The Dunedin Study - DMHDRU

Publications

All peer reviewed publications are listed below.

Displaying page 2 of 22.

A polygenic score for age-at-first-birth predicts disinhibition | 2020
Leah S. Richmond‐Rakerd, Terrie E. Moffitt, Louise Arseneault, Daniel W. Belsky , Jennie Connor , ... Show all » David L. Corcoran , HonaLee Harrington, Renate M. Houts, Richie Poulton , Joey A. Prinz, Sandhya Ramrakha , Karen Sugden, Jasmin Wertz, Benjamin S. Williams, Avshalom Caspi « Hide
Journal of Child Psychology and Psychiatry, 2020, .
https://doi.org/10.1111/jcpp.13224
download pdf Our ref: RO727
Show abstract » Background: A recent genome‐wide association study identified molecular‐genetic associations with age‐at‐first‐birth. However, the meaning of these genetic discoveries is unclear. Drawing on evidence linking early pregnancy withdisinhibitory behavior, we tested the hypothesis that genetic discoveries for age‐at‐first‐birth predict disinhibition.Methods: We included participants with genotype data from the two‐decade‐long Environmental Risk (E‐Risk) Study(N = 1,999) and the four‐decade‐long Dunedin Study (N = 918). We calculated a genome‐wide polygenic score for age‐at‐first‐birth and tested whether it was associated with a range of disinhibitory outcomes across the life course,including low childhood self‐control; risk for externalizing psychopathology; officially recorded criminal offending;substance dependence; informant reports of disinhibitory problems; and number of lifetime sexual partners. We
further tested whether associations were attributable to accelerated pubertal maturation. Results: In both cohorts,the age‐at‐first‐birth polygenic score predicted low childhood self‐control, externalizing psychopathology, officially recorded criminal offending, substance dependence, and number of sexual partners. Associations were modest, butrobust across replication. Childhood disinhibition partly mediated associations between the polygenic scoreand reproductive behaviors. In contrast, associations were not attributable to accelerated pubertal timing.Conclusions: Genomic discoveries for age‐at‐first‐birth are about more than reproductive biology: They provideinsight into the disinhibitory traits and behaviors that accompany early parenthood. Age‐at‐first‐birth is a usefulproxy phenotype for researchers interested in disinhibition. Further, interventions that improve self‐regulationabilities may benefit young parents and their children. Keywords: Reproductive behavior; self‐control; risk‐taking;genetics; longitudinal.

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The Dunedin Multidisciplinary Health and Development Study: oral health findings and their implications | 2020
Chuen Lin Hong, Jonathan M. Broadbent, W. Murray Thomson, Richie Poulton
Journal of the Royal Society of New Zealand, 2020, 50(1), .
https://doi.org/10.1080/03036758.2020.1716816
download pdf Our ref: NZ96
Show abstract » Longitudinal research is needed to better understand the natural history of oral conditions and long-term health and social outcomes. Oral health data has been collected periodically in the Dunedin Multidisciplinary Health and Development Study for over 40 years. To date, 70+ peer-review articles on the Study’s oral health-related findings have been published, providing insight into the natural history of oral conditions, risk factors, impacts on quality of life, and disparities in oral health. Some of these report new findings, while others build upon the existing body of evidence. This paper provides an overview of these findings and reflects on their public health implications and policy utility in New Zealand.
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A risk calculator to predict adult attention-deficit/hyperactivity disorder: generation and external validation in three birth cohorts and one clinical sample | 2019
Caye, Arthur; Jessica Agnew-Blais; Louise Arseneault; Ives Cavalcante-Passos; Helen Gonçalves; Christian Kieling; Kate Langley; Ana M. B. Menezes; Terrie E Moffitt; Anita Thapar; Thiago Botter-Maio Rocha; Margaret Sibley; James M. Swanson; Fernando Wehrmeister; Luis Augusto Rohde.
Epidemiology and Psychiatric Sciences, 2019, 29(37), .
https://doi.org/10.1017/s2045796019000283
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Our ref: RO756
Show abstract » Aim: Few personalised medicine investigations have been conducted for mental health. We aimed to generate and validate a risk tool that predicts adult attention-deficit/hyperactivity disorder (ADHD).

Methods: Using logistic regression models, we generated a risk tool in a representative population cohort (ALSPAC - UK, 5113 participants, followed from birth to age 17) using childhood clinical and sociodemographic data with internal validation. Predictors included sex, socioeconomic status, single-parent family, ADHD symptoms, comorbid disruptive disorders, childhood maltreatment, ADHD symptoms, depressive symptoms, mother's depression and intelligence quotient. The outcome was defined as a categorical diagnosis of ADHD in young adulthood without requiring age at onset criteria. We also tested Machine Learning approaches for developing the risk models: Random Forest, Stochastic Gradient Boosting and Artificial Neural Network. The risk tool was externally validated in the E-Risk cohort (UK, 2040 participants, birth to age 18), the 1993 Pelotas Birth Cohort (Brazil, 3911 participants, birth to age 18) and the MTA clinical sample (USA, 476 children with ADHD and 241 controls followed for 16 years from a minimum of 8 and a maximum of 26 years old).

Results: The overall prevalence of adult ADHD ranged from 8.1 to 12% in the population-based samples, and was 28.6% in the clinical sample. The internal performance of the model in the generating sample was good, with an area under the curve (AUC) for predicting adult ADHD of 0.82 (95% confidence interval (CI) 0.79-0.83). Calibration plots showed good agreement between predicted and observed event frequencies from 0 to 60% probability. In the UK birth cohort test sample, the AUC was 0.75 (95% CI 0.71-0.78). In the Brazilian birth cohort test sample, the AUC was significantly lower -0.57 (95% CI 0.54-0.60). In the clinical trial test sample, the AUC was 0.76 (95% CI 0.73-0.80). The risk model did not predict adult anxiety or major depressive disorder. Machine Learning approaches did not outperform logistic regression models. An open-source and free risk calculator was generated for clinical use and is available online at https://ufrgs.br/prodah/adhd-calculator/.

Conclusions: The risk tool based on childhood characteristics specifically predicts adult ADHD in European and North-American population-based and clinical samples with comparable discrimination to commonly used clinical tools in internal medicine and higher than most previous attempts for mental and neurological disorders. However, its use in middle-income settings requires caution.

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Psychiatry’s Opportunity to Prevent the Rising Burden of Age-Related Disease | 2019
Terrie E. Moffitt, Avshalom Caspi
JAMA Psychiatry, 2019, 76(5), 461–462.
https://doi.org/10.1001/jamapsychiatry.2019.0037
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Our ref: RO755
Show abstract » Three demographic trends are colliding to form a perfect storm: the postretirement portion of the population is swelling, the human life span is lengthening, and the birth rate is dropping. The result is that the balance of young to old in the population is shifting, leaving fewer young workers to drive the economy and pay taxes to support aging citizens. These 3 trends mean more stress for the young and less support for the old, bringing 2 opportunities for the mental health field. First, an opportunity to prevent disability among young people, which would enhance their well-being and capacity to shoulder the burden of the dependent older population. Young people tend to be physically healthy but can experience behavioral problems, emotional problems, substance abuse, and cognitive impairments. These conditions respond to mental health treatments. Second, an opportunity to prevent ill health among older people, which would reduce the burden of age-related disability. Here, we argue that psychiatry is well situated to prevent disability among older people by doing something it does well: treat young people. Risk-prediction research shows that the same people who have poor mental and cognitive health while young tend to have age-related diseases years later.1,2 Moreover, the timing is right. Mental disorders peak in adolescence and young adulthood, whereas noninfectious diseases peak in midlife and neurodegenerative conditions peak in late life.
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Brain-age in midlife is associated with accelerated biological aging and cognitive decline in a longitudinal birth cohort | 2019
Elliot, M.L. Belsky, D.W., Knodt, A.R., ... Show all » Ireland, D., Melzer, T.R., Poulton, R., Ramrakha, S., Caspi, A., Moffitt, T.E., Hariri, A.R « Hide
Molecular Psychiatry, 2019, .
https://doi.org/10.1038/s41380-019-0626-7
download pdf Our ref: RO733
Show abstract » An individual’s brainAGE is the difference between chronological age and age predicted from machine-learning models of brain-imaging data. BrainAGE has been proposed as a biomarker of age-related deterioration of the brain. Having an older brainAGE has been linked to Alzheimer’s, dementia, and mortality. However, these findings are largely based on crosssectional associations which can confuse age differences with cohort differences. To illuminate the validity of brainAGE as a biomarker of accelerated brain aging, a study is needed of a large cohort all born in the same year who nevertheless vary on brainAGE. In the Dunedin Study, a population-representative 1972–73 birth cohort, we measured brainAGE at age 45 years, as well as the pace of biological aging and cognitive decline in longitudinal data from childhood to midlife (N = 869). In this cohort, all chronological age 45 years, brainAGE was measured reliably (ICC = 0.81) and ranged from 24 to 72 years. Those with older midlife brainAGEs tended to have poorer cognitive function in both adulthood and childhood, as well as impaired brain health at age 3. Furthermore, those with older brainAGEs had an accelerated pace of biological aging, older facial appearance, and early signs of cognitive decline from childhood to midlife. These findings help to validate brainAGE as a potential surrogate biomarker for midlife intervention studies that seek to measure dementia-prevention efforts in midlife. However, the findings also caution against the assumption that brainAGE scores represent only age-related deterioration of the brain as they may also index central nervous system variation present since childhood.
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White matter hyperintensities are common in midlife and already associated with cognitive decline | 2019
Tracy d’Arbeloff, Maxwell L. Elliott, Annchen R. Knodt, Tracy R. Melzer, Ross Keenan, ... Show all » David Ireland, Sandhya Ramrakha, Richie Poulton, Tim Anderson, Avshalom Caspi, Terrie E. Moffitt, Ahmad R. Hariri « Hide
Brain Communications, 2019, 1(1), .
https://doi.org/10.1093/braincomms/fcz041
download pdf Our ref: RO728
Show abstract » White matter hyperintensities proliferate as the brain ages and are associated with increased risk for cognitive decline as well as Alzheimer’s disease and related dementias. As such, white matter hyperintensities have been targeted as a surrogate biomarker in intervention trials with older adults. However, it is unclear at what stage of aging white matter hyperintensities begin to relate to cognition and if they may be a viable target for early prevention. In the Dunedin Study, a population-representative cohort followed since birth, we measured white matter hyperintensities in 843 45-year-old participants using T2-weighted magnetic resonance imaging and we assessed cognitive decline from childhood to midlife. We found that white matter hyperintensities were common at age 45 and that white matter hyperintensity volume was modestly associated with both lower childhood (ß = −0.08, P = 0.013) and adult IQ (ß=−0.15, P < 0.001). Moreover, white matter hyperintensity volume was associated with greater cognitive decline from childhood to midlife (ß=−0.09, P < 0.001). Our results demonstrate that a link between white matter hyperintensities and early signs of cognitive decline is detectable decades before clinical symptoms of dementia emerge. Thus, white matter hyperintensities may be a useful surrogate biomarker for identifying individuals in midlife at risk for future accelerated cognitive decline and selecting participants for dementia prevention trials.
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Replicability of structural brain alterations associated with general psychopathology: evidence from a population-representative birth cohort | 2019
Romer, A. L., Knodt, A. R., Sison, ... Show all » M., Ireland, D., Ramrakha, S., Poulton, R., Keenan, R., Melzer, T. R., Moffitt, T. E., Caspi, A., Hariri, A. R. « Hide
Molecular Psychiatry, 2019, .
https://doi.org/10.1038/s41380-019-0621-z
download pdf Our ref: RO726
Show abstract » Transdiagnostic research has identified a general psychopathology factor – often called the ‘p’
factor – that accounts for shared liability to internalizing, externalizing, and thought disorders in
diverse samples. It has been argued that the p factor may reflect dysfunctional thinking present
in serious mental illness. In support of this, we previously used a theory-free, data-driven
multimodal neuroimaging approach to find that higher p factor scores are associated with
structural deficits within a cerebello-thalamo-cortical circuit (CTCC) and visual association
cortex, both of which are important for monitoring and coordinating information processing in
the service of executive control. Here we attempt to replicate these associations by conducting
region-of-interest analyses of the CTCC and visual association cortex using data from 831
members of the Dunedin Multidisciplinary Health and Development Study, a five-decade
longitudinal study of a population-representative birth cohort now 45 years old. We further
sought to replicate a more recent report that p factor scores can be predicted by patterns of
distributed cerebellar morphology as estimated through independent component analysis. We
successfully replicated associations between higher p factor scores and both reduced grey
matter volume of the visual association cortex and fractional anisotropy of pontine white
matter pathways within the CTCC. In contrast, we failed to replicate prior associations between
cerebellar structure and p factor scores. Collectively, our findings encourage further focus on
the CTCC and visual association cortex as core neural substrates and potential biomarkers of
transdiagnostic risk for mental illness.

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Epigenome-wide Association Study of Attention-Deficit/Hyperactivity Disorder Symptoms in Adults | 2019
Jenny van Dongen, Nuno R. Zilhão, Karen Sugden, BIOS Consortium, Eilis J. Hannon, ... Show all » Jonathan Mill, Avshalom Caspi, Jessica Agnew-Blais, Louise Arseneault, David L. Corcoran, Terrie E. Moffitt, Richie Poulton, Barbara Franke, Dorret I. Boomsma « Hide
Biological Psychiatry, 2019, 86(8), 559-607.
https://doi.org/10.1016/j.biopsych.2019.02.016
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Our ref: RO720
Show abstract » Background
Previous studies have reported associations between attention-deficit/hyperactivity disorder symptoms and DNA methylation in children. We report the first epigenome-wide association study meta-analysis of adult attention-deficit/hyperactivity disorder symptoms, based on peripheral blood DNA methylation (Infinium HumanMethylation450K array) in three population-based adult cohorts.

Methods
An epigenome-wide association study was performed in the Netherlands Twin Register (N = 2258, mean age 37 years), Dunedin Multidisciplinary Health and Development Study (N = 800, age 38 years), and Environmental Risk Longitudinal Twin Study (N = 1631, age 18 years), and results were combined through meta-analysis (total sample size N = 4689). Region-based analyses accounting for the correlation between nearby methylation sites were also performed.

Results
One epigenome-wide significant differentially methylated position was detected in the Dunedin study, but meta-analysis did not detect differentially methylated positions that were robustly associated across cohorts. In region-based analyses, six significant differentially methylation regions (DMRs) were identified in the Netherlands Twin Register, 19 in the Dunedin study, and none in the Environmental Risk Longitudinal Twin Study. Of these DMRs, 92% were associated with methylation quantitative trait loci, and 68% showed moderate to large blood-brain correlations for DNA methylation levels. DMRs included six nonoverlapping DMRs (three in the Netherlands Twin Register, three in the Dunedin study) in the major histocompatibility complex, which were associated with expression of genes in the major histocompatibility complex, including C4A and C4B, previously implicated in schizophrenia.

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Genetics of nurture: A test of the hypothesis that parents' genetics predict their observed caregiving | 2019
Wertz J Belsky J Moffitt TE Belsky DW., Harrington H., Avinun R., Poulton R., Ramrakha S., ... Show all » Caspi A. « Hide
Development Psychology, 2019, 55(7), 1461–1472.
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Our ref: RO716
Show abstract » Twin studies have documented that parenting behavior is partly heritable, but it is unclear how parents' genetics shape their caregiving. Using tools of molecular genetics, the present study investigated this process by testing hypotheses about associations between a genome-wide polygenic score for educational attainment and parental caregiving in 702 members of the Dunedin Study, a population-representative birth cohort. Data have been prospectively collected from when Study members were born through to midlife, and include assessments of the caregiving they provided once they became parents. Results showed that parents' polygenic scores predicted warm, sensitive, and stimulating caregiving, both in personal interactions with their young children (as captured on video) and through the home environments they created for their families (as observed by home visitors). The magnitude of this effect was small. Polygenic-score associations were independent of well-established predictors of parenting, such as parents' own childhood experiences of parenting and the age at which they became parents. Polygenic-score associations were mediated by parents' early-emerging cognitive abilities and self-control skills. Findings have implications for theory and research about genetic influences on caregiving and child development. (PsycINFO Database Record (c) 2019 APA, all rights reserved).
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Association of Neurocognitive and Physical Function With Gait Speed in Midlife | 2019
Line Jee Hartmann Rasmussen, Avshalom Caspi, Antony Ambler, Jonathan M. Broadbent, Harvey J. Cohen, ... Show all » Tracy d’Arbeloff, Maxwell Elliott, Robert J. Hancox, HonaLee Harrington, Sean Hogan, Renate Houts, David Ireland, Annchen R. Knodt, Kim Meredith-Jones, Miriam C. Morey, Lynda Morrison, Richie Poulton, Sandhya Ramrakha, Leah Richmond-Rakerd, Maria L. Sison, Kate Sneddon, W. Murray Thomson, Ahmad R. Hariri, Terrie E. Moffitt « Hide
JAMA Network Open, 2019, .
10.1001/jamanetworkopen.2019.13123
download pdfLink to full publication »
Our ref: RO725
Show abstract » IMPORTANCE Gait speed is a well-known indicator of risk of functional decline and mortality in older adults, but little is known about the factors associated with gait speed earlier in life.
OBJECTIVES To test the hypothesis that slow gait speed reflects accelerated biological aging at midlife, as well as poor neurocognitive functioning in childhood and cognitive decline from childhood to midlife.

DESIGN, SETTING, AND PARTICIPANTS This cohort study uses data from the Dunedin Multidisciplinary Health and Development Study, a population-based study of a representative 1972
to 1973 birth cohort in New Zealand that observed participants to age 45 years (until April 2019). Data analysis was performed from April to June 2019.

EXPOSURES Childhood neurocognitive functions and accelerated aging, brain structure, and concurrent physical and cognitive functions in adulthood.

MAIN OUTCOMES AND MEASURES Gait speed at age 45 years, measured under 3 walking conditions: usual, dual task, and maximum gait speeds.

RESULTS Of the 1037 original participants (91% of eligible births; 535 [51.6%] male), 997 were alive at age 45 years, of whom 904 (90.7%) had gait speed measured (455 [50.3%] male; 93%white). The mean (SD) gait speeds were 1.30 (0.17) m/s for usual gait, 1.16 (0.23) m/s for dual task gait, and 1.99 (0.29) m/s for maximum gait. Adults with more physical limitations (standardized regression coefficient [β], −0.27; 95%CI, −0.34 to −0.21; P < .001), poorer physical functions (ie, weak grip strength [β, 0.36; 95%CI, 0.25 to 0.46], poor balance [β, 0.28; 95%CI, 0.21 to 0.34], poor visualmotor coordination [β, 0.24; 95%CI, 0.17 to 0.30], and poor performance on the chair-stand [β, 0.34; 95%CI, 0.27 to 0.40] or 2-minute step tests [β, 0.33; 95%CI, 0.27 to 0.39]; all P < .001), accelerated biological aging across multiple organ systems (β, −0.33; 95%CI, −0.40 to −0.27; P < .001), older facial appearance (β, −0.25; 95%CI, −0.31 to −0.18; P < .001), smaller brain volume (β, 0.15; 95%CI, 0.06 to 0.23; P < .001), more cortical thinning (β, 0.09; 95%CI, 0.02 to 0.16; P = .01), smaller cortical surface area (β, 0.13; 95%CI, 0.04 to 0.21; P = .003), and more white matter hyperintensities (β, −0.09; 95%CI, −0.15 to −0.02; P = .01) had slower gait speed. Participants with lower IQ in midlife (β, 0.38; 95%CI, 0.32 to 0.44; P < .001) and participants who exhibited cognitive
decline from childhood to adulthood (β, 0.10; 95%CI, 0.04 to 0.17; P < .001) had slower gait at age 45 years. Those with poor neurocognitive functioning as early as age 3 years had slower gait in midlife (β, 0.26; 95%CI, 0.20 to 0.32; P < .001).

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Childhood and adolescent television viewing and internalising disorders in adulthood | 2019
Helena M McAnally, Tamara Young, Robert J Hancox
Preventive Medicine Reports, 2019, 15 100890.
https://doi.org/10.1016/j.pmedr.2019.100890
download pdf Our ref: RO722
Show abstract » Time spent watching television during childhood and adolescence has been linked to socio-emotional and physical health problems in adulthood. It is unclear whether excessive television viewing is a risk factor for internalising mental health disorders such as anxiety and depression. Longitudinal associations between television viewing in childhood and adult diagnoses of anxiety and depression were investigated in a population-based birth cohort from Dunedin, New Zealand. Mean weekday television viewing time was reported by parents and adolescents between ages 5 and 15 years (1977-1987). Diagnoses of any anxiety disorder and major depression were made using standard criteria from symptoms reported for the previous year at ages 18, 21, 26, 32, and 38 years (between 1990 and 2012). Analyses adjusted for sex, parent and teacher reports of worry/fearfulness at age 5, and socioeconomic status during childhood. Diagnoses were counted if present at any of these assessments. Approximately half of all participants met criteria for anxiety disorder or depression during at least one adult assessment. Participants who had watched more television during childhood and adolescence were more likely to have a diagnosis of anxiety in sex-adjusted analyses (OR [95% CI] 1.22 [1.05, 1.41], p=0.01), although this association weakened after adjustment for early childhood worry/fearfulness and socioeconomic status. There was no association between television viewing and depression in sex- or fully-adjusted analyses. Excessive television viewing during childhood and adolescence may be a risk factor for developing an anxiety disorder in adulthood, but does not appear to influence the long-term risk for major depression.
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Associations between lung and endothelial function in early middle age | 2019
Robert J. Hancox, Lathan Thomas, Michael J.A. Williams, Malcolm R. Sears
Respirology, 2019, .
https://doi.org/10.1111/resp.13556
download pdf Our ref: RO723
Show abstract » Background and objective
Chronic lung disease is associated with impaired endothelial function and this may be a risk factor for poor cardiovascular health. It is unknown if there is an association between lung and endothelial function in the general population. We investigated associations between lung and endothelial function in a population‐based cohort of 38‐year‐old men and women.

Methods
Systemic endothelial function was measured using peripheral arterial tonometry to calculate the Framingham reactive hyperaemia index. Lung function was assessed using spirometry, plethysmographic lung volumes, airway conductance and gas transfer. Associations between lung and endothelial function were assessed with and without adjustment for potential confounding factors using regression analyses.

Results
Sex modified the association between lung and endothelial function. Among women, lower values of pre‐ and post‐bronchodilator spirometry, total lung capacity and functional residual capacity (FRC) were associated with worse endothelial function (P < 0.05). These associations persisted after adjustment for smoking, asthma diagnoses, fitness and body mass index. Associations were weaker among men: only FRC, airway conductance and post‐bronchodilator forced expiratory volume in 1 s (FEV1)/forced vital capacity (FVC) ratios were associated with endothelial function. Endothelial function was not associated with gas transfer in either sex.

Conclusion
Lower lung volumes and airflow obstruction are associated with endothelial dysfunction among women. There is weaker evidence for an association between airway and endothelial function in men. These findings may partly explain the increased risk of cardiovascular disease among people with poor lung function, but suggest that there are sex differences in this association.

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Smoking does not accelerate leucocyte telomere attrition: a meta-analysis of 18 longitudinal cohorts | 2019
Melissa Bateson, Abraham Aviv, Laila Bendix, Athanase Benetos, Yoav Ben-Shlomo, ... Show all » Stig E. Bojesen, Cyrus Cooper, Rachel Cooper, Ian J. Deary, Sara Hagg, Sarah E. Harris, Jeremy D. Kark, Florian Kronenberg, Diana Kuh, Carlos Labat, Carmen M. Martin-Ruiz, Craig Meyer, Børge G. Nordestgaard, Brenda W. J. H. Penninx, Gillian V. Pepper, Dora Revesz, M. Abdullah Said, John M. Starr, Holly Syddall, William Murray Thomson, Pim van der Harst, Mary Whooley, Thomas von Zglinicki, Peter Willeit, Yiqiang Zhan, Daniel Nettle « Hide
The Royal Society Open Science, 2019, 6(6), .
https://doi.org/10.1098/rsos.190420
download pdf Our ref: RO721
Show abstract » Smoking is associated with shorter leucocyte telomere length (LTL), a biomarker of increased morbidity and reduced longevity. This association is widely interpreted as evidence that smoking causes accelerated LTL attrition in adulthood, but the evidence for this is inconsistent. We analysed the association between smoking and LTL dynamics in 18 longitudinal cohorts. The dataset included data from 12 579 adults (4678 current smokers and 7901 non-smokers) over a mean follow-up interval of 8.6 years. Meta-analysis confirmed a cross-sectional difference in LTL between smokers and non-smokers, with mean LTL 84.61 bp shorter in smokers (95% CI: 22.62 to 146.61). However, LTL attrition was only 0.51 bp yr−1 faster in smokers than in non-smokers (95% CI: −2.09 to 1.08), a difference that equates to only 1.32% of the estimated age-related loss of 38.33 bp yr−1. Assuming a linear effect of smoking, 167 years of smoking would be required to generate the observed cross-sectional difference in LTL. Therefore, the difference in LTL between smokers and non-smokers is extremely unlikely to be explained by a linear, causal effect of smoking. Selective adoption, whereby individuals with short telomeres are more likely to start smoking, needs to be considered as a more plausible explanation for the observed pattern of telomere dynamics.
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General functional connectivity: Shared features of resting-state and task fMRI drive reliable and heritable individual differences in functional brain networks | 2019
Maxwell L. Elliott, Annchen R. Knodt, Megan Cooke, M. Justin Kim, Tracy R. Melzer, ... Show all » Ross Keenan, David Ireland, Sandhya Ramrakha, Richie Poulton, Avshalom Caspi, Terrie E. Moffitt, Ahmad R. Hariri « Hide
NeuroImage, 2019, 189 516-532.
https://doi.org/10.1016/j.neuroimage.2019.01.068
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Our ref: RO719
Show abstract » Intrinsic connectivity, measured using resting-state fMRI, has emerged as a fundamental tool in the study of the human brain. However, due to practical limitations,
many studies do not collect enough resting-state data to generate reliable measures of intrinsic connectivity necessary for studying individual differences. Here we
present general functional connectivity (GFC) as a method for leveraging shared features across resting-state and task fMRI and demonstrate in the Human Connectome
Project and the Dunedin Study that GFC offers better test-retest reliability than intrinsic connectivity estimated from the same amount of resting-state data
alone. Furthermore, at equivalent scan lengths, GFC displayed higher estimates of heritability than resting-state functional connectivity. We also found that predictions
of cognitive ability from GFC generalized across datasets, performing as well or better than resting-state or task data alone. Collectively, our work suggests that GFC can improve the reliability of intrinsic connectivity estimates in existing datasets and, subsequently, the opportunity to identify meaningful correlates of individual differences in behavior. Given that task and resting-state data are often collected together, many researchers can immediately derive more reliable measures of intrinsic connectivity through the adoption of GFC rather than solely using resting-state data. Moreover, by better capturing heritable variation in intrinsic connectivity, GFC represents a novel endophenotype with broad applications in clinical neuroscience and biomarker discovery.

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A Polygenic Score for Higher Educational Attainment is Associated with Larger Brains | 2019
Elliott, M. L. Belsky, D. W. Anderson, K. Corcoran, D. L. Ge, ... Show all » T. Knodt, A. Prinz, J. A. Sugden, K. Williams, B. Ireland, D. Poulton, R. Caspi, A. Holmes, A. Moffitt, T.E. Hariri, A. R. « Hide
Cerebal Cortex, 2019, 1-9.
https://doi.org/10.1093/cercor/bhy219
download pdf Our ref: RO706
Show abstract » People who score higher on intelligence tests tend to have larger brains. Twin studies suggest the same genetic factors influence both brain size and intelligence. This has led to the hypothesis that genetics influence intelligence partly by contributing to development of larger brains. We tested this hypothesis with molecular genetic data using discoveries from a genome-wide association study (GWAS) of educational attainment, a correlate of intelligence. We analyzed genetic, brain imaging, and cognitive test data from the UK Biobank, the Dunedin Study, the Brain Genomics Superstruct Project (GSP), and the Duke Neurogenetics Study (DNS) (combined N=8,271). We measured genetics using polygenic scores based on published GWAS. We conducted meta-analysis to test associations among participants' genetics, total brain volume (i.e., brain size), and cognitive test performance. Consistent with previous findings, participants with higher polygenic scores achieved higher scores on cognitive tests, as did participants with larger brains. Participants with higher polygenic scores also had larger brains. We found some evidence that brain size partly mediated associations between participants' education polygenic scores and their cognitive test performance. Effect-sizes were larger in the population-based UK Biobank and Dunedin samples than in the GSP and DNS samples. Sensitivity analysis suggested this effect-size difference partly reflected restricted range of cognitive performance in the GSP and DNS samples. Recruitment and retention of population-representative samples should be a priority for neuroscience research. Findings suggest promise for studies integrating GWAS discoveries with brain imaging data to understand neurobiology linking genetics with individual differences in cognitive performance.
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Childhood IQ predicts age-38 oral disease experience and service-use | 2019
Thomson WM, Broadbent JM, Caspi A, Poulton R, Moffitt TE
Community Dentistry and Oral Epidemiology, 2019, 47(3), 252-258.
https://doi.org/10.1111/cdoe.12451
Our ref: RO718
Show abstract » OBJECTIVES:
Given that people with higher intelligence have been shown to live longer, enjoy better health and have more favourable health behaviours, we investigated the association between childhood IQ and a range of important dental health and service-use indicators at age 38.

METHODS:
Long-standing prospective study of a complete birth cohort, with childhood IQ (assessed at ages 7, 9, 11 and 13 years) used to allocate participants (N = 818) to one of four ordinal categories of childhood IQ.

RESULTS:
There were distinct and consistent gradients by childhood IQ in almost all of the dental caries experience measures (with the exception of filled teeth) whereby each was most severe in the lowest child IQ category and least severe in the highest; the exception was the mean FT score, for which there was no discernible gradient. Indicators of self-care and periodontal disease experience showed similar gradients, and multivariate modelling using the continuous IQ score confirmed the observed patterns.

CONCLUSIONS:
Childhood cognitive function is a key determinant of oral health and dental service-use by midlife, with those of lower cognitive capacity as children likely to have poorer oral health, less favourable oral health-related beliefs, and more detrimental self-care and dental visiting practices by age 38. There is a need to shape dental clinical services and public health interventions so that people with the poorest cognitive function do not continue to be disadvantaged.

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Establishing a generalized polyepigenetic biomarker for tobacco smoking | 2019
Sugden K, Hannon E J, Arseneault L, Belsky DW, Broadbent JM, ... Show all » Corcoran DL Hancox RJ Houts RM Moffitt TE Poulton R Prinz JA Thomson WM, Williams BS Wong CCY Mill J Caspi A « Hide
Translational Psychiatry, 2019, 9 .
https://doi.org/10.1038/s41398-019-0430-9
Our ref: RO717
Show abstract » Large-scale epigenome-wide association meta-analyses have identified multiple ‘signatures’’ of smoking. Drawing on these findings, we describe the construction of a polyepigenetic DNA methylation score that indexes smoking behavior and that can be utilized for multiple purposes in population health research. To validate the score, we use data from two birth cohort studies: The Dunedin Longitudinal Study, followed to age-38 years, and the Environmental Risk Study, followed to age-18 years. Longitudinal data show that changes in DNA methylation accumulate with increased exposure to tobacco smoking and attenuate with quitting. Data from twins discordant for smoking behavior show that smoking influences DNA methylation independently of genetic and environmental risk factors. Physiological data show that changes in DNA methylation track smoking-related changes in lung function and gum health over time. Moreover, DNA methylation changes predict corresponding changes in gene expression in pathways related to inflammation, immune response, and cellular trafficking. Finally, we present prospective data about the link between adverse childhood experiences (ACEs) and epigenetic modifications; these findings document the importance of controlling for smoking-related DNA methylation changes when studying biological embedding of stress in life-course research. We introduce the polyepigenetic DNA methylation score as a tool both for discovery and theory-guided research in epigenetic epidemiology
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Effect modification of FADS2 polymorphisms on the association between breastfeeding and intelligence: results from a collaborative meta-analysis | 2019
Hartwig FP, Davies NM, Horta BL, Ahluwalia TS, Bisgaard H, ... Show all » Bønnelykke K, Caspi A, Moffitt TE, Poulton R, Sajjad A, Tiemeier HW, Dalmau-Bueno A, Guxens M, Bustamante M, Santa-Marina L, Parker N, Paus T, Pausova Z, Lauritzen L, Schnurr TM, Michaelsen KF, Hansen T, Oddy W, Pennell CE, Warrington NM, Davey Smith G, Victora CG « Hide
International Journal of Epidemiology, 2019, 48(1), 45–57.
https://doi.org/10.1093/ije/dyy273
Our ref: RO715
Show abstract » BACKGROUND:
Accumulating evidence suggests that breastfeeding benefits children's intelligence, possibly due to long-chain polyunsaturated fatty acids (LC-PUFAs) present in breast milk. Under a nutritional adequacy hypothesis, an interaction between breastfeeding and genetic variants associated with endogenous LC-PUFAs synthesis might be expected. However, the literature on this topic is controversial.

METHODS:
We investigated this gene × environment interaction through a collaborative effort. The primary analysis involved >12 000 individuals and used ever breastfeeding, FADS2 polymorphisms rs174575 and rs1535 coded assuming a recessive effect of the G allele, and intelligence quotient (IQ) in Z scores.

RESULTS:
There was no strong evidence of interaction, with pooled covariate-adjusted interaction coefficients (i.e. difference between genetic groups of the difference in IQ Z scores comparing ever with never breastfed individuals) of 0.12[(95% confidence interval (CI): -0.19; 0.43] and 0.06 (95% CI: -0.16; 0.27) for the rs174575 and rs1535 variants, respectively. Secondary analyses corroborated these results. In studies with ≥5.85 and <5.85 months of breastfeeding duration, pooled estimates for the rs174575 variant were 0.50 (95% CI: -0.06; 1.06) and 0.14 (95% CI: -0.10; 0.38), respectively, and 0.27 (95% CI: -0.28; 0.82) and -0.01 (95% CI: -0.19; 0.16) for the rs1535 variant.

CONCLUSIONS:
Our findings did not support an interaction between ever breastfeeding and FADS2 polymorphisms. However, subgroup analysis suggested that breastfeeding may supply LC-PUFAs requirements for cognitive development if breastfeeding lasts for some (currently unknown) time. Future studies in large individual-level datasets would allow properly powered subgroup analyses and further improve our understanding on the breastfeeding × FADS2 interaction.

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Association of Childhood Lead Exposure With Adult Personality Traits and Lifelong Mental Health | 2019
Reuben, Aaron Schaefer, Jonathan Moffitt, Terrie Broadbent, Jonathan Harrington, ... Show all » Honalee Houts, Renate Ramrakha, Sandhya Poulton, Richie Caspi, Avshalom « Hide
JAMA Psychiatry, 2019, 76(4), 418-425.
10.1001/jamapsychiatry.2018.4192
download pdf Our ref: RO714
Show abstract » Importance: Millions of adults now entering middle age were exposed to high levels of lead, a developmental neurotoxin, as children. Although childhood lead exposure has been linked to disrupted behavioral development, the long-term consequences for adult mental and behavioral health have not been fully characterized. Objective: To examine whether childhood lead exposure is associated with greater psychopathology across the life course and difficult adult personality traits. Design, setting, and participants: This prospective cohort study was based on a population-representative birth cohort of individuals born between April 1, 1972, and March 31, 1973, in Dunedin, New Zealand, the Dunedin Multidisciplinary Health and Development Study. Members were followed up in December 2012 when they were 38 years of age. Data analysis was performed from March 14, 2018, to October 24, 2018. Exposures: Childhood lead exposure ascertained as blood lead levels measured at 11 years of age. Blood lead levels were unrelated to family socioeconomic status. Main outcomes and measures: Primary outcomes were adult mental health disorder symptoms assessed through clinical interview at 18, 21, 26, 32, and 38 years of age and transformed through confirmatory factor analysis into continuous measures of general psychopathology and internalizing, externalizing, and thought disorder symptoms (all standardized to a mean [SD] of 100 [15]) and adult personality assessed through informant report using the Big Five Personality Inventory (assessing neuroticism, extraversion, openness to experience, agreeableness, and conscientiousness) at 26, 32, and 38 years of age (all scores standardized to a mean [SD] of 0 [1]). Hypotheses were formulated after data collection; an analysis plan was posted in advance. Results: Of 1037 original study members, 579 (55.8%) were tested for lead exposure at 11 years of age (311 [53.7%] male). The mean (SD) blood lead level was 11.08 (4.96) μg/dL. After adjusting for study covariates, each 5-μg/dL increase in childhood blood lead level was associated with a 1.34-point increase (95% CI, 0.11-2.57; P = .03) in general psychopathology, driven by internalizing (b = 1.41; 95% CI, 0.19-2.62; P = .02) and thought disorder (b = 1.30; 95% CI, 0.06-2.54; P = .04) symptoms. Each 5-μg/dL increase in childhood blood lead level was also associated with a 0.10-SD increase in neuroticism (95% CI, 0.02-0.08; P = .02), a 0.09-SD decrease in agreeableness (95% CI, -0.18 to -0.01; P = .03), and a 0.14-SD decrease in conscientiousness (95% CI, -0.25 to -0.03; P = .01). There were no statistically significant associations with informant-rated extraversion (b = -0.09; 95% CI, -0.17 to 0.004; P = .06) and openness to experience (b = -0.07; 95% CI, -0.17 to 0.03; P = .15). Conclusions and relevance: In this multidecade, longitudinal study of lead-exposed children, higher childhood blood lead level was associated with greater psychopathology across the life course and difficult adult personality traits. Childhood lead exposure may have long-term consequences for adult mental health and personality
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Cumulative childhood risk is associated with a new measure of chronic inflammation in adulthood | 2019
Rasmussen, L.J.H., Moffitt, T.E., Eugen-Olsen, ... Show all » J., Belsky, D.W., Danese, A., Harrington, H., Houts R.M., Poulton, R., Sugden, K., Williams, B., Caspi, A. « Hide
Journal of Child Psychology and Psychiatry, 2019, 60(2), 199-208.
10.1111/jcpp.12928
download pdfLink to full publication »
Our ref: RO708
Show abstract » Background:Childhood risk factors are associated with elevated inflammatory biomarkers in adulthood, but it isunknown whether these risk factors are associated with increased adult levels of the chronic inflammation markersoluble urokinase plasminogen activator receptor (suPAR). We aimed to test the hypothesis that childhood exposureto risk factors for adult disease is associated with elevated suPAR in adulthood and to compare suPAR with the oft-reported inflammatory biomarker C-reactive protein (CRP).Methods:Prospective study of a population-representa-tive 1972–1973 birth cohort; the Dunedin Multidisciplinary Health and Development Study observed participants toage 38 years. Main childhood predictors were poor health, socioeconomic disadvantage, adverse childhoodexperiences (ACEs), low IQ, and poor self-control. Main adult outcomes were adulthood inflammation measuredas suPAR and high-sensitivity CRP (hsCRP).Results:Participants with available plasma samples at age 38 wereincluded (N=837, 50.5% male). suPAR (mean 2.40 ng/ml;SD0.91) was positively correlated with hsCRP (r0.15,p<.001). After controlling for sex, body mass index (BMI), and smoking, children who experienced more ACEs, lowerIQ, or had poorer self-control showed elevated adult suPAR. When the five childhood risks were aggregated into aCumulative Childhood Risk index, and controlling for sex, BMI, and smoking, Cumulative Childhood Risk wasassociated with higher suPAR (b0.10; SE 0.03;p=.002). Cumulative Childhood Risk predicted elevated suPAR, aftercontrolling for hsCRP (b0.18; SE 0.03;p<.001).Conclusions:Exposure to more childhood risk factors wasassociated with higher suPAR levels, independent of CRP. suPAR is a useful addition to studies connecting childhoodrisk to adult inflammatory burden.
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Does physical fitness enhance lung function in children and young adults? | 2018
Robert J. Hancox, Finn Rasmussen
European Respiratory Journal, 2018, 51(2), .
https://doi.org/10.1183/13993003.01374-2017
Our ref: RO713
Show abstract » Although physical activity is important for lung health, it is unclear whether physical fitness influences lung function. We investigated associations between lung function and fitness in two population-based cohort studies of children and young adults.

Aerobic fitness was measured using a maximal cycle ergometer test at ages 9, 15, 21 and 29 years in Odense, Denmark and using a submaximal cycle test at ages 15, 26, 32 and 38 years in Dunedin, New Zealand.

Aerobic fitness was positively associated with forced expiratory volume in 1 s (FEV1) and forced vital capacity (FVC) in cross-sectional analyses at all ages in both cohorts, independently of height, weight, sex, asthma and smoking. Each standard deviation difference in fitness was associated with 2–3% predicted higher values of FEV1 and FVC. Improvements in fitness during childhood and adolescence were associated with growth in lung volumes in longitudinal analyses. These associations tended to be stronger in males than females. No longitudinal associations were found after peak adult lung function had been attained. Fitness was not significantly associated with FEV1/FVC ratios.

Aerobic fitness is positively associated with lung volumes. Improving fitness during childhood and adolescence is associated with greater adult lung volumes, but not with airway calibre.

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Intergenerational changes in adolescents’ physical fitness and weight in New Zealand | 2018
McAnally HM, Reeves LM, Sligo JL, Hancox RJ
The New Zealand medical journal, 2018, 131(1482), 16-28.
Link to full publication »
Our ref: NZ95
Show abstract » AIMS:
This research examines fitness and body weight in two cohorts of adolescents, to determine continuity and changes in these measures across two generations.

METHODS:
Height, weight and fitness were measured in a population-based cohort of 15 year-olds in 1986/7 (Dunedin Study, n=968). The same measures were obtained for their 15-16 year-old children between 2007 and 2015 (Next Generation Study, n=343). Fitness was defined as maximal aerobic capacity (V'O2max). Height and weight were measured in all participants and fitness was adjusted for weight (V'O2max/kg).

RESULTS:
The Next Generation participants were, on average, heavier than the Dunedin Study participants had been, and had higher body mass index values (kg/m2). Unadjusted V'O2max values for boys did not differ between generations, but were lower in Next Generation girls compared to Dunedin Study girls. For both sexes, the Next Generation participants had lower weight-adjusted V'O2max values than the Dunedin Study participants. Compared to their parents, weight-adjusted V'O2max values were approximately 25% lower in girls and 15% lower in boys.

CONCLUSIONS:
Overall adolescents today appear to be less fit and heavier than their parents were at the same age. The decline in fitness over a generation is particularly evident in adolescent girls, although boys also have lower levels of fitness once body weight has been taken into account.

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Periodontitis and multiple markers of cardiometabolic risk in the fourth decade: A cohort study | 2018
Shearer, D. M. Thomson, W. M. Cameron, C. M. Ramrakha, S. Wilson, ... Show all » G. Wong, T. Y. Williams, M. J. A. McLean, R. Theodore, R. Poulton, R. « Hide
Community Dentistry and Oral Epidemiology, 2018, 46(6), 615-623.
download pdfLink to full publication »
Our ref: RO712
Show abstract » OBJECTIVES: To examine associations between periodontitis at ages 32 and 38 and a range of early cardiometabolic risk biomarkers at age 38. METHODS: Periodontal probing depth and bleeding on probing data collected during the age-32 and age-38 assessments in the Dunedin Multidisciplinary Health and Development Study were used to quantify periodontal inflammatory load. Retinal microvascular abnormalities, endothelial dysfunction, and metabolic syndrome data were collected during the age-38 assessment. Regression models were used to examine associations between these cardiometabolic risk markers and (1) the inflammatory load at age 38 and (2) the change in inflammatory load between ages 32 and 38. RESULTS: Periodontal inflammatory load was recorded for 890 Study members at age 32, 891 at age 38, and 856 at both ages. Retinal vessel data were available for 922, endothelial dysfunction data for 909 and metabolic syndrome data for 905 at age 38. Neither the inflammatory load of periodontitis at 38 nor the changes in inflammatory load 32-38 were found to be associated with any of the three cardiometabolic risk markers. CONCLUSIONS: Periodontitis was not associated with markers of cardiometabolic risk at this relatively early stage in the life course. It is possible that any influence of periodontitis on cardiometabolic health develops later in life, or periodontitis is not involved in the putative causal chain comprising systemic inflammation, cardiometabolic risk markers, and subsequent cardiovascular risk.
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Genetic analysis of social mobility in five longitudinal studies | 2018
Belsky, D.W. Domingue, B.W Wedow, R Arseneault, L. Boardman, ... Show all » J Caspi, A. Conley, D Fletcher, J.M Freese, J Herd, P Moffitt, T. E Poulton, R. Sicinski, K Wertz, J. Mullan Harris, K « Hide
PNAS (Proceedings of the National Academy of Sciences of the USA), 2018, 115(13), E7275-E7284.
https://doi.org/10.1073/pnas.1817958115
Our ref: RO702
Show abstract » A summary genetic measure, called a “polygenic score,” derived from a genome-wide association study (GWAS) of education can modestly predict a person’s educational and economic success. This prediction could signal a biological mechanism: Educationlinked genetics could encode characteristics that help people get ahead in life. Alternatively, prediction could reflect social history: People from well-off families might stay well-off for social reasons, and these families might also look alike genetically. A key test to distinguish biological mechanism from social history is if people with higher education polygenic scores tend to climb the social ladder beyond their parents’ position. Upward mobility would indicate education-linked genetics encodes characteristics that foster success. We tested if education-linked polygenic scores predicted social mobility in >20,000 individuals in five longitudinal studies in the United States, Britain, and New Zealand. Participants with higher polygenic scores achieved more education and career success and accumulated more wealth. However, they also tended to come from better-off families. In the key test, participants with higher polygenic scores tended to be upwardly mobile compared with their parents. Moreover, in sibling-difference analysis, the sibling with the higher polygenic score was more upwardly mobile. Thus, education GWAS discoveries are not mere correlates of privilege; they influence social mobility within a life. Additional analyses revealed that a mother’s polygenic score predicted her child’s attainment over and above the child’s own polygenic score, suggesting parents’ genetics can also affect their children’s attainment through environmental pathways. Education GWAS discoveries affect socioeconomic attainment through influence on individuals’ family-oforigin environments and their social mobility.
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Genetics and Crime: Integrating New Genomic Discoveries Into Psychological Research About Antisocial Behavior | 2018
Wertz, J. Caspi, A. Belsky, D. W. Beckley, A. L. Arseneault, ... Show all » L. Barnes, J. C. Corcoran, D. L. Hogan, S. Houts, R. Morgan, N. Odgers, C. L. Prinz, Joseph A. Sugden, K. Williams, B.S. Poulton, R. Moffitt, T. E « Hide
Psychological Science, 2018, 29(5), 791-803.
download pdfLink to full publication »
Our ref: RO703
Show 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.
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Eleven Telomere, Epigenetic Clock, and Biomarker-Composite Quantifications of Biological Aging: Do They Measure the Same Thing? | 2018
Belsky, D. W. Moffitt, T.E. Cohen, A.A. Corcoran, D. L. Levine, ... Show all » M.E. Prinz, J. A. Schaefer, J. Sugden, K. Williams, B. Poulton, R. Caspi, A. « Hide
American Journal of Epidemiology, 2018, 187(6), 1220-1230.
http://dx.doi.org/10.1093/aje/kwx346
Our ref: RO700
Show abstract » The geroscience hypothesis posits that therapies to slow biological processes of aging can prevent disease and extend healthy years of life. To test such “gero-protective” therapies in humans, outcome measures are needed that can assess extension of disease-free lifespan. This need has spurred development of different methods to quantify biological aging. But different methods have not been systematically compared in the same humans. We implemented seven methods to quantify biological aging using repeated-measures physiological and genomic data in 964 middle-aged humans in the Dunedin Study. We studied telomere-length and erosion, three epigenetic-clocks and their ticking rates, and three biomarker-composites, 11 measures in total. Contrary to expectation, we found low agreement between different measures of biological aging. We next compared associations between biological aging measures and outcomes gero-protective therapies seek to modify: physical functioning, cognitive decline, and subjective signs of aging, including aged facial appearance. The 71-CpG epigenetic clock and biomarker composites were consistently related to these aging-related outcomes. However, effect-sizes were modest. Results suggests that various proposed approaches to quantifying biological aging may not measure the same aspects of the aging process. Further systematic evaluation and refinement of measures of biological aging is needed to furnish outcomes for geroprotector trials.
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Analysis of DNA Methylation in Young People: Limited Evidence for an Association Between Victimization Stress and Epigenetic Variation in Blood | 2018
Marzi, S. J. Sugden, K. Arseneault, L. Belsky, D. W. Burrage, ... Show all » J. Corcoran, D. L. Danese, A. Fisher, H. L. Hannon, E. Moffitt, T. E. Odgers, C. L. Pariante, C. Poulton, R. Williams, B. S. Wong, C. C. Y. Mill, J. Caspi, A. « Hide
American Journal of Psychiatry, 2018, 175(6), 517-529.
https://doi.org/10.1176/appi.ajp.2017.17060693
Our ref: RO705
Show abstract » Objective:DNA methylation has been proposed as an epigenetic mechanism by which early-life experiences become “embedded” in the genome and alter transcriptional processes to compromise health. The authors sought to investigate whether early-life victimization stress is associated with genome-wide DNA methylation.Method:The authors tested the hypothesis that victimization is associated with DNA methylation in the Environmental Risk (E-Risk) Longitudinal Study, a nationally representative 1994–1995 birth cohort of 2,232 twins born in England and Wales and assessed at ages 5, 7, 10, 12, and 18 years. Multiple forms of victimization were ascertained in childhood and adolescence (including physical, sexual, and emotional abuse; neglect; exposure to intimate-partner violence; bullying; cyber-victimization; and crime).Results:Epigenome-wide analyses of polyvictimization across childhood and adolescence revealed few significant associations with DNA methylation in peripheral blood at age 18, but these analyses were confounded by tobacco smoking and/or did not survive co-twin control tests. Secondary analyses of specific forms of victimization revealed sparse associations with DNA methylation that did not replicate across different operationalizations of the same putative victimization experience. Hypothesis-driven analyses of six candidate genes in the stress response (NR3C1, FKBP5, BDNF, AVP, CRHR1, SLC6A4) did not reveal predicted associations with DNA methylation in probes annotated to these genes.Conclusions:Findings from this epidemiological analysis of the epigenetic effects of early-life stress do not support the hypothesis of robust changes in DNA methylation in victimized young people. We need to come to terms with the possibility that epigenetic epidemiology is not yet well matched to experimental, nonhuman models in uncovering the biological embedding of stress.
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The high societal costs of childhood conduct problems: evidence from administrative records up to age 38 in a longitudinal birth cohort | 2018
Rivenbark, Joshua G. Odgers, Candice L. Caspi, Avshalom Harrington, HonaLee Hogan, ... Show all » Sean Houts, Renate M. Poulton, Richie Moffitt, Terrie E. « Hide
Journal of Child Psychology and Psychiatry, 2018, 59(6), 703-710.
https://doi.org/10.1111/jcpp.12850
Our ref: RO701
Show abstract » Children with conduct problems that persist into adulthood are at increased risk for future behavioral, health, and social problems. However, the longer term public service usage among these children has not been fully documented. To aid public health and intervention planning, adult service usage across criminal justice, health care, and social welfare domains is compared among all individuals from a representative cohort who followed different conduct problem trajectories from childhood into adulthood. Participants are from the Dunedin Multidisciplinary Health and Development Study, a prospective, representative cohort of consecutive births (N = 1,037) from April 1972 to March 1973 in Dunedin, New Zealand. Regression analyses were used to compare levels of public service usage up to age 38, gathered via administrative and electronic medical records, between participants who displayed distinct subtypes of childhood conduct problems (low, childhood-limited, adolescent-onset, and life-course persistent). Children exhibiting life-course persistent conduct problems used significantly more services as adults than those with low levels of childhood conduct problems. Although this group comprised only 9.0% of the population, they accounted for 53.3% of all convictions, 15.7% of emergency department visits, 20.5% of prescription fills, 13.1% of injury claims, and 24.7% of welfare benefit months. Half of this group (50.0%) also accrued high service use across all three domains of criminal justice, health, and social welfare services, as compared to only 11.3% of those with low conduct problems (OR = 7.27, 95% CI = 4.42–12.0). Conduct problems in childhood signal high future costs in terms of service utilization across multiple sectors. Future evaluations of interventions aimed at conduct problems should also track potential reductions in health burden and service usage that stretch into midlife.
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Association of childhood blood lead levels with criminal offending | 2018
Beckley, A. L. Caspi, A. Broadbent, J. Harrington, HL Houts, ... Show all » R. Poulton, R. Ramrakha, S. Reuben, A. Moffitt , T.E. « Hide
JAMA Pediatrics, 2018, 172(2), 166-173.
http://dx.doi.org/10.1001/jamapediatrics.2017.4005
Our ref: RO707
Show abstract » Importance  Lead is a neurotoxin with well-documented effects on health. Research suggests that lead may be associated with criminal behavior. This association is difficult to disentangle from low socioeconomic status, a factor in both lead exposure and criminal offending.Objective  To test the hypothesis that a higher childhood blood lead level (BLL) is associated with greater risk of criminal conviction, recidivism (repeat conviction), conviction for violent offenses, and variety of self-reported criminal offending in a setting where BLL was not associated with low socioeconomic status.Design, Setting, and Participants  A total of 553 individuals participated in a prospective study based on a population-representative cohort born between April 1, 1972, and March 31, 1973, from New Zealand; the Dunedin Multidisciplinary Health and Development Study observed participants to age 38 years (December 2012). Statistical analysis was performed from November 10, 2016, to September 5, 2017.Exposures  Blood lead level measured at age 11 years.Main Outcomes and Measures  Official criminal conviction cumulative to age 38 years (data collected in 2013), single conviction or recidivism, conviction for nonviolent or violent crime, and self-reported variety of crime types at ages 15, 18, 21, 26, 32, and 38 years.Results  Participants included 553 individuals (255 female and 298 male participants) who had their blood tested for lead at age 11 years. The mean (SD) BLL at age 11 years was 11.01 (4.62) μg/dL. A total of 154 participants (27.8%) had a criminal conviction, 86 (15.6%) had recidivated, and 53 (9.6%) had a violent offense conviction. Variety scores for self-reported offending ranged from 0 to 10 offense types at each assessment; higher numbers indicated greater crime involvement. Self-reported offending followed the well-established age-crime curve (ie, the mean [SD] variety of self-reported offending increased from 1.99 [2.82] at age 15 years to its peak of 4.24 [3.15] at age 18 years and 4.22 [3.02] at age 21 years and declined thereafter to 1.10 [1.59] at age 38 years). Blood lead level was a poor discriminator between no conviction and conviction (area under the curve, 0.58). Overall, associations between BLL and conviction outcomes were weak. The estimated effect of BLL was lower for recidivism than for single convictions and lower for violent offending than for nonviolent offending. Sex-adjusted associations between BLL reached statistical significance for only 1 of the 6 self-reported offending outcomes at age 15 years (r = 0.10; 95% CI, 0.01-0.18; P = .02).Conclusions and Relevance  This study overcomes past limitations of studies of BLL and crime by studying the association in a place and time where the correlation was not confounded by childhood socioeconomic status. Findings failed to support a dose-response association between BLL and consequential criminal offending.
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Non-suicidal self-injury and suicide attempts in a New Zealand birth cohort | 2017
Coppersmith, D. D. L. Nada-Raja, S. Beautrais, A. L.
Journal of Affective Disorders, 2017, 221 89-96.
10.1016/j.jad.2017.06.029
download pdfLink to full publication »
Our ref: RO711
Show abstract » Background: Non-suicidal self-injury (NSSI) and suicide attempts are related, but distinct behaviors. The primary aim of the current study was to identify factors that distinguish those with different lifetime histories of selfinjury. A secondary aim was to test whether lifetime history of self-injury at age 26 predicted current suicide ideation at age 32.
Methods: Participants were 26 year olds from a large birth cohort with a lifetime history of no self-injury (n = 466), a lifetime history of NSSI (n = 191), or a lifetime history of NSSI and a suicide attempt (NSSI+ SA; n = 52). They were compared on a history of psychiatric disorders, 12-month suicide ideation, lifetime history of childhood sexual abuse, and lifetime exposure to suicide.
Results: An anxiety disorder, a substance dependence disorder, suicide ideation, and a history of childhood sexual abuse distinguished the NSSI+ SA and NSSI only groups. Longitudinal results demonstrated that a history of NSSI predicted future suicide ideation after adjusting for other selected risk factors.
Limitations: The majority of analyses are cross-sectional which limits inferences about causality. The retrospective self-report for lifetime behavior could be subject to reporting biases.
Conclusions: Adults with a history of NSSI and adults with a history of NSSI and a suicide attempt are clinically distinct groups that are both at risk of future suicide ideation. Identifying and treating NSSI could be a key preventive factor in reducing subsequent suicide risk.

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Life-Course Relationship between Socioeconomic Circumstances and Timing of First Birth in a Birth Cohort | 2017
van Roode, T. Sharples, K. Dickson, N. Paul, C.
PLoS One, 2017, 12(1), e0170170.
10.1371/journal.pone.0170170
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Our ref: RO709
Show abstract » OBJECTIVES: This study examines the influence of socioeconomic circumstances in childhood (childhood SES) and adulthood (adult SES) on timing of first birth by age 37. METHODS: A longitudinal study of a 1972-1973 New Zealand birth cohort collected information on socioeconomic characteristics from age 3-32 and reproductive histories at 21, 26, 32 and 38; information on first birth was available from 978 of the original 1037. Relative Risks (RR) and 95% Confidence Intervals (CI) were calculated using Poisson regression to examine first live birth prior to age 21, from 21-25, from 26-31, and from 32-37, by socioeconomic characteristics at different ages. RESULTS: Overall, 68.5% of men had fathered a child and 75.9% of women had given birth, by age 37; with overall differences in parenthood to age 31 for men, and 37 for women evident by childhood SES. While parenthood by age 20 was strongly associated with lower childhood SES for both sexes, first entry into motherhood from 32-37 was more likely with higher adult SES at age 32 (RR = 1.8, 95% CI 1.1-3.0 for medium and RR = 1.9, 95% CI 1.1-3.3 for high compared with low). Education also differientated age at parenthood, with those with higher education more likely to defer fatherhood past age 31, and motherhood past age 25 followed by a period of increased likelihood of motherhood for women with higher levels of education from age 32-37 (RR = 1.4, 95% CI 0.87-2.2 and RR = 1.7, 95% CI 1.1-2.6 for medium and high respectively compared with low). CONCLUSIONS: SES varies across the lifecourse, and SES at the time has the strongest association with first births at that time. Low childhood SES drives adolescent parenthood, with resulting cumulative differences in parenthood past age 30. Those with more education and higher adult SES are deferring parenthood but attempt to catch up in the mid to late thirties.
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How much atopy is attributable to common childhood environmental exposures? A population-based birth cohort study followed to adulthood | 2017
Shin HH., Lynch SJ., Gray AR., Sears MR., Hancox RJ.
International Journal of Epidemiology, 2017, 46(6), 2009-2016.
https://doi.org/10.1093/ije/dyx098
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Our ref: RO724
Show abstract » BACKGROUND:
The rising prevalence of atopic diseases implies a strong influence of environmental determinants. Epidemiological studies have identified several early life exposures that appear to influence the risk of developing atopic sensitization, but the combined influence of these exposures is unknown. We sought to estimate the proportion of atopy that could be attributed to common childhood exposures associated with atopic sensitization in adolescence and young adulthood.

METHODS:
Atopic sensitization was measured by skin-prick tests for common aeroallergens in a population-based New Zealand birth cohort at ages 13 and 32 years. The independent effects of previously identified risk and protective factors for atopic sensitization were assessed using multiple logistic regression. Population attributable fractions were calculated for atopic sensitization in childhood and adulthood.

RESULTS:
Tobacco smoke exposure, dog and cat ownership, nail-biting and thumb-sucking, attending pre-school day care, and household crowding were associated with a lower risk of atopic sensitization whereas breastfeeding was associated with a higher risk. Population attributable fractions for combined effects of these environmental factors suggest that they may account for 58% of atopic sensitization at age 13 and 49% at age 32 years.

CONCLUSIONS:
A substantial proportion of atopic sensitization appears to be attributable to common childhood environmental and lifestyle factors, and the influence of these exposures persists into adulthood. The absolute risks attributable to these exposures will be different in other cohorts and we cannot assume that these associations are necessarily causal. Nevertheless, the findings suggest that identifiable childhood environmental factors contribute substantially to atopic sensitization.

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Is low cognitive functioning a predictor or consequence of major depressive disorder? A test in two longitudinal birth cohorts | 2017
Schaefer, J. D. Scult, M. A. Caspi, A. Arseneault, L. Belsky, ... Show all » D. W. Hariri, A. R. Harrington, H. Houts, R. Ramrakha, S. Poulton, R. Moffitt, T. E. « Hide
Development and Psychopathology, 2017, 16 1-15.
https://doi.org/10.1017/S095457941700164X
download pdf Our ref: RO710
Show 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.
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Impact of early personal-history characteristics on the Pace of Aging: implications for clinical trials of therapies to slow aging and extend healthspan | 2017
Belsky, D. W., Caspi, A., Cohen, ... Show all » H. J., Kraus, W. E., Ramrakha, S., Poulton, R., Moffitt, T. E. « Hide
Aging Cell, 2017, 16(4), 644-651.
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Our ref: RO699
Show 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.
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Childhood body mass index and endothelial dysfunction evaluated by peripheral arterial tonometry in early midlife | 2017
Williams, M. J. A., Milne, B. J., Ambler, ... Show all » A., Theodore, R., Ramrakha, S., Caspi, A., Moffitt, T. E., Poulton, R. « Hide
International Journal of Obesity, 2017, 41(9), 1355-1360.
DOI: 10.1038/ijo.2017.108
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Our ref: RO698
Show abstract » BACKGROUND/OBJECTIVES: Endothelial dysfunction predicts mortality but it is unknown whether childhood obesity predicts adult endothelial dysfunction. The aim of this study was to determine whether anthropometric indices of body fat in childhood, adolescence and early midlife are associated with endothelial dysfunction in early midlife. SUBJECTS/METHODS: Participants belonged to a representative birth cohort of 1037 individuals born in Dunedin, New Zealand in 1972 and 1973 and followed to age 38 years, with 95% retention (the Dunedin Multidisciplinary Health and Development Study). We assessed anthropometric indices of obesity at ages 3, 5, 7, 9, 11, 13, 15, 18, 21, 26, 32 and 38 years. We tested associations between endothelial function assessed by peripheral arterial tonometry (PAT) at age 38 and; age 38 cardiovascular risk factors; age 3 body mass index (BMI); and four BMI trajectory groups from childhood to early midlife. RESULTS: Early midlife endothelial dysfunction was associated with BMI, large waist circumference, low high-density lipoprotein cholesterol, low cardiorespiratory fitness and increased high-sensitivity C-reactive protein. After adjustment for sex and childhood socioeconomic status, 3-year-olds with BMI 1 s.d. above the mean had Framingham-reactive hyperemia index (F-RHI) ratios that were 0.10 below those with normal BMI (beta=-0.10, 95% confidence interval (CI) -0.17 to -0.03, P=0.007) at age 38. Cohort members in the 'overweight', 'obese' and 'morbidly obese' trajectories had F-RHI ratios that were 0.08 (beta=-0.08, 95% CI -0.14 to -0.03, P=0.003), 0.13 (beta=-0.13, 95% CI -0.21 to -0.06, P<0.001) and 0.17 (beta=-0.17, 95% CI -0.33 to -0.01, P=0.033), respectively, below age-peers in the 'normal' trajectory. CONCLUSIONS: Childhood BMI and the trajectories of BMI from childhood to early midlife predict endothelial dysfunction evaluated by PAT in early midlife.
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The Origins of Cognitive Deficits in Victimized Children: Implications for Neuroscientists and Clinicians | 2017
Danese, A., Moffitt, T. E., Arseneault, ... Show all » L., Bleiberg, B. A., Dinardo, P. B., Gandelman, S. B., Houts, R., Ambler, A., Fisher, H. L., Poulton, R., Caspi, A. « Hide
Am J Psychiatry, 2017, 174(4), 349-361.
DOI: 10.1176/appi.ajp.2016.16030333
Our ref: RO697
Show abstract » OBJECTIVE: Individuals reporting a history of childhood violence victimization have impaired brain function. However, the clinical significance, reproducibility, and causality of these findings are disputed. The authors used data from two large cohort studies to address these research questions directly. METHOD: The authors tested the association between prospectively collected measures of childhood violence victimization and cognitive functions in childhood, adolescence, and adulthood among 2,232 members of the U.K. E-Risk Study and 1,037 members of the New Zealand Dunedin Study who were followed up from birth until ages 18 and 38 years, respectively. Multiple measures of victimization and cognition were used, and comparisons were made of cognitive scores for twins discordant for victimization. RESULTS: Individuals exposed to childhood victimization had pervasive impairments in clinically relevant cognitive functions, including general intelligence, executive function, processing speed, memory, perceptual reasoning, and verbal comprehension in adolescence and adulthood. However, the observed cognitive deficits in victimized individuals were largely explained by cognitive deficits that predated childhood victimization and by confounding genetic and environmental risks. CONCLUSIONS: Findings from two population-representative birth cohorts totaling more than 3,000 individuals and born 20 years and 20,000 km apart suggest that the association between childhood violence victimization and later cognition is largely noncausal, in contrast to conventional interpretations. These findings support the adoption of a more circumspect approach to causal inference in the neuroscience of stress. Clinically, cognitive deficits should be conceptualized as individual risk factors for victimization as well as potential complicating features during treatment.
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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 | 2017
Reuben, A., Caspi, A., Belsky, ... Show all » D. W., Broadbent, J., Harrington, H., Sugden, K., Houts, R. M., Ramrakha, S., Poulton, R., Moffitt, T. E. « Hide
JAMA, 2017, 317(12), 1244-1251.
DOI: 10.1001/jama.2017.1712
Our ref: RO696
Show abstract » mportance: 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. Objective: 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. Design, Setting, and Participants: 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). Exposures: 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. Main Outcomes and Measures: 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]). Results: 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) microg/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-microg/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-microg/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. Conclusions and Relevance: 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.
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The Longitudinal Study of Aging in Human Young Adults: Knowledge Gaps and Research Agenda | 2017
Moffitt, T. E., Belsky, D. W., Danese, ... Show all » A., Poulton, R., Caspi, A. « Hide
J Gerontol A Biol Sci Med Sci, 2017, 72(2), 210-215.
DOI: 10.1093/gerona/glw191
Our ref: RO695
Show 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. METHOD: 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). RESULTS: 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. CONCLUSIONS: 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.
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Enduring mental health: Prevalence and prediction | 2017
Schaefer, J. D., Caspi, A., Belsky, ... Show all » D. W., Harrington, H., Houts, R., Horwood, L, J., Hussong, A., Ramrakha, S., Poulton, R., Moffitt, T. E. « Hide
J Abnorm Psychol, 2017, 126(2), 212-224.
DOI: 10.1037/abn0000232
download pdf Our ref: RO694
Show 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
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Periodontitis is not associated with metabolic risk during the fourth decade of life | 2017
Shearer, D, M., Thomson, W. M., ... Show all » Broadbent, J, M., Mann, J., Poulton, R. « Hide
Journal of Clinical Periodontology, 2017, 44(1), 22-30.
DOI: 10.1111/jcpe.12641
Our ref: RO693
Show abstract » Aim: To examine associations between periodontitis and developmental trajectories of glycated haemoglobin (HbA1c) during the third and fourth decades in an initially healthy sample. Materials and methods: HbA1c data collected at ages 26, 32 and 38 in the prospective Dunedin Multidisciplinary Health and Development Study were used to assign study members (n = 893) to trajectories applying group-based trajectory modelling (GBTM). The model allowed the statistical linking of baseline demographic, smoking and waist-height ratio covariates to group membership probability; and added a time-varying covariate (periodontitis) to the trajectories themselves to examine whether events that occurred during the course of the trajectory altered its course. Results: Three HbA1c trajectory groups were identified: “Low” (n = 98, 11.0%); “Medium” (n = 482, 54.0%); and “High” (n = 313, 35.0%) with mean HbA1c of 29.6, 34.1 and 38.7 mmol/mol, respectively, at age 38. Having periodontitis at 32 and 38 was associated with an upward shift in the trajectories. However, none of the associations were statistically significant. Conclusions: Periodontitis was not found to be associated with dysglycaemia over 12 years from early adulthood into early middle age. This suggests that any influence periodontitis may have on dysglycaemia develops later in life.
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