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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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