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Psychology and Neuroscience
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Publications of Daniel W Belsky    :chronological  alphabetical  combined listing:

%% Journal Articles   
@article{fds333731,
   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},
   Pages = {956797617744542},
   Year = {2018},
   Month = {March},
   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 = {fds333731}
}

@article{fds332056,
   Author = {Domingue, BW and Belsky, DW and Fletcher, JM and Conley, D and Boardman,
             JD and Harris, KM},
   Title = {The social genome of friends and schoolmates in the National
             Longitudinal Study of Adolescent to Adult
             Health.},
   Journal = {Proceedings of the National Academy of Sciences of
             USA},
   Volume = {115},
   Number = {4},
   Pages = {702-707},
   Year = {2018},
   Month = {January},
   url = {http://dx.doi.org/10.1073/pnas.1711803115},
   Abstract = {Humans tend to form social relationships with others who
             resemble them. Whether this sorting of like with like arises
             from historical patterns of migration, meso-level social
             structures in modern society, or individual-level selection
             of similar peers remains unsettled. Recent research has
             evaluated the possibility that unobserved genotypes may play
             an important role in the creation of homophilous
             relationships. We extend this work by using data from 5,500
             adolescents from the National Longitudinal Study of
             Adolescent to Adult Health (Add Health) to examine genetic
             similarities among pairs of friends. Although there is some
             evidence that friends have correlated genotypes, both at the
             whole-genome level as well as at trait-associated loci (via
             polygenic scores), further analysis suggests that meso-level
             forces, such as school assignment, are a principal source of
             genetic similarity between friends. We also observe apparent
             social-genetic effects in which polygenic scores of an
             individual's friends and schoolmates predict the
             individual's own educational attainment. In contrast, an
             individual's height is unassociated with the height genetics
             of peers.},
   Doi = {10.1073/pnas.1711803115},
   Key = {fds332056}
}

@article{fds327153,
   Author = {Belsky, DW and Huffman, KM and Pieper, CF and Shalev, I and Kraus,
             WE},
   Title = {Change in the Rate of Biological Aging in Response to
             Caloric Restriction: CALERIE Biobank Analysis.},
   Journal = {Journals of Gerontology: Series A},
   Volume = {73},
   Number = {1},
   Pages = {4-10},
   Year = {2017},
   Month = {December},
   url = {http://dx.doi.org/10.1093/gerona/glx096},
   Abstract = {Biological aging measures have been proposed as proxies for
             extension of healthy life span in trials of geroprotective
             therapies that aim to slow aging. Several methods to measure
             biological aging show promise but it is not known if these
             methods are sensitive to changes caused by geroprotective
             therapy. We conducted analysis of two proposed methods to
             quantify biological aging using data from a recently
             concluded trial of an established geroprotector, caloric
             restriction. We obtained data from the National Institute on
             Aging CALERIE randomized trial through its public-access
             biobank (https://calerie.duke.edu/). The CALERIE trial
             randomized N = 220 nonobese adults to 25% caloric
             restriction (n = 145; 11.7% caloric restriction was
             achieved, on average) or to maintain current diet (n = 75)
             for 2 years. We analyzed biomarker data collected at
             baseline, 12-, and 24-month follow-up assessments. We
             applied published biomarker algorithms to these data to
             calculate two biological age measures, Klemera-Doubal Method
             Biological Age and homeostatic dysregulation.
             Intent-to-treat analysis using mixed-effects growth models
             of within-person change over time tested if caloric
             restriction slowed increase in measures of biological aging
             across follow-up. Analyses of both measures indicated
             caloric restriction slowed biological aging. Weight loss did
             not account for the observed effects. Results suggest future
             directions for testing of geroprotective therapies in
             humans.},
   Doi = {10.1093/gerona/glx096},
   Key = {fds327153}
}

@article{fds331420,
   Author = {Hastings, WJ and Shalev, I and Belsky, DW},
   Title = {Translating measures of biological aging to test
             effectiveness of geroprotective interventions: What can we
             learn from research on telomeres?},
   Journal = {Frontiers in Genetics},
   Volume = {8},
   Number = {NOV},
   Year = {2017},
   Month = {November},
   url = {http://dx.doi.org/10.3389/fgene.2017.00164},
   Abstract = {© 2017 Hastings, Shalev and Belsky. Intervention studies in
             animals suggest molecular changes underlying age-related
             disease and disability can be slowed or reversed. To speed
             translation of these so-called "geroprotective" therapies to
             prevent age-related disease and disability in humans,
             biomarkers are needed that can track changes in the rate of
             human aging over the course of intervention trials.
             Algorithm methods that measure biological processes of aging
             from combinations of DNA methylation marks or clinical
             biomarkers show promise. To identify next steps for
             establishing utility of these algorithm-based measures of
             biological aging for geroprotector trials, we considered the
             history a candidate biomarker of aging that has received
             substantial research attention, telomere length. Although
             telomere length possesses compelling biology to recommend it
             as a biomarker of aging, mixed research findings have
             impeded clinical and epidemiologic translation. Strengths of
             telomeres that should be established for algorithm
             biomarkers of aging are correlation with chronological age
             across the lifespan, prediction of disease, disability, and
             early death, and responsiveness to risk and protective
             exposures. Key challenges in telomere research that
             algorithm biomarkers of aging must address are measurement
             precision and reliability, establishing links between
             longitudinal rates of change across repeated measurements
             and aging outcomes, and clarity over whether the biomarker
             is a causal mechanism of aging. These strengths and
             challenges suggest a research agenda to advance translation
             of algorithm-based aging biomarkers: establish validity in
             young-adult and midlife individuals; test responsiveness to
             exposures that shorten or extend healthy lifespan; and
             conduct repeated-measures longitudinal studies to test
             differential rates of change.},
   Doi = {10.3389/fgene.2017.00164},
   Key = {fds331420}
}

@article{fds330421,
   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 = {fds330421}
}

@article{fds328924,
   Author = {Domingue, BW and Liu, H and Okbay, A and Belsky, DW},
   Title = {Genetic Heterogeneity in Depressive Symptoms Following the
             Death of a Spouse: Polygenic Score Analysis of the U.S.
             Health and Retirement Study.},
   Journal = {American Journal of Psychiatry},
   Volume = {174},
   Number = {10},
   Pages = {963-970},
   Year = {2017},
   Month = {October},
   url = {http://dx.doi.org/10.1176/appi.ajp.2017.16111209},
   Abstract = {Experience of stressful life events is associated with risk
             of depression. Yet many exposed individuals do not become
             depressed. A controversial hypothesis is that genetic
             factors influence vulnerability to depression following
             stress. This hypothesis is often tested with a
             "diathesis-stress" model, in which genes confer excess
             vulnerability. The authors tested an alternative formulation
             of this model: genes may buffer against depressogenic
             effects of life stress.The hypothesized genetic buffer was
             measured using a polygenic score derived from a published
             genome-wide association study of subjective well-being. The
             authors tested whether married older adults who had higher
             polygenic scores were less vulnerable to depressive symptoms
             following the death of their spouse compared with
             age-matched peers who had also lost their spouse and who had
             lower polygenic scores. Data were analyzed from 8,588
             non-Hispanic white adults in the Health and Retirement Study
             (HRS), a population-representative longitudinal study of
             older adults in the United States.HRS adults with higher
             well-being polygenic scores experienced fewer depressive
             symptoms during follow-up. Those who survived the death of
             their spouses (N=1,647) experienced a sharp increase in
             depressive symptoms following the death and returned toward
             baseline over the following 2 years. Having a higher
             well-being polygenic score buffered against increased
             depressive symptoms following a spouse's death.The effects
             were small, and the clinical relevance is uncertain,
             although polygenic score analyses may provide clues to
             behavioral pathways that can serve as therapeutic targets.
             Future studies of gene-environment interplay in depression
             may benefit from focus on genetics discovered for putative
             protective factors.},
   Doi = {10.1176/appi.ajp.2017.16111209},
   Key = {fds328924}
}

@article{fds328923,
   Author = {Belsky, DW and Snyder-Mackler, N},
   Title = {Invited Commentary: Integrating Genomics and Social
             Epidemiology-Analysis of Late-Life Low Socioeconomic Status
             and the Conserved Transcriptional Response to
             Adversity.},
   Journal = {American Journal of Epidemiology},
   Volume = {186},
   Number = {5},
   Pages = {510-513},
   Year = {2017},
   Month = {September},
   url = {http://dx.doi.org/10.1093/aje/kwx145},
   Abstract = {Socially disadvantaged children face increased morbidity and
             mortality as they age. Understanding mechanisms through
             which social disadvantage becomes biologically embedded and
             devising measurements that can track this embedding are
             critical priorities for research to address social gradients
             in health. The analysis by Levine et al. (Am J Epidemiol.
             2017;186(5):503-509) of genome-wide gene expression in a
             subsample of US Health and Retirement Study participants
             suggests important new directions for the field.
             Specifically, findings suggest promise in integrating gene
             expression data into population studies and provide further
             evidence for the conserved transcriptional response to
             adversity as a marker of biological embedding of social
             disadvantage. The study also highlights methodological
             issues related to the analysis of gene expression data and
             social gradients in health and a need to examine the
             conserved transcriptional response to adversity alongside
             other proposed measurements of biological embedding. Looking
             to the future, advances in genome science are opening new
             opportunities for sociogenomic epidemiology.},
   Doi = {10.1093/aje/kwx145},
   Key = {fds328923}
}

@article{fds326223,
   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 = {fds326223}
}

@article{fds327274,
   Author = {Domingue, BW and Belsky, DW and Harrati, A and Conley, D and Weir, DR and Boardman, JD},
   Title = {Mortality selection in a genetic sample and implications for
             association studies},
   Journal = {International Journal of Epidemiology},
   Volume = {46},
   Number = {4},
   Pages = {1285-1294},
   Year = {2017},
   Month = {August},
   url = {http://dx.doi.org/10.1093/ije/dyx041},
   Doi = {10.1093/ije/dyx041},
   Key = {fds327274}
}

@article{fds327272,
   Author = {Belsky, DW},
   Title = {Translating Polygenic Analysis for Prevention},
   Journal = {Circulation: Cardiovascular Genetics},
   Volume = {10},
   Number = {3},
   Pages = {e001798-e001798},
   Year = {2017},
   Month = {June},
   url = {http://dx.doi.org/10.1161/CIRCGENETICS.117.001798},
   Doi = {10.1161/CIRCGENETICS.117.001798},
   Key = {fds327272}
}

@article{fds327273,
   Author = {Richmond-Rakerd, LS and Belsky, DW},
   Title = {Swedish Register Analysis of Divorce and Alcohol Use
             Disorder Highlights Social Relationships as a Target for
             Preventive Psychiatry and Genetic Research.},
   Journal = {American Journal of Psychiatry},
   Volume = {174},
   Number = {5},
   Pages = {411-413},
   Year = {2017},
   Month = {May},
   url = {http://dx.doi.org/10.1176/appi.ajp.2017.17020170},
   Doi = {10.1176/appi.ajp.2017.17020170},
   Key = {fds327273}
}

@article{fds328283,
   Author = {Domingue, BW and Belsky, DW},
   Title = {The social genome: Current findings and implications for the
             study of human genetics.},
   Journal = {PLoS genetics},
   Volume = {13},
   Number = {3},
   Pages = {e1006615},
   Year = {2017},
   Month = {March},
   url = {http://dx.doi.org/10.1371/journal.pgen.1006615},
   Doi = {10.1371/journal.pgen.1006615},
   Key = {fds328283}
}

@article{fds325853,
   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 : the journal of the American Medical
             Association},
   Volume = {317},
   Number = {12},
   Pages = {1244-1251},
   Year = {2017},
   Month = {March},
   url = {http://dx.doi.org/10.1001/jama.2017.1712},
   Abstract = {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.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.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).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.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]).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.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 = {fds325853}
}

@article{fds328103,
   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 = {Journals of Gerontology: Series A},
   Volume = {72},
   Number = {2},
   Pages = {210-215},
   Year = {2017},
   Month = {February},
   url = {http://dx.doi.org/10.1093/gerona/glw191},
   Abstract = {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.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).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.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 = {fds328103}
}

@article{fds324457,
   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 = {fds324457}
}

@article{fds324523,
   Author = {Moskalev, A and Anisimov, V and Aliper, A and Artemov, A and Asadullah,
             K and Belsky, D and Baranova, A and de Grey, A and Dixit, VD and Debonneuil, E and Dobrovolskaya, E and Fedichev, P and Fedintsev, A and Fraifeld, V and Franceschi, C and Freer, R and Fülöp, T and Feige, J and Gems, D and Gladyshev, V and Gorbunova, V and Irincheeva, I and Jager,
             S and Jazwinski, SM and Kaeberlein, M and Kennedy, B and Khaltourina, D and Kovalchuk, I and Kovalchuk, O and Kozin, S and Kulminski, A and Lashmanova, E and Lezhnina, K and Liu, G-H and Longo, V and Mamoshina,
             P and Maslov, A and Pedro de Magalhaes and J et al.},
   Title = {A review of the biomedical innovations for healthy
             longevity.},
   Journal = {Aging},
   Volume = {9},
   Number = {1},
   Pages = {7-25},
   Year = {2017},
   Month = {January},
   url = {http://dx.doi.org/10.18632/aging.101163},
   Doi = {10.18632/aging.101163},
   Key = {fds324523}
}

@article{fds270476,
   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 = {Journals of Gerontology: Series B},
   Volume = {71},
   Number = {6},
   Pages = {968-977},
   Year = {2016},
   Month = {November},
   ISSN = {1079-5014},
   url = {http://dx.doi.org/10.1093/geronb/gbv035},
   Abstract = {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.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.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.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 = {fds270476}
}

@article{fds323892,
   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 = {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.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.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.Childhood bullying victimization
             predicts overweight in young adulthood.},
   Doi = {10.1097/psy.0000000000000388},
   Key = {fds323892}
}

@article{fds323792,
   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 = {The 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 = {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.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.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.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 = {fds323792}
}

@article{fds319052,
   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 = {fds319052}
}

@article{fds316497,
   Author = {Conley, D and Laidley, T and Belsky, DW and Fletcher, JM and Boardman,
             JD and Domingue, BW},
   Title = {Assortative mating and differential fertility by phenotype
             and genotype across the 20th century.},
   Journal = {Proceedings of the National Academy of Sciences of
             USA},
   Volume = {113},
   Number = {24},
   Pages = {6647-6652},
   Publisher = {National Academy of Sciences},
   Year = {2016},
   Month = {June},
   ISSN = {1091-6490},
   url = {http://www.pnas.org/content/early/2016/05/25/1523592113.abstract},
   Abstract = {This study asks two related questions about the shifting
             landscape of marriage and reproduction in US society over
             the course of the last century with respect to a range of
             health and behavioral phenotypes and their associated
             genetic architecture: (i) Has assortment on measured genetic
             factors influencing reproductive and social fitness traits
             changed over the course of the 20th century? (ii) Has the
             genetic covariance between fitness (as measured by total
             fertility) and other traits changed over time? The answers
             to these questions inform our understanding of how the
             genetic landscape of American society has changed over the
             past century and have implications for population trends. We
             show that husbands and wives carry similar loadings for
             genetic factors related to education and height. However,
             the magnitude of this similarity is modest and has been
             fairly consistent over the course of the 20th century. This
             consistency is particularly notable in the case of
             education, for which phenotypic similarity among spouses has
             increased in recent years. Likewise, changing patterns of
             the number of children ever born by phenotype are not
             matched by shifts in genotype-fertility relationships over
             time. Taken together, these trends provide no evidence that
             social sorting is becoming increasingly genetic in nature or
             that dysgenic dynamics have accelerated.},
   Doi = {10.1073/pnas.1523592113},
   Key = {fds316497}
}

@article{fds319053,
   Author = {Belsky, DW},
   Title = {Invited Commentary: Lessons for Research on Cognitive Aging
             From a Study of Children.},
   Journal = {American Journal of Epidemiology},
   Volume = {183},
   Number = {12},
   Pages = {1083-1085},
   Year = {2016},
   Month = {June},
   url = {http://dx.doi.org/10.1093/aje/kww029},
   Abstract = {As the population ages, the burden of disease from cognitive
             decline and dementing illness is rising. In the absence of
             treatments to reverse cognitive decline, prevention is a
             public health priority. Physical fitness and physical
             activity have emerged as prevention targets based on
             evidence of "neuroprotective" benefits in observational
             studies. However, observational studies linking active
             lifestyle with successful cognitive aging might be subject
             to bias from "neuroselection," in which adults with better
             cognitive functioning are more likely to engage in healthy
             behaviors and avoid unhealthy ones. In their analysis of
             longitudinal data on several thousand children from the
             United Kingdom's Millennium Cohort Study, Aggio et al. (Am J
             Epidemiol. 2016;183(12):1075-1082) revealed that this
             pattern of neuroselection is already apparent in childhood.
             However, they also report data that suggest there are
             cognitive benefits to engaging in certain types of active
             behaviors over and above this selection. Their findings
             argue for greater attention to confounding by neuroselection
             in research on cognitive aging, and they suggest the
             possibility that early interventions to promote certain
             health behaviors may instill a virtuous cycle with benefits
             that accumulate across the lifespan.},
   Doi = {10.1093/aje/kww029},
   Key = {fds319053}
}

@article{fds316211,
   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},
   ISSN = {0033-2917},
   url = {http://dx.doi.org/10.1017/s0033291715002482},
   Abstract = {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.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.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).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 = {fds316211}
}

@article{fds316214,
   Author = {Steinsbekk, S and Belsky, D and Guzey, IC and Wardle, J and Wichstrøm,
             L},
   Title = {Polygenic Risk, Appetite Traits, and Weight Gain in Middle
             Childhood: A Longitudinal Study.},
   Journal = {JAMA Pediatrics},
   Volume = {170},
   Number = {2},
   Pages = {e154472},
   Year = {2016},
   Month = {February},
   ISSN = {2168-6203},
   url = {http://hdl.handle.net/10161/12078 Duke open
             access},
   Abstract = {Genome-wide association studies have identified genetic
             risks for obesity. These genetic risks influence development
             of obesity partly by accelerating weight gain in childhood.
             Research is needed to identify mechanisms to inform
             intervention. Cross-sectional studies suggest appetite
             traits as a candidate mechanism. Longitudinal studies are
             needed to test whether appetite traits mediate genetic
             influences on children's weight gain.To test whether genetic
             risk for obesity predicts accelerated weight gain in middle
             childhood (ages 4-8 years) and whether genetic association
             with accelerated weight gain is mediated by appetite
             traits.Longitudinal study of a representative birth cohort
             at the Trondheim Early Secure Study, Trondheim, Norway,
             enrolled at age 4 years during 2007 to 2008, with follow-ups
             at ages 6 and 8 years. Participants were sampled from all
             children born in 2003 or 2004 who attended regular community
             health checkups for 4-year-olds (97.2% attendance; 82.0%
             consent rate, n = 2475). Nine hundred ninety-five children
             participated at age 4 years, 795 at age 6 years, and 699 at
             age 8 years. Analyses included 652 children with genotype,
             adiposity, and appetite data.Outcomes were body mass index
             and body-fat phenotypes measured from anthropometry (ages 4,
             6, and 8 years) and bioelectrical impedance (ages 6 and 8
             years). Genetic risk for obesity was measured using a
             genetic risk score composed of 32 single-nucleotide
             polymorphisms previously discovered in genome-wide
             association studies of adult body mass index. Appetite
             traits were measured at age 6 years with the Children's
             Eating Behavior Questionnaire.Of the 652 genotyped child
             participants, 323 (49.5%) were female, 58 (8.9%) were
             overweight, and 1 (0.2%) was obese. Children at higher
             genetic risk for obesity had higher baseline body mass index
             and fat mass compared with lower genetic risk peers, and
             they gained weight and fat mass more rapidly during
             follow-up. Each SD increase in genetic risk score was
             associated with a 0.22-point increase in BMI at age-4
             baseline (for the intercept, unstandardized path coefficient
             B = 0.22 [95% CI, 0.06-0.38]; P = .008. Children with higher
             genetic risk scores also gained BMI points more rapidly from
             ages 4 to 6 years (B = 0.11 [95% CI, 0.03-0.20]; P = .01 ;
             β = 0.12) and from 6 to 8 years (B = 0.09 [95% CI,
             0.00-0.19]; P = .05; β = 0.10), compared with their lower
             genetic risk peers. Children at higher genetic risk had
             higher levels of alleged obesogenic appetite traits than
             peers with lower genetic risk at age 6 years, but appetite
             traits did not mediate genetic associations with weight
             gain. The sum of the 5 indirect effects was B = -0.001 (95%
             CI, -0.02 -0.01); P = .86; β = 0.00.Genetic risk for
             obesity is associated with accelerated childhood weight
             gain. Interventions targeting childhood weight gain may
             provide one path to mitigating genetic risk. However, middle
             childhood appetite traits may not be a promising target for
             such interventions. Studies of early-childhood samples are
             needed to test whether appetite traits explain how genetic
             risks accelerate growth earlier in development.},
   Doi = {10.1001/jamapediatrics.2015.4472},
   Key = {fds316214}
}

@article{fds328925,
   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},
   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 = {fds328925}
}

@article{fds316213,
   Author = {Belsky, DW},
   Title = {Reply to Newman: Quantification of biological aging in young
             adults is not the same thing as the onset of
             obesity.},
   Journal = {Proceedings of the National Academy of Sciences of
             USA},
   Volume = {112},
   Number = {52},
   Pages = {E7164-E7165},
   Year = {2015},
   Month = {December},
   ISSN = {0027-8424},
   url = {http://hdl.handle.net/10161/12079 Duke open
             access},
   Doi = {10.1073/pnas.1518878112},
   Key = {fds316213}
}

@article{fds270477,
   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 = {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 = {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.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.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.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 = {fds270477}
}

@article{fds270478,
   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 = {Proceedings of the National Academy of Sciences of
             USA},
   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 = {fds270478}
}

@article{fds316212,
   Author = {Domingue, BW and Belsky, DW and Conley, D and Harris, KM and Boardman,
             JD},
   Title = {Polygenic Influence on Educational Attainment},
   Journal = {AERA open},
   Volume = {1},
   Number = {3},
   Pages = {233285841559997-233285841559997},
   Year = {2015},
   Month = {July},
   url = {http://hdl.handle.net/10161/12080 Duke open
             access},
   Doi = {10.1177/2332858415599972},
   Key = {fds316212}
}

@article{fds270481,
   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 = {Annals of Neurology},
   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 = {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.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.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.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 = {fds270481}
}

@article{fds270479,
   Author = {Albert, D and Belsky, DW and Crowley, DM and Bates, JE and Pettit, GS and Lansford, JE and Dick, D and Dodge, KA},
   Title = {Developmental mediation of genetic variation in response to
             the Fast Track prevention program.},
   Journal = {Development and Psychopathology},
   Volume = {27},
   Number = {1},
   Pages = {81-95},
   Year = {2015},
   Month = {February},
   ISSN = {0954-5794},
   url = {http://dx.doi.org/10.1017/s095457941400131x},
   Abstract = {We conducted a developmental analysis of genetic moderation
             of the effect of the Fast Track intervention on adult
             externalizing psychopathology. The Fast Track intervention
             enrolled 891 children at high risk to develop externalizing
             behavior problems when they were in kindergarten. Half of
             the enrolled children were randomly assigned to receive 10
             years of treatment, with a range of services and resources
             provided to the children and their families, and the other
             half to usual care (controls). We previously showed that the
             effect of the Fast Track intervention on participants' risk
             of externalizing psychopathology at age 25 years was
             moderated by a variant in the glucocorticoid receptor gene.
             Children who carried copies of the A allele of the single
             nucleotide polymorphism rs10482672 had the highest risk of
             externalizing psychopathology if they were in the control
             arm of the trial and the lowest risk of externalizing
             psychopathology if they were in the treatment arm. In this
             study, we test a developmental hypothesis about the origins
             of this for better and for worse Gene × Intervention
             interaction (G × I): that the observed G × I effect on
             adult psychopathology is mediated by the proximal impact of
             intervention on childhood externalizing problems and
             adolescent substance use and delinquency. We analyzed
             longitudinal data tracking the 270 European American
             children in the Fast Track randomized control trial with
             available genetic information (129 intervention children,
             141 control group peers, 69% male) from kindergarten through
             age 25 years. Results show that the same pattern of for
             better and for worse susceptibility to intervention observed
             at the age 25 follow-up was evident already during
             childhood. At the elementary school follow-ups and at the
             middle/high school follow-ups, rs10482672 predicted better
             adjustment among children receiving the Fast Track
             intervention and worse adjustment among children in the
             control condition. In turn, these proximal G × I effects
             early in development mediated the ultimate G × I effect on
             externalizing psychopathology at age 25 years. We discuss
             the contribution of these findings to the growing literature
             on genetic susceptibility to environmental
             intervention.},
   Doi = {10.1017/s095457941400131x},
   Key = {fds270479}
}

@article{fds270480,
   Author = {Albert, D and Belsky, DW and Crowley, DM and Latendresse, SJ and Aliev,
             F and Riley, B and Sun, C and Conduct Problems Prevention Research
             Group, and Dick, DM and Dodge, KA},
   Title = {Can Genetics Predict Response to Complex Behavioral
             Interventions? Evidence from a Genetic Analysis of the Fast
             Track Randomized Control Trial.},
   Journal = {Journal of Policy Analysis and Management},
   Volume = {34},
   Number = {3},
   Pages = {497-518},
   Year = {2015},
   Month = {January},
   ISSN = {0276-8739},
   url = {http://hdl.handle.net/10161/9365 Duke open
             access},
   Abstract = {Early interventions are a preferred method for addressing
             behavioral problems in high-risk children, but often have
             only modest effects. Identifying sources of variation in
             intervention effects can suggest means to improve
             efficiency. One potential source of such variation is the
             genome. We conducted a genetic analysis of the Fast Track
             randomized control trial, a 10-year-long intervention to
             prevent high-risk kindergarteners from developing adult
             externalizing problems including substance abuse and
             antisocial behavior. We tested whether variants of the
             glucocorticoid receptor gene NR3C1 were associated with
             differences in response to the Fast Track intervention. We
             found that in European-American children, a variant of NR3C1
             identified by the single-nucleotide polymorphism rs10482672
             was associated with increased risk for externalizing
             psychopathology in control group children and decreased risk
             for externalizing psychopathology in intervention group
             children. Variation in NR3C1 measured in this study was not
             associated with differential intervention response in
             African-American children. We discuss implications for
             efforts to prevent externalizing problems in high-risk
             children and for public policy in the genomic
             era.},
   Doi = {10.1002/pam.21811},
   Key = {fds270480}
}

@article{fds270518,
   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 of
             USA},
   Volume = {111},
   Number = {48},
   Pages = {17087-17092},
   Year = {2014},
   Month = {December},
   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 = {fds270518}
}

@article{fds270494,
   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 = {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.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.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.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 = {fds270494}
}

@article{fds270485,
   Author = {Belsky, DW and Suppli, NP and Israel, S},
   Title = {Gene-environment interaction research in psychiatric
             epidemiology: a framework and implications for study
             design.},
   Journal = {Social Psychiatry and Psychiatric Epidemiology},
   Volume = {49},
   Number = {10},
   Pages = {1525-1529},
   Year = {2014},
   Month = {October},
   ISSN = {0933-7954},
   url = {http://dx.doi.org/10.1007/s00127-014-0954-5},
   Doi = {10.1007/s00127-014-0954-5},
   Key = {fds270485}
}

@article{fds270483,
   Author = {Danese, A and Dove, R and Belsky, DW and Henchy, J and Williams, B and Ambler, A and Arseneault, L},
   Title = {Leptin deficiency in maltreated children.},
   Journal = {Translational Psychiatry},
   Volume = {4},
   Number = {9},
   Pages = {e446},
   Year = {2014},
   Month = {September},
   url = {http://dx.doi.org/10.1038/tp.2014.79},
   Abstract = {Consistent with findings from experimental research in
             nonhuman primates exposed to early-life stress, children
             exposed to maltreatment are at high risk of detrimental
             physical health conditions, such as obesity and systemic
             inflammation. Because leptin is a key molecule involved in
             the regulation of both energy balance and immunity, we
             investigated abnormalities in leptin physiology among
             maltreated children. We measured leptin, body mass index and
             C-reactive protein in 170 12-year-old children members of
             the Environmental-Risk Longitudinal Twin Study, for whom we
             had prospectively-collected information on maltreatment
             exposure. We found that maltreated children exhibited
             blunted elevation in leptin levels in relation to increasing
             levels of physiological stimuli, adiposity and inflammation,
             compared with a group of non-maltreated children matched for
             gender, zygosity and socioeconomic status. These findings
             were also independent of key potential artifacts and
             confounders, such as time of day at sample collection,
             history of food insecurity, pubertal maturation and
             depressive symptoms. Furthermore, using birth weight as a
             proxy measure for leptin, we found that physiological
             abnormalities were presumably not present at birth in
             children who went on to be maltreated but only emerged over
             the course of childhood, after maltreatment exposure. Leptin
             deficiency may contribute to onset, persistence and
             progression of physical health problems in maltreated
             children.},
   Doi = {10.1038/tp.2014.79},
   Key = {fds270483}
}

@article{fds270493,
   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 = {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.To test whether chronic asthma is
             associated with a proposed biomarker of accelerated aging,
             leukocyte telomere length.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.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.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 = {fds270493}
}

@article{fds270487,
   Author = {Belsky, DW},
   Title = {Appetite for prevention: genetics and developmental
             epidemiology join forces in obesity research.},
   Journal = {JAMA Pediatrics},
   Volume = {168},
   Number = {4},
   Pages = {309-311},
   Year = {2014},
   Month = {April},
   ISSN = {2168-6203},
   url = {http://dx.doi.org/10.1001/jamapediatrics.2013.5291},
   Doi = {10.1001/jamapediatrics.2013.5291},
   Key = {fds270487}
}

@article{fds270489,
   Author = {Belsky, DW and Sears, MR},
   Title = {The potential to predict the course of childhood
             asthma.},
   Journal = {Expert review of respiratory medicine},
   Volume = {8},
   Number = {2},
   Pages = {137-141},
   Year = {2014},
   Month = {April},
   ISSN = {1747-6348},
   url = {http://dx.doi.org/10.1586/17476348.2014.879826},
   Abstract = {Many children experience pre-school or early childhood
             wheezing. In a significant proportion symptoms disappear as
             the child grows, but others have persistent and troublesome
             asthma which can be life-long. Tools to predict course of
             disease in young children are a priority for families and
             clinicians. This review summarizes evidence from several
             longitudinal population-based birth-cohort studies that have
             identified risk factors for persistence and remission of
             childhood asthma. These factors include clinical
             characteristics, environmental and other exposures, familial
             factors, biomarkers of allergic inflammation, measurements
             of lung function and airway responsiveness, and genetic
             variants. This review also introduces the concept of
             polygenic risk and genetic risk scores, and describes
             results from a recent study that suggests promise for the
             use of genetic information in predicting the course of
             childhood asthma. We conclude with a discussion of
             implications and future directions.},
   Doi = {10.1586/17476348.2014.879826},
   Key = {fds270489}
}

@article{fds270488,
   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},
   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 = {fds270488}
}

@article{fds270501,
   Author = {Israel, S and Moffitt, TE and Belsky, DW and Hancox, RJ and Poulton, R and Roberts, B and Thomson, WM 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},
   Month = {March},
   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 = {fds270501}
}

@article{fds270484,
   Author = {Belsky, DW and Israel, S},
   Title = {Integrating genetics and social science: genetic risk
             scores.},
   Journal = {Biodemography and Social Biology},
   Volume = {60},
   Number = {2},
   Pages = {137-155},
   Year = {2014},
   Month = {January},
   ISSN = {1948-5565},
   url = {http://dx.doi.org/10.1080/19485565.2014.946591},
   Abstract = {The sequencing of the human genome and the advent of
             low-cost genome-wide assays that generate millions of
             observations of individual genomes in a matter of hours
             constitute a disruptive innovation for social science. Many
             public use social science datasets have or will soon add
             genome-wide genetic data. With these new data come technical
             challenges, but also new possibilities. Among these, the
             lowest-hanging fruit and the most potentially disruptive to
             existing research programs is the ability to measure
             previously invisible contours of health and disease risk
             within populations. In this article, we outline why now is
             the time for social scientists to bring genetics into their
             research programs. We discuss how to select genetic variants
             to study. We explain how the polygenic architecture of
             complex traits and the low penetrance of individual genetic
             loci pose challenges to research integrating genetics and
             social science. We introduce genetic risk scores as a method
             of addressing these challenges and provide guidance on how
             genetic risk scores can be constructed. We conclude by
             outlining research questions that are ripe for social
             science inquiry.},
   Doi = {10.1080/19485565.2014.946591},
   Key = {fds270484}
}

@article{fds270490,
   Author = {Domingue, BW and Belsky, DW and Harris, KM and Smolen, A and McQueen,
             MB and Boardman, JD},
   Title = {Polygenic risk predicts obesity in both white and black
             young adults.},
   Journal = {PloS one},
   Volume = {9},
   Number = {7},
   Pages = {e101596},
   Editor = {Uddin, M},
   Year = {2014},
   Month = {January},
   url = {http://dx.doi.org/10.1371/journal.pone.0101596},
   Abstract = {To test transethnic replication of a genetic risk score for
             obesity in white and black young adults using a national
             sample with longitudinal data.A prospective longitudinal
             study using the National Longitudinal Study of Adolescent
             Health Sibling Pairs (n = 1,303). Obesity phenotypes
             were measured from anthropometric assessments when study
             members were aged 18-26 and again when they were 24-32.
             Genetic risk scores were computed based on published
             genome-wide association study discoveries for obesity.
             Analyses tested genetic associations with body-mass index
             (BMI), waist-height ratio, obesity, and change in BMI over
             time.White and black young adults with higher genetic risk
             scores had higher BMI and waist-height ratio and were more
             likely to be obese compared to lower genetic risk age-peers.
             Sibling analyses revealed that the genetic risk score was
             predictive of BMI net of risk factors shared by siblings. In
             white young adults only, higher genetic risk predicted
             increased risk of becoming obese during the study period. In
             black young adults, genetic risk scores constructed using
             loci identified in European and African American samples had
             similar predictive power.Cumulative information across the
             human genome can be used to characterize individual level
             risk for obesity. Measured genetic risk accounts for only a
             small amount of total variation in BMI among white and black
             young adults. Future research is needed to identify
             modifiable environmental exposures that amplify or mitigate
             genetic risk for elevated BMI.},
   Doi = {10.1371/journal.pone.0101596},
   Key = {fds270490}
}

@article{fds270486,
   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 = {American Journal of Psychiatry},
   Volume = {170},
   Number = {12},
   Pages = {1451-1459},
   Year = {2013},
   Month = {December},
   ISSN = {0002-953X},
   url = {http://dx.doi.org/10.1176/appi.ajp.2013.13020234},
   Abstract = {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.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.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.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 = {fds270486}
}

@article{fds270503,
   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},
   ISSN = {0002-9262},
   url = {http://dx.doi.org/10.1093/aje/kwt135},
   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 = {fds270503}
}

@article{fds270495,
   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},
   Pages = {S73-S83},
   Year = {2013},
   Month = {October},
   ISSN = {0090-0036},
   url = {http://dx.doi.org/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 = {fds270495}
}

@article{fds270491,
   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://dx.doi.org/10.1017/s0954579413000175},
   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 = {fds270491}
}

@article{fds325885,
   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},
   url = {http://dx.doi.org/10.1017/S0954579413000175},
   Doi = {10.1017/S0954579413000175},
   Key = {fds325885}
}

@article{fds270515,
   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},
   ISSN = {2168-622X},
   url = {http://dx.doi.org/10.1001/jamapsychiatry.2013.736},
   Abstract = {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.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.A 38-year, prospective, longitudinal study of a
             representative birth cohort.The Dunedin Multidisciplinary
             Health and Development Study of New Zealand.The study
             included 1037 male and female participants.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.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.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.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 = {fds270515}
}

@article{fds270500,
   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 and Social Biology},
   Volume = {59},
   Number = {1},
   Pages = {85-100},
   Year = {2013},
   Month = {January},
   ISSN = {1948-5565},
   url = {http://dx.doi.org/10.1080/19485565.2013.774628},
   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 = {fds270500}
}

@article{fds270513,
   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 = {453-461},
   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. Funding: US National
             Institute on Aging and UK Medical Research Council. © 2013
             Elsevier Ltd.},
   Doi = {10.1016/S2213-2600(13)70101-2},
   Key = {fds270513}
}

@article{fds270514,
   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 = {Archives of Pediatrics and Adolescent Medicine},
   Volume = {166},
   Number = {6},
   Pages = {515-521},
   Year = {2012},
   Month = {June},
   ISSN = {1072-4710},
   url = {http://dx.doi.org/10.1001/archpediatrics.2012.131},
   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 = {fds270514}
}

@article{fds270502,
   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 (Clinical research ed.)},
   Volume = {344},
   Pages = {e2683},
   Year = {2012},
   Month = {April},
   ISSN = {0959-8138},
   url = {http://dx.doi.org/10.1136/bmj.e2683},
   Abstract = {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.The Environmental Risk (E-Risk)
             longitudinal study of a nationally representative UK cohort
             of 1116 twin pairs born in 1994-95 (2232 children).England
             and Wales, United Kingdom.Children assessed at 5, 7, 10, and
             12 years of age.Relative risks of children's self harming
             behaviour in the six months before their 12th birthday.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.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 = {fds270502}
}

@article{fds270508,
   Author = {Ricketts, TC and Belsky, DW},
   Title = {Medicare costs and surgeon supply in hospital service
             areas.},
   Journal = {Annals of Surgery},
   Volume = {255},
   Number = {3},
   Pages = {474-477},
   Year = {2012},
   Month = {March},
   ISSN = {0003-4932},
   url = {http://dx.doi.org/10.1097/sla.0b013e31822f2021},
   Abstract = {OBJECTIVE: To quantify the correlates of variations of
             Medicare per beneficiary costs at the hospital service area
             level and determine whether physician supply and the
             specialty of physicians has a significant relationship with
             cost variation. BACKGROUND: The American Medical Association
             Masterfile data on physician and surgeon location,
             characteristics and specialty; Census derived
             sociodemographic data from 2006 ZIP code level Claritas
             PopFacts database; and Medicare per beneficiary costs from
             the Dartmouth Atlas of Health Care project. METHODS: A
             correlational analysis using bivariate plots and fixed
             effects linear regression models controlling for hospital
             service area sociodemographics and the number and
             characteristics of the physician supply. Data were
             aggregated to the Dartmouth hospital service area level from
             ZIP code level files. RESULTS: We found that costs are
             strongly related to the sociodemographic character of the
             hospital service areas and the overall supply of physicians
             but a mixed correlation to the specialist supply depending
             on the interaction of the proportion of the physician supply
             who are international medical graduates. The ratio of
             general surgeons and surgical subspecialists to population
             are associated with lower costs in the models, again with
             difference depending on the influence of international
             medical graduates. There is a strong association between
             higher costs and the local proportion of physician supply
             made up of graduates of non-US or Canadian medical schools
             and female graduates. CONCLUSIONS: These results suggest
             that strategies to reduce overall costs by changing
             physician supply must consider more than just overall
             numbers.},
   Doi = {10.1097/sla.0b013e31822f2021},
   Key = {fds270508}
}

@article{fds270517,
   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},
   ISSN = {0954-5794},
   url = {http://dx.doi.org/10.1017/s0954579411000812},
   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 = {fds270517}
}

@article{fds270506,
   Author = {Sloan, FA and Costanzo, PR and Belsky, D and Holmberg, E and Malone, PS and Wang, Y and Kertesz, S},
   Title = {Heavy drinking in early adulthood and outcomes at mid
             life.},
   Journal = {Journal of Epidemiology and Community Health},
   Volume = {65},
   Number = {7},
   Pages = {600-605},
   Year = {2011},
   Month = {July},
   ISSN = {0143-005X},
   url = {http://dx.doi.org/10.1136/jech.2009.102228},
   Abstract = {BACKGROUND: Heavy drinking in early adulthood among Blacks,
             but not Whites, has been found to be associated with more
             deleterious health outcomes, lower labor market success and
             lower educational attainment at mid-life. This study
             analysed psychosocial pathways underlying racial differences
             in the impact of early heavy alcohol use on occupational and
             educational attainment at mid-life. METHODS: Outcomes in
             labor market participation, occupational prestige and
             educational attainment were measured in early and
             mid-adulthood. A mixture model was used to identify
             psychosocial classes that explain how race-specific
             differences in the relationship between drinking in early
             adulthood and occupational outcomes in mid-life operate.
             Data came from Coronary Artery Risk Development in Young
             Adults, a longitudinal epidemiologic study. RESULTS:
             Especially for Blacks, heavy drinking in early adulthood was
             associated with a lower probability of being employed in
             mid-life. Among employed persons, there was a link between
             heavy drinking for both Whites and Blacks and decreased
             occupational attainment at mid-life. We grouped individuals
             into three distinct distress classes based on external
             stressors and indicators of internally generated stress.
             Blacks were more likely to belong to the higher distressed
             classes as were heavy drinkers in early adulthood.
             Stratifying the data by distress class, relationships
             between heavy drinking, race and heavy drinking-race
             interactions were overall weaker than in the pooled
             analysis. CONCLUSIONS: Disproportionate intensification of
             life stresses in Blacks renders them more vulnerable to
             long-term effects of heavy drinking.},
   Doi = {10.1136/jech.2009.102228},
   Key = {fds270506}
}

@article{fds270509,
   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
             USA},
   Volume = {108},
   Number = {7},
   Pages = {2693-2698},
   Year = {2011},
   Month = {February},
   ISSN = {0027-8424},
   url = {http://dx.doi.org/10.1073/pnas.1010076108},
   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 = {fds270509}
}

@article{fds270497,
   Author = {Poley, S and Ricketts, T and Belsky, D and Gaul, K},
   Title = {Pediatric surgeons: subspecialists increase faster than
             generalists.},
   Journal = {Bulletin of the American College of Surgeons},
   Volume = {95},
   Number = {10},
   Pages = {35-38},
   Year = {2010},
   Month = {October},
   ISSN = {0002-8045},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/21449276},
   Key = {fds270497}
}

@article{fds270516,
   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},
   ISSN = {0002-9262},
   url = {http://dx.doi.org/10.1093/aje/kwq201},
   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 = {fds270516}
}

@article{fds270492,
   Author = {Belsky, D and Ricketts, T and Poley, S and Gaul, K},
   Title = {Surgical deserts in the U.S.: counties without
             surgeons.},
   Journal = {Bulletin of the American College of Surgeons},
   Volume = {95},
   Number = {9},
   Pages = {32-35},
   Year = {2010},
   Month = {September},
   ISSN = {0002-8045},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/21449298},
   Key = {fds270492}
}

@article{fds270482,
   Author = {Frank, DA and Chilton, M and Casey, PH and Black, MM and Cook, JT and Cutts, DB and Meyers, AF},
   Title = {Nutritional-Assistance Programs Play a Critical Role in
             Reducing Food Insecurity},
   Journal = {Pediatrics},
   Volume = {125},
   Number = {5},
   Pages = {e1267-e1267},
   Year = {2010},
   Month = {May},
   ISSN = {0031-4005},
   url = {http://dx.doi.org/10.1542/peds.2010-0808},
   Doi = {10.1542/peds.2010-0808},
   Key = {fds270482}
}

@article{fds302546,
   Author = {Melchior, M and Caspi, A and Belsky, D and Moffitt,
             TE},
   Title = {In Reply},
   Journal = {Pediatrics},
   Volume = {125},
   Number = {5},
   Pages = {e1267-e1268},
   Year = {2010},
   Month = {May},
   ISSN = {0031-4005},
   url = {http://dx.doi.org/10.1542/peds.2010-0808a},
   Doi = {10.1542/peds.2010-0808a},
   Key = {fds302546}
}

@article{fds270499,
   Author = {Fraher, E and Belsky, DW and Gaul, K and Carpenter,
             J},
   Title = {Factors affecting attrition from associate degree nursing
             programs in North Carolina.},
   Journal = {Cahiers de Sociologie et de Demographie Medical},
   Volume = {50},
   Number = {2},
   Pages = {213-246},
   Year = {2010},
   Month = {April},
   ISSN = {0007-9995},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/20653220},
   Abstract = {Projected nursing shortfalls have spurred the state of North
             Carolina to initiate a series of strategies to increase the
             number of graduates from pre-licensure Registered Nurse (RN)
             programs. These efforts have been largely successful, but
             attrition rates from Associate Degree Nursing (ADN) programs
             remain high. Only 58% of students entering ADN programs
             complete the degree. While policy makers are keenly aware
             that attrition from ADN programs is problematic, there is a
             lack of empirical evidence to identify the specific factors
             contributing to student attrition. In late 2007, the North
             Carolina Community College System (NCCCS) asked the Cecil G.
             Sheps Center for Health Services Research to conduct a study
             of Associate Degree Nursing program attrition and its
             causes. This paper summarizes the findings from that study
             and identifies the student- and program-level
             characteristics associated with more and less successful ADN
             programs. While this study was conducted in a single state
             in the US, the substantive findings--as well as the
             methodological approach--may be useful to other states and
             other countries. The study revealed that socioeconomically
             disadvantaged students (those with GEDs and those who
             received Pell Grants), non-white students, and younger and
             older students were less likely to graduate on-time. When
             programs were grouped into high and low performance
             categories on the basis of risk adjusted graduation rates,
             high performing programs were distinguished by more
             stringent admissions policies and better educated faculties.
             Nursing shortages have garnered significant attention and
             resources from state and national workforce planners in
             recent years. But to date, investments in expanding program
             capacity have not been matched by attention to program
             completion rates, with the result that we have enlarged the
             pipeline without fixing the leaks. Faculty shortages and
             recession-induced resource constraints limit further program
             expansion. Addressing attrition problems can expand RN
             production in the short-term at relatively lower
             costs.},
   Key = {fds270499}
}

@article{fds270498,
   Author = {Poley, S and Belsky, D and Gaul, K and Ricketts, T and Fraher, E and Sheldon, G},
   Title = {Longitudinal trends in the U.S. surgical workforce,
             1981-2006.},
   Journal = {Bulletin of the American College of Surgeons},
   Volume = {94},
   Number = {8},
   Pages = {27-31},
   Year = {2009},
   Month = {August},
   ISSN = {0002-8045},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/19715005},
   Key = {fds270498}
}

@article{fds270505,
   Author = {Sloan, FA and Belsky, D and Ruiz, D and Lee, P},
   Title = {Changes in incidence of diabetes mellitus-related eye
             disease among US elderly persons, 1994-2005.},
   Journal = {Archives of Ophthalmology},
   Volume = {126},
   Number = {11},
   Pages = {1548-1553},
   Year = {2008},
   Month = {November},
   ISSN = {0003-9950},
   url = {http://dx.doi.org/10.1001/archopht.126.11.1548},
   Abstract = {To determine if diabetic eye disease has changed over time
             among older Americans and to explore possibilities for
             observed change.We performed a longitudinal analysis of
             nationally representative Medicare data, the Medicare 5%
             sample, collected from January 1, 1991, through December 31,
             2004, using standard claims data algorithms and
             cross-sectional analysis of the Medicare Current Beneficiary
             Survey.Compared with Medicare beneficiaries first diagnosed
             with diabetes mellitus in 1994, those first diagnosed with
             diabetes in 1999 and in 2003 showed lower rates of
             background and proliferative diabetic retinopathy within 1
             year after diagnosis and during 6 years of follow-up among
             the 1999 cohort. Six-year rates of surgical procedures for
             retinopathy were lower among beneficiaries in the 1999
             cohort than in the 1994 cohort, and rates of glucose, lipid,
             and cholesterol monitoring were higher. In addition,
             hypertension was diagnosed more frequently among the 1999
             cohort during 6 years. Data from the Medicare Current
             Beneficiary Survey showed higher rates of antihypertensive
             drug use among persons diagnosed with diabetes in 1999
             compared with 1994.Decreases in rates of diabetic
             retinopathy among persons newly diagnosed with diabetes
             enrolled in Medicare from 1994 to 2004 and concurrent
             improvements in primary care for diabetes suggest that
             better primary care has had an effect on the Medicare
             population, despite increasing rates of other adverse
             outcomes.},
   Doi = {10.1001/archopht.126.11.1548},
   Key = {fds270505}
}

@article{fds270504,
   Author = {Stein, JD and Ruiz, D and Belsky, D and Lee, PP and Sloan,
             FA},
   Title = {Longitudinal rates of postoperative adverse outcomes after
             glaucoma surgery among medicare beneficiaries 1994 to
             2005.},
   Journal = {Ophthalmology: Journal of The American Academy of
             Ophthalmology},
   Volume = {115},
   Number = {7},
   Pages = {1109-1116.e7},
   Year = {2008},
   Month = {July},
   ISSN = {0161-6420},
   url = {http://dx.doi.org/10.1016/j.ophtha.2008.03.033},
   Abstract = {To determine longitudinal rates of postoperative adverse
             outcomes after incisional glaucoma surgery in a nationally
             representative longitudinal sample.Retrospective,
             longitudinal cohort analysis.Medicare beneficiaries >or=68
             years who underwent a primary trabeculectomy (PT),
             trabeculectomy with scarring (TS), or glaucoma drainage
             device (GDD) implantation from 1994 to 2003 with follow-up
             through 2005.Primary trabeculectomy, TS, and GDD were
             identified from International Classification of Diseases
             (ICD-9-CM) and Current Procedural Terminology (CPT)
             procedure codes. Change in rates of postoperative adverse
             outcomes associated with these 3 surgical interventions was
             analyzed by cumulative incidence rates and Cox proportional
             hazards model regression; regression analysis controlled for
             prior adverse outcome measures (3-year run-up) and
             demographic variables.First-, second-, and sixth-year
             cumulative rates and probability of experiencing serious
             adverse outcomes (retinal detachment, endophthalmitis,
             suprachoroidal hemorrhage), less serious adverse outcomes
             (choroidal detachment, corneal edema, hypotony), and receipt
             of additional glaucoma surgery were identified through
             Medicare claims for each treatment group.At the 1-year
             follow-up, rates of severe adverse outcomes were higher
             among beneficiaries in the GDD group (2.0%) relative to the
             PT (0.6%) and TS groups (1.3%). Controlling for prior
             adverse outcomes to the surgery and demographic factors in
             Cox proportional analysis, differences were often reduced,
             but generally remained statistically and clinically
             significant. Rates of severe outcomes, less severe outcomes,
             corneal edema, and low vision/blindness were higher for
             persons undergoing GDD than PT or TS. However, rates of
             reoperation were higher for TS than GDD.The risk for adverse
             outcomes was higher in GDD than in PT surgery or TS,
             controlling for a number of important case mix and
             demographic factors.},
   Doi = {10.1016/j.ophtha.2008.03.033},
   Key = {fds270504}
}

@article{fds270496,
   Author = {Sloan, FA and Belsky, DW and Boly, IA},
   Title = {Prevalence of major eye diseases among US Civil War
             veterans, 1890-1910.},
   Journal = {Archives of Ophthalmology},
   Volume = {126},
   Number = {2},
   Pages = {246-250},
   Year = {2008},
   Month = {February},
   ISSN = {0003-9950},
   url = {http://dx.doi.org/10.1001/archophthalmol.2007.34},
   Abstract = {To estimate the prevalence of major eye diseases and low
             vision or blindness in a national sample of male US Union
             Army veterans from 1890 to 1910 and to compare these
             prevalence rates with contemporary rates for the same
             diseases and visual status.Longitudinal histories of 16,022
             white Union Army veterans receiving disability pensions from
             1890 to 1910 were developed from pension board examination
             records. Prevalence rates of trachoma, corneal opacities,
             cataract, diseases of the retina and optic nerve, and low
             vision or blindness were calculated in 1895 and 1910.
             Changes in prevalence by age were examined.By 1910, 11.9% of
             veterans had low vision or were blind in both eyes.
             Prevalence of cataract increased with age, resulting in
             13.1% of veterans having had cataract in one or both eyes.
             Rates of trachoma were 3.2% in 1895 and 4.8% in 1910. Rates
             of corneal opacity were 3.0% and 5.1%, respectively.
             Glaucoma was rarely diagnosed from 1890 to 1910, but
             diseases of the optic nerve were reported in 2.0% of
             veterans in 1895 and 3.6% in 1910.This study documents
             substantial reductions in the prevalence of low vision or
             blindness and changes in the composition of eye diseases
             from an era in which there were few effective therapies for
             eye diseases to the present.},
   Doi = {10.1001/archophthalmol.2007.34},
   Key = {fds270496}
}

@article{fds270511,
   Author = {Costanzo, PR and Malone, PS and Belsky, D and Kertesz, S and Pletcher,
             M and Sloan, FA},
   Title = {Longitudinal differences in alcohol use in early
             adulthood.},
   Journal = {Journal of studies on alcohol and drugs},
   Volume = {68},
   Number = {5},
   Pages = {727-737},
   Year = {2007},
   Month = {September},
   ISSN = {1937-1888},
   Abstract = {OBJECTIVE: Research with college populations suggests that
             elevated levels of heavy drinking do not generally persist
             into later adulthood for most individuals. The aims of this
             study were to determine whether this pattern applies to the
             population as a whole and to identify those for whom heavy
             drinking in early adulthood does lead to continued high
             levels of consumption throughout the life course. METHOD:
             Patterns of heavy drinking were assessed, and a mixture
             model was used to evaluate relationships between
             psychological profiles and trajectories of heavy drinking in
             early to middle adulthood for race-gender groups. Subjects
             (N = 5,115; 55% women) were drawn from the longitudinal
             study of Coronary Artery Risk Development in Young Adults
             (CARDIA) conducted in four major U.S. cities from 1985 to
             1995. RESULTS: Patterns of heavy drinking differed by race
             and gender, with higher rates observed among whites and men.
             Heavy drinking was generally most common in the early 20s
             and dropped sharply thereafter. For a subset with
             psychological profiles characterized by elevated levels of
             hostility, anxiety, and depressive symptoms, high rates of
             heavy drinking persisted into later adulthood; 20% of whites
             and 50% of blacks in the overall sample were in this subset.
             Rates of heavy drinking in this group were similar for
             blacks and whites. CONCLUSIONS: At a population level, heavy
             drinking in early adulthood tends not to continue into later
             life. For a subset of psychologically vulnerable
             individuals, however, early adult heavy drinking persists
             into the middle adulthood years.},
   Key = {fds270511}
}

@article{fds270512,
   Author = {Bethel, MA and Sloan, FA and Belsky, D and Feinglos,
             MN},
   Title = {Longitudinal incidence and prevalence of adverse outcomes of
             diabetes mellitus in elderly patients.},
   Journal = {Archives of internal medicine},
   Volume = {167},
   Number = {9},
   Pages = {921-927},
   Year = {2007},
   Month = {May},
   ISSN = {0003-9926},
   url = {http://dx.doi.org/10.1001/archinte.167.9.921},
   Abstract = {BACKGROUND: The natural history of type 2 diabetes mellitus
             (DM) in the elderly has not been previously described in a
             national longitudinal sample. METHODS: This national
             longitudinal analysis (January 1, 1991, to December 31,
             2004) examines mortality and morbidity rates in a
             representative sample of elderly patients newly diagnosed as
             having DM. Medicare beneficiaries diagnosed as having DM in
             1994 (n=33,772) were compared with a control group
             (n=25,563) regarding death, lower extremity complications,
             nephropathy, retinopathy, cardiovascular complications, and
             cerebrovascular complications. RESULTS: The DM group had
             excess mortality of 9.2% by year 11 compared with the
             control group. By 2004, 91.8% of the DM group experienced an
             adverse complication compared with 72.0% of the control
             group. The DM group had a higher prevalence and incidence of
             microvascular and macrovascular complications at all time
             points compared with controls. Patients with DM were at
             increased risk for all lower extremity complications,
             particularly those requiring surgical intervention
             (gangrene, debridement, and amputation). Cardiovascular
             complications were a leading cause of morbidity, with 57.6%
             of the DM group diagnosed as having heart failure compared
             with 34.1% of the controls. CONCLUSION: Elderly persons
             newly diagnosed as having DM experienced high rates of
             complications during 10-year follow-up, far in excess of
             elderly persons without this diagnosis, implying a
             substantial burden on the individual and on the health care
             system.},
   Doi = {10.1001/archinte.167.9.921},
   Key = {fds270512}
}

@article{fds270510,
   Author = {Humphreys, M and Costanzo, P and Haynie, KL and Ostbye, T and Boly, I and Belsky, D and Sloan, F},
   Title = {Racial disparities in diabetes a century ago: evidence from
             the pension files of US Civil War veterans.},
   Journal = {Social Science & Medicine},
   Volume = {64},
   Number = {8},
   Pages = {1766-1775},
   Year = {2007},
   Month = {April},
   ISSN = {0277-9536},
   url = {http://dx.doi.org/10.1016/j.socscimed.2006.12.004},
   Abstract = {Using a comprehensive database constructed from the pension
             files of US Civil War veterans, we explore characteristics
             and occurrence of type 2 diabetes among older black and
             white males, living circa 1900. We find that rates of
             diagnosed diabetes were much lower among males in this
             period than a century later. In contrast to the late 20th
             Century, the rates of diagnosed diabetes were lower among
             black than among white males, suggesting that the reverse
             pattern is of relatively recent origin. Two-thirds of both
             white and black veterans had body-mass indexes (BMIs) in the
             currently recommended weight range, a far higher proportion
             than documented by recent surveys. Longevity among persons
             with diabetes was not reduced among Civil War veterans, and
             those with diabetes suffered comparatively few sequelae of
             the condition. Over 90% of black veterans engaged in low
             paying, high-physical effort jobs, as compared to about half
             of white veterans. High rates of work-related physical
             activity may provide a partial explanation of low rates of
             diagnosed diabetes among blacks. We found no evidence of
             discrimination in testing by race, as indicated by rates of
             examinations in which a urinalysis was performed. This
             dataset is valuable for providing a national benchmark
             against which to compare modern diabetes prevalence
             patterns.},
   Doi = {10.1016/j.socscimed.2006.12.004},
   Key = {fds270510}
}

@article{fds270507,
   Author = {Salm, M and Belsky, D and Sloan, FA},
   Title = {Trends in cost of major eye diseases to Medicare, 1991 to
             2000.},
   Journal = {American Journal of Ophthalmology},
   Volume = {142},
   Number = {6},
   Pages = {976-982},
   Year = {2006},
   Month = {December},
   ISSN = {0002-9394},
   url = {http://dx.doi.org/10.1016/j.ajo.2006.07.057},
   Abstract = {PURPOSE: To estimate impacts of physician-diagnosed eye
             diseases (age-related macular degeneration (AMD), cataract,
             diabetic retinopathy, and glaucoma) on Medicare payments in
             the periods 1991 to 1995 and 1996 to 2000. DESIGN: A
             retrospective cohort study to estimate program payments per
             capita and in total for each of the major eye diseases and
             the four eye diseases in total. METHODS: Data from the 1994
             and 1999 National Long-Term Care Survey (NLTCS) and medical
             claims to Medicare from 1991 to 2000 were merged with the
             NLTCS. Medicare payments for eye-related procedures on
             persons with and without major eye diseases as reported on
             Medicare claims and self-reported data from NLTCS. RESULTS:
             Overall, the burden of major eye diseases was to increase
             Medicare spending by 4.8 billion dollars (1999 USD) in 1991
             to 1995 and by 4.5 billion dollars in 1996 to 2000. The most
             expensive eye disease was cataract, costing Medicare 3.8
             billion dollars in 1991 to 1995 and 3 billion dollars in
             1996 to 2000. CONCLUSIONS: Prevalence of major eye diseases
             increased over time, but the effect of major eye diseases on
             Medicare payments decreased, mainly as a result of lower
             payments for cataract surgery in the later
             years.},
   Doi = {10.1016/j.ajo.2006.07.057},
   Key = {fds270507}
}


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