Study, a representative birth cohort of 2,232
             children, mothers were interviewed and teachers completed
             mailed questionnaires to assess children's past 6-month CD
             symptoms. A follow-up assessment was conducted when children
             were 10 years old.<h4>Results</h4>CD-diagnosed 5-year-olds
             were significantly more likely than controls to have
             behavioural and educational difficulties at age 10.
             Increased risk for age-10 educational difficulties persisted
             after controlling for age-5 IQ and ADHD diagnosis. Although
             the majority of CD-diagnosed 5-year-olds had no CD symptoms
             at age 10, findings suggest that these "remitted" children
             continued to experience behavioural and educational problems
             5 years later despite their apparent remission from
             CD.<h4>Conclusions</h4>DSM-IV CD symptoms validly identify
             preschool-aged children who continue to have behavioural and
             educational problems in middle-childhood.},
   Doi = {10.1007/s00787-008-0729-1},
   Key = {fds253285}
}

@article{fds253288,
   Author = {Bowes, L and Arseneault, L and Maughan, B and Taylor, A and Caspi, A and Moffitt, TE},
   Title = {School, neighborhood, and family factors are associated with
             children's bullying involvement: a nationally representative
             longitudinal study.},
   Journal = {Journal of the American Academy of Child and Adolescent
             Psychiatry},
   Volume = {48},
   Number = {5},
   Pages = {545-553},
   Year = {2009},
   Month = {May},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/19325496},
   Abstract = {<h4>Objective</h4>To test whether school, neighborhood, and
             family factors are independently associated with children's
             involvement in bullying, over and above their own behaviors
             that may increase their risk for becoming involved in
             bullying.<h4>Method</h4>We examined bullying in the
             Environmental Risk (E-Risk) Longitudinal Twin Study, a
             nationally representative 1994-1995 birth cohort of 2,232
             children. We used mother and teacher reports to identify
             children who experienced bullying between the ages of 5 and
             7 years either as victims, bullies, or bully-victims. We
             collected information about school characteristics from the
             Department for Children, Schools and Families. We collected
             reports from mothers about children's neighborhood and home
             environments and reports from mothers and teachers about
             children's internalizing and externalizing problems when
             they were 5 years old.<h4>Results</h4>Multinomial logistic
             regressions showed that over and above other
             socioenvironmental factors and children's behavior problems,
             school size was associated with an increased risk for being
             a victim of bullying, problems with neighbors was associated
             with an increased risk for being a bully-victim, and family
             factors (e.g., child maltreatment, domestic violence) were
             associated with all groups of children involved in
             bullying.<h4>Conclusions</h4>Socioenvironmental factors are
             associated with children's risk for becoming involved in
             bullying over and above their own behaviors. Intervention
             programs aimed at reducing bullying should extend their
             focus beyond schools to include local communities and
             families.},
   Doi = {10.1097/chi.0b013e31819cb017},
   Key = {fds253288}
}

@article{fds253289,
   Author = {Gregory, AM and Caspi, A and Moffitt, TE and Milne, BJ and Poulton, R and Sears, MR},
   Title = {Links between anxiety and allergies: psychobiological
             reality or possible methodological bias?},
   Journal = {Journal of personality},
   Volume = {77},
   Number = {2},
   Pages = {347-362},
   Year = {2009},
   Month = {April},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/19192077},
   Abstract = {The objective of the study was to examine the link between
             anxiety and allergies to establish whether it reflects a
             psychobiological reality or a possible methodological bias.
             A cohort of 1,037 children enrolled in the study. Anxiety
             disorders were assessed between 11 and 21 years. Anxious
             personality was assessed at 18 years. Allergies were
             examined at 21 years by (a) self reports, (b) skin pricks,
             and (c) serum total immunoglobulin E (IgE). Self-reported
             allergies were predicted by recurrent anxiety disorders (OR
             [95% CI]=1.56 [1.06-2.30], p=.023) and self-reports of
             anxious personality (OR [95% CI]=1.67 [1.17-2.37], p=.004):
             Objectively verified allergies were not. These results
             suggest that the link between anxiety and allergies may
             reflect a methodological artifact rather than a
             psychobiological reality.},
   Doi = {10.1111/j.1467-6494.2008.00550.x},
   Key = {fds253289}
}

@article{fds253291,
   Author = {Gregory, AM and Caspi, A and Moffitt, TE and Poulton,
             R},
   Title = {Sleep problems in childhood predict neuropsychological
             functioning in adolescence.},
   Journal = {Pediatrics},
   Volume = {123},
   Number = {4},
   Pages = {1171-1176},
   Year = {2009},
   Month = {April},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/19336377},
   Abstract = {<h4>Objectives</h4>Our goal was to examine the association
             between parent-rated sleep problems during childhood and
             neuropsychological functioning during adolescence.<h4>Participants
             and methods</h4>Longitudinal prospective data on an entire
             birth cohort from Dunedin, New Zealand, were obtained. One
             thousand thirty-seven children were enrolled in the study
             (52% male). Parents reported on sleep problems when the
             study members were 5, 7, and 9 years of age.
             Neuropsychological functioning was assessed by using 7 tests
             when the participants were 13 years of age.<h4>Results</h4>After
             adjusting for gender and socioeconomic status, persistent
             sleep problems during childhood predicted scores on 2
             neuropsychological tests: the copy score of the
             Rey-Osterrieth Complex Figure Test and 2 measures of
             performance on the Halstead Trail Making Test. These results
             were substantively replicated when sleep was assessed at the
             5- and 9-year (but not 7-year) assessments
             separately.<h4>Conclusions</h4>Sleep problems during
             childhood may be associated with certain aspects of
             neuropsychological functioning during adolescence. This adds
             to the growing body of literature suggesting that childhood
             sleep problems may be a risk indicator of later
             difficulties.},
   Doi = {10.1542/peds.2008-0825},
   Key = {fds253291}
}

@article{fds253290,
   Author = {Fullana, MA and Mataix-Cols, D and Caspi, A and Harrington, H and Grisham, JR and Moffitt, TE and Poulton, R},
   Title = {Obsessions and compulsions in the community: prevalence,
             interference, help-seeking, developmental stability, and
             co-occurring psychiatric conditions.},
   Journal = {The American journal of psychiatry},
   Volume = {166},
   Number = {3},
   Pages = {329-336},
   Year = {2009},
   Month = {March},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/19188283},
   Abstract = {<h4>Objective</h4>It is unclear how many people in the
             community have obsessions and compulsions and associated
             levels of interference. It is also unknown what variables
             predict help-seeking for these symptoms, whether they are
             developmentally stable, and whether they increase the risk
             of mental disorders.<h4>Method</h4>The authors analyzed data
             from the prospective longitudinal Dunedin study of an
             unselected birth cohort. The presence of obsessions and
             compulsions and mental disorders was assessed using the
             Diagnostic Interview Schedule (DIS) at ages 11, 26, and 32.
             Data on interference and help-seeking were obtained at ages
             26 and 32.<h4>Results</h4>Obsessions and compulsions were
             frequent in individuals with mental disorders other than
             obsessive-compulsive disorder (OCD) and among people without
             mental disorders. Even in the latter group, these symptoms
             caused significant interference. The presence of
             anxiety/depression and of obsessions (particularly
             aggressive and shameful thoughts), but not compulsions, was
             associated with help-seeking. Harm/checking was the most
             prevalent symptom dimension. Symptom dimensions were
             temporally stable and associated with increased comorbidity.
             Obsessive-compulsive symptoms at age 11 predicted a high
             risk of an adult OCD diagnosis as well as elevated adult
             symptom dimensions.<h4>Conclusions</h4>Obsessions and
             compulsions are common in the adult population, have their
             roots in childhood, and are associated with interference,
             risk for disorders, and help-seeking. Subclinical obsessions
             and compulsions should be taken into account in research,
             intervention, and DSM-V.},
   Doi = {10.1176/appi.ajp.2008.08071006},
   Key = {fds253290}
}

@article{fds253148,
   Author = {Moffitt, TE and Scott, S},
   Title = {Conduct Disorders of Childhood and Adolescence},
   Pages = {543-564},
   Publisher = {BLACKWELL PUBLISHING LTD},
   Year = {2009},
   Month = {February},
   url = {http://dx.doi.org/10.1002/9781444300895.ch35},
   Doi = {10.1002/9781444300895.ch35},
   Key = {fds253148}
}

@article{fds253159,
   Author = {Melchior, M and Moffitt, TE and Poulton, R and Sugden, K and Caspi,
             A},
   Title = {HIGH WORK DEMANDS AND DEPRESSION: THE MODERATING ROLE OF THE
             SEROTONIN TRANSPORTER GENE (5-HTT) AND WORK
             CONTROL},
   Journal = {EUROPEAN PSYCHIATRY},
   Volume = {24},
   Pages = {1 pages},
   Publisher = {ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES
             ELSEVIER},
   Year = {2009},
   Month = {January},
   ISSN = {0924-9338},
   url = {http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000208663800660&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=47d3190e77e5a3a53558812f597b0b92},
   Key = {fds253159}
}

@article{fds253207,
   Author = {Koenen, KC and Moffitt, TE and Roberts, AL and Martin, LT and Kubzansky,
             L and Harrington, H and Poulton, R and Caspi, A},
   Title = {Childhood IQ and adult mental disorders: a test of the
             cognitive reserve hypothesis.},
   Journal = {The American journal of psychiatry},
   Volume = {166},
   Number = {1},
   Pages = {50-57},
   Year = {2009},
   Month = {January},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/19047325},
   Abstract = {<h4>Objective</h4>Cognitive reserve has been proposed as
             important in the etiology of neuropsychiatric disorders.
             However, tests of the association between premorbid IQ and
             adult mental disorders other than schizophrenia have been
             limited and inconclusive. The authors tested the hypothesis
             that low childhood IQ is associated with increased risk and
             severity of adult mental disorders.<h4>Method</h4>Participants
             were members of a representative 1972-1973 birth cohort of
             1,037 males and females in Dunedin, New Zealand, who were
             followed up to age 32 with 96% retention. WISC-R IQ was
             assessed at ages 7, 9, and 11. Research diagnoses of DSM
             mental disorders were made at ages 18, 21, 26, and
             32.<h4>Results</h4>Lower childhood IQ was associated with
             increased risk of developing schizophrenia spectrum
             disorder, adult depression, and adult anxiety. Lower
             childhood IQ was also associated with greater comorbidity
             and with persistence of depression; the association with
             persistence of generalized anxiety disorder was nearly
             significant. Higher childhood IQ predicted increased risk of
             adult mania.<h4>Conclusions</h4>Lower cognitive reserve, as
             reflected by childhood IQ, is an antecedent of several
             common psychiatric disorders and also predicts persistence
             and comorbidity. Thus, many patients who seek mental health
             treatment may have lower cognitive ability; this should be
             considered in prevention and treatment planning.},
   Doi = {10.1176/appi.ajp.2008.08030343},
   Key = {fds253207}
}

@article{fds253208,
   Author = {Milne, BJ and Caspi, A and Crump, R and Poulton, R and Rutter, M and Sears,
             MR and Moffitt, TE},
   Title = {The validity of the family history screen for assessing
             family history of mental disorders.},
   Journal = {American journal of medical genetics. Part B,
             Neuropsychiatric genetics : the official publication of the
             International Society of Psychiatric Genetics},
   Volume = {150B},
   Number = {1},
   Pages = {41-49},
   Year = {2009},
   Month = {January},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/18449865},
   Abstract = {There is a need to collect psychiatric family history
             information quickly and economically (e.g., for genome-wide
             studies and primary care practice). We sought to evaluate
             the validity of family history reports using a brief
             screening instrument, the Family History Screen (FHS). We
             assessed the validity of parents' reports of seven
             psychiatric disorders in their adult children probands from
             the Dunedin Study (n = 959, 52% male), using the proband's
             diagnosis as the criterion outcome. We also investigated
             whether there were informant characteristics that enhanced
             accuracy of reporting or were associated with reporting
             biases. Using reports from multiple informants, we obtained
             sensitivities ranging from 31.7% (alcohol dependence) to
             60.0% (conduct disorder) and specificities ranging from
             76.0% (major depressive episode) to 97.1% (suicide attempt).
             There was little evidence that any informant characteristics
             enhanced accuracy of reporting. However, three reporting
             biases were found: the probability of reporting disorder in
             the proband was greater for informants with versus without a
             disorder, for female versus male informants, and for younger
             versus older informants. We conclude that the FHS is as
             valid as other family history instruments (e.g., the FH-RDC,
             FISC), and its brief administration time makes it a
             cost-effective method for collecting family history data. To
             avoid biasing results, researchers who aim to compare groups
             in terms of their family history should ensure that the
             informants reporting on these groups do not differ in terms
             of age, sex or personal history of disorder.},
   Doi = {10.1002/ajmg.b.30764},
   Key = {fds253208}
}

@article{fds253252,
   Author = {Lynam, DR and Charnigo, R and Moffitt, TE and Raine, A and Loeber, R and Stouthamer-Loeber, M},
   Title = {The stability of psychopathy across adolescence.},
   Journal = {Development and psychopathology},
   Volume = {21},
   Number = {4},
   Pages = {1133-1153},
   Year = {2009},
   Month = {January},
   ISSN = {0954-5794},
   url = {http://dx.doi.org/10.1017/s0954579409990083},
   Abstract = {The current diagnostic system suggests that personality
             disorder categories be applied to children and adolescents
             in rare circumstances because of expected changes in
             personality pathology across development. The present study
             examined the stability in personality pathology,
             specifically psychopathy, across childhood and adolescence.
             Using a short form of the CPS and mixed models incorporating
             fixed and random effects, we examined the reliability,
             individual stability, mean-level stability, and predictive
             utility of juvenile psychopathy as a function of age (i.e.,
             from 7 to 17 years old) in over 1,500 boys from the three
             cohorts of the Pittsburgh Youth Study. If adolescent
             development contributes to instability in personality
             pathology, large age-related fluctuations in reliability,
             stability, and predictive utility should be observed,
             particularly in the latter part of adolescence when
             normative changes are hypothesized to influence levels of
             psychopathy. Such fluctuations were not observed. In
             general, juvenile psychopathy could be reliably assessed
             beginning in childhood, was fairly stable across short and
             long intervals, showed little mean-level fluctuation, and
             predicted delinquency across adolescence. These results
             suggest that concerns about large changes in personality
             pathology across childhood and adolescence may be
             overstated. Implications and future directions are
             discussed.},
   Doi = {10.1017/s0954579409990083},
   Key = {fds253252}
}

@article{fds168663,
   Author = {Danese, A. and Moffitt, T.E. and Harrington, HL. and Milne, B. and Polanczyk, G. and Pariente, C. and Poulton, R. and Caspi,
             A.},
   Title = {Adverse childhood experiences predict adult risk factors for
             age-related disease: depression, inflammation, and
             clustering of metabolic risk markers},
   Journal = {Archives of Pediatric and Adolescent Medicine},
   Volume = {163},
   Pages = {1135-1143},
   Year = {2009},
   Key = {fds168663}
}

@article{fds140041,
   Author = {Baker, T and Moffitt, T.E. and Caspi, A.},
   Title = {Phenotypes & Endophenotypes},
   Journal = {Foundations for Genetic Studies of Nicotine Use and
             Dependence},
   Booktitle = {NCI tobacco Control Monograph},
   Year = {2009},
   Key = {fds140041}
}

@article{fds253170,
   Author = {Lussier, P and Farrington, D and Moffitt, TE},
   Title = {Is the antisocial child father of the abusive man? A 40-year
             prospective longitudinal study on the development
             antecedents of intimate partner violence.},
   Journal = {Criminology},
   Volume = {47},
   Number = {3},
   Pages = {401-440},
   Publisher = {WILEY},
   Year = {2009},
   ISSN = {0011-1384},
   url = {http://dx.doi.org/10.1111/j.1745-9125.2009.00160.x},
   Abstract = {This prospective longitudinal study examined whether early
             childhood risk factors contributed to explaining and
             predicting intimate partner violence (IPV) in midadulthood.
             Participants included 202 men from the Cambridge
             longitudinal study who were in an intimate relationship in
             their mid-40s. Neuropsychological deficits and the presence
             of a criminogenic family environment were measured between
             ages 8 and 10. Antisocial behavior was measured between ages
             8 and 18. IPV was measured at age 48 using a self-report
             instrument completed by the participants' female partners.
             Perpetration and victimization rates were relatively high;
             violence was mostly mutual, and men were more likely to be
             victims than perpetrators. Findings indicate that a
             criminogenic environment increases the risk of IPV by
             fostering the development of antisocial behavior and
             neuropsychological deficits. A link also exists between a
             high level of antisocial behavior during adolescence and the
             risk of IPV later in life. The results suggest the presence
             of both continuity and discontinuity of antisocial behavior
             as childhood risk factors that increase the likelihood of
             future involvement in IPV, but the role of these risk
             factors is modest. © 2009 American Society of
             Criminology.},
   Doi = {10.1111/j.1745-9125.2009.00160.x},
   Key = {fds253170}
}

@article{fds253254,
   Author = {Melchior, M and Caspi, A and Moffitt, TE},
   Title = {The mental health context of food insecurity},
   Journal = {Pediatrics},
   Volume = {124},
   Pages = {564-572},
   Year = {2009},
   Key = {fds253254}
}

@article{fds253279,
   Author = {Milne, BJ and Caspi, A and Harrington, HL and Poulton, R and Rutter, M and Moffitt, TE},
   Title = {Does family history indicate a more serious form of illness?
             The case for depression, anxiety, alcohol dependence and
             drug dependence},
   Journal = {Archives of General Psychiatry},
   Volume = {66},
   Number = {7},
   Pages = {738-747},
   Year = {2009},
   Key = {fds253279}
}

@article{fds253286,
   Author = {Hancox, RJ and Poulton, R and Welch, D and Olova, N and McLachlan, CR and Greene, JM and Sears, MR and Caspi, A and Moffitt, TE and Robertson, SP and Braithwaite, AW},
   Title = {Accelerated decline in lung function in cigarette smokers is
             associated with TP53/HDM2 polymorphisms.},
   Journal = {Human Genetics},
   Volume = {126},
   Number = {4},
   Pages = {559-565},
   Year = {2009},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/19521721},
   Abstract = {In vitro studies have shown that p53 mediates a protective
             response against DNA damage by causing either cell-cycle
             arrest and DNA repair, or apoptosis. These responses have
             not yet been demonstrated in humans. A common source of DNA
             damage in humans is cigarette smoke, which should activate
             p53 repair mechanisms. As the level of p53 is regulated by
             MDM2, which targets p53 for degradation, the G-allele of a
             polymorphism in intron 1 of MDM2 (rs2279744:G/T), that
             results in higher MDM2 levels, should be associated with a
             reduced p53 response and hence more DNA damage and
             corresponding tissue destruction. Similarly, the alleles of
             rs1042522 in TP53 that encode arginine (G-allele) or proline
             (C-allele) at codon 72, which cause increased pro-apoptotic
             (G-allele) or cell-cycle arrest activities (C-allele),
             respectively, may moderate p53's ability to prevent DNA
             damage. To test these hypotheses, we examined lung function
             in relation to cumulative history of smoking in a
             population-based cohort. The G-alleles in MDM2 and TP53 were
             found to be associated with accelerated smoking-related
             decline in lung function. These data support the hypothesis
             that p53 protects from DNA damage in humans and provides a
             potential explanation for the variation in lung function
             impairment amongst smokers.},
   Doi = {10.1007/s00439-009-0704-z},
   Key = {fds253286}
}

@article{fds336542,
   Author = {Milne, BJ and Caspi, A and Crump, R and Poulton, R and Rutter, M and Sears,
             MR and Moffitt, TE},
   Title = {The validity of a breif economical screening instrument for
             assessing family history of mental disorders.},
   Journal = {American Journal of Medical Genetics Part B:
             Neuropsychiatric Genetics},
   Volume = {150B},
   Pages = {41-49},
   Year = {2009},
   Key = {fds336542}
}

@article{fds253301,
   Author = {Milne, BJ and Moffitt, TE and Crump, R and Poulton, R and Rutter, M and Sears, MR and Taylor, A and Caspi, A},
   Title = {How should we construct psychiatric family history scores? A
             comparison of alternative approaches from the Dunedin Family
             Health History Study.},
   Journal = {Psychological medicine},
   Volume = {38},
   Number = {12},
   Pages = {1793-1802},
   Year = {2008},
   Month = {December},
   ISSN = {0033-2917},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/18366822},
   Abstract = {<h4>Background</h4>There is increased interest in assessing
             the family history of psychiatric disorders for both genetic
             research and public health screening. It is unclear how best
             to combine family history reports into an overall score. We
             compare the predictive validity of different family history
             scores.<h4>Method</h4>Probands from the Dunedin Study
             (n=981, 51% male) had their family history assessed for nine
             different conditions. We computed four family history scores
             for each disorder: (1) a simple dichotomous categorization
             of whether or not probands had any disordered first-degree
             relatives; (2) the observed number of disordered
             first-degree relatives; (3) the proportion of first-degree
             relatives who are disordered; and (4) Reed's score, which
             expressed the observed number of disordered first-degree
             relatives in terms of the number expected given the age and
             sex of each relative. We compared the strength of
             association between each family history score and probands'
             disorder outcome.<h4>Results</h4>Each score produced
             significant family history associations for all disorders.
             The scores that took account of the number of disordered
             relatives within families (i.e. the observed, proportion,
             and Reed's scores) produced significantly stronger
             associations than the dichotomous score for conduct
             disorder, alcohol dependence and smoking. Taking account of
             family size (i.e. using the proportion or Reed's score)
             produced stronger family history associations depending on
             the prevalence of the disorder among family
             members.<h4>Conclusions</h4>Dichotomous family history
             scores can be improved upon by considering the number of
             disordered relatives in a family and the population
             prevalence of the disorder.},
   Doi = {10.1017/s0033291708003115},
   Key = {fds253301}
}

@article{fds253278,
   Author = {Odgers, CL and Caspi, A and Nagin, DS and Piquero, AR and Slutske, WS and Milne, BJ and Dickson, N and Poulton, R and Moffitt,
             TE},
   Title = {Is it important to prevent early exposure to drugs and
             alcohol among adolescents?},
   Journal = {Psychological science},
   Volume = {19},
   Number = {10},
   Pages = {1037-1044},
   Year = {2008},
   Month = {October},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/19000215},
   Abstract = {Exposure to alcohol and illicit drugs during early
             adolescence has been associated with poor outcomes in
             adulthood. However, many adolescents with exposure to these
             substances also have a history of conduct problems, which
             raises the question of whether early exposure to alcohol and
             drugs leads to poor outcomes only for those adolescents who
             are already at risk. In a 30-year prospective study, we
             tested whether there was evidence that early substance
             exposure can be a causal factor for adolescents' future
             lives. After propensity-score matching, early-exposed
             adolescents remained at an increased risk for a number of
             poor outcomes. Approximately 50% of adolescents exposed to
             alcohol and illicit drugs prior to age 15 had no
             conduct-problem history, yet were still at an increased risk
             for adult substance dependence, herpes infection, early
             pregnancy, and crime. Efforts to reduce or delay early
             substance exposure may prevent a wide range of adult health
             problems and should not be restricted to adolescents who are
             already at risk.},
   Doi = {10.1111/j.1467-9280.2008.02196.x},
   Key = {fds253278}
}

@article{fds340548,
   Author = {Danese, A and Moffitt, TE and Pariante, CM and Ambler, A and Poulton, R and Caspi, A},
   Title = {Elevated inflammation levels in depressed adults with a
             history of childhood maltreatment (vol 65, pg 409,
             2008)},
   Journal = {ARCHIVES OF GENERAL PSYCHIATRY},
   Volume = {65},
   Number = {6},
   Pages = {725-725},
   Publisher = {AMER MEDICAL ASSOC},
   Year = {2008},
   Month = {June},
   Key = {fds340548}
}

@article{UNKNOWN,
   Author = {Koenen, KC and Moffitt, TE and Caspi, A and Gregory, A and Harrington,
             H and Poulton, R},
   Title = {The developmental mental-disorder histories of adults with
             posttraumatic stress disorder: a prospective longitudinal
             birth cohort study.},
   Journal = {Journal of abnormal psychology},
   Volume = {117},
   Number = {2},
   Pages = {460-466},
   Year = {2008},
   Month = {May},
   ISSN = {0021-843X},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/18489223},
   Keywords = {posttraumatic stress disorder trauma comorbidity birth
             cohort epidemiology national-comorbidity-survey dsm-iv
             disorders psychiatric-disorders prevalence childhood
             lifetime anxiety mood},
   Abstract = {Clinical and epidemiologic studies have established that
             posttraumatic stress disorder (PTSD) is highly comorbid with
             other mental disorders. However, such studies have largely
             relied on adults' retrospective reports to ascertain
             comorbidity. The authors examined the developmental mental
             health histories of adults with PTSD using data on mental
             disorders assessed across the first 3 decades of life among
             members of the longitudinal Dunedin Multidisciplinary Health
             and Development Study; 100% of those diagnosed with
             past-year PTSD and 93.5% of those with lifetime PTSD at age
             26 had met criteria for another mental disorder between ages
             11 and 21. Most other mental disorders had first onsets by
             age 15. Of new cases of PTSD arising between ages 26 and 32,
             96% had a prior mental disorder and 77% had been diagnosed
             by age 15. These data suggest PTSD almost always develops in
             the context of other mental disorders. Research on the
             etiology of PTSD may benefit from taking lifetime
             developmental patterns of comorbidity into consideration.
             Juvenile mental-disorder histories may help indicate which
             individuals are most likely to develop PTSD in populations
             at high risk of trauma exposure.},
   Doi = {10.1037/0021-843x.117.2.460},
   Key = {UNKNOWN}
}

@article{UNKNOWN,
   Author = {Danese, A and Moffitt, TE and Pariante, CM and Ambler, A and Poulton, R and Caspi, A},
   Title = {Elevated inflammation levels in depressed adults with a
             history of childhood maltreatment.},
   Journal = {Archives of general psychiatry},
   Volume = {65},
   Number = {4},
   Pages = {409-415},
   Year = {2008},
   Month = {April},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/18391129},
   Keywords = {c-reactive protein coronary-heart-disease early-life stress
             major depression cardiovascular-disease myocardial-infarction
             responses abuse association comorbidity},
   Abstract = {<h4>Context</h4>The association between depression and
             inflammation is inconsistent across research
             samples.<h4>Objective</h4>To test whether a history of
             childhood maltreatment could identify a subgroup of
             depressed individuals with elevated inflammation levels,
             thus helping to explain previous inconsistencies.<h4>Design</h4>Prospective
             longitudinal cohort study.<h4>Setting</h4>New
             Zealand.<h4>Participants</h4>A representative birth cohort
             of 1000 individuals was followed up to age 32 years as part
             of the Dunedin Multidisciplinary Health and Development
             Study. Study members were assessed for history of childhood
             maltreatment and current depression.<h4>Main outcome
             measures</h4>Inflammation was assessed using a clinically
             relevant categorical measure of high-sensitivity C-reactive
             protein (>3 mg/L) and a dimensional inflammation factor
             indexing the shared variance of continuous measures of
             high-sensitivity C-reactive protein, fibrinogen, and white
             blood cells.<h4>Results</h4>Although depression was
             associated with high levels of high-sensitivity C-reactive
             protein (relative risk,1.45; 95% confidence
             interval,1.06-1.99), this association was significantly
             attenuated and no longer significant when the effect of
             childhood maltreatment was taken into account. Individuals
             with current depression and a history of childhood
             maltreatment were more likely to have high levels of
             high-sensitivity C-reactive protein compared with control
             subjects (n = 27; relative risk, 2.07; 95% confidence
             interval, 1.23-3.47). In contrast, individuals with current
             depression only had a nonsignificant elevation in risk (n =
             109; relative risk, 1.40; 95% confidence interval,
             0.97-2.01). Results were generalizable to the inflammation
             factor. The elevated inflammation levels in individuals who
             were both depressed and maltreated were not explained by
             correlated risk factors such as depression recurrence, low
             socioeconomic status in childhood or adulthood, poor health,
             or smoking.<h4>Conclusions</h4>A history of childhood
             maltreatment contributes to the co-occurrence of depression
             and inflammation. Information about experiences of childhood
             maltreatment may help to identify depressed individuals with
             elevated inflammation levels and, thus, at greater risk of
             cardiovascular disease.},
   Doi = {10.1001/archpsyc.65.4.409},
   Key = {UNKNOWN}
}

@article{UNKNOWN,
   Author = {Ordoñana, JR and Caspi, A and Moffitt, TE},
   Title = {Unintentional injuries in a twin study of preschool
             children: environmental, not genetic, risk
             factors.},
   Journal = {Journal of pediatric psychology},
   Volume = {33},
   Number = {2},
   Pages = {185-194},
   Year = {2008},
   Month = {March},
   ISSN = {0146-8693},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/17569713},
   Keywords = {environmental factors genetic predisposition injury-prone
             twins unintentional injuries caregiver supervision behavior
             disorders vital-statistics childhood hyperactivity
             temperament population toddlers history mothers},
   Abstract = {<h4>Objective</h4>To analyze the relative contribution of
             latent genetic and environmental factors to differences in
             the injury liability of children, and to examine the
             association between measured socio-economic, family, and
             child-behavior variables and unintentional injury
             risk.<h4>Methods</h4>Unintentional injuries from birth to
             age 5, together with information regarding measured risk
             variables, were reported by mothers in a sample of 1027
             same-sex twin pairs from a nationally representative
             1994-1995 birth cohort.<h4>Results</h4>Child-specific
             environmental factors accounted for most of the variance
             (86.4%) in the likelihood of ever having an injury. When
             considering the risk of two or more injuries child-specific
             environmental factors explained 60.2% of the variance and
             family-wide environmental influence 39.8%. Measured
             socio-economic, family, and child-behavior factors predicted
             frequent injury.<h4>Conclusions</h4>Results give little
             support to the concept of a heritable injury-prone trait in
             preschool children; environmental influences accounted for
             most of the injury variance in this sample. However,
             behavioral variables, especially the child's externalizing
             problem behaviors, are also important in explaining
             unintentional injuries.},
   Doi = {10.1093/jpepsy/jsm041},
   Key = {UNKNOWN}
}

@article{fds253281,
   Author = {Arseneault, L and Milne, BJ and Taylor, A and Adams, F and Delgado, K and Caspi, A and Moffitt, TE},
   Title = {Being bullied as an environmentally mediated contributing
             factor to children's internalizing problems: a study of
             twins discordant for victimization.},
   Journal = {Archives of pediatrics & adolescent medicine},
   Volume = {162},
   Number = {2},
   Pages = {145-150},
   Year = {2008},
   Month = {February},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/18250239},
   Abstract = {<h4>Objective</h4>To test whether the experience of being
             bullied has an environmentally mediated effect on
             internalizing symptoms in young children.<h4>Design</h4>A
             genetically informative, longitudinal 1994-1995 birth
             cohort.<h4>Setting</h4>A nationally representative sample
             from the United Kingdom.<h4>Participants</h4>We examined
             1116 twin pairs who are participants in the Environmental
             Risk Longitudinal Twin Study. Main Exposure The experience
             of being bullied between the ages of 7 and 9 years.<h4>Main
             outcome measures</h4>Mothers' and teachers' reports of
             children's internalizing problems at 7 and 10 years of
             age.<h4>Results</h4>Monozygotic twins who had been bullied
             had more internalizing symptoms (mean, 0.23; SD, 1.00)
             compared with their co-twin who had not been bullied (mean,
             -0.13; SD, 0.86), indicating that being bullied has an
             environmentally mediated effect on children's internalizing
             problems (beta, 0.36 [95% confidence interval (CI),
             0.18-0.54]). This effect remained significant after
             controlling for preexisting internalizing problems (beta,
             0.26 [95% CI, 0.09-0.44]).<h4>Conclusions</h4>Being bullied
             at a young age is an environmentally mediated contributing
             factor to children's internalizing problems. Intervention
             programs aimed at reducing bullying behavior in schools and
             in the community have the potential to influence children's
             early symptoms of mental health problems.},
   Doi = {10.1001/archpediatrics.2007.53},
   Key = {fds253281}
}

@article{UNKNOWN,
   Author = {Caspi, A and Langley, K and Milne, B and Moffitt, TE and O'Donovan, M and Owen, MJ and Polo Tomas and M and Poulton, R and Rutter, M and Taylor, A and Williams, B and Thapar, A},
   Title = {A replicated molecular genetic basis for subtyping
             antisocial behavior in children with attention-deficit/hyperactivity
             disorder.},
   Journal = {Archives of general psychiatry},
   Volume = {65},
   Number = {2},
   Pages = {203-210},
   Year = {2008},
   Month = {February},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/18250258},
   Keywords = {catechol-o-methyltransferase deficit-hyperactivity-disorder
             val(158)met genotype prefrontal function conduct disorder
             human brain comt adhd predictors modulation},
   Abstract = {<h4>Context</h4>Attention-deficit/hyperactivity disorder
             (ADHD) is a heterogeneous neurodevelopmental disorder that
             in some cases is accompanied by antisocial
             behavior.<h4>Objective</h4>To test if variations in the
             catechol O-methyltransferase gene (COMT) would prove useful
             in identifying the subset of children with ADHD who exhibit
             antisocial behavior.<h4>Design</h4>Three independent samples
             composed of 1 clinical sample of ADHD cases and 2 birth
             cohort studies.<h4>Participants</h4>Participants in the
             clinical sample were drawn from child psychiatry and child
             health clinics in England and Wales. The 2 birth cohort
             studies included 1 sample of 2232 British children born in
             1994-1995 and a second sample of 1037 New Zealander children
             born in 1972-1973.<h4>Main outcome measures</h4>Diagnosis of
             ADHD and measures of antisocial behavior.<h4>Results</h4>We
             present replicated evidence that the COMT valine/methionine
             polymorphism at codon 158 (COMT Val158Met) was associated
             with phenotypic variation among children with ADHD. Across
             the 3 samples, valine/valine homozygotes had more symptoms
             of conduct disorder, were more aggressive, and were more
             likely to be convicted of criminal offenses compared with
             methionine carriers.<h4>Conclusions</h4>The findings confirm
             the presence of genetic heterogeneity in ADHD and illustrate
             how genetic information may provide biological evidence
             pointing to clinical subtypes.},
   Doi = {10.1001/archgenpsychiatry.2007.24},
   Key = {UNKNOWN}
}

@article{UNKNOWN,
   Author = {Thomson, WM and Poulton, R and Broadbent, JM and Moffitt, TE and Caspi,
             A and Beck, JD and Welch, D and Hancox, RJ},
   Title = {Cannabis smoking and periodontal disease among young
             adults.},
   Journal = {JAMA},
   Volume = {299},
   Number = {5},
   Pages = {525-531},
   Year = {2008},
   Month = {February},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/18252882},
   Keywords = {self-reported smoking cigarette-smoking new-zealand validity
             index},
   Abstract = {<h4>Context</h4>Tobacco smoking is a recognized behavioral
             risk factor for periodontal disease (through its systemic
             effects), and cannabis smoking may contribute in a similar
             way.<h4>Objective</h4>To determine whether cannabis smoking
             is a risk factor for periodontal disease.<h4>Design and
             setting</h4>Prospective cohort study of the general
             population, with cannabis use determined at ages 18, 21, 26,
             and 32 years and dental examinations conducted at ages 26
             and 32 years. The most recent data collection (at age 32
             years) was completed in June 2005.<h4>Participants</h4>A
             complete birth cohort born in 1972 and 1973 in Dunedin, New
             Zealand, and assessed periodically (with a 96% follow-up
             rate of the 1015 participants who survived to age 32 years).
             Complete data for this analysis were available from 903
             participants (comprising 89.0% of the surviving birth
             cohort).<h4>Main outcome measure</h4>Periodontal disease
             status at age 32 years (and changes from ages 26 to 32
             years) determined from periodontal combined attachment loss
             (CAL) measured at 3 sites per tooth.<h4>Results</h4>Three
             cannabis exposure groups were determined: no exposure (293
             individuals, or 32.3%), some exposure (428; 47.4%), and high
             exposure (182; 20.2%). At age 32 years, 265 participants
             (29.3%) had 1 or more sites with 4 mm or greater CAL, and
             111 participants (12.3%) had 1 or more sites with 5 mm or
             greater CAL. Incident attachment loss between the ages of 26
             and 32 years in the none, some, and high cannabis exposure
             groups was 6.5%, 11.2%, and 23.6%, respectively. After
             controlling for tobacco smoking (measured in pack-years),
             sex, irregular use of dental services, and dental plaque,
             the relative risk estimates for the highest cannabis
             exposure group were as follows: 1.6 (95% confidence interval
             [CI], 1.2-2.2) for having 1 or more sites with 4 mm or
             greater CAL; 3.1 (95% CI, 1.5-6.4) for having 1 or more
             sites with 5 mm or greater CAL; and 2.2 (95% CI, 1.2-3.9)
             for having incident attachment loss (in comparison with
             those who had never smoked cannabis). Tobacco smoking was
             strongly associated with periodontal disease experience, but
             there was no interaction between cannabis use and tobacco
             smoking in predicting the condition's occurrence.<h4>Conclusion</h4>Cannabis
             smoking may be a risk factor for periodontal disease that is
             independent of the use of tobacco.},
   Doi = {10.1001/jama.299.5.525},
   Key = {UNKNOWN}
}

@article{UNKNOWN,
   Author = {Moffitt, TE and Arseneault, L and Jaffee, SR and Kim-Cohen, J and Koenen, KC and Odgers, CL and Slutske, WS and Viding,
             E},
   Title = {Research review: DSM-V conduct disorder: research needs for
             an evidence base.},
   Journal = {Journal of child psychology and psychiatry, and allied
             disciplines},
   Volume = {49},
   Number = {1},
   Pages = {3-33},
   Year = {2008},
   Month = {January},
   ISSN = {0021-9630},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/18181878},
   Keywords = {conduct disorder dsm-v oppositional defiant disorder
             antisocial personality-disorder callous-unemotional traits
             great-smoky mountains deficit hyperactivity disorder
             disruptive behavior disorders alcohol epidemiologic survey
             life-course-persistent family history method iv field
             trials},
   Abstract = {This article charts a strategic research course toward an
             empirical foundation for the diagnosis of conduct disorder
             in the forthcoming DSM-V. Since the DSM-IV appeared in 1994,
             an impressive amount of new information about conduct
             disorder has emerged. As a result of this new knowledge,
             reasonable rationales have been put forward for adding to
             the conduct disorder diagnostic protocol: a
             childhood-limited subtype, family psychiatric history,
             callous-unemotional traits, female-specific criteria,
             preschool-specific criteria, early substance use, and
             biomarkers from genetics, neuroimaging, and physiology
             research. This article reviews the evidence for these and
             other potential changes to the conduct disorder diagnosis.
             We report that although there is a great deal of exciting
             research into each of the topics, very little of it provides
             the precise sort of evidence base required to justify any
             alteration to the DSM-V. We outline specific research
             questions and study designs needed to build the lacking
             evidence base for or against proposed changes to DSM-V
             conduct disorder.},
   Doi = {10.1111/j.1469-7610.2007.01823.x},
   Key = {UNKNOWN}
}

@article{UNKNOWN,
   Author = {Viding, E and Jones, AP and Frick, PJ and Moffitt, TE and Plomin,
             R},
   Title = {Heritability of antisocial behaviour at 9: do
             callous-unemotional traits matter?},
   Journal = {Developmental science},
   Volume = {11},
   Number = {1},
   Pages = {17-22},
   Year = {2008},
   Month = {January},
   ISSN = {1363-755X},
   url = {http://dx.doi.org/10.1111/j.1467-7687.2007.00648.x},
   Keywords = {psychopathic personality-traits twins early development
             conduct problems children multivariate 7-year-olds childhood
             community cognition etiology},
   Abstract = {A previous finding from our group indicated that
             teacher-rated antisocial behaviour (AB) among 7-year-olds is
             particularly heritable in the presence of
             callous-unemotional (CU) traits. Using a sample of 1865
             same-sex twin pairs, we employed DeFries-Fulker extremes
             analysis to investigate whether teacher-rated AB
             with/without CU traits also shows aetiological differences
             among 9-year-olds. Furthermore, we assessed whether the
             differences in the magnitude of heritability would be
             evident even when hyperactive symptoms were controlled for
             in the statistical analysis. AB among 9-year-olds was more
             heritable with than without concomitant CU. The heritability
             difference was even more pronounced in magnitude when
             hyperactive symptoms were controlled. CU traits thus appear
             to index one valid way of sub-typing children with
             early-onset AB.},
   Doi = {10.1111/j.1467-7687.2007.00648.x},
   Key = {UNKNOWN}
}

@article{UNKNOWN,
   Author = {Odgers, CL and Moffitt, TE and Broadbent, JM and Dickson, N and Hancox,
             RJ and Harrington, H and Poulton, R and Sears, MR and Thomson, WM and Caspi, A},
   Title = {Female and male antisocial trajectories: from childhood
             origins to adult outcomes.},
   Journal = {Development and psychopathology},
   Volume = {20},
   Number = {2},
   Pages = {673-716},
   Year = {2008},
   Month = {January},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/18423100},
   Keywords = {life-course-persistent information maximum-likelihood
             developmental trajectories conduct disorder young-adults
             birth cohort adolescent delinquency offending trajectories
             measurement invariance methodological issues},
   Abstract = {This article reports on the childhood origins and adult
             outcomes of female versus male antisocial behavior
             trajectories in the Dunedin longitudinal study. Four
             antisocial behavior trajectory groups were identified among
             females and males using general growth mixture modeling and
             included life-course persistent (LCP), adolescent-onset,
             childhood-limited, and low trajectory groups. During
             childhood, both LCP females and males were characterized by
             social, familial and neurodevelopmental risk factors,
             whereas those on the adolescent-onset pathway were not. At
             age 32, women and men on the LCP pathway were engaging in
             serious violence and experiencing significant mental health,
             physical health, and economic problems. Females and males on
             the adolescent-onset pathway were also experiencing
             difficulties at age 32, although to a lesser extent.
             Although more males than females followed the LCP
             trajectory, findings support similarities across gender with
             respect to developmental trajectories of antisocial behavior
             and their associated childhood origins and adult
             consequences. Implications for theory, research, and
             practice are discussed.},
   Doi = {10.1017/s0954579408000333},
   Key = {UNKNOWN}
}

@article{fds304720,
   Author = {Ball, HA and Arseneault, L and Taylor, A and Maughan, B and Caspi, A and Moffitt, TE},
   Title = {Genetic and environmental influences on victims, bullies and
             bully-victims in childhood.},
   Journal = {Journal of child psychology and psychiatry, and allied
             disciplines},
   Volume = {49},
   Number = {1},
   Pages = {104-112},
   Year = {2008},
   Month = {January},
   ISSN = {0021-9630},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/18181884},
   Abstract = {<h4>Background</h4>Three groups of children are involved in
             bullying: victims, bullies and bully-victims who are both
             bullies and victims of bullying. Understanding the origins
             of these groups is important since they have elevated
             emotional and behavioural problems, especially the
             bully-victims. No research has examined the genetic and
             environmental influences on these social
             roles.<h4>Method</h4>Mother and teacher reports of
             victimisation and bullying were collected in a nationally
             representative cohort of 1,116 families with 10-year-old
             twins. Model-fitting was used to examine the relative
             influence of genetics and environments on the liability to
             be a victim, a bully or a bully-victim.<h4>Results</h4>Twelve
             percent of children were severely bullied as victims, 13%
             were frequent bullies, and 2.5% were heavily involved as
             bully-victims. Genetic factors accounted for 73% of the
             variation in victimisation and 61% of the variation in
             bullying, with the remainder explained by environmental
             factors not shared between the twins. The covariation
             between victim and bully roles (r = .25), which
             characterises bully-victims, was accounted for by genetic
             factors only. Some genetic factors influenced both
             victimisation and bullying, although there were also genetic
             factors specific to each social role.<h4>Conclusions</h4>Children's
             genetic endowments, as well as their surrounding
             environments, influence which children become victims,
             bullies and bully-victims. Future research identifying
             mediating characteristics that link the genetic and
             environmental influences to these social roles could provide
             targets for intervention.},
   Doi = {10.1111/j.1469-7610.2007.01821.x},
   Key = {fds304720}
}

@article{UNKNOWN,
   Author = {Milne, B.J. and Moffitt, T.E. and Crump, R. and Poulton, R. and Rutter, M. and Sears, M.?R. and Taylor, A. and Caspi,
             A.},
   Title = {How should we construct psychiatric family history scores? A
             comparison of alternative approaches from the Dunedin Family
             Health History Study},
   Journal = {Psychological Medicine},
   Volume = {38},
   Number = {12},
   Pages = {1793-1802},
   Year = {2008},
   Abstract = {BackgroundThere is increased interest in assessing the
             family history of psychiatric disorders for both genetic
             research and public health screening. It is unclear how best
             to combine family history reports into an overall score. We
             compare the predictive validity of different family history
             scores.MethodProbands from the Dunedin Study (n=981, 51%
             male) had their family history assessed for nine different
             conditions. We computed four family history scores for each
             disorder: (1) a simple dichotomous categorization of whether
             or not probands had any disordered first-degree relatives;
             (2) the observed number of disordered first-degree
             relatives; (3) the proportion of first-degree relatives who
             are disordered; and (4) Reed's score, which expressed the
             observed number of disordered first-degree relatives in
             terms of the number expected given the age and sex of each
             relative. We compared the strength of association between
             each family history score and probands' disorder
             outcome.ResultsEach score produced significant family
             history associations for all disorders. The scores that took
             account of the number of disordered relatives within
             families (i.e. the observed, proportion, and Reed's scores)
             produced significantly stronger associations than the
             dichotomous score for conduct disorder, alcohol dependence
             and smoking. Taking account of family size (i.e. using the
             proportion or Reed's score) produced stronger family history
             associations depending on the prevalence of the disorder
             among family members.ConclusionsDichotomous family history
             scores can be improved upon by considering the number of
             disordered relatives in a family and the population
             prevalence of the disorder.},
   Key = {UNKNOWN}
}

@article{fds140042,
   Author = {Danese, A. and Moffitt, T.E. and Pariente, C. and Poulton, R. and Caspi, A.},
   Title = {Elevated inflammation levels in depressed adults with a
             history of childhood maltreatment},
   Journal = {Archives of General Psychiatry},
   Volume = {65},
   Pages = {409-416},
   Year = {2008},
   Key = {fds140042}
}

@article{fds336543,
   Author = {Ordonana, J and Caspi, A and Moffitt, TE},
   Title = {Unintentional injuries in preschool children: Environmental,
             not genetic, risk factors in a twin study},
   Journal = {JPedPsychology},
   Pages = {185-194},
   Year = {2008},
   Key = {fds336543}
}

@article{fds253255,
   Author = {Ball, H and Arseneault, L and Taylor, A and Maughan, B and Caspi, A and Moffitt, TE},
   Title = {Genetic and environmental influences on victims, bullies and
             bully-victims in childhood},
   Journal = {JCPP},
   Volume = {49},
   Number = {1},
   Pages = {145-150},
   Year = {2008},
   ISSN = {0021-9630},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/18181884},
   Abstract = {BACKGROUND: Three groups of children are involved in
             bullying: victims, bullies and bully-victims who are both
             bullies and victims of bullying. Understanding the origins
             of these groups is important since they have elevated
             emotional and behavioural problems, especially the
             bully-victims. No research has examined the genetic and
             environmental influences on these social roles. METHOD:
             Mother and teacher reports of victimisation and bullying
             were collected in a nationally representative cohort of
             1,116 families with 10-year-old twins. Model-fitting was
             used to examine the relative influence of genetics and
             environments on the liability to be a victim, a bully or a
             bully-victim. RESULTS: Twelve percent of children were
             severely bullied as victims, 13% were frequent bullies, and
             2.5% were heavily involved as bully-victims. Genetic factors
             accounted for 73% of the variation in victimisation and 61%
             of the variation in bullying, with the remainder explained
             by environmental factors not shared between the twins. The
             covariation between victim and bully roles (r = .25), which
             characterises bully-victims, was accounted for by genetic
             factors only. Some genetic factors influenced both
             victimisation and bullying, although there were also genetic
             factors specific to each social role. CONCLUSIONS:
             Children's genetic endowments, as well as their surrounding
             environments, influence which children become victims,
             bullies and bully-victims. Future research identifying
             mediating characteristics that link the genetic and
             environmental influences to these social roles could provide
             targets for intervention.},
   Doi = {10.1111/j.1469-7610.2007.01821.x},
   Key = {fds253255}
}

@article{fds336544,
   Author = {Koenen, and K, and al, TEME},
   Title = {Childhood IQ and adult mental disorders},
   Journal = {American J of Psychiatry},
   Volume = {166},
   Pages = {50-57},
   Year = {2008},
   Key = {fds336544}
}

@article{fds253205,
   Author = {Caspi, A and Williams, B and Kim-Cohen, J and Craig, IW and Milne, BJ and Poulton, R and Schalkwyk, LC and Taylor, A and Werts, H and Moffitt,
             TE},
   Title = {Moderation of breastfeeding effects on the IQ by genetic
             variation in fatty acid metabolism.},
   Journal = {Proceedings of the National Academy of Sciences of the
             United States of America},
   Volume = {104},
   Number = {47},
   Pages = {18860-18865},
   Year = {2007},
   Month = {November},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/17984066},
   Abstract = {Children's intellectual development is influenced by both
             genetic inheritance and environmental experiences.
             Breastfeeding is one of the earliest such postnatal
             experiences. Breastfed children attain higher IQ scores than
             children not fed breast milk, presumably because of the
             fatty acids uniquely available in breast milk. Here we show
             that the association between breastfeeding and IQ is
             moderated by a genetic variant in FADS2, a gene involved in
             the genetic control of fatty acid pathways. We confirmed
             this gene-environment interaction in two birth cohorts, and
             we ruled out alternative explanations of the finding
             involving gene-exposure correlation, intrauterine growth,
             social class, and maternal cognitive ability, as well as
             maternal genotype effects on breastfeeding and breast milk.
             The finding shows that environmental exposures can be used
             to uncover novel candidate genes in complex phenotypes. It
             also shows that genes may work via the environment to shape
             the IQ, helping to close the nature versus nurture
             debate.},
   Doi = {10.1073/pnas.0704292104},
   Key = {fds253205}
}

@article{fds253204,
   Author = {Melchior, M and Moffitt, TE and Milne, BJ and Poulton, R and Caspi,
             A},
   Title = {Why do children from socioeconomically disadvantaged
             families suffer from poor health when they reach adulthood?
             A life-course study.},
   Journal = {American journal of epidemiology},
   Volume = {166},
   Number = {8},
   Pages = {966-974},
   Year = {2007},
   Month = {October},
   ISSN = {0002-9262},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/17641151},
   Abstract = {The authors investigated what risk factors contribute to an
             excess risk of poor adult health among children who
             experience socioeconomic disadvantage. Data came from 1,037
             children born in Dunedin, New Zealand, in 1972-1973, who
             were followed from birth to age 32 years (2004-2005).
             Childhood socioeconomic status (SES) was measured at
             multiple points between birth and age 15 years. Risk factors
             evaluated included a familial liability to poor health,
             childhood/adolescent health characteristics, low childhood
             intelligence quotient (IQ), exposure to childhood
             maltreatment, and adult SES. Adult health outcomes evaluated
             at age 32 years were major depressive disorder, anxiety
             disorders, tobacco dependence, alcohol or drug dependence,
             and clustering of cardiovascular disease risk factors.
             Results showed that low childhood SES was associated with an
             increased risk of substance dependence and poor physical
             health in adulthood (for tobacco dependence, sex-adjusted
             relative risk (RR) = 2.27, 95% confidence interval (CI):
             1.41, 3.65; for alcohol or drug dependence, RR = 2.11, 95%
             CI: 1.16, 3.84; for cardiovascular risk factor status, RR =
             2.55, 95% CI: 1.46, 4.46). Together, the risk factors
             studied here accounted for 55-67% of poor health outcomes
             among adults exposed to low SES as children. No single risk
             factor emerged as the prime explanation, suggesting that the
             processes mediating the link between childhood low SES and
             adult poor health are multifactorial.},
   Doi = {10.1093/aje/kwm155},
   Key = {fds253204}
}

@article{fds253260,
   Author = {Ramrakha, S and Bell, ML and Paul, C and Dickson, N and Moffitt, TE and Caspi, A},
   Title = {Childhood behavior problems linked to sexual risk taking in
             young adulthood: a birth cohort study.},
   Journal = {Journal of the American Academy of Child and Adolescent
             Psychiatry},
   Volume = {46},
   Number = {10},
   Pages = {1272-1279},
   Year = {2007},
   Month = {October},
   ISSN = {0890-8567},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/17885568},
   Abstract = {<h4>Objective</h4>To study whether behavioral and emotional
             problems during childhood predicted early sexual debut,
             risky sex at age 21 years, and sexually transmitted
             infections up to age 21 years. Some possible mediational
             pathways were also explored.<h4>Method</h4>Participants were
             enrolled in the Dunedin Multidisciplinary Health and
             Development Study (n = 1,037), a prospective, longitudinal
             study of a New Zealand birth cohort born in 1972-1973. Data
             obtained at ages 5, 7, 9, 11, 13, 15, and 21 years were
             used. Adjustment was made for gender, socioeconomic status,
             parenting factors, and residence changes.<h4>Results</h4>High
             levels of antisocial behavior between age 5 and 11 years
             were associated with increased odds of early sexual debut
             (adjusted odds ratio [AOR] 2.17, 95% confidence [CI]
             1.34-3.54) and risky sex (AOR 1.88, 95% CI 1.04-3.40). No
             relationship was observed between hyperactivity and later
             sexual health outcomes. In contrast, high levels of anxiety
             were associated with reduced odds of risky sex (AOR 0.45,
             95% CI 0.25-0.80) and sexually transmitted infections (AOR
             0.34, 95% CI 0.17-0.70). Involvement with delinquent peers
             explained some of the association between antisocial
             behavior and early sexual debut and risky sex. A poor
             relationship with parents also explained some of the
             association between antisocial behavior and early sexual
             debut.<h4>Conclusions</h4>The findings demonstrate links
             between behavioral and emotional problems occurring early in
             life and later deleterious sexual health outcomes. Targeting
             antisocial behavior and teaching accurate appraisals of
             danger during childhood may help mitigate these negative
             consequences.},
   Doi = {10.1097/chi.0b013e3180f6340e},
   Key = {fds253260}
}

@article{fds253299,
   Author = {Odgers, CL and Milne, BJ and Caspi, A and Crump, R and Poulton, R and Moffitt, TE},
   Title = {Predicting prognosis for the conduct-problem boy: can family
             history help?},
   Journal = {Journal of the American Academy of Child and Adolescent
             Psychiatry},
   Volume = {46},
   Number = {10},
   Pages = {1240-1249},
   Year = {2007},
   Month = {October},
   ISSN = {0890-8567},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/17885565},
   Abstract = {<h4>Objective</h4>Many children with conduct disorder
             develop life-course persistent antisocial behavior; however,
             other children exhibit childhood-limited or
             adolescence-limited conduct disorder symptoms and escape
             poor adult outcomes. Prospective prediction of long-term
             prognosis in pediatric and adolescent clinical settings is
             difficult. Improved prognosis prediction would support wise
             allocation of limited treatment resources. The purpose of
             this article is to evaluate whether family history of
             psychiatric disorder can statically predict long-term
             prognosis among conduct-problem children.<h4>Method</h4>Participants
             were male members of the Dunedin Study, a birth cohort of
             1,037 children (52% male). Conduct-problem subtypes were
             defined using prospective assessments between ages 7 and 26
             years. Family history interviews assessed mental disorders
             for three generations: the participants' grandparents,
             parents, and siblings.<h4>Results</h4>Family history of
             externalizing disorders distinguished life-course persistent
             antisocial males from other conduct-problem children and
             added significant incremental validity beyond family and
             child risk factors. A simple three-item family history
             screen of maternal-reported alcohol abuse was associated
             with life-course persistent prognosis in our research
             setting and should be evaluated in clinical
             practice.<h4>Conclusions</h4>: Family history of
             externalizing disorders distinguished between life-course
             persistent versus childhood-limited and adolescent-onset
             conduct problems. Brief family history questions may assist
             clinicians in pediatric settings to refine the diagnosis of
             conduct disorder and identify children who most need
             treatment.},
   Doi = {10.1097/chi.0b013e31813c6c8d},
   Key = {fds253299}
}

@article{fds253257,
   Author = {Roberts, BW and Harms, PD and Caspi, A and Moffitt,
             TE},
   Title = {Predicting the counterproductive employee in a
             child-to-adult prospective study.},
   Journal = {The Journal of applied psychology},
   Volume = {92},
   Number = {5},
   Pages = {1427-1436},
   Year = {2007},
   Month = {September},
   ISSN = {0021-9010},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/17845095},
   Abstract = {The present research tested the relations between a battery
             of background factors and counterproductive work behaviors
             in a 23-year longitudinal study of young adults (N = 930).
             Background information, such as diagnosed adolescent conduct
             disorder, criminal conviction records, intelligence, and
             personality traits, was assessed before participants entered
             the labor force. These background factors were combined with
             work conditions at age 26 to predict counterproductive work
             behaviors at age 26. The results showed that people
             diagnosed with childhood conduct disorder were more prone to
             commit counterproductive work behaviors in young adulthood
             and that these associations were partially mediated by
             personality traits measured at age 18. Contrary to
             expectations, criminal convictions that occurred prior to
             entering the workforce were unrelated to counterproductive
             work behaviors. Job conditions and personality traits had
             independent effects on counterproductive work behaviors,
             above and beyond background factors.},
   Doi = {10.1037/0021-9010.92.5.1427},
   Key = {fds253257}
}

@article{fds253302,
   Author = {Newcombe, R and Milne, BJ and Caspi, A and Poulton, R and Moffitt,
             TE},
   Title = {Birthweight predicts IQ: fact or artefact?},
   Journal = {Twin research and human genetics : the official journal of
             the International Society for Twin Studies},
   Volume = {10},
   Number = {4},
   Pages = {581-586},
   Year = {2007},
   Month = {August},
   ISSN = {1832-4274},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/17708699},
   Abstract = {It has been shown that lower birthweight is associated with
             lower IQ, but it remains unclear whether this association is
             causal or spurious. We examined the relationship between
             birthweight and IQ in two prospective longitudinal birth
             cohorts: a UK cohort of 1116 twin pairs (563 monozygotic
             [MZ] pairs), born in 1994-95, and a New Zealand cohort of
             1037 singletons born in 1972-73. IQ was tested with the
             Wechsler Intelligence Scales for Children. Birthweight
             differences within MZ twin pairs predicted IQ differences
             within pairs, ruling out genetic and shared environmental
             explanations for the association. Birthweight predicted IQ
             similarly in the twin and nontwin cohorts after controlling
             for social disadvantage, attesting that the association
             generalized beyond twins. An increase of 1000 g in
             birthweight was associated with a 3 IQ point increase.
             Results from two cohorts add to evidence that low
             birthweight is a risk factor for compromised neurological
             health. Our finding that birthweight differences predict IQ
             differences within MZ twin pairs provides new evidence that
             the mechanism can be narrowed to an environmental effect
             during pregnancy, rather than any familial environmental
             influence shared by siblings, or genes. With the increasing
             numbers of low-birthweight infants, our results support the
             contention that birthweight could be a target for early
             preventive intervention to reduce the number of children
             with compromised IQ.},
   Doi = {10.1375/twin.10.4.581},
   Key = {fds253302}
}

@article{fds253303,
   Author = {Melchior, M and Caspi, A and Milne, BJ and Danese, A and Poulton, R and Moffitt, TE},
   Title = {Work stress precipitates depression and anxiety in young,
             working women and men.},
   Journal = {Psychological medicine},
   Volume = {37},
   Number = {8},
   Pages = {1119-1129},
   Year = {2007},
   Month = {August},
   ISSN = {0033-2917},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/17407618},
   Abstract = {<h4>Background</h4>Rates of depression have been rising, as
             have rates of work stress. We tested the influence of work
             stress on diagnosed depression and anxiety in young working
             adults.<h4>Method</h4>Participants were enrolled in the
             Dunedin study, a 1972-1973 longitudinal birth cohort
             assessed most recently in 2004-2005, at age 32 (n=972, 96%
             of 1015 cohort members still alive). Work stress
             (psychological job demands, work decision latitude, low work
             social support, physical work demands) was ascertained by
             interview. Major depressive disorder (MDD) and generalized
             anxiety disorder (GAD) were ascertained using the Diagnostic
             Interview Schedule (DIS) and diagnosed according to DSM-IV
             criteria.<h4>Results</h4>Participants exposed to high
             psychological job demands (excessive workload, extreme time
             pressures) had a twofold risk of MDD or GAD compared to
             those with low job demands. Relative risks (RRs) adjusting
             for all work characteristics were: 1.90 [95% confidence
             interval (CI) 1.22-2.98] in women, and 2.00 (95% CI
             1.13-3.56) in men. Analyses ruled out the possibility that
             the association between work stress and disorder resulted
             from study members' socio-economic position, a personality
             tendency to report negatively, or a history of psychiatric
             disorder prior to labour-market entry. Prospective
             longitudinal analyses showed that high-demand jobs were
             associated with the onset of new depression and anxiety
             disorder in individuals without any pre-job history of
             diagnosis or treatment for either disorder.<h4>Conclusions</h4>Work
             stress appears to precipitate diagnosable depression and
             anxiety in previously healthy young workers. Helping workers
             cope with work stress or reducing work stress levels could
             prevent the occurrence of clinically significant depression
             and anxiety.},
   Doi = {10.1017/s0033291707000414},
   Key = {fds253303}
}

@article{fds253168,
   Author = {Moffitt, TE and Melchior, M},
   Title = {Why does the worldwide prevalence of childhood attention
             deficit hyperactivity disorder matter?},
   Journal = {The American journal of psychiatry},
   Volume = {164},
   Number = {6},
   Pages = {856-858},
   Year = {2007},
   Month = {June},
   ISSN = {0002-953X},
   url = {http://dx.doi.org/10.1176/ajp.2007.164.6.856},
   Doi = {10.1176/ajp.2007.164.6.856},
   Key = {fds253168}
}

@article{fds253305,
   Author = {Moffitt, TE and Harrington, H and Caspi, A and Kim-Cohen, J and Goldberg, D and Gregory, AM and Poulton, R},
   Title = {Depression and generalized anxiety disorder: cumulative and
             sequential comorbidity in a birth cohort followed
             prospectively to age 32 years.},
   Journal = {Archives of general psychiatry},
   Volume = {64},
   Number = {6},
   Pages = {651-660},
   Year = {2007},
   Month = {June},
   ISSN = {0003-990X},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/17548747},
   Abstract = {<h4>Context</h4>The close association between generalized
             anxiety disorder (GAD) and major depressive disorder (MDD)
             prompts questions about how to characterize this association
             in future diagnostic systems. Most information about GAD-MDD
             comorbidity comes from patient samples and retrospective
             surveys.<h4>Objective</h4>To revisit the sequential and
             cumulative comorbidity between GAD and MDD using data from a
             prospective longitudinal cohort.<h4>Design</h4>Prospective
             longitudinal cohort study.<h4>Setting</h4>New
             Zealand.<h4>Participants</h4>The representative 1972-1973
             Dunedin birth cohort of 1037 members was followed up to age
             32 years with 96% retention.<h4>Main outcome
             measures</h4>Research diagnoses of anxiety and depression
             were made at ages 11, 13, 15, 18, 21, 26, and 32 years.
             Mental health services were reported on a life history
             calendar.<h4>Results</h4>Sequentially, anxiety began before
             or concurrently in 37% of depression cases, but depression
             began before or concurrently in 32% of anxiety cases.
             Cumulatively, 72% of lifetime anxiety cases had a history of
             depression, but 48% of lifetime depression cases had
             anxiety. During adulthood, 12% of the cohort had comorbid
             GAD + MDD, of whom 66% had recurrent MDD, 47% had recurrent
             GAD, 64% reported using mental health services, 47% took
             psychiatric medication, 8% were hospitalized, and 11%
             attempted suicide. In this comorbid group, depression onset
             occurred first in one third of the participants, anxiety
             onset occurred first in one third, and depression and
             anxiety onset began concurrently in one third.<h4>Conclusions</h4>Challenging
             the prevailing notion that generalized anxiety usually
             precedes depression and eventually develops into depression,
             these findings show that the reverse pattern occurs almost
             as often. The GAD-MDD relation is strong, suggesting that
             the disorders could be classified in 1 category of distress
             disorders. Their developmental relation seems more
             symmetrical than heretofore presumed, suggesting that MDD is
             not necessarily primary over GAD in diagnostic hierarchy.
             This prospective study suggests that the lifetime prevalence
             of GAD and MDD may be underestimated by retrospective
             surveys and that comorbid GAD + MDD constitutes a greater
             mental health burden than previously thought.},
   Doi = {10.1001/archpsyc.64.6.651},
   Key = {fds253305}
}

@article{fds304719,
   Author = {Odgers, CL and Caspi, A and Broadbent, JM and Dickson, N and Hancox, RJ and Harrington, H and Poulton, R and Sears, MR and Thomson, WM and Moffitt,
             TE},
   Title = {Prediction of differential adult health burden by conduct
             problem subtypes in males.},
   Journal = {Archives of general psychiatry},
   Volume = {64},
   Number = {4},
   Pages = {476-484},
   Year = {2007},
   Month = {April},
   ISSN = {0003-990X},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/17404124},
   Abstract = {<h4>Context</h4>A cardinal feature of the DSM-IV diagnostic
             criteria for conduct disorder is the distinction between
             childhood- vs adolescent-onset subtypes. Whether such
             developmental subtypes exist in the population and have
             different prognoses should be rigorously tested to inform
             the DSM-V.<h4>Objectives</h4>To evaluate the epidemiological
             validity of childhood- vs adolescent-onset conduct problems
             in a prospective birth cohort, and to assess whether
             life-course-persistent conduct problems are associated with
             a greater adult health burden.<h4>Design, setting, and
             participants</h4>Our sample includes 526 male study members
             in the Dunedin Multidisciplinary Health and Development
             Study, a 1-year birth cohort (April 1, 1972, through March
             30, 1973). Developmental trajectories were defined using
             prospective ratings of conduct problems at 7, 9, 11, 13, 15,
             18, 21, and 26 years of age.<h4>Main outcome
             measures</h4>Health burden was assessed as mental and
             physical health problems at 32 years of age measured via
             diagnostic interviews and physical examinations.<h4>Results</h4>We
             identified the following 4 developmental subtypes of conduct
             problems through general growth mixture modeling: (1)
             childhood-onset/life-course-persistent, (2) adolescent
             onset, (3) childhood limited, and (4) low. At 32 years of
             age, study members with the life-course-persistent subtype
             experienced the worst health burden. To a lesser extent,
             those with the adolescent-onset subtype also experienced
             health problems. A childhood-limited subtype not specified
             by DSM-IV was revealed; its adult health outcomes were
             within the range of the cohort norm.<h4>Conclusions</h4>Results
             support the epidemiological validity of the DSM-IV conduct
             disorder distinction based on age of onset but highlight the
             need to also consider long-term persistence to refine
             diagnosis. Preventing and treating conduct problems has the
             potential to reduce the adult health burden.},
   Doi = {10.1001/archpsyc.64.4.476},
   Key = {fds304719}
}

@article{fds253304,
   Author = {Moffitt, TE and Caspi, A and Harrington, H and Milne, BJ and Melchior,
             M and Goldberg, D and Poulton, R},
   Title = {Generalized anxiety disorder and depression: childhood risk
             factors in a birth cohort followed to age
             32.},
   Journal = {Psychological medicine},
   Volume = {37},
   Number = {3},
   Pages = {441-452},
   Year = {2007},
   Month = {March},
   ISSN = {0033-2917},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/17201999},
   Abstract = {<h4>Background</h4>The close association between generalized
             anxiety disorder (GAD) and major depressive disorder (MDD)
             prompts questions about how to characterize them in future
             diagnostic systems. We tested whether risk factors for MDD
             and GAD are similar or different.<h4>Method</h4>The
             representative 1972-73 Dunedin birth cohort of 1037 males
             and females was followed to age 32 with 96% retention. Adult
             GAD and MDD were diagnosed at ages 18, 21, 26, and 32 years,
             and juvenile anxiety/depression were also taken into
             account. Thirteen prospective risk measures indexed domains
             of family history, adverse family environment, childhood
             behavior, and adolescent self-esteem and personality
             traits.<h4>Results</h4>Co-morbid MDD+GAD was antedated by
             highly elevated risk factors broadly across all domains.
             MDD+GAD was further characterized by the earliest onset,
             most recurrence, and greatest use of mental health services
             and medication. Pure GAD had levels of risk factors similar
             to the elevated levels for co-morbid MDD+GAD; generally,
             pure MDD did not. Pure GAD had risks during childhood not
             shared by pure MDD, in domains of adverse family environment
             (low SES, somewhat more maltreatment) and childhood behavior
             (internalizing problems, conduct problems, somewhat more
             inhibited temperament). Pure MDD had risks not shared by
             pure GAD, in domains of family history (of depression) and
             personality (low positive emotionality).<h4>Conclusions</h4>Specific
             antecedent risk factors for pure adult MDD versus GAD may
             suggest partly different etiological pathways. That GAD and
             co-morbid MDD+GAD share many risk markers suggests that the
             presence of GAD may signal a pathway toward relatively more
             severe internalizing disorder.},
   Doi = {10.1017/s0033291706009640},
   Key = {fds253304}
}

@article{fds253256,
   Author = {Piquero, AR and Moffitt, TE and Wright, BE},
   Title = {Self-control and criminal career dimensions},
   Journal = {Journal of Contemporary Criminal Justice},
   Volume = {23},
   Number = {1},
   Pages = {72-89},
   Publisher = {SAGE Publications},
   Year = {2007},
   Month = {February},
   ISSN = {1043-9862},
   url = {http://dx.doi.org/10.1177/1043986206298949},
   Abstract = {The criminal career paradigm parcels offenders' careers into
             multiple dimensions, including participation, frequency,
             persistence, seriousness, career length, and desistance, and
             each dimension may have different causes. In a forceful
             critique of this perspective, Gottfredson and Hirschi claim
             that low self-control equally predicts all dimensions of
             criminal behavior and that its effect holds steady across
             types of people, including both men and women. This study
             examines the link between low self-control and the career
             dimensions of participation, frequency, persistence, and
             desistance from crime. Analyses also investigate whether
             self-control distinguishes between persistence and
             desistance. Using data from 985 participants in the Dunedin
             Multidisciplinary Health and Human Development Study, the
             authors found overall support for Gottfredson and Hirschi's
             position. © 2007 Sage Publications.},
   Doi = {10.1177/1043986206298949},
   Key = {fds253256}
}

@article{fds253306,
   Author = {Lynam, DR and Caspi, A and Moffitt, TE and Loeber, R and Stouthamer-Loeber, M},
   Title = {Longitudinal evidence that psychopathy scores in early
             adolescence predict adult psychopathy.},
   Journal = {Journal of abnormal psychology},
   Volume = {116},
   Number = {1},
   Pages = {155-165},
   Year = {2007},
   Month = {February},
   ISSN = {0021-843X},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/17324026},
   Abstract = {This study examined the relation between psychopathy
             assessed at age 13 by using the mother-reported Childhood
             Psychopathy Scale (D. R. Lynam, 1997) and psychopathy
             assessed at age 24 by using the interviewer-rated
             Psychopathy Checklist: Screening Version (PCL:SV; S. D.
             Hart, D. N. Cox, & R. D. Hare, 1995). Data from over 250
             participants of the middle sample of the Pittsburgh Youth
             Study were used to examine this relation; approximately 9%
             of the sample met criteria for a possible PCL:SV diagnosis.
             Despite the long time lag, different sources, and different
             methods, psychopathy from early adolescence into young
             adulthood was moderately stable (r=.31). The relation was
             present for the PCL:SV total and facet scores, was not
             moderated by initial risk status or initial psychopathy
             level, and held even after controlling for other age 13
             variables. Diagnostic stability was somewhat lower. Both
             specificity and negative predictive power were good, and
             sensitivity was adequate, but positive predictive power was
             poor. This constitutes the first demonstration of the
             relative stability of psychopathy from adolescence into
             adulthood and provides evidence for the incremental utility
             of the adolescent psychopathy construct. Implications and
             future directions are discussed.},
   Doi = {10.1037/0021-843x.116.1.155},
   Key = {fds253306}
}

@article{fds253307,
   Author = {Koenen, KC and Moffitt, TE and Poulton, R and Martin, J and Caspi,
             A},
   Title = {Early childhood factors associated with the development of
             post-traumatic stress disorder: results from a longitudinal
             birth cohort.},
   Journal = {Psychological medicine},
   Volume = {37},
   Number = {2},
   Pages = {181-192},
   Year = {2007},
   Month = {February},
   ISSN = {0033-2917},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/17052377},
   Abstract = {<h4>Background</h4>Childhood factors have been associated
             with increased risk of developing post-traumatic stress
             disorder (PTSD). Previous studies assessed only a limited
             number of childhood factors retrospectively. We examined the
             association between childhood neurodevelopmental,
             temperamental, behavioral and family environmental
             characteristics assessed before age 11 years and the
             development of PTSD up to age 32 years in a birth
             cohort.<h4>Method</h4>Members of a 1972-73 New Zealand birth
             cohort (n=1037) who were assessed at ages 26 and 32 years
             for PTSD as defined by DSM-IV.<h4>Results</h4>We identified
             two sets of childhood risk factors. The first set of risk
             factors was associated both with increased risk of trauma
             exposure and with PTSD assessed at age 26. These included
             childhood externalizing characteristics and family
             environmental stressors, specifically maternal distress and
             loss of a parent. The second set of risk factors affected
             risk for PTSD only and included low IQ and chronic
             environmental adversity. The effect of cumulative childhood
             factors on risk of PTSD at age 26 was substantial; over 58%
             of cohort members in the highest risk quartile for three
             developmental factors had PTSD as compared to only 25% of
             those not at high risk on any factors. Low IQ at age 5,
             antisocial behavior, and poverty before age 11 continued to
             predict PTSD related to traumatic events that occurred
             between the ages of 26 and 32.<h4>Conclusions</h4>Developmental
             capacities and conditions of early childhood may increase
             both risk of trauma exposure and the risk that individuals
             will respond adversely to traumatic exposures. Rather than
             being solely a response to trauma, PTSD may have
             developmental origins.},
   Doi = {10.1017/s0033291706009019},
   Key = {fds253307}
}

@article{fds253308,
   Author = {Gregory, AM and Caspi, A and Moffitt, TE and Koenen, K and Eley, TC and Poulton, R},
   Title = {Juvenile mental health histories of adults with anxiety
             disorders.},
   Journal = {The American journal of psychiatry},
   Volume = {164},
   Number = {2},
   Pages = {301-308},
   Year = {2007},
   Month = {February},
   ISSN = {0002-953X},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/17267794},
   Abstract = {<h4>Objective</h4>Information about the psychiatric
             histories of adults with anxiety disorders was examined to
             further inform nosology and etiological/ preventive
             efforts.<h4>Method</h4>The authors used data from a
             prospective longitudinal study of a representative birth
             cohort (N=1,037) from ages 11 to 32 years, making
             psychiatric diagnoses according to DSM criteria. For adults
             with anxiety disorders at 32 years, follow-back analyses
             ascertained first diagnosis of anxiety and other juvenile
             disorders.<h4>Results</h4>Of adults with each type of
             anxiety disorder, approximately half had been diagnosed with
             a psychiatric disorder (one-third with an anxiety disorder)
             by age 15. The juvenile histories of psychiatric problems
             for adults with different types of anxiety disorders were
             largely nonspecific, partially reflecting comorbidity at 32
             years. Histories of anxiety and depression were most common.
             There was also specificity. For example, adults with panic
             disorder did not have histories of juvenile disorders,
             whereas those with other anxiety disorders did. Adults with
             posttraumatic stress disorder had histories of conduct
             disorder, whereas those with other anxiety disorders did
             not. Adults with specific phobia had histories of juvenile
             phobias but not other anxiety disorders.<h4>Conclusions</h4>Strong
             comorbidity between different anxiety disorders and lack of
             specificity in developmental histories of adults with
             anxiety disorders supports a hierarchical approach to
             classification, with a broad class of anxiety disorders
             having individual disorders within it. The early first
             diagnosis of psychiatric difficulties in individuals with
             anxiety disorders suggests the need to target research
             examining the etiology of anxiety disorders and prevention
             early in life.},
   Doi = {10.1176/ajp.2007.164.2.301},
   Key = {fds253308}
}

@article{fds199252,
   Author = {Moffitt, T.E. and Caspi, A. and Harrington, HL and Milne, B. and Melchior, M. and Goldberg, D. and Poulton, R.},
   Title = {Generalized anxiety disorder and depression: Childhood risk
             factors in a birth cohort followed to age
             32.},
   Journal = {Psychological Medicine},
   Volume = {37},
   Pages = {441-452.},
   Year = {2007},
   Key = {fds199252}
}

@article{fds140033,
   Author = {Caspi, A. and Williams, B. and Kim-Cohen, J. and Craig, I. W. and Milne, B.J. and Poulton, R. and Schalkwyk, L. C. and Taylor, A. and Werts, H. and Moffitt, T. E},
   Title = {Nature, nurture, and the IQ: Genetic variation in fatty acid
             metabolism moderates the association between breastfeeding
             and children’s cognitive development},
   Journal = {PNAS Proceeding of the National Academy of
             Sciences},
   Volume = {104},
   Pages = {18860-18865},
   Year = {2007},
   Key = {fds140033}
}

@article{fds253202,
   Author = {Jaffee, S and Caspi, A and Moffitt, TE and Polo Tomas and M and Taylor,
             A},
   Title = {Individual, family, and neighborhood factors predict
             children’s resilience to maltreatment: A cumulative
             stressors model},
   Journal = {Child Abuse & Neglect},
   Volume = {31},
   Number = {3},
   Pages = {231-253},
   Year = {2007},
   ISSN = {0145-2134},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/17395260},
   Abstract = {<h4>Objective</h4>Children who are physically maltreated are
             at risk of a range of adverse outcomes in childhood and
             adulthood, but some children who are maltreated manage to
             function well despite their history of adversity. Which
             individual, family, and neighborhood characteristics
             distinguish resilient from non-resilient maltreated
             children? Do children's individual strengths promote
             resilience even when children are exposed to multiple family
             and neighborhood stressors (cumulative stressors
             model)?<h4>Methods</h4>Data were from the Environmental Risk
             Longitudinal Study which describes a nationally
             representative sample of 1,116 twin pairs and their
             families. Families were home-visited when the twins were 5
             and 7 years old, and teachers provided information about
             children's behavior at school. Interviewers rated the
             likelihood that children had been maltreated based on
             mothers' reports of harm to the child and child welfare
             involvement with the family.<h4>Results</h4>Resilient
             children were those who engaged in normative levels of
             antisocial behavior despite having been maltreated. Boys
             (but not girls) who had above-average intelligence and whose
             parents had relatively few symptoms of antisocial
             personality were more likely to be resilient versus
             non-resilient to maltreatment. Children whose parents had
             substance use problems and who lived in relatively high
             crime neighborhoods that were low on social cohesion and
             informal social control were less likely to be resilient
             versus non-resilient to maltreatment. Consistent with a
             cumulative stressors model of children's adaptation,
             individual strengths distinguished resilient from
             non-resilient children under conditions of low, but not
             high, family and neighborhood stress.<h4>Conclusion</h4>These
             findings suggest that for children residing in multi-problem
             families, personal resources may not be sufficient to
             promote their adaptive functioning.},
   Doi = {10.1016/j.chiabu.2006.03.011},
   Key = {fds253202}
}

@article{fds253259,
   Author = {Caspi, A and Williams, B and Kim Cohen and J and Craig, IW and Milne, BJ and Poulton, R and Schalkwyk, LC and Taylor, A and Werts, H and Moffitt,
             TE},
   Title = {Nature, nuture, & the IQ: Genetic variation in fatty acid
             metabolism moderates the association between breastfeeding
             and children's cognitive development},
   Journal = {Proceedings of the National Academy of Sciences
             (PNAS)},
   Volume = {104},
   Pages = {18860-18865},
   Year = {2007},
   Key = {fds253259}
}

@article{fds253300,
   Author = {Odgers, C and Caspi, A and Broadbent, JM and Dickson, N and Hancox, B and Harrington, H and Poulton, R and Sears, MR and Thompson, M and Moffitt,
             TE},
   Title = {Conduct problems subtypes in males predict differential
             adult health burden},
   Journal = {Archives of General Psychiatry},
   Volume = {64},
   Number = {4},
   Pages = {476-484},
   Year = {2007},
   ISSN = {0003-990X},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/17404124},
   Abstract = {CONTEXT: A cardinal feature of the DSM-IV diagnostic
             criteria for conduct disorder is the distinction between
             childhood- vs adolescent-onset subtypes. Whether such
             developmental subtypes exist in the population and have
             different prognoses should be rigorously tested to inform
             the DSM-V. OBJECTIVES: To evaluate the epidemiological
             validity of childhood- vs adolescent-onset conduct problems
             in a prospective birth cohort, and to assess whether
             life-course-persistent conduct problems are associated with
             a greater adult health burden. DESIGN, SETTING, AND
             PARTICIPANTS: Our sample includes 526 male study members in
             the Dunedin Multidisciplinary Health and Development Study,
             a 1-year birth cohort (April 1, 1972, through March 30,
             1973). Developmental trajectories were defined using
             prospective ratings of conduct problems at 7, 9, 11, 13, 15,
             18, 21, and 26 years of age. MAIN OUTCOME MEASURES: Health
             burden was assessed as mental and physical health problems
             at 32 years of age measured via diagnostic interviews and
             physical examinations. RESULTS: We identified the following
             4 developmental subtypes of conduct problems through general
             growth mixture modeling: (1) childhood-onset/life-course-persistent,
             (2) adolescent onset, (3) childhood limited, and (4) low. At
             32 years of age, study members with the life-course-persistent
             subtype experienced the worst health burden. To a lesser
             extent, those with the adolescent-onset subtype also
             experienced health problems. A childhood-limited subtype not
             specified by DSM-IV was revealed; its adult health outcomes
             were within the range of the cohort norm. CONCLUSIONS:
             Results support the epidemiological validity of the DSM-IV
             conduct disorder distinction based on age of onset but
             highlight the need to also consider long-term persistence to
             refine diagnosis. Preventing and treating conduct problems
             has the potential to reduce the adult health
             burden.},
   Doi = {10.1001/archpsyc.64.4.476},
   Key = {fds253300}
}

@article{fds336545,
   Author = {Melchior, M and Moffitt, TE and Milne, BJ and Poulton, R and Caspi,
             A},
   Title = {Why do children from socioeconomically disadvantaged
             families suffer poor health when they reach adulthood?
             Longitudinal results from the Dunedin birth cohort
             study},
   Journal = {American Journal of Epidemiology},
   Volume = {66},
   Pages = {966-974},
   Year = {2007},
   Key = {fds336545}
}

@article{fds336992,
   Author = {Moffitt, TE and Melchior, M},
   Title = {Why does the worldwide prevalence of childhood ADHD matter?
             Editorial},
   Journal = {American Journal of Psychiatry},
   Volume = {164},
   Pages = {856-858},
   Year = {2007},
   Key = {fds336992}
}

@article{fds304717,
   Author = {Cannon, M and Moffitt, TE and Caspi, A and Murray, RM and Harrington, H and Poulton, R},
   Title = {Neuropsychological performance at the age of 13 years and
             adult schizophreniform disorder: prospective birth cohort
             study.},
   Journal = {The British journal of psychiatry : the journal of mental
             science},
   Volume = {189},
   Pages = {463-464},
   Year = {2006},
   Month = {November},
   ISSN = {0007-1250},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/17077440},
   Abstract = {We examined neuropsychological functioning at age 13 years
             in adolescents who later developed schizophreniform
             disorder, compared with healthy controls and with
             adolescents diagnosed as having had a manic episode or
             depression or anxiety disorder. Participants were from an
             unselected birth cohort. Attentional, executive and motor
             impairments at age 13 were found in those who later
             fulfilled diagnostic criteria for schizophreniform disorder,
             suggesting that these impairments may be the earliest
             emerging neuropsychological impairments in
             schizophrenia-related disorders.},
   Doi = {10.1192/bjp.bp.105.020552},
   Key = {fds304717}
}

@article{fds304718,
   Author = {Koenen, KC and Caspi, A and Moffitt, TE and Rijsdijk, F and Taylor,
             A},
   Title = {Genetic influences on the overlap between low IQ and
             antisocial behavior in young children.},
   Journal = {Journal of abnormal psychology},
   Volume = {115},
   Number = {4},
   Pages = {787-797},
   Year = {2006},
   Month = {November},
   ISSN = {0021-843X},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/17100536},
   Abstract = {The well-documented relation between the phenotypes of low
             IQ and childhood antisocial behavior could be explained by
             either common genetic influences or environmental
             influences. These competing explanations were examined
             through use of the Environmental Risk Longitudinal Twin
             Study 1994-1995 cohort (Moffitt & the E-Risk Study Team,
             2002) of 1,116 twin pairs and their families. Children's IQ
             was assessed via individual testing at age 5 years. Mothers
             and teachers reported on children's antisocial behavior at
             ages 5 and 7 years. Low IQ was related to antisocial
             behavior at age 5 years and predicted relatively higher
             antisocial behavior scores at age 7 years when antisocial
             behavior at age 5 years was controlled. This association was
             significantly stronger among boys than among girls. Genetic
             influences common to both phenotypes explained 100% of the
             low IQ-antisocial behavior relation in boys. Findings
             suggest that specific candidate genes and neurobiological
             processes should be tested in relation to both
             phenotypes.},
   Doi = {10.1037/0021-843x.115.4.787},
   Key = {fds304718}
}

@article{fds304716,
   Author = {Kim-Cohen, J and Caspi, A and Taylor, A and Williams, B and Newcombe, R and Craig, IW and Moffitt, TE},
   Title = {MAOA, maltreatment, and gene-environment interaction
             predicting children's mental health: new evidence and a
             meta-analysis.},
   Journal = {Molecular psychiatry},
   Volume = {11},
   Number = {10},
   Pages = {903-913},
   Year = {2006},
   Month = {October},
   ISSN = {1359-4184},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/16801953},
   Abstract = {Previous research on adults has shown that a functional
             polymorphism in the promoter region of the monoamine oxidase
             A (MAOA) gene moderates the impact of childhood maltreatment
             on risk for developing antisocial behavior. Thus far,
             attempts to replicate this finding have been mixed. The
             current study (i) presents new data investigating this
             finding in a sample of 975 seven-year-old boys, and (ii)
             evaluates the extant data by conducting a meta-analysis of
             published findings. We replicated the original finding by
             showing that the MAOA polymorphism moderates the development
             of psychopathology after exposure to physical abuse, we
             extended the finding to childhood closer in time to the
             maltreatment experience, and we ruled-out the possibility of
             a spurious finding by accounting for passive and evocative
             gene-environment correlation. Moreover, meta-analysis
             demonstrated that across studies, the association between
             maltreatment and mental health problems is significantly
             stronger in the group of males with the genotype conferring
             low vs high MAOA activity. These findings provide the
             strongest evidence to date suggesting that the MAOA gene
             influences vulnerability to environmental stress, and that
             this biological process can be initiated early in
             life.},
   Doi = {10.1038/sj.mp.4001851},
   Key = {fds304716}
}

@article{fds253311,
   Author = {Caspi, A and Harrington, H and Moffitt, TE and Milne, BJ and Poulton,
             R},
   Title = {Socially isolated children 20 years later: risk of
             cardiovascular disease.},
   Journal = {Archives of pediatrics & adolescent medicine},
   Volume = {160},
   Number = {8},
   Pages = {805-811},
   Year = {2006},
   Month = {August},
   ISSN = {1072-4710},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/16894079},
   Abstract = {<h4>Objective</h4>To test the hypothesis that children who
             occupy peripheral or isolated roles in their peer groups
             (isolated children) are at risk of poor adult
             health.<h4>Design</h4>Longitudinal study of an entire birth
             cohort.<h4>Setting</h4>Dunedin, New Zealand.<h4>Participants</h4>A
             total of 1037 children who were followed up from birth to
             age 26 years.<h4>Interventions</h4>Measurement of social
             isolation in childhood, adolescence, and adulthood.<h4>Main
             outcome measures</h4>When study members were 26 years old,
             we measured adult cardiovascular multifactorial risk status
             (overweight, elevated blood pressure, elevated total
             cholesterol level, low high-density lipoprotein level,
             elevated glycated hemoglobin concentration, and low maximum
             oxygen consumption).<h4>Results</h4>Socially isolated
             children were at significant risk of poor adult health
             compared with nonisolated children (risk ratio, 1.37; 95%
             confidence interval, 1.17-1.61). This association was
             independent of other well-established childhood risk factors
             for poor adult health (low childhood socioeconomic status,
             low childhood IQ, childhood overweight), was not accounted
             for by health-damaging behaviors (lack of exercise, smoking,
             alcohol misuse), and was not attributable to greater
             exposure to stressful life events. In addition, longitudinal
             findings showed that chronic social isolation across
             multiple developmental periods had a cumulative,
             dose-response relationship to poor adult health (risk ratio,
             2.58; 95% confidence interval, 1.46-4.56).<h4>Conclusions</h4>Longitudinal
             findings about children followed up to adulthood suggest
             that social isolation has persistent and cumulative
             detrimental effects on adult health. The findings underscore
             the usefulness of a life-course approach to health research,
             by focusing attention on the effect of the timing of
             psychosocial risk factors in relation to adult
             health.},
   Doi = {10.1001/archpedi.160.8.805},
   Key = {fds253311}
}

@article{fds253312,
   Author = {Gregory, AM and Caspi, A and Moffitt, TE and Poulton,
             R},
   Title = {Family conflict in childhood: a predictor of later
             insomnia.},
   Journal = {Sleep},
   Volume = {29},
   Number = {8},
   Pages = {1063-1067},
   Year = {2006},
   Month = {August},
   ISSN = {0161-8105},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/16944675},
   Abstract = {<h4>Study objectives</h4>To examine the association between
             childhood exposure to family conflict and insomnia at 18
             years of age.<h4>Design</h4>Longitudinal prospective data on
             an entire birth cohort were obtained. Parents completed the
             Conflict subscale of the Moos Family Environment Scale when
             the study members were 7, 9, 13, and 15 years of age.
             Insomnia was examined in a standardized interview when the
             participants were aged 18 years.<h4>Setting</h4>Participants
             were born in Dunedin, New Zealand, and were interviewed at
             this location.<h4>Patients or participants</h4>One thousand
             thirty-seven children born between April 1, 1972, and March
             31, 1973, enrolled in the study (52% male). At age 18 years,
             993 (97% of living cohort members) provided
             data.<h4>Interventions</h4>N/A.<h4>Measurements and
             results</h4>The mean level of family conflict at age 7 to 15
             years predicted insomnia at 18 years after controlling for
             sex, socioeconomic status, sleep problems at 9 years, and
             self-reported health (odds ratio [95% confidence interval] =
             1.42 [1.17-1.73], p < .001). There was a dose-response
             relationship, whereby the more assessments at which families
             scored in the top 25% for conflict, the greater the young
             person's likelihood of developing insomnia at age 18 years.
             This association was present even after controlling for
             depression at 18 years.<h4>Conclusions</h4>This study
             demonstrates a modest but robust longitudinal link between
             family conflict during childhood and insomnia experienced at
             18 years of age. Future work needs to replicate this finding
             in different populations and to elucidate the mechanisms
             underlying this association.},
   Doi = {10.1093/sleep/29.8.1063},
   Key = {fds253312}
}

@article{fds253313,
   Author = {Arseneault, L and Walsh, E and Trzesniewski, K and Newcombe, R and Caspi, A and Moffitt, TE},
   Title = {Bullying victimization uniquely contributes to adjustment
             problems in young children: a nationally representative
             cohort study.},
   Journal = {Pediatrics},
   Volume = {118},
   Number = {1},
   Pages = {130-138},
   Year = {2006},
   Month = {July},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/16818558},
   Abstract = {<h4>Objective</h4>It has been shown that bullying
             victimization is associated with behavior and school
             adjustment problems, but it remains unclear whether the
             experience of bullying uniquely contributes to those
             problems after taking into account preexisting adjustment
             problems.<h4>Methods</h4>We examined bullying in the
             Environmental Risk Study, a nationally representative
             1994-1995 birth cohort of 2232 children. We identified
             children who experienced bullying between the ages of 5 and
             7 years either as pure victims or bully/victims. We
             collected reports from mothers and teachers about children's
             behavior problems and school adjustment when they were 5
             years old and again when they were age 7.<h4>Results</h4>Compared
             with control children, pure victims showed more
             internalizing problems and unhappiness at school when they
             were 5 and 7 years. Girls who were pure victims also showed
             more externalizing problems than controls. Compared with
             controls and pure victims, bully/victims showed more
             internalizing problems, more externalizing problems, and
             fewer prosocial behaviors when they were 5 and 7 years. They
             also were less happy at school compared with control
             children at 7 years of age. Pure victims and bully/victims
             showed more behavior and school adjustment problems at 7
             years of age, even after controlling for preexisting
             adjustment problems at 5 years of age.<h4>Conclusions</h4>Being
             the victim of a bully during the first years of schooling
             contributes to maladjustment in young children. Prevention
             and intervention programs aimed at reducing mental health
             problems during childhood should target bullying as an
             important risk factor.},
   Doi = {10.1542/peds.2005-2388},
   Key = {fds253313}
}

@article{fds253323,
   Author = {Caspi, A and Moffitt, TE},
   Title = {Gene-environment interactions in psychiatry: joining forces
             with neuroscience.},
   Journal = {Nature reviews. Neuroscience},
   Volume = {7},
   Number = {7},
   Pages = {583-590},
   Year = {2006},
   Month = {July},
   ISSN = {1471-003X},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/16791147},
   Abstract = {Gene-environment interaction research in psychiatry is new,
             and is a natural ally of neuroscience. Mental disorders have
             known environmental causes, but there is heterogeneity in
             the response to each causal factor, which gene-environment
             findings attribute to genetic differences at the DNA
             sequence level. Such findings come from epidemiology, an
             ideal branch of science for showing that a gene-environment
             interactions exist in nature and affect a significant
             fraction of disease cases. The complementary discipline of
             epidemiology, experimental neuroscience, fuels
             gene-environment hypotheses and investigates underlying
             neural mechanisms. This article discusses opportunities and
             challenges in the collaboration between psychiatry,
             epidemiology and neuroscience in studying gene-environment
             interactions.},
   Doi = {10.1038/nrn1925},
   Key = {fds253323}
}

@article{fds253315,
   Author = {Kim-Cohen, J and Caspi, A and Rutter, M and Tomás, MP and Moffitt,
             TE},
   Title = {The caregiving environments provided to children by
             depressed mothers with or without an antisocial
             history.},
   Journal = {The American journal of psychiatry},
   Volume = {163},
   Number = {6},
   Pages = {1009-1018},
   Year = {2006},
   Month = {June},
   ISSN = {0002-953X},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/16741201},
   Abstract = {<h4>Objective</h4>Many depressed women have a history of
             antisocial behavior, but research into maternal depression
             has not ascertained if this has implications for children of
             depressed mothers. This study compared the developmental
             outcomes in and caregiving environments provided to children
             by depressed mothers with or without an antisocial
             history.<h4>Method</h4>In the Environmental Risk
             Longitudinal Twin Study, a nationally representative study
             of 1,106 families, mothers were administered the Diagnostic
             Interview Schedule for Major Depressive Disorder and
             interviewed about their lifetime history of antisocial
             personality disorder symptoms. Mothers and teachers provided
             information regarding the children's behavior problems at 5
             and 7 years of age. The authors assessed the quality of the
             caregiving environment through maternal reports and
             interviewer observations.<h4>Results</h4>Compared with
             children of mothers with depression only, the children of
             depressed and antisocial mothers had significantly higher
             levels of antisocial behavior and rates of DSM-IV conduct
             disorder, even after the authors controlled for numbers of
             symptoms and chronicity of maternal major depressive
             disorder. The children of depressed and antisocial mothers
             were at an elevated risk of experiencing multiple caregiving
             abuses, including physical maltreatment, high levels of
             maternal hostility, and exposure to domestic
             violence.<h4>Conclusions</h4>If one ignores the common
             co-occurrence of an antisocial history in depressed mothers,
             it may obscure the significantly elevated risks in
             children's development. Clinicians treating women's
             depression should be aware that children of depressed and
             antisocial mothers constitute a group at extremely high risk
             for early-onset psychopathology.},
   Doi = {10.1176/ajp.2006.163.6.1009},
   Key = {fds253315}
}

@article{fds304715,
   Author = {Ehrensaft, MK and Moffitt, TE and Caspi, A},
   Title = {Is domestic violence followed by an increased risk of
             psychiatric disorders among women but not among men? A
             longitudinal cohort study.},
   Journal = {Am J Psychiatry},
   Volume = {163},
   Number = {5},
   Pages = {885-892},
   Year = {2006},
   Month = {May},
   ISSN = {0002-953X},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/16648331},
   Abstract = {OBJECTIVE: The association between violence between intimate
             partners and psychiatric disorders is assumed to reflect a
             causal link. This assumption is now questioned because
             several longitudinal studies have documented that
             adolescents with psychiatric disorders grow up to be
             overrepresented among adults involved in partner violence.
             METHOD: The study followed a representative birth cohort
             prospectively. Adolescent mental disorders were diagnosed at
             age 18 years. Between ages 24 and 26 years, the authors
             identified individuals involved in nonabusive relationships
             versus those involved in clinically abusive relationships
             (i.e., resulting in injury and/or official intervention). At
             age 26 years, mental disorders were again diagnosed.
             RESULTS: Male and female adolescents with psychiatric
             disorders were at greatest risk of becoming involved in
             abusive adult relationships. After the authors controlled
             for earlier psychiatric history, women who were involved in
             abusive relationships, but not men, had an increased risk of
             adult psychiatric morbidity. CONCLUSIONS: 1) Psychiatric
             disorders pose risk for involvement in abusive relationships
             for both sexes; 2) partner abuse is a contributing source of
             psychiatric disorders among women but not among
             men.},
   Doi = {10.1176/ajp.2006.163.5.885},
   Key = {fds304715}
}

@article{fds253321,
   Author = {Vermeiren, R and Jespers, I and Moffitt, T},
   Title = {Mental health problems in juvenile justice
             populations.},
   Journal = {Child and adolescent psychiatric clinics of North
             America},
   Volume = {15},
   Number = {2},
   Pages = {333-viii},
   Year = {2006},
   Month = {April},
   ISSN = {1056-4993},
   url = {http://dx.doi.org/10.1016/j.chc.2005.11.008},
   Abstract = {The limited literature on mental health problems in juvenile
             justice population has reported that most youth in juvenile
             justice hold psychiatric pathology. Although conduct
             disorder and substance abuse are the most prevalent
             conditions in this population, many other diagnoses can be
             found at alarmingly high rates; research on other diagnoses
             (eg, autism, psychosis) is limited. This finding underscores
             the necessity of implementing adequate diagnostic assessment
             within forensic settings and of developing interventions
             programs that take into account the presence of psychiatric
             problems.},
   Doi = {10.1016/j.chc.2005.11.008},
   Key = {fds253321}
}

@article{fds304714,
   Author = {Mill, J and Caspi, A and Williams, BS and Craig, I and Taylor, A and Polo-Tomas, M and Berridge, CW and Poulton, R and Moffitt,
             TE},
   Title = {Prediction of heterogeneity in intelligence and adult
             prognosis by genetic polymorphisms in the dopamine system
             among children with attention-deficit/hyperactivity
             disorder: evidence from 2 birth cohorts.},
   Journal = {Archives of general psychiatry},
   Volume = {63},
   Number = {4},
   Pages = {462-469},
   Year = {2006},
   Month = {April},
   ISSN = {0003-990X},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/16585476},
   Abstract = {<h4>Context</h4>The study and treatment of psychiatric
             disorders is made difficult by the fact that patients with
             identical symptoms often differ markedly in their clinical
             features and presumably in their etiology. A principal aim
             of genetic research is to provide new information that can
             resolve such clinical heterogeneity and that can be
             incorporated into diagnostic practice.<h4>Objective</h4>To
             test the hypothesis that the DRD4 seven-repeat allele and
             DAT1 ten-repeat allele would prove useful in identifying a
             subset of children with attention-deficit/hyperactivity
             disorder (ADHD) who have compromised intellectual
             functions.<h4>Design</h4>Longitudinal epidemiologic
             investigation of 2 independent birth cohorts.<h4>Setting</h4>Britain
             and New Zealand.<h4>Participants</h4>The first cohort was
             born in Britain in 1994-1995 and includes 2232 children; the
             second cohort was born in New Zealand in 1972-1973 and
             includes 1037 children.<h4>Main outcome measures</h4>Evaluation
             of ADHD, IQ, and adult psychosocial adjustment.<h4>Results</h4>We
             present replicated evidence that polymorphisms in the DRD4
             and DAT1 genes were associated with variation in
             intellectual functioning among children diagnosed as having
             ADHD, apart from severity of their symptoms. We further show
             longitudinal evidence that these polymorphisms predicted
             which children with ADHD were at greatest risk for poor
             adult prognosis.<h4>Conclusion</h4>The findings indicate
             that genetic information of this nature may prove useful for
             etiology-based psychiatric nosologies.},
   Doi = {10.1001/archpsyc.63.4.462},
   Key = {fds304714}
}

@article{fds253319,
   Author = {Rutter, M and Moffitt, TE and Caspi, A},
   Title = {Gene-environment interplay and psychopathology: multiple
             varieties but real effects.},
   Journal = {Journal of child psychology and psychiatry, and allied
             disciplines},
   Volume = {47},
   Number = {3-4},
   Pages = {226-261},
   Year = {2006},
   Month = {March},
   ISSN = {0021-9630},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/16492258},
   Abstract = {Gene-environment interplay is a general term that covers
             several divergent concepts with different meanings and
             different implications. In this review, we evaluate research
             evidence on four varieties of gene-environment interplay.
             First, we consider epigenetic mechanisms by which
             environmental influences alter the effects of genes. Second,
             we focus on variations in heritability according to
             environmental circumstances. Third, we discuss what is known
             about gene-environment correlations. Finally, we assess
             concepts and findings on the interaction between specific
             identified genes and specific measured environmental risks.
             In order to provide an understanding of what may be involved
             in gene-environment interplay, we begin our presentation
             with a brief historical review of prevailing views about the
             role of genetic and environmental factors in the causation
             of mental disorders, and we provide a simplified account of
             some of the key features of how genes 'work'.},
   Doi = {10.1111/j.1469-7610.2005.01557.x},
   Key = {fds253319}
}

@article{fds253320,
   Author = {Trzesniewski, KH and Donnellan, MB and Moffitt, TE and Robins, RW and Poulton, R and Caspi, A},
   Title = {Low self-esteem during adolescence predicts poor health,
             criminal behavior, and limited economic prospects during
             adulthood.},
   Journal = {Developmental psychology},
   Volume = {42},
   Number = {2},
   Pages = {381-390},
   Year = {2006},
   Month = {March},
   ISSN = {0012-1649},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/16569175},
   Abstract = {Using prospective data from the Dunedin Multidisciplinary
             Health and Development Study birth cohort, the authors found
             that adolescents with low self-esteem had poorer mental and
             physical health, worse economic prospects, and higher levels
             of criminal behavior during adulthood, compared with
             adolescents with high self-esteem. The long-term
             consequences of self-esteem could not be explained by
             adolescent depression, gender, or socioeconomic status.
             Moreover, the findings held when the outcome variables were
             assessed using objective measures and informant reports;
             therefore, the findings cannot be explained by shared method
             variance in self-report data. The findings suggest that low
             self-esteem during adolescence predicts negative real-world
             consequences during adulthood.},
   Doi = {10.1037/0012-1649.42.2.381},
   Key = {fds253320}
}

@article{fds253322,
   Author = {Moffitt, TE and Caspi, A and Rutter, M},
   Title = {Measured Gene-Environment Interactions in Psychopathology:
             Concepts, Research Strategies, and Implications for
             Research, Intervention, and Public Understanding of
             Genetics.},
   Journal = {Perspectives on psychological science : a journal of the
             Association for Psychological Science},
   Volume = {1},
   Number = {1},
   Pages = {5-27},
   Year = {2006},
   Month = {March},
   ISSN = {1745-6916},
   url = {http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000207449900002&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=47d3190e77e5a3a53558812f597b0b92},
   Abstract = {There is much curiosity about interactions between genes and
             environmental risk factors for psychopathology, but this
             interest is accompanied by uncertainty. This article aims to
             address this uncertainty. First, we explain what is and is
             not meant by gene-environment interaction. Second, we
             discuss reasons why such interactions were thought to be
             rare in psychopathology, and argue instead that they ought
             to be common. Third, we summarize emerging evidence about
             gene-environment interactions in mental disorders. Fourth,
             we argue that research on gene-environment interactions
             should be hypothesis driven, and we put forward strategies
             to guide future studies. Fifth, we describe potential
             benefits of studying measured gene-environment interactions
             for basic neuroscience, gene hunting, intervention, and
             public understanding of genetics. We suggest that
             information about nurture might be harnessed to make new
             discoveries about the nature of psychopathology.},
   Doi = {10.1111/j.1745-6916.2006.00002.x},
   Key = {fds253322}
}

@article{fds313457,
   Author = {Moffitt, T and Caspi, A},
   Title = {Evidence from behavioral genetics for environmental
             contributions to antisocial conduct},
   Pages = {108-152},
   Publisher = {Cambridge University Press},
   Year = {2006},
   Month = {January},
   url = {http://dx.doi.org/10.1017/CBO9780511489341.005},
   Abstract = {Despite assiduous efforts to eliminate it, antisocial
             behavior is still a problem. Approximately 20 percent of
             people in the developed world experience victimization by
             perpetrators of violent and non-violent illegal behavior
             each year (US Bureau of Justice Statistics, 2002). The World
             Report on Violence and Health (World Health Organization,
             2002) tallies the staggering burden of mortality, disease,
             disability, and compromised well-being brought about by
             perpetrators of family violence and other violent crimes.
             Behavioral science needs to achieve a more complete
             understanding of the causes of antisocial behavior to
             provide an evidence base for effectively controlling and
             preventing it. A new wave of intervention research in the
             last decade has demonstrated clear success for a number of
             programs designed to prevent antisocial behavior
             (http://www.preventingcrime.org/; Heinrich, Brown, & Aber,
             1999; Sherman et al., 1999; Weissberg, Kumpfer, & Seligman,
             2003). Nevertheless, the reduction in antisocial behavior
             brought about by even the best prevention programs is, on
             average, modest (Olds et al., 1998; Wasserman & Miller,
             1998; Heinrich, Brown, & Aber, 1999; Wilson, Gottfredson, &
             Najaka, 2001; Dodge, 2003; Wandersman & Florin, 2003). The
             best-designed intervention programs reduce serious juvenile
             offenders' recidivism by only about 12 percent (Lipsey &
             Wilson, 1998). This modest success of interventions that
             were theory-driven, well-designed, and amply funded sends a
             clear message that we do not yet understand the causes of
             antisocial behavior well enough to prevent
             it.},
   Doi = {10.1017/CBO9780511489341.005},
   Key = {fds313457}
}

@article{fds70011,
   Author = {Caspi, A. and Harrington, HL and Moffitt, TE and Milne, B. and Poulton,
             R},
   Title = {Socially isolated children 20 years later: risk for
             cardiovascular disease},
   Journal = {Archives of Pediatric and Adolescent Medicine},
   Volume = {160},
   Pages = {805-811},
   Year = {2006},
   Key = {fds70011}
}

@article{fds253194,
   Author = {Trzesniewski, KH and Moffitt, TE and Caspi, A and Taylor, A and Maughan,
             B},
   Title = {Revisiting the association between reading ability and
             antisocial behavior: New evidence from a longitudinal
             behavior genetics study},
   Journal = {Child Development},
   Volume = {77},
   Number = {1},
   Pages = {72-88},
   Year = {2006},
   ISSN = {0009-3920},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/16460526},
   Abstract = {Previous studies have reported, but not explained, the
             reason for a robust association between reading achievement
             and antisocial behavior. This association was investigated
             using the Environmental Risk (E-Risk) Longitudinal Twin
             Study, a nationally representative 1994-1995 birth cohort of
             5- and 7-year-olds. Results showed that the association
             resulted primarily from environmental factors common to both
             reading and antisocial behavior and was stronger in boys.
             Environmental factors also explained the relation between
             reading disability and conduct disorder. Leading candidate
             environmental risk factors weakly mediated the association.
             For boys the best explanation was a reciprocal causation
             model: poor reading led to antisocial behavior, and vice
             versa. In contrast, the relation between reading achievement
             and attention deficit hyperactivity disorder was best
             explained by common genetic influences.},
   Doi = {10.1111/j.1467-8624.2006.00857.x},
   Key = {fds253194}
}

@article{fds253196,
   Author = {Jaffee, S and Belsky, J and Sligo, J and Harrington, HL and Caspi, A and Moffitt, TE},
   Title = {When parents have a history of adolescent conduct disorder:
             parenting, offspring behavior, and the caregiving
             environment},
   Journal = {Journal of Abnormal Psychology},
   Volume = {115},
   Number = {2},
   Pages = {309-319},
   Year = {2006},
   ISSN = {0021-843X},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/16737395},
   Abstract = {Individuals with early-emerging conduct problems are likely
             to become parents who expose their children to considerable
             adversity. The current study tested the specificity of and
             alternative explanations for this trajectory. The sample
             included 246 members of a prospective, 30-year cohort study
             and their 3-year-old children. Parents who had a history of
             conduct disorder were specifically at elevated risk for
             socioeconomic disadvantage and relationship violence, but
             suboptimal parenting and offspring temperament problems were
             common to parents with any history of disorder. Recurrent
             disorder, comorbidity, and adversity in the family of origin
             did not fully account for these findings. The cumulative
             consequences of early-onset conduct disorder and assortative
             mating for antisocial behavior may explain the long-term
             effects of conduct disorder on young adult
             functioning.},
   Doi = {10.1037/0021-843x.115.2.309},
   Key = {fds253196}
}

@article{fds253198,
   Author = {Mill, J and Dempster, E and Caspi, A and Williams, B and Moffitt, TE and Craig, I},
   Title = {Evidence for monozygotic twin (MZ) discordance in
             methylation level at two CpG sites in the promoter region of
             the Catechol-O-Methyltransferase (COMT) gene},
   Journal = {American Journal of Medical Genetics},
   Volume = {141B},
   Number = {4},
   Pages = {319-433},
   Year = {2006},
   ISSN = {1552-4841},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/16583437},
   Abstract = {Monozygotic (MZ) twin concordance for a range of psychiatric
             conditions is rarely 100%. It has been suggested that
             epigenetic factors, such as DNA methylation, may account for
             a proportion of the variation in behavioral traits observed
             between these genetically identical individuals. In this
             study we have quantitatively assessed the methylation status
             of two CpG sites in the promoter region of the COMT gene in
             12 MZ twins-pairs discordant for birth weight, but otherwise
             clinically unaffected. DNA was obtained at age 5-years using
             buccal swabs, and modified using sodium-bisulfite treatment.
             Methylation profiles were assessed using Pyrosequencing, a
             technology enabling the precise degree of methylation to be
             assessed at any CpG site. We found that the degree of
             methylation at the two CpG sites was highly correlated, but
             there was considerable variation in the concordance of
             methylation levels between MZ twin-pairs. Some MZ twin-pairs
             showed a high degree of methylation concordance, whereas
             others differed markedly in their methylation profiles. Such
             epigenetic variation between genetically identical
             individuals may play a key role in the etiology of
             psychopathology, and explain the incomplete phenotypic
             concordance observed in MZ twins.},
   Doi = {10.1002/ajmg.b.30316},
   Key = {fds253198}
}

@article{fds253309,
   Author = {Koenen, KC and Moffitt, TE and Caspi, A and Rijsdijk,
             F},
   Title = {Genetic influences on the overlap between low IQ and
             antisocial behavior in young children},
   Journal = {Journal of Abnormal Psychology},
   Volume = {115},
   Number = {4},
   Pages = {782-797},
   Year = {2006},
   ISSN = {0021-843X},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/17100536},
   Abstract = {The well-documented relation between the phenotypes of low
             IQ and childhood antisocial behavior could be explained by
             either common genetic influences or environmental
             influences. These competing explanations were examined
             through use of the Environmental Risk Longitudinal Twin
             Study 1994-1995 cohort (Moffitt & the E-Risk Study Team,
             2002) of 1,116 twin pairs and their families. Children's IQ
             was assessed via individual testing at age 5 years. Mothers
             and teachers reported on children's antisocial behavior at
             ages 5 and 7 years. Low IQ was related to antisocial
             behavior at age 5 years and predicted relatively higher
             antisocial behavior scores at age 7 years when antisocial
             behavior at age 5 years was controlled. This association was
             significantly stronger among boys than among girls. Genetic
             influences common to both phenotypes explained 100% of the
             low IQ-antisocial behavior relation in boys. Findings
             suggest that specific candidate genes and neurobiological
             processes should be tested in relation to both
             phenotypes.},
   Doi = {10.1037/0021-843X.115.4.787},
   Key = {fds253309}
}

@article{fds253310,
   Author = {Cannon, M and Moffitt, TE and Caspi, A and Harrington, HL and Murray,
             RM and Poulton, R},
   Title = {Neuropsychological test scores at age 13 and later
             schizophreniform disorder: a prospective longitudinal birth
             cohort study},
   Journal = {British Journal of Psychiatry},
   Volume = {189},
   Pages = {463-464},
   Year = {2006},
   ISSN = {0007-1250},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/17077440},
   Abstract = {We examined neuropsychological functioning at age 13 years
             in adolescents who later developed schizophreniform
             disorder, compared with healthy controls and with
             adolescents diagnosed as having had a manic episode or
             depression or anxiety disorder. Participants were from an
             unselected birth cohort. Attentional, executive and motor
             impairments at age 13 were found in those who later
             fulfilled diagnostic criteria for schizophreniform disorder,
             suggesting that these impairments may be the earliest
             emerging neuropsychological impairments in
             schizophrenia-related disorders.},
   Doi = {10.1192/bjp.bp.105.020552},
   Key = {fds253310}
}

@article{fds253314,
   Author = {Kim Cohen and J and Caspi, A and Taylor, A and Williams, B and Newcombe, R and Craig, IW and Moffitt, TE},
   Title = {MAOA, early adversity, and gene-environment interaction
             predicting children's mental health: New evidence and a
             meta-analysis},
   Journal = {Molecular Psychiatry},
   Volume = {11},
   Number = {10},
   Pages = {903-913},
   Year = {2006},
   ISSN = {1359-4184},
   url = {http://www.psychiatryonline.org/},
   Abstract = {Previous research on adults has shown that a functional
             polymorphism in the promoter region of the monoamine oxidase
             A (MAOA) gene moderates the impact of childhood maltreatment
             on risk for developing antisocial behavior. Thus far,
             attempts to replicate this finding have been mixed. The
             current study (i) presents new data investigating this
             finding in a sample of 975 seven-year-old boys, and (ii)
             evaluates the extant data by conducting a meta-analysis of
             published findings. We replicated the original finding by
             showing that the MAOA polymorphism moderates the development
             of psychopathology after exposure to physical abuse, we
             extended the finding to childhood closer in time to the
             maltreatment experience, and we ruled-out the possibility of
             a spurious finding by accounting for passive and evocative
             gene-environment correlation. Moreover, meta-analysis
             demonstrated that across studies, the association between
             maltreatment and mental health problems is significantly
             stronger in the group of males with the genotype conferring
             low vs high MAOA activity. These findings provide the
             strongest evidence to date suggesting that the MAOA gene
             influences vulnerability to environmental stress, and that
             this biological process can be initiated early in
             life.},
   Doi = {10.1038/sj.mp.4001851},
   Key = {fds253314}
}

@article{fds253316,
   Author = {Ehrensaft, M and Moffitt, TE and Caspi, A},
   Title = {Domestic violence increases risk of psychiatric disorder in
             women but not in men: A longitudinal cohort
             study},
   Journal = {American Journal of Psychiatry},
   Volume = {163},
   Number = {5},
   Pages = {885-892},
   Year = {2006},
   ISSN = {0002-953X},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/16648331},
   Abstract = {OBJECTIVE: The association between violence between intimate
             partners and psychiatric disorders is assumed to reflect a
             causal link. This assumption is now questioned because
             several longitudinal studies have documented that
             adolescents with psychiatric disorders grow up to be
             overrepresented among adults involved in partner violence.
             METHOD: The study followed a representative birth cohort
             prospectively. Adolescent mental disorders were diagnosed at
             age 18 years. Between ages 24 and 26 years, the authors
             identified individuals involved in nonabusive relationships
             versus those involved in clinically abusive relationships
             (i.e., resulting in injury and/or official intervention). At
             age 26 years, mental disorders were again diagnosed.
             RESULTS: Male and female adolescents with psychiatric
             disorders were at greatest risk of becoming involved in
             abusive adult relationships. After the authors controlled
             for earlier psychiatric history, women who were involved in
             abusive relationships, but not men, had an increased risk of
             adult psychiatric morbidity. CONCLUSIONS: 1) Psychiatric
             disorders pose risk for involvement in abusive relationships
             for both sexes; 2) partner abuse is a contributing source of
             psychiatric disorders among women but not among
             men.},
   Doi = {10.1176/ajp.2006.163.5.885},
   Key = {fds253316}
}

@article{fds253317,
   Author = {Piquero, AR and Brame, R and Fagan, J and Moffitt,
             TE},
   Title = {Assessing the offending activity of criminal domestic
             violence suspects},
   Journal = {Public Health Reports},
   Volume = {121},
   Number = {4},
   Pages = {1-21},
   Year = {2006},
   url = {http://dx.doi.org/10.1177/003335490612100409},
   Abstract = {<h4>Objective</h4>Over the past quarter century, intimate
             partner violence research has occupied an increasingly
             important position in the research agenda of criminology,
             public policy, and public health. Yet, a number of questions
             about the criminal careers of domestic violence offenders
             remain unresolved. This study attempts to determine (1) the
             extent to which criminal domestic violence offenders
             specialize in violence, and (2) whether the severity of an
             offender's attacks against the same victim increase,
             decrease, or stay about the same over time.<h4>Methods</h4>Data
             from the Spouse Assault Replication Program (SARP) are used
             to address two questions corresponding to different features
             of the criminal careers of domestic violence
             offenders.<h4>Results</h4>The specialization analysis
             reveals that the majority of domestic violence offenders
             with prior official criminal records have been involved in
             nonviolent forms of criminal behavior in addition to
             domestic violence. The escalation analysis identifies groups
             of escalators and de-escalators as well as individuals who
             engage in stable low-level aggression and stable high-level
             aggression.<h4>Conclusions</h4>Few SARP domestic violence
             offenders have been specializing exclusively in violence.
             There is also a heterogeneous mix of offenders who escalate
             and de-escalate the severity of their attacks over the
             short-term follow-up periods. Few studies have presented
             data consistent with the present study's findings. A
             longitudinal analysis of the criminal careers of domestic
             violence offender subtypes is critical for future
             research.},
   Doi = {10.1177/003335490612100409},
   Key = {fds253317}
}

@article{fds253318,
   Author = {Mill, J and Caspi, A and Williams, BS and Craig, I and Taylor, A and Polo
             Tomas, M and Berridge, C and Poulton, R and Moffitt,
             TE},
   Title = {Genetic polymorphisms in the dopamine system predict
             heterogeneity in intelligence and adult prognosis among
             children with attention-deficit hyperactivity disorder:
             Evidence from two birth cohorts},
   Journal = {Archives of General Psychiatry},
   Volume = {63},
   Number = {4},
   Pages = {462-469},
   Year = {2006},
   ISSN = {0003-990X},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/16585476},
   Abstract = {CONTEXT: The study and treatment of psychiatric disorders is
             made difficult by the fact that patients with identical
             symptoms often differ markedly in their clinical features
             and presumably in their etiology. A principal aim of genetic
             research is to provide new information that can resolve such
             clinical heterogeneity and that can be incorporated into
             diagnostic practice. OBJECTIVE: To test the hypothesis that
             the DRD4 seven-repeat allele and DAT1 ten-repeat allele
             would prove useful in identifying a subset of children with
             attention-deficit/hyperactivity disorder (ADHD) who have
             compromised intellectual functions. DESIGN: Longitudinal
             epidemiologic investigation of 2 independent birth cohorts.
             SETTING: Britain and New Zealand. PARTICIPANTS: The first
             cohort was born in Britain in 1994-1995 and includes 2232
             children; the second cohort was born in New Zealand in
             1972-1973 and includes 1037 children. MAIN OUTCOME MEASURES:
             Evaluation of ADHD, IQ, and adult psychosocial adjustment.
             RESULTS: We present replicated evidence that polymorphisms
             in the DRD4 and DAT1 genes were associated with variation in
             intellectual functioning among children diagnosed as having
             ADHD, apart from severity of their symptoms. We further show
             longitudinal evidence that these polymorphisms predicted
             which children with ADHD were at greatest risk for poor
             adult prognosis. CONCLUSION: The findings indicate that
             genetic information of this nature may prove useful for
             etiology-based psychiatric nosologies.},
   Doi = {10.1001/archpsyc.63.4.462},
   Key = {fds253318}
}

@article{fds253324,
   Author = {Silver, E and Arseneault, L and Langley, J and Caspi, A and Moffitt,
             TE},
   Title = {Mental disorder and violent victimization in a total birth
             cohort.},
   Journal = {American journal of public health},
   Volume = {95},
   Number = {11},
   Pages = {2015-2021},
   Year = {2005},
   Month = {November},
   ISSN = {0090-0036},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/16254233},
   Abstract = {<h4>Objective</h4>We examined the association between mental
             disorder and violent victimization in a general population
             sample.<h4>Methods</h4>We performed a multivariate analysis
             of violent victimization in a 12-month period on a total
             birth cohort with follow-up data that assessed, during their
             21st year, males and females born in Dunedin, New Zealand,
             in the early 1970s.<h4>Results</h4>Compared with people with
             no mental disorder, (1) people with anxiety disorders
             experienced more sexual assaults, (2) people with
             schizophreniform disorders experienced more threatened and
             completed physical assaults, (3) people with alcohol
             dependence disorders experienced more completed physical
             assaults, and (4) people with marijuana dependence disorders
             experienced more attempted physical assaults. These results
             held after control for psychiatric comorbidity, demographic
             characteristics, and the study participants' own violent
             behavior.<h4>Conclusion</h4>Mentally disordered young adults
             tend to experience more violent victimization in the
             community than those without a mental disorder.},
   Doi = {10.2105/ajph.2003.021436},
   Key = {fds253324}
}

@article{fds253326,
   Author = {Arseneault, L and Kim-Cohen, J and Taylor, A and Caspi, A and Moffitt,
             TE},
   Title = {Psychometric evaluation of 5- and 7-year-old children's
             self-reports of conduct problems.},
   Journal = {Journal of abnormal child psychology},
   Volume = {33},
   Number = {5},
   Pages = {537-550},
   Year = {2005},
   Month = {October},
   ISSN = {0091-0627},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/16195949},
   Abstract = {Past research suggests that young children are incapable of
             reporting information about their own behavior problems. To
             test this, we examined the validity and the usefulness of
             children's self-reports in the E-Risk Study, a nationally
             representative birth cohort of 2,232 children. We used the
             Berkeley Puppet Interview to obtain children's self-reports
             of conduct problems when they were 5-years old and the
             Dominic-R when they were 7-years old. We also collected
             information about the children and their families by
             interviewing mothers, sending questionnaires to teachers,
             and rating examiners' observations during home visits.
             Results indicate that when children's self-reports are
             gathered with structured and developmentally appropriate
             instruments, they are shown to be valid measures: conduct
             problems reported by the children themselves were associated
             with known correlates including individual characteristics
             (e.g., IQ), related behaviors (e.g., hyperactivity), and
             family variables (e.g., economic disadvantages). Observed
             correlations closely matched effect sizes reported in the
             literature using adults' reports of children's behavioral
             problems. In addition, children's self-reports can be
             useful: both measures distinguished children meeting DSM-IV
             criteria for research diagnoses of conduct disorder.
             Children's reports also contributed unique information not
             provided by adults. For research and clinical purposes,
             young children's self-reports can be viewed as a valuable
             complement to adults' ratings and observational measures of
             children's behavior problems.},
   Doi = {10.1007/s10802-005-6736-5},
   Key = {fds253326}
}

@article{fds253327,
   Author = {Lynam, DR and Caspi, A and Moffitt, TE and Raine, A and Loeber, R and Stouthamer-Loeber, M},
   Title = {Adolescent psychopathy and the big five: results from two
             samples.},
   Journal = {Journal of abnormal child psychology},
   Volume = {33},
   Number = {4},
   Pages = {431-443},
   Year = {2005},
   Month = {August},
   ISSN = {0091-0627},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/16118990},
   Abstract = {The present study examines the relation between psychopathy
             and the Big Five dimensions of personality in two samples of
             adolescents. Specifically, the study tests the hypothesis
             that the aspect of psychopathy representing selfishness,
             callousness, and interpersonal manipulation (Factor 1) is
             most strongly associated with low Agreeableness, whereas the
             aspect of psychopathy representing impulsivity, instability,
             and social deviance (Factor 2) is associated with low
             Agreeableness, low Conscientiousness, and high Neuroticism.
             Data from 13- and 16-year-old boys and their mothers from
             two samples of the Pittsburgh Youth Study are used to test
             these hypotheses. Results were consistent across age and
             rating source in supporting the initial hypotheses,
             providing support for the construct of juvenile psychopathy
             and the interpretation of psychopathy as a constellation of
             traits drawn from a general model of personality
             functioning.},
   Doi = {10.1007/s10648-005-5724-0},
   Key = {fds253327}
}

@article{fds253325,
   Author = {Slutske, WS and Caspi, A and Moffitt, TE and Poulton,
             R},
   Title = {Personality and problem gambling: a prospective study of a
             birth cohort of young adults.},
   Journal = {Archives of general psychiatry},
   Volume = {62},
   Number = {7},
   Pages = {769-775},
   Year = {2005},
   Month = {July},
   ISSN = {0003-990X},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/15997018},
   Abstract = {<h4>Context</h4>Individual differences in dimensions of
             personality may play an important role in explaining risk
             for disordered gambling behavior as well as the comorbidity
             between disordered gambling behavior and other
             substance-related addictive disorders.<h4>Objectives</h4>To
             identify the personality correlates of problem gambling in a
             representative non-treatment-seeking sample, as well as to
             determine whether these are similar to the personality
             correlates of other substance-related addictive disorders
             and whether individual differences in personality might
             account for the comorbidity between disordered gambling
             behavior and other substance-related addictive
             disorders.<h4>Design</h4>Longitudinal population-based
             study.<h4>Participants</h4>A complete birth cohort of young
             adults born in Dunedin, New Zealand, between April 1, 1972,
             and March 31, 1973 (N = 939; 475 men, 464 women).<h4>Main
             outcome measures</h4>Multidimensional Personality
             Questionnaire assessments of personality were obtained at
             age 18 years; structured interview-based diagnoses of
             past-year problem gambling and alcohol, cannabis, and
             nicotine dependence were obtained at age 21
             years.<h4>Results</h4>Problem gambling at age 21 years was
             associated with higher scores on the higher-order
             personality dimension of negative emotionality (d = 0.90)
             and with lower scores on the personality dimension of
             constraint (d = -0.72) measured at age 18 years compared
             with control subjects who did not have a past-year addictive
             disorder at age 21 years. Problem gambling was also
             associated with Multidimensional Personality Questionnaire
             indicators of risk-taking (d = 0.50) and impulsivity (d =
             0.56). The personality profile associated with problem
             gambling was similar to the profiles associated with
             alcohol, cannabis, and nicotine dependence. The relations
             between problem gambling and the substance-related addictive
             disorders (odds ratios = 3.32-3.61) were reduced after
             controlling for individual differences in personality (odds
             ratios = 1.90-2.32).<h4>Conclusions</h4>From the perspective
             of personality, problem gambling has much in common with the
             addictive disorders, as well as with the larger class of
             "externalizing" or "disinhibitory" disorders. Knowledge
             gained from the study of common personality underpinnings
             may be helpful in determining where disordered gambling
             behavior should reside in our diagnostic classification
             system.},
   Doi = {10.1001/archpsyc.62.7.769},
   Key = {fds253325}
}

@article{fds253341,
   Author = {Moffitt, TE},
   Title = {The new look of behavioral genetics in developmental
             psychopathology: gene-environment interplay in antisocial
             behaviors.},
   Journal = {Psychological bulletin},
   Volume = {131},
   Number = {4},
   Pages = {533-554},
   Year = {2005},
   Month = {July},
   ISSN = {0033-2909},
   url = {http://dx.doi.org/10.1037/0033-2909.131.4.533},
   Abstract = {This article reviews behavioral-genetic research to show how
             it can help address questions of causation in developmental
             psychopathology. The article focuses on studies of
             antisocial behavior, because these have been leading the way
             in investigating environmental as well as genetic influences
             on psychopathology. First, the article illustrates how
             behavioral-genetic methods are being newly applied to detect
             the best candidates for genuine environmental causes among
             the many risk factors for antisocial behavior. Second, the
             article examines findings of interaction between genes and
             environments (G x E) associated with antisocial behavior,
             outlining steps for testing hypotheses of measured G x E.
             Third, the article envisages future work on gene-environment
             interplay, arguing that it is an interesting and profitable
             way forward for psychopathology research.},
   Doi = {10.1037/0033-2909.131.4.533},
   Key = {fds253341}
}

@article{fds253328,
   Author = {Kim-Cohen, J and Arseneault, L and Caspi, A and Tomás, MP and Taylor,
             A and Moffitt, TE},
   Title = {Validity of DSM-IV conduct disorder in 41/2-5-year-old
             children: a longitudinal epidemiological
             study.},
   Journal = {The American journal of psychiatry},
   Volume = {162},
   Number = {6},
   Pages = {1108-1117},
   Year = {2005},
   Month = {June},
   ISSN = {0002-953X},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/15930059},
   Abstract = {<h4>Objective</h4>This longitudinal study of a nonreferred,
             population-based sample tested the concurrent, convergent,
             and predictive validity of DSM-IV conduct disorder in
             children 4(1/2)-5 years of age.<h4>Method</h4>In the
             Environmental Risk Longitudinal Twin Study, a representative
             birth cohort of 2,232 children, the children's mothers were
             interviewed and the teachers completed mailed questionnaires
             to assess the children's past 6-month conduct disorder
             symptoms. Children with three or more symptoms were
             diagnosed with conduct disorder, and a subset with five or
             more symptoms was diagnosed with "moderate-to-severe"
             conduct disorder.<h4>Results</h4>The prevalence of conduct
             disorder and moderate-to-severe conduct disorder were 6.6%
             and 2.5%, respectively. Children diagnosed with conduct
             disorder were significantly more likely than comparison
             subjects to self-report antisocial behaviors, to behave
             disruptively during observational assessment, and to have
             risk factors known to be associated with conduct disorder in
             older children (effect sizes ranging from 0.26 to 1.24).
             Five-year-olds diagnosed with conduct disorder were
             significantly more likely than comparison subjects to have
             behavioral and educational difficulties at age 7. Increased
             risk for educational difficulties at age 7 persisted after
             control for IQ and attention deficit hyperactivity disorder
             diagnosis at age 5.<h4>Conclusions</h4>Behavioral problems
             of preschool-age children meeting diagnostic criteria for
             conduct disorder should not be ignored. Appropriate
             intervention should be provided to prevent ongoing
             behavioral and academic problems.},
   Doi = {10.1176/appi.ajp.162.6.1108},
   Key = {fds253328}
}

@article{fds253329,
   Author = {Viding, E and Blair, RJR and Moffitt, TE and Plomin,
             R},
   Title = {Evidence for substantial genetic risk for psychopathy in
             7-year-olds.},
   Journal = {Journal of child psychology and psychiatry, and allied
             disciplines},
   Volume = {46},
   Number = {6},
   Pages = {592-597},
   Year = {2005},
   Month = {June},
   url = {http://dx.doi.org/10.1111/j.1469-7610.2004.00393.x},
   Abstract = {<h4>Background</h4>Individuals with early warning signs of
             life-long psychopathy, callous-unemotional traits (CU) and
             high levels of antisocial behaviour (AB) can be identified
             in childhood. We report here the first twin study of high
             levels of psychopathic tendencies in young
             children.<h4>Methods</h4>At the end of the first school
             year, teachers provided ratings of CU and AB for 3687 twin
             pairs from the Twins Early Development Study (TEDS). For the
             analyses of extreme CU, we selected same-sex twin pairs
             where at least one twin scored 1.3 or more standard
             deviations above the mean on the CU scale (612 probands, 459
             twin pairs). For the analysis of extreme AB, we selected
             same-sex twin pairs where at least one twin scored 1.3 or
             more standard deviations above the mean on AB scale (444
             probands, 364 twin pairs). Furthermore, the extreme AB
             sample was divided into those who were also extreme on CU
             (children with psychopathic tendencies; 234 probands, 187
             twin pairs) and those who did not score in the extreme for
             CU (children without psychopathic tendencies; 210 probands,
             177 twin pairs).<h4>Results</h4>DeFries-Fulker extremes
             analysis indicated that exhibiting high levels of CU is
             under strong genetic influence. Furthermore, separating
             children with AB into those with high and low levels of CU
             showed striking results: AB in children with high levels of
             CU is under extremely strong genetic influence and no
             influence of shared environment, whereas AB in children with
             low levels of CU shows moderate genetic and shared
             environmental influence.<h4>Conclusions</h4>The remarkably
             high heritability for CU, and for AB children with CU,
             suggests that molecular genetic research on antisocial
             behaviour should focus on the CU core of psychopathy. Our
             findings also raise questions for public policy on
             interventions for antisocial behaviour.},
   Doi = {10.1111/j.1469-7610.2004.00393.x},
   Key = {fds253329}
}

@article{fds253330,
   Author = {Piquero, AR and Brame, R and Moffitt, TE},
   Title = {Extending the study of continuity and change: Gender
             differences in the linkage between adolescent and adult
             offending},
   Journal = {Journal of Quantitative Criminology},
   Volume = {21},
   Number = {2},
   Pages = {219-243},
   Publisher = {Springer Nature},
   Year = {2005},
   Month = {June},
   ISSN = {0748-4518},
   url = {http://dx.doi.org/10.1007/s10940-005-2494-3},
   Abstract = {Recently, Paternoster et∈al. used data from the Cambridge
             Study in Delinquent Development, a longitudinal study of 411
             South London boys mostly born in 1953, to investigate the
             linkage between adolescent and adult offending and found
             that variations in adult offending were consistent with a
             random process after conditioning on adolescent offending.
             In this paper, we test the robustness of this early study
             across data sources and genders. Here, we use data from the
             Dunedin New Zealand 1972 birth cohort study to replicate
             previous findings regarding stability and change in criminal
             offending between the adolescent and adult years. In
             particular, our interest centers on the stochastic
             properties of the adolescent and adult conviction
             distribution in the cohort and whether the structure of this
             distribution is similar for males and females. This
             replication and extension of prior work is especially
             important since criminologists have little understanding of
             the pattern of female adolescent offending or how the
             patterns are linked to adult offending for women. The
             analysis reveals that variation in adult offending after
             conditioning on adolescent offending is consistent with a
             random (Poisson) process. Furthermore, this pattern is
             evident for both the males and the females in the Dunedin
             New Zealand 1972 birth cohort. © 2005 Springer
             Science+Business Media, Inc.},
   Doi = {10.1007/s10940-005-2494-3},
   Key = {fds253330}
}

@article{fds253331,
   Author = {Jaffee, SR and Harrington, H and Cohen, P and Moffitt,
             TE},
   Title = {Cumulative prevalence of psychiatric disorder in
             youths.},
   Journal = {Journal of the American Academy of Child and Adolescent
             Psychiatry},
   Volume = {44},
   Number = {5},
   Pages = {406-407},
   Year = {2005},
   Month = {May},
   url = {http://dx.doi.org/10.1097/01.chi.0000155317.38265.61},
   Doi = {10.1097/01.chi.0000155317.38265.61},
   Key = {fds253331}
}

@article{fds253336,
   Author = {Caspi, A and Moffitt, TE and Cannon, M and McClay, J and Murray, R and Harrington, H and Taylor, A and Arseneault, L and Williams, B and Braithwaite, A and Poulton, R and Craig, IW},
   Title = {Moderation of the effect of adolescent-onset cannabis use on
             adult psychosis by a functional polymorphism in the
             catechol-O-methyltransferase gene: longitudinal evidence of
             a gene X environment interaction.},
   Journal = {Biological psychiatry},
   Volume = {57},
   Number = {10},
   Pages = {1117-1127},
   Year = {2005},
   Month = {May},
   ISSN = {0006-3223},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/15866551},
   Abstract = {<h4>Background</h4>Recent evidence documents that cannabis
             use by young people is a modest statistical risk factor for
             psychotic symptoms in adulthood, such as hallucinations and
             delusions, as well as clinically significant schizophrenia.
             The vast majority of cannabis users do not develop
             psychosis, however, prompting us to hypothesize that some
             people are genetically vulnerable to the deleterious effects
             of cannabis.<h4>Methods</h4>In a longitudinal study of a
             representative birth cohort followed to adulthood, we tested
             why cannabis use is associated with the emergence of
             psychosis in a minority of users, but not in
             others.<h4>Results</h4>A functional polymorphism in the
             catechol-O-methyltransferase (COMT) gene moderated the
             influence of adolescent cannabis use on developing adult
             psychosis. Carriers of the COMT valine158 allele were most
             likely to exhibit psychotic symptoms and to develop
             schizophreniform disorder if they used cannabis. Cannabis
             use had no such adverse influence on individuals with two
             copies of the methionine allele.<h4>Conclusions</h4>These
             findings provide evidence of a gene x environment
             interaction and suggest that a role of some susceptibility
             genes is to influence vulnerability to environmental
             pathogens.},
   Doi = {10.1016/j.biopsych.2005.01.026},
   Key = {fds253336}
}

@article{fds253339,
   Author = {Moffitt, TE and Caspi, A and Rutter, M},
   Title = {Strategy for investigating interactions between measured
             genes and measured environments.},
   Journal = {Archives of general psychiatry},
   Volume = {62},
   Number = {5},
   Pages = {473-481},
   Year = {2005},
   Month = {May},
   ISSN = {0003-990X},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/15867100},
   Abstract = {The purpose of this article is to promote research that
             tests hypotheses of measured gene-environment interaction
             (GxE). A GxE occurs when the effect of exposure to an
             environmental pathogen on health is conditional on a
             person's genotype (or conversely, when environmental
             experience moderates genes' effects on health).
             Gene-environment interactions were thought to be rare in
             psychiatry, but empirical findings of measured GxEs are now
             emerging. However, the current high level of curiosity about
             GxE is accompanied by uncertainty about the feasibility of
             GxE research and by pragmatic questions about how to carry
             out good GxE studies. First, we summarize emerging evidence
             about GxE in psychiatric disorders. Second, we describe 7
             strategic steps that may be used to organize further
             hypothesis-driven studies of GxE. Third, we explain the
             potential benefits of the measured-GxE approach for basic
             neuroscience and for gene hunting. We suggest that in
             psychiatric genetics, ignoring nurture handicaps the field's
             capacity to make new discoveries about nature.},
   Doi = {10.1001/archpsyc.62.5.473},
   Key = {fds253339}
}

@article{fds253332,
   Author = {Donnellan, MB and Trzesniewski, KH and Robins, RW and Moffitt, TE and Caspi, A},
   Title = {Low self-esteem is related to aggression, antisocial
             behavior, and delinquency.},
   Journal = {Psychological science},
   Volume = {16},
   Number = {4},
   Pages = {328-335},
   Year = {2005},
   Month = {April},
   ISSN = {0956-7976},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/15828981},
   Abstract = {The present research explored the controversial link between
             global self-esteem and externalizing problems such as
             aggression, antisocial behavior, and delinquency. In three
             studies, we found a robust relation between low self-esteem
             and externalizing problems. This relation held for measures
             of self-esteem and externalizing problems based on
             self-report, teachers' ratings, and parents' ratings, and
             for participants from different nationalities (United States
             and New Zealand) and age groups (adolescents and college
             students). Moreover, this relation held both
             cross-sectionally and longitudinally and after controlling
             for potential confounding variables such as supportive
             parenting, parent-child and peer relationships,
             achievement-test scores, socioeconomic status, and IQ. In
             addition, the effect of self-esteem on aggression was
             independent of narcissism, an important finding given recent
             claims that individuals who are narcissistic, not low in
             self-esteem, are aggressive. Discussion focuses on
             clarifying the relations among self-esteem, narcissism, and
             externalizing problems.},
   Doi = {10.1111/j.0956-7976.2005.01535.x},
   Key = {fds253332}
}

@article{fds253333,
   Author = {Gregory, AM and Caspi, A and Eley, TC and Moffitt, TE and Oconnor, TG and Poulton, R},
   Title = {Prospective longitudinal associations between persistent
             sleep problems in childhood and anxiety and depression
             disorders in adulthood.},
   Journal = {Journal of abnormal child psychology},
   Volume = {33},
   Number = {2},
   Pages = {157-163},
   Year = {2005},
   Month = {April},
   ISSN = {0091-0627},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/15839494},
   Abstract = {The objective of this study was to examine the associations
             between persistent childhood sleep problems and adulthood
             anxiety and depression. Parents of 943 children (52% male)
             participating in the Dunedin Multidisciplinary Health and
             Development Study provided information on their children's
             sleep and internalizing problems at ages 5, 7, and 9 years.
             When the participants were 21 and 26 years, adult anxiety
             and depression were diagnosed using a standardized
             diagnostic interview. After controlling for childhood
             internalizing problems, sex, and socioeconomic status,
             persistent sleep problems in childhood predicted adulthood
             anxiety disorders (OR (95% CI) = 1.60 (1.05-2.45), p = .030)
             but not depressive disorders (OR (95% CI) = .99 (.63-1.56),
             p = .959). Persistent sleep problems in childhood may be an
             early risk indicator of anxiety in adulthood.},
   Doi = {10.1007/s10802-005-1824-0},
   Key = {fds253333}
}

@article{fds253334,
   Author = {Hughes, C and Jaffee, SR and Happé, F and Taylor, A and Caspi, A and Moffitt, TE},
   Title = {Origins of individual differences in theory of mind: from
             nature to nurture?},
   Journal = {Child development},
   Volume = {76},
   Number = {2},
   Pages = {356-370},
   Year = {2005},
   Month = {March},
   ISSN = {0009-3920},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/15784087},
   Abstract = {In this study of the origins of individual differences in
             theory of mind (ToM), the Environmental Risk (E-Risk)
             Longitudinal Twin Study sample of 1,116 sixty-month-old twin
             pairs completed a comprehensive battery of ToM tasks.
             Individual differences in ToM were striking and strongly
             associated with verbal ability. Behavioral genetic models of
             the data showed that environmental factors explained the
             majority of the variance in ToM performance in this sample.
             Shared environmental influences on verbal ability had a
             common impact on ToM and explained more than half the
             phenotypic correlation between these two skills. Possible
             underlying proximal mechanisms are discussed, including
             maternal speech and mind-mindedness, sibling interactions,
             and peer influences.},
   Doi = {10.1111/j.1467-8624.2005.00850.x},
   Key = {fds253334}
}

@article{fds253335,
   Author = {Raine, A and Moffitt, TE and Caspi, A and Loeber, R and Stouthamer-Loeber, M and Lynam, D},
   Title = {Neurocognitive impairments in boys on the life-course
             persistent antisocial path.},
   Journal = {Journal of abnormal psychology},
   Volume = {114},
   Number = {1},
   Pages = {38-49},
   Year = {2005},
   Month = {February},
   ISSN = {0021-843X},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/15709810},
   Abstract = {This study addresses 5 unresolved issues in the
             neuropsychology of antisocial behavior using a community
             sample of 325 school boys in whom neurocognitive measures
             were assessed at age 16-17 years. Antisocial behavior
             measures collected from age 7-17 years were cluster analyzed
             and produced 4 groups: control, childhood-limited,
             adolescent-limited, and life-course persistent. Those on the
             lifecourse persistent path and also on the childhood-limited
             path were particularly impaired on spatial and memory
             functions. Impairments were independent of abuse,
             psychosocial adversity, head injury, and hyperactivity.
             Findings provide some support for the life-course persistent
             versus adolescent-limited theory of antisocial behavior and
             suggest that (a) neurocognitive impairments are profound and
             not artifactual and (b) childhood-limited antisocials may
             not be free of long-lasting functional impairment.},
   Doi = {10.1037/0021-843x.114.1.38},
   Key = {fds253335}
}

@article{fds253338,
   Author = {Kim-Cohen, J and Moffitt, TE and Taylor, A and Pawlby, SJ and Caspi,
             A},
   Title = {Maternal depression and children's antisocial behavior:
             nature and nurture effects.},
   Journal = {Archives of general psychiatry},
   Volume = {62},
   Number = {2},
   Pages = {173-181},
   Year = {2005},
   Month = {February},
   ISSN = {0003-990X},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/15699294},
   Abstract = {<h4>Background</h4>Children of depressed mothers have
             elevated conduct problems, presumably because maternal
             depression disrupts the caregiving environment.
             Alternatively, the association between maternal depression
             and children's antisocial behavior (ASB) may come about
             because (1) depressed women are likely to have comorbid
             antisocial personality traits, (2) depressed women are
             likely to mate and bear children with antisocial men, or (3)
             children of depressed mothers inherit a genetic liability
             for psychopathology.<h4>Method</h4>We used data from the
             E-Risk Study, a representative British cohort of 1116 twin
             pairs assessed at 5 and 7 years of age. We tested for
             environmental mediation of the association between maternal
             depression during the children's first 5 years of life and
             children's ASB at age 7 years, free from familial liability
             for ASB.<h4>Results</h4>Maternal depression occurring after,
             but not before, the twins' birth was associated with child
             ASB and showed a significant dose-response relationship with
             child ASB at 7 years of age. Parental history of ASPD
             symptoms accounted for approximately one third of the
             observed association between maternal depression and
             children's ASB, but maternal depression continued to
             significantly predict children's ASB. Intraindividual change
             analyses indicated that children exposed to their mother's
             depression between ages 5 and 7 years showed a subsequent
             increase in ASB by age 7 years. The combination of
             depression and ASPD symptoms in mothers posed the greatest
             risk for children's ASB.<h4>Conclusions</h4>Studies ignoring
             genetic transmission overestimate social transmission
             effects because both genetic and environmental processes are
             involved in creating risk for ASB in children of depressed
             mothers. Interventions for depressed mothers aiming to
             reduce conduct problems in their children should address
             parents' antisocial personality, as well as mothers'
             depression.},
   Doi = {10.1001/archpsyc.62.2.173},
   Key = {fds253338}
}

@article{fds253108,
   Author = {Moffitt, TE and Caspi, A},
   Title = {Life-course persistent and adolescence-limited antisocial
             males: Longitudinal followup to adulthood},
   Pages = {161-186},
   Booktitle = {Developmental Psychobiology of Aggression},
   Publisher = {Cambridge University Press},
   Editor = {D.M. Stoff and E.J. Susman},
   Year = {2005},
   Month = {January},
   url = {http://dx.doi.org/10.1017/CBO9780511499883.009},
   Abstract = {This chapter tests and refines a developmental taxonomy of
             antisocial behavior, which proposed two primary hypothetical
             prototypes: life-course persistent offenders whose
             antisocial behavior begins in childhood and continues
             worsening thereafter, versus adolescence-limited offenders
             whose antisocial behavior begins in adolescence and desists
             in young adulthood (Moffitt, 1993). Two of our previous
             reports have described clinically defined groups of
             childhood-onset and adolescence-onset antisocial youths in
             the Dunedin birth cohort during childhood (Moffitt & Caspi,
             2001) and at age 18 (Moffitt, Caspi, Dickson, Silva, &
             Stanton, 1996). Recently we followed up the cohort at age
             26, and here we describe how the two groups of males fared
             in adulthood. In so doing we test a hypothesis critical to
             the theory: that childhood-onset, but not adolescent-onset,
             antisocial behavior is associated in adulthood with
             antisocial personality, violence, and continued serious
             antisocial behavior that expands into maladjustment in work
             life and victimization of partners and children (Moffitt,
             1993). The Two Prototypes and Their Predicted Adult
             Outcomes: According to the theory, life-course persistent
             antisocials are few, persistent, and pathological.
             Adolescence-limited antisocials are common, relatively
             temporary, and near normative. The developmental typology
             hypothesized that childhood-onset versus adolescent-onset
             conduct problems have different etiologies. In addition, the
             typology differed from other developmental crime theories by
             predicting different outcome pathways for the two types
             across the adult life-course (Caspi & Moffitt, 1995;
             Moffitt, 1993, 1994, 1997).},
   Doi = {10.1017/CBO9780511499883.009},
   Key = {fds253108}
}

@article{fds253337,
   Author = {Jaffee, SR and Caspi, A and Moffitt, TE and Dodge, KA and Rutter, M and Taylor, A and Tully, LA},
   Title = {Nature X nurture: genetic vulnerabilities interact with
             physical maltreatment to promote conduct
             problems.},
   Journal = {Development and psychopathology},
   Volume = {17},
   Number = {1},
   Pages = {67-84},
   Year = {2005},
   Month = {January},
   ISSN = {0954-5794},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/15971760},
   Abstract = {Maltreatment places children at risk for psychiatric
             morbidity, especially conduct problems. However, not all
             maltreated children develop conduct problems. We tested
             whether the effect of physical maltreatment on risk for
             conduct problems was strongest among those who were at high
             genetic risk for these problems using data from the E-risk
             Study, a representative cohort of 1,116 5-year-old British
             twin pairs and their families. Children's conduct problems
             were ascertained via parent and teacher interviews. Physical
             maltreatment was ascertained via parent report. Children's
             genetic risk for conduct problems was estimated as a
             function of their co-twin's conduct disorder status and the
             pair's zygosity. The effect of maltreatment on risk for
             conduct problems was strongest among those at high genetic
             risk. The experience of maltreatment was associated with an
             increase of 2% in the probability of a conduct disorder
             diagnosis among children at low genetic risk for conduct
             disorder but an increase of 24% among children at high
             genetic risk. Prediction of behavioral pathology can attain
             greater accuracy if both pathogenic environments and genetic
             risk are ascertained. Certain genotypes may promote
             resistance to trauma. Physically maltreated children whose
             first-degree relatives engage in antisocial behavior warrant
             priority for therapeutic intervention.},
   Doi = {10.1017/s0954579405050042},
   Key = {fds253337}
}

@article{fds253340,
   Author = {Moffitt, TE},
   Title = {Genetic and environmental influences on antisocial
             behaviors: evidence from behavioral-genetic
             research.},
   Journal = {Advances in genetics},
   Volume = {55},
   Pages = {41-104},
   Year = {2005},
   Month = {January},
   ISSN = {0065-2660},
   url = {http://dx.doi.org/10.1016/s0065-2660(05)55003-x},
   Abstract = {This article reviews behavioral-genetic research into human
             antisocial behavior. The focus is on studies of antisocial
             behavior that have been leading the way in investigating
             environmental and genetic influences on human behavior. The
             first generation of studies, which provided quantitative
             estimates attesting that genes and environments each
             influence about half of the population's variation in
             antisocial behaviors is interpreted. Then how
             behavioral-genetic methods are being applied to test
             developmental theory and to detect environmental causes of
             antisocial behavior is illustrated. Evidence for
             interactions between genes and the environment in the
             etiology of antisocial behavior is also examined. The
             article ends by envisioning future work on gene-environment
             interplay in the etiology of antisocial behavior.},
   Doi = {10.1016/s0065-2660(05)55003-x},
   Key = {fds253340}
}

@article{fds253342,
   Author = {Moffitt, TE},
   Title = {Grandma Macon},
   Journal = {Our State: The Magazine of North Carolina},
   Year = {2005},
   Month = {January},
   Key = {fds253342}
}

@article{fds340552,
   Author = {Caspi, A and McClay, J and Moffitt, TE and Mill, J and Martin, J and Craig,
             IW and Taylor, A and Poulton, R},
   Title = {Role of genotype in the cycle of violence in maltreated
             children - Fears of the future in children und young
             people},
   Journal = {ZEITSCHRIFT FUR SOZIOLOGIE DER ERZIEHUNG UND
             SOZIALISATION},
   Volume = {25},
   Number = {2},
   Pages = {133-145},
   Publisher = {JUVENTA VERLAG GMBH},
   Year = {2005},
   Month = {January},
   Key = {fds340552}
}

@article{fds253345,
   Author = {Jaffee, SR and Caspi, A and Moffitt, TE and Polo-Tomas, M and Price, TS and Taylor, A},
   Title = {The limits of child effects: evidence for genetically
             mediated child effects on corporal punishment but not on
             physical maltreatment.},
   Journal = {Developmental psychology},
   Volume = {40},
   Number = {6},
   Pages = {1047-1058},
   Year = {2004},
   Month = {November},
   ISSN = {0012-1649},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/15535755},
   Abstract = {Research on child effects has demonstrated that children's
             difficult and coercive behavior provokes harsh discipline
             from adults. Using a genetically sensitive design, the
             authors tested the limits of child effects on adult behavior
             that ranged from the normative (corporal punishment) to the
             nonnormative (physical maltreatment). The sample was a
             1994-1995 nationally representative birth cohort of 1,116
             twins and their families who participated in the
             Environmental Risk Longitudinal Study. Results showed that
             environmental factors accounted for most of the variation in
             corporal punishment and physical maltreatment. However,
             corporal punishment was genetically mediated in part, and
             the genetic factors that influenced corporal punishment were
             largely the same as those that influenced children's
             antisocial behavior, suggesting a child effect. The authors
             conclude that risk factors for maltreatment are less likely
             to reside within the child and more likely to reside in
             characteristics that differ between families.},
   Doi = {10.1037/0012-1649.40.6.1047},
   Key = {fds253345}
}

@article{fds253346,
   Author = {Maughan, B and Taylor, A and Caspi, A and Moffitt,
             TE},
   Title = {Prenatal smoking and early childhood conduct problems:
             testing genetic and environmental explanations of the
             association.},
   Journal = {Archives of general psychiatry},
   Volume = {61},
   Number = {8},
   Pages = {836-843},
   Year = {2004},
   Month = {August},
   ISSN = {0003-990X},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/15289282},
   Abstract = {<h4>Background</h4>Extensive evidence now supports a
             statistical association between prenatal smoking and
             increased risk for antisocial outcomes in offspring. Though
             this statistical link may signal a causal association,
             commentators have urged caution in interpreting findings
             because of the likelihood of confounding.<h4>Methods</h4>We
             used data from the Environmental Risk Longitudinal Twin
             Study, a representative British sample of 1116 twin pairs
             studied at ages 5 and 7 years, to assess associations
             between prenatal smoking and early childhood conduct
             problems net of the effects of both heritable and
             environmental risks for child antisocial
             outcomes.<h4>Results</h4>Prenatal smoking showed a strong,
             dose-response relationship with child conduct problems at
             ages 5 and 7 years. Around half of this association was
             attributable to correlated genetic effects. Mothers who
             smoked during pregnancy differed from other mothers in a
             number of ways. They were more likely to be antisocial, had
             children with more antisocial men, were bringing up their
             children in more disadvantaged circumstances, and were more
             likely to have had depression. Controlling for antisocial
             behavior in both parents, depression in mothers, family
             disadvantage, and genetic influences, estimates for the
             effects of prenatal smoking were reduced by between 75% and
             the entire initial effects.<h4>Conclusions</h4>Observed
             associations between prenatal smoking and childhood conduct
             problems are likely to be heavily confounded with other
             known risks for children's behavioral development. As a
             result, tests of any causal influence of prenatal smoking
             must await findings from experimental studies.},
   Doi = {10.1001/archpsyc.61.8.836},
   Key = {fds253346}
}

@article{fds253351,
   Author = {Moffitt, TE},
   Title = {Reply to Russell Barkley},
   Journal = {APA Monitor on Psychology},
   Year = {2004},
   Month = {August},
   Key = {fds253351}
}

@article{fds253350,
   Author = {Wright, BRE and Caspi, A and Moffitt, TE and Paternoster,
             R},
   Title = {Does the perceived risk of punishment deter criminally prone
             individuals? Rational choice, self-control, and
             crime},
   Journal = {Journal of Research in Crime and Delinquency},
   Volume = {41},
   Number = {2},
   Pages = {180-213},
   Publisher = {SAGE Publications},
   Year = {2004},
   Month = {May},
   ISSN = {0022-4278},
   url = {http://dx.doi.org/10.1177/0022427803260263},
   Abstract = {Society's efforts to deter crime with punishment may be
             ineffective because those individuals most prone to commit
             crime often act impulsively, with little thought for the
             future, and so they may be unmoved by the threat of later
             punishment. Deterrence messages they receive, therefore, may
             fall on deaf ears. This article examines this issue by
             testing the relationship between criminal propensity,
             perceived risks and costs of punishment, and criminal
             behavior. The authors analyzed data from the Dunedin (New
             Zealand) Study, a longitudinal study of individuals from
             birth through age 26 (N = 1,002). They found that in fact,
             deterrence perceptions had their greatest impact on
             criminally prone study members.},
   Doi = {10.1177/0022427803260263},
   Key = {fds253350}
}

@article{fds253352,
   Author = {Kim-Cohen, J and Moffitt, TE and Caspi, A and Taylor,
             A},
   Title = {Genetic and environmental processes in young children's
             resilience and vulnerability to socioeconomic
             deprivation.},
   Journal = {Child development},
   Volume = {75},
   Number = {3},
   Pages = {651-668},
   Year = {2004},
   Month = {May},
   ISSN = {0009-3920},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/15144479},
   Abstract = {Some children exposed to socioeconomic (SES) deprivation are
             resilient and function better than expected, given the level
             of deprivation they have experienced. The present study
             tested genetic and environmental contributions to young
             children's resilience and vulnerability to SES deprivation.
             Children's resilience was assessed by the difference between
             their actual score and the score predicted by their level of
             SES deprivation in the E-Risk Study, an epidemiological
             cohort of 1,116 five-year-old twin pairs. Consistent with
             previous research, results showed that maternal warmth,
             stimulating activities, and children's outgoing temperament
             appeared to promote positive adjustment in children exposed
             to SES deprivation. Findings add new information by
             demonstrating that resilience is partly heritable and that
             protective processes operate through both genetic and
             environmental effects.},
   Doi = {10.1111/j.1467-8624.2004.00699.x},
   Key = {fds253352}
}

@article{fds304713,
   Author = {Ehrensaft, MK and Moffitt, TE and Caspi, A},
   Title = {Clinically abusive relationships in an unselected birth
             cohort: men's and women's participation and developmental
             antecedents.},
   Journal = {J Abnorm Psychol},
   Volume = {113},
   Number = {2},
   Pages = {258-270},
   Year = {2004},
   Month = {May},
   ISSN = {0021-843X},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/15122946},
   Abstract = {In an unselected birth cohort (N=980, age 24-26 years),
             individuals in abusive relationships causing injury and/or
             official intervention (9% prevalence) were compared with
             participants reporting physical abuse without clinical
             consequences and with control participants who reported no
             abuse, on current characteristics and prospective
             developmental risks. In nonclinically abusive relationships,
             perpetrators were primarily women. In clinically abusive
             relationships, men and women used physical abuse, although
             more women needed medical treatment for injury. Women in
             clinically abusive relationships had childhood family
             adversity, adolescent conduct problems, and aggressive
             personality; men had disinhibitory psychopathology since
             childhood and extensive personality deviance. These findings
             counter the hibitory assumption that if clinical abuse was
             ascertained in epidemiological samples, it would be
             primarily man-to-woman, explained by patriarchy rather than
             psychopathology.},
   Doi = {10.1037/0021-843X.113.2.258},
   Key = {fds304713}
}

@article{fds253190,
   Author = {Tully, LA and Arseneault, L and Caspi, A and Moffitt, TE and Morgan,
             J},
   Title = {Does maternal warmth moderate the effects of birth weight on
             twins' attention-deficit/hyperactivity disorder (ADHD)
             symptoms and low IQ?},
   Journal = {Journal of consulting and clinical psychology},
   Volume = {72},
   Number = {2},
   Pages = {218-226},
   Year = {2004},
   Month = {April},
   ISSN = {0022-006X},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/15065956},
   Abstract = {The moderating effect of maternal warmth on the association
             between low birth weight and children's attention-deficit/hyperactivity
             disorder (ADHD) symptoms and low IQ was studied in 2,232
             twins. Half of 5-year-old children had low birth weights,
             below 2,500 g. Maternal warmth, a component of expressed
             emotion, was coded from mothers' audiotaped descriptions of
             each child. Both parents and teachers rated children's ADHD
             symptoms, and the children were administered an IQ test.
             Results showed a significant interaction between children's
             birth weight and maternal warmth in predicting mothers' and
             teachers' ratings of ADHD. The interaction was not
             significant for IQ. The findings suggest that the effect of
             children's birth weight on their ADHD symptoms can be
             moderated by maternal warmth and that enhancing maternal
             warmth may prevent behavior problems among the increasing
             population of low-birth- weight children.},
   Doi = {10.1037/0022-006x.72.2.218},
   Key = {fds253190}
}

@article{fds304711,
   Author = {Tully, LA and Moffitt, TE and Caspi, A and Taylor, A and Kiernan, H and Andreou, P},
   Title = {What effect does classroom separation have on twins'
             behavior, progress at school, and reading
             abilities?},
   Journal = {Twin research : the official journal of the International
             Society for Twin Studies},
   Volume = {7},
   Number = {2},
   Pages = {115-124},
   Year = {2004},
   Month = {April},
   ISSN = {1369-0523},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/15169595},
   Abstract = {We investigated the effects of classroom separation on
             twins' behavior, progress at school, and reading abilities.
             This investigation was part of a longitudinal study of a
             nationally-representative sample of twins (the E-risk Study)
             who were assessed at the start of school (age 5) and
             followed up (age 7). We examined three groups of twins:
             pairs who were in the same class at both ages; pairs who
             were in separate classes at both ages; and pairs who were in
             the same class at age 5, but separated by age 7. When
             compared to those not separated, those separated early had
             significantly more teacher-rated internalizing problems and
             those separated later showed more internalizing problems and
             lower reading scores. Monozygotic (MZ) twins showed more
             problems as a result of separation than dizygotic (DZ)
             twins. No group differences emerged for externalizing
             problems, ADHD or prosocial behaviors. The implications of
             the findings for parents and teachers of twins, and for
             school practices about separating twins, are
             discussed.},
   Doi = {10.1375/136905204323016087},
   Key = {fds304711}
}

@article{fds304712,
   Author = {Rutter, M and Caspi, A and Fergusson, D and Horwood, LJ and Goodman, R and Maughan, B and Moffitt, TE and Meltzer, H and Carroll,
             J},
   Title = {Sex differences in developmental reading disability: new
             findings from 4 epidemiological studies.},
   Journal = {JAMA},
   Volume = {291},
   Number = {16},
   Pages = {2007-2012},
   Year = {2004},
   Month = {April},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/15113820},
   Abstract = {<h4>Context</h4>An influential article published in 1990
             claimed that the increased rate of reading disability in
             boys was a consequence of referral bias.<h4>Objectives</h4>To
             summarize the history of research on sex differences in
             reading disability and to provide new evidence from 4
             independent epidemiological studies about the nature,
             extent, and significance of sex differences in reading
             disability.<h4>Design, setting, and participants</h4>The
             Dunedin Multidisciplinary Health and Development Study
             comprised 989 individuals (52.1% male) in a cohort born
             between April 1972 and March 1973 in Dunedin, New Zealand,
             and followed up from age 3 years; reading performance and IQ
             were assessed at ages 7, 9, and 11 years using the Burt Word
             Reading Test and the Wechsler Intelligence Scale for
             Children-Revised (WISC-R), respectively. The Christchurch
             Health and Development Study comprised 895 individuals (50%
             male) in a prospectively studied cohort born in the
             Christchurch, New Zealand, region during a 4-month period in
             1977; reading performance and IQ were assessed at ages 8 to
             10 years using the Burt Word Reading Test and the WISC-R.
             The Office for National Statistics (ONS) Study comprised a
             UK nationally representative sample of 5752 children (50.1%
             male) aged 9 to 15 years in 1999; reading was assessed on
             the British Ability Scales II and IQ on the British Picture
             Vocabulary Scales II. The Environmental Risk Longitudinal
             Twin Study (E-Risk) comprised 2163 twin children from
             England and Wales (49.1% male) identified at birth in 1994
             and 1995 and included administration of the Test of Word
             Reading Efficiency at age 7 years and the Wechsler Preschool
             and Primary Scale of Intelligence-Revised as a test of IQ at
             age 5 years.<h4>Main outcome measure</h4>Reading performance
             by sex in the lowest 15% of the distribution for all 4
             studies, with and without taking IQ into
             account.<h4>Results</h4>In all 4 studies, the rates of
             reading disability were significantly higher in boys. For
             non-IQ-referenced reading disability: Dunedin study, 21.6%
             in boys vs 7.9% in girls (odds ratio [OR], 3.19; 95%
             confidence interval [CI], 2.15-4.17); Christchurch study,
             20.6% in boys vs 9.8% in girls (OR, 2.38; 95% CI,
             1.62-3.50); ONS study, 17.6% in boys vs 13.0% in girls (OR,
             1.43; 95% CI, 1.23-1.65); and E-Risk, 18.0% in boys vs 13.0%
             in girls (OR, 1.39; 95% CI, 1.04-1.86). The rates for
             IQ-referenced reading disabilities were similar.<h4>Conclusion</h4>Reading
             disabilities are clearly more frequent in boys than in
             girls.},
   Doi = {10.1001/jama.291.16.2007},
   Key = {fds304712}
}

@article{fds253355,
   Author = {Caspi, A and Moffitt, TE and Morgan, J and Rutter, M and Taylor, A and Arseneault, L and Tully, L and Jacobs, C and Kim-Cohen, J and Polo-Tomas, M},
   Title = {Maternal expressed emotion predicts children's antisocial
             behavior problems: using monozygotic-twin differences to
             identify environmental effects on behavioral
             development.},
   Journal = {Developmental psychology},
   Volume = {40},
   Number = {2},
   Pages = {149-161},
   Year = {2004},
   Month = {March},
   ISSN = {0012-1649},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/14979757},
   Abstract = {If maternal expressed emotion is an environmental risk
             factor for children's antisocial behavior problems, it
             should account for behavioral differences between siblings
             growing up in the same family even after genetic influences
             on children's behavior problems are taken into account. This
             hypothesis was tested in the Environmental Risk Longitudinal
             Twin Study with a nationally representative 1994-1995 birth
             cohort of twins. The authors interviewed the mothers of 565
             five-year-old monozygotic (MZ) twin pairs and established
             which twin in each family received more negative emotional
             expression and which twin received more warmth. Within MZ
             pairs, the twin receiving more maternal negativity and less
             warmth had more antisocial behavior problems. Qualitative
             interviews were used to generate hypotheses about why
             mothers treat their children differently. The results
             suggest that maternal emotional attitudes toward children
             may play a causal role in the development of antisocial
             behavior and illustrate how genetically informative research
             can inform tests of socialization hypotheses.},
   Doi = {10.1037/0012-1649.40.2.149},
   Key = {fds253355}
}

@article{fds253354,
   Author = {Jaffee, SR and Caspi, A and Moffitt, TE and Taylor,
             A},
   Title = {Physical maltreatment victim to antisocial child: evidence
             of an environmentally mediated process.},
   Journal = {Journal of abnormal psychology},
   Volume = {113},
   Number = {1},
   Pages = {44-55},
   Year = {2004},
   Month = {February},
   ISSN = {0021-843X},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/14992656},
   Abstract = {The well-documented finding that child physical maltreatment
             predicts later antisocial behavior has at least 2
             explanations: (a). Physical maltreatment causes antisocial
             behavior, and (b). genetic factors transmitted from parents
             to children influence the likelihood that parents will be
             abusive and that children will engage in antisocial
             behavior. The authors tested these hypotheses in the
             representative Environmental-Risk cohort of 1116 twin pairs
             and their families, who were assessed when the twins were 5
             and 7 years old. Mothers reported on children's experience
             of physical maltreatment, and mothers and teachers reported
             on children's antisocial behavior. The findings support the
             hypothesis that physical maltreatment plays a causal role in
             the development of children's antisocial behavior and that
             preventing maltreatment can prevent its violent
             sequelae.},
   Doi = {10.1037/0021-843x.113.1.44},
   Key = {fds253354}
}

@article{fds253344,
   Author = {Hussong, AM and Curran, PJ and Moffitt, TE and Caspi, A and Carrig,
             MM},
   Title = {Substance abuse hinders desistance in young adults'
             antisocial behavior.},
   Journal = {Development and psychopathology},
   Volume = {16},
   Number = {4},
   Pages = {1029-1046},
   Year = {2004},
   Month = {January},
   ISSN = {0954-5794},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/15704826},
   Abstract = {We examined two hypotheses about the developmental relation
             between substance abuse and individual differences in
             desistance from antisocial behavior during young adulthood.
             The "snares" hypothesis posits that substance abuse should
             result in time-specific elevations in antisocial behavior
             relative to an individual's own developmental trajectory of
             antisocial behavior, whereas the "launch" hypothesis posits
             that substance abuse early in young adulthood slows an
             individual's overall pattern of crime desistance relative to
             the population norm during this developmental period. We
             conducted latent trajectory analyses to test these
             hypotheses using interview data about antisocial behaviors
             and substance abuse assessed at ages 18, 21, and 26 in men
             from the Dunedin Multidisciplinary Health and Development
             Study (N = 461). We found significant individual variability
             in initial levels and rates of change in antisocial behavior
             over time as well as support for both the snares hypothesis
             and the launch hypothesis as explanations for the
             developmental relation between substance abuse and crime
             desistance in young men.},
   Doi = {10.1017/s095457940404012x},
   Key = {fds253344}
}

@article{fds253349,
   Author = {Skegg, K and Nada-Raja, S and Moffitt, TE},
   Title = {Minor self-harm and psychiatric disorder: a population-based
             study.},
   Journal = {Suicide & life-threatening behavior},
   Volume = {34},
   Number = {2},
   Pages = {187-196},
   Year = {2004},
   Month = {January},
   url = {http://dx.doi.org/10.1521/suli.34.2.187.32790},
   Abstract = {Little is known about the extent to which minor self-harm in
             the general population is associated with psychiatric
             disorder. A population-based sample of 980 young adults was
             interviewed independently about past-year suicidal and
             self-harm behavior and thoughts, and psychiatric disorders.
             Self-harm included self-harmful behaviors such as
             self-battery, as well as traditional methods of suicide (ICD
             [International Classification of Diseases] self-harm). All
             with ICD self-harm and most with other self-harmful behavior
             met the criteria for DSM-IV disorder. Suicidal/self-harmful
             thoughts increased the odds for self-harm, even in men
             without psychiatric disorder (odds ratio 4.9, 95% confidence
             interval 1.3-17.9). Young adults engaging in even minor
             self-harm warrant screening for psychiatric
             disorder.},
   Doi = {10.1521/suli.34.2.187.32790},
   Key = {fds253349}
}

@article{fds253356,
   Author = {Kuntsi, J and Eley, TC and Taylor, A and Hughes, C and Asherson, P and Caspi, A and Moffitt, TE},
   Title = {Co-occurrence of ADHD and low IQ has genetic
             origins.},
   Journal = {American journal of medical genetics. Part B,
             Neuropsychiatric genetics : the official publication of the
             International Society of Psychiatric Genetics},
   Volume = {124B},
   Number = {1},
   Pages = {41-47},
   Year = {2004},
   Month = {January},
   ISSN = {1552-4841},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/14681911},
   Abstract = {Previous studies show that the symptoms of attention deficit
             hyperactivity disorder (ADHD) and lower intelligence
             quotient (IQ) covary in children. We investigated the
             aetiology of this association in a large population-based
             sample of 5-year-old twins. The twins were individually
             assessed on an IQ test, and data on ADHD symptoms were
             obtained from mother interviews and teacher ratings.
             Confirming previous studies, the phenotypic correlation
             between ADHD symptom scores and IQ was -0.3 and, in a
             categorical analysis, children with a Diagnostic and
             Statistical Manual of Mental Disorders (DSM-IV) ADHD
             research diagnosis obtained IQ scores nine points lower, on
             average, than comparison children. We show here that the
             co-occurrence of ADHD and lower IQ has genetic origins: 86%
             of the association between ADHD symptom scores and IQ, and
             100% of the association between ADHD diagnosis and IQ, was
             accounted for by genetic influences that are shared by ADHD
             and IQ. Some candidate genes for ADHD could also contribute
             to variation in IQ or vice versa.},
   Doi = {10.1002/ajmg.b.20076},
   Key = {fds253356}
}

@article{fds69953,
   Author = {Kuntsi, J. and Eley, T. C. and Taylor, A. and Hughes, C. and Asherson, P. and Caspi, A. and Moffitt, T. E},
   Title = {The co-occurrence of ADHD and low IQ has genetic
             origins},
   Journal = {American Journal of Medical Genetics (Neuropsychiatric
             Genetics)},
   Volume = {124B},
   Pages = {41-47},
   Year = {2004},
   Key = {fds69953}
}

@article{fds336546,
   Author = {Tully, L and Arseneault, L and Caspi, A and Moffitt, TE and Morgan,
             J},
   Title = {Does maternal warmth moderate the effects of birth weight on
             twins’ ADHD symptoms and low IQ?},
   Journal = {Journal of Consulting and Clinical Psychology},
   Volume = {72},
   Pages = {218-226},
   Year = {2004},
   Key = {fds336546}
}

@article{fds253343,
   Author = {Lynam, DR and Piquero, A and Moffitt, TE},
   Title = {Specialization and the propensity to violence: Support from
             self-reports but not official records},
   Journal = {Journal of Contemporary Criminal Justice},
   Volume = {20},
   Pages = {215-228},
   Year = {2004},
   Key = {fds253343}
}

@article{fds253347,
   Author = {Rutter, M and Caspi, A and Fergusson, DM and Horwood, LJ and Goodman, R and Maughan, B and Moffitt, TE and Meltzer, H and Carroll,
             J},
   Title = {Gender differences in reading difficulties: New findings
             from four epidemiological studies},
   Journal = {JAMA},
   Volume = {291},
   Number = {16},
   Pages = {2007-2012},
   Year = {2004},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/15113820},
   Abstract = {CONTEXT: An influential article published in 1990 claimed
             that the increased rate of reading disability in boys was a
             consequence of referral bias. OBJECTIVES: To summarize the
             history of research on sex differences in reading disability
             and to provide new evidence from 4 independent
             epidemiological studies about the nature, extent, and
             significance of sex differences in reading disability.
             DESIGN, SETTING, AND PARTICIPANTS: The Dunedin
             Multidisciplinary Health and Development Study comprised 989
             individuals (52.1% male) in a cohort born between April 1972
             and March 1973 in Dunedin, New Zealand, and followed up from
             age 3 years; reading performance and IQ were assessed at
             ages 7, 9, and 11 years using the Burt Word Reading Test and
             the Wechsler Intelligence Scale for Children-Revised
             (WISC-R), respectively. The Christchurch Health and
             Development Study comprised 895 individuals (50% male) in a
             prospectively studied cohort born in the Christchurch, New
             Zealand, region during a 4-month period in 1977; reading
             performance and IQ were assessed at ages 8 to 10 years using
             the Burt Word Reading Test and the WISC-R. The Office for
             National Statistics (ONS) Study comprised a UK nationally
             representative sample of 5752 children (50.1% male) aged 9
             to 15 years in 1999; reading was assessed on the British
             Ability Scales II and IQ on the British Picture Vocabulary
             Scales II. The Environmental Risk Longitudinal Twin Study
             (E-Risk) comprised 2163 twin children from England and Wales
             (49.1% male) identified at birth in 1994 and 1995 and
             included administration of the Test of Word Reading
             Efficiency at age 7 years and the Wechsler Preschool and
             Primary Scale of Intelligence-Revised as a test of IQ at age
             5 years. MAIN OUTCOME MEASURE: Reading performance by sex in
             the lowest 15% of the distribution for all 4 studies, with
             and without taking IQ into account. RESULTS: In all 4
             studies, the rates of reading disability were significantly
             higher in boys. For non-IQ-referenced reading disability:
             Dunedin study, 21.6% in boys vs 7.9% in girls (odds ratio
             [OR], 3.19; 95% confidence interval [CI], 2.15-4.17);
             Christchurch study, 20.6% in boys vs 9.8% in girls (OR,
             2.38; 95% CI, 1.62-3.50); ONS study, 17.6% in boys vs 13.0%
             in girls (OR, 1.43; 95% CI, 1.23-1.65); and E-Risk, 18.0% in
             boys vs 13.0% in girls (OR, 1.39; 95% CI, 1.04-1.86). The
             rates for IQ-referenced reading disabilities were similar.
             CONCLUSION: Reading disabilities are clearly more frequent
             in boys than in girls.},
   Doi = {10.1001/jama.291.16.2007},
   Key = {fds253347}
}

@article{fds253348,
   Author = {Ehrensaft, M and Moffitt, TE and Caspi, A},
   Title = {Clinically abusive relationships and their developmental
             antecedents in an unselected birth cohort},
   Journal = {Journal of Abnormal Psychology},
   Volume = {113},
   Number = {2},
   Pages = {258-270},
   Year = {2004},
   ISSN = {0021-843X},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/15122946},
   Abstract = {In an unselected birth cohort (N=980, age 24-26 years),
             individuals in abusive relationships causing injury and/or
             official intervention (9% prevalence) were compared with
             participants reporting physical abuse without clinical
             consequences and with control participants who reported no
             abuse, on current characteristics and prospective
             developmental risks. In nonclinically abusive relationships,
             perpetrators were primarily women. In clinically abusive
             relationships, men and women used physical abuse, although
             more women needed medical treatment for injury. Women in
             clinically abusive relationships had childhood family
             adversity, adolescent conduct problems, and aggressive
             personality; men had disinhibitory psychopathology since
             childhood and extensive personality deviance. These findings
             counter the hibitory assumption that if clinical abuse was
             ascertained in epidemiological samples, it would be
             primarily man-to-woman, explained by patriarchy rather than
             psychopathology.},
   Doi = {10.1037/0021-843X.113.2.258},
   Key = {fds253348}
}

@article{fds253353,
   Author = {Tully, L and Moffitt, TE and Caspi, A and Taylor, A and Kiernan, H and Andreou, P},
   Title = {Classroom separation and twins’ behaviour and cognitive
             abilities},
   Journal = {Twin Research},
   Volume = {7},
   Number = {2},
   Pages = {115-124},
   Year = {2004},
   ISSN = {1369-0523},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/15169595},
   Abstract = {We investigated the effects of classroom separation on
             twins' behavior, progress at school, and reading abilities.
             This investigation was part of a longitudinal study of a
             nationally-representative sample of twins (the E-risk Study)
             who were assessed at the start of school (age 5) and
             followed up (age 7). We examined three groups of twins:
             pairs who were in the same class at both ages; pairs who
             were in separate classes at both ages; and pairs who were in
             the same class at age 5, but separated by age 7. When
             compared to those not separated, those separated early had
             significantly more teacher-rated internalizing problems and
             those separated later showed more internalizing problems and
             lower reading scores. Monozygotic (MZ) twins showed more
             problems as a result of separation than dizygotic (DZ)
             twins. No group differences emerged for externalizing
             problems, ADHD or prosocial behaviors. The implications of
             the findings for parents and teachers of twins, and for
             school practices about separating twins, are
             discussed.},
   Doi = {10.1375/136905204323016087},
   Key = {fds253353}
}

@article{fds253360,
   Author = {Arseneault, L and Cannon, M and Murray, R and Poulton, R and Caspi, A and Moffitt, TE},
   Title = {Childhood origins of violent behaviour in adults with
             schizophreniform disorder.},
   Journal = {The British journal of psychiatry : the journal of mental
             science},
   Volume = {183},
   Pages = {520-525},
   Year = {2003},
   Month = {December},
   ISSN = {0007-1250},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/14645023},
   Abstract = {<h4>Background</h4>People with psychosis have an elevated
             risk of violence.<h4>Aims</h4>To examine whether violent
             behaviour in adults with psychosis can be accounted for by
             psychotic symptoms or physical aggression in
             childhood.<h4>Method</h4>We used data from a prospective
             longitudinal study of a complete birth cohort born in New
             Zealand. When cohort members were 26 years old, information
             was obtained on past-year psychiatric diagnosis of
             schizophreniform disorder and on violent behaviour.
             Childhood psychotic symptoms were measured at age 11 years
             using a diagnostic interview, and childhood physical
             aggression was assessed by teachers when cohort members were
             aged 7, 9 and 11 years.<h4>Results</h4>Participants with
             schizophreniform disorder were more likely to be violent
             than participants without, even after controlling for
             sociodemographic variables and concurrent substance
             dependence disorders. Childhood psychotic symptoms were a
             strong risk factor for violence in adults with
             schizophreniform disorder, as was childhood physical
             aggression, although to a lesser extent.<h4>Conclusions</h4>Violence
             by individuals with schizophreniform disorder could be
             prevented by monitoring early signs of psychotic symptoms
             and by controlling childhood physical aggression.},
   Doi = {10.1192/bjp.183.6.520},
   Key = {fds253360}
}

@article{fds304710,
   Author = {Belsky, J and Jaffee, SR and Caspi, A and Moffitt, T and Silva,
             PA},
   Title = {Intergenerational relationships in young adulthood and their
             life course, mental health, and personality
             correlates.},
   Journal = {Journal of family psychology : JFP : journal of the Division
             of Family Psychology of the American Psychological
             Association (Division 43)},
   Volume = {17},
   Number = {4},
   Pages = {460-471},
   Year = {2003},
   Month = {December},
   ISSN = {0893-3200},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/14640797},
   Abstract = {To evaluate effects of life-course events and experiences of
             young adults, as well as personality and mental-health
             history on intergenerational relationships in young
             adulthood, the authors examined dyadic relationship data
             drawn from a sample of more than 900 New Zealand
             26-year-olds and their mothers and fathers. Results
             indicated that intergenerational relations were more
             positive when young adults were childless, not unemployed,
             married, and living away from home, but these factors did
             not interact with family relationship history in predicting
             relationship outcomes. Intergenerational relationships were
             less positive when children scored low on positive
             emotionality and constraint and high on negative
             emotionality and mental disorders, though these attributes
             did not account for the effect of life-course factors.
             Results are discussed in terms of the openness of the
             parent-child relationship in adulthood to further
             development.},
   Doi = {10.1037/0893-3200.17.4.460},
   Key = {fds304710}
}

@article{fds253370,
   Author = {Rutter, M and Caspi, A and Moffitt, TE},
   Title = {Using sex differences in psychopathology to study causal
             mechanisms: unifying issues and research
             strategies.},
   Journal = {Journal of child psychology and psychiatry, and allied
             disciplines},
   Volume = {44},
   Number = {8},
   Pages = {1092-1115},
   Year = {2003},
   Month = {November},
   ISSN = {0021-9630},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/14626453},
   Abstract = {<h4>Background</h4>Although there is an extensive
             literature, both speculative and empirical, on postulated
             differences between males and females in their rates of
             particular types of disorder, very little is known about the
             mechanisms that underlie these sex differences. The study of
             mechanisms is important because it may provide clues on
             aetiological processes. The review seeks to outline what is
             known, what are the methodological hazards that must be
             dealt with, and the research strategies that may be
             employed.<h4>Methods</h4>We note the need for representative
             general samples, and for adequate measurement and
             significance testing if valid conclusions are to be drawn.
             We put forward three levels of causes that have to be
             considered: a genetically determined distal basic starting
             point; the varied consequences of being male or female; and
             the proximal risk or protective factors that are more
             directly implicated in the causal mechanisms that predispose
             to psychopathology. In delineating these, we argue that
             three key sets of evidential criteria have to be met: a)
             that the risk factors differ between males and females; b)
             that they provide for risk or protection within each sex;
             and c) that when introduced into a causal model, they
             eliminate or reduce the sex differences in the disorders
             being studied.<h4>Results</h4>A male excess mainly applies
             to early onset disorders that involve some kind of
             neurodevelopmental impairment. A female excess mainly
             applies to adolescent-onset emotional disorders. No
             variables have yet met all the necessary criteria but some
             good leads are available. The possible research strategies
             that may be employed are reviewed.<h4>Conclusions</h4>The
             systematic investigation of sex differences constitutes an
             invaluable tool for the study of the causal processes
             concerned with psychopathology.},
   Doi = {10.1111/1469-7610.00194},
   Key = {fds253370}
}

@article{fds253361,
   Author = {Arseneault, L and Moffitt, TE and Caspi, A and Taylor, A and Rijsdijk,
             FV and Jaffee, SR and Ablow, JC and Measelle, JR},
   Title = {Strong genetic effects on cross-situational antisocial
             behaviour among 5-year-old children according to mothers,
             teachers, examiner-observers, and twins'
             self-reports.},
   Journal = {Journal of child psychology and psychiatry, and allied
             disciplines},
   Volume = {44},
   Number = {6},
   Pages = {832-848},
   Year = {2003},
   Month = {September},
   ISSN = {0021-9630},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/12959492},
   Abstract = {<h4>Background</h4>Early childhood antisocial behaviour is a
             strong prognostic indicator for poor adult mental health.
             Thus, information about its etiology is needed. Genetic
             etiology is unknown because most research with young
             children focuses on environmental risk factors, and the few
             existing studies of young twins used only mothers' reports
             of behaviour, which may be biased.<h4>Method</h4>We
             investigated genetic influences on antisocial behaviour in a
             representative-plus-high-risk sample of 1116 pairs of
             5-year-old twins using data from four independent sources:
             mothers, teachers, examiner-observers previously
             unacquainted with the children, and the children
             themselves.<h4>Results</h4>Children's antisocial behaviour
             was reliably measured by all four informants; no bias was
             detected in mothers', teachers', examiners', or children's
             reports. Variation in antisocial behaviour that was agreed
             upon by all informants, and thus was pervasive across
             settings, was influenced by genetic factors (82%) and
             experiences specific to each child (18%). Variation in
             antisocial behaviour that was specific to each informant was
             meaningful variation, as it was also influenced by genetic
             factors (from 33% for the children's report to 71% for the
             teachers' report).<h4>Conclusions</h4>This study and four
             others of very young twins show that genetic risks
             contribute strongly to population variation in antisocial
             behaviour that emerges in early childhood. In contrast,
             genetic risk is known to be relatively modest for adolescent
             antisocial behaviour, suggesting that the early-childhood
             form has a distinct etiology, particularly if it is
             pervasive across situations.},
   Doi = {10.1111/1469-7610.00168},
   Key = {fds253361}
}

@article{fds253369,
   Author = {Sluyter, F and Arseneault, L and Moffitt, TE and Veenema, AH and de
             Boer, S and Koolhaas, JM},
   Title = {Toward an animal model for antisocial behavior: parallels
             between mice and humans.},
   Journal = {Behavior genetics},
   Volume = {33},
   Number = {5},
   Pages = {563-574},
   Year = {2003},
   Month = {September},
   url = {http://dx.doi.org/10.1023/a:1025730901955},
   Abstract = {The goal of this article is to examine whether mouse lines
             genetically selected for short and long attack latencies are
             good animal models for antisocial behavior in humans. To
             this end, we compared male Short and Long Attack Latency
             mice (SAL and LAL, respectively) with the extremes of the
             Dunedin Multidisciplinary Health and Development Study (men
             who persistently displayed antisocial behavior [Persisters]
             and men who never manifested antisocial behavior
             [Abstainers]). Groups were compared on the basis of five
             distinct domains: aggression/violence, reproduction,
             cognition, behavioral disorders, and endophenotypes. Our
             observations point to considerable parallels between, on one
             side, SAL and Persisters, and, on the other side, between
             LAL and Abstainers (but to a lesser extent). We believe that
             SAL and LAL are good mouse models to study the development
             of antisocial behavior and will yield valuable and testable
             hypotheses with regard to the neurobiological and genetical
             architecture of antisocial behavior.},
   Doi = {10.1023/a:1025730901955},
   Key = {fds253369}
}

@article{fds253367,
   Author = {Caspi, A and Harrington, H and Milne, B and Amell, JW and Theodore, RF and Moffitt, TE},
   Title = {Children's behavioral styles at age 3 are linked to their
             adult personality traits at age 26.},
   Journal = {Journal of personality},
   Volume = {71},
   Number = {4},
   Pages = {495-513},
   Year = {2003},
   Month = {August},
   ISSN = {0022-3506},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/12901429},
   Abstract = {We observed 1,000 3-year-old children who exhibited five
             temperament types: Undercontrolled, Inhibited, Confident,
             Reserved, and Well-adjusted. Twenty-three years later, we
             reexamined 96% of the children as adults, using multiple
             methods of comprehensive personality assessment, including
             both self- and informant-reports. These longitudinal data
             provide the longest and strongest evidence to date that
             children's early-emerging behavioral styles can foretell
             their characteristic behaviors, thoughts, and feelings as
             adults, pointing to the foundations of the human personality
             in the early years of life.},
   Doi = {10.1111/1467-6494.7104001},
   Key = {fds253367}
}

@article{fds253368,
   Author = {Richardson, LP and Davis, R and Poulton, R and McCauley, E and Moffitt,
             TE and Caspi, A and Connell, F},
   Title = {A longitudinal evaluation of adolescent depression and adult
             obesity.},
   Journal = {Archives of pediatrics & adolescent medicine},
   Volume = {157},
   Number = {8},
   Pages = {739-745},
   Year = {2003},
   Month = {August},
   ISSN = {1072-4710},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/12912778},
   Abstract = {<h4>Background</h4>Prior studies have had conflicting
             results regarding the relationship between adolescent
             depression and adult obesity.<h4>Objective</h4>To test the
             hypothesis that depression in adolescence would increase the
             risk for obesity in early adulthood.<h4>Methods</h4>We used
             data from a longitudinal study of a birth cohort of children
             born between April 1, 1972, and March 31, 1973, in Dunedin,
             New Zealand (N = 1037). These data included regular
             diagnostic mental health interviews and height/weight
             measurements throughout childhood and adolescence. We
             performed logistic regression analyses to assess the
             relationship between major depression in early or late
             adolescence and the risk for obesity at 26 years of
             age.<h4>Results</h4>Major depression occurred in 7% of the
             cohort during early adolescence (11, 13, and 15 years of
             age) and 27% during late adolescence (18 and 21 years of
             age). At 26 years of age, 12% of study members were obese.
             After adjusting for each individual's baseline body mass
             index (calculated as the weight in kilograms divided by the
             square of height in meters), depressed late adolescent girls
             were at a greater than 2-fold increased risk for obesity in
             adulthood compared with their nondepressed female peers
             (relative risk, 2.32; 95% confidence interval, 1.29-3.83). A
             dose-response relationship between the number of episodes of
             depression during adolescence and risk for adult obesity was
             also observed in female subjects. The association was not
             observed for late adolescent boys or for early adolescent
             boys or girls.<h4>Conclusions</h4>Depression in late
             adolescence is associated with later obesity, but only among
             girls. Future studies should address reasons for these age
             and sex differences and the potential for intervention to
             reduce the risk for adult obesity in depressed older
             adolescent girls.},
   Doi = {10.1001/archpedi.157.8.739},
   Key = {fds253368}
}

@article{fds253358,
   Author = {Kim-Cohen, J and Caspi, A and Moffitt, TE and Harrington, H and Milne,
             BJ and Poulton, R},
   Title = {Prior juvenile diagnoses in adults with mental disorder:
             developmental follow-back of a prospective-longitudinal
             cohort.},
   Journal = {Archives of general psychiatry},
   Volume = {60},
   Number = {7},
   Pages = {709-717},
   Year = {2003},
   Month = {July},
   ISSN = {0003-990X},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/12860775},
   Abstract = {<h4>Background</h4>If most adults with mental disorders are
             found to have a juvenile psychiatric history, this would
             shift etiologic research and prevention policy to focus more
             on childhood mental disorders.<h4>Method</h4>Our prospective
             longitudinal study followed up a representative birth cohort
             (N = 1037). We made psychiatric diagnoses according to DSM
             criteria at 11, 13, 15, 18, 21, and 26 years of age. Adult
             disorders were defined in the following 3 ways: (1) cases
             diagnosed using a standardized diagnostic interview, (2) the
             subset using treatment, and (3) the subset receiving
             intensive mental health services. Follow-back analyses
             ascertained the proportion of adult cases who had juvenile
             diagnoses and the types of juvenile diagnoses they
             had.<h4>Results</h4>Among adult cases defined via the
             Diagnostic Interview Schedule, 73.9% had received a
             diagnosis before 18 years of age and 50.0% before 15 years
             of age. Among treatment-using cases, 76.5% received a
             diagnosis before 18 years of age and 57.5% before 15 years
             of age. Among cases receiving intensive mental health
             services, 77.9% received a diagnosis before 18 years of age
             and 60.3% before 15 years of age. Adult disorders were
             generally preceded by their juvenile counterparts (eg, adult
             anxiety was preceded by juvenile anxiety), but also by
             different disorders. Specifically, adult anxiety and
             schizophreniform disorders were preceded by a broad array of
             juvenile disorders. For all adult disorders, 25% to 60% of
             cases had a history of conduct and/or oppositional defiant
             disorder.<h4>Conclusions</h4>Most adult disorders should be
             reframed as extensions of juvenile disorders. In particular,
             juvenile conduct disorder is a priority prevention target
             for reducing psychiatric disorder in the adult
             population.},
   Doi = {10.1001/archpsyc.60.7.709},
   Key = {fds253358}
}

@article{fds253366,
   Author = {Caspi, A and Sugden, K and Moffitt, TE and Taylor, A and Craig, IW and Harrington, H and McClay, J and Mill, J and Martin, J and Braithwaite,
             A and Poulton, R},
   Title = {Influence of life stress on depression: moderation by a
             polymorphism in the 5-HTT gene.},
   Journal = {Science (New York, N.Y.)},
   Volume = {301},
   Number = {5631},
   Pages = {386-389},
   Year = {2003},
   Month = {July},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/12869766},
   Abstract = {In a prospective-longitudinal study of a representative
             birth cohort, we tested why stressful experiences lead to
             depression in some people but not in others. A functional
             polymorphism in the promoter region of the serotonin
             transporter (5-HT T) gene was found to moderate the
             influence of stressful life events on depression.
             Individuals with one or two copies of the short allele of
             the 5-HT T promoter polymorphism exhibited more depressive
             symptoms, diagnosable depression, and suicidality in
             relation to stressful life events than individuals
             homozygous for the long allele. This epidemiological study
             thus provides evidence of a gene-by-environment interaction,
             in which an individual's response to environmental insults
             is moderated by his or her genetic makeup.},
   Doi = {10.1126/science.1083968},
   Key = {fds253366}
}

@article{fds253363,
   Author = {Roberts, BW and Caspi, A and Moffitt, TE},
   Title = {Work experiences and personality development in young
             adulthood.},
   Journal = {Journal of personality and social psychology},
   Volume = {84},
   Number = {3},
   Pages = {582-593},
   Year = {2003},
   Month = {March},
   ISSN = {0022-3514},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/12635918},
   Abstract = {This longitudinal study provides an analysis of the
             relationship between personality traits and work experiences
             with a special focus on the relationship between changes in
             personality and work experiences in young adulthood.
             Longitudinal analyses uncovered 3 findings. First, measures
             of personality taken at age 18 predicted both objective and
             subjective work experiences at age 26. Second, work
             experiences were related to changes in personality traits
             from age 18 to 26. Third, the predictive and change
             relations between personality traits and work experiences
             were corresponsive: Traits that "selected" people into
             specific work experiences were the same traits that changed
             in response to those same work experiences. The relevance of
             the findings to theories of personality development is
             discussed.},
   Doi = {10.1037/0022-3514.84.3.582},
   Key = {fds253363}
}

@article{fds253364,
   Author = {Tully, LA and Moffitt, TB and Caspi, A},
   Title = {Maternal adjustment, parenting and child behaviour in
             families of school-aged twins conceived after IVF and
             ovulation induction.},
   Journal = {Journal of child psychology and psychiatry, and allied
             disciplines},
   Volume = {44},
   Number = {3},
   Pages = {316-325},
   Year = {2003},
   Month = {March},
   ISSN = {0021-9630},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/12635963},
   Abstract = {<h4>Background</h4>Previous studies that have examined the
             long-term effects of infertility and assisted reproductive
             technology on parenting and child behaviour in families with
             twins have suffered from methodological problems. This study
             compared measures of parental adjustment, parenting and
             child behaviour in families with 5-year-old twins who were
             conceived after in vitro fertilisation (IVF) or ovulation
             induction (OI) with families whose twins were naturally
             conceived (NC).<h4>Methods</h4>The families who conceived
             via IVF/OI (N = 121) were identified from an epidemiological
             study of twins and matched to families who were conceived
             naturally (N = 121) on the basis of eleven child and family
             variables. Mothers were interviewed in their homes for the
             study.<h4>Results</h4>No significant differences were
             observed between the IVF/OI families and the NC families on
             measures of parental adjustment or parent and teacher
             ratings of the twins' behaviour. IVF/OI mothers and their
             partners agreed with each other about discipline more than
             NC couples, but otherwise no other differences in parenting
             were found.<h4>Conclusions</h4>Overall, this study provides
             evidence that families who conceive twins following IVF/OI
             are functioning well and that the experience of fertility
             treatment does not lead to long-term difficulties for
             parents or children.},
   Doi = {10.1111/1469-7610.00124},
   Key = {fds253364}
}

@article{fds253107,
   Author = {Moffitt, TE and Caspi, A},
   Title = {Preventing the Inter-Generational continuity of antisocial
             behaviour: Implications of partner violence},
   Pages = {109-129},
   Publisher = {Cambridge University Press},
   Year = {2003},
   Month = {January},
   url = {http://dx.doi.org/10.1017/CBO9780511489259.005},
   Abstract = {Antisocial behaviour is highly stable across the life course
             of individuals (Farrington, 1995; Loeber, 1982), and it runs
             strongly from generation to generation within families
             (Huesmann et al., 1984; Rowe and Farrington, 1997). Indeed,
             the correlation between measures of fathers’ and sons’
             antisocial behaviour appears to be about as high as the
             correlation between measures of antisocial behaviour taken
             at two points in the life course of the same individual.
             Behavioural genetic studies reveal that less than half of
             this inter-generational continuity can be ascribed to
             heritable factors (Carey, 1994; Miles and Carey, 1997).
             Moreover, behavioural genetic studies estimate that
             environmental factors shared by family members must account
             for as much as one-third of the population variance in
             children’s antisocial behaviour (averaged across six
             large-scale twin studies available when this chapter was
             written: Edelbrock et al., 1995; Eley, Lichtenstein and
             Stevenson, 1999; Gjone et al., 1996; Schmitz et al., 1995;
             Silberg et al., 1994; Thapar, 1995). The antisocial
             behaviour of almost all seriously antisocial adults first
             emerged during early childhood in the context of the family
             home (Moffitt, 1993; Moffitt, Caspi, Dickson, Silva and
             Stanton, 1996; Robins, 1978). When official crime records
             are searched for all of the mothers, fathers, sisters, and
             brothers in a large sample of families, over 50 per cent of
             the offences are concentrated in only 5 per cent of the
             families (Farrington, Barnes and Lambert,
             1996).},
   Doi = {10.1017/CBO9780511489259.005},
   Key = {fds253107}
}

@article{fds253359,
   Author = {Koenen, KC and Moffitt, TE and Caspi, A and Taylor, A and Purcell,
             S},
   Title = {Domestic violence is associated with environmental
             suppression of IQ in young children.},
   Journal = {Development and psychopathology},
   Volume = {15},
   Number = {2},
   Pages = {297-311},
   Year = {2003},
   Month = {January},
   ISSN = {0954-5794},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/12931829},
   Abstract = {Research suggests that exposure to extreme stress in
             childhood, such as domestic violence, affects children's
             neurocognitive development, leading to lower intelligence.
             But studies have been unable to account for genetic
             influences that might confound the association between
             domestic violence and lower intelligence. This twin study
             tested whether domestic violence had environmentally
             mediated effects on young children's intelligence.
             Children's IQs were assessed for a population sample of 1116
             monozygotic and dizygotic 5-year-old twin pairs in England.
             Mothers reported their experience of domestic violence in
             the previous 5 years. Ordinary least squares regression
             showed that domestic violence was uniquely associated with
             IQ suppression in a dose-response relationship. Children
             exposed to high levels of domestic violence had IQs that
             were, on average, 8 points lower than unexposed children.
             Structural equation models showed that adult domestic
             violence accounted for 4% of the variation, on average, in
             child IQ, independent of latent genetic influences. The
             findings are consistent with animal experiments and human
             correlational studies documenting the harmful effects of
             extreme stress on brain development Programs that
             successfully reduce domestic violence should also have
             beneficial effects on children's cognitive
             development.},
   Doi = {10.1017/s0954579403000166},
   Key = {fds253359}
}

@article{fds253362,
   Author = {Eley, TC and Lichtenstein, P and Moffitt, TE},
   Title = {A longitudinal behavioral genetic analysis of the etiology
             of aggressive and nonaggressive antisocial
             behavior.},
   Journal = {Development and psychopathology},
   Volume = {15},
   Number = {2},
   Pages = {383-402},
   Publisher = {Cambridge University Press (CUP)},
   Year = {2003},
   Month = {January},
   ISSN = {0954-5794},
   url = {http://dx.doi.org/10.1017/s095457940300021x},
   Abstract = {Developmental studies of antisocial behavior (ASB) have
             found two subgroups of behaviors, roughly described as
             aggressive and nonaggressive ASB. Theoretical accounts
             predict that aggressive ASB, which shows greater stability,
             should have high heritability. In contrast, nonaggressive
             ASB is very common in adolescence, shows less continuity,
             and should be influenced both by genes and shared
             environment. This study explored the genetic and
             environmental influences on aggressive and nonaggressive ASB
             in over 1,000 twin pairs aged 8-9 years and again at 13-14
             years. Threshold models were fit to the data to incorporate
             the skew. In childhood, aggressive ASB was highly heritable
             and showed little influence of shared environment, whereas
             nonaggressive ASB was significantly influenced both by genes
             and shared environment. In adolescence, both variables were
             influenced both by genes and shared envirnmment. The
             continuity in aggressive antisocial behavior symptoms from
             childhood to adolescence was largely mediated by genetic
             influences, whereas continuity in nonaggressive antisocial
             behavior was mediated both by the shared environment and
             genetic influences. These data are in agreement with the
             hypothesis that aggressive ASB is a stable heritable trait
             as compared to nonaggressive behavior, which is more
             strongly influenced by the environment and shows less
             genetic stability over time.},
   Doi = {10.1017/s095457940300021x},
   Key = {fds253362}
}

@article{fds253365,
   Author = {Jaffee, SR and Moffitt, TE and Caspi, A and Taylor,
             A},
   Title = {Life with (or without) father: the benefits of living with
             two biological parents depend on the father's antisocial
             behavior.},
   Journal = {Child development},
   Volume = {74},
   Number = {1},
   Pages = {109-126},
   Year = {2003},
   Month = {January},
   ISSN = {0009-3920},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/12625439},
   Abstract = {The salutary effects of being raised by two married,
             biological parents depend on the quality of care parents can
             provide. Using data from an epidemiological sample of 1,116
             5-year-old twin pairs and their parents, this study found
             that the less time fathers lived with their children, the
             more conduct problems their children had, but only if the
             fathers engaged in low levels of antisocial behavior. In
             contrast, when fathers engaged in high levels of antisocial
             behavior, the more time they lived with their children, the
             more conduct problems their children had. Behavioral genetic
             analyses showed that children who resided with antisocial
             fathers received a "double whammy" of genetic and
             environmental risk for conduct problems. Marriage may not be
             the answer to the problems faced by some children living in
             single-parent families unless their fathers can become
             reliable sources of emotional and economic
             support.},
   Doi = {10.1111/1467-8624.t01-1-00524},
   Key = {fds253365}
}

@article{fds69940,
   Author = {Roberts, B. W. and Caspi, A. and Moffitt, T.
             E},
   Title = {Work experiences and personality change in young
             adulthood},
   Journal = {Journal of Personality and Social Psychology},
   Volume = {84},
   Pages = {582-593},
   Year = {2003},
   Key = {fds69940}
}

@article{fds69943,
   Author = {Arseneault, L. and Moffitt, T.E. and Caspi, A. and Taylor, A. and Rijsdijk, F. and Jaffee, S and Ablow, JC and Measelle,
             J.R},
   Title = {Strong genetic effects on cross-situational antisocial
             behavior among 5-year-old children, according to mothers,
             teachers, examiners, and twin’s self-reports},
   Journal = {Journal of Child Psychiatry and Psychology},
   Volume = {44},
   Pages = {832-848},
   Year = {2003},
   Key = {fds69943}
}

@article{fds253173,
   Author = {Broidy, and LM, and Nagin, and DS, and Tremblay, and RE, IAO and Brame, and B, and Dodge, and K, and Fergusson, and D, and Horwood, and J, and Loeber, and R, and Laird, and Lynam, and Moffitt, and TE},
   Title = {Developmental trajectories of childhood disruptive behavior
             disorders and adolescent delinquency: A six-nation
             replication},
   Journal = {Developmental Psychology},
   Volume = {39},
   Number = {2},
   Pages = {222-245},
   Year = {2003},
   url = {http://dx.doi.org/10.1037//0012-1649.39.2.222},
   Abstract = {This study used data from 6 sites and 3 countries to examine
             the developmental course of physical aggression in childhood
             and to analyze its linkage to violent and nonviolent
             offending outcomes in adolescence. The results indicate that
             among boys there is continuity in problem behavior from
             childhood to adolescence and that such continuity is
             especially acute when early problem behavior takes the form
             of physical aggression. Chronic physical aggression during
             the elementary school years specifically increases the risk
             for continued physical violence as well as other nonviolent
             forms of delinquency during adolescence. However, this
             conclusion is reserved primarily for boys, because the
             results indicate no clear linkage between childhood physical
             aggression and adolescent offending among female samples
             despite notable similarities across male and female samples
             in the developmental course of physical aggression in
             childhood.},
   Doi = {10.1037//0012-1649.39.2.222},
   Key = {fds253173}
}

@article{fds253357,
   Author = {Belsky, J and Jaffee, SR and Caspi, A and Moffitt, TE and Silva,
             PA},
   Title = {Patterns of intergenerational relations in young adulthood
             and their life-course and mental-health correlates},
   Journal = {Journal of Family Psychology},
   Volume = {17},
   Number = {4},
   Pages = {460-471},
   Year = {2003},
   ISSN = {0893-3200},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/14640797},
   Abstract = {To evaluate effects of life-course events and experiences of
             young adults, as well as personality and mental-health
             history on intergenerational relationships in young
             adulthood, the authors examined dyadic relationship data
             drawn from a sample of more than 900 New Zealand
             26-year-olds and their mothers and fathers. Results
             indicated that intergenerational relations were more
             positive when young adults were childless, not unemployed,
             married, and living away from home, but these factors did
             not interact with family relationship history in predicting
             relationship outcomes. Intergenerational relationships were
             less positive when children scored low on positive
             emotionality and constraint and high on negative
             emotionality and mental disorders, though these attributes
             did not account for the effect of life-course factors.
             Results are discussed in terms of the openness of the
             parent-child relationship in adulthood to further
             development.},
   Doi = {10.1037/0893-3200.17.4.460},
   Key = {fds253357}
}

@article{fds253371,
   Author = {Robins, RW and Caspi, A and Moffitt, TE},
   Title = {It's not just who you're with, it's who you are: personality
             and relationship experiences across multiple
             relationships.},
   Journal = {Journal of personality},
   Volume = {70},
   Number = {6},
   Pages = {925-964},
   Year = {2002},
   Month = {December},
   ISSN = {0022-3506},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/12498360},
   Abstract = {The present study examined the influence of stable
             personality traits on romantic relationships using
             longitudinal data on a large, representative sample of young
             adults. Relationship experiences (quality, conflict, and
             abuse) showed relatively small mean-level changes over time
             and significant levels of rank-order stability, even across
             different relationship partners. Antecedent personality
             traits (assessed at age 18) predicted relationship
             experiences at age 26 and change in relationship experiences
             from age 21 to 26. Conversely, relationship experiences also
             predicted change in personality. Importantly, these findings
             generally held across relationship partners, suggesting that
             some people tend to be generally happy (or unhappy) across
             relationships, and this is due, in part, to stable
             individual differences in personality. Discussion focuses on
             the broader implications of the findings, in particular the
             need for relationship researchers to consider the importance
             of personality for why relationships thrive or fail and the
             need for personality researchers to consider the impact of
             relationship experiences on intraindividual personality
             development.},
   Doi = {10.1111/1467-6494.05028},
   Key = {fds253371}
}

@article{fds253187,
   Author = {Arseneault, L and Cannon, M and Poulton, R and Murray, R and Caspi, A and Moffitt, TE},
   Title = {Cannabis use in adolescence and risk for adult psychosis:
             longitudinal prospective study.},
   Journal = {BMJ (Clinical research ed.)},
   Volume = {325},
   Number = {7374},
   Pages = {1212-1213},
   Year = {2002},
   Month = {November},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/12446537},
   Doi = {10.1136/bmj.325.7374.1212},
   Key = {fds253187}
}

@article{fds253372,
   Author = {Poulton, R and Caspi, A and Milne, BJ and Thomson, WM and Taylor, A and Sears, MR and Moffitt, TE},
   Title = {Association between children's experience of socioeconomic
             disadvantage and adult health: a life-course
             study.},
   Journal = {Lancet (London, England)},
   Volume = {360},
   Number = {9346},
   Pages = {1640-1645},
   Year = {2002},
   Month = {November},
   ISSN = {0140-6736},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/12457787},
   Abstract = {<h4>Background</h4>Research into social inequalities in
             health has tended to focus on low socioeconomic status in
             adulthood. We aimed to test the hypothesis that children's
             experience of socioeconomic disadvantage is associated with
             a wide range of health risk factors and outcomes in adult
             life.<h4>Methods</h4>We studied an unselected cohort of 1000
             children (born in New Zealand during 1972-73) who had been
             assessed at birth and ages 3, 5, 7, 9, 11, 13, and 15 years.
             At age 26 years, we assessed these individuals for health
             outcomes including body-mass index, waist:hip ratio, blood
             pressure, cardiorespiratory fitness, dental caries, plaque
             scores, gingival bleeding, periodontal disease, major
             depression, and tobacco and alcohol dependence, and tested
             for associations between these variables and childhood and
             adult socioeconomic status.<h4>Findings</h4>Compared with
             those from high socioeconomic status backgrounds, children
             who grew up in low socioeconomic status families had poorer
             cardiovascular health. Significant differences were also
             found on all dental health measures, with a threefold
             increase in adult periodontal disease (31.1% vs 11.9%) and
             caries level (32.2% vs 9.9%) in low versus high childhood
             socioeconomic status groups. Substance abuse resulting in
             clinical dependence was related in a similar way to
             childhood socioeconomic status (eg, 21.5% vs 12.1% for adult
             alcohol dependence). The longitudinal associations could not
             be attributed to life-course continuity of low socioeconomic
             status, and upward mobility did not mitigate or reverse the
             adverse effects of low childhood socioeconomic status on
             adult health.<h4>Interpretation</h4>Protecting children
             against the effects of socioeconomic adversity could reduce
             the burden of disease experienced by adults. These findings
             provide strong impetus for policy makers, practitioners, and
             researchers to direct energy and resources towards childhood
             as a way of improving population health.},
   Doi = {10.1016/s0140-6736(02)11602-3},
   Key = {fds253372}
}

@article{fds253373,
   Author = {Jaffee, SR and Moffitt, TE and Caspi, A and Taylor, A and Arseneault,
             L},
   Title = {Influence of adult domestic violence on children's
             internalizing and externalizing problems: an environmentally
             informative twin study.},
   Journal = {Journal of the American Academy of Child and Adolescent
             Psychiatry},
   Volume = {41},
   Number = {9},
   Pages = {1095-1103},
   Year = {2002},
   Month = {September},
   ISSN = {0890-8567},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/12218431},
   Abstract = {<h4>Objective</h4>Externalizing and internalizing problems
             may aggregate in families because (1) siblings share genetic
             risks for problem behaviors or (2) siblings are exposed to
             similar environmental risks. A genetically sensitive design
             was used to determine whether domestic violence accounted
             significantly for the variation and covariation of
             externalizing and internalizing problems, independent of
             additive genetic effects on these behavior
             problems.<h4>Method</h4>Using the Achenbach family of
             instruments, mothers and teachers reported internalizing and
             externalizing problems for 1,116 monozygotic and dizygotic
             5-year-old twin pairs in the United Kingdom (93% response
             rate). Mothers reported their experiences of domestic
             violence in the previous 5 years. Structural equation models
             were tested to determine the effect of mothers' experiences
             of domestic violence on children's emotional and conduct
             problems, controlling for latent genetic and environmental
             effects on these behaviors.<h4>Results</h4>A multivariate
             model showed that adult domestic violence accounted for 2%
             and 5% of the variation in children's internalizing and
             externalizing problems, respectively, independent of genetic
             effects. The co-occurrence of externalizing and
             internalizing scores was accounted for by genetic (62.6%)
             and shared environmental (29.2%) factors and by domestic
             violence (8%).<h4>Conclusions</h4>Because domestic violence
             affects children's behavior problems beyond genetic
             influences, programs that successfully reduce domestic
             violence should also prevent children's psychopathology.},
   Doi = {10.1097/00004583-200209000-00010},
   Key = {fds253373}
}

@article{fds304709,
   Author = {Moffitt, TE and E-Risk Study Team},
   Title = {Teen-aged mothers in contemporary Britain.},
   Journal = {Journal of child psychology and psychiatry, and allied
             disciplines},
   Volume = {43},
   Number = {6},
   Pages = {727-742},
   Year = {2002},
   Month = {September},
   url = {http://dx.doi.org/10.1111/1469-7610.00082},
   Abstract = {<h4>Background</h4>This paper describes the circumstances of
             contemporary young mothers and their children from a
             nationally representative sample, and compares them to the
             circumstances of mothers who delayed childbearing beyond age
             20.<h4>Methods</h4>The participants are members of the
             Environmental Risk (E-risk) Longitudinal Twin Study, which
             follows an epidemiological sample of 1,116 women who became
             mothers in England and Wales in 1994-95, and their children,
             and contains an over-sample of young mothers. Home visits
             were conducted when the children were aged 5 years. Data
             were collected from mothers via interviews, from children
             via experimental tasks and observations, and from teachers
             via postal questionnaires.<h4>Results</h4>Young mothers
             encountered more socio-economic deprivation, had
             significantly less human and social capital, and experienced
             more mental health difficulties. Their partners were less
             reliable and supportive, both economically and emotionally,
             and were more antisocial and abusive. The children of young
             mothers showed reduced educational attainment, were rated by
             multiple informants as having more emotional and behavioural
             problems, were at increased risk of maltreatment or harm,
             and showed higher rates of illnesses, accidents, and
             injuries.<h4>Conclusions</h4>Young mothers today face
             difficulties known to have long-lasting effects for women
             and their children. Preventions that target young mothers
             may reduce harm to the physical health, mental health, and
             social status of future generations.},
   Doi = {10.1111/1469-7610.00082},
   Key = {fds304709}
}

@article{fds253374,
   Author = {Taylor, DR and Fergusson, DM and Milne, BJ and Horwood, LJ and Moffitt,
             TE and Sears, MR and Poulton, R},
   Title = {A longitudinal study of the effects of tobacco and cannabis
             exposure on lung function in young adults.},
   Journal = {Addiction (Abingdon, England)},
   Volume = {97},
   Number = {8},
   Pages = {1055-1061},
   Year = {2002},
   Month = {August},
   ISSN = {0965-2140},
   url = {http://dx.doi.org/10.1046/j.1360-0443.2002.00169.x},
   Abstract = {<h4>Aim</h4>To assess the possible effects of tobacco and
             cannabis smoking on lung function in young adults between
             the ages of 18 and 26.<h4>Setting and participants</h4>A
             group of over 900 young adults derived from a birth cohort
             of 1037 subjects born in Dunedin, New Zealand in 1972/73
             were studied at age 18, 21 and 26 years.<h4>Measurements</h4>Cannabis
             and tobacco smoking were documented at each age using a
             standardized interview. Lung function, as measured by the
             forced expiratory volume in one second/vital capacity
             (FEV1/VC) ratio, was obtained by simple spirometry. A fixed
             effects regression model was used to analyse the data to
             take account of confounding factors.<h4>Findings</h4>When
             the sample was stratified for cumulative use, there was
             evidence of a linear relationship between cannabis use and
             FEV1/VC (P < 0.05). In the absence of adjusting for other
             variables, increasing cannabis use over time was associated
             with a decline in FEV1/VC with time; the mean FEV1/VC among
             subjects using cannabis on 900 or more occasions was 7.2%,
             2.6% and 5.0% less than non-users at ages 18, 21 and 26,
             respectively. After controlling for potential confounding
             factors (age, tobacco smoking and weight) the negative
             effect of cumulative cannabis use on mean FEV1/VC was only
             marginally significant (P < 0.09). Age (P < 0.001),
             cigarette smoking (P < 0.05) and weight (P < 0.001) were all
             significant predictors of FEV1/VC. Cannabis use and daily
             cigarette smoking acted additively to influence
             FEV1/VC.<h4>Conclusions</h4>Longitudinal observations over 8
             years in young adults revealed a dose-dependent relationship
             between cumulative cannabis consumption and decline in
             FEV1/VC. However, when confounders were accounted for the
             effect was reduced and was only marginally significant, but
             given the limited time frame over which observations were
             made, the trend suggests that continued cannabis smoking has
             the potential to result in clinically important impairment
             of lung function.},
   Doi = {10.1046/j.1360-0443.2002.00169.x},
   Key = {fds253374}
}

@article{fds253379,
   Author = {Caspi, A and McClay, J and Moffitt, TE and Mill, J and Martin, J and Craig,
             IW and Taylor, A and Poulton, R},
   Title = {Role of genotype in the cycle of violence in maltreated
             children.},
   Journal = {Science (New York, N.Y.)},
   Volume = {297},
   Number = {5582},
   Pages = {851-854},
   Year = {2002},
   Month = {August},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/12161658},
   Abstract = {We studied a large sample of male children from birth to
             adulthood to determine why some children who are maltreated
             grow up to develop antisocial behavior, whereas others do
             not. A functional polymorphism in the gene encoding the
             neurotransmitter-metabolizing enzyme monoamine oxidase A
             (MAOA) was found to moderate the effect of maltreatment.
             Maltreated children with a genotype conferring high levels
             of MAOA expression were less likely to develop antisocial
             problems. These findings may partly explain why not all
             victims of maltreatment grow up to victimize others, and
             they provide epidemiological evidence that genotypes can
             moderate children's sensitivity to environmental
             insults.},
   Doi = {10.1126/science.1072290},
   Key = {fds253379}
}

@article{fds253375,
   Author = {Hughes, C and Oksanen, H and Taylor, A and Jackson, J and Murray, L and Caspi, A and Moffitt, TE},
   Title = {'I'm gonna beat you!' SNap!: an observational paradigm for
             assessing young children's disruptive behaviour in
             competitive play.},
   Journal = {Journal of child psychology and psychiatry, and allied
             disciplines},
   Volume = {43},
   Number = {4},
   Pages = {507-516},
   Year = {2002},
   Month = {May},
   ISSN = {0021-9630},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/12030596},
   Abstract = {<h4>Background</h4>This study focuses on a novel
             observational paradigm (SNAP) involving a rigged competitive
             card game (Murray, Woolgar, Cooper, & Hipwell, 2001)
             designed to expose children to the threat of losing. Recent
             work suggests that this paradigm is useful for assessing
             disruptive behaviour in young children (Hughes, Cutting, &
             Dunn, 2001).<h4>Method</h4>We report on a large study
             (involving 800 five-year-olds) that compares observational
             ratings of disruptive behaviour on the SNAP game with mother
             and teacher reports of externalising behaviour on the CBCL
             and TRF (Achenbach, 1991a, 1991b). To ensure independence of
             data, playmates were randomly assigned to two different
             sub-samples. The validity of this rigged game for examining
             individual differences in disruptive behaviour was supported
             (in both sub-samples) by modest but significant correlations
             with both mother and teacher ratings of externalising
             problems, and by significantly elevated SNAP ratings among
             children rated by mothers and teachers as showing extreme (>
             or = 95th%) levels of externalising problems, compared with
             the remaining majority of children.<h4>Results</h4>Significant
             gender differences in disruptive behaviour were found on all
             three measures: observational SNAP ratings and
             mother/teacher questionnaire ratings. Factors that may
             contribute to this gender difference are
             discussed.<h4>Conclusions</h4>Our findings emphasise the
             importance of multi-method, multi-informant measures of
             disruptive behaviour, and suggest that the rigged card game
             used in this study is a valuable adjunct to more standard
             methods of rating disruptive behaviour.},
   Doi = {10.1111/1469-7610.00041},
   Key = {fds253375}
}

@article{fds253376,
   Author = {Cannon, M and Caspi, A and Moffitt, TE and Harrington, H and Taylor, A and Murray, RM and Poulton, R},
   Title = {Evidence for early-childhood, pan-developmental impairment
             specific to schizophreniform disorder: results from a
             longitudinal birth cohort.},
   Journal = {Archives of general psychiatry},
   Volume = {59},
   Number = {5},
   Pages = {449-456},
   Year = {2002},
   Month = {May},
   ISSN = {0003-990X},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/11982449},
   Abstract = {<h4>Background</h4>Childhood developmental abnormalities
             have been previously described in schizophrenia. It is not
             known, however, whether childhood developmental impairment
             is specific to schizophrenia or is merely a marker for a
             range of psychiatric outcomes.<h4>Methods</h4>A 1-year birth
             cohort (1972-1973) of 1037 children enrolled in the Dunedin
             Multidisciplinary Health and Development Study was assessed
             at biennial intervals between ages 3 and 11 years on
             emotional, behavioral, and interpersonal problems, motor and
             language development, and intelligence. At age 11 years,
             children were asked about psychotic symptoms. At age 26
             years, DSM-IV diagnoses were made using the Diagnostic
             Interview Schedule. Study members having schizophreniform
             disorder (n = 36 [3.7%]) were compared with healthy controls
             and also with groups diagnosed as having mania (n = 20 [2%])
             and nonpsychotic anxiety or depression disorders (n = 278
             [28.5%]) on childhood variables.<h4>Results</h4>Emotional
             problems and interpersonal difficulties were noted in
             children who later fulfilled diagnostic criteria for any of
             the adult psychiatric outcomes assessed. However,
             significant impairments in neuromotor, receptive language,
             and cognitive development were additionally present only
             among children later diagnosed as having schizophreniform
             disorder. Developmental impairments also predicted
             self-reported psychotic symptoms at age 11 years. These
             impairments were independent of the effects of
             socioeconomic, obstetric, and maternal factors.<h4>Conclusions</h4>The
             results provide evidence for an early-childhood, persistent,
             pan-developmental impairment that is specifically associated
             with schizophreniform disorder and that predicts psychotic
             symptoms in childhood and adulthood.},
   Doi = {10.1001/archpsyc.59.5.449},
   Key = {fds253376}
}

@article{fds253377,
   Author = {Jaffee, SR and Moffitt, TE and Caspi, A and Fombonne, E and Poulton, R and Martin, J},
   Title = {Differences in early childhood risk factors for
             juvenile-onset and adult-onset depression.},
   Journal = {Archives of general psychiatry},
   Volume = {59},
   Number = {3},
   Pages = {215-222},
   Year = {2002},
   Month = {March},
   ISSN = {0003-990X},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/11879158},
   Abstract = {<h4>Background</h4>Family and twin studies suggest that
             juvenile-onset major depressive disorder (MDD) may be
             etiologically distinct from adult-onset MDD. This study is
             the first to distinguish prospectively between juvenile- and
             adult-onset cases of MDD in a representative birth cohort
             followed up from childhood into adulthood.<h4>Method</h4>The
             study followed a representative birth cohort prospectively
             from birth to age 26 years. Early childhood risk factors
             covered the period from birth to age 9 years. Diagnoses of
             MDD were made according to DSM criteria at 3 points prior to
             adulthood (ages 11, 13, and 15 years) and 3 points during
             adulthood (ages 18, 21, and 26 years). Four groups were
             defined as (1) individuals first diagnosed as having MDD in
             childhood, but not in adulthood (n = 21); (2) individuals
             first diagnosed as having MDD in adulthood (n = 314); (3)
             individuals first diagnosed in childhood whose depression
             recurred in adulthood by age 26 years (n = 34); and (4)
             never-depressed individuals (n = 629).<h4>Results</h4>The 2
             juvenile-onset groups had similar high-risk profiles on the
             childhood measures. Compared with the adult-depressed group,
             the juvenile-onset groups experienced more perinatal insults
             and motor skill deficits, caretaker instability,
             criminality, and psychopathology in their family-of-origin,
             and behavioral and socioemotional problems. The adult-onset
             group's risk profile was similar to that of the
             never-depressed group with the exception of elevated
             childhood sexual abuse.<h4>Conclusions</h4>Heterogeneity
             within groups of psychiatric patients poses problems for
             theory, research, and treatment. The present study
             illustrates that the distinction between juvenile vs
             adult-onset MDD is important for understanding heterogeneity
             within depression.},
   Doi = {10.1001/archpsyc.59.3.215},
   Key = {fds253377}
}

@article{fds253186,
   Author = {Arseneault, L and Moffit, TE and Caspi, A and Taylor,
             A},
   Title = {The targets of violence committed by young offenders with
             alcohol dependence, marijuana dependence and
             schizophrenia-spectrum disorders: findings from a birth
             cohort.},
   Journal = {Criminal behaviour and mental health : CBMH},
   Volume = {12},
   Number = {2},
   Pages = {155-168},
   Year = {2002},
   Month = {January},
   ISSN = {0957-9664},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/12459816},
   Abstract = {<h4>Background</h4>Estimates of who is most at risk from
             violence by people with mental illness rest mainly on
             identified patient samples. This study, without such
             selection bias, examined the targets of violence committed
             by young adults with as-yet untreated alcohol dependence,
             marijuana dependence, or schizophrenia-spectrum disorders,
             to determine the extent to which their victims were
             co-residents or non-household members.<h4>Methods</h4>In a
             total birth cohort of 21-year-olds (n=956), past-year
             prevalence of alcohol dependence, marijuana dependence and
             schizophrenia-spectrum disorders were diagnosed using
             standardized DSM-III-R interviews. None of the people with
             schizophrenia-spectrum disorder has been hospitalized in the
             past year. Past-year violence and victim targets were
             measured using self-reports.<h4>Results</h4>Compared with
             controls, cohort members with substance dependence or
             schizophrenia-spectrum disorders had higher prevalence and
             frequency rates of assault against co-residents, against
             non-household members, and also robbery and gang fights. Out
             of 39, five individuals with schizophrenia-spectrum disorder
             committed violent street crimes. Persons with substance
             dependence had similar proportions of violence against
             co-resident and non-household members, but persons with
             schizophrenia-spectrum disorders tended to victimize
             co-residents more than others.<h4>Conclusions</h4>At the age
             when they are most likely to contribute to the community's
             violence burden, young untreated offenders with alcohol or
             marijuana dependence or with schizophrenia-spectrum
             disorders assault not only co-residents, but others as well,
             and commit violent street crimes. Families, schoolteachers
             and primary care physicians have an important potentially
             preventive role in early identification and treatment of the
             disorders.},
   Doi = {10.1002/cbm.493},
   Key = {fds253186}
}

@article{fds253378,
   Author = {Mill, JS and Caspi, A and McClay, J and Sugden, K and Purcell, S and Asherson, P and Craig, I and McGuffin, P and Braithwaite, A and Poulton,
             R and Moffitt, TE},
   Title = {The dopamine D4 receptor and the hyperactivity phenotype: a
             developmental-epidemiological study.},
   Journal = {Molecular psychiatry},
   Volume = {7},
   Number = {4},
   Pages = {383-391},
   Year = {2002},
   Month = {January},
   ISSN = {1359-4184},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/11986982},
   Abstract = {Attention-deficit hyperactivity disorder (ADHD) affects 2-6%
             of school-age children and is a precursor of behavioural
             problems in adolescence and adulthood. Underlying the
             categorical definition of ADHD are the quantitative traits
             of activity, impulsivity, and inattention which vary
             continuously in the population. Both ADHD and quantitative
             measures of hyperactivity are heritable, and influenced by
             multiple genes of small effect. Several studies have
             reported an association between clinically defined ADHD and
             the seven-repeat allele of a 48-bp tandem repeat
             polymorphism in the third exon of the dopamine D4 receptor
             gene (DRD4). We tested this association in a large,
             unselected birth cohort (n = 1037) using multiple measures
             of the hyperactivity phenotype taken at multiple assessment
             ages across 20 years. This longitudinal approach allowed us
             to ascertain whether or not DRD4 has a general effect on the
             diagnosed (n = 49) or continuously distributed hyperactivity
             phenotype, and related personality traits. We found no
             evidence to support this association.},
   Doi = {10.1038/sj.mp.4000984},
   Key = {fds253378}
}

@article{fds253381,
   Author = {Moffitt, TE and Caspi, A and Harrington, H and Milne,
             BJ},
   Title = {Males on the life-course-persistent and adolescence-limited
             antisocial pathways: follow-up at age 26
             years.},
   Journal = {Development and psychopathology},
   Volume = {14},
   Number = {1},
   Pages = {179-207},
   Year = {2002},
   Month = {January},
   ISSN = {0954-5794},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/11893092},
   Abstract = {This article reports a comparison on outcomes of 26-year-old
             males who were defined several years ago in the Dunedin
             longitudinal study as exhibiting childhood-onset versus
             adolescent-onset antisocial behavior and who were
             indistinguishable on delinquent offending in adolescence.
             Previous studies of these groups in childhood and
             adolescence showed that childhood-onset delinquents had
             inadequate parenting, neurocognitive problems,
             undercontrolled temperament, severe hyperactivity,
             psychopathic personality traits, and violent behavior.
             Adolescent-onset delinquents were not distinguished by these
             features. Here followed to age 26 years, the childhood-onset
             delinquents were the most elevated on psychopathic
             personality traits, mental-health problems, substance
             dependence, numbers of children, financial problems, work
             problems, and drug-related and violent crime, including
             violence against women and children. The adolescent-onset
             delinquents at 26 years were less extreme but elevated on
             impulsive personality traits, mental-health problems,
             substance dependence, financial problems, and property
             offenses. A third group of men who had been aggressive as
             children but not very delinquent as adolescents emerged as
             low-level chronic offenders who were anxious, depressed,
             socially isolated, and had financial and work problems.
             These findings support the theory of life-course-persistent
             and adolescence-limited antisocial behavior but also extend
             it. Findings recommend intervention with all aggressive
             children and with all delinquent adolescents, to prevent a
             variety of maladjustments in adult life.},
   Doi = {10.1017/s0954579402001104},
   Key = {fds253381}
}

@article{fds69914,
   Author = {Moffitt, T.E. and Caspi, A. and Harrington, H. and Milne,
             B},
   Title = {Males on the life-course persistent and adolescence-limited
             antisocial pathways: Follow-up at age 26},
   Journal = {Development and Psychopathology},
   Volume = {14},
   Pages = {179-206},
   Year = {2002},
   Key = {fds69914}
}

@article{fds69920,
   Author = {Jaffee, SR, Moffitt and TE, Caspi and A, Fombonne and E., Martin and J. and Poulton, R},
   Title = {Differences in early childhood risk factors for
             juvenile-onset versus adult-onset depression},
   Journal = {Archives of General Psychiatry},
   Volume = {58},
   Pages = {215-222},
   Year = {2002},
   Key = {fds69920}
}

@article{fds69924,
   Author = {Jaffee, S. R. and Moffitt, T. E. and Caspi, A. and Taylor, A. and Arseneault, L},
   Title = {The influence of adult domestic violence on children's
             internalizing and externalizing problems: An
             environmentally-informative twin study},
   Journal = {Journal of the American Academy of Child and Adolescent
             Psychiatry},
   Volume = {41},
   Pages = {1095-1103},
   Year = {2002},
   Key = {fds69924}
}

@article{fds253380,
   Author = {Moffitt, and TE, and authors, TE-RST},
   Title = {Contemporary teen-aged mothers in Britain},
   Journal = {Journal of Child Psychology and Psychiatry},
   Volume = {43},
   Number = {6},
   Pages = {727-742},
   Year = {2002},
   url = {http://dx.doi.org/10.1111/1469-7610.00082},
   Abstract = {Background: This paper describes the circumstances of
             contemporary young mothers and their children from a
             nationally representative sample, and compares them to the
             circumstances of mothers who delayed childbearing beyond age
             20. Methods: The participants are members of the
             Environmental Risk (E-risk) Longitudinal Twin Study, which
             follows an epidemiological sample of 1,116 women who became
             mothers in England and Wales in 1994-95, and their children,
             and contains an over-sample of young mothers. Home visits
             were conducted when the children were aged 5 years. Data
             were collected from mothers via interviews, from children
             via experimental tasks and observations, and from teachers
             via postal questionnaires. Results: Young mothers
             encountered more socio-economic deprivation, had
             significantly less human and social capital, and experienced
             more mental health difficulties. Their partners were less
             reliable and supportive, both economically and emotionally,
             and were more antisocial and abusive. The children of young
             mothers showed reduced educational attainment, were rated by
             multiple informants as having more emotional and behavioural
             problems, were at increased risk of maltreatment or harm,
             and showed higher rates of illnesses, accidents, and
             injuries. Conclusions: Young mothers today face difficulties
             known to have long-lasting effects for women and their
             children. Preventions that target young mothers may reduce
             harm to the physical health, mental health, and social
             status of future generations.},
   Doi = {10.1111/1469-7610.00082},
   Key = {fds253380}
}

@article{fds336547,
   Author = {Arseneault, L and Cannon, M and Poulton, R and Murray, R and Caspi, A and Moffitt, TE},
   Title = {Cannabis use in adolescence and risk for adult
             psychosis},
   Journal = {British Medical Journal},
   Volume = {325},
   Pages = {1212-1213},
   Year = {2002},
   Key = {fds336547}
}

@article{fds336548,
   Author = {Arseneault, A and Moffitt, TE and Caspi, A and Taylor,
             A},
   Title = {The targets of violence committed by young offenders with a
             mental disorder: Findings from a birth cohort},
   Journal = {Criminal Behavior and Mental Health},
   Volume = {12},
   Pages = {155-168},
   Year = {2002},
   Key = {fds336548}
}

@article{fds253382,
   Author = {Loeber, R and Farrington, DP and Stouthamer-Loeber, M and Moffitt,
             TE and Caspi, A and Lynam, D},
   Title = {Male mental health problems, psychopathy, and personality
             traits: key findings from the first 14 years of the
             Pittsburgh Youth Study.},
   Journal = {Clinical child and family psychology review},
   Volume = {4},
   Number = {4},
   Pages = {273-297},
   Year = {2001},
   Month = {December},
   ISSN = {1096-4037},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/11837460},
   Abstract = {This paper reviews key findings on juvenile mental health
             problems in boys, psychopathy, and personality traits,
             obtained in the first 14 years of studies using data from
             the Pittsburgh Youth Study. This is a study of 3 samples,
             each of about 500 boys initially randomly drawn from boys in
             the 1st, 4th, and 7th grades of public schools in
             Pittsburgh. The boys have been followed regularly, initially
             each half year, and later at yearly intervals. Currently,
             the oldest boys are about 25 years old, whereas the youngest
             boys are about 19. Findings are presented on the prevalence
             and interrelation of disruptive behaviors, ADHD, and
             depressed mood. Results concerning risk factors for these
             outcomes are reviewed. Psychological factors such as
             psychopathy, impulsivity, and personality are described. The
             paper closes with findings on service delivery of boys with
             mental health problems.},
   Doi = {10.1023/a:1013574903810},
   Key = {fds253382}
}

@article{fds253383,
   Author = {Poulton, R and Moffitt, TE and Harrington, H and Milne, BJ and Caspi,
             A},
   Title = {Persistence and perceived consequences of cannabis use and
             dependence among young adults: implications for
             policy.},
   Journal = {The New Zealand medical journal},
   Volume = {114},
   Number = {1145},
   Pages = {544-547},
   Year = {2001},
   Month = {December},
   ISSN = {0028-8446},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/11833947},
   Abstract = {<h4>Aims</h4>To document patterns of cannabis use and
             dependence from late-adolescence through to the
             mid-twenties; to describe perceived consequences of cannabis
             use among young people; and to consider policy implications
             of these findings.<h4>Methods</h4>This was a longitudinal
             study of the Dunedin Multidisciplinary Health and
             Development Study birth cohort with repeated measures of
             cannabis use at ages 18, 21 and 26 years.<h4>Results</h4>Twelve
             month prevalence rates of cannabis use (just over 50%) and
             dependence (just under 10%) remained stable between age 21
             and 26 years, contrary to an expected decline. Cannabis
             dependence, as distinct from occasional use, was associated
             with high rates of harder drug use, selling of drugs and
             drug conviction. Cumulatively, almost 3/4 of our cohort had
             tried cannabis by age 26. Young people thought the risk of
             getting caught using cannabis was trivial, and that using
             cannabis had few negative social consequences.<h4>Conclusions</h4>The
             persistent high rates of cannabis use and dependence among
             young New Zealand adults raises important issues for policy
             makers. Current laws are not particularly effective in
             deterring use. Whereas occasional use does not appear to
             present a serious problem, cannabis dependence among users
             is a serious public health issue that warrants immediate
             action.},
   Key = {fds253383}
}

@article{fds253184,
   Author = {Mill, J and Caspi, A and McClay, J and Poulton, R and Braithewaite, A and Asherson, P and Moffitt, T},
   Title = {The dopamine D4 receptor (DRD4) gene, behaviour, and
             psychopathology: A developmental-epidemiological
             study},
   Journal = {American Journal of Medical Genetics - Neuropsychiatric
             Genetics},
   Volume = {105},
   Number = {7},
   Pages = {576},
   Year = {2001},
   Month = {October},
   ISSN = {1552-4841},
   Abstract = {Variation at the DRD4 locus has been postulated to be
             associated with a wide range of personality traits and
             psychopathologies. Most notably, the association between the
             7-repeat allele of the exon-3 VNTR and ADHD is one of the
             most replicated findings in psychiatric genetics. Whilst
             considerable work has been done on DRD4 in small clinical
             samples, the relationship between alleles of this gene and
             quantitative measures of behaviour in a large
             population-based sample have never been studied. We have
             genotyped participants in the Dunedin Multidisciplinary
             Health and Development Study, a 26-year longitudinal study
             of a phenotypically well-characterised birth cohort (N=
             1037) for the 48 bp VNTR in exon 3 of DRD4. Our findings
             play down the role of DRD4 in hyperactivity, but support an
             association with quantitative and categorical measures of
             alcoholism as well as negative emotionality personality
             traits. We are currently replicating these findings in
             another large population-based sample comprising of 3000
             twin pairs.},
   Key = {fds253184}
}

@article{fds253185,
   Author = {Roberts, BW and Caspi, A and Moffitt, TE},
   Title = {The kids are alright: growth and stability in personality
             development from adolescence to adulthood.},
   Journal = {Journal of personality and social psychology},
   Volume = {81},
   Number = {4},
   Pages = {670-683},
   Year = {2001},
   Month = {October},
   ISSN = {0022-3514},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/11642353},
   Abstract = {This longitudinal study provides a comprehensive analysis of
             continuity and change in personality functioning from age 18
             to age 26 in a birth cohort (N = 921) using the
             Multidimensional Personality Questionnaire (A. Tellegen,
             1982). Data were analyzed using 4 different methods:
             differential continuity, mean-level change, individual
             differences in change, and ipsative change. Convergent
             evidence pointing toward personality continuity, as opposed
             to change, was found. The personality changes that did take
             place from adolescence to adulthood reflected growth in the
             direction of greater maturity; many adolescents became more
             controlled and socially more confident and less angry and
             alienated. Consistent with this, greater initial levels of
             maturity were associated with less personality change over
             time. The results indicate that the transition from
             adolescence to young adulthood is marked by continuity of
             personality and growth toward greater maturity.},
   Doi = {10.1037/0022-3514.81.4.670},
   Key = {fds253185}
}

@article{fds253384,
   Author = {Milne, BJ and Poulton, R and Caspi, A and Moffitt,
             TE},
   Title = {Brain drain or OE? Characteristics of young New Zealanders
             who leave.},
   Journal = {The New Zealand medical journal},
   Volume = {114},
   Number = {1141},
   Pages = {450-453},
   Year = {2001},
   Month = {October},
   ISSN = {0028-8446},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/11700773},
   Abstract = {<h4>Aims</h4>To characterise the emigration patterns of
             young New Zealanders.<h4>Methods</h4>The 980 members of the
             Dunedin Multidisciplinary Health and Development Study
             participating in the "age-26" (1998-1999) assessment
             provided information about emigration behaviour,
             qualifications, aspects of physical and mental health and
             personality.<h4>Results</h4>26% of the sample had moved
             overseas to live between the ages of 18 and 26, with the
             United Kingdom and Australia being the most common
             destinations. Compared to non-emigrants, emigrants had
             higher IQ scores, were better qualified, leaner and fitter,
             and had happier and less stress-prone personalities. Based
             on their planned return date, 63% of emigrants were
             considered to be on their OE overseas experience (OE, return
             in <5 years), 18% were defined as brain-drain emigrants
             (return in >5 years or never) and 18% were uncertain about
             their return. Brain-drain emigrants were more likely than OE
             emigrants to leave for better work opportunities, and they
             were also more likely to go to Australia. However, there
             were no differences in terms of qualifications, intelligence
             and personality between OE and brain-drain
             emigrants.<h4>Conclusions</h4>Most young New Zealanders in
             this cohort who left for overseas were embarking on their
             OE. Brain-drain emigrants make up a sizeable minority of
             emigrants, but appear to possess no more skills than those
             who plan or choose to return.},
   Key = {fds253384}
}

@article{fds253387,
   Author = {Caspi, A and Taylor, A and Smart, M and Jackson, J and Tagami, S and Moffitt, TE},
   Title = {Can women provide reliable information about their
             children's fathers? cross-informant agreement about men's
             lifetime antisocial behaviour.},
   Journal = {Journal of child psychology and psychiatry, and allied
             disciplines},
   Volume = {42},
   Number = {7},
   Pages = {915-920},
   Year = {2001},
   Month = {October},
   ISSN = {0021-9630},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/11693586},
   Abstract = {It is difficult to study the contribution of fathers'
             antisocial behaviour to children's development because
             fathers with behavioural problems are often absent or
             reluctant to participate in research. This study examines
             whether mothers' reports about their children's fathers'
             antisocial behaviour can be substituted for interviews with
             fathers. Both members of 67 couples (N = 134) were
             interviewed separately and independently about the men's
             lifetime antisocial behaviour. There was strong relative
             agreement: the women's reports about men's antisocial
             behaviour and the men's self-reports about the same
             behaviour were highly correlated. However, there was poor
             agreement about absolute level: compared to men's
             self-reports, women reported fewer of the men's antisocial
             behaviours. Women's reports provide a reliable index of
             men's relative standing in a distribution and can be used in
             research about their children's fathers, but should not be
             used to make diagnostic decisions about men's antisocial
             disorders.},
   Doi = {10.1111/1469-7610.00787},
   Key = {fds253387}
}

@article{fds253388,
   Author = {Jaffee, SR and Caspi, A and Moffitt, TE and Taylor, A and Dickson,
             N},
   Title = {Predicting early fatherhood and whether young fathers live
             with their children: prospective findings and policy
             reconsiderations.},
   Journal = {Journal of child psychology and psychiatry, and allied
             disciplines},
   Volume = {42},
   Number = {6},
   Pages = {803-815},
   Year = {2001},
   Month = {September},
   ISSN = {0021-9630},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/11583253},
   Abstract = {This prospective study of a birth cohort addressed three
             questions. Which individual and family-of-origin
             characteristics predict the age at which young men make the
             transition to fatherhood? Do these same characteristics
             predict how long young men live with their child? Are
             individual differences in the amount of time fathers spend
             living with their child associated with the father's
             psychosocial characteristics in young adulthood? In this
             unique study, it was found that by age 26, 19% of the 499
             study men had become fathers. Individual and
             family-of-origin characteristics were assessed from birth
             until age 15 and contemporaneous characteristics were
             assessed at age 26. Young men who experienced a stressful
             rearing environment and a history of conduct problems were
             more likely to become fathers at an early age and to spend
             less time living with their child. Of those who experienced
             none of the risk factors, fewer than 10% had become fathers
             by age 26 compared to more than 60% of those who experienced
             five risk factors. Fathers who lived apart from their child
             reported the most social and psychological difficulties in
             young adulthood. These findings point to individual and
             family-of-origin characteristics that might be targeted in
             order to delay fatherhood and increase levels of paternal
             involvement. However, given their troubled life histories
             and poor social-psychological adjustment in young adulthood,
             some absent fathers might have difficulties providing
             positive parenting and partnering unless policy initiatives
             to promote intact families also support young
             fathers.},
   Doi = {10.1111/1469-7610.00777},
   Key = {fds253388}
}

@article{fds253386,
   Author = {Entner Wright and BR and Caspi, A and Moffitt, TE and Silva,
             PA},
   Title = {The effects of social ties on crime vary by criminal
             propensity: A life-course model of interdependence},
   Journal = {Criminology},
   Volume = {39},
   Number = {2},
   Pages = {321-348},
   Publisher = {WILEY},
   Year = {2001},
   Month = {January},
   url = {http://dx.doi.org/10.1111/j.1745-9125.2001.tb00925.x},
   Abstract = {Previous studies have explained the transition from criminal
             propensity in youth to criminal behavior in adulthood with
             hypotheses of enduring criminal propensity, unique social
             causation, and cumulative social disadvantage. In this
             article we develop an additional hypothesis derived from the
             life-course concept of interdependence: The effects of
             social ties on crime vary as a function of individuals'
             propsensity for crime. We tested these four hypotheses with
             data from the Dunedin Study. In support of life-course
             interdependence, prosocial ties, such as education,
             employment, family ties, and partnerships, deterred crime,
             and antisocial ties, such as delinquent peers, promoted
             crime, most strongly among low self-control individuals. Our
             findings bear implications for theories and policies of
             crime.},
   Doi = {10.1111/j.1745-9125.2001.tb00925.x},
   Key = {fds253386}
}

@article{fds253389,
   Author = {Jaffee, S and Caspi, A and Moffitt, TE and Belsky, J and Silva,
             P},
   Title = {Why are children born to teen mothers at risk for adverse
             outcomes in young adulthood? Results from a 20-year
             longitudinal study.},
   Journal = {Development and psychopathology},
   Volume = {13},
   Number = {2},
   Pages = {377-397},
   Year = {2001},
   Month = {January},
   ISSN = {0954-5794},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/11393652},
   Abstract = {This 20-year longitudinal study showed that the young adult
             offspring of teen mothers are at risk for a range of adverse
             outcomes including early school leaving, unemployment, early
             parenthood, and violent offending. We tested how much the
             effect of teen childbearing on offspring outcomes could be
             accounted for by social selection (in which a woman's
             characteristics that make her an inadequate parent also make
             her likely to bear children in her teens) versus social
             influence (in which the consequences of becoming a teen
             mother also bring harm to her children, apart from any
             characteristics of her own). The results provided support
             for both mechanisms. Across outcomes, maternal
             characteristics and family circumstances together accounted
             for approximately 39% of the effect of teen childbearing on
             offspring outcomes. Consistent with a social-selection
             hypothesis, maternal characteristics accounted for
             approximately 18% of the effect of teen childbearing on
             offspring outcomes; consistent with a social-influence
             hypothesis, family circumstances accounted for 21% of the
             teen childbearing effect after controlling for maternal
             characteristics. These results suggest that public policy
             initiatives should be targeted not only at delaying
             childbearing in the population but at supporting individual
             at-risk mothers and their children.},
   Doi = {10.1017/s0954579401002103},
   Key = {fds253389}
}

@article{fds253390,
   Author = {Moffitt, TE and Caspi, A},
   Title = {Childhood predictors differentiate life-course persistent
             and adolescence-limited antisocial pathways among males and
             females.},
   Journal = {Development and psychopathology},
   Volume = {13},
   Number = {2},
   Pages = {355-375},
   Year = {2001},
   Month = {January},
   ISSN = {0954-5794},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/11393651},
   Abstract = {This article reports a comparison on childhood risk factors
             of males and females exhibiting childhood-onset and
             adolescent-onset antisocial behavior, using data from the
             Dunedin longitudinal study. Childhood-onset delinquents had
             childhoods of inadequate parenting, neurocognitive problems,
             and temperament and behavior problems, whereas
             adolescent-onset delinquents did not have these pathological
             backgrounds. Sex comparisons showed a male-to-female ratio
             of 10:1 for childhood-onset delinquency but a sex ratio of
             only 1.5:1 for adolescence-onset delinquency. Showing the
             same pattern as males, childhood-onset females had high-risk
             backgrounds but adolescent-onset females did not. These
             findings are consistent with core predictions from the
             taxonomic theory of life-course persistent and
             adolescence-limited antisocial behavior.},
   Doi = {10.1017/s0954579401002097},
   Key = {fds253390}
}

@article{fds69904,
   Author = {Caspi, A. and Taylor, A. and Smart, M.A. and Jackson, J. and Tagami, S. and Moffitt, T.E},
   Title = {Can women provide reliable information about their
             children’s fathers? Cross-informant agreement about
             men’s antisocial behaviour},
   Journal = {Journal of Child Psychology and Psychiatry},
   Volume = {42},
   Pages = {915-920},
   Year = {2001},
   Key = {fds69904}
}

@article{fds69910,
   Author = {Loeber, R. and Farrington, D.P. and Stouthamer-Loeber, M. and Moffitt, T.E. and Caspi, A. and Lynam, D},
   Title = {Male mental health problems, psychopathy and personality
             traits: Key findings from the first fourteen years of the
             Pittsburgh Youth Study},
   Journal = {Clinical Child and Family Psychology Review},
   Volume = {4},
   Pages = {273-279},
   Year = {2001},
   Key = {fds69910}
}

@article{fds253385,
   Author = {Moffitt, TE and Robins, RW and Caspi, A},
   Title = {A couples analysis of partner abuse with implications for
             abuse prevention},
   Journal = {Criminology and Public Policy},
   Volume = {1},
   Pages = {5-36},
   Year = {2001},
   Key = {fds253385}
}

@article{fds336549,
   Author = {Roberts, BW and Caspi, A and Moffitt, TE},
   Title = {The kids are alright: Personality change in the transition
             from adolescence to young adulthood},
   Journal = {Journal of Personality and Social Psychology},
   Volume = {81},
   Pages = {670-683},
   Year = {2001},
   Key = {fds336549}
}

@article{fds253180,
   Author = {Arseneault, L and Moffitt, TE and Caspi, A},
   Title = {Mental Disorders and Violence in a Total,::Birth Cohorts
             Results from the Dunedin Study},
   Journal = {Primary Care Companion to the Journal of Clinical
             Psychiatry},
   Volume = {2},
   Number = {6},
   Pages = {231-232},
   Year = {2000},
   Month = {December},
   ISSN = {1523-5998},
   Abstract = {Background: Because most individuals with mental illness are
             not hospitalized and most violent individuals are not
             convicted of crimes, hospital-and prison-based research
             underestimates the rates of mental illness and violence
             found in the general population. This study examined the
             overlap of mental disorders and violence in a birth cohort.
             Method: A total of 961 individuals born in Dunedin, New
             Zealand, from April 1, 1972, through March 31, 1973, (i.e.,
             94% of the total city birth cohort) were studied. DSM-III-R
             interviews were used to identify pastyear prevalence of
             mental disorders, and self-report of criminal offense and
             search of official conviction records were employed to
             measure past-year violence. The variables of substance use
             before the violent offense, excessive threat perception, and
             adolescent conduct disorder were studied as possible
             explanations for the link between mental disorders and
             violence. Results: Individuals with DSM-III-R alcohol
             dependence were 1.9 times (95% confidence interval [CI] =
             1.0 to 3.5), those with marijuana dependence were 3.8 times
             (95% CI = 2.2 to 6.8), and those with schizophrenia-spectrum
             disorder were 2.5 times (95% CI = 1.1 to 5.7) more likely to
             be violent than individuals without a psychiatric disorder.
             Although individuals with at least 1 of these disorders
             committed half of the violent crimes reported in this study
             (one tenth of the violence accounted uniquely for by
             patients with schizophrenia-spectrum disorder), they
             constituted only one fifth of the study cohort. Substance
             use before the violent event accounted for the violence in
             individuals with alcohol dependence. Adolescent history of
             conduct disorder best explained violence in individuals with
             marijuana dependence. Both excessive threat perception and
             adolescent history of conduct disorder accounted for
             violence in individuals with schizophrenia-spectrum
             disorder. Conclusions: Individuals with mental illness were
             responsible for a substantial percentage of the violent acts
             committed by persons within their age group. Because the
             explanations for violence varied between groups of
             individuals with different mental disorders, multiple
             treatment and intervention strategies may be necessary to
             prevent the occurrence of violent acts.},
   Key = {fds253180}
}

@article{fds253392,
   Author = {Krueger, RF and Caspi, A and Moffitt, TE},
   Title = {Epidemiological personology: the unifying role of
             personality in population-based research on problem
             behaviors.},
   Journal = {Journal of personality},
   Volume = {68},
   Number = {6},
   Pages = {967-998},
   Year = {2000},
   Month = {December},
   ISSN = {0022-3506},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/11130741},
   Abstract = {Epidemiological personology refers to a paradigm in which a
             developmental perspective on individual differences is
             paired with a population-based sampling frame to yield
             insights about the role of personality in consequential
             social outcomes. We review our work in epidemiological
             personology, linking personality to diverse, problematic
             social outcomes: Mental disorders, health-risk behaviors,
             and violence. We conclude that broad-band personality
             measurement is both feasible and fruitful in large-scale
             research on problem behaviors, and we call for increased
             collaboration between personality psychologists and
             researchers in fields such as public health, epidemiology,
             and sociology.},
   Doi = {10.1111/1467-6494.00123},
   Key = {fds253392}
}

@article{fds253391,
   Author = {Lynam, DR and Caspi, A and Moffitt, TE and Wikström, PO and Loeber, R and Novak, S},
   Title = {The interaction between impulsivity and neighborhood context
             on offending: the effects of impulsivity are stronger in
             poorer neighborhoods.},
   Journal = {Journal of abnormal psychology},
   Volume = {109},
   Number = {4},
   Pages = {563-574},
   Year = {2000},
   Month = {November},
   ISSN = {0021-843X},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/11195980},
   Abstract = {This research blends 2 traditions of theorizing on the
             causes of crime, one focused on the role of individual
             differences and the other focused on structural and
             contextual variables. Two related studies examined the
             relations among impulsivity, neighborhood context, and
             juvenile offending. The first, cross-sectional study uses a
             large sample of 13-year-old inner-city boys, whereas the
             second, longitudinal study offers a conceptual replication
             using 17-year-old inner-city boys who are a subset of the
             original sample. Across both studies, results indicate that
             the effects of impulsivity on juvenile offending are
             stronger in poorer neighborhoods. Furthermore, nonimpulsive
             boys in poor neighborhoods were at no greater risk for
             delinquency than nonimpulsive boys in better-off
             neighborhoods.},
   Doi = {10.1037//0021-843x.109.4.563},
   Key = {fds253391}
}

@article{fds253394,
   Author = {Taylor, DR and Poulton, R and Moffitt, TE and Ramankutty, P and Sears,
             MR},
   Title = {The respiratory effects of cannabis dependence in young
             adults.},
   Journal = {Addiction (Abingdon, England)},
   Volume = {95},
   Number = {11},
   Pages = {1669-1677},
   Year = {2000},
   Month = {November},
   url = {http://dx.doi.org/10.1046/j.1360-0443.2000.951116697.x},
   Abstract = {<h4>Aim</h4>To evaluate the relationship between cannabis
             dependence and respiratory symptoms and lung function in
             young adults, while controlling for the effects of tobacco
             smoking.<h4>Setting and participants</h4>Nine hundred and
             forty-three young adults from a birth cohort of 1037
             subjects born in Dunedin, New Zealand in 1972/1973 were
             studied at age 21.<h4>Measurements</h4>Standardized
             respiratory symptom questionnaires were administered.
             Spirometry and methacholine challenge tests were undertaken.
             Cannabis dependence was determined using DSM-III-R criteria.
             Descriptive analyses and comparisons between
             cannabis-dependent, tobacco-smoking and non-smoking groups
             were undertaken. Adjusted odds ratios for respiratory
             symptoms, lung function and airway hyper-responsiveness
             (PC20) were measured.<h4>Findings</h4>Ninety-one subjects
             (9.7%) were cannabis-dependent and 264 (28.1%) were current
             tobacco smokers. After controlling for tobacco use,
             respiratory symptoms associated with cannabis dependence
             included: wheezing apart from colds, exercise-induced
             shortness of breath, nocturnal wakening with chest tightness
             and early morning sputum production. These were increased by
             61%, 65%, 72% (all p < 0.05) and 144% (p < 0.01)
             respectively, compared to non-tobacco smokers. The frequency
             of respiratory symptoms in cannabis-dependent subjects was
             similar to tobacco smokers of 1-10 cigarettes/day. The
             proportion of cannabis-dependent study members with an
             FEV1/FVC ratio of < 80% was 36% compared to 20% for
             non-smokers (p = 0.04). These outcomes occurred
             independently of co-existing bronchial asthma.<h4>Conclusion</h4>Significant
             respiratory symptoms and changes in spirometry occur in
             cannabis-dependent individuals at age 21 years, even
             although the cannabis smoking history is of relatively short
             duration.},
   Doi = {10.1046/j.1360-0443.2000.951116697.x},
   Key = {fds253394}
}

@article{fds253396,
   Author = {Poulton, R and Caspi, A and Moffitt, TE and Cannon, M and Murray, R and Harrington, H},
   Title = {Children's self-reported psychotic symptoms and adult
             schizophreniform disorder: a 15-year longitudinal
             study.},
   Journal = {Archives of general psychiatry},
   Volume = {57},
   Number = {11},
   Pages = {1053-1058},
   Year = {2000},
   Month = {November},
   ISSN = {0003-990X},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/11074871},
   Abstract = {<h4>Background</h4>Childhood risk factors for the
             development of adult schizophrenia have proved to have only
             modest and nonspecific effects, and most seem unrelated to
             the adult phenotype. We report the first direct examination
             of the longitudinal relationship between psychotic symptoms
             in childhood and adulthood.<h4>Methods</h4>We analyzed
             prospective data from a birth cohort (N = 761), in which
             children were asked about delusional beliefs and
             hallucinatory experiences at age 11 years, and then followed
             up to age 26 years. Structured diagnostic interviews were
             employed at both ages and self-report of schizophreniform
             symptoms was augmented by other data sources at age 26
             years.<h4>Results</h4>Self-reported psychotic symptoms at
             age 11 years predicted a very high risk of a
             schizophreniform diagnosis at age 26 years (odds ratio,
             16.4; 95% confidence interval, 3.9-67.8). In terms of
             attributable risk, 42% of the age-26 schizophreniform cases
             in the cohort had reported 1 or more psychotic symptoms at
             age 11 years. Age-11 psychotic symptoms did not predict
             mania or depression at age 26 years, suggesting specificity
             of prediction to schizophreniform disorder. The link between
             child and adult psychotic symptoms was not simply the result
             of general childhood psychopathology.<h4>Conclusion</h4>These
             findings provide the first evidence for continuity of
             psychotic symptoms from childhood to adulthood.},
   Doi = {10.1001/archpsyc.57.11.1053},
   Key = {fds253396}
}

@article{fds304708,
   Author = {Arseneault, L and Moffitt, TE and Caspi, A and Taylor, PJ and Silva,
             PA},
   Title = {Mental disorders and violence in a total birth cohort:
             results from the Dunedin Study.},
   Journal = {Archives of general psychiatry},
   Volume = {57},
   Number = {10},
   Pages = {979-986},
   Year = {2000},
   Month = {October},
   ISSN = {0003-990X},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/11015816},
   Abstract = {<h4>Background</h4>We report on mental disorders and
             violence for a birth cohort of young adults, regardless of
             their contact with the health or justice
             systems.<h4>Methods</h4>We studied 961 young adults who
             constituted 94% of a total-city birth cohort in New Zealand,
             April 1, 1972, through March 31, 1973. Past-year prevalence
             of mental disorders was measured using standardized
             DSM-III-R interviews. Past-year violence was measured using
             self-reports of criminal offending and a search of official
             conviction records. We also tested whether substance use
             before the violent offense, adolescent excessive perceptions
             of threat, and a juvenile history of conduct disorder
             accounted for the link between mental disorders and
             violence.<h4>Results</h4>Individuals meeting diagnostic
             criteria for alcohol dependence, marijuana dependence, and
             schizophrenia-spectrum disorder were 1.9 (95% confidence
             interval [CI], 1.0-3.5), 3.8 (95% CI, 2.2-6.8), and 2.5 (95%
             CI, 1.1-5.7) times, respectively, more likely than control
             subjects to be violent. Persons with at least 1 of these 3
             disorders constituted one fifth of the sample, but they
             accounted for half of the sample's violent crimes (10% of
             violence risk was uniquely attributable to
             schizophrenia-spectrum disorder). Among alcohol-dependent
             individuals, violence was best explained by substance use
             before the offense; among marijuana-dependent individuals,
             by a juvenile history of conduct disorder; and among
             individuals with schizophrenia-spectrum disorder, by
             excessive perceptions of threat and a history of conduct
             disorder.<h4>Conclusions</h4>In the age group committing
             most violent incidents, individuals with mental disorders
             account for a considerable amount of violence in the
             community. Different mental disorders are linked to violence
             via different core explanations, suggesting
             multiple-targeted prevention strategies.},
   Doi = {10.1001/archpsyc.57.10.979},
   Key = {fds304708}
}

@article{fds253183,
   Author = {McClay, J and Caspi, A and Moffitt, TE and Poulton, R and Craig,
             I},
   Title = {A holistic approach to variation in dopamine
             genes},
   Journal = {American Journal of Medical Genetics - Neuropsychiatric
             Genetics},
   Volume = {96},
   Number = {4},
   Pages = {554},
   Year = {2000},
   Month = {August},
   ISSN = {1552-4841},
   Abstract = {Many behavioral disorders have a multifactorial etiology,
             with a genetic contribution provided by multiple
             Quantitative Trait Loci (QTLs). It is probable that such
             QTLs will be functionally related and interacting
             (epistatic). To investigate this general hypothesis, we have
             focused on variation in those genes concerned with the
             receptors and metabolic pathway of a single
             neurotransmitter, thereby achieving an "Integrated Pathway
             Genotype Analysis", IPGA. The target for our first holistic
             approach of this type is the dopamine system. To improve the
             efficiency of the integrated pathway approach, we have
             developed a multiplex PCR, whereby six polymorphic repeat
             markers associated with the following loci are amplified and
             analyzed simultaneously: monoamine oxidases A and B (MAOA,
             MAOB), dopamine beta hydroxylase (DBH), phenylalanine
             hydroxylase (PAH), tyrosine hydroxylase (TH) & the dopamine
             receptor 5 (DRD5) - coupled with SNP analysis at the COMT,
             DRD1, DRD2 & DRD3 loci. In a first in-depth investigation
             employing this approach, we are genotyping approximately
             1000 individuals from a birth cohort now reaching the 27th
             year of a longitudinal study based in Dunedin, New Zealand
             (Moffitt, Caspi, Rutter, & Silva, 1999, Findings from the
             first two decades of the Dunedin Longitudinal Study). The
             genotype data will be examined in the context of life-course
             persistent, high scores on measures of depression,
             antisocial behavior, and personality traits.},
   Key = {fds253183}
}

@article{fds253393,
   Author = {Robins, RW and Caspi, A and Moffitt, TE},
   Title = {Two personalities, one relationship: both partners'
             personality traits shape the quality of their
             relationship.},
   Journal = {Journal of personality and social psychology},
   Volume = {79},
   Number = {2},
   Pages = {251-259},
   Year = {2000},
   Month = {August},
   ISSN = {0022-3514},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/10948978},
   Abstract = {This research tested 6 models of the independent and
             interactive effects of stable personality traits on each
             partner's reports of relationship satisfaction and quality.
             Both members of 360 couples (N = 720) completed the
             Multidimensional Personality Questionnaire and were
             interviewed about their relationship. Findings show that a
             woman's relationship happiness is predicted by her partner's
             low Negative Emotionality, high Positive Emotionality, and
             high Constraint, whereas a man's relationship happiness is
             predicted only by his partner's low Negative Emotionality.
             Findings also show evidence of additive but not interactive
             effects: Each partner's personality contributed
             independently to relationship outcomes but not in a
             synergistic way. These results are discussed in relation to
             models that seek to integrate research on individual
             differences in personality traits with research on
             interpersonal processes in intimate relationships.},
   Doi = {10.1037//0022-3514.79.2.251},
   Key = {fds253393}
}

@article{fds253182,
   Author = {Ramrakha, S and Caspi, A and Dickson, N and Moffitt, TE and Paul,
             C},
   Title = {Psychiatric disorders and risky sexual behaviour in young
             adulthood: cross sectional study in birth
             cohort.},
   Journal = {BMJ (Clinical research ed.)},
   Volume = {321},
   Number = {7256},
   Pages = {263-266},
   Year = {2000},
   Month = {July},
   ISSN = {0959-8138},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/10915126},
   Abstract = {<h4>Objective</h4>To determine if risky sexual intercourse,
             sexually transmitted diseases, and sexual intercourse at an
             early age are associated with psychiatric
             disorder.<h4>Design</h4>Cross sectional study of a birth
             cohort at age 21 years with assessments presented by
             computer (for sexual behaviour) and by trained interviewers
             (for psychiatric disorder).<h4>Setting</h4>New Zealand in
             1993-4.<h4>Participants</h4>992 study members (487 women)
             from the Dunedin multidisciplinary health and development
             study. Complete data were available on both measures for 930
             study members.<h4>Main outcome measures</h4>Psychiatric
             disorders (anxiety, depression, eating disorder, substance
             dependence, antisocial disorder, mania, schizophrenia
             spectrum) and measures of sexual behaviour.<h4>Results</h4>Young
             people diagnosed with substance dependence, schizophrenia
             spectrum, and antisocial disorders were more likely to
             engage in risky sexual intercourse, contract sexually
             transmitted diseases, and have sexual intercourse at an
             early age (before 16 years). Unexpectedly, so were young
             people with depressive disorders. Young people with mania
             were more likely to report risky sexual intercourse and have
             sexually transmitted diseases. The likelihood of risky
             behaviour was increased by psychiatric comorbidity.<h4>Conclusions</h4>There
             is a clear association between risky sexual behaviour and
             common psychiatric disorders. Although the temporal relation
             is uncertain, the results indicate the need to coordinate
             sexual medicine with mental health services in the treatment
             of young people.},
   Doi = {10.1136/bmj.321.7256.263},
   Key = {fds253182}
}

@article{fds253397,
   Author = {Caspi, A and Taylor, A and Moffitt, TE and Plomin,
             R},
   Title = {Neighborhood deprivation affects children's mental health:
             environmental risks identified in a genetic
             design.},
   Journal = {Psychological science},
   Volume = {11},
   Number = {4},
   Pages = {338-342},
   Year = {2000},
   Month = {July},
   ISSN = {0956-7976},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/11273396},
   Abstract = {The possibility that neighborhood conditions affect
             children's development has captured much attention because
             of its implications for prevention. But does growing up in
             deprived neighborhoods matter above and beyond a genetic
             liability to behavior problems, if genetically vulnerable
             families tend to concentrate in poor neighborhoods? A
             nationwide study of 2-year-old twins shows that children in
             deprived neighborhoods were at increased risk for emotional
             and behavioral problems over and above any genetic
             liability. Environmental factors shared by members of a
             family accounted for 20% of the population variation in
             children's behavior problems, and neighborhood deprivation
             accounted for 5% of this family-wide environmental effect.
             The results suggest that the link between poor neighborhoods
             and children's mental health may be a true environmental
             effect, and demonstrate that genetic designs are
             environmentally informative and can be used to identify
             modifiable risk factors for promoting child
             health.},
   Doi = {10.1111/1467-9280.00267},
   Key = {fds253397}
}

@article{fds253398,
   Author = {McGee, R and Williams, S and Poulton, R and Moffitt,
             T},
   Title = {A longitudinal study of cannabis use and mental health from
             adolescence to early adulthood.},
   Journal = {Addiction (Abingdon, England)},
   Volume = {95},
   Number = {4},
   Pages = {491-503},
   Year = {2000},
   Month = {April},
   url = {http://dx.doi.org/10.1046/j.1360-0443.2000.9544912.x},
   Abstract = {<h4>Aims</h4>To examine the longitudinal association between
             cannabis use and mental health.<h4>Design</h4>Information
             concerning cannabis use and mental health from 15 to 21
             years was available for a large sample of individuals as
             part of a longitudinal study from childhood to
             adulthood.<h4>Participants</h4>Participants were enrolled in
             the Dunedin Multidisciplinary Health and Development Study,
             a research programme on the health, development and
             behaviour of a large group of New Zealanders born between 1
             April 1972 and 31 March 1973.<h4>Measurements</h4>Cannabis
             use and identification of mental disorder was based upon
             self-report as part of a general assessment of mental health
             using a standard diagnostic interview. Daily smoking and
             alcohol use at age 15 were assessed by self-report. Indices
             of family socio-economic status, family climate and
             parent-child interaction were formed using information
             gathered from parent report and behavioural observations
             over early childhood. Childhood behaviour problems were
             assessed by parent and teacher report. Attachment to parents
             was assessed in adolescence.<h4>Findings</h4>Cross-sectional
             associations between cannabis use and mental disorder were
             significant at all three ages. Both outcome variables shared
             similar pathways of low socio-economic status and history of
             behaviour problems in childhood, and low parental attachment
             in adolescence. Mental disorder at age 15 led to a small but
             significantly elevated risk of cannabis use at age 18; by
             contrast, cannabis use at age 18 elevated the risk of mental
             disorder at age 21. The latter association reflected the
             extent to which cannabis dependence and other externalizing
             disorders at age 21 were predicted by earlier level of
             involvement with cannabis.<h4>Conclusions</h4>The findings
             suggest that the primary causal direction leads from mental
             disorder to cannabis use among adolescents and the reverse
             in early adulthood. Both alcohol use and cigarette smoking
             had independent associations with later mental health
             disorder.},
   Doi = {10.1046/j.1360-0443.2000.9544912.x},
   Key = {fds253398}
}

@article{fds336550,
   Author = {Ramrakha, S and Caspi, A and Dickson, N and Moffitt, TE and Paul,
             C},
   Title = {Psychiatric disorders and risky sex in young
             people},
   Journal = {British Medical Journal},
   Volume = {321},
   Pages = {263-266},
   Year = {2000},
   Key = {fds336550}
}

@article{fds253181,
   Author = {Moffitt, TE and Krueger, RF and Caspi, A and Fagan,
             J},
   Title = {Partner abuse and general crime: How are they the same? How
             are they different?},
   Journal = {Criminology},
   Volume = {38},
   Number = {1},
   Pages = {201-235},
   Publisher = {WILEY},
   Year = {2000},
   url = {http://dx.doi.org/10.1111/j.1745-9125.2000.tb00888.x},
   Abstract = {Both partner abuse and general crime violate the rights and
             safety of victims. But are these phenomena the same or are
             they distinct, demanding their own research and intervention
             specialties? Are persons who abuse their partners the same
             people who commit other criminal behavior? Do partner abuse
             and general crime share the same correlates? We investigated
             these questions in a birth cohort of over 800 young adults,
             by testing whether a personality model known to predict
             general crime would also predict partner abuse. Personality
             data were gathered at age 18, and self-reported partner
             abuse and general criminal offending were measured at age
             21. Results from modeling latent constructs showed that
             partner abuse and general crime represent different
             constructs that are moderately related; they are not merely
             two expressions of the same underlying antisocial
             propensity. Group comparisons showed many, but not all,
             partner abusers also engaged in violence against
             nonintimates. Personality analyses showed that partner abuse
             and general crime shared a strong propensity from a trait
             called Negative Emotionality. However, crime was related to
             weak Constraint (low self-control), but partner abuse was
             not. All findings applied to women as well as to men,
             suggesting that women's partner abuse may be motivated by
             the same intra-personal features that motivate men's abuse.
             The results are consistent with theoretical and applied
             arguments about the "uniqueness" of partner violence
             relative to other crime and violence.},
   Doi = {10.1111/j.1745-9125.2000.tb00888.x},
   Key = {fds253181}
}

@article{fds253395,
   Author = {Arseneault, L and Moffitt, TE and Caspi, A and Taylor, PJ and Silva,
             PA},
   Title = {Mental disorder and violence in a total birth
             cohort},
   Journal = {Archives of General Psychiatry},
   Volume = {57},
   Number = {10},
   Pages = {979-986},
   Year = {2000},
   ISSN = {0003-990X},
   url = {http://www.kompas.com/health/klinikpria},
   Abstract = {BACKGROUND: We report on mental disorders and violence for a
             birth cohort of young adults, regardless of their contact
             with the health or justice systems. METHODS: We studied 961
             young adults who constituted 94% of a total-city birth
             cohort in New Zealand, April 1, 1972, through March 31,
             1973. Past-year prevalence of mental disorders was measured
             using standardized DSM-III-R interviews. Past-year violence
             was measured using self-reports of criminal offending and a
             search of official conviction records. We also tested
             whether substance use before the violent offense, adolescent
             excessive perceptions of threat, and a juvenile history of
             conduct disorder accounted for the link between mental
             disorders and violence. RESULTS: Individuals meeting
             diagnostic criteria for alcohol dependence, marijuana
             dependence, and schizophrenia-spectrum disorder were 1.9
             (95% confidence interval [CI], 1.0-3.5), 3.8 (95% CI,
             2.2-6.8), and 2.5 (95% CI, 1.1-5.7) times, respectively,
             more likely than control subjects to be violent. Persons
             with at least 1 of these 3 disorders constituted one fifth
             of the sample, but they accounted for half of the sample's
             violent crimes (10% of violence risk was uniquely
             attributable to schizophrenia-spectrum disorder). Among
             alcohol-dependent individuals, violence was best explained
             by substance use before the offense; among
             marijuana-dependent individuals, by a juvenile history of
             conduct disorder; and among individuals with
             schizophrenia-spectrum disorder, by excessive perceptions of
             threat and a history of conduct disorder. CONCLUSIONS: In
             the age group committing most violent incidents, individuals
             with mental disorders account for a considerable amount of
             violence in the community. Different mental disorders are
             linked to violence via different core explanations,
             suggesting multiple-targeted prevention strategies.},
   Key = {fds253395}
}

@article{fds253399,
   Author = {Henry, B and Caspi, A and Moffitt, TE and Harrington, HL and Silva,
             PA},
   Title = {Staying in school protects boys with poor self-regulation in
             childhood from later crime: A longitudinal
             study},
   Journal = {International Journal of Behavioral Development},
   Volume = {23},
   Number = {4},
   Pages = {1049-1073},
   Publisher = {SAGE Publications},
   Year = {1999},
   Month = {January},
   ISSN = {0165-0254},
   url = {http://dx.doi.org/10.1080/016502599383667},
   Abstract = {Based on a theoretical model that emphasises the distinction
             between individual and contextual determinants of antisocial
             behaviour, the current study examined whether school
             attendance throughout adolescence acted as a protective
             factor for individuals at risk for criminal behaviour in
             early adulthood. Specifically, Lack of Control, an index of
             self-regulation which has previously been shown to predict
             later criminal behaviour, was expected to interact with
             early school leaving to predict self-reports and official
             records of criminal behaviour collected at age 21.
             Multivariate regression analyses revealed a significant
             three-way interaction between school attendance,
             self-regulation, and sex. Among males, after controlling for
             the effects of socioeconomic status and IQ, the main effects
             for Lack of Control and school attendance were found to be
             significant; additionally, the interaction between Lack of
             Control and school attendance was significant, indicating
             that the strength of the relation between Lack of Control
             and criminal outcomes was moderated by school attendance.
             The main effects for Lack of Control and school attendance
             were significant for females, but the interaction between
             Lack of Control and school attendance was not significant.
             The protective effect of school attendance among males could
             not be accounted for by differences in familial disruption
             or adolescent delinquency. © 1999 The International Society
             for the Study of Behavioural Development.},
   Doi = {10.1080/016502599383667},
   Key = {fds253399}
}

@article{fds253400,
   Author = {Entner Wright and BRE and Caspi, A and Moffitt, TE and Silva,
             PA},
   Title = {Low self-control, social bonds, and crime: Social causation,
             social selection, or both?},
   Journal = {Criminology},
   Volume = {37},
   Number = {3},
   Pages = {479-514},
   Publisher = {WILEY},
   Year = {1999},
   Month = {January},
   url = {http://dx.doi.org/10.1111/j.1745-9125.1999.tb00494.x},
   Abstract = {This article examines the social-selection and
             social-causation processes that generate criminal behavior.
             We describe these processes with three theoretical models: a
             social-causation model that links crime to contemporaneous
             social relationships; a social-selection model that links
             crime to personal characteristics formed in childhood; and a
             mixed selection-causation model that links crime to social
             relationships and childhood characteristics. We tested these
             models with a longitudinal study in Dunedin, New Zealand, of
             individuals followed from birth through age 21. We analyzed
             measures of childhood and adolescent low self-control as
             well as adolescent and adult social bonds and criminal
             behavior. In support of social selection, we found that low
             self-control in childhood predicted disrupted social bonds
             and criminal offending later in life. In support of social
             causation, we found that social bonds and adolescent
             delinquency predicted later adult crime and, further, that
             the effect of self-control on crime was largely mediated by
             social bonds. In support of both selection and causation, we
             found that the social-causation effects remained significant
             even when controlling for preexisting levels of
             self-control, but that their effects diminished. Taken
             together, these findings support theoretical models that
             incorporate social-selection and social-causation
             processes.},
   Doi = {10.1111/j.1745-9125.1999.tb00494.x},
   Key = {fds253400}
}

@article{fds253401,
   Author = {Entner Wright and BR and Caspi, A and Moffitt, TE and Miech, RA and Silva,
             PA},
   Title = {Reconsidering the relationship between SES and delinquency:
             Causation but not correlation},
   Journal = {Criminology},
   Volume = {37},
   Number = {1},
   Pages = {175-194},
   Publisher = {WILEY},
   Year = {1999},
   Month = {January},
   url = {http://dx.doi.org/10.1111/j.1745-9125.1999.tb00483.x},
   Abstract = {Many theories of crime have linked low levels of
             socioeconomic status (SES) to high levels of delinquency.
             However, empirical studies have consistently found weak or
             nonexistent correlations between individuals' SES and their
             self-reported delinquent behavior. Drawing upon recent
             theoretical innovations (Hagan et al., 1985; Jensen, 1993;
             Tittle, 1995), we propose that this apparent contradiction
             between theory and data may be reconciled by recognizing
             that SES has both a negative and a positive indirect effect
             upon delinquency that, in tandem, results in little overall
             correlation between the two. We tested this proposal with
             longitudinal data from the Dunedin Multidisciplinary Health
             and Development Study. We used measures of parental SES
             recorded at study members' birth through age 15,
             social-psychological characteristics at age 18, and
             self-reported delinquency at ages 18 and 21. We found that
             low SES promoted delinquency by increasing individuals'
             alienation, financial strain, and aggression and by
             decreasing educational and occupational aspirations, whereas
             high SES promoted individuals' delinquency by increasing
             risk taking and social power and by decreasing conventional
             values. These findings suggest a reconciliation between
             theory and data, and they underscore the conceptual
             importance of elucidating the full range of causal linkages
             between SES and delinquency.},
   Doi = {10.1111/j.1745-9125.1999.tb00483.x},
   Key = {fds253401}
}

@article{fds253178,
   Author = {Miech, RA and Caspi, A and Moffitt, TE and Wright, BE and Silva,
             PA},
   Title = {Low socio-economic status and mental disorders: A
             longitudinal study of causation and selection},
   Journal = {American Journal of Sociology},
   Volume = {104},
   Number = {4},
   Pages = {1096-1131},
   Publisher = {University of Chicago Press},
   Year = {1999},
   ISSN = {0002-9602},
   url = {http://dx.doi.org/10.1086/210137},
   Abstract = {This article examines low socioeconomic staus (SES) as both
             a cause and a consequence of mental illnesses by
             investigating the mutual influence of mental disorders and
             educational attainment, a core element of SES. The analyses
             are based on a longitudinal panel design and focus on four
             disorders: anxiety, depression, antisocial disorder, and
             attention deficit disorder. The article shows that each
             disorder has a unique relationship with SES, highlighting
             the need for greater consideration of antisocial disorders
             in the status attainment process and for further theoretical
             development in the sociology of mental disorders to account
             for disorder-specific relations with SES.},
   Doi = {10.1086/210137},
   Key = {fds253178}
}

@article{fds253403,
   Author = {Magdol, L and Moffitt, TE and Caspi, A and Silva,
             PA},
   Title = {Developmental antecedents of partner abuse: a
             prospective-longitudinal study.},
   Journal = {Journal of abnormal psychology},
   Volume = {107},
   Number = {3},
   Pages = {375-389},
   Year = {1998},
   Month = {August},
   ISSN = {0021-843X},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/9715573},
   Abstract = {Prospective measures of risk factors for partner abuse were
             obtained from a large birth cohort in 4 domains:
             socioeconomic resources, family relations, educational
             achievements, and problem behaviors. Partner abuse outcomes
             were measured at age 21. Results showed that antecedents of
             abuse included risk factors from all 4 domains. Risk factors
             were similar for men and women. Some age 3 antecedents were
             significant, but the strongest correlations were from age
             15. In multivariate analyses, the most consistent predictor
             was the presence of early problem behaviors. In a
             cross-validation tests, abuse was moderately predictable by
             the same antecedents, whether the outcome measure was
             self-report or reports from partners of sample members.
             Findings suggest that theories of partner abuse should
             account for developmental influences from multiple life
             domains and that primary prevention of partner abuse should
             begin in adolescence.},
   Doi = {10.1037//0021-843x.107.3.375},
   Key = {fds253403}
}

@article{fds253405,
   Author = {Bardone, AM and Moffitt, TE and Caspi, A and Dickson, N and Stanton, WR and Silva, PA},
   Title = {Adult physical health outcomes of adolescent girls with
             conduct disorder, depression, and anxiety.},
   Journal = {Journal of the American Academy of Child and Adolescent
             Psychiatry},
   Volume = {37},
   Number = {6},
   Pages = {594-601},
   Year = {1998},
   Month = {June},
   ISSN = {0890-8567},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/9628079},
   Abstract = {<h4>Objective</h4>To examine the young adult physical health
             outcomes of adolescent girls with behavior
             problems.<h4>Method</h4>Girls with conduct disorder, girls
             with depression, girls with anxiety, and healthy girls (N =
             459) who had been evaluated at age 15 years were followed up
             at age 21, when general physical health, substance
             dependence, and reproductive health were
             assessed.<h4>Results</h4>After control for potentially
             confounding variables including prior health, adolescent
             conduct disorder predicted more medical problems, poorer
             self-reported overall health, lower body mass index, alcohol
             and/or marijuana dependence, tobacco dependence, daily
             smoking, more lifetime sexual partners, sexually transmitted
             disease, and early pregnancy. Adolescent depression
             predicted only adult tobacco dependence and more medical
             problems; adolescent anxiety predicted more medical
             problems.<h4>Conclusions</h4>The robust link between female
             adolescent conduct disorder and poor physical health in
             adulthood suggests that intervention with girls who have
             conduct disorder may be a strategy for preventing subsequent
             health problems.},
   Doi = {10.1097/00004583-199806000-00009},
   Key = {fds253405}
}

@article{fds253406,
   Author = {Newman, DL and Moffitt, TE and Caspi, A and Silva,
             PA},
   Title = {Comorbid mental disorders: implications for treatment and
             sample selection.},
   Journal = {Journal of abnormal psychology},
   Volume = {107},
   Number = {2},
   Pages = {305-311},
   Year = {1998},
   Month = {May},
   ISSN = {0021-843X},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/9604559},
   Abstract = {Disorders from the Diagnostic and Statistical Manual of
             Mental Disorders (3rd ed., rev.; American Psychiatric
             Association, 1987) were assessed in a birth cohort of 961
             young adults. Comorbid cases exceeded single-disordered
             cases in chronic history of mental illness, use of
             treatments, physical health problems, functional
             interference in daily life, and impaired adaptation across
             domains such as work, education, health, and social-support
             networks. Single-disorder cases were also more impaired than
             nondisordered cases, but comorbid cases were the most
             severely impaired. Our findings suggest that (a) samples
             that underrepresent comorbidity (pure single-disorder cases
             or student samples) will underestimate effect sizes for
             relations between a disorder and its correlates, whereas
             samples that overrepresent comorbidity (clinical or
             adjudicated samples) will overestimate effect sizes, (b)
             comorbidity is accompanied by complications that challenge
             treatment planning, compliance, and coordination of service
             delivery, and (c) comorbidity is associated with physical,
             educational, and economic problems that make it a broad
             societal concern.},
   Doi = {10.1037//0021-843x.107.2.305},
   Key = {fds253406}
}

@article{fds253407,
   Author = {Krueger, RF and Caspi, A and Moffitt, TE and Silva,
             PA},
   Title = {The structure and stability of common mental disorders
             (DSM-III-R): a longitudinal-epidemiological
             study.},
   Journal = {Journal of abnormal psychology},
   Volume = {107},
   Number = {2},
   Pages = {216-227},
   Year = {1998},
   Month = {May},
   ISSN = {0021-843X},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/9604551},
   Abstract = {The latent structure and stability of 10 common mental
             disorders were examined in a birth cohort at ages 18 and 21.
             A 2-factor model, in which some disorders were presumed to
             reflect internalizing problems and others were presumed to
             reflect externalizing problems, provided a more optimal fit
             to the data than either a 1- or a 4-factor model. To a
             significant extent, persons in the sample retained their
             relative positions on the latent factors across the 3-year
             period from age 18 to age 21. Results offer potential
             clarification of the meaning of comorbidity in
             psychopathology research by suggesting that comorbidity may
             results from common mental disorders being reliable,
             covariant indicators of stable, underlying "core
             psychopathological processes."},
   Doi = {10.1037//0021-843x.107.2.216},
   Key = {fds253407}
}

@article{fds253408,
   Author = {Martin, J and Nada-Raja, S and Langley, J and Feehan, M and McGee, R and Clarke, J and Begg, D and Hutchinson-Cervantes, M and Moffitt, T and Rivara, F},
   Title = {Physical assault in New Zealand: the experience of 21 year
             old men and women in a community sample.},
   Journal = {The New Zealand medical journal},
   Volume = {111},
   Number = {1065},
   Pages = {158-160},
   Year = {1998},
   Month = {May},
   ISSN = {0028-8446},
   Abstract = {<h4>Aim</h4>To obtain epidemiological information on
             physical assault in a high risk group of New
             Zealanders.<h4>Method</h4>Rates of physical assault in the
             preceding twelve months were ascertained by interview in a
             cohort of 21 year old, Dunedin-born men (n = 482) and women
             (n = 462).<h4>Results</h4>Forty-five percent of the men and
             one quarter of the women reported at least one physical
             assault, either completed, attempted or threatened. A small
             proportion of these received medical treatment. Most serious
             assaults were by a perpetrator who was thought to have been
             drinking alcohol. Most assaults on men were by strangers but
             partners carried out more assaults against women, especially
             those receiving medical treatment. One quarter of all
             assaults on women were by other women, compared to 15% of
             the assaults on men. Differences between patterns of
             assaults on women and on men are discussed.<h4>Conclusion</h4>It
             is important for doctors to be aware of the widespread
             occurrence of interpersonal violence in New Zealand and its
             underreporting.},
   Key = {fds253408}
}

@article{fds253409,
   Author = {Krueger, RF and Moffitt, TE and Caspi, A and Bleske, A and Silva,
             PA},
   Title = {Assortative mating for antisocial behavior: developmental
             and methodological implications.},
   Journal = {Behavior genetics},
   Volume = {28},
   Number = {3},
   Pages = {173-186},
   Year = {1998},
   Month = {May},
   ISSN = {0001-8244},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/9670593},
   Abstract = {Do people mate assortatively for antisocial behavior? If so,
             what are the implications for the development and
             persistence of antisocial behavior? We investigated
             assortative mating for antisocial behavior and its
             correlates in a sample of 360 couples from Dunedin, New
             Zealand. We found substantial assortative mating for
             self-reports of antisocial behavior per se and for
             self-reports of couple members' tendencies to associate with
             antisocial peers (0.54 on average). Perceptions about the
             likelihood of social sanctions for antisocial behavior
             (e.g., being caught by the authorities or losing the respect
             of one's family) showed moderate assortative mating (0.32 on
             average). However, assortative mating for personality traits
             related to antisocial behavior was low (0.15 on average).
             These findings suggest that, whereas assortative mating for
             many individual-difference variables (such as personality
             traits) is low, assortative mating for actual antisocial
             behaviors is substantial. We conclude that future family
             studies of antisocial behavior should endeavor to measure
             and understand the influence of assortative mating. In
             addition, we outline a testable behavior-genetic model for
             the development of antisocial behavior, in which genes and
             environments promoting or discouraging antisocial behavior
             become concentrated within families (due to assortative
             mating), giving rise to widely varying individual
             developmental trajectories that are, nevertheless, similar
             within families.},
   Doi = {10.1023/a:1021419013124},
   Key = {fds253409}
}

@article{fds253411,
   Author = {Moffitt, TE and Brammer, GL and Caspi, A and Fawcett, JP and Raleigh, M and Yuwiler, A and Silva, P},
   Title = {Whole blood serotonin relates to violence in an
             epidemiological study.},
   Journal = {Biological psychiatry},
   Volume = {43},
   Number = {6},
   Pages = {446-457},
   Year = {1998},
   Month = {March},
   ISSN = {0006-3223},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/9532350},
   Abstract = {<h4>Background</h4>Clinical and animal studies suggest that
             brain serotonergic systems may regulate aggressive behavior;
             however, the serotonin/violence hypothesis has not been
             assessed at the epidemiological level. For study of an
             epidemiological sample we examined blood serotonin, because
             certain physiological and behavioral findings suggested that
             it might serve as an analog marker for serotonergic
             function.<h4>Methods</h4>Whole blood serotonin was measured
             in a representative birth cohort of 781 21-year-old women
             (47%) and men (53%). Violence was measured using cumulative
             court conviction records and participants' self-reports.
             Potential intervening factors addressed were: gender, age,
             diurnal variation, diet, psychiatric medications, illicit
             drug history, season of phlebotomy, plasma tryptophan,
             platelet count, body mass, suicide attempts, psychiatric
             diagnoses, alcohol, tobacco, socioeconomic status, IQ, and
             overall criminal offending.<h4>Results</h4>Whole blood
             serotonin related to violence among men but not women.
             Violent men's mean blood serotonin level was 0.48 SD above
             the male population norm and 0.56 SD above the mean of
             nonviolent men. The finding was specific to violence, as
             opposed to general crime, and it was robust across two
             different methods of measuring violence. Together, the
             intervening variables accounted for 25% of the relation
             between blood serotonin and violence.<h4>Conclusions</h4>To
             our knowledge, this is the first demonstration that an index
             of serotonergic function is related to violence in the
             general population.},
   Doi = {10.1016/s0006-3223(97)00340-5},
   Key = {fds253411}
}

@article{fds253177,
   Author = {Moffitt, TE and Caspi, A},
   Title = {Annotation: implications of violence between intimate
             partners for child psychologists and psychiatrists.},
   Journal = {Journal of child psychology and psychiatry, and allied
             disciplines},
   Volume = {39},
   Number = {2},
   Pages = {137-144},
   Year = {1998},
   Month = {February},
   ISSN = {0021-9630},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/9669227},
   Doi = {10.1111/1469-7610.00308},
   Key = {fds253177}
}

@article{fds253413,
   Author = {Hankin, BL and Abramson, LY and Moffitt, TE and Silva, PA and McGee, R and Angell, KE},
   Title = {Development of depression from preadolescence to young
             adulthood: emerging gender differences in a 10-year
             longitudinal study.},
   Journal = {Journal of abnormal psychology},
   Volume = {107},
   Number = {1},
   Pages = {128-140},
   Year = {1998},
   Month = {February},
   ISSN = {0021-843X},
   url = {http://dx.doi.org/10.1037//0021-843x.107.1.128},
   Abstract = {The authors investigated the emergence of gender differences
             in clinical depression and the overall development of
             depression from preadolescence to young adulthood among
             members of a complete birth cohort using a prospective
             longitudinal approach with structured diagnostic interviews
             administered 5 times over the course of 10 years. Small
             gender differences in depression (females greater than
             males) first began to emerge between the ages of 13 and 15.
             However, the greatest increase in this gender difference
             occurred between ages 15 and 18. Depression rates and
             accompanying gender differences for a university student
             subsample were no different than for a nonuniversity
             subsample. There was no gender difference for depression
             recurrence or for depression symptom severity. The peak
             increase in both overall rates of depression and new cases
             of depression occurred between the ages of 15 and 18.
             Results suggest that middle-to-late adolescence (ages 15-18)
             may be a critical time for studying vulnerability to
             depression because of the higher depression rates and the
             greater risk for depression onset and dramatic increase in
             gender differences in depression during this
             period.},
   Doi = {10.1037//0021-843x.107.1.128},
   Key = {fds253413}
}

@article{fds253404,
   Author = {Caspi, A and Moffitt, TE and Entner Wright and BR and Suva,
             PA},
   Title = {Early failure in the labor market: childhood and adolescent
             predictors of unemployment in the transition to
             adulthood},
   Journal = {American Sociological Review},
   Volume = {63},
   Number = {3},
   Pages = {424-451},
   Publisher = {SAGE Publications},
   Year = {1998},
   Month = {January},
   ISSN = {0003-1224},
   url = {http://dx.doi.org/10.2307/2657557},
   Abstract = {We investigate the childhood and adolescent predictors of
             youth unemployment in a US longitudinal study of young
             adults who have been studied for the 21 years since their
             births in 1972-1973. We test hypotheses about the predictors
             of youth unemployment using information about each
             individual's human capital, social capital, and personal
             capital. In the human capital domain, lack of high-school
             qualifications, poor reading skills, low IQ scores, and
             limited parental resources significantly increased the risk
             of unemployment. In the social capital domain, growing up in
             a single-parent family, family conflict, and lack of
             attachment to school also increased the risk of
             unemployment. In the personal capital domain, children
             involved in antisocial behavior had an increased risk of
             unemployment. These predictors of unemployment reached back
             to early childhood, suggesting that they began to shape
             labor-market outcomes years before these youths entered the
             work force. In addition, these effects remained significant
             after controlling for the duration of education and
             educational attainment, suggesting that many early personal
             and family characteristics affect labor-market outcomes, not
             only because they restrict the accumulation of human capital
             (e.g., education), but also because they directly affect
             labor-market behaviors. Failure to account for prior social,
             psychological, and economic risk factors may lead to
             inflated estimates of the effects of unemployment on future
             outcomes.},
   Doi = {10.2307/2657557},
   Key = {fds253404}
}

@article{fds253410,
   Author = {Entner Wright and BR and Caspi, A and Moffitt, TE and Silva,
             PA},
   Title = {Factors Associated with Doubled-Up Housing - A Common
             Precursor to Homelessness},
   Journal = {Social Service Review},
   Volume = {72},
   Number = {1},
   Pages = {92-111},
   Publisher = {University of Chicago Press},
   Year = {1998},
   Month = {January},
   url = {http://dx.doi.org/10.1086/515747},
   Abstract = {Previous research on housing problems has concentrated on
             the more visible homelessness rather than more intermediate
             forms of housing problems such as doubled-up housing. This
             article expands this research by analyzing entrance into
             doubled-up housing among a sample of adolescents. This
             common type of vulnerable housing has been linked to various
             social and psychological problems. It commonly precedes
             homelessness, and it potentially increases the risk of
             homelessness. We find that doubled-up housing frequently
             occurs during young adulthood and is predicted by
             insufficient human capital, broken social ties, and personal
             disabilities.},
   Doi = {10.1086/515747},
   Key = {fds253410}
}

@article{fds253412,
   Author = {Magdol, L and Moffitt, TE and Caspi, A and Silva,
             PA},
   Title = {Hitting without a license: Testing explanations for
             differences in partner abuse between young adult daters and
             cohabitors},
   Journal = {Journal of Marriage and Family},
   Volume = {60},
   Number = {1},
   Pages = {41-55},
   Publisher = {JSTOR},
   Year = {1998},
   Month = {January},
   url = {http://dx.doi.org/10.2307/353440},
   Abstract = {We compared partner abuse by cohabitors and daters among
             21-year-olds. Cohabitors were significantly more likely than
             daters to perform abusive behaviors. We identified factors
             that differentiate cohabitors from daters and tested whether
             these factors explained the difference in partner abuse. As
             controls in regression models predicting abuse, none of
             these factors individually explained the difference in
             partner abuse between cohabitors and daters. With all
             factors added to the model simultaneously, the effect of
             cohabitation remained significant, but was substantially
             reduced. These findings have intervention implications
             because premarital cohabitation is a risk factor for abuse
             after marriage.},
   Doi = {10.2307/353440},
   Key = {fds253412}
}

@article{fds253414,
   Author = {Danielson, KK and Moffitt, TE and Caspi, A and Silva,
             PA},
   Title = {Comorbidity between abuse of an adult and DSM-III-R mental
             disorders: evidence from an epidemiological
             study.},
   Journal = {The American journal of psychiatry},
   Volume = {155},
   Number = {1},
   Pages = {131-133},
   Year = {1998},
   Month = {January},
   ISSN = {0002-953X},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/9433353},
   Abstract = {<h4>Objective</h4>The purpose of this study was to report
             the prevalence, risk, and implications of comorbidity
             between partner violence and psychiatric
             disorders.<h4>Method</h4>Data were obtained from a
             representative birth cohort of 941 young adults through use
             of the Conflict Tactics Scales and Diagnostic Interview
             Schedule.<h4>Results</h4>Half of those involved in partner
             violence had a psychiatric disorder; one-third of those with
             a psychiatric disorder were involved in partner violence.
             Individuals involved in severe partner violence had elevated
             rates of a wide spectrum of disorders.<h4>Conclusions</h4>The
             findings support the importance of mental health clinicians
             screening for partner violence and treating victims and
             perpetrators before injury occurs.},
   Doi = {10.1176/ajp.155.1.131},
   Key = {fds253414}
}

@article{fds69875,
   Author = {Bardone, A. and Moffitt, T.E. and Caspi, A. and Dickson, N. and Stanton, W. and Silva, P.A},
   Title = {Adult physical health outcomes of adolescent girls with
             conduct disorder, depression or anxiety},
   Journal = {Journal of the American Academy of Child and Adolescent
             Psychiatry},
   Volume = {37},
   Pages = {594-601},
   Year = {1998},
   Key = {fds69875}
}

@article{fds253402,
   Author = {Loeber, R and Farrington, DP and Stouthamer Loeber and M and Moffitt,
             TE and Caspi, A},
   Title = {The development of male offending: Key findings from the
             first decade of the Pittsburgh Youth Study},
   Journal = {Studies on Crime and Prevention},
   Volume = {7},
   Pages = {1-31},
   Year = {1998},
   Key = {fds253402}
}

@article{fds253415,
   Author = {Moffitt, TE and Caspi, A},
   Title = {Implications of violence between intimate partners for child
             psychologists and psychiatrists},
   Journal = {Journal of Child Psychology and Psychiatry},
   Volume = {39},
   Pages = {137-144},
   Year = {1998},
   Key = {fds253415}
}

@article{fds253417,
   Author = {Caspi, A and Begg, D and Dickson, N and Harrington, H and Langley, J and Moffitt, TE and Silva, PA},
   Title = {Personality differences predict health-risk behaviors in
             young adulthood: evidence from a longitudinal
             study.},
   Journal = {Journal of personality and social psychology},
   Volume = {73},
   Number = {5},
   Pages = {1052-1063},
   Year = {1997},
   Month = {November},
   ISSN = {0022-3514},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/9364760},
   Abstract = {In a longitudinal study of a birth cohort, the authors
             identified youth involved in each of 4 different health-risk
             behaviors at age 21: alcohol dependence, violent crime,
             unsafe sex, and dangerous driving habits. At age 18, the
             Multidimensional Personality Questionnaire (MPQ) was used to
             assess 10 distinct personality traits. At age 3,
             observational measures were used to classify children into
             distinct temperament groups. Results showed that a similar
             constellation of adolescent personality traits, with
             developmental origins in childhood, is linked to different
             health-risk behaviors at 21. Associations between the same
             personality traits and different health-risk behaviors were
             not an artifact of the same people engaging in different
             health-risk behaviors; rather, these associations implicated
             the same personality type in different but related
             behaviors. In planning campaigns, health professionals may
             need to design programs that appeal to the unique
             psychological makeup of persons most at risk for health-risk
             behaviors.},
   Doi = {10.1037//0022-3514.73.5.1052},
   Key = {fds253417}
}

@article{fds304706,
   Author = {Moffitt, TE},
   Title = {Helping poor mothers and children.},
   Journal = {JAMA},
   Volume = {278},
   Number = {8},
   Pages = {680-681},
   Year = {1997},
   Month = {August},
   ISSN = {0098-7484},
   url = {http://dx.doi.org/10.1001/jama.1997.03550080090046},
   Doi = {10.1001/jama.1997.03550080090046},
   Key = {fds304706}
}

@article{fds253419,
   Author = {Moffitt, TE and Caspi, A and Krueger, RF and Magdol, L and Margolin, G and Silva, PA and Sydney, R},
   Title = {Do partners agree about abuse in their relationship? A
             psychometric evaluation of interpartner agreement},
   Journal = {Psychological Assessment},
   Volume = {9},
   Number = {1},
   Pages = {47-56},
   Publisher = {American Psychological Association (APA)},
   Year = {1997},
   Month = {March},
   ISSN = {1040-3590},
   url = {http://dx.doi.org/10.1037/1040-3590.9.1.47},
   Abstract = {This study tested whether partners can be relied on to
             provide congruent reports about abuse in their relationship.
             The authors examined whether interpartner agreement (IA)
             varies as a function of whether the perpetrator is the man
             or the woman, and by whether the abusive behavior being
             reported is physical or psychological. Guided by
             psychometric test theory, the authors examined whether weak
             14 about specific behaviors can be improved by aggregating
             behavior items into scales and by controlling for random
             measurement error. A representative sample of 360 young
             couples was studied. IA did not vary with the perpetrator's
             gender or with the nature of the abusive behaviors, but
             victims (both men and women) reported somewhat more abuse
             than did their perpetrators. IA about specific abusive
             behaviors was only poor to fair, but it became very good
             when items were aggregated into scales and even better when
             measurement errors were removed from the reports. The
             findings suggest that reports of abuse can be aggregated to
             form internally consistent scales that show strong IA,
             thereby fulfilling criteria for reliability. Moreover under
             research conditions that guarantee confidentiality, either
             abuser reports or victim reports are suitable methods for
             use in research on partner abuse.},
   Doi = {10.1037/1040-3590.9.1.47},
   Key = {fds253419}
}

@article{fds253421,
   Author = {Newman, DL and Caspi, A and Moffitt, TE and Silva,
             PA},
   Title = {Antecedents of adult interpersonal functioning: effects of
             individual differences in age 3 temperament.},
   Journal = {Developmental psychology},
   Volume = {33},
   Number = {2},
   Pages = {206-217},
   Year = {1997},
   Month = {March},
   ISSN = {0012-1649},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/9147830},
   Abstract = {We examined whether temperamental differences at age 3 are
             linked to interpersonal functioning in young adulthood. In a
             sample of over 900 children, we identified 5 distinct groups
             of children based on behavioral observations: Well-adjusted,
             undercontrolled, reserved, confident, and inhibited. At age
             21, we assessed the children's interpersonal functioning in
             4 social contexts: in the social network, at home, in
             romantic relationships, and at work. We found three patterns
             of relations: (a) Well-adjusted, reserved, and confident
             children defined a heterogeneous range of normative adult
             interpersonal behavior, (b) inhibited children had lower
             levels of social support but normative adjustment in
             romantic relationships and at work, and (c) undercontrolled
             children had lower levels of adjustment and greater
             interpersonal conflict across adult social
             contexts.},
   Doi = {10.1037//0012-1649.33.2.206},
   Key = {fds253421}
}

@article{fds253423,
   Author = {Poulton, RG and Brooke, M and Moffitt, TE and Stanton, WR and Silva,
             PA},
   Title = {Prevalence and correlates of cannabis use and dependence in
             young New Zealanders.},
   Journal = {The New Zealand medical journal},
   Volume = {110},
   Number = {1039},
   Pages = {68-70},
   Year = {1997},
   Month = {March},
   Abstract = {<h4>Aims</h4>To determine change in patterns of cannabis use
             in New Zealand in an unselected birth cohort and investigate
             the relationship between level of cannabis use, violent
             behaviour and employment history.<h4>Method</h4>Prospective
             longitudinal design using members of the Dunedin
             Multidisciplinary Health and Development Study at ages 15,
             18 and 21 years.<h4>Results</h4>Rates of cannabis use
             increased from 15% (n = 144) at age 15 years to more than
             half of the sample seen at age 21 years (n = 497; 52.4%).
             DSM-III-R defined cannabis dependence assessed at age 18 and
             21 years increased from 6.6% (n = 61) to 9.6% (n = 91).
             Males were more likely to use and be dependent on cannabis
             than females. Early use substantially increased the risk for
             the development of cannabis dependence in young adulthood.
             Cross-sectional analysis at age 21 found levels of cannabis
             use and dependence to be higher among the unemployed and
             those with a history of violent behaviour.<h4>Conclusions</h4>Prevalence
             rates of cannabis use in young New Zealanders were found to
             be higher than previously reported. A history of
             unemployment or of violent behaviour was associated with
             more frequent cannabis use at age 21. Males were more likely
             than females to use cannabis frequently and to meet
             DSM-III-R criteria for dependence at age 21. It is suggested
             that drug education campaigns should specifically target
             young males.},
   Key = {fds253423}
}

@article{fds253422,
   Author = {Magdol, L and Moffitt, TE and Caspi, A and Newman, DL and Fagan, J and Silva, PA},
   Title = {Gender differences in partner violence in a birth cohort of
             21-year-olds: bridging the gap between clinical and
             epidemiological approaches.},
   Journal = {Journal of consulting and clinical psychology},
   Volume = {65},
   Number = {1},
   Pages = {68-78},
   Year = {1997},
   Month = {February},
   ISSN = {0022-006X},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/9103736},
   Abstract = {This study describes partner violence in a representative
             sample of young adults. Physical violence perpetration was
             reported by 37.2% of women and 21.8% of men. Correlates of
             involvement in severe physical violence differed by gender.
             Severe physical violence was more strongly associated with
             unemployment, low educational attainment, few social support
             resources, polydrug use, antisocial personality disorder
             symptoms, depression symptoms, and violence toward strangers
             for men than for women. Women who were victims of severe
             physical violence were more likely than men who were victims
             to experience symptoms of anxiety. The findings converge
             with community studies showing that more women than men are
             physically violent toward a partner and with clinical
             studies highlighting violence perpetrated against women by
             men with deviant characteristics.},
   Doi = {10.1037//0022-006x.65.1.68},
   Key = {fds253422}
}

@article{fds253420,
   Author = {Jeglum Bartusch and DR and Lynam, DR and Moffitt, TE and Silva,
             PA},
   Title = {Is age important? Testing a general versus a developmental
             theory of antisocial behavior},
   Journal = {Criminology},
   Volume = {35},
   Number = {1},
   Pages = {13-48},
   Publisher = {WILEY},
   Year = {1997},
   Month = {January},
   url = {http://dx.doi.org/10.1111/j.1745-9125.1997.tb00869.x},
   Abstract = {We tested competing hypotheses derived from Gottfredson and
             Hirschi's (1990) general theory and Moffitt's (1993a)
             developmental theory of antisocial behavior. The
             developmental theory argues that different factors give rise
             to antisocial behavior at different points in the life
             course. In contrast, the general theory maintains that the
             factor underlying antisocial behavior (i.e., criminal
             propensity) is the same at all ages. To test these competing
             predictions, we used longitudinal data spanning from age 5
             to age 18 for the male subjects in the Dunedin
             Multidisciplinary Health and Development Study. Using
             reports from three sources (parents, teachers, and the boys
             themselves), we estimated second-order confirmatory factor
             models of antisocial behavior. These models provided
             consistent support for the developmental theory, showing
             that separate latent factors underlie childhood and
             adolescent antisocial behavior. Moreover, we found that
             these childhood and adolescent factors related in ways
             predicted by Moffitt's developmental theory to four
             correlates of antisocial behavior: Childhood antisocial
             behavior was related more strongly than adolescent
             antisocial behavior to low verbal ability, hyperactivity,
             and negative/impulsive personality, whereas adolescent
             antisocial behavior was related more strongly than childhood
             antisocial behavior to peer delinquency. The two underlying
             latent factors also showed the predicted differential
             relations to later criminal convictions: Childhood
             antisocial behavior was significantly more strongly
             associated with convictions for violence, while adolescent
             antisocial behavior was significantly more strongly
             associated with convictions for nonviolent
             offenses.},
   Doi = {10.1111/j.1745-9125.1997.tb00869.x},
   Key = {fds253420}
}

@article{fds69854,
   Author = {Magdol, L. and Moffitt, T.E. and Caspi, A. and Newman, D.L. and Fagan, J. and Silva, P.A},
   Title = {Gender differences in partner violence in a birth cohort of
             21-years-olds: Bridging the gap between clinical and
             epidemiological approaches},
   Journal = {Journal of Consulting and Clinical Psychology},
   Volume = {65},
   Pages = {68-78},
   Year = {1997},
   Key = {fds69854}
}

@article{fds69859,
   Author = {Caspi, A. and Begg, D. and Dickson, N. and Harrington, H. and Langley, J.D. and Moffitt, T.E. and Silva, P.A},
   Title = {Personality traits predicts health-risk behaviors in young
             adulthood: Evidence from a longitudinal study},
   Journal = {Journal of Personality and Social Psychology},
   Volume = {73},
   Pages = {1052-1063},
   Year = {1997},
   Key = {fds69859}
}

@article{fds253416,
   Author = {Caspi, A and Wright, B and Moffitt, TE and Silva,
             PA},
   Title = {Predictors of youth unemployment},
   Journal = {Focus},
   Volume = {19},
   Number = {1},
   Pages = {34-35},
   Year = {1997},
   Key = {fds253416}
}

@article{fds253418,
   Author = {Moffitt, TE},
   Title = {Editorial: Helping poor mothers and children},
   Journal = {Journal of the American Medical Association},
   Volume = {278},
   Number = {8},
   Pages = {680-681},
   Year = {1997},
   ISSN = {0098-7484},
   Key = {fds253418}
}

@article{fds340560,
   Author = {Begg, DJ and Langley, JD and Moffitt, T and Marshall,
             SW},
   Title = {Sport and delinquency: an examination of the deterrence
             hypothesis in a longitudinal study.},
   Journal = {British journal of sports medicine},
   Volume = {30},
   Number = {4},
   Pages = {335-341},
   Year = {1996},
   Month = {December},
   url = {http://dx.doi.org/10.1136/bjsm.30.4.335},
   Abstract = {<h4>Objective</h4>To determine whether involvement in
             sporting activity in mid-adolescence would deter delinquent
             behaviour in late adolescence.<h4>Methods</h4>Members of a
             longitudinal cohort study were interviewed at ages 15 and 18
             years and, among other topics, were asked questions relating
             to involvement in physical activity and delinquent
             behaviour. Logistic regression models were used to examine
             the relation between sports involvement and delinquency at
             age 15 years and delinquency at age 18.<h4>Results</h4>After
             controlling for delinquent behaviour and psychosocial
             factors at age 15, females with moderate or high levels of
             sporting activity, and males with high levels of sporting
             activity, were significantly more likely to be delinquent at
             age 18 years than those with low levels of sporting
             activity. No significant association was found between
             sporting activity and aggressive behaviour, team sport
             participation and delinquency, and team sport participation
             and aggressive behaviour.<h4>Conclusions</h4>This study did
             not support the deterrence hypothesis and showed that high
             involvement in sporting activity, but not team sport, was
             associated with a subsequent increase in delinquent
             behaviour.},
   Doi = {10.1136/bjsm.30.4.335},
   Key = {fds340560}
}

@article{fds253427,
   Author = {Caspi, A and Moffitt, TE and Newman, DL and Silva,
             PA},
   Title = {Behavioral observations at age 3 years predict adult
             psychiatric disorders. Longitudinal evidence from a birth
             cohort.},
   Journal = {Archives of general psychiatry},
   Volume = {53},
   Number = {11},
   Pages = {1033-1039},
   Year = {1996},
   Month = {November},
   ISSN = {0003-990X},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/8911226},
   Abstract = {<h4>Background</h4>This study provides, to our knowledge,
             the first empirical test of whether behavioral differences
             among children in the first 3 years of life are linked to
             specific adult psychiatric disorders: anxiety and mood
             disorders, antisocial personality disorder, recidivistic and
             violent crime, alcoholism, and suicidal behavior.<h4>Methods</h4>In
             a longitudinal-epidemiological study, 3-year-old children
             were classified into groups based on examiner observations
             of their behavior. At age 21 years, they were reassessed for
             psychopathologic functioning using standardized interviews
             based on DSM-III-R criteria.<h4>Results</h4>Although effect
             sizes were small, undercontrolled (includes children who are
             impulsive, restless and distractible) and inhibited
             (includes children who are shy, fearful, and easily upset)
             children differed significantly from comparison children in
             young adulthood. Under-controlled 3-year-olds were more
             likely at 21 years to meet diagnostic criteria for
             antisocial personality disorder and to be involved in crime.
             Inhibited 3-year-olds were more likely at 21 years to meet
             diagnostic criteria for depression. Both groups were more
             likely to attempt suicide, and boys in both groups had
             alcohol-related problems. Controls for family social class
             did not change the findings.<h4>Conclusion</h4>Some forms of
             adult psychopathologic abnormality are meaningfully linked,
             albeit weakly, to behavioral differences observed among
             children in the third year of life.},
   Doi = {10.1001/archpsyc.1996.01830110071009},
   Key = {fds253427}
}

@article{fds253426,
   Author = {Krueger, RF and Caspi, A and Moffitt, TE and Silva, PA and McGee,
             R},
   Title = {Personality traits are differentially linked to mental
             disorders: a multitrait-multidiagnosis study of an
             adolescent birth cohort.},
   Journal = {Journal of abnormal psychology},
   Volume = {105},
   Number = {3},
   Pages = {299-312},
   Year = {1996},
   Month = {August},
   ISSN = {0021-843X},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/8772001},
   Abstract = {The authors assessed the relation between personality and
             mental disorder in a representative birth cohort of 897 men
             and women. Personality was assessed at age 18 with the
             Multidimensional Personality Questionnaire (MPQ; A.
             Tellegen, 1982), and 4 types of mental disorder (affective,
             anxiety, substance dependence, and conduct disorder) were
             assessed at ages 15, 18 and 21, using age-appropriate
             standardized diagnostic interviews. All disorder groups had
             MPQ profiles that were very different from those of
             controls. When comorbid cases were excluded, fewer
             significant differences between diagnosed cases and controls
             remained. Relations between personality and mental disorder
             were not affected by the measurement of disorder as
             continuous versus discrete, gender, or the age at which
             disorder was diagnosed. Relations between personality and
             mental disorders appear to be robust, and individual
             personality differences may be particularly relevant to
             understanding the most severe (comorbid) expressions of
             psychopathology.},
   Doi = {10.1037//0021-843x.105.3.299},
   Key = {fds253426}
}

@article{fds253430,
   Author = {Newman, DL and Moffitt, TE and Caspi, A and Magdol, L and Silva, PA and Stanton, WR},
   Title = {Psychiatric disorder in a birth cohort of young adults:
             prevalence, comorbidity, clinical significance, and new case
             incidence from ages 11 to 21.},
   Journal = {Journal of consulting and clinical psychology},
   Volume = {64},
   Number = {3},
   Pages = {552-562},
   Year = {1996},
   Month = {June},
   ISSN = {0022-006X},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/8698949},
   Abstract = {Mental health data were gathered at ages 11, 13, 15, 18, and
             21 in an epidemiological sample using standardized
             diagnostic assessments. Prevalence of Diagnostic and
             Statistical Manual of Mental Disorders (3rd ed. revised;
             American Psychiatric Association, 1987) mental disorders
             increased longitudinally from late childhood (18%) through
             mid-(22%) to late-adolescence (41%) and young adulthood
             (40%). Nearly half of age-21 cases had comorbid diagnoses;
             and comorbidity was associated with severity of impairment.
             The incidence of cases with adult onset was only 10.6%:
             73.8% of adults diagnosed at age 21 had a developmental
             history of mental disorder. Relative to new cases, those
             with developmental histories were more severely impaired and
             more likely to have comorbid diagnoses. The high prevalence
             rate and significant impairment associated with a diagnosis
             of mental disorder suggests that treatment resources need to
             target the young adult sector of the population. The low
             new-case incidence in young adulthood, however, suggests
             that primary prevention and etiological research efforts
             need to target children and adolescents.},
   Doi = {10.1037//0022-006x.64.3.435},
   Key = {fds253430}
}

@article{fds253431,
   Author = {Krueger, RF and Caspi, A and Moffitt, TE and White, J and Stouthamer-Loeber, M},
   Title = {Delay of gratification, psychopathology, and personality: is
             low self-control specific to externalizing
             problems?},
   Journal = {Journal of personality},
   Volume = {64},
   Number = {1},
   Pages = {107-129},
   Year = {1996},
   Month = {March},
   ISSN = {0022-3506},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/8656312},
   Abstract = {We assessed the delay of gratification behavior of 428
             twelve- and thirteen-year-old boys, half of whom were known
             to manifest symptoms of behavioral disturbance. Consistent
             with the hypothesis that low self-control is a risk factor
             specific to externalizing (aggressive and delinquent)
             disorders, boys who showed signs of externalizing disorders
             tended to seek immediate gratification in a laboratory task
             more often than both nondisordered boys and boys who showed
             signs of internalizing (anxious and depressed) disorders. In
             addition, children who were able to delay immediate
             gratification were described by their mothers as ego
             controlled, ego resilient, conscientious, open to
             experience, and agreeable. These results suggest that poor
             delay of gratification may be one of a select number of
             specific risk factors for externalizing disorder, and that
             good delay of gratification is linked to multiple adaptive
             tendencies in early adolescence.},
   Doi = {10.1111/j.1467-6494.1996.tb00816.x},
   Key = {fds253431}
}

@article{fds304727,
   Author = {Moffitt, TE},
   Title = {Measuring children's antisocial behaviors.},
   Journal = {JAMA},
   Volume = {275},
   Number = {5},
   Pages = {403-404},
   Year = {1996},
   Month = {February},
   ISSN = {0098-7484},
   url = {http://dx.doi.org/10.1001/jama.1996.03530290073041},
   Doi = {10.1001/jama.1996.03530290073041},
   Key = {fds304727}
}

@article{fds253424,
   Author = {Bardone, AM and Moffitt, TE and Caspi, A and Dickson, N and Silva,
             PA},
   Title = {Adult mental health and social outcomes of adolescent girls
             with depression and conduct disorder},
   Journal = {Development and Psychopathology},
   Volume = {8},
   Number = {4},
   Pages = {811-829},
   Publisher = {Cambridge University Press (CUP)},
   Year = {1996},
   Month = {January},
   url = {http://dx.doi.org/10.1017/s0954579400007446},
   Abstract = {Follow-up studies of adolescent depression and conduct
             disorder have pointed to homotypic continuity, but less
             information exists about outcomes beyond mental disorders
             and about the extent to which adolescents with different
             disorders experience different versus similar difficulties
             during the transition to adulthood. We assessed the
             continuity of adolescent disorder by following girls in a
             complete birth cohort who at age 15 were depressed (n = 27),
             conduct disordered (n = 37), or without a mental health
             disorder (n = 341) into young adulthood (age 21) to identify
             their outcomes in three domains: mental health and illegal
             behavior, human capital, and relationship and family
             formation. We found homotypic continuity; in general,
             depressed girls became depressed women and conduct
             disordered girls developed antisocial personality disorder
             symptoms by age 21. Conduct disorder exclusively predicted
             at age 21: antisocial personality disorder, substance
             dependence, illegal behavior, dependence on multiple welfare
             sources, early home leaving, multiple cohabitation partners,
             and physical partner violence. Depression exclusively
             predicted depression at age 21. Examples of equifinality
             (where alternate pathways lead to the same outcome)
             surfaced, as both adolescent disorders predicted at age 21:
             anxiety disorder, multiple drug use, early school leaving,
             low school attainment, any cohabitation, pregnancy, and
             early child bearing.},
   Doi = {10.1017/s0954579400007446},
   Key = {fds253424}
}

@article{fds253428,
   Author = {Caspi, A and Moffitt, TE and Thornton, A and Freedman, D and Amell, JW and Harrington, H and Smeijers, J and Silva, PA},
   Title = {The Life History Calendar: A Research and clinical
             assessment method for collecting retrospective event-history
             data},
   Journal = {International Journal of Methods in Psychiatric
             Research},
   Volume = {6},
   Number = {2},
   Pages = {101-114},
   Publisher = {WILEY},
   Year = {1996},
   Month = {January},
   ISSN = {1049-8931},
   url = {http://dx.doi.org/10.1002/(SICI)1234-988X(199607)6:2<101::AID-MPR156>3.3.CO;2-},
   Abstract = {This article describes the Life History Calendar (LHC), a
             data-collection method for obtaining reliable retrospective
             data about life events and activities. The LHC method was
             developed in the context of longitudinal research to record
             central events that can occur in a respondent's life. The
             LHC can be used as both a research and a clinical assessment
             method. As a research instrument, the LHC can be used to
             collect detailed event-history data for analyzing
             life-course dynamics. As a clinical instrument, the LHC can
             be used both as an assessment tool and as a therapeutic
             guide. In this article, we explain the need for a LHC when
             studying life-course dynamics; describe the advantages of
             the LHC method; present data about the validity of the LHC;
             describe research and clinical uses of the LHC; and discuss
             the design of the LHC and offer suggestions about how to
             tailor LHC's for unique research and clinical purposes. ©
             1996 by John Wiley & Sons, Ltd.},
   Doi = {10.1002/(SICI)1234-988X(199607)6:2<101::AID-MPR156>3.3.CO;2-},
   Key = {fds253428}
}

@article{fds253429,
   Author = {Henry, B and Caspi, A and Moffitt, TE and Silva, PA},
   Title = {Temperamental and familial predictors of violent and
             nonviolent criminal convictions: Age 3 to age
             18},
   Journal = {Developmental Psychology},
   Volume = {32},
   Number = {4},
   Pages = {614-623},
   Publisher = {American Psychological Association (APA)},
   Year = {1996},
   Month = {January},
   ISSN = {0012-1649},
   url = {http://dx.doi.org/10.1037/0012-1649.32.4.614},
   Abstract = {This study examined the relations between family
             characteristics, childhood temperament, and convictions for
             violent and nonviolent offenses at age 18 in a
             representative birth cohort of men who are part of a
             longitudinal study. Three groups of men were identified on
             the basis of their conviction status at age 18: Participants
             who had never been convicted (n = 404), participants who had
             been convicted for nonviolent offenses only (n = 50), and
             participants who had been convicted for violent offenses (n
             = 21). Multivariate analysis of variance and logistic
             regression analyses indicated that family factors were
             associated with both types of conviction outcomes, whereas
             childhood temperament was associated primarily with
             convictions for violent offenses. The potentially distinct
             roles of social- and self-regulation in the development of
             antisocial behavior are discussed.},
   Doi = {10.1037/0012-1649.32.4.614},
   Key = {fds253429}
}

@article{fds253433,
   Author = {Moffitt, TE and Caspi, A and Dickson, N and Silva, P and Stanton,
             W},
   Title = {Childhood-onset versus adolescent-onset antisocial conduct
             problems in males: Natural history from ages 3 to 18
             years},
   Journal = {Development and Psychopathology},
   Volume = {8},
   Number = {2},
   Pages = {399-424},
   Publisher = {Cambridge University Press (CUP)},
   Year = {1996},
   Month = {January},
   url = {http://dx.doi.org/10.1017/s0954579400007161},
   Abstract = {We report data that support the distinction between
             childhood-onset and adolescent-onset type conduct problems.
             Natural histories are described from a representative birth
             cohort of 457 males studied longitudinally from age 3 to 18
             years. Childhood- and adolescent-onset cases differed on
             temperament as early as age 3 years, but almost half of
             childhood-onset cases did not become seriously delinquent.
             Type comparisons were consistent with our contention that
             males whose antisocial behavior follows a
             life-course-persistent path differ from males who follow an
             adolescence-limited path. As adolescents, the two types
             differed on convictions for violent crime, personality
             profiles, school leaving, and bonds to family. These
             differences can be attributed to developmental history
             because the two groups were well matched on measures of
             antisocial conduct at age 18 years: parent-reports,
             self-reports, and adjudication records. By age 18 years,
             many conduct-problem boys had encountered factors that could
             ensnare them in an antisocial future: substance dependence,
             unsafe sex, dangerous driving habits, delinquent friends,
             delinquent perceptions, and unemployment. Implications for
             theory, research design, prevention, and therapeutic
             treatment of conduct problems are highlighted.},
   Doi = {10.1017/s0954579400007161},
   Key = {fds253433}
}

@article{fds253434,
   Author = {Robins, RW and John, OP and Caspi, A and Moffitt, TE and Stouthamer-Loeber, M},
   Title = {Resilient, overcontrolled, and undercontrolled boys: three
             replicable personality types.},
   Journal = {Journal of personality and social psychology},
   Volume = {70},
   Number = {1},
   Pages = {157-171},
   Year = {1996},
   Month = {January},
   ISSN = {0022-3514},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/8558407},
   Abstract = {Three replicable personality types were identified in a
             sample of 300 adolescent boys and shown to generalize across
             African Americans and Caucasians. The types had conceptually
             coherent relations with the Big Five dimensions, ego
             resiliency, and ego control, and converged with three of the
             types identified by J. Block (1971). The behavioral
             implications of the types were explored using several
             independent data sources. Resilients were intelligent,
             successful in school, unlikely to be delinquents, and
             relatively free of psychopathology; Overcontrollers shared
             some of these characteristics but were also prone to
             internalizing problems; and Undercontrollers showed a
             general pattern of academic, behavioral, and emotional
             problems. This research demonstrates that replicable and
             generalizable personality types can be identified
             empirically, and that the unique constellation of traits
             defining an individual has important consequences for a wide
             range of outcomes.},
   Doi = {10.1037//0022-3514.70.1.157},
   Key = {fds253434}
}

@article{fds253435,
   Author = {Fergusson, DM and Horwood, LJ and Caspi, A and Moffitt, TE and Silva,
             PA},
   Title = {The (artefactual) remission of reading disability:
             Psychometric lessons in the study of stability and change in
             behavioral development},
   Journal = {Developmental Psychology},
   Volume = {32},
   Number = {1},
   Pages = {132-140},
   Publisher = {American Psychological Association (APA)},
   Year = {1996},
   Month = {January},
   ISSN = {0012-1649},
   url = {http://dx.doi.org/10.1037/0012-1649.32.1.132},
   Abstract = {Patterns of reading disability were examined in 2
             longitudinal studies. The major findings were (a) that on
             the basis of the observed data, remission of reading
             disability was relatively common with up to 37% of
             reading-disabled children showing remission of this
             disability within a 2-year period, and (b) when the data
             were analyzed with a latent Markov model that took account
             of measurement errors in test scores, the estimated true
             rate of remission of reading disability was between 15% and
             19% over a 2-year period. The presence of measurement error
             in reading disability classifications may lead to an
             inflated and misleading impression of the rate of remission
             of these problems. General implications of these findings
             for interpreting patterns of stability and change in
             longitudinal-developmental data were discussed. Copyright
             1996 by the American Psychological Association,
             Inc.},
   Doi = {10.1037/0012-1649.32.1.132},
   Key = {fds253435}
}

@article{fds69842,
   Author = {Newman, D. and Moffitt, T.E. and Caspi, A. Magdol and L., Silva and P.A. and Stanton, W},
   Title = {Psychiatric disorder in a birth cohort of young adults:
             Prevalence, co-morbidity, clinical significance, and new
             case incidence from age 11 to 21},
   Journal = {Journal of Consulting and Clinical Psychology},
   Volume = {64},
   Pages = {552-562},
   Year = {1996},
   Key = {fds69842}
}

@article{fds253425,
   Author = {Begg, DJ and Langley, JD and Moffitt, TE and Marshall,
             SW},
   Title = {Sport and delinquency: A longitudinal study of the
             deterrence hypothesis},
   Journal = {British Journal of Sports Medicine},
   Volume = {30},
   Pages = {1-7},
   Year = {1996},
   Key = {fds253425}
}

@article{fds253432,
   Author = {Moffitt, TE},
   Title = {Editorial: Measuring children's antisocial
             behaviors},
   Journal = {Journal of the American Medical Association},
   Volume = {275},
   Number = {5},
   Pages = {403-404},
   Year = {1996},
   ISSN = {0098-7484},
   url = {http://dx.doi.org/10.1001/jama.275.5.403},
   Doi = {10.1001/jama.275.5.403},
   Key = {fds253432}
}

@article{fds253437,
   Author = {Keltner, D and Moffitt, TE and Stouthamer-Loeber,
             M},
   Title = {Facial expressions of emotion and psychopathology in
             adolescent boys.},
   Journal = {Journal of abnormal psychology},
   Volume = {104},
   Number = {4},
   Pages = {644-652},
   Year = {1995},
   Month = {November},
   ISSN = {0021-843X},
   url = {http://dx.doi.org/10.1037//0021-843x.104.4.644},
   Abstract = {On the basis of the widespread belief that emotions underpin
             psychological adjustment, the authors tested 3 predicted
             relations between externalizing problems and anger,
             internalizing problems and fear and sadness, and the absence
             of externalizing problems and social-moral emotion
             (embarrassment). Seventy adolescent boys were classified
             into 1 of 4 comparison groups on the basis of teacher
             reports using a behavior problem checklist: internalizers,
             externalizers, mixed (both internalizers and externalizers),
             and nondisordered boys. The authors coded the facial
             expressions of emotion shown by the boys during a structured
             social interaction. Results supported the 3 hypotheses: (a)
             Externalizing adolescents showed increased facial
             expressions of anger, (b) on 1 measure internalizing
             adolescents showed increased facial expressions of fear, and
             (c) the absence of externalizing problems (or nondisordered
             classification) was related to increased displays of
             embarrassment. Discussion focused on the relations of these
             findings to hypotheses concerning the role of impulse
             control in antisocial behavior.},
   Doi = {10.1037//0021-843x.104.4.644},
   Key = {fds253437}
}

@article{fds253438,
   Author = {Douglass, HM and Moffitt, TE and Dar, R and McGee, R and Silva,
             P},
   Title = {Obsessive-compulsive disorder in a birth cohort of
             18-year-olds: prevalence and predictors.},
   Journal = {Journal of the American Academy of Child and Adolescent
             Psychiatry},
   Volume = {34},
   Number = {11},
   Pages = {1424-1431},
   Year = {1995},
   Month = {November},
   url = {http://dx.doi.org/10.1097/00004583-199511000-00008},
   Abstract = {<h4>Objective</h4>To report descriptive epidemiological
             information on obsessive-compulsive disorder (OCD) in an
             unselected birth cohort of 930 males and females, aged 18
             years.<h4>Method</h4>An epidermiological study of the
             prevalence of self-reported OCD at age 18, and a
             longitudinal analysis of the prospective predictors of
             OCD.<h4>Results</h4>Using the Diagnostic Interview Schedule,
             the authors found a 1-year prevalence rate of 4%, with a
             male-female ratio of 0.7:1. The majority of OCD cases met
             criteria for a comorbid disorder, most commonly depression
             (62%), social phobia (38%), and substance dependence
             (alcohol 24%, marijuana 19%).<h4>Conclusions</h4>Data
             collected on the sample from birth to age 18 years indicated
             that many childhood risk factors theorized in the literature
             did not predict OCD in this sample. However, a history of
             depression and substance use were prospective risk factors
             for OCD.},
   Doi = {10.1097/00004583-199511000-00008},
   Key = {fds253438}
}

@article{fds253442,
   Author = {Caspi, A and Henry, B and McGee, RO and Moffitt, TE and Silva,
             PA},
   Title = {Temperamental origins of child and adolescent behavior
             problems: from age three to age fifteen.},
   Journal = {Child development},
   Volume = {66},
   Number = {1},
   Pages = {55-68},
   Year = {1995},
   Month = {February},
   ISSN = {0009-3920},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/7497829},
   Abstract = {We assessed relations between early temperament and behavior
             problems across 12 years in an unselected sample of over 800
             children. Temperament measures were drawn from behavior
             ratings made by examiners who observed children at ages 3,
             5, 7, and 9. Factor analyses revealed 3 dimensions at each
             age: Lack of Control, Approach, and Sluggishness.
             Temperament dimensions at ages 3 and 5 were correlated in
             theoretically coherent ways with behavior problems that were
             independently evaluated by parents and teachers at ages 9
             and 11, and by parents at ages 13 and 15. Lack of Control
             was more strongly associated with later externalizing
             behavior problems than with internalizing problems; Approach
             was associated with fewer internalizing problems among boys;
             and Sluggishness was weakly associated with both anxiety and
             inattention, especially among girls. Lack of Control and
             Sluggishness were also associated with fewer adolescent
             competencies. These results suggest that early temperament
             may have predictive specificity for the development of later
             psychopathology.},
   Doi = {10.1111/j.1467-8624.1995.tb00855.x},
   Key = {fds253442}
}

@article{fds253436,
   Author = {Caspi, A and Begg, D and Dickson, N and Langley, J and Moffitt, TE and McGee, R and Silva, PA},
   Title = {Identification of personality types at risk for poor health
             and injury in late adolescence},
   Journal = {Criminal Behaviour and Mental Health},
   Volume = {5},
   Number = {4},
   Pages = {330-350},
   Publisher = {WILEY},
   Year = {1995},
   Month = {January},
   url = {http://dx.doi.org/10.1002/cbm.1995.5.4.330},
   Abstract = {In an unselected general birth cohort of 862 18-year-olds,
             we sought to identify the personality characteristics
             associated with involvement in each of five afferent
             health-risk behaviours (unprotected sexual intercourse with
             multiple partners, dangerous driving habits, violent crime,
             alcohol dependence and marijuana dependence) as well as the
             personality characteristics associated with a syndrome of
             multiple health-risk behaviours. A unique configuration of
             traits differentiated youth involved in any given single
             health-risk behaviour from youth who were not. These youth
             were more impulsive, aggressive, alienated and tended to
             experience negative emotions in response to daily hassles. A
             different unique configuration of traits differentiated
             youth involved in a syndrome of multiple health-risk
             behaviours from youth involved in a single or in no
             health-risk behaviours. These youth were distinguished by a
             rejection of social norms, danger-seeking, impulsivity, a
             very low threshold for negative emotional responses such as
             anger, irritability and nervous tension, and by little need
             or capacity for connection to other people. In planning
             health campaigns, health professionals need to consider the
             unique psychological make-up of persons most at risk for
             health-risk behaviours and design programmes that will
             appeal to them.},
   Doi = {10.1002/cbm.1995.5.4.330},
   Key = {fds253436}
}

@article{fds253439,
   Author = {Lynam, DR and Moffitt, TE},
   Title = {Delinquency and Impulsivity and IQ: A Reply to Block
             (1995)},
   Journal = {Journal of Abnormal Psychology},
   Volume = {104},
   Number = {2},
   Pages = {399-401},
   Publisher = {American Psychological Association (APA)},
   Year = {1995},
   Month = {January},
   ISSN = {0021-843X},
   url = {http://dx.doi.org/10.1037/0021-843X.104.2.399},
   Abstract = {Although J. Block's critique (J. Block, 1995) of the D.
             Lynam, T. Moffitt, and M. Stouthamer-Loeber report (D.
             Lynam, T. Moffitt, and M. Stouthamer-Loeber, 1993) contains
             several interesting points, many of his criticisms are not
             valid and resulted from miscommunications,
             misunderstandings, and simple preferences. Specifically, the
             authors believe the criticisms to be the results of
             mistaking a single hypothesis for an organizing principle, a
             misunderstanding of the reported path analyses, and a simple
             preference for impulsivity over IQ as an explanatory
             construct. An attempt is made to address the
             misinterpretation through clarification of the predicted
             relations between IQ, executive dysfunction, impulsivity,
             and delinquency. The original path analyses are reviewed and
             are shown to refute not only the original self-control
             hypothesis (Lynam et al., 1993), as reported, but also
             Block's more recent version. Finally, evidence marshalled by
             Block to support his emphasis on impulsive personality over
             low IQ is argued to have inadequacies from empirical and
             social policy perspectives.},
   Doi = {10.1037/0021-843X.104.2.399},
   Key = {fds253439}
}

@article{fds253441,
   Author = {Poulton, RG and Moffitt, TE},
   Title = {The Rey-Osterreith Complex Figure Test: norms for young
             adolescents and an examination of validity.},
   Journal = {Archives of clinical neuropsychology : the official journal
             of the National Academy of Neuropsychologists},
   Volume = {10},
   Number = {1},
   Pages = {47-56},
   Publisher = {Oxford University Press (OUP)},
   Year = {1995},
   Month = {January},
   ISSN = {0887-6177},
   url = {http://dx.doi.org/10.1093/arclin/10.1.47},
   Abstract = {Although recent studies have investigated theoretically
             relevant aspects of performance and psychometric properties
             of the Rey-Osterreith Complex Figure Test (ROCFT), there is
             no documentation of the instrument's construct and
             predictive validity in an unselected, nonclinical
             population. This is necessary because knowledge of base
             rates of poor performance in the general population is
             required to evaluate the significance of performance
             deficits in clinical populations. The ROCFT was administered
             to 740 children aged 13 years who are members of an
             unselected birth cohort, representative of the general
             population. Normative findings are presented. Correlational
             analysis indicated that performance on the ROCFT was closely
             related to performance on the Block Design and Object
             Assembly subtests of the WISC-R. The first documentation was
             obtained of the ROCFT's predictive validity. Subjects in an
             unselected nonclinical sample who had a history of central
             nervous system health problems scored below the rest of the
             sample. Implications for the continued use of this
             instrument are discussed.},
   Doi = {10.1093/arclin/10.1.47},
   Key = {fds253441}
}

@article{fds69832,
   Author = {Caspi, A. and Begg, D. and Dickson, N. and Langley, J. and Moffitt, T.E. and McGee, R.O. and Silva, P.A},
   Title = {Identification of a personality type at risk for injury and
             health outcomes in adolescence},
   Journal = {Criminal Behavior and Mental Health},
   Volume = {5},
   Pages = {330-350},
   Year = {1995},
   Key = {fds69832}
}

@article{fds253440,
   Author = {Nagin, DS and Farrington, DP and Moffitt, TE},
   Title = {Life-course trajectories of different types of
             offenders},
   Journal = {Criminology},
   Volume = {33},
   Number = {1},
   Pages = {111-140},
   Publisher = {WILEY},
   Year = {1995},
   url = {http://dx.doi.org/10.1111/j.1745-9125.1995.tb01173.x},
   Abstract = {The point of departure for this paper is Nagin and Land
             (1993), who identified four distinctive offending
             trajectories in a sample of 403 British males—a group
             without any convictions, “adolescence‐limiteds,”“high‐level
             chronics,” and “low‐level chronics.” We build upon
             that study with a detailed analysis of the distinguishing
             individual characteristics, behaviors, and social
             circumstances from ages 10 through 32 of these four groups.
             The most salient findings concern the adolescence‐limiteds.
             By age 32 the work records of the adolescence‐limiteds
             were indistinguishable from the never‐convicted and
             substantially better than those of the chronic offenders.
             The adolescence‐limiteds also seem to have established
             better relationships with their spouses than the chronics.
             The seeming reformation of the adolescence‐limiteds,
             however, was less than complete. They continued to drink
             heavily and use drugs, get into fights, and commit criminal
             acts (according to self‐reports). Copyright © 1995, Wiley
             Blackwell. All rights reserved},
   Doi = {10.1111/j.1745-9125.1995.tb01173.x},
   Key = {fds253440}
}

@article{fds253446,
   Author = {White, JL and Moffitt, TE and Caspi, A and Bartusch, DJ and Needles, DJ and Stouthamer-Loeber, M},
   Title = {Measuring impulsivity and examining its relationship to
             delinquency.},
   Journal = {Journal of abnormal psychology},
   Volume = {103},
   Number = {2},
   Pages = {192-205},
   Year = {1994},
   Month = {May},
   ISSN = {0021-843X},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/8040489},
   Abstract = {A multimethod, multisource assessment of impulsivity was
             conducted in a sample of more than 400 boys who were members
             of a longitudinal study of the development of antisocial
             behavior. Exploratory and confirmatory factor analysis of
             the 11 different impulsivity measures revealed two
             impulsivity factors: Cognitive and Behavioral. Cognitive and
             behavioral impulsivity had similar correlations with
             socioeconomic status. Cognitive impulsivity was more
             strongly related to IQ than was behavioral impulsivity.
             Behavioral impulsivity was more strongly related to
             delinquency at ages 10 and 12-13 than was cognitive
             impulsivity. Consistent with theoretical prediction, our
             results also indicate that behavioral impulsivity was
             especially related to serious delinquency that is stable
             over time.},
   Doi = {10.1037//0021-843x.103.2.192},
   Key = {fds253446}
}

@article{fds304707,
   Author = {Krueger, RF and Schmutte, PS and Caspi, A and Moffitt, TE and Campbell,
             K and Silva, PA},
   Title = {Personality traits are linked to crime among men and women:
             evidence from a birth cohort.},
   Journal = {Journal of abnormal psychology},
   Volume = {103},
   Number = {2},
   Pages = {328-338},
   Year = {1994},
   Month = {May},
   ISSN = {0021-843X},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/8040502},
   Abstract = {Is there a relationship between personality and criminal
             behavior? We addressed this question in a representative
             birth cohort of 862 male and female 18-year-olds.
             Personality was assessed with the Multidimensional
             Personality Questionnaire (MPQ). The MPQ measures 10
             relatively independent personality traits and was not
             designed to identify offenders. Delinquency was assessed via
             3 data sources: self-reports, informant reports, and
             official records. Variable-centered analyses revealed that
             MPQ scales indexing negative emotionality and behavioral
             constraint were consistent predictors of delinquency across
             the 3 data sources. Person-centered analyses revealed that
             youths abstaining from delinquency were uniquely
             characterized by low interpersonal potency. Youths involved
             in extensive delinquency were uniquely characterized by
             feelings of alienation, lack of social closeness, and risk
             taking. Advances in understanding criminal behavior can be
             made through research that places the personality-delinquency
             link in a developmental context.},
   Doi = {10.1037//0021-843x.103.2.328},
   Key = {fds304707}
}

@article{fds253166,
   Author = {Moffitt, TE and Lynam, D},
   Title = {The neuropsychology of conduct disorder and delinquency:
             implications for understanding antisocial
             behavior.},
   Journal = {Progress in experimental personality & psychopathology
             research},
   Pages = {233-262},
   Year = {1994},
   Month = {January},
   Key = {fds253166}
}

@article{fds253443,
   Author = {Henry, B and Moffitt, TE and Caspi, A and Langley, J and Silva,
             PA},
   Title = {On the "Remembrance of Things Past": A Longitudinal
             Evaluation of the Retrospective Method},
   Journal = {Psychological Assessment},
   Volume = {6},
   Number = {2},
   Pages = {92-101},
   Publisher = {American Psychological Association (APA)},
   Year = {1994},
   Month = {January},
   ISSN = {1040-3590},
   url = {http://dx.doi.org/10.1037/1040-3590.6.2.92},
   Abstract = {This study examines the extent of agreement between
             retrospective and prospective measures of variables in 7
             different content domains: Residence changes,
             anthropometrics, injuries, reading ability, family
             characteristics, behavior problems, and delinquency. The
             authors evaluated retrospective reports using data from a
             large sample of 18-year-old youth who have been studied
             prospectively since their births. The findings suggested
             that (a) psychosocial variables (e.g., reports about
             subjective psychological states and family processes)
             revealed the lowest level of agreement between prospective
             and retrospective measures, and (b) even when retrospective
             reports correlated significantly with prospective data, the
             absolute level of agreement between the 2 data sources was
             quite poor. It appears that reliance on retrospective
             reports about psychosocial variables should be approached
             with caution. Moreover, it is suggested that the use of
             retrospective reports should be limited to testing
             hypotheses about the relative standing of individuals in a
             distribution and should not be used to test hypotheses that
             demand precision in estimating event frequencies and event
             dates.},
   Doi = {10.1037/1040-3590.6.2.92},
   Key = {fds253443}
}

@article{fds253444,
   Author = {MOFFITT, TE and LYNAM, DR and SILVA, PA},
   Title = {NEUROPSYCHOLOGICAL TESTS PREDICTING PERSISTENT MALE
             DELINQUENCY},
   Journal = {Criminology},
   Volume = {32},
   Number = {2},
   Pages = {277-300},
   Publisher = {WILEY},
   Year = {1994},
   Month = {January},
   url = {http://dx.doi.org/10.1111/j.1745-9125.1994.tb01155.x},
   Abstract = {This article reports the first longitudinal evidence that
             prospective measures of neuropsychological status predict
             antisocial outcomes. We studied data for a birth cohort of
             several hundred New Zealand males from age 13 to age 18.
             Age‐13 neuropsychological scores predicted later
             delinquency measured via multiple sources: police, courts,
             and self‐report. Poor neuropsychological scores were
             associated with early onset of delinquency. The results fit
             our predictions about two trajectories of delinquent
             involvement: (1) Poor neuropsychological status predicted
             specifically male offending that began before age 13 and
             persisted at high levels thereafter. (2) By contrast, in
             this sample neuropsychological status was unrelated to
             delinquency that began in adolescence. Copyright © 1994,
             Wiley Blackwell. All rights reserved},
   Doi = {10.1111/j.1745-9125.1994.tb01155.x},
   Key = {fds253444}
}

@article{fds253445,
   Author = {CASPI, A and MOFFITT, TE and SILVA, PA and STOUTHAMER‐LOEBER, M and KRUEGER, RF and SCHMUTTE, PS},
   Title = {ARE SOME PEOPLE CRIME‐PRONE? REPLICATIONS OF THE
             PERSONALITY‐CRIME RELATIONSHIP ACROSS COUNTRIES, GENDERS,
             RACES, AND METHODS},
   Journal = {Criminology},
   Volume = {32},
   Number = {2},
   Pages = {163-196},
   Publisher = {WILEY},
   Year = {1994},
   Month = {January},
   url = {http://dx.doi.org/10.1111/j.1745-9125.1994.tb01151.x},
   Abstract = {We examined the relation between personality traits and
             crime in two studies. In New Zealand we studied
             18‐year‐old males and females from an entire birth
             cohort. In Pittsburgh we studied an ethnically diverse group
             of 12‐ and 13‐year‐old boys. In both studies we
             gathered multiple and independent measures of personality
             and delinquent involvement. The personality correlates of
             delinquency were robust in different nations, in different
             age cohorts, across gender, and across race: greater
             delinquent participation was associated with a personality
             configuration characterized by high Negative Emotionality
             and weak Constraint. We suggest that when Negative
             Emotionality (the tendency to experience aversive affective
             states) is accompanied by weak Constraint (difficulty in
             impulse control), negative emotions may be translated more
             readily into antisocial acts. We review additional evidence
             about the developmental origins and consequences of this
             personality configuration and discuss its implications for
             theories about antisocial behavior. Copyright © 1994, Wiley
             Blackwell. All rights reserved},
   Doi = {10.1111/j.1745-9125.1994.tb01151.x},
   Key = {fds253445}
}

@article{fds253175,
   Author = {John, OP and Caspi, A and Robins, RW and Moffitt, TE and Stouthamer
             Loeber, M},
   Title = {The "Little Five": Exploring the five-factor model of
             personality in adolescent boys},
   Journal = {Child Development},
   Volume = {65},
   Number = {1},
   Pages = {160-178},
   Year = {1994},
   ISSN = {0009-3920},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/8131645},
   Abstract = {The California Child Q-set (CCQ) was used to explore the
             structure of personality in early adolescence and to develop
             scales to measure the "Big Five" dimensions: Extraversion,
             Agreeableness, Conscientiousness, Neuroticism, and Openness
             to Experience. Mothers provided Q-sorts of 350 ethnically
             diverse boys between 12 and 13 years old. Analyses of the
             construct validity of the scales provided a nomological
             network relating the Big Five to theoretically and socially
             important criterion variables, such as juvenile delinquency,
             Externalizing and Internalizing disorders of childhood
             psychopathology, school performance, IQ, SES, and race.
             These effects were obtained using diverse methods, including
             self-reports from the boys, ratings by their mothers and
             their teachers, and objective-test data. In addition to the
             Big Five, analyses also suggested 2 possibly age-specific
             dimensions of personality in early adolescence. Discussion
             is focused on the changing manifestations of personality
             traits throughout development.},
   Doi = {10.1111/j.1467-8624.1994.tb00742.x},
   Key = {fds253175}
}

@article{fds253447,
   Author = {Krueger, R and Schmutte, PS and Caspi, A and Moffitt, T and Campbell, K and Silva, PA},
   Title = {Personality traits are linked to crime: Evidence from a
             birth cohort},
   Journal = {Journal of Abnormal Psychology},
   Volume = {103},
   Number = {2},
   Pages = {328-338},
   Year = {1994},
   ISSN = {0021-843X},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/8040502},
   Abstract = {Is there a relationship between personality and criminal
             behavior? We addressed this question in a representative
             birth cohort of 862 male and female 18-year-olds.
             Personality was assessed with the Multidimensional
             Personality Questionnaire (MPQ). The MPQ measures 10
             relatively independent personality traits and was not
             designed to identify offenders. Delinquency was assessed via
             3 data sources: self-reports, informant reports, and
             official records. Variable-centered analyses revealed that
             MPQ scales indexing negative emotionality and behavioral
             constraint were consistent predictors of delinquency across
             the 3 data sources. Person-centered analyses revealed that
             youths abstaining from delinquency were uniquely
             characterized by low interpersonal potency. Youths involved
             in extensive delinquency were uniquely characterized by
             feelings of alienation, lack of social closeness, and risk
             taking. Advances in understanding criminal behavior can be
             made through research that places the personality-delinquency
             link in a developmental context.},
   Key = {fds253447}
}

@article{fds253164,
   Author = {Lynam, D and Moffitt, T and Stouthamer-Loeber,
             M},
   Title = {Erratum: Explaining the relation between IQ and delinquency:
             Class, race, test motivation, school failure, or
             self-control? (Journal of Abnormal Psychology (1993) 102:2
             (187-196))},
   Journal = {Journal of Abnormal Psychology},
   Volume = {102},
   Number = {4},
   Pages = {552},
   Publisher = {American Psychological Association (APA)},
   Year = {1993},
   Month = {November},
   ISSN = {0021-843X},
   url = {http://dx.doi.org/10.1037/0021-843X.102.4.552},
   Doi = {10.1037/0021-843X.102.4.552},
   Key = {fds253164}
}

@article{fds253451,
   Author = {Henry, B and Feehan, M and McGee, R and Stanton, W and Moffitt, TE and Silva, P},
   Title = {The importance of conduct problems and depressive symptoms
             in predicting adolescent substance use.},
   Journal = {Journal of abnormal child psychology},
   Volume = {21},
   Number = {5},
   Pages = {469-480},
   Year = {1993},
   Month = {October},
   ISSN = {0091-0627},
   url = {http://dx.doi.org/10.1007/bf00916314},
   Abstract = {The current study assessed the relative importance of
             conduct problems and depressive symptoms, measured at two
             ages (11 and 15), for predicting substance use at age 15 in
             an unselected birth cohort of New Zealand adolescents. Among
             males, when the relative predictive utility of both conduct
             problems and depressive symptoms was assessed, only
             pre-adolescent depressive symptoms were found to predict
             multiple drug use 4 years later. No predictive relation was
             found between early symptomatology and later substance use
             among females. The strongest association between predictors
             and substance use emerged between age 15 multiple drug use
             and concurrent conduct problems for both males and females.
             Finally, both conduct problems and depressive symptoms at
             age 15 were also found to be associated with concurrent
             "self-medication" among females.},
   Doi = {10.1007/bf00916314},
   Key = {fds253451}
}

@article{fds253454,
   Author = {Caspi, A and Moffitt, TE},
   Title = {When Do Individual Differences Matter? A Paradoxical Theory
             of Personality Coherence},
   Journal = {Psychological Inquiry},
   Volume = {4},
   Number = {4},
   Pages = {247-271},
   Publisher = {Informa UK Limited},
   Year = {1993},
   Month = {October},
   url = {http://dx.doi.org/10.1207/s15327965pli0404_1},
   Abstract = {We propose that individual differences in personality should
             be studied during periods of environmental change because
             these periods provide an opportunity to discern the general
             mechanisms that govern the functions and processes of
             personality. We delineate the circumstances wherein
             personality differences are accentuated and then specify the
             conditions whereby change is produced. Personality
             differences are likely to be revealed during transitions
             into unpredictable new situations, when there is a press to
             behave but no information about how to behave adaptively.
             Dispositional differences are thus accentuated as each
             person seeks to transform novel, ambiguous, and uncertain
             circumstances into familiar, clear, and expectable social
             encounters. Our theory also accounts for turning points in
             behavioral development: Systematic change is likely to occur
             during transitions into new situations, when there is a
             press to behave and when previous responses are actively
             discouraged while clear information is provided about how to
             behave adaptively. © 1993, Taylor & Francis Group, LLC. All
             rights reserved.},
   Doi = {10.1207/s15327965pli0404_1},
   Key = {fds253454}
}

@article{fds253449,
   Author = {Lynam, D and Moffitt, T and Stouthamer-Loeber,
             M},
   Title = {Explaining the relation between IQ and delinquency: class,
             race, test motivation, school failure, or
             self-control?},
   Journal = {Journal of abnormal psychology},
   Volume = {102},
   Number = {2},
   Pages = {187-196},
   Year = {1993},
   Month = {May},
   ISSN = {0021-843X},
   url = {http://dx.doi.org/10.1037//0021-843x.102.2.187},
   Abstract = {An inverse relation between IQ and delinquency has been well
             established, but the direction of effect remains to be
             specified. Differing explanatory accounts of the relation
             were empirically examined in the present study using data on
             13-year-old boys involved in a high-risk longitudinal study.
             Accounts that interpreted the relation as spurious or that
             posited that delinquency-related factors lead to low IQ
             scores received no support; findings were most consistent
             with the hypothesis that the direction of effect runs from
             low IQ to delinquency. The IQ-delinquency relation was
             robust after race, class, and observed test motivation were
             controlled statistically. Additionally, the effect of IQ was
             mediated by school performance for Black youth but not for
             White youth.},
   Doi = {10.1037//0021-843x.102.2.187},
   Key = {fds253449}
}

@article{fds253456,
   Author = {Moffitt, TE and Caspi, A and Harkness, AR and Silva,
             PA},
   Title = {The natural history of change in intellectual performance:
             who changes? How much? Is it meaningful?},
   Journal = {Journal of child psychology and psychiatry, and allied
             disciplines},
   Volume = {34},
   Number = {4},
   Pages = {455-506},
   Year = {1993},
   Month = {May},
   ISSN = {0021-9630},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/8509490},
   Abstract = {A prerequisite step for studying the magnitude and meaning
             of IQ change is to distinguish between true IQ change that
             is a researchable phenomenon and IQ "change" that can be
             accounted for by measurement error. We studied the
             reliability, magnitude and meaning of IQ change using scores
             on the WISC--R obtained from a representative sample of 794
             children at ages 7, 9, 11 and 13. The findings suggest that,
             in the majority of children, IQ change is either negligible
             in amount, unreliably measured or both. In a nontrivial
             minority of children, naturalistic IQ change is marked and
             real, but this change is variable in its timing,
             idiosyncratic in its source and transient in its course. We
             discuss the implications of these findings for interventions
             that aspire to improve IQ scores.},
   Doi = {10.1111/j.1469-7610.1993.tb01031.x},
   Key = {fds253456}
}

@article{fds253450,
   Author = {Moffitt, TE},
   Title = {The neuropsychology of conduct disorder},
   Journal = {Development and Psychopathology},
   Volume = {5},
   Number = {1-2},
   Pages = {135-151},
   Publisher = {Cambridge University Press (CUP)},
   Year = {1993},
   Month = {January},
   url = {http://dx.doi.org/10.1017/S0954579400004302},
   Abstract = {This article reviews evidence from neuropsychological tests
             that brain dysfunction is a correlate of conduct disorder.
             Most studies report consistent findings of differential
             neuropsychological deficits for antisocial samples in verbal
             and “executive” functions. Neuropsychological measures
             are related to some of the best indicators of poor outcome
             for children with conduct symptoms, such as early onset,
             stability across time, hyperactive symptoms, and
             aggressiveness. Neuropsychological tests statistically
             predict variance in antisocial behavior independently of
             appropriate control variables. This article argues that
             neuropsychological variables warrant further study as
             possible causal factors for conduct disorder and presents
             one developmental perspective on how neuropsychological
             problems might contribute risk for conduct disorder. ©
             1993, Congress on Research in Dance. All rights
             reserved.},
   Doi = {10.1017/S0954579400004302},
   Key = {fds253450}
}

@article{fds253452,
   Author = {Henry, B and Moffitt, T and Robins, L and Earls, F and Silva,
             P},
   Title = {Early family predictors of child and adolescent atisocial
             behviour: Who are the mothers of delinquents?},
   Journal = {Criminal Behaviour and Mental Health},
   Volume = {3},
   Number = {2},
   Pages = {97-118},
   Publisher = {WILEY},
   Year = {1993},
   Month = {January},
   url = {http://dx.doi.org/10.1002/cbm.1993.3.2.97},
   Abstract = {This study tested the utility of 29 maternal and familial
             characteristics for the purpose of prospectively identifying
             children who are at high risk for antisocial and delinquent
             outcomes. The family data were drawn from the archives of
             the Dunedin Multidisciplinary Health and Development Study.
             The study's design offers certain methodological advantages:
             the sample is a representative unselected birth cohort; the
             family measures were taken very early in childhood;
             information about the child's antisocial behaviour was
             collected from many different sources and at many different
             ages; a comparison group of children with other behaviour
             disorders was included, and it was posible to examine the
             influence of possible 'confounding variables'. Three groups
             of 11-year-old children (antisocial (n = 50), other
             disorders (n = 37), and non-disordered (n = 220)) were
             compared on family variables. Nine family variables
             differentiated the antisocial children from the
             non-disordered children, the most important of which were
             parental disagreement about how to discipline the 5-year-old
             child, and many changes of the child's primary caretaker by
             age 15, prospective family variablse accounted for
             significant amounts of the variance in number of police
             contacts and age at first police contact.},
   Doi = {10.1002/cbm.1993.3.2.97},
   Key = {fds253452}
}

@article{fds253455,
   Author = {Caspi, A and Lynam, D and Moffitt, TE and Silva, PA},
   Title = {Unraveling Girls' Delinquency: Biological, Dispositional,
             and Contextual Contributions to Adolescent
             Misbehavior},
   Journal = {Developmental Psychology},
   Volume = {29},
   Number = {1},
   Pages = {19-30},
   Publisher = {American Psychological Association (APA)},
   Year = {1993},
   Month = {January},
   ISSN = {0012-1649},
   url = {http://dx.doi.org/10.1037/0012-1649.29.1.19},
   Abstract = {We examined processes linking biological and behavioral
             changes in different contexts during adolescence by studying
             an unselected cohort of New Zealand girls from childhood
             through adolescence when they entered either mixed-sex or
             all-girl secondary schools. The impact of menarcheal timing
             on female delinquency was moderated by the sex composition
             of schools; early-maturing girls in mixed-sex settings were
             at greatest risk for delinquency. Individual differences in
             delinquency were also significantly more stable among girls
             in mixed-sex schools than among those in all-girl schools.
             These contextual variations are interpreted in terms of the
             differential distribution of reinforcements and
             opportunities for delinquency.},
   Doi = {10.1037/0012-1649.29.1.19},
   Key = {fds253455}
}

@article{fds304705,
   Author = {Moffitt, TE},
   Title = {Adolescence-limited and life-course-persistent antisocial
             behavior: A developmental taxonomy.},
   Journal = {Psychological Review},
   Volume = {100},
   Number = {4},
   Pages = {674-701},
   Publisher = {American Psychological Association (APA)},
   Year = {1993},
   url = {http://dx.doi.org/10.1037//0033-295x.100.4.674},
   Abstract = {A dual taxonomy is presented to reconcile 2 incongruous
             facts about antisocial behavior: (a) It shows impressive
             continuity over age, but (b) its prevalence changes
             dramatically over age, increasing almost 10-fold temporarily
             during adolescence. This article suggests that delinquency
             conceals 2 distinct categories of individuals, each with a
             unique natural history and etiology: A small group engages
             in antisocial behavior of 1 sort or another at every life
             stage, whereas a larger group is antisocial only during
             adolescence. According to the theory of life-course-persistent
             antisocial behavior, children's neuropsychological problems
             interact cumulatively with their criminogenic environments
             across development, culminating in a pathological
             personality. According to the theory of adolescence-limited
             antisocial behavior, a contemporary maturity gap encourages
             teens to mimic antisocial behavior in ways that are
             normative and adjustive.},
   Doi = {10.1037//0033-295x.100.4.674},
   Key = {fds304705}
}

@article{fds253448,
   Author = {Moffitt, TE},
   Title = {"Life-course-persistent" and "adolescence-limited"
             antisocial behavior: A developmental taxonomy},
   Journal = {Psychological Review},
   Volume = {100},
   Number = {4},
   Pages = {674-701},
   Year = {1993},
   Abstract = {A dual taxonomy is presented to reconcile 2 incongruous
             facts about antisocial behavior: (a) It shows impressive
             continuity overage, but (b) its prevalence changes
             dramatically overage, increasing almost 10-fold temporarily
             during adolescence. This article suggests that delinquency
             conceals 2 distinct categories of individuals, each with a
             unique natural history and etiology: A small group engages
             in antisocial behavior of 1 sort or another at every life
             stage, whereas a larger group is antisocial only during
             adolescence. According to the theory of life-course-persistent
             antisocial behavior, children's neuropsychological problems
             interact cumulatively with their criminogenic environments
             across development, culminating in a pathological
             personality. According to the theory of adolescence-limited
             antisocial behavior, a contemporary maturity gap encourages
             teens to mimic antisocial behavior in ways that are
             normative and adjustive.},
   Key = {fds253448}
}

@article{fds253453,
   Author = {Caspi, A and Moffitt, TE},
   Title = {Paradox regained},
   Journal = {Psychological Inquiry},
   Volume = {4},
   Number = {4},
   Pages = {313-321},
   Publisher = {Informa UK Limited},
   Year = {1993},
   url = {http://dx.doi.org/10.1207/s15327965pli0404_16},
   Doi = {10.1207/s15327965pli0404_16},
   Key = {fds253453}
}

@article{fds253163,
   Author = {White, JL and Moffitt, TE and Silva, PA},
   Title = {Neuropsychological and socio-emotional correlates of
             specific-arithmetic disability},
   Journal = {Archives of Clinical Neuropsychology},
   Volume = {7},
   Number = {1},
   Pages = {1-13},
   Publisher = {Oxford University Press (OUP)},
   Year = {1992},
   Month = {January},
   ISSN = {0887-6177},
   url = {http://dx.doi.org/10.1016/0887-6177(92)90014-E},
   Abstract = {Neuropsychological and socio-emotional factors associated
             with specific-arithmetic disability were investigated in an
             unselected sample of New Zealand children. Subjects were 17
             specific-arithmetic disabled, 27 specific-reading disabled,
             63 generally disabled, and 50 nondisabled 13 year olds.
             Evidence was sought for an association between
             specific-arithmetic disability and the neuropsychological
             and socio-emotional correlates of Nonverbal Learning
             Disability syndrome (NLD). NLD is characterized by a pattern
             of nonverbal and verbal neuropsychological strengths and
             weaknesses, and appears to place individuals at greater risk
             for internalizing psychopathology, than other learning
             disabilities. Only specific-arithmetic disabled subjects
             were found to show a neuropsychological profile reminiscent
             of NLD. Evidence of poor socio-emotional adjustment was
             found across all three learning-disabled groups, and was
             greatest among generally disabled subjects. We found that
             the specific-arithmetic-disabled subjects exhibited the
             greatest degree of overlap between internalizing
             psychopathology and a NLD neuropsychological profile. The
             results are interpreted as providing some support for the
             idea that specific-arithmetic-disabled individuals may be at
             greater risk for the NLD syndrome than either generally
             disabled or specific-reading-disabled individuals. ©
             1992.},
   Doi = {10.1016/0887-6177(92)90014-E},
   Key = {fds253163}
}

@article{fds253463,
   Author = {Caspi, A and Block, J and Block, JH and Klopp, B and Lynam, D and Moffitt,
             TE and Stouthamer-Loeber, M},
   Title = {A "Common-Language" Version of the California Child Q-Set
             for Personality Assessment},
   Journal = {Psychological Assessment},
   Volume = {4},
   Number = {4},
   Pages = {512-523},
   Publisher = {American Psychological Association (APA)},
   Year = {1992},
   Month = {January},
   ISSN = {1040-3590},
   url = {http://dx.doi.org/10.1037/1040-3590.4.4.512},
   Abstract = {J. Block and J.H. Block's (1980) California Child Q-Set
             (CCQ), a unique instrument used by professional observers to
             assess children's personalities, has contributed important
             information about the nature of personality development. The
             authors of this article introduce language-simplifying
             modifications to the items in the original CCQ for this
             assessment procedure to be used with a wide range of
             nonprofessional observers (e.g., parents with little formal
             education). Reliability and validity assessments show that
             the "common-language" version of the CCQ can be used with
             lay persons to yield reliable, valid, and valuable
             information about the links between personality functioning
             and problems in adaptive functioning in diverse
             populations.},
   Doi = {10.1037/1040-3590.4.4.512},
   Key = {fds253463}
}

@article{fds253174,
   Author = {Moffitt, TE and Caspi, A and Belsky, J and Silva,
             PA},
   Title = {Childhood experience and the onset of menarche},
   Journal = {Child Development},
   Volume = {63},
   Number = {1},
   Pages = {47-58},
   Year = {1992},
   ISSN = {0009-3920},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/1551329},
   Abstract = {We tested predictions about psychosocial factors in the
             onset of menarche using data from a longitudinal study of
             16-year-old girls. Belsky, Steinberg, and Draper have
             proposed a model that seeks to explain individual
             differences in maturational timing in terms of stressful
             childhood experiences. Their model hypothesizes that (1)
             individuals who grow up under conditions of family stress
             (2) experience behavioral and psychological problems which
             (3) provoke earlier reproductive readiness. In this study,
             the effect of family stressors on menarche was mediated by
             neither behavior problems nor weight, contrary to the
             predictions. However, the most provocative proposition
             advanced by Belsky et al. received empirical support. Family
             conflict and father absence in childhood predicted an
             earlier age of menarche, and these factors in combination
             with weight showed some evidence of an additive influence on
             menarche. A genetic inheritance model may provide a more
             parsimonious account of these data than does a conditional
             adaptation model derived from sociobiology.},
   Doi = {10.1111/j.1467-8624.1992.tb03594.x},
   Key = {fds253174}
}

@article{fds253457,
   Author = {White, J and Moffitt, TE and Silva, PA},
   Title = {Specific arithmetic disability: neuropsychological and
             socio-emotional correlates},
   Journal = {Archives of Neuropsychology},
   Volume = {7},
   Pages = {1-16},
   Year = {1992},
   Key = {fds253457}
}

@article{fds253458,
   Author = {Henry, B and Moffitt, TE and Silva, PA},
   Title = {Disentangling delinquency and learning disability:
             Neuropsychological function and social support},
   Journal = {The International Journal of Clinical Neuropsychology},
   Volume = {13},
   Pages = {1-6},
   Year = {1992},
   Key = {fds253458}
}

@article{fds253460,
   Author = {Caspi, A and Moffitt, TE},
   Title = {Individual differences are accentuated during periods of
             social change: the sample case of girls at
             puberty.},
   Journal = {Journal of personality and social psychology},
   Volume = {61},
   Number = {1},
   Pages = {157-168},
   Year = {1991},
   Month = {July},
   ISSN = {0022-3514},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/1890586},
   Abstract = {The emergence of new behaviors and the reorganization of
             psychological structures are often attributed to critical
             events and crises in the life course. A fundamentally
             different perspective is offered: Potentially disruptive
             transitions produce personality continuity, not change. The
             behavioral responses of adolescent girls to the onset of
             menarche was studied in a longitudinal study of an
             unselected birth cohort. Predictions from 3 rival hypotheses
             about the relation between pubertal change and social
             psychological change were first tested: the stressful
             change, off time, and early-timing hypotheses. The results
             supported the early-timing hypothesis. Whether stressful,
             early menarche generated new behavioral problems or
             accentuated premenarcheal dispositions was then tested. The
             results supported an accentuation model: Stressful
             transitions accentuated behavioral problems among girls who
             were predisposed to behavioral problems earlier in
             childhood. Speculations are offered for a broader theory
             about the role of individual differences in the life
             course.},
   Doi = {10.1037//0022-3514.61.1.157},
   Key = {fds253460}
}

@article{fds253459,
   Author = {Henry, B and Moffitt, TE and Silva, PA and McGee,
             R},
   Title = {Anxiety and cognitive task performance: A longitudinal
             perspective},
   Journal = {Child Study Journal},
   Volume = {21},
   Pages = {167-184},
   Year = {1991},
   Key = {fds253459}
}

@article{fds253462,
   Author = {Moffitt, TE},
   Title = {Juvenile delinquency and attention deficit disorder: boys'
             developmental trajectories from age 3 to age
             15.},
   Journal = {Child development},
   Volume = {61},
   Number = {3},
   Pages = {893-910},
   Publisher = {JSTOR},
   Year = {1990},
   Month = {June},
   url = {http://dx.doi.org/10.1111/j.1467-8624.1990.tb02830.x},
   Abstract = {This article describes a longitudinal analysis of the
             behavior of a birth cohort of 435 boys. 4 groups were
             defined at age 13 on the basis of both self-reported
             delinquent behavior and professional diagnosis of Attention
             Deficit Disorder: ADD + delinquent, ADD only, delinquent
             only, and nondisordered. Biennial correlates of delinquency
             (antisocial behavior problems, verbal intelligence, reading
             difficulty, and family adversity) were traced across
             childhood. The ADD + delinquent boys consistently fared the
             worst on the assessments of family adversity, verbal
             intelligence, and reading. Their antisocial behavior began
             before school age, escalated at school entry, and persisted
             into adolescence. The ADD-only boys had normal family,
             intelligence, and reading scores, and showed only mild
             antisocial behavior in middle childhood. The delinquent-only
             boys showed no early risk from family, low intelligence, or
             reading deficit, and remained relatively free of conduct
             problems until they initiated delinquency at age 13.
             Persistence of criminal offending beyond adolescence is
             predicted for the ADD + delinquent boys.},
   Doi = {10.1111/j.1467-8624.1990.tb02830.x},
   Key = {fds253462}
}

@article{fds253464,
   Author = {Feehan, M and Stanton, WR and McGee, R and Silva, PA and Moffitt,
             TE},
   Title = {Is there an association between lateral preference and
             delinquent behavior?},
   Journal = {Journal of abnormal psychology},
   Volume = {99},
   Number = {2},
   Pages = {198-201},
   Year = {1990},
   Month = {May},
   ISSN = {0021-843X},
   url = {http://dx.doi.org/10.1037//0021-843x.99.2.198},
   Abstract = {Results of recent research suggests an association between
             left lateral preference and delinquent behavior. In this
             study the lateral preferences of 881 seven-year-old children
             were determined using behavioral indicators of hand and foot
             use. Mixed-handedness was associated with parent-reported
             problem behavior scores and self-reported delinquency scores
             at ages 13 and 15. However, preference for left hand and
             foot use was found to be unrelated to the delinquency
             measures. The distribution of lateral preferences in an
             identified delinquent group was not significantly different
             from the distribution in the sample remainder. The lack of
             an association between left preference and delinquency may
             be accounted for by an increased cultural acceptance of
             individual preference.},
   Doi = {10.1037//0021-843x.99.2.198},
   Key = {fds253464}
}

@article{fds253461,
   Author = {WHITE, JL and MOFFITT, TE and EARLS, F and ROBINS, L and SILVA,
             PA},
   Title = {HOW EARLY CAN WE TELL?: PREDICTORS OF CHILDHOOD CONDUCT
             DISORDER AND ADOLESCENT DELINQUENCY},
   Journal = {Criminology},
   Volume = {28},
   Number = {4},
   Pages = {507-535},
   Publisher = {WILEY},
   Year = {1990},
   Month = {January},
   url = {http://dx.doi.org/10.1111/j.1745-9125.1990.tb01337.x},
   Abstract = {It is often argued that intervention efforts can benefit
             from the early identification of children at risk for
             antisocial disorders. Little is known, however about the
             predictive efficacy of early predictors This study examined
             the predictive power of a variety of characteristics of the
             preschool child for antisocial outcome at ages 11 and 15.
             The subjects were 1,037 members of a longitudinal
             investigation of a New Zealand birth cohort. Groups with no
             disorders (n = 837), disorders other than antisocial
             disorders (n =37), and antisocial disorders (n = SO) were
             defined. Preschool descriptors were screened for their
             predictive power. A discriminant function analysis was
             computed with the jive most promising preschool variables.
             The function correctly classified 81 % of subjects as
             antisocial, or not. at age 11, and 66% of subjects as
             delinquent, or not, at age 15. Having preschool behavior
             problems was the single best predictor of antisocial
             disorders at age 11. This result is consistent with earlier
             findings that, among measures assessed in childhood,
             behavior problems are the best predictor of later antisocial
             outcome. Copyright © 1990, Wiley Blackwell. All rights
             reserved},
   Doi = {10.1111/j.1745-9125.1990.tb01337.x},
   Key = {fds253461}
}

@article{fds340562,
   Author = {Moffitt, TE},
   Title = {The Neuropsychology of Juvenile Delinquency: A Critical
             Review},
   Journal = {Crime and Justice},
   Volume = {12},
   Pages = {99-169},
   Publisher = {University of Chicago Press},
   Year = {1990},
   Month = {January},
   url = {http://dx.doi.org/10.1086/449165},
   Doi = {10.1086/449165},
   Key = {fds340562}
}

@article{fds253465,
   Author = {White, JL and Moffitt, TE and Silva, PA},
   Title = {A prospective replication of the protective effects of IQ in
             subjects at high risk for juvenile delinquency.},
   Journal = {Journal of consulting and clinical psychology},
   Volume = {57},
   Number = {6},
   Pages = {719-724},
   Year = {1989},
   Month = {December},
   ISSN = {0022-006X},
   url = {http://dx.doi.org/10.1037//0022-006x.57.6.719},
   Abstract = {The purpose of the study was to test the replicability of a
             protective effect of high IQ against criminality. Support
             has been found in prior studies for the hypotheses that Ss
             at high risk would have an elevated risk of serious criminal
             involvement, that seriously criminal Ss would have a lower
             mean IQ score than noncriminal Ss, and that Ss at high risk
             who had not become involved in serious criminal behavior
             would have the highest IQs. This report tests these
             hypotheses in a prospective design. Subjects were 1,037
             members of a longitudinal investigation of a New Zealand
             birth cohort. IQs were examined for male and female Ss who
             were divided into 4 groups formed on the basis of risk
             status at age 5 years and delinquency outcome at ages 13 and
             15. Analyses were conducted with and without mild
             delinquents excluded from the nondelinquent groups. We found
             that male and female delinquents showed significantly lower
             IQ scores than nondelinquents. By varying S selection
             procedures, we also found that a very high IQ may help boys,
             even those at risk, to stay free of delinquency
             altogether.},
   Doi = {10.1037//0022-006x.57.6.719},
   Key = {fds253465}
}

@article{fds253468,
   Author = {Frost, LA and Moffitt, TE and McGee, R},
   Title = {Neuropsychological correlates of psychopathology in an
             unselected cohort of young adolescents.},
   Journal = {Journal of abnormal psychology},
   Volume = {98},
   Number = {3},
   Pages = {307-313},
   Year = {1989},
   Month = {August},
   ISSN = {0021-843X},
   url = {http://dx.doi.org/10.1037//0021-843x.98.3.307},
   Abstract = {Members of a birth cohort were assessed for psychopathology
             and neuropsychological dysfunction at age 13. Ss who met
             DSM-III criteria for a single disorder, multiple disorders,
             and no disorder were compared on 5 composite
             neuropsychological measures. The multiple disorders group
             performed significantly worse than did the nondisordered
             group on the Verbal, Visuospatial, Verbal Memory, and
             Visual-Motor Integration factors. They also showed the
             highest rate of neuropsychological impairment. The
             attention-deficit disorder group performed significantly
             worse than did the nondisordered group on the Verbal Memory
             and Visual-Motor Integration factors, and the anxiety
             disorder group performed significantly worse than did the
             nondisordered group on the Visual-Motor Integration factor.
             Results suggest that neuropsychological dysfunction is more
             often associated with multiple rather than single,
             psychiatric disorders in adolescents. The problem of
             comorbidity in studies of neuropsychological function in
             childhood and adolescent psychopathology is
             highlighted.},
   Doi = {10.1037//0021-843x.98.3.307},
   Key = {fds253468}
}

@article{fds304726,
   Author = {Baker, LA and Mack, W and Moffitt, TE and Mednick,
             S},
   Title = {Sex differences in property crime in a Danish adoption
             cohort.},
   Journal = {Behavior genetics},
   Volume = {19},
   Number = {3},
   Pages = {355-370},
   Year = {1989},
   Month = {May},
   ISSN = {0001-8244},
   url = {http://dx.doi.org/10.1007/bf01066164},
   Abstract = {Sex differences in genetic and environmental influences on
             criminal behavior against property were studied in a birth
             cohort of 6129 male and 7065 female Danish adoptees and
             their biological and adoptive parents. Both genetic and
             environmental factors were found to contribute to variation
             in liability to property criminality, the relative
             proportions of variance explained being similar in males and
             females. Important shared- and nonshared-family
             environmental factors were present. In separate analyses of
             average liability toward property criminality, however,
             convicted females appeared to be more genetically
             predisposed than convicted males, a conclusion based on the
             finding that female property offenders were more likely than
             male offenders to have convicted biological (but
             adopted-away) offspring. On the other hand,
             property-offending males and females did not appear to
             differ in their average shared-family environmental
             liabilities, since conviction rates did not differ for
             adoptees of convicted adoptive mothers and fathers. Also,
             social class in the adoptive parents of convicted sons and
             daughters were comparable, further indicating that average
             shared-family environmental liabilities do not differ
             between the sexes.},
   Doi = {10.1007/bf01066164},
   Key = {fds304726}
}

@article{fds253469,
   Author = {McGee, R and Williams, S and Moffitt, T and Anderson,
             J},
   Title = {A comparison of 13-year-old boys with attention deficit
             and/or reading disorder on neuropsychological
             measures.},
   Journal = {Journal of abnormal child psychology},
   Volume = {17},
   Number = {1},
   Pages = {37-53},
   Year = {1989},
   Month = {February},
   url = {http://dx.doi.org/10.1007/bf00910769},
   Abstract = {This study compared 13-year-old boys with attention deficit
             disorder (ADD) and/or reading disability (RD), and controls
             with neither disorder on a battery of verbal and nonverbal
             neuropsychological measures. The aim was to examine whether
             ADD was associated with a qualitatively distinct pattern of
             deficits compared with RD. None of the measures
             differentiated the boys with ADD-only from the controls; the
             only deficit associated with ADD was slightly lower IQ. RD,
             on the other hand, was associated with deficits in memory
             and verbal skills.},
   Doi = {10.1007/bf00910769},
   Key = {fds253469}
}

@article{fds253466,
   Author = {Baker, LA and Mack, W and Moffitt, TE and Mednick,
             SA},
   Title = {Etiology of sex differences in criminal convictions in a
             Danish adoption cohort},
   Journal = {Behavior Genetics},
   Volume = {19},
   Number = {3},
   Pages = {355-370},
   Year = {1989},
   ISSN = {0001-8244},
   url = {http://dx.doi.org/10.1007/BF01066164},
   Abstract = {Sex differences in genetic and environmental influences on
             criminal behavior against property were studied in a birth
             cohort of 6129 male and 7065 female Danish adoptees and
             their biological and adoptive parents. Both genetic and
             environmental factors were found to contribute to variation
             in liability to property criminality, the relative
             proportions of variance explained being similar in males and
             females. Important shared- and nonshared-family
             environmental factors were present. In separate analyses of
             average liability toward property criminality, however,
             convicted females appeared to be more genetically
             predisposed than convicted males, a conclusion based on the
             finding that female property offenders were more likely than
             male offenders to have convicted biological (but
             adopted-away) offspring. On the other hand,
             property-offending males and females did not appear to
             differ in their average shared-family environmental
             liabilities, since conviction rates did not differ for
             adoptees of convicted adoptive mothers and fathers. Also,
             social class in the adopitive parents of convicted sons and
             daughters were comparable, further indicating that average
             shared-family environmental liabilities do not differ
             between the sexes. © 1989 Plenum Publishing
             Corporation.},
   Doi = {10.1007/BF01066164},
   Key = {fds253466}
}

@article{fds253467,
   Author = {Moffitt, TE and Henry, B},
   Title = {Neuropsychological assessment of executive functions in
             self-reported delinquents},
   Journal = {Development and Psychopathology},
   Volume = {1},
   Number = {2},
   Pages = {105-118},
   Publisher = {Cambridge University Press (CUP)},
   Year = {1989},
   url = {http://dx.doi.org/10.1017/S0954579400000298},
   Abstract = {Deficits in “executive” neuropsychological functions
             have been proposed to underlie the development of antisocial
             behavior such as juvenile delinquency. Results of research
             into the executive functions of delinquents have been mixed,
             and studies have been hampered by reliance on small samples
             of adjudicated subjects and questionable validity of the
             tests administered. This research examined the performance
             of a large unselected birth cohort of adolescent boys and
             girls on five tests of executive function that have
             documented reliability and validity. It is the first such
             study to use self-reports of antisocial behavior. Executive
             deficits were shown only by a subgroup of delinquent
             subjects with childhood comorbidity of antisocial behavior
             and attention deficit disorder; that subgroup's behavior was
             also rated as more aggressive and impulsive than comparison
             groups'. Group differences on executive measures remained
             significant after the effects of overall IQ were
             statistically controlled. Also, delinquents who had been
             detected by police did not show poorer executive functions
             than subjects with equivalent self-reports of delinquent
             behavior who had evaded official detection, suggesting that
             executive deficits are related to the development of
             antisocial behavior itself, and not simply to risk of
             detection. © 1989, Cambridge University Press. All rights
             reserved.},
   Doi = {10.1017/S0954579400000298},
   Key = {fds253467}
}

@article{fds253471,
   Author = {Moffitt, TE and Silva, PA},
   Title = {Self-reported delinquency, neuropsychological deficit, and
             history of attention deficit disorder.},
   Journal = {Journal of abnormal child psychology},
   Volume = {16},
   Number = {5},
   Pages = {553-569},
   Year = {1988},
   Month = {October},
   url = {http://dx.doi.org/10.1007/bf00914266},
   Abstract = {This study was designed to evaluate the possibility that a
             pattern of cognitive deficit is associated with delinquent
             behavior, while avoiding some of the methodological problems
             of previous research. The Self-Report Early Delinquency
             instrument and a research battery of neuropsychological
             tests were administered blindly to an unselected cohort of
             678 13-year-olds. Because the diagnosis of attention deficit
             disorder (ADD) was found at markedly elevated rates in the
             backgrounds of these delinquents, the possibility was
             examined that the neuropsychological deficits of delinquents
             might be limited to delinquents with histories of ADD.
             Although delinquents with past ADD were more cognitively
             impaired than non-ADD delinquents, both groups scored
             significantly below nondelinquents on verbal, visuospatial,
             and visual-motor integration skills. In addition, ADD
             delinquents scored poorly on memory abilities. Subjects with
             ADD who had not developed delinquent behavior were not as
             cognitively impaired as ADD delinquents, suggesting that it
             is the specific comorbidity of ADD and delinquency that
             bears neuropsychological study.},
   Doi = {10.1007/bf00914266},
   Key = {fds253471}
}

@article{fds253473,
   Author = {Moffitt, TE and Silva, PA},
   Title = {IQ and delinquency: a direct test of the differential
             detection hypothesis.},
   Journal = {Journal of abnormal psychology},
   Volume = {97},
   Number = {3},
   Pages = {330-333},
   Year = {1988},
   Month = {August},
   ISSN = {0021-843X},
   url = {http://dx.doi.org/10.1037//0021-843x.97.3.330},
   Abstract = {A number of studies have reported that juvenile delinquency
             is negatively related to IQ scores. The IQ/delinquency
             relation has been questioned on the basis of the
             differential detection confound, which attributes the
             apparent relation to biased likelihood of detection, and
             thus inclusion in research, of low-IQ delinquents. A direct
             test of the differential detection hypothesis was conducted
             by comparing the mean IQ scores of two groups of delinquent
             subjects from the same birth cohort. Group 1 had been
             detected in delinquent acts by police. Group 2 was not known
             to police, but was equivalent to group 1 on amount and
             seriousness of self-reported delinquency. The two groups did
             not differ significantly on IQ, but both groups scored
             significantly below nondelinquent cohort members. Results
             were inconsistent with the prediction of group differences
             posed by the differential detection hypothesis.},
   Doi = {10.1037//0021-843x.97.3.330},
   Key = {fds253473}
}

@article{fds253475,
   Author = {Share, DL and Moffitt, TE and Silva, PA},
   Title = {Factors associated with arithmetic-and-reading disability
             and specific arithmetic disability.},
   Journal = {Journal of learning disabilities},
   Volume = {21},
   Number = {5},
   Pages = {313-320},
   Year = {1988},
   Month = {May},
   url = {http://dx.doi.org/10.1177/002221948802100515},
   Doi = {10.1177/002221948802100515},
   Key = {fds253475}
}

@article{fds253474,
   Author = {Moffitt, TE and Silva, PA},
   Title = {Neuropsychological deficit and self-reported delinquency in
             an unselected birth cohort.},
   Journal = {Journal of the American Academy of Child and Adolescent
             Psychiatry},
   Volume = {27},
   Number = {2},
   Pages = {233-240},
   Year = {1988},
   Month = {March},
   url = {http://dx.doi.org/10.1097/00004583-198803000-00017},
   Abstract = {The Self-Report Early Deliquency instrument and a research
             battery of neuropsychological tests were administered
             blindly to a large unselected cohort of 13-year-old male and
             female subjects. Findings were cross-validated using split
             halves of the cohort. A pattern of verbal,
             visuospatial-motor integration, and memory deficits
             contributed variance to deliquency beyond that explained by
             social disadvantage, suggesting that some patterns of
             cognitive deficit may be associated with delinquent
             behavior. The significance of such a finding in a young
             cohort, not yet actively involved in or influenced by a life
             of delinquency, is discussed.},
   Doi = {10.1097/00004583-198803000-00017},
   Key = {fds253474}
}

@article{fds321674,
   Author = {Moffitt, TE and Silva, PA},
   Title = {Neuropsychological deficit and self-reported delinquency in
             an unselected birth cohort.},
   Journal = {Journal of the American Academy of Child and Adolescent
             Psychiatry},
   Volume = {27},
   Number = {2},
   Pages = {233-240},
   Year = {1988},
   Month = {March},
   Abstract = {The Sell-Report Early Delinquency instrument and a research
             battery of neuropsychological tests were administered
             blindly to a large unselected cohort of 13-year-old male and
             female subjects. Findings were cross-validated using split
             halves of the cohort. A pattern of verbal,
             visuospatial-motor integration, and memory deficits
             contributed variance to delinquency beyond that explained by
             social disadvantage, suggesting that some patterns of
             cognitive deficit may be associated with delinquent
             behavior. The significance of such a finding in a young
             cohort, not yet actively involved in or influenced by a life
             of delinquency, is discussed. © 1988 American Academy of
             Child and Adolescent Psychiatry.},
   Key = {fds321674}
}

@article{fds253472,
   Author = {Stevens, DE and Moffitt, TE},
   Title = {Neuropsychological profile of an Asperger's syndrome case
             with exceptional calculating ability},
   Journal = {Clinical Neuropsychologist},
   Volume = {2},
   Number = {3},
   Pages = {228-238},
   Publisher = {Informa UK Limited},
   Year = {1988},
   Month = {January},
   url = {http://dx.doi.org/10.1080/13854048808520105},
   Doi = {10.1080/13854048808520105},
   Key = {fds253472}
}

@article{fds253470,
   Author = {Moffitt, TE and Silva, PA},
   Title = {Self-reported delinquency: Results from an instrument for
             New Zealand},
   Journal = {Australian and New Zealand Journal of Criminology},
   Volume = {21},
   Number = {4},
   Pages = {227-240},
   Publisher = {SAGE Publications},
   Year = {1988},
   url = {http://dx.doi.org/10.1177/000486588802100405},
   Doi = {10.1177/000486588802100405},
   Key = {fds253470}
}

@article{fds253476,
   Author = {Moffitt, TE},
   Title = {Parental mental disorder and offspring criminal behavior: an
             adoption study.},
   Journal = {Psychiatry},
   Volume = {50},
   Number = {4},
   Pages = {346-360},
   Year = {1987},
   Month = {November},
   url = {http://dx.doi.org/10.1080/00332747.1987.11024366},
   Abstract = {It is not unreasonable to expect that some biological
             predisposition toward antisocial behavior may characterize
             the most serious of recidivistic and violent criminal
             offenders. This study used the adoption method to examine
             the contribution of mental disorder in adoptees' biological
             backgrounds to their recidivistic and violent criminal
             offending. Multiple recidivistic nonviolent criminal
             behavior was found at a significantly elevated rate in
             adopted-away sons when mental disorder and criminal
             involvement were characteristic of the adoptees' biological
             families. A similar, but nonsignificant, elevation was found
             for rates of violence. Parental diagnostic types associated
             most strongly with sons' later criminal involvement were
             drug abuse, alcohol abuse, and personality disorders.
             Parental psychoses were not related to offspring recidivism
             or violence in this cohort. Possible confounding effects of
             missing data, institutionalization prior to adoption,
             information given to adoptive parents by the adoption
             agencies about the child's biological background, historical
             period, perinatal factors, and selective placement were
             considered. Perinatal factors could not be discounted as
             contributors to the findings.},
   Doi = {10.1080/00332747.1987.11024366},
   Key = {fds253476}
}

@article{fds253477,
   Author = {Moffitt, TE and Silva, PA},
   Title = {WISC-R verbal and performance IQ discrepancy in an
             unselected cohort: clinical significance and longitudinal
             stability.},
   Journal = {Journal of consulting and clinical psychology},
   Volume = {55},
   Number = {5},
   Pages = {768-774},
   Year = {1987},
   Month = {October},
   ISSN = {0022-006X},
   url = {http://dx.doi.org/10.1037//0022-006x.55.5.768},
   Abstract = {This study examined children from an unselected birth cohort
             who had Wechsler Intelligence Scale for Children-Revised
             (WISC-R) verbal and performance IQ discrepancies that placed
             them beyond the 90th percentile. It was hypothesized that,
             relative to their cohort peers, these children would be
             characterized by greater frequency of perinatal
             difficulties, early childhood neurological abnormalities,
             health problems of neurological significance, and
             concussion. Additionally, it was hypothesized that such
             children would exhibit more behavior problems, lower
             academic achievement, and poorer motor skills. Generally,
             the null hypotheses were not rejected by the results.
             Longitudinal investigation of the stability of the verbal
             and performance IQ discrepancy revealed that about 23% of
             discrepant cases were discrepant at two or more ages.
             Depressed verbal IQ relative to performance IQ was found to
             be more common than the reverse pattern. Children with
             performance IQ greater than verbal IQ scored significantly
             lower than children for whom this pattern was reversed on
             measures of academic achievement. Results show that cautious
             interpretation is needed of verbal and performance IQ
             discrepancy in the general (nonneurological) assessment
             setting. © 1987 American Psychological Association.},
   Doi = {10.1037//0022-006x.55.5.768},
   Key = {fds253477}
}

@article{fds253478,
   Author = {Mednick, SA and Moffitt, TE and Gabrielli, WF and Hutchings,
             B},
   Title = {Genetic influenc-es on criminal behavior. Evidence from an
             adoption cohort},
   Journal = {Tijdschrift voor Criminologie},
   Volume = {27},
   Pages = {34-51},
   Year = {1985},
   Key = {fds253478}
}

@article{fds253479,
   Author = {Moffitt, TE},
   Title = {Implications for delinquency deterrence from the learning
             theory model of punishment},
   Journal = {Criminal Justice and Behavior},
   Volume = {10},
   Number = {2},
   Pages = {131-158},
   Publisher = {SAGE Publications},
   Year = {1983},
   url = {http://dx.doi.org/10.1177/0093854883010002001},
   Abstract = {Both the experimental laboratory model of punishment and the
             juvenile justice system's negative sanctioning process have
             a common goal of suppressing undesired behavior. The
             psychological literature on the experimental model of
             punishment contains a number of principles that have been
             demonstrated to improve the effectivenss of punishment in
             suppressing behaviors under controlled study. This article
             presents five of these principles, which yield predictions
             about deterrence of illegal acts by the use of negative
             sactions in the form of testable hypotheses. The principles
             are (1) intensity, (2) temporal proximity, (3) availability
             of reward, (4) schedule of delivery, and (5) availability of
             alternative behaviors. Following discussion of these
             principles and their implications for juvenile sanctioning,
             cautionary comments are made. The article concludes with the
             reminder that application of any of the principles of
             punishment would be premature without research aimed at
             exploration of the numerous issues brought up in the course
             of this exploratory article. © 1983, SAGE PUBLICATIONS. All
             rights reserved.},
   Doi = {10.1177/0093854883010002001},
   Key = {fds253479}
}

@article{fds253481,
   Author = {Moffitt, TE and Gabrielli, WF and Mednick, SA and Schulsinger,
             F},
   Title = {Socioeconomic status, IQ, and delinquency.},
   Journal = {Journal of abnormal psychology},
   Volume = {90},
   Number = {2},
   Pages = {152-156},
   Year = {1981},
   Month = {April},
   ISSN = {0021-843X},
   url = {http://dx.doi.org/10.1037//0021-843x.90.2.152},
   Abstract = {A number of studies have found a negative relationship
             between IQ and delinquent involvement. Some researchers
             maintain that IQ is a spurious variable in the relationship
             between socioeconomic status (SES) and delinquency, whereas
             others assert that IQ bears a causal relationship to
             delinquency that is independent of the effects of SES.
             Results from 2 Danish prospective longitudinal studies are
             presented that support the latter view. Ss in the 1st study
             were 129 males born between September, 1959 and December,
             1961; all male offspring born between 1944 and 1947 served
             as Ss in Study 2 (N = 31,436). In each study, a significant
             negative correlation between IQ and level of delinquent
             involvement remained after SES effects were partialled out.
             It is posited that low IQ children may be likely to engage
             in delinquent behavior because their poor verbal abilities
             limit their opportunities to obtain rewards in the school
             environment. (34 ref) (PsycINFO Database Record (c) 2006
             APA, all rights reserved). © 1981 American Psychological
             Association.},
   Doi = {10.1037//0021-843x.90.2.152},
   Key = {fds253481}
}

@article{fds253480,
   Author = {Parnas, J and Mednick, SA and Moffitt, TE and Crapuche,
             F},
   Title = {Perinatal complications and adult schizophrenia},
   Journal = {Trends in Neurosciences},
   Volume = {4},
   Number = {C},
   Pages = {262-264},
   Publisher = {Elsevier BV},
   Year = {1981},
   Month = {January},
   ISSN = {0166-2236},
   url = {http://dx.doi.org/10.1016/0166-2236(81)90082-5},
   Abstract = {Although the existence of a genetic predisposition in the
             etiology of schizophrenia is well established, little is
             known concerning environmental factors which contribute to
             schizophrenic breakdown. In this review the etiological
             significance of pregnancy and birth complications is
             considered, with special emphasis on the interactive roles
             of genetics and environmental insult. ©
             1981.},
   Doi = {10.1016/0166-2236(81)90082-5},
   Key = {fds253480}
}

@article{fds253482,
   Author = {Moffitt, TE},
   Title = {Vocabulary and arithmetic performance of father-absent
             boys},
   Journal = {Child Study Journal},
   Volume = {10},
   Number = {4},
   Pages = {233-241},
   Publisher = {SUNY-STATE UNIV NY BUFFALO, DEPT EDUCATIONAL
             FDN},
   Year = {1981},
   Key = {fds253482}
}

@article{fds253483,
   Author = {Mitchell, D and Winter, W and Moffitt, T},
   Title = {Cross-modality contrast: Exteroceptive context habituation
             enhances taste neophobia and conditioned taste
             aversions},
   Journal = {Animal Learning & Behavior},
   Volume = {8},
   Number = {4},
   Pages = {524-528},
   Publisher = {Springer Nature},
   Year = {1980},
   Month = {December},
   ISSN = {0090-4996},
   url = {http://dx.doi.org/10.3758/BF03197764},
   Abstract = {The relationship between absolute and relative stimulus
             novelty was examined within the context of the conditioned
             taste aversion paradigm in which the relative novelty of the
             conditioned interoceptive stimulus was manipulated by
             differential exteroceptive context habituation. Rats
             received similar isolation histories but either 5 or 30 days
             of habituation to the test environment prior to treatment.
             One group was administered lithium chloride following
             saccharin consumption, a second group was administered
             isotonic saline following saccharin consumption, and a third
             group was administered saline after water consumption. The
             animals habituated for 30 days exhibited greater conditioned
             avoidance and greater neophobic avoidance of saccharin than
             did animals habituated for only 5 days. The results are
             interpreted in terms of a cross-modality stimulus contrast
             effect which implicates context habituation as an important
             parameter of both taste neophobia and taste aversion
             learning. © 1980 Psychonomic Society, Inc.},
   Doi = {10.3758/BF03197764},
   Key = {fds253483}
}

@article{fds321675,
   Author = {Schulsinger, F and Mednick, SA and Walker, EF and Cudeck, R and Moffitt,
             T},
   Title = {Biosocial implications growing from high‐risk
             research},
   Journal = {Acta Psychiatrica Scandinavica},
   Volume = {62},
   Series = {Acta Psychiatrica Scandinavica Supplement 285, Vol.
             62,},
   Number = {285 S},
   Pages = {112-120},
   Booktitle = {Epidemiological research as basis of the organization of
             extramural psychiatry},
   Publisher = {WILEY},
   Editor = {E. Stromgren and A. Dupont and J.A. Nielsen},
   Year = {1980},
   Month = {January},
   url = {http://dx.doi.org/10.1111/j.1600-0447.1980.tb07681.x},
   Abstract = {A brief report of Mednick & Schulsinger's high‐risk study
             of schizophrenia is given. Path analyses of social and
             biological variables in the study demonstrate sex
             differences with implications for the etiology of
             schizophrenia. Sex is discussed as a possible
             non‐descriptive, biological addition to the traditional
             descriptive way of conceptualizing schizophrenia. Evidence
             for other social or psychological extensions of the
             definition of schizophrenia is mentioned. Copyright © 1980,
             Wiley Blackwell. All rights reserved},
   Doi = {10.1111/j.1600-0447.1980.tb07681.x},
   Key = {fds321675}
}


%% Books   
@book{fds69952,
   Author = {National Academy of Sciences Panel},
   Title = {Firearms and violence: A critical review},
   Publisher = {Washington, D.C. National Academcy of Sciences},
   Year = {2004},
   Key = {fds69952}
}

@book{fds140018,
   Author = {B. Lahey and T.E. Moffitt and A Caspi},
   Title = {The causes of Conduct Disorder},
   Year = {2003},
   Key = {fds140018}
}

@book{fds69912,
   Author = {Working party on genetics and human behaviour},
   Title = {Genetics and human behaviour: The ethical
             context},
   Publisher = {London: Nuffield Council on Bioethics},
   Year = {2002},
   Key = {fds69912}
}

@book{fds69900,
   Author = {Moffitt, T.E. and Caspi, A. and Rutter, M. and Silva,
             P.A},
   Title = {Sex differences in antisocial behaviour: Conduct disorder,
             delinquency, and violence in the Dunedin longitudinal
             study},
   Publisher = {Cambridge: Cambridge University Press},
   Year = {2001},
   Key = {fds69900}
}

@book{fds69887,
   Author = {Moffitt, T. E. and Caspi, A},
   Title = {Findings about partner violence in the Dunedin
             Multidisciplinary Health & Development Study},
   Series = {National Institute of Justice Research in
             Brief},
   Publisher = {Washington, D.C.: US Department of Justice},
   Year = {1999},
   url = {http://www.ncjrs.org},
   Key = {fds69887}
}


%% Chapters in Books   
@misc{fds358970,
   Author = {Lewis, SJ and Koenen, KC and Ambler, A and Arseneault, L and Caspi, A and Fisher, HL and Moffitt, TE and Danese, A},
   Title = {Psychopathology and cognitive deficits in young people
             exposed to complex trauma},
   Journal = {BJPsych Open},
   Volume = {7},
   Number = {S1},
   Pages = {S36-S37},
   Publisher = {Royal College of Psychiatrists},
   Year = {2021},
   Month = {June},
   url = {http://dx.doi.org/10.1192/bjo.2021.149},
   Abstract = {<jats:sec id="S2056472421001496_sec_a1"><jats:title>Aims</jats:title><jats:p>Complex
             traumas are traumatic experiences that involve multiple
             interpersonal threats during childhood or adolescence, such
             as repeated abuse. This type of trauma is hypothesized to
             lead to more severe psychopathology and poorer cognitive
             function than other non-complex traumas, such as road
             traffic accidents. However, empirical testing of this
             hypothesis has been limited to clinical or convenience
             samples and cross-sectional designs. To better understand
             this topic, we aimed to investigate psychopathology and
             cognitive function in young people exposed to complex,
             non-complex, or no trauma from a population-representative
             longitudinal cohort, and to consider the role of
             pre-existing vulnerabilities.</jats:p></jats:sec><jats:sec
             id="S2056472421001496_sec_a2"><jats:title>Method</jats:title><jats:p>Participants
             were from the Environmental Risk (E-Risk) Longitudinal Twin
             Study, a population-representative birth-cohort of 2,232
             children born in England and Wales in 1994-95. At age 18
             years (93% participation), we assessed lifetime exposure to
             complex and non-complex trauma. We also assessed past-year
             psychopathology including general psychopathology ‘p’
             and several psychiatric disorders, as well as current
             cognitive function including IQ, executive function, and
             processing speed. Additionally, we prospectively assessed
             early childhood vulnerabilities including internalizing and
             externalizing symptoms at age 5, IQ at age 5, family history
             of mental illness, family socioeconomic status, and
             sex.</jats:p></jats:sec><jats:sec id="S2056472421001496_sec_a3"><jats:title>Result</jats:title><jats:p>We
             found that participants who had been exposed to complex
             trauma had more severe psychopathology and poorer cognitive
             function across wide-ranging measures at age 18, compared to
             both trauma-unexposed participants and those exposed to
             non-complex trauma. Early childhood vulnerabilities had an
             important role in these presentations, as they predicted
             risk of later complex trauma exposure, and largely explained
             associations of complex trauma with cognitive deficits, but
             not with psychopathology.</jats:p></jats:sec><jats:sec
             id="S2056472421001496_sec_a4"><jats:title>Conclusion</jats:title><jats:p>By
             conflating complex and non-complex traumas, current research
             and clinical practice under-estimate the severity of
             psychopathology and cognitive deficits linked with complex
             trauma, as well as the role of pre-existing vulnerabilities.
             A better understanding of the mental health needs of people
             exposed to complex trauma and underlying mechanisms could
             inform the development of new effective interventions.</jats:p></jats:sec>},
   Doi = {10.1192/bjo.2021.149},
   Key = {fds358970}
}

@misc{fds359349,
   Author = {Bourassa, KJ and Caspi, A and Moffitt, TE},
   Title = {ADVERSE CHILDHOOD EXPERIENCES AND POORER HEALTH IN MIDLIFE:
             INVESTIGATING PSYCHOSOCIAL MECHANISMS OF
             ACTION},
   Journal = {PSYCHOSOMATIC MEDICINE},
   Volume = {83},
   Number = {7},
   Pages = {A22-A23},
   Year = {2021},
   Key = {fds359349}
}

@misc{fds361149,
   Author = {Agnew-Blais, J and Belsky, DW and Danese, A and Polanczyk, GV and Sugden, K and Wertz, J and Williams, B and Lewis, CM and Arseneault, L and Moffitt, TE},
   Title = {Household Chaos and Childhood ADHD Symptoms: A
             Gene-Environment Correlation Study},
   Journal = {BEHAVIOR GENETICS},
   Volume = {51},
   Number = {6},
   Pages = {687-688},
   Year = {2021},
   Key = {fds361149}
}

@misc{fds351565,
   Author = {Bourassa, KJ and Caspi, A and Harrington, H and Houts, R and Poulton, R and Ramrakha, S and Moffitt, TE},
   Title = {Intimate partner violence and lower relationship quality are
             associated with faster biological aging.},
   Journal = {Psychology and aging},
   Volume = {35},
   Number = {8},
   Pages = {1127-1139},
   Year = {2020},
   Month = {December},
   url = {http://dx.doi.org/10.1037/pag0000581},
   Abstract = {The characteristics of people's relationships have relevance
             to health-high quality romantic relationships are associated
             with improved health whereas intimate partner violence is
             associated with poorer health. Recently, increased attention
             has been focused on the biological processes underpinning
             these associations. A geroscience approach-examining whether
             close relationship characteristics are associated with
             biological aging-would complement previous research focused
             on individual disease pathways. This study used participants
             from the Dunedin Study (<i>N</i> = 974) to investigate
             relationship characteristics and biological aging across
             almost 20 years, from age 26 to 45. Being involved in
             romantic relationships was associated with slower biological
             aging, β = -0.12, <i>p</i> < .001. This difference
             represented 2.9 years of aging over the two decades. Greater
             relationship quality was also associated with slower
             biological aging, β = -0.19, <i>p</i> < .001, whereas
             higher levels of partner violence were associated with
             faster biological aging, β = 0.25, <i>p</i> < .001. A 1 SD
             difference in these characteristics was associated with a
             difference of 1.0 and 1.3 years of aging over the two
             decades, respectively. Secondary analyses suggested that
             experiencing violence from a partner was more strongly
             associated with biological aging than perpetrating violence,
             and that the experience of physical violence was more
             strongly associated with aging than psychological violence.
             These findings suggest that the characteristics of romantic
             relationships have relevance for biological aging in
             midlife. Interventions designed to increase relationship
             quality and decrease partner violence could reduce future
             morbidity and early mortality by slowing people's biological
             aging. (PsycInfo Database Record (c) 2020 APA, all rights
             reserved).},
   Doi = {10.1037/pag0000581},
   Key = {fds351565}
}

@misc{fds351566,
   Author = {Bourassa, KJ and Moffitt, TE and Caspi, A},
   Title = {ARE PEOPLE WITH GREATER CARDIOVASCULAR REACTIVITY SMARTER,
             HAPPIER, AND HEALTHIER? COUNTERINTUITIVE FINDINGS IN THE
             DUNEDIN AND MIDUS STUDIES},
   Journal = {PSYCHOSOMATIC MEDICINE},
   Volume = {82},
   Number = {6},
   Pages = {A225-A225},
   Year = {2020},
   Key = {fds351566}
}

@misc{fds354341,
   Author = {van Dongen, J and Hagenbeek, FA and Suderman, M and Roetman, P and Sugden, K and Chiocchetti, AG and Ismail, K and Mulder, RH and Hafferty,
             J and Adams, MJ and Walker, RM and Morris, SW and Lahti, J and Kupers, LK and Escaramis, G and Alemany, S and Bonder, MJ and Meijer, M and Ip, HF and Jansen, R and Baselmans, BML and Parmar, P and Lowry, E and Streit, F and Sirignano, L and Send, T and Frank, J and Jylhava, J and Wang, Y and Mishra, PP and Colins, OF and Corcoran, D and Poulton, R and Mill, J and Hannon, EJ and Arseneault, L and Korhonen, T and Vuoksimaa, E and Felix,
             J and Bakermans-Kranenburg, M and Campbell, A and Czamara, D and Binder,
             E and Corpeleijn, E and Ramon Gonzalez and J and Grazuleviciene, R and Gutzkow, KB and Evandt, J and Vafeiadi, M and Klein, M and van der Meer,
             D and Ligthart, L and Kluft, C and Davies, GE and Hakulinen, C and Keltikangas-Jarvinen, L and Franke, B and Freitag, CM and Konrad, K and Hervas, A and Fernandez-Rivas, A and Vetro, A and Raitakari, O and Lehtimaki, T and Vermeiren, R and Strandberg, T and Raikkonen, K and Snieder, H and Witt, SH and Deuschle, M and Pedersen, NL and Hagg, S and Sunyer, J and Franke, L and Kaprio, J and Ollikainen, M and Moffitt, TE and Tiemeier, H and van Ijzendoorn, MH and Relton, C and Vrijheid, M and Sebert, S and Jarvelin, M-R and Caspi, A and Evans, KL and McIntosh, AM and Bartels, M and Boomsma, D},
   Title = {DNA methylation signatures of a broad spectrum of aggressive
             behavior: a meta-analysis of epigenome-wide studies across
             the lifespan},
   Journal = {BEHAVIOR GENETICS},
   Volume = {50},
   Number = {6},
   Pages = {485-487},
   Year = {2020},
   Key = {fds354341}
}

@misc{fds370502,
   Author = {Wertz, J and Caspi, A and Arseneault, L and Belsky, DW and Richmond-Rakerd, L and Moffitt, TE},
   Title = {Young-adult outcomes of adolescent Borderline personality
             disorder symptoms: Results from a longitudinal twin cohort
             study},
   Journal = {PERSONALITY AND INDIVIDUAL DIFFERENCES},
   Volume = {157},
   Year = {2020},
   Key = {fds370502}
}

@misc{fds370503,
   Author = {Wertz, J and Moffitt, TE and Agnew-Blais, J and Arseneault, L and Belsky, DW and Corcoran, DL and Houts, R and Matthews, T and Prinz, JA and Richmond-Rakerd, L and Sugden, K and Williams, B and Caspi,
             A},
   Title = {Using DNA from mothers and children to study parental
             investment in children's educational attainment},
   Journal = {PERSONALITY AND INDIVIDUAL DIFFERENCES},
   Volume = {157},
   Year = {2020},
   Key = {fds370503}
}

@misc{fds340544,
   Author = {Fisher, H and Marzi, S and Arseneault, L and Wong, C and Kandaswamy, R and Moffitt, T and Roberts, S and Mill, J and Caspi, A},
   Title = {16.1 EPIGENETIC SIGNATURES OF CHILDHOOD AND ADOLESCENT
             VICTIMISATION USING A GENETICALLY SENSITIVE LONGITUDINAL
             COHORT STUDY.},
   Journal = {Schizophrenia Bulletin},
   Volume = {44},
   Number = {suppl_1},
   Pages = {S25-S25},
   Publisher = {Oxford University Press (OUP)},
   Year = {2018},
   Month = {April},
   url = {http://dx.doi.org/10.1093/schbul/sby014.060},
   Doi = {10.1093/schbul/sby014.060},
   Key = {fds340544}
}

@misc{fds340545,
   Author = {Crush, E and Arseneault, L and Moffitt, T and Danese, A and Caspi, A and Jaffee, S and Fisher, H},
   Title = {O12.3. PROTECTIVE FACTORS FOR PSYCHOTIC EXPERIENCES AMONGST
             ADOLESCENTS EXPOSED TO MULTIPLE FORMS OF
             VICTIMIZATION},
   Journal = {Schizophrenia Bulletin},
   Volume = {44},
   Number = {suppl_1},
   Pages = {S110-S110},
   Publisher = {Oxford University Press (OUP)},
   Year = {2018},
   Month = {April},
   url = {http://dx.doi.org/10.1093/schbul/sby015.271},
   Doi = {10.1093/schbul/sby015.271},
   Key = {fds340545}
}

@misc{fds340546,
   Author = {Trotta, A and Arseneault, L and Caspi, A and Danese, A and Moffitt, T and Pariante, C and Fisher, H},
   Title = {O8.3. CLINICAL AND FUNCTIONAL OUTCOMES IN YOUNG ADULTHOOD OF
             CHILDREN WITH PSYCHOTIC SYMPTOMS: A LONGITUDINAL TWIN COHORT
             STUDY},
   Journal = {Schizophrenia Bulletin},
   Volume = {44},
   Number = {suppl_1},
   Pages = {S97-S97},
   Publisher = {Oxford University Press (OUP)},
   Year = {2018},
   Month = {April},
   url = {http://dx.doi.org/10.1093/schbul/sby015.239},
   Doi = {10.1093/schbul/sby015.239},
   Key = {fds340546}
}

@misc{fds343480,
   Author = {Matthews, T and Danese, A and Caspi, A and Fisher, HL and Goldman-Mellor, S and Kepa, A and Moffitt, TE and Odgers, CL and Arsencault, L},
   Title = {Loneliness in young adulthood: Findings from an
             epidemiological cohort study},
   Journal = {EUROPEAN PSYCHIATRY},
   Volume = {48},
   Pages = {S34-S35},
   Publisher = {ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES
             ELSEVIER},
   Year = {2018},
   Month = {March},
   Key = {fds343480}
}

@misc{fds345886,
   Author = {Moffitt, TE},
   Title = {Adolescence-limited and life-course-persistent offending: A
             complementary pair of developmental theories},
   Pages = {11-54},
   Booktitle = {Developmental Theories of Crime and Delinquency},
   Year = {2018},
   Month = {February},
   ISBN = {9780765808301},
   Key = {fds345886}
}

@misc{fds341892,
   Author = {McGee, TR and Moffitt, TE},
   Title = {The developmental taxonomy},
   Pages = {149-158},
   Booktitle = {The Oxford Handbook of Developmental and Life-Course
             Criminology},
   Year = {2018},
   Month = {January},
   ISBN = {9780190201371},
   url = {http://dx.doi.org/10.1093/oxfordhb/9780190201371.013.9},
   Abstract = {This chapter considers whether the peak in the age–crime
             curve is a function of active offenders committing more
             crime during adolescence or a function of more individuals
             actively offending in the peak years. It discusses the two
             main and most empirically tested typological groupings: the
             life-course persistent group and the adolescence limited
             group. The chapter then reviews the evidence on a
             theoretically interesting grouping: those who abstain from
             antisocial and offending behavior. It focuses on the debate
             regarding whether those who were originally thought to
             recover from early-onset antisocial behavior have
             childhood-limited antisocial behavior or exhibit low-level
             chronic antisocial behavior across the life course. Finally,
             the chapter discusses how the theory it introduces accounts
             for adult-onset offending and considers whether there are
             gender differences that need to be accounted for by the
             theory.},
   Doi = {10.1093/oxfordhb/9780190201371.013.9},
   Key = {fds341892}
}

@misc{fds361151,
   Author = {Danese, A},
   Title = {The origins of cognitive deficits in victimized
             children},
   Journal = {Psychoneuroendocrinology},
   Volume = {83},
   Pages = {7-7},
   Publisher = {Elsevier BV},
   Year = {2017},
   Month = {September},
   url = {http://dx.doi.org/10.1016/j.psyneuen.2017.07.257},
   Doi = {10.1016/j.psyneuen.2017.07.257},
   Key = {fds361151}
}

@misc{fds341516,
   Author = {Moffitt, TE},
   Title = {Life-course-persistent versus adolescence-limited antisocial
             behavior},
   Pages = {75-103},
   Booktitle = {Developmental and Life-course Criminological
             Theories},
   Year = {2017},
   Month = {July},
   ISBN = {9780754629641},
   url = {http://dx.doi.org/10.4324/9781315094908},
   Doi = {10.4324/9781315094908},
   Key = {fds341516}
}

@misc{fds346407,
   Author = {Moffitt, TE},
   Title = {Adolescence-limited and life-course-persistent antisocial
             behavior: A developmental taxonomy},
   Pages = {405-432},
   Booktitle = {The Termination of Criminal Careers},
   Year = {2017},
   Month = {July},
   ISBN = {9780754620853},
   Abstract = {A dual taxonomy is presented to reconcile 2 incongruous
             facts about antisocial behavior: (a) It shows impressive
             continuity over age, but (b) its prevalence changes
             dramatically over age, increasing almost 10-fold temporarily
             during adolescence. This article suggests that delinquency
             conceals 2 distinct categories of individuals, each with a
             unique natural history and etiology: A small group engages
             in antisocial behavior of 1 sort or another at every life
             stage, whereas a larger group is antisocial only during
             adolescence. According to the theory of life-course-persistent
             antisocial behavior, children's neuropsychological problems
             interact cumulatively with their criminogenic environments
             across development, culminating in a pathological
             personality. According to the theory of adolescence-limited
             antisocial behavior, a contemporary maturity gap encourages
             teens to mimic antisocial behavior in ways that are
             normative and adjustive.},
   Key = {fds346407}
}

@misc{fds363845,
   Author = {Caspi, A and McClay, J and Moffitt, TE and Mill, J and Martin, J and Craig,
             IW and Taylor, A and Poulton, R},
   Title = {Role of genotype in the cycle of violence in maltreated
             children},
   Pages = {205-208},
   Booktitle = {Biosocial Theories of Crime},
   Year = {2017},
   Month = {July},
   ISBN = {9780754629191},
   Abstract = {We studied a large sample of male children from birth to
             adulthood to determine why some children who are maltreated
             grow up to develop antisocial behavior, whereas others do
             not. A functional polymorphism in the gene encoding the
             neurotransmitter-metabolizing enzyme monoamine oxidase A
             (MAOA) was found to moderate the effect of maltreatment.
             Maltreated children with a genotype conferring high levels
             of MAOA expression were less likely to develop antisocial
             problems. These findings may partly explain why not all
             victims of maltreatment grow up to victimize others, and
             they provide epidemiological evidence that genotypes can
             moderate children's sensitivity to environmental
             insults.},
   Key = {fds363845}
}

@misc{fds363843,
   Author = {Moffitt, TE},
   Title = {Adolescence-limited and life-course-persistent antisocial
             behavior: A developmental taxonomy},
   Pages = {69-96},
   Booktitle = {Biosocial Theories of Crime},
   Year = {2017},
   Month = {July},
   ISBN = {9780754629191},
   Abstract = {A dual taxonomy is presented to reconcile 2 incongruous
             facts about antisocial behavior: (a) It shows impressive
             continuity over age, but (b) its prevalence changes
             dramatically over age, increasing almost 10-fold temporarily
             during adolescence. This article suggests that delinquency
             conceals 2 distinct categories of individuals, each with a
             unique natural history and etiology: A small group engages
             in antisocial behavior of 1 sort or another at every life
             stage, whereas a larger group is antisocial only during
             adolescence. According to the theory of life-course-persislent
             antisocial behavior, children's neuropsychological problems
             interact cumulatively with their criminogenic environments
             across development, culminating in a pathological
             personality. According to the theory of adolescence-limited
             antisocial behavior, a contemporary maturity gap encourages
             teens to mimic antisocial behavior in ways that are
             normative and adjustive.},
   Key = {fds363843}
}

@misc{fds363844,
   Author = {Moffitt, TE},
   Title = {The new look of behavioral genetics in developmental
             psychopathology: Gene-environment interplay in antisocial
             behaviors},
   Pages = {183-204},
   Booktitle = {Biosocial Theories of Crime},
   Year = {2017},
   Month = {July},
   ISBN = {9780754629191},
   Abstract = {This article reviews behavioral-genetic research to show how
             it can help address questions o f causation in developmental
             psychopathology. The article focuses on studies of
             antisocial behavior, because these have been leading the way
             in investigating environmental as w ell as genetic
             influences on psychopathology. First, the article
             illustrates how behavioral-genetic methods are being newly
             applied to detect the best candidates for genuine
             environmental causes among the many risk factors for
             antisocial behavior. Second, the article examines findings o
             f interaction between genes and environments (G X E)
             associated with antisocial behavior, outlining steps for
             testing hypotheses o f measured G X E. Third, the article
             envisages future work on gene-environm ent interplay,
             arguing that it is an interesting and profitable way forward
             for psychopathology research.},
   Key = {fds363844}
}

@misc{fds366199,
   Author = {Piquero, AR and Moffitt, TE},
   Title = {Explaining the Facts of Crime: How the Developmental
             Taxonomy Replies to Farrington’s Invitation},
   Volume = {14},
   Pages = {51-72},
   Booktitle = {Integrated Developmental and Life-course Theories of
             Offending: Advances in Criminological Theory: Volume
             14},
   Year = {2017},
   Month = {January},
   ISBN = {9781412807999},
   url = {http://dx.doi.org/10.4324/9780203788431-3},
   Abstract = {The relationship between age and crime has been one of the
             most well-documented (Quetelet, 1831; Hirschi and
             Gottfredson, 1983) and contentious (Steffensmeier et al.,
             1989; Britt, 1992) of all criminological facts. Researchers
             studying the relationship between age and crime have
             typically observed that the aggregate pattern is such that
             criminal activity tends to peak in the late teens through
             the mid-twenties, and then declines throughout
             adulthood.},
   Doi = {10.4324/9780203788431-3},
   Key = {fds366199}
}

@misc{fds368961,
   Author = {Moffitt, TE},
   Title = {A Review of Research on the Taxonomy of Life-Course
             Persistent Versus Adolescence-Limited Antisocial
             Behavior},
   Volume = {15},
   Pages = {277-312},
   Booktitle = {Taking Stock: The Status of Criminological Theory: Advances
             in Criminological Theory: Volume 15},
   Year = {2017},
   Month = {January},
   ISBN = {9781315130620},
   url = {http://dx.doi.org/10.4324/9781315130620-11},
   Abstract = {This chapter reviews ten years of research into a
             developmental taxonomy of antisocial behavior that proposed
             two primary hypothetical prototypes: life-course persistent
             versus adolescence-limited offenders. According to the
             taxonomic theory, life-course persistent offenders’
             antisocial behavior has its origins in the
             neurodevelopmental processes beginning in childhood and
             continuing persistently thereafter. In contrast,
             adolescence-limited offenders’ antisocial behavior has its
             origins in social processes beginning in adolescence, and
             desists in young adulthood. According to the theory,
             life-course persistent antisocial individuals are few,
             persistent, and pathological. Adolescence-limited antisocial
             individuals are common, relatively transient, and near
             normative. The chapter shows that the adolescence-limited
             path is more strongly associated with delinquent peers, as
             compared against the life-course persistent path. However,
             one study that traced peer-affiliation trajectories
             concluded that peers were as influential for childhood-onset
             persistent offenders as for adolescent-onset offenders. The
             most direct test of the adolescence-limited etiological
             hypothesis was carried out in the Youth in Transition Survey
             of 2, 000 males.},
   Doi = {10.4324/9781315130620-11},
   Key = {fds368961}
}

@misc{fds366966,
   Author = {Moffitt, TE},
   Title = {How Individuals' Future Orientation Makes a Difference to
             Their Society: Self-control in a Four-decade Study of 1000
             Children},
   Volume = {27},
   Pages = {137-156},
   Booktitle = {FORESIGHT},
   Year = {2017},
   Key = {fds366966}
}

@misc{fds342822,
   Author = {Belsky, DW and Caspi, A and Poulton, R and Moffitt,
             T},
   Title = {BEYOND MICE: PARTICIPANT CHARACTERISTICS TO MEASURE IN HUMAN
             HEALTHSPAN EXTENSION TRIALS},
   Journal = {GERONTOLOGIST},
   Volume = {56},
   Pages = {348-348},
   Publisher = {OXFORD UNIV PRESS INC},
   Year = {2016},
   Month = {November},
   Key = {fds342822}
}

@misc{fds324441,
   Author = {Newbury, J and Arseneault, L and Caspi, A and Moffitt, TE and Odgers,
             CL and Fisher, HL},
   Title = {Neighbourhood Adversity, Crime Victimisation and Adolescent
             Psychotic Experiences: Findings from a Longitudinal Cohort
             Study},
   Journal = {EARLY INTERVENTION IN PSYCHIATRY},
   Volume = {10},
   Pages = {65-65},
   Publisher = {WILEY-BLACKWELL},
   Year = {2016},
   Month = {October},
   Key = {fds324441}
}

@misc{fds336533,
   Author = {Caspi, A and Moffitt, TE},
   Title = {Longitudinal cohort research: Sowing, nurturing, waiting,
             harvesting},
   Pages = {249-255},
   Booktitle = {Scientists Making a Difference: One Hundred Eminent
             Behavioral and Brain Scientists Talk about their Most
             Important Contributions},
   Publisher = {Cambridge University Press},
   Year = {2016},
   Month = {August},
   ISBN = {9781107127135},
   url = {http://dx.doi.org/10.1017/CBO9781316422250.055},
   Doi = {10.1017/CBO9781316422250.055},
   Key = {fds336533}
}

@misc{fds324774,
   Author = {Shalev, I and Caspi, A and Moffitt, TE},
   Title = {PERINATAL COMPLICATIONS PREDICT SUBJECTIVE AND OBJECTIVE
             AGING INDICATORS BY MIDLIFE},
   Journal = {The Gerontologist},
   Volume = {55},
   Number = {Suppl_2},
   Pages = {197-197},
   Publisher = {Oxford University Press (OUP)},
   Year = {2015},
   Month = {November},
   url = {http://dx.doi.org/10.1093/geront/gnv554.07},
   Doi = {10.1093/geront/gnv554.07},
   Key = {fds324774}
}

@misc{fds344830,
   Author = {Caspi, A and Lynam, D and Moffitt, TE and Silva, PA},
   Title = {Unraveling girls’ delinquency: Biological, dispositional,
             and contextual contributions to adolescent
             misbehavior},
   Pages = {293-304},
   Booktitle = {Risks and Problem Behaviors in Adolescence},
   Year = {2014},
   Month = {January},
   ISBN = {9780815332947},
   Abstract = {We examined processes linking biological and behavioral
             changes in different contexts during adolescence by studying
             an unselected cohort of New Zealand girls from childhood
             through adolescence when they entered either mixed-sex or
             all-girl secondary schools. The impact of menarcheal timing
             on female delinquency was moderated by the sex composition
             of schools: early-maturing girls in mixed-sex settings were
             at greatest risk for delinquency. Individual differences in
             delinquency were also significantly more stable among girls
             in mixed-sex schools than among those in all-girl schools.
             These contextual variations are interpreted in terms of the
             differential distribution of reinforcements and
             opportunities for delinquency.},
   Key = {fds344830}
}

@misc{fds365873,
   Author = {Taylor, PJ and van den Bree, MBM and Williams, N and Moffitt,
             TE},
   Title = {Genetic influences on antisocial behaviour, problem
             substance use and schizophrenia: Evidence from quantitative
             genetic and molecular genetic studies},
   Pages = {186-210},
   Booktitle = {Forensic Psychiatry: clinical, legal and ethical issues,
             Second Edition},
   Year = {2014},
   Month = {January},
   ISBN = {9780340806289},
   url = {http://dx.doi.org/10.1201/b15462-8},
   Abstract = {This chapter considers the genetic contribution in more
             detail. It provides a basic introduction to concepts and an
             overview of research methods in the fields of most relevance
             to forensic psychiatry. The chapter presents a summary of
             quantitative genetic and molecular genetic findings in these
             areas. Adoption and twin studies yield information about the
             relative contributions of genes and environment to
             antisocial behaviour, problem substance use and
             schizophrenia, but molecular genetic studies are needed to
             elucidate their genetic architecture. The importance of
             gene-environment interplay on complex traits has gained
             increasing recognition. Adoption and twin studies yield
             information about the relative contributions of genes and
             environment to antisocial behaviour, problem substance use
             and schizophrenia, but molecular genetic studies are needed
             to elucidate their genetic architecture. The serotonergic
             system has been implicated in a variety of traits, including
             impulsivity, addictive behaviour, suicide, mood regulation,
             sexual activity, appetite and eating disorder as well as
             cognition, sensory processing and motor activity.},
   Doi = {10.1201/b15462-8},
   Key = {fds365873}
}

@misc{fds345887,
   Author = {Moffitt, TE},
   Title = {Adolescence-limited and life-course-persistent antisocial
             behavior: A developmental taxonomy},
   Pages = {90-117},
   Booktitle = {The Science of Mental Health: Volume 7: Personality and
             Personality Disorder},
   Year = {2013},
   Month = {January},
   ISBN = {9780815337508},
   Abstract = {A dual taxonomy is presented to reconcile 2 incongruous
             facts about antisocial behavior: (a) It shows impressive
             continuity over age, but (b) its prevalence changes
             dramatically over age, increasing almost I Q-fold
             temporarily during adolescence. This article suggests that
             delinquency conceals 2 distinct categories of individuals.
             each with a unique natural history and etiology: A small
             group engages in antisocial behavior of I sort or another at
             every life stage, whereas a larger group is anti social only
             during adolescence. According to the theory of
             life-collrse-persistenl antisocial behavior, children’s
             neuropsychological problems interact cumulatively with their
             criminogenic environments across development. culminating in
             a pathologicaJ personality. According to the theory of
             adolescence- limited antisocial behavior. a contemporary
             maturity gap encourages teens to mimic antisocial behavior
             in ways that are normative and adjustive.},
   Key = {fds345887}
}

@misc{fds213238,
   Author = {T.E. Moffitt},
   Title = {Preface},
   Booktitle = {Handbook of Life-course Criminology},
   Publisher = {Springer Verlag},
   Editor = {C. Gibson and M. Krohn},
   Year = {2013},
   ISBN = {978-1-4614-5113-6},
   url = {http://www.springer.com/social+sciences/criminology/book/978-1-4614-5112-9},
   Keywords = {Crime Prevention and Intervention • Criminal Policy
             • Domestic Violence • Drug Abuse Prevention •
             Emerging Adulthood • Quantitative Criminology •
             Youth Gangs},
   Key = {fds213238}
}

@misc{fds372072,
   Author = {Fisher, H and Caspi, A and Poulton, R and Meier, M and Houts, R and Harrington, H and Arseneault, L and Moffitt, T},
   Title = {Specificity of childhood psychotic symptoms for predicting
             schizophrenia by 38 years of age: a birth cohort
             study},
   Journal = {EUROPEAN CHILD & ADOLESCENT PSYCHIATRY},
   Volume = {22},
   Pages = {S129-S129},
   Year = {2013},
   Key = {fds372072}
}

@misc{fds253126,
   Author = {Moffitt, TE},
   Title = {Self-Control, Then and Now},
   Pages = {40-45},
   Booktitle = {The Future of Criminology},
   Publisher = {Oxford University Press},
   Year = {2012},
   Month = {September},
   ISBN = {9780199917938},
   url = {http://dx.doi.org/10.1093/acprof:oso/9780199917938.003.0005},
   Abstract = {This chapter advances the need to improve the physical and
             financial health of populations and reduce crime. It focuses
             on the role of poor self-control in predicting delinquency,
             health outcomes, substance use dependence, and financial
             wealth, providing supporting data from the Dunedin
             longitudinal study and the Environmental-Risk Longitudinal
             Twin Study. The role of sibling comparisons is stressed to
             examine differences in self-control among siblings reared in
             the same family environment. The findings are highly
             relevant for future intervention programs aimed at enhancing
             self-control at all levels in the population.},
   Doi = {10.1093/acprof:oso/9780199917938.003.0005},
   Key = {fds253126}
}

@misc{fds213239,
   Author = {T.E. Moffitt},
   Title = {Childhood self-control and the population's crime rate,
             health, and wealth},
   Booktitle = {Festschrift for David Farrington, The Future of
             Criminology},
   Publisher = {Oxford University Press},
   Editor = {R. Loeber},
   Year = {2012},
   Key = {fds213239}
}

@misc{fds370504,
   Author = {Ouellet-Morin, I and Odgers, C and Danese, A and Bowes, L and Shakoor,
             S and Papadopoulos, AS and Caspi, A and Moffitt, TE and Arsenault,
             L},
   Title = {Blunted cortisol responses to stress signals social and
             behavioural problems among maltreated/bullied 12 year-old
             children},
   Journal = {EUROPEAN CHILD & ADOLESCENT PSYCHIATRY},
   Volume = {20},
   Number = {1},
   Pages = {S90-S90},
   Publisher = {SPRINGER},
   Year = {2011},
   Month = {June},
   Key = {fds370504}
}

@misc{fds372023,
   Author = {Davidson, M and Reichenberg, AA and Levine, SZ and Rabinowitz, J and Keefe, R and Murray, R and Moffitt, T and Caspi, A},
   Title = {MODELING THE EXPRESSION AND COURSE OF DEVELOPMENTAL
             ABNORMALITIES PRECEDING ADULT SCHIZOPHRENIA:
             CHARACTERIZATION OF A NEW DEVELOPMENTAL ULTRA-HIGH-RISK
             GROUP IN 2 BIRTH COHORTS},
   Journal = {SCHIZOPHRENIA BULLETIN},
   Volume = {37},
   Pages = {49-50},
   Publisher = {OXFORD UNIV PRESS},
   Year = {2011},
   Month = {March},
   Key = {fds372023}
}

@misc{fds199384,
   Author = {T.E. Moffitt and S. Ross},
   Title = {Self control, health, wealth and public safety},
   Booktitle = {Controlling CrimeL strategies and tradeoffs,},
   Publisher = {Univ of Chicago Press},
   Editor = {PJ cook, J Ludwig and J McCrary},
   Year = {2011},
   Key = {fds199384}
}

@misc{fds198963,
   Author = {VandenBree, M. and Moffitt, T.E.},
   Title = {Developmental pathways into antisocial behaviour: Genes and
             experience.},
   Volume = {in press},
   Booktitle = {Forensic Psychiatry},
   Publisher = {Oxford University Press},
   Editor = {J. Gunn and P. Taylor},
   Year = {2011},
   Key = {fds198963}
}

@misc{fds198730,
   Author = {Caspi, A. and Holmes, A and Uher, R and Hariri, A and Moffitt,
             TE},
   Title = {Genetic sensitivity to the environment: The case of the
             serotonin transporter gene (5-HTT), and is implications for
             studying complex diseases and traits.},
   Booktitle = {Gene–Environment Interactions in Developmental
             Psychopathology.},
   Publisher = {Guilford Publications},
   Editor = {K Dodge and M Rutter},
   Year = {2011},
   Key = {fds198730}
}

@misc{fds198731,
   Author = {Moffitt, TE. and Ross, S.},
   Title = {Self-control, Health, Wealth and Public Safety},
   Booktitle = {Controlling Crime: Strategies and Tradeoffs},
   Publisher = {Chicago: University of Chicago Press},
   Editor = {PJ Cook and J Ludwig and J McCrary},
   Year = {2011},
   Key = {fds198731}
}

@misc{fds168815,
   Author = {Piquero, A. and Moffitt T.E.},
   Title = {The personal history of the developmental taxonomy of
             antisocial behavior: An interview with Terrie
             Moffitt},
   Booktitle = {The Origins of Criminology: Advances in Criminological
             Theory},
   Editor = {F.T. Cullen},
   Year = {2011},
   Key = {fds168815}
}

@misc{fds253128,
   Author = {Piquero, AR and Moffitt, TE},
   Title = {Life-course persistent offending},
   Pages = {201-222},
   Booktitle = {Forensic Psychology: Concepts, Debates and Practice: Second
             Edition},
   Publisher = {Willan},
   Year = {2010},
   Month = {July},
   ISBN = {9780203833308},
   url = {http://dx.doi.org/10.4324/9780203833308},
   Doi = {10.4324/9780203833308},
   Key = {fds253128}
}

@misc{fds287926,
   Author = {Reichenberg, A and Caspi, A and Harrington, H and Houts, R and Keefe,
             RS and Murray, RM and Poulton, R and Moffitt, TE},
   Title = {Static and Dynamic Cognitive Deficits in Childhood Precede
             Adult Schizophrenia: A 30-Year Study},
   Journal = {BIOLOGICAL PSYCHIATRY},
   Volume = {67},
   Number = {9},
   Pages = {12S-12S},
   Publisher = {ELSEVIER SCIENCE INC},
   Year = {2010},
   Month = {May},
   ISSN = {0006-3223},
   url = {http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000277064200039&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=47d3190e77e5a3a53558812f597b0b92},
   Key = {fds287926}
}

@misc{fds342724,
   Author = {Reichenberg, A and Caspi, A and Harrington, H and Houts, R and Keefe, R and Murray, R and Poulton, R and Moffitt, T},
   Title = {STATIC AND DYNAMIC COGNITIVE DEFICITS IN CHILDHOOD PRECEDE
             ADULT SCHIZOPHRENIA: A 30-YEAR STUDY},
   Journal = {Schizophrenia Research},
   Volume = {117},
   Number = {2-3},
   Pages = {175-175},
   Publisher = {Elsevier BV},
   Year = {2010},
   Month = {April},
   url = {http://dx.doi.org/10.1016/j.schres.2010.02.207},
   Doi = {10.1016/j.schres.2010.02.207},
   Key = {fds342724}
}

@misc{fds168818,
   Author = {Moffitt, T.E. and Ross, S. and Raine, A.},
   Title = {Crime and biology},
   Booktitle = {Crime, 2nd edition},
   Publisher = {Oxford University Press},
   Editor = {J.Q.Wilson and J.Petersilia},
   Year = {2010},
   Key = {fds168818}
}

@misc{fds168812,
   Author = {Moffitt, T.E. and Caspi, A. and Harrington,
             HL.},
   Title = {Life-course persistent and adolescence-limited antisocial
             males followed to adulthood.},
   Booktitle = {A developmental approach to antisocial behaviour},
   Publisher = {The Hague: North Holland Publishers},
   Editor = {W.Koops, R.Loeber and W.Slot},
   Year = {2009},
   Key = {fds168812}
}

@misc{fds168665,
   Author = {Moffitt, T.E. and Caspi, A. and Harrington, HL. and Milne, B. and Melchior, M. and Goldberg, D. and Poulton, R.},
   Title = {Generalized anxiety disorder and depression: Childhood risk
             factors in a birth cohort followed to age
             32.},
   Booktitle = {Diagnostic Issues in Depression and Generalized Anxiety
             Disorder: Refining the Research Agenda for
             DSM-IV.},
   Publisher = {Arlington, VA: American Psychiatric Association},
   Editor = {Goldberg, D. and Kendler, K.S. and Sirovatka, P. and Regier, D.A.},
   Year = {2009},
   Key = {fds168665}
}

@misc{fds349444,
   Author = {Slutske, WS and Caspi, A and Moffitt, TE and Piasecki, TM and Sher, KJ and Poulton, R},
   Title = {Developmentally-limited versus persistent alcohol
             dependence: A longitudinal birth cohort study},
   Journal = {ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH},
   Volume = {31},
   Number = {6},
   Pages = {312A-312A},
   Publisher = {BLACKWELL PUBLISHING},
   Year = {2007},
   Month = {June},
   Key = {fds349444}
}

@misc{fds70026,
   Author = {Moffitt, T. E. and Caspi, A},
   Title = {Evidence from behavioral genetics for environmental
             contributions to antisocial conduct},
   Pages = {96-123},
   Booktitle = {Handbook of Socialization},
   Publisher = {New York: Guilford Press},
   Editor = {J. Grusec and P. Hastings},
   Year = {2007},
   Key = {fds70026}
}

@misc{fds70027,
   Author = {Moffitt, T.E},
   Title = {A review of research on the taxonomy of life-course
             persistent and adolescence-limited offending},
   Booktitle = {The Cambridge handbook of violent behavior},
   Publisher = {New York: Cambridge University Press},
   Editor = {D. Flannery and A .Vazonsyi and I. Waldman},
   Year = {2007},
   Key = {fds70027}
}

@misc{fds70028,
   Author = {Moffitt, T. E. and Caspi, A},
   Title = {Evidence from behavioral genetics for environmental
             contributions to antisocial conduct},
   Pages = {45-82},
   Booktitle = {Crime and Schizophrenia: Causes & Cures},
   Publisher = {New York: Nova Science Publishers},
   Editor = {A. Raine},
   Year = {2007},
   Key = {fds70028}
}

@misc{fds70040,
   Author = {Moffitt, T.E. and Caspi, A. and Harrington, HL},
   Title = {Life-course persistent and adolescence-limited antisocial
             males followed to adulthood},
   Booktitle = {A developmental approach to antisocial behaviour},
   Publisher = {The Hague: North Holland Publishers},
   Editor = {W.Koops, R.Loeber and W.Slot},
   Year = {2007},
   Key = {fds70040}
}

@misc{fds70041,
   Author = {Hussong, A.M. and Curran, P.J. and Moffitt, T.E. and Caspi,
             A},
   Title = {A test of developmental snares using latent growth
             trajectory models},
   Booktitle = {Turning points: Developmental stages, secular trends, and
             individual change: Theoretical considerations, research
             designs, and alternative methods of analysis},
   Editor = {P. Cohen and B. Cudeck and B. Pruzek},
   Year = {2007},
   Key = {fds70041}
}

@misc{fds70042,
   Author = {Moffitt, T.E. and Scott, S},
   Title = {Conduct Disorder},
   Series = {4th edition},
   Booktitle = {Rutter’s Child and Adolescent Psychiatry},
   Publisher = {London: Blackwell's},
   Year = {2007},
   Key = {fds70042}
}

@misc{fds70043,
   Author = {VandenBree, M. and Moffitt, T.E},
   Title = {Developmental pathways into antisocial behaviour: Genes and
             experience},
   Booktitle = {Forensic Psychiatry},
   Publisher = {London: Hodder Arnold},
   Editor = {J. Gunn and P. Taylor},
   Year = {2007},
   Key = {fds70043}
}

@misc{fds366198,
   Author = {Moffitt, TE},
   Title = {A Review of Research on the Taxonomy of Life-Course
             Persistent Versus Adolescence-Limited Antisocial
             Behavior},
   Pages = {49-74},
   Booktitle = {CAMBRIDGE HANDBOOK OF VIOLENT BEHAVIOR AND
             AGGRESSION},
   Year = {2007},
   Key = {fds366198}
}

@misc{fds340549,
   Author = {Gregory, AM and Caspi, A and Moffitt, TE and Poulton,
             R},
   Title = {Family conflict in childhood: a predictor of later
             insomnia},
   Journal = {JOURNAL OF SLEEP RESEARCH},
   Volume = {15},
   Pages = {154-154},
   Publisher = {BLACKWELL PUBLISHING},
   Year = {2006},
   Month = {September},
   Key = {fds340549}
}

@misc{fds372024,
   Author = {Murray, R and Arseneault, L and Caspi, A and Moffitt, T and Cannon, M and Boydell, J and Thirtalli, J},
   Title = {Adolescent cannabis use and later psychosis},
   Journal = {AUSTRALIAN AND NEW ZEALAND JOURNAL OF PSYCHIATRY},
   Volume = {40},
   Pages = {A106-A106},
   Publisher = {BLACKWELL PUBLISHING},
   Year = {2006},
   Month = {August},
   Key = {fds372024}
}

@misc{fds253140,
   Author = {Moffitt, TE and Caspi, A},
   Title = {Evidence from behavioral genetics for environmental
             contributions to antisocial conduct},
   Pages = {45-81},
   Booktitle = {The explanation of crime: Context, mechanisms, and
             development},
   Publisher = {Cambridge UK: Cambridge University Press},
   Editor = {P.O. Wikstrom and Rob J. Sampson},
   Year = {2006},
   Month = {January},
   ISBN = {9781594546099},
   url = {http://dx.doi.org/10.1017/CBO9780511489341.005},
   Abstract = {This chapter reviews recent behavioral-genetic research that
             is helping to address questions about the non-genetic,
             environmental causes of antisocial conduct. We illustrate
             how behavioral-genetic methods are being newly applied to
             detect the genuine environmental influences among the many
             risk factors for antisocial behavior. We further examine
             interactions between genes and environments, in which
             environmental effects may be stronger than previously
             assumed, within genetically vulnerable children. Despite
             assiduous efforts to eliminate it, antisocial behavior is
             still a problem. Approximately 20% of people in the
             developed world experience victimization by perpetrators of
             violent and non-violent illegal behavior each year (U.S.
             Bureau of Justice Statistics, 2002). The World Report on
             Violence and Health (WHO, 2002) tallies the staggering
             burden of mortality, disease, disability, and compromised
             well-being brought about by perpetrators of family violence
             and other violent crimes. Behavioral science needs to
             achieve a more complete understanding of the causes of
             antisocial behavior to provide an evidence base for
             effectively controlling and preventing antisocial behavior.
             A new wave of intervention research in the last decade has
             demonstrated clear success for a number of programs designed
             to prevent antisocial behavior (http://www.preventingcrime.org;
             Heinrich, Brown and Aber, 1999; Sherman et al., 1999;
             Weissberg, Kumpfer and Seligman, 2003). Nevertheless, the
             reduction in antisocial behavior brought about by even the
             best prevention programs is, on average, modest (Dodge,
             2003; Wasserman and Miller, 1998; Olds et al., 1998;
             Heinrich, Brown and Aber, 1999; Wandersman and Florin, 2003;
             Wilson, Gottfredson and Najaka, 2001). The best-designed
             intervention programs reduce serious juvenile offenders'
             recidivism only by about 12% (Lipsey and Wilson, 1998). This
             modest success of interventions that were theory-driven,
             well-designed and amply-funded sends a clear message that we
             do not yet understand the causes of antisocial behavior well
             enough to prevent it. © 2006 by Nova Science Publishers,
             Inc. All rights reserved.},
   Doi = {10.1017/CBO9780511489341.005},
   Key = {fds253140}
}

@misc{fds340550,
   Author = {Sugden, K and Caspi, A and Moffitt, TE and Craig,
             IW},
   Title = {S.03.02 Gene-environment interaction in depression},
   Journal = {European Neuropsychopharmacology},
   Volume = {16},
   Pages = {S168-S168},
   Publisher = {Elsevier BV},
   Year = {2006},
   Month = {January},
   url = {http://dx.doi.org/10.1016/s0924-977x(06)70024-4},
   Doi = {10.1016/s0924-977x(06)70024-4},
   Key = {fds340550}
}

@misc{fds321673,
   Author = {Moffitt, TE},
   Title = {Life-Course-Persistent versus Adolescence-Limited Antisocial
             Behavior},
   Volume = {3},
   Series = {2nd edition},
   Pages = {570-598},
   Booktitle = {Developmental Psychopathology: Second Edition},
   Publisher = {JOHN WILEY & SONS INC},
   Editor = {D. Cicchetti and D. J. Cohen},
   Year = {2006},
   Month = {January},
   ISBN = {9780471237389},
   url = {http://dx.doi.org/10.1002/9780470939406.ch15},
   Abstract = {This chapter reviews 10 years of research into a
             developmental taxonomy of antisocial behavior that proposed
             two primary hypothetical prototypes: life-course-persistent
             versus adolescence-limited offenders. According to the
             taxonomic theory, life-course-persistent offenders'
             antisocial behavior has its origins in neurodevelopmental
             processes; it begins in childhood and continues persistently
             thereafter. In contrast, adolescence- limited offenders'
             antisocial behavior has its origins in social processes; it
             begins in adolescence and desists in young adulthood.
             Life-course-persistent antisocial behavior originates early
             in life, when the difficult behavior of a high-risk young
             child is exacerbated by a high-risk social environment. The
             chapter presents four groups of existing studies, which
             suggests that the pattern of antisocial behavior that begins
             early in life, is pervasive across settings, is
             characterized by aggressive personality traits, includes
             physical aggression, and persists into adulthood is
             associated with relatively more genetic influence than is
             the pattern of later-onset, situational, transient
             delinquency.},
   Doi = {10.1002/9780470939406.ch15},
   Key = {fds321673}
}

@misc{fds70016,
   Author = {Moffitt, T. E. and Caspi, A},
   Title = {Facteurs de risque associes aux trajectoires
             developpementales des conduites antisociales chez les
             garcons et les filles},
   Pages = {79-120},
   Booktitle = {Les conduites antisociales des filles},
   Publisher = {Press de l’Universite du Quebec},
   Editor = {P. Verlaan and M. Dery},
   Year = {2006},
   Key = {fds70016}
}

@misc{fds70017,
   Author = {Moffitt, T.E},
   Title = {A review of research on the taxonomy of life-course
             persistent and adolescence-limited offending},
   Pages = {502-521},
   Booktitle = {Taking Stock: The Status of Criminological
             Theory},
   Publisher = {New Brunswick, NJ: Transactions Publishers},
   Editor = {F.T. Cullen and J.P. Wright and M. Coleman},
   Year = {2006},
   Key = {fds70017}
}

@misc{fds372073,
   Author = {Murray, R and Arseneault, L and Caspi, A and Moffitt, T and Cannon, M and Boydell, J and Thirtalli, J},
   Title = {Adolescent cannabis use and later psychosis},
   Journal = {SCHIZOPHRENIA RESEARCH},
   Volume = {81},
   Pages = {10-11},
   Year = {2006},
   Key = {fds372073}
}

@misc{fds340551,
   Author = {Cannon, M and Moffitt, TE and Caspi, A and Harrington, HL and Murray,
             RA and Poulton, R},
   Title = {Neuropsychological deficits at age 13 and later
             schizophreniform disorder: A longitudinal birth cohort
             study},
   Journal = {SCHIZOPHRENIA BULLETIN},
   Volume = {31},
   Number = {2},
   Pages = {319-320},
   Publisher = {OXFORD UNIV PRESS},
   Year = {2005},
   Month = {April},
   Key = {fds340551}
}

@misc{fds69993,
   Author = {Piquero, A. and Moffitt, T.E},
   Title = {Explaining the facts of crime: How development taxonomy
             replies to Farrington’s invitation},
   Volume = {14},
   Booktitle = {Integrated Developmental and Life-Course Theories of
             Offiending:Advances in Criminological Theory},
   Publisher = {New Brunswick, NJ: Transactions Press},
   Editor = {D.P. Farrington},
   Year = {2005},
   Key = {fds69993}
}

@misc{fds69994,
   Author = {Piquero, AR and Moffitt, TE and Lawton, B},
   Title = {Race and Crime: The contribution of individual, familial,
             and neighborhood level risk factors to life-course-persistent
             offending},
   Booktitle = {Our children, your children: Confronting race and ethnicity
             in the American juvenile justice system},
   Publisher = {Chicago, IL: University of Chicago Press},
   Editor = {D Hawkins and K Kempf-Leonard},
   Year = {2005},
   Key = {fds69994}
}

@misc{fds370505,
   Author = {Mill, J and Caspi, A and Dempster, EL and Williams, BS and Moffitt, TE and Craig, I},
   Title = {Methylation analysis of a NGF1-A transcription factor
             binding-site in the promoter region of the human
             glucocorticoid receptor gene (NR3C1)},
   Journal = {AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC
             GENETICS},
   Volume = {138B},
   Number = {1},
   Pages = {89-89},
   Year = {2005},
   Key = {fds370505}
}

@misc{fds370506,
   Author = {Mill, J and Caspi, A and Williams, BS and Craig, I and Taylor, A and Polo-Tomas, M and Berridge, C and Poulton, R and Moffitt,
             TE},
   Title = {Genetic polymorphisms predict variationiin intelligence and
             adult prognosis among children with attention-deficit
             hyperactivity disorder},
   Journal = {AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC
             GENETICS},
   Volume = {138B},
   Number = {1},
   Pages = {59-59},
   Year = {2005},
   Key = {fds370506}
}

@misc{fds340553,
   Author = {Cannon, M and Moffitt, TE and Caspi, A and Harrington, HL and Murray,
             RM and Poulton, R},
   Title = {Neuropsychological function at age 13 and later
             schizophreniform disorder: A longitudinal birth cohort
             study},
   Journal = {AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC
             GENETICS},
   Volume = {130B},
   Number = {1},
   Pages = {15-15},
   Publisher = {WILEY-LISS},
   Year = {2004},
   Month = {September},
   Key = {fds340553}
}

@misc{fds340554,
   Author = {Cannon, M and Moffitt, TE and Caspi, A and Harrington, HL and Murray,
             RM and Poulton, R},
   Title = {Neuropsychological function at age 13 and later
             schizophreniform disorder in a longitudinal birth
             cohort},
   Journal = {EUROPEAN PSYCHIATRY},
   Volume = {19},
   Pages = {65S-65S},
   Publisher = {EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER},
   Year = {2004},
   Month = {April},
   Key = {fds340554}
}

@misc{fds340555,
   Author = {Cannon, M and Moffitt, TE and Caspi, A and Harrington, HL and Murray,
             RM and Poulton, R},
   Title = {Poor executive function at age 13 predicts later
             schizophreniform disorder: A longitudinal birth cohort
             study},
   Journal = {SCHIZOPHRENIA RESEARCH},
   Volume = {67},
   Number = {1},
   Pages = {19-19},
   Publisher = {ELSEVIER SCIENCE BV},
   Year = {2004},
   Month = {February},
   Key = {fds340555}
}

@misc{fds69969,
   Author = {Piquero, A. and Moffitt, T.E},
   Title = {Life-course-persistent and adolescence-limited
             offending},
   Booktitle = {Forensic Psychology Debates, Concepts, &
             Practice},
   Publisher = {Devon: Willan Publishing},
   Editor = {Joanna Adler},
   Year = {2004},
   Key = {fds69969}
}

@misc{fds69970,
   Author = {Loeber, R. and Farrington, D.P. and Stouthamer-Loeber, M. and Moffitt, T. E. and Caspi, A. and White, H.R. and Wei, E.H. and Beyers,
             J.M},
   Title = {The development of male offending: Key findings from 14
             years of the Pittsburgh Youth Study},
   Booktitle = {Longitudinal research in the social and behavioral
             sciences},
   Publisher = {New York: Kluwer/Plenum},
   Editor = {T. Thornberry and M. Krohn},
   Year = {2004},
   Key = {fds69970}
}

@misc{fds69968,
   Author = {Moffitt, T.E},
   Title = {Developmental course of health-risking behaviors},
   Booktitle = {Preventing Violence and Related Health-risking Behaviors in
             Adolescents: An NIH State of the Science
             Consensus},
   Publisher = {Bethesda, MD: National Institutes of Health},
   Year = {2004},
   Key = {fds69968}
}

@misc{fds340556,
   Author = {Cannon, M and Arseneault, L and Poulton, R and Murray, RM and Caspi, A and Moffitt, TE},
   Title = {Cannabis use in adolescence and risk for adult psychosis: A
             birth cohort study},
   Journal = {Schizophrenia Research},
   Volume = {60},
   Number = {1},
   Pages = {35-35},
   Publisher = {Elsevier BV},
   Year = {2003},
   Month = {March},
   url = {http://dx.doi.org/10.1016/s0920-9964(03)80102-0},
   Doi = {10.1016/s0920-9964(03)80102-0},
   Key = {fds340556}
}

@misc{fds69948,
   Author = {Moffitt, T.E},
   Title = {Life-course persistent and adolescence-limited antisocial
             behaviour: A 10- year research review and a research
             agenda},
   Booktitle = {The causes of conduct disorder and serious juvenile
             delinquency},
   Publisher = {New York: Guilford},
   Editor = {B. Lahey and T. Moffitt and A.Caspi},
   Year = {2003},
   Key = {fds69948}
}

@misc{fds69950,
   Author = {Moffitt, T.E. and Walsh, A},
   Title = {The adolescence-limited/life course persistent theory of
             antisocial behavior: What have we learned?},
   Booktitle = {Biosocial Criminology: Challenging environmentalism’s
             supremacy},
   Publisher = {New York: Anderson Publishing.},
   Editor = {A. Walsh and L. Ellis},
   Year = {2003},
   Key = {fds69950}
}

@misc{fds69951,
   Author = {Loeber, R. and Farrington, D.F. and Stouthamer-Loeber, M. and Moffitt, T.E. and Caspi, A. and White, H.R. and Wei, E.H. and Beyers,
             J.M},
   Title = {The development of male offending: Key findings from 14
             years of the Pittsburgh Youth Study},
   Pages = {93-136},
   Booktitle = {Taking stock of delinquency: An overview of findings from
             contemporary longitudinal studies},
   Publisher = {New York: Kluwer/Plenum},
   Editor = {T. Thornberry and M. Krohn},
   Year = {2003},
   Key = {fds69951}
}

@misc{fds69949,
   Author = {Moffitt, T. E. and Caspi, A},
   Title = {Preventing the inter-generational continuity of antisocial
             behavior: Implications from partner violence
             research},
   Booktitle = {Primary prevention of antisocial behavior},
   Publisher = {New York: Cambridge University Press},
   Editor = {D. Farrington and J. Coid},
   Year = {2003},
   Key = {fds69949}
}

@misc{fds349445,
   Author = {Jaffee, SR and Moffitt, TE and Caspi, A},
   Title = {Life with (and without) father: The double-whammy of genetic
             and environmental risk for children raised by antisocial
             fathers},
   Journal = {BEHAVIOR GENETICS},
   Volume = {32},
   Number = {6},
   Pages = {471-471},
   Publisher = {KLUWER ACADEMIC/PLENUM PUBL},
   Year = {2002},
   Month = {November},
   Key = {fds349445}
}

@misc{fds69929,
   Author = {Moffitt, T. E. and Caspi, A},
   Title = {Como prevenir a continuidade intergeracional do
             comportamento anti-socialimplicações da violência entre
             companheiros},
   Pages = {373-396},
   Booktitle = {Comportamento Anti-social e FamíliaUma abordagem
             científica},
   Publisher = {Coimbra: Livraria Almedina},
   Editor = {A. C. Fonseca},
   Year = {2002},
   Key = {fds69929}
}

@misc{fds69930,
   Author = {Moffitt, T.E},
   Title = {Quantitative behavioural genetic research into human
             antisocial behaviour},
   Booktitle = {Genetics and human behaviour: the ethical
             context},
   Publisher = {London: Nuffield Council on Bioethics},
   Year = {2002},
   Key = {fds69930}
}

@misc{fds69931,
   Author = {McGuffin, P. and Thapar, A. and Moffitt, T.E},
   Title = {Personality disorders},
   Booktitle = {Psychiatric genetics and genomics},
   Publisher = {Oxford: Oxford University Press},
   Editor = {P. McGuffin and M. Owen and I.I. Gottesman},
   Year = {2002},
   Key = {fds69931}
}

@misc{fds370507,
   Author = {Cannon, M and Caspi, A and Moffitt, TE and Harrington, HL and Taylor, A and Murray, M and Poulton, R},
   Title = {Evidence for early childhood, pan-developmental impairment
             specific to schizophreniform disorder: results from a
             longitudinal birth cohort},
   Journal = {ACTA PSYCHIATRICA SCANDINAVICA},
   Volume = {105},
   Pages = {33-33},
   Year = {2002},
   Key = {fds370507}
}

@misc{fds340557,
   Author = {Arseneault, L and Moffitt, TE and Caspi, A},
   Title = {Is the general public a target of violent mentally
             disordered individuals? Findings from a young adult birth
             cohort},
   Journal = {AGGRESSIVE BEHAVIOR},
   Volume = {27},
   Number = {3},
   Pages = {226-227},
   Publisher = {WILEY-LISS},
   Year = {2001},
   Month = {January},
   Key = {fds340557}
}

@misc{fds340558,
   Author = {Moffitt, T and Caspi, A and Fawcett, P and Brammer, GL and Raleigh, M and Yuwiler, A and Silva, P},
   Title = {Whole blood serotonin and family background relate to male
             violence},
   Journal = {BIOSOCIAL BASES OF VIOLENCE},
   Volume = {292},
   Pages = {231-249},
   Booktitle = {Biosocial bases of violence},
   Publisher = {PLENUM PRESS DIV PLENUM PUBLISHING CORP},
   Editor = {Raine, A and Brennan, PA and Farrington, DP and Mednick,
             SA},
   Year = {1997},
   Month = {January},
   ISBN = {0-306-45601-X},
   Key = {fds340558}
}

@misc{fds340559,
   Author = {Henry, B and Caspi, A and Moffitt, T and Silva, P},
   Title = {Temperamental and familial predictors of criminal
             conviction},
   Journal = {BIOSOCIAL BASES OF VIOLENCE},
   Volume = {292},
   Pages = {305-307},
   Booktitle = {Biosocial bases of violence},
   Publisher = {PLENUM PRESS DIV PLENUM PUBLISHING CORP},
   Editor = {Raine, A and Brennan, PA and Farrington, DP and Mednick,
             SA},
   Year = {1997},
   Month = {January},
   ISBN = {0-306-45601-X},
   Key = {fds340559}
}

@misc{fds69864,
   Author = {Moffitt, T.E},
   Title = {Neuropsychology, antisocial behavior, and neighborhood
             context},
   Booktitle = {Violence and childhood in the inner city},
   Publisher = {New York: Cambridge University Press},
   Editor = {J. McCord},
   Year = {1997},
   Key = {fds69864}
}

@misc{fds69861,
   Author = {Henry, B. and Moffitt, T.E},
   Title = {Neuropsychological and Neuroimaging Studies on Juvenile
             Delinquency and Adult Criminal Behavior},
   Pages = {280-288},
   Booktitle = {Handbook of antisocial behavior},
   Publisher = {New York: Wiley},
   Editor = {D. Stoff and J. Breiling and J. Maser},
   Year = {1997},
   Key = {fds69861}
}

@misc{fds69850,
   Author = {Moffitt, T.E},
   Title = {Adolescence-limited and life-course-persistent offending: A
             complementary pair of developmental theories},
   Pages = {11-54},
   Booktitle = {Advances in criminological theory: Developmental theories of
             crime and delinquency},
   Publisher = {London: Transactions Publishers},
   Editor = {T. Thornberry},
   Year = {1996},
   Key = {fds69850}
}

@misc{fds69851,
   Author = {Caspi, A. and Harkness, A. and Moffitt, T.E. and Silva,
             P.A},
   Title = {Continuity and change in human development: Lessons learnt
             from the study of intellectual performance},
   Pages = {59-74},
   Booktitle = {From child to adulthood: The Dunedin study},
   Publisher = {Oxford: Oxford University Press},
   Editor = {P.A. Silva and W.A. Stanton},
   Year = {1996},
   Key = {fds69851}
}

@misc{fds69852,
   Author = {Moffitt, T.E. and Harrington, H.L},
   Title = {Delinquency across development: The natural history of
             antisocial behavior},
   Booktitle = {From child to adulthood: The Dunedin study},
   Publisher = {Oxford: Oxford University Press},
   Editor = {P.A. Silva and W.A. Stanton},
   Year = {1996},
   Key = {fds69852}
}

@misc{fds69833,
   Author = {Moffitt, T.E. and Caspi, A. and Silva, P.A. and Stouthamer-Loeber,
             M},
   Title = {Individual differences in personality and intelligence are
             linked to crime: Cross-context evidence from nations,
             neighborhoods, genders, races, and age-cohorts},
   Series = {Vol. 4 of "Current Perspectives on Aging and the life
             cycle"},
   Pages = {1-34},
   Booktitle = {Delinquency and disrepute in the life course: Contextual and
             dynamic analyses},
   Publisher = {Greenwich, CT: JAI Press},
   Editor = {J. Hagan},
   Year = {1995},
   Key = {fds69833}
}

@misc{fds69834,
   Author = {Caspi, A. and Moffitt, T. E},
   Title = {The continuity of maladaptive behavior},
   Volume = {2},
   Pages = {472-511},
   Booktitle = {Manual of developmental psychopathology},
   Publisher = {New York, NY: Wiley},
   Editor = {D. Cicchetti and D. Cohen},
   Year = {1995},
   Key = {fds69834}
}

@misc{fds340561,
   Author = {MOFFITT, TE},
   Title = {NATURAL HISTORIES OF DELINQUENCY},
   Journal = {CROSS-NATIONAL LONGITUDINAL RESEARCH ON HUMAN DEVELOPMENT
             AND CRIMINAL BEHAVIOR},
   Volume = {76},
   Pages = {3-61},
   Booktitle = {Cross-national longitudinal research on human development
             and criminal behavior},
   Publisher = {KLUWER ACADEMIC PUBL},
   Editor = {Weitekamp, EGM and Kerner, HJ},
   Year = {1994},
   Month = {January},
   ISBN = {0-7923-2620-2},
   Key = {fds340561}
}

@misc{fds69820,
   Author = {Moffitt, T.E. and Lynam, D},
   Title = {Neuropsychology of delinquent behavior: Implications for
             understanding the psychopath},
   Volume = {18},
   Series = {Progress in Experimental Personality and Psychopathology
             Research},
   Pages = {233-262},
   Booktitle = {Psychopathy and antisocial personality: A developmental
             perspective,},
   Publisher = {New York: Springer},
   Editor = {D. Fowles and P. Sutker and S. Goodman},
   Year = {1994},
   Key = {fds69820}
}

@misc{fds69822,
   Author = {Moffitt, T.E. and Silva, P.A. and Lynam, D.R. and Henry,
             B},
   Title = {Self-Reported Delinquency at Age 18: New Zealand's Dunedin
             Multidisciplinary Health and Development
             Study},
   Pages = {356-371},
   Booktitle = {The international self-report delinquency
             project},
   Publisher = {Den Haag: Ministry of Justice of the Netherlands},
   Editor = {J. Junger-Tas and G. J. Terlouw},
   Year = {1994},
   Key = {fds69822}
}

@misc{fds69788,
   Author = {Moffitt, T.E. and Henry, B},
   Title = {Neuropsychological studies of juvenile delinquency and
             violence: A review},
   Pages = {67-91},
   Booktitle = {The neuropsychology of aggression},
   Publisher = {Norwell, MA: Kluwer Academic Publishers},
   Editor = {J. Milner},
   Year = {1991},
   Key = {fds69788}
}

@misc{fds69785,
   Author = {Moffitt, T.E},
   Title = {The neuropsychology of delinquency: A critical review of
             theory and research},
   Volume = {12},
   Pages = {99-169},
   Booktitle = {Crime and justice: An annual review of research},
   Publisher = {Chicago, IL: University of Chicago Press},
   Editor = {N. Morris and M. Tonry},
   Year = {1990},
   Key = {fds69785}
}

@misc{fds340563,
   Author = {MOFFITT, TE},
   Title = {ACCOMMODATING SELF-REPORT METHODS TO A LOW-DELINQUENCY
             CULTURE - A LONGITUDINAL-STUDY FROM NEW-ZEALAND},
   Journal = {CROSS-NATIONAL RESEARCH IN SELF-REPORTED CRIME AND
             DELINQUENCY},
   Volume = {50},
   Pages = {43-66},
   Publisher = {KLUWER ACADEMIC PUBL},
   Editor = {KLEIN, MW},
   Year = {1989},
   Month = {January},
   ISBN = {0-7923-0345-8},
   Key = {fds340563}
}

@misc{fds69774,
   Author = {Moffitt, T.E},
   Title = {Accommodating self-report methods to a low-delinquency
             culture: Experience from New Zealand},
   Pages = {43-66},
   Booktitle = {Cross-national research in self-reported crime and
             delinquency},
   Publisher = {Dordrecht: Kluwer Academic Press},
   Editor = {M.W. Klein},
   Year = {1989},
   Key = {fds69774}
}

@misc{fds69775,
   Author = {Moffitt, T.E. and Mednick S.A. and Gabrielli,
             W.F},
   Title = {Predicting criminal violence: Descriptive data and
             predispositional factors},
   Pages = {13-34},
   Booktitle = {Current approaches to the prediction of violence},
   Publisher = {New York, NY: American Psychiatric Association
             Press},
   Editor = {D. Brizer and M. Crowner},
   Year = {1989},
   Key = {fds69775}
}

@misc{fds342823,
   Author = {FROST, LA and MOFFITT, TE and MCGEE, R},
   Title = {NEUROPSYCHOLOGICAL CORRELATES OF EARLY ADOLESCENT
             PSYCHOPATHOLOGY},
   Journal = {JOURNAL OF CLINICAL AND EXPERIMENTAL NEUROPSYCHOLOGY},
   Volume = {10},
   Number = {1},
   Pages = {72-72},
   Publisher = {SWETS ZEITLINGER PUBLISHERS},
   Year = {1988},
   Month = {January},
   Key = {fds342823}
}

@misc{fds69765,
   Author = {Moffitt, T.E},
   Title = {Neuropsychology and self-reported early delinquency in an
             unselected birth cohort: A preliminary report from New
             Zealand},
   Pages = {89-112},
   Booktitle = {Biological contributions to crime causation},
   Publisher = {New York, NY: Martinus Nijhoff Press},
   Editor = {T.E. Moffitt and S.A. Mednick},
   Year = {1988},
   Key = {fds69765}
}

@misc{fds69766,
   Author = {McGee, R. and Share, D. and Moffitt, T.E. and Williams, S. and Silva,
             P.A},
   Title = {Reading disability, behavior problems and juvenile
             delinquency},
   Pages = {158-172},
   Booktitle = {Individual differences in children and adolescents:
             International research perspectives},
   Publisher = {New York, NY: Hodder and Stoughton},
   Editor = {D. Saklofske and S. Eysenck},
   Year = {1988},
   Key = {fds69766}
}

@misc{fds69753,
   Author = {Mednick, S.A. and Moffitt, T.E. and Gabrielli, W.F. and Hutchings,
             B},
   Title = {Genetic factors in criminal behavior: A review},
   Booktitle = {The development of antisocial and prosocial
             behavior},
   Publisher = {New York, NY: Academic Press, Inc.},
   Editor = {J. Block and D. Olweus and M.R. Yarrow},
   Year = {1986},
   Key = {fds69753}
}

@misc{fds69754,
   Author = {Moffitt, T.E. and Mednick, S.A. and Volavka,
             J},
   Title = {Psychobiological factors in the relationships between crime
             and mental illness},
   Volume = {2},
   Pages = {173-224},
   Booktitle = {Law and mental health: International perspectives},
   Publisher = {New York, NY: Pergamon Press},
   Editor = {D. Weisstub},
   Year = {1986},
   Key = {fds69754}
}

@misc{fds69749,
   Author = {Moffitt, T.E. and Mednick, S.A. and Cudeck, R},
   Title = {Methodological issues in high risk research: The prospective
             longitudinal approach},
   Booktitle = {The child at risk},
   Publisher = {New York, NY: Oxford University Press},
   Editor = {R.E. Tarter},
   Year = {1983},
   Key = {fds69749}
}

@misc{fds69750,
   Author = {Mednick, S.A. and Moffitt, T.E. and Pollock, V. and Talovic, S. and Gabrielli, W.F},
   Title = {The inheritance of human deviance},
   Booktitle = {Human development: An interactional perspective},
   Publisher = {New York, NY: Academic Press, Inc.},
   Editor = {D. Magnusson and V.L. Allen},
   Year = {1983},
   Key = {fds69750}
}

@misc{fds69747,
   Author = {Mednick, S.A. and Harway, M. and Mednick, B. and Moffitt,
             T.E},
   Title = {Longitudinal research: North American data
             sets},
   Booktitle = {Child development, information and formation of public
             policy},
   Publisher = {St. Louis, MO: University of Missouri Press},
   Editor = {T.E. Jordan},
   Year = {1981},
   Key = {fds69747}
}

@misc{fds253484,
   Author = {TILSON, HA and CABE, PA and MITCHELL, D and MOFFITT, T and RHODERICK,
             R},
   Title = {SOME NEUROTOXIC EFFECTS OF POLYBROMINATED BIPHENYL (PBB)
             COMPOUNDS IN RODENTS},
   Journal = {ENVIRONMENTAL HEALTH PERSPECTIVES},
   Volume = {20},
   Number = {OCT},
   Pages = {244-244},
   Publisher = {US DEPT HEALTH HUMAN SERVICES PUBLIC HEALTH
             SERVICE},
   Year = {1977},
   Month = {January},
   Key = {fds253484}
}


%% Commentaries/Book Reviews   
@article{fds198976,
   Author = {T.E. Moffitt},
   Title = {Foreward. In Victoria Costello, A Lethal Inheritance: A
             Mother Uncovers the Science Behind Three Generations of
             Mental Illness.},
   Publisher = {NY: Prometheus Books.},
   Year = {2012},
   Key = {fds198976}
}


%% Edited Volumes   
@misc{fds69758,
   Title = {Biological contributions to crime causation},
   Publisher = {Dordrecht:Martinus-Nijhoff Press},
   Editor = {Moffitt, T.E. and Mednick, S.A},
   Year = {1988},
   Key = {fds69758}
}

@misc{fds69755,
   Title = {The causes of crime: New biological approaches},
   Publisher = {New York, NY: Cambridge University Press},
   Editor = {Mednick, S.A. and Moffitt, T.E. and Stack, S.A},
   Year = {1987},
   Key = {fds69755}
}


%% Reprinted Articles   
@article{fds69915,
   Author = {Moffitt, T.E. and Caspi, A. and Harrington, H. and Milne,
             B},
   Title = {Males on the life-course persistent and adolescence-limited
             antisocial pathways: Follow-up at age 26},
   Series = {3rd edition},
   Booktitle = {Crime: Readings},
   Publisher = {Sage Publications},
   Editor = {Robert Crutchfield and Georges Bridges and Joseph Weis and Charis
             Kubrin},
   Year = {2007},
   Key = {fds69915}
}

@article{fds69975,
   Author = {Moffitt, T. E. and Caspi, A. and Rutter, M},
   Title = {Strategy for investigating interaction between measured
             genes and measured environments.},
   Booktitle = {Beyond Nature & Nurture in Psychiatry: Genes, Environment, &
             their Interplay},
   Publisher = {Taylor and Francis Publishers},
   Editor = {J. MacCabe et al.},
   Year = {2006},
   Key = {fds69975}
}

@article{fds69977,
   Author = {Kim-Cohen, J},
   Title = {Maternal depression and children’s antisocial behaviour:
             More than just genetics},
   Pages = {39-49},
   Booktitle = {ACAMH Occasional Papers No. 25. Genetics: Impact on Current
             Child and Adolescent Mental Health},
   Publisher = {London: Association for Child and Adolescent Mental
             Health},
   Editor = {W. Yule},
   Year = {2006},
   Key = {fds69977}
}

@article{fds69817,
   Author = {Caspi, A. Moffitt and T.E., Silva and P.A., Stouthamer-Loeber and M., Schmutte. P. and Krueger, R},
   Title = {Are some people crime-prone? Replications of the
             personality-crime relationship across countries, genders,
             races, and methods.},
   Booktitle = {Sociology of deviance},
   Publisher = {Mason, OH: Thomson Custom Publishing},
   Editor = {J.G. Weis},
   Year = {2003},
   Key = {fds69817}
}

@article{fds69809,
   Author = {Moffitt, T.E},
   Title = {"Life-course-persistent" and "adolescence-limited"
             antisocial behavior: A developmental taxonomy,},
   Booktitle = {Criminological Theory: Past and Present},
   Publisher = {Los Angeles: Sage},
   Editor = {S. Cody},
   Year = {2002},
   Key = {fds69809}
}

@article{fds69889,
   Author = {Moffitt, T.E. and Krueger, R.F. and Caspi, A. and Fagan, J},
   Title = {Partner abuse and general crime: How are they the same? How
             are they different?},
   Booktitle = {The International Library of Criminology, Criminal Justice,
             and Penology},
   Publisher = {Ashgate Publishing},
   Editor = {D. Nelken and G. Mars},
   Year = {2002},
   Key = {fds69889}
}

@article{fds69808,
   Author = {Moffitt, T.E},
   Title = {"Life-course-persistent" and "adolescence-limited"
             antisocial behavior: A developmental taxonomy,},
   Booktitle = {Boundaries: Readings in Crime, Deviance, and Criminal
             Justice},
   Publisher = {Boston: Pearson Custom Publishing & NY: Wadsworth
             Publishing},
   Year = {2001},
   Key = {fds69808}
}

@article{fds69810,
   Author = {Moffitt, T.E},
   Title = {"Life-course-persistent" and "adolescence-limited"
             antisocial behavior: A developmental taxonomy,},
   Booktitle = {The Science of Mental Health},
   Publisher = {Routledge/Taylor & Francis Group},
   Editor = {Steven Hyman},
   Year = {2001},
   Key = {fds69810}
}

@article{fds69811,
   Author = {Moffitt, T.E},
   Title = {"Life-course-persistent" and "adolescence-limited"
             antisocial behavior: A developmental taxonomy,},
   Series = {2nd edition},
   Booktitle = {Criminologial theory: Past to Present},
   Publisher = {Los Angeles: Roxbury},
   Editor = {F. Cullen and R. Agnew},
   Year = {2001},
   Key = {fds69811}
}

@article{fds69882,
   Author = {Wright, B.R.E. and Caspi, A. and Moffitt, T.E. and Silva,
             P.A},
   Title = {Reconsidering the relationship between SES and delinquency:
             Causation but not correlation.},
   Series = {2nd edition},
   Booktitle = {Juvenile Delinquency Readings},
   Publisher = {Boston: Pine Forge Press},
   Editor = {J.G. Weis and R.D. Crutchfield and G.S. Bridges},
   Year = {2001},
   Key = {fds69882}
}

@article{fds69883,
   Author = {Wright, B.R.E. and Caspi, A. and Moffitt, T.E. and Silva,
             P.A},
   Title = {Reconsidering the relationship between SES and delinquency:
             Causation but not correlation.},
   Booktitle = {Boundaries: Readings in Crime, Deviance, and
             Justice},
   Publisher = {Boston: Pearson Publishing},
   Editor = {B.R.E. Wright and R. McNeal},
   Year = {2001},
   Key = {fds69883}
}

@article{fds69879,
   Author = {Loeber, Rolf and Farrington, David P and Stouthamer-Loeber, Magda and Moffitt, Terrie E and Caspi, Avshalom},
   Title = {The development of male offending: Key findings from the
             first decade of the Pittsburgh Youth Study.},
   Series = {Essential readings in developmental psychology.},
   Pages = {336-378},
   Booktitle = {Children and the law: The essential readings},
   Publisher = {Malden, ME, US: Blackwell Publishers Inc.. xiii,
             432pp.},
   Editor = {Ray Bull},
   Year = {2001},
   Key = {fds69879}
}

@article{fds69806,
   Author = {Moffitt, T.E},
   Title = {"Life-course-persistent" and "adolescence-limited"
             antisocial behavior: A developmental taxonomy,},
   Booktitle = {The international library of criminology, criminal justice,
             and penology},
   Publisher = {Aldershot, UK: Ashgate Publishers},
   Editor = {D. Nelken and G. Mars},
   Year = {2000},
   Key = {fds69806}
}

@article{fds69807,
   Author = {Moffitt, T.E},
   Title = {"Life-course-persistent" and "adolescence-limited"
             antisocial behavior: A developmental taxonomy,},
   Booktitle = {Life course criminology: Contemporary and classic
             readings},
   Publisher = {NY: Wadsworth publishing},
   Editor = {P. Mazerolle and A. Piquero},
   Year = {2000},
   Key = {fds69807}
}

@article{fds69827,
   Author = {Nagin, D.S. and Farrington, D.P. and Moffitt, T.
             E},
   Title = {Life-course trajectories of different types of
             offenders,},
   Booktitle = {Life course criminology: Contemporary and classic
             readings},
   Publisher = {New York: Wadsworth Publishing},
   Editor = {P. Mazerolle and A. Piquero},
   Year = {2000},
   Key = {fds69827}
}

@article{fds69839,
   Author = {Moffitt, T. E. and Caspi, A},
   Title = {Comportamento anti-social persistente ao longo da vida e
             comportamento anti-social limitado a adolescencia:seus
             preditores e suas etiologias},
   Journal = {Revista Portugesa de Pedagogia},
   Volume = {3},
   Pages = {65-106},
   Year = {2000},
   Key = {fds69839}
}

@article{fds69794,
   Author = {Caspi, A. and Lynam, D. and Moffitt, T.E. and Silva,
             P.A},
   Title = {Unraveling girls' delinquency: Biological, dispositional,
             and contextual contributions to adolescent
             misbehaviour.},
   Booktitle = {Adolescence: Development, diversity and context},
   Publisher = {Hamden, CT: Garland},
   Editor = {R. Lerner},
   Year = {1999},
   Key = {fds69794}
}

@article{fds69804,
   Author = {Moffitt, T.E},
   Title = {"Life-course-persistent" and "adolescence-limited"
             antisocial behavior: A developmental taxonomy,},
   Booktitle = {Crime & criminals: Classic and contemporary
             readings},
   Publisher = {Los Angeles: Roxbury Publishing},
   Editor = {F.R., Scarpitti and A.L. Nielsen},
   Year = {1998},
   Key = {fds69804}
}

@article{fds69805,
   Author = {Moffitt, T.E},
   Title = {"Life-course-persistent" and "adolescence-limited"
             antisocial behavior: A developmental taxonomy,},
   Booktitle = {Uses of Criminal Statistics},
   Publisher = {Aldershot, UK: Ashgate Publishers},
   Editor = {K. Pease},
   Year = {1998},
   Key = {fds69805}
}

@article{fds69816,
   Author = {Caspi, A. Moffitt and T.E., Silva and P.A., Stouthamer-Loeber and M., Schmutte. P. and Krueger, R},
   Title = {Are some people crime-prone? Replications of the
             personality-crime relationship across countries, genders,
             races, and methods.},
   Booktitle = {The criminology theory reader},
   Publisher = {New York: New York University Press},
   Editor = {S. Henry and W. Einstadter},
   Year = {1998},
   Key = {fds69816}
}

@article{fds69846,
   Author = {Caspi, A. and Moffitt, T. E. and Newman, D. L. and Silva, P.
             A},
   Title = {Behavioral observations at age 3 predict adult psychiatric
             disorders: Longitudinal evidence from a birth
             cohort.},
   Volume = {30},
   Booktitle = {Annual progress in child psychiatry and child
             development},
   Publisher = {Bristol, PA: Brunner/Mazel},
   Editor = {M.E. Hertzig and A. Farber},
   Year = {1998},
   Key = {fds69846}
}

@article{fds69803,
   Author = {T.E. Moffitt},
   Title = {"Life-course-persistent" and "adolescence-limited"
             antisocial behavior: A developmental taxonomy,},
   Booktitle = {Criminological Theory: Past to Present},
   Publisher = {Los Angeles: Roxbury Publishing},
   Editor = {R. Agnew and F. Cullen},
   Year = {1997},
   Key = {fds69803}
}

@article{fds69831,
   Author = {Keltner, D. and Moffitt, T.E. and Stouthamer-Loeber,
             M},
   Title = {Facial expressions of emotion and psychopathology in
             adolescent males,},
   Booktitle = {What facial expression reveals about emotion, development,
             psychopathology, and health},
   Publisher = {New York: Oxford University Press},
   Editor = {P. Ekman and E. Rosenberg},
   Year = {1997},
   Key = {fds69831}
}

@article{fds69800,
   Author = {Moffitt, T.E},
   Title = {The neuropsychology of conduct disorder,},
   Booktitle = {Contemporary criminological theory},
   Publisher = {Northwestern University Press},
   Editor = {L. Seigel},
   Year = {1996},
   Key = {fds69800}
}

@article{fds69770,
   Author = {Moffitt, T.E. and Henry, B},
   Title = {Neuropsychological assessment of executive functions in
             self-reported delinquents,},
   Booktitle = {The international library of criminology and criminal
             justice},
   Publisher = {Aldershot, UK: Dartmouth Pub. Co. Ltd.},
   Year = {1994},
   Key = {fds69770}
}

@article{fds69778,
   Author = {Caspi, A. and Block, J. and Block, J. H. and Klopp, B. and Lynam, D. and Moffitt, T. E. and Stouthamer-Loeber, M. A},
   Title = {A "common language" version of the California Child Q-Sort
             for personality assessment,},
   Volume = {26},
   Booktitle = {Annual Progress in Child Psychiatry and Child
             Development},
   Editor = {Hertzig and Farber},
   Year = {1994},
   Key = {fds69778}
}

@article{fds69782,
   Author = {Moffitt, T.E},
   Title = {Juvenile delinquency and Attention Deficit Disorder:
             Developmental trajectories from age 3 to
             15,},
   Booktitle = {Yearbook of Psychiatry and Applied Mental
             Health},
   Publisher = {Chicago, IL: Mosby},
   Editor = {J.E. Schowalter},
   Year = {1992},
   Key = {fds69782}
}

@article{fds69781,
   Author = {Moffitt, T.E},
   Title = {Juvenile delinquency and Attention Deficit Disorder:
             Developmental trajectories from age 3 to
             15,},
   Volume = {3},
   Booktitle = {Forum on Corrections Research},
   Year = {1991},
   Key = {fds69781}
}

@article{fds69784,
   Author = {White, J. and Moffitt, T.E. and Earls, F. and Robins, L.N. and Silva,
             P.A},
   Title = {How early can we tell? Preschool predictors of boys' conduct
             disorder and delinquency,},
   Volume = {3},
   Booktitle = {Forum on Corrections Research},
   Year = {1991},
   Key = {fds69784}
}

@article{fds69773,
   Author = {White, J. and Moffitt, T.E. and Silva, P.A},
   Title = {A prospective replication of the protective effects of IQ in
             subjects at high risk for juvenile delinquency},
   Volume = {8},
   Booktitle = {Youth Update},
   Editor = {J. Shamsie},
   Year = {1990},
   Key = {fds69773}
}

@article{fds69780,
   Author = {Moffitt, T.E},
   Title = {Juvenile delinquency and Attention Deficit Disorder:
             Developmental trajectories from age 3 to
             15,},
   Volume = {8},
   Booktitle = {Youth Update},
   Editor = {J. Shamsie},
   Year = {1990},
   Key = {fds69780}
}


%% Other   
@misc{fds213372,
   Author = {T.E. Moffitt},
   Title = {Video: American Society of Criminology Oral History
             Project},
   Year = {2012},
   Key = {fds213372}
}

@misc{fds198977,
   Author = {In collaboration and Razorfilms New Zealand},
   Title = {Documentary Film: The Science of Us: The 1037 most studied
             people in the world.},
   Year = {2011},
   Key = {fds198977}
}

@misc{fds198978,
   Author = {T.E. Moffitt},
   Title = {Video interview about our research by the Jacobs Foundation,
             10 minutes},
   Year = {2011},
   Key = {fds198978}
}

@misc{fds198979,
   Author = {T.E. Moffitt},
   Title = {Video interview about our research by NARSAD, the Brain and
             Behavior Research Foundation, 5 minutes},
   Year = {2011},
   Key = {fds198979}
}

@misc{fds185934,
   Author = {Rutter, M and Griffiths, S and Belsky, J and Brown G and Dunn, J and D’Onofrio, B and Eekelaar, J and Ermisch, J and Moffitt, TE and Gardner, F and Weale, A and Witherspoon, S.},
   Title = {Social Science and Family Policies},
   Publisher = {The British Academy},
   Address = {London},
   Year = {2010},
   Month = {October},
   Key = {fds185934}
}

@misc{fds185935,
   Author = {Reuter, P. et al.},
   Title = {Understanding the Demand for Illegal Drugs},
   Publisher = {Washington, DC: National Academy of Sciences},
   Year = {2010},
   Month = {October},
   Key = {fds185935}
}

@misc{fds185936,
   Author = {Moffitt, TE and Caspi, A.},
   Title = {Blog: Childhood stress and lifelong health},
   Journal = {Psychology Today},
   Year = {2010},
   Key = {fds185936}
}

@misc{fds168664,
   Author = {Baker, T. and Moffitt, T.E. and Caspi, A.},
   Title = {The Nicotine-dependence phenotype: Translating theoretical
             perspective and extant data into recommendations for genetic
             mapping.},
   Journal = {Phenotypes and Endophenotypes: Foundations for Genetic
             Studies of Nicotine Use and Dependence., National Cancer
             Institute, Tobacco Control Monograph 22},
   Year = {2009},
   Key = {fds168664}
}

@misc{fds70019,
   Author = {Moffitt, T.E},
   Title = {Nature’s Great Experiment},
   Year = {2007},
   url = {http://www.naturesgreatexperiment.com},
   Key = {fds70019}
}

@misc{fds70024,
   Author = {Moffitt, TE and Arseneault, L and Jaffee, SR, Kim-Cohen and J, Koenen and KC, Odgers and CL, Slutske and WS and Viding,
             E},
   Title = {DSM-V Conduct Disorder: Research needs for an evidence
             base},
   Year = {2007},
   url = {http://www\advancingdx.psych.org},
   Key = {fds70024}
}

@misc{fds69995,
   Author = {Moffitt, T.E},
   Title = {The 'Ethical Emporium'},
   Year = {2006},
   url = {http://www.windfalldigital.com/ethicalemporium/},
   Key = {fds69995}
}

@misc{fds69913,
   Author = {Moffitt, T.E. and Britten, B. and Busoni, F. and Puccini, G. and Purcell, H. and Stravinsky, I. and Verdi, G. and Wagner,
             R},
   Title = {The king of forensic psychiatry: An opera on the occasion of
             John Gunn’s retirement},
   Journal = {Criminal Behavior and Mental Health},
   Volume = {12},
   Pages = {s93-s96},
   Year = {2002},
   Key = {fds69913}
}

@misc{fds69911,
   Author = {Poulton, R. and Moffitt, T. E},
   Title = {Submission to the Parliamentary Select Committee on Health:
             Inquiry into health strategies relating to cannabis use:
             Cannabis use findings from the Dunedin Multidisciplinary
             Health and Development Study (DMHDS)},
   Publisher = {Otago, NZ: University of Otago, Dunedin School of
             Medicine},
   Year = {2001},
   Key = {fds69911}
}

@misc{fds69835,
   Author = {Moffitt, T.E},
   Title = {Partner Violence Among Young Adults},
   Year = {1995},
   Key = {fds69835}
}

@misc{fds69823,
   Author = {Moffitt, T.E},
   Title = {Juvenile delinquency: Seed of a career in violent crime,
             just sowing wild oats - or both?},
   Year = {1994},
   Key = {fds69823}
}

@misc{fds69751,
   Author = {Moffitt, T.E},
   Title = {Genetic influence of parental psychiatric illness on violent
             and recidivistic criminal behavior: The Danish adoption
             study},
   Publisher = {Los Angeles: University of Southern California},
   Year = {1984},
   Key = {fds69751}
}


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