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18 results on '"O'Donnell, K.J."'

1. Maternal sensitivity and child internalizing and externalizing behavior: A mediating role for glucocorticoid receptor gene (NR3C1) methylation?

Author

Creasey, N.L., Beijers, R., O'Donnell, K.J., Weerth, C. de, Tollenaar, M.S., Creasey, N.L., Beijers, R., O'Donnell, K.J., Weerth, C. de, and Tollenaar, M.S.

Abstract

10 maart 2023, Item does not contain fulltext, The early caregiving environment can have lasting effects on child mental health. Animal models suggest that glucocorticoid receptor gene (NR3C1) DNA methylation plays a mediating role in linking more responsive caregiving to improved behavioral outcomes by its impact on the stress regulatory system. In this longitudinal study, we examined whether children's NR3C1 methylation levels mediate an effect of maternal sensitivity in infancy on levels of child internalizing and externalizing behavior in a community sample. Maternal sensitivity of 145 mothers was rated at infant age 5 weeks, 12 months, and 30 months by observing mother–infant interactions. Buccal DNA methylation was assessed in the same children at age 6 years and maternal-reported internalizing and externalizing behavior was assessed at age 6 and 10 years. Higher sensitivity at age 5 weeks significantly predicted lower DNA methylation levels at two NR3C1 CpG loci, although methylation levels at these loci did not mediate an effect of maternal sensitivity on levels of child internalizing and externalizing behavior. Overall, the study provides evidence that maternal sensitivity in early infancy is associated with DNA methylation levels at loci involved in stress regulation, but the significance of this finding for child mental health remains unclear.

Published
2023

2. Cumulative risk exposure and child cellular aging in a Dutch low-risk community sample

Author

Beijers, R., Thije, I. ten, Bolhuis, E., O'Donnell, K.J., Tollenaar, M.S., Shalev, I., Hastings, W.J., MacIsaac, J.L., Lin, D.T.S., Meaney, M.J., Kobor, M.S., Belsky, J., Weerth, C. de, Beijers, R., Thije, I. ten, Bolhuis, E., O'Donnell, K.J., Tollenaar, M.S., Shalev, I., Hastings, W.J., MacIsaac, J.L., Lin, D.T.S., Meaney, M.J., Kobor, M.S., Belsky, J., and Weerth, C. de

Abstract

Contains fulltext : 283811.pdf (Publisher’s version ) (Open Access), One of the proposed mechanisms linking childhood stressor exposure to negative mental and physical health outcomes in later life is cellular aging. In this prospective, longitudinal, and pre-registered study, we examined the association between a cumulative pattern of childhood risk exposure from age 6 to age 10 (i.e., poor maternal mental health, parental relationship problems, family/friend death, bullying victimization, poor quality friendships) and change in two biomarkers of cellular aging (i.e., telomere length, epigenetic age) from age 6 to age 10 in a Dutch low-risk community sample (n = 193). We further examined the moderating effect of cortisol reactivity at age 6. Ordinary Least Squares regression analyses revealed no significant main effects of childhood risk exposure on change in cellular aging, nor a moderation effect of child cortisol reactivity. Secondary findings showed a positive correlation between telomere length and cortisol reactivity at age 6, warranting further investigation. More research in similar communities is needed before drawing strong conclusions based on the null results.

Published
2023

3. Maternal sensitivity and child internalizing and externalizing behavior

Author

Creasey, N., Beijers, R., O'Donnell, K.J., de Weerth, C., and Tollenaar, M.S.

Subjects
Psychiatry and Mental health, Developmental and Educational Psychology, Social Development
Abstract

The early caregiving environment can have lasting effects on child mental health. Animal models suggest that glucocorticoid receptor gene (NR3C1) DNA methylation plays a mediating role in linking more responsive caregiving to improved behavioral outcomes by its impact on the stress regulatory system. In this longitudinal study, we examined whether children’s NR3C1 methylation levels mediate an effect of maternal sensitivity in infancy on levels of child internalizing and externalizing behavior in a community sample. Maternal sensitivity of 145 mothers was rated at infant age 5 weeks, 12 months, and 30 months by observing mother–infant interactions. Buccal DNA methylation was assessed in the same children at age 6 years and maternal-reported internalizing and externalizing behavior was assessed at age 6 and 10 years. Higher sensitivity at age 5 weeks significantly predicted lower DNA methylation levels at two NR3C1 CpG loci, although methylation levels at these loci did not mediate an effect of maternal sensitivity on levels of child internalizing and externalizing behavior. Overall, the study provides evidence that maternal sensitivity in early infancy is associated with DNA methylation levels at loci involved in stress regulation, but the significance of this finding for child mental health remains unclear.

Published
2023
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4. Maternal prenatal anxiety and the fetal origins of epigenetic aging

Author

McGill, M.G., Pokhvisneva, I., Clappison, A.S., McEwen, L.M., Beijers, R., Tollenaar, M.S., Pham, H., Kee, M., Garg, E., De Mendonca Filho, E.J., Karnani, N., Silveira, P.P., Kobor, M.S., Weerth, C. de, Meaney, M.J., O'Donnell, K.J., McGill, M.G., Pokhvisneva, I., Clappison, A.S., McEwen, L.M., Beijers, R., Tollenaar, M.S., Pham, H., Kee, M., Garg, E., De Mendonca Filho, E.J., Karnani, N., Silveira, P.P., Kobor, M.S., Weerth, C. de, Meaney, M.J., and O'Donnell, K.J.

Abstract

Item does not contain fulltext, Background: The Fetal Origins of Mental Health is a well-established framework that currently lacks a robust index of the biological embedding of prenatal adversity. The Pediatric Buccal Epigenetic (PedBE) clock is a novel epigenetic tool that associates with aspects of the prenatal environment but additional validation in longitudinal datasets is required. Likewise, the relationship between prenatal maternal mental health and the PedBE clock has not been described. Methods: Longitudinal cohorts from the Netherlands (BIBO: N = 165) and Singapore (GUSTO: N = 340) provided data on prenatal maternal anxiety and longitudinal assessments of buccal cell-derived genome-wide DNA methylation assessed at 6 and 10 years of age in BIBO and at 3, 9, and 48 months of age in GUSTO. Measures of epigenetic age acceleration were calculated using the PedBE clock and benchmarked against an established multi-tissue epigenetic predictor. Results: Prenatal maternal anxiety predicted child PedBE epigenetic age acceleration in both cohorts with effects largely restricted to males and not females. These results were independent of obstetric, socioeconomic, and genetic risk factors, with a larger effect size for prenatal anxiety than depression. PedBE age acceleration predicted increased externalizing symptoms in males from mid- to late-childhood in the BIBO cohort only. Conclusions: These findings point to the fetal origins of epigenetic age acceleration and reveal an increased sensitivity in males. Convergent evidence underscores the societal importance of providing timely and effective mental health support to pregnant women, which may have lasting consequences for both mother and child.

Published
2022

5. Reply to: Crossing the 'birth border' for epigenetic effects

Author

McGill, M.G., Pokhvisneva, I., Clappison, A.S., McEwen, L.M., Beijers, R., Tollenaar, M.S., Pham, H., Kee, M., Garg, E., De Mendonca Filho, E.J., Karnani, N., Silveira, P.P., Kobor, M.S., Weerth, C. de, Meaney, M.J., O'Donnell, K.J., McGill, M.G., Pokhvisneva, I., Clappison, A.S., McEwen, L.M., Beijers, R., Tollenaar, M.S., Pham, H., Kee, M., Garg, E., De Mendonca Filho, E.J., Karnani, N., Silveira, P.P., Kobor, M.S., Weerth, C. de, Meaney, M.J., and O'Donnell, K.J.

Abstract

03 maart 2022, Item does not contain fulltext

Published
2022

6. Attachment insecurity and the biological embedding of reproductive strategies: Investigating the role of cellular aging

Author

Bolhuis, E., Belsky, J., Frankenhuis, W.E., Shalev, I., Hastings, W.J., Tollenaar, M.S., O'Donnell, K.J., McGill, M.G., Pokhvisneva, I., Lin, D.T.S., MacIsaac, J.L., Kobor, M.S., Weerth, C. de, Beijers, R., Bolhuis, E., Belsky, J., Frankenhuis, W.E., Shalev, I., Hastings, W.J., Tollenaar, M.S., O'Donnell, K.J., McGill, M.G., Pokhvisneva, I., Lin, D.T.S., MacIsaac, J.L., Kobor, M.S., Weerth, C. de, and Beijers, R.

Abstract

Contains fulltext : 283552.pdf (Publisher’s version ) (Open Access), Evolutionary-developmental psychologists have posited that individuals who grow up in stressful rearing circumstances follow faster life history strategies, thereby increasing their chances of reproduction. This preregistered study tested this stress-acceleration hypothesis in a low-risk longitudinal sample of 193 Dutch mother-child dyads, by investigating whether infant-mother attachment insecurity at 12 months of age predicted earlier pubertal onset and more callous-unemotional traits, aggression and risk-taking about a decade later. Also evaluated were the possible mediating roles of two biomarkers of accelerated aging (i.e., telomere length, epigenetic aging) at age 6. Structural equation modelling revealed no effects of attachment insecurity on biomarkers, pubertal timing or behavior. These null findings suggest that the explanatory value of evolutionary-developmental thinking might be restricted to high-risk samples, though unexplored variation in susceptibility to environmental influences might also explain the null findings.

Published
2022

7. Cumulative risk exposure and child cellular aging in a Dutch low-risk community sample

Author

Beijers, R., Thije, I. ten, Bolhuis, E., O'Donnell, K.J., Tollenaar, M.S., Shalev, I., Hastings, W.J., MacIsaac, J.L., Lin, D.T.S., Meaney, M.J., Kobor, M.S., Belsky, J., Weerth, C. de, Beijers, R., Thije, I. ten, Bolhuis, E., O'Donnell, K.J., Tollenaar, M.S., Shalev, I., Hastings, W.J., MacIsaac, J.L., Lin, D.T.S., Meaney, M.J., Kobor, M.S., Belsky, J., and Weerth, C. de

Abstract

02 november 2022, Contains fulltext : 283811.pdf (Publisher’s version ) (Open Access), One of the proposed mechanisms linking childhood stressor exposure to negative mental and physical health outcomes in later life is cellular aging. In this prospective, longitudinal, and pre-registered study, we examined the association between a cumulative pattern of childhood risk exposure from age 6 to age 10 (i.e., poor maternal mental health, parental relationship problems, family/friend death, bullying victimization, poor quality friendships) and change in two biomarkers of cellular aging (i.e., telomere length, epigenetic age) from age 6 to age 10 in a Dutch low-risk community sample (n = 193). We further examined the moderating effect of cortisol reactivity at age 6. Ordinary Least Squares regression analyses revealed no significant main effects of childhood risk exposure on change in cellular aging, nor a moderation effect of child cortisol reactivity. Secondary findings showed a positive correlation between telomere length and cortisol reactivity at age 6, warranting further investigation. More research in similar communities is needed before drawing strong conclusions based on the null results.

Published
2022

8. Maternal antenatal depression and child mental health

Author

Chen, L.M., Tollenaar, M.S., Dass, S.H.A., Bouvette-Turcot, A.A., Pokhvisneva, I., Gaudreau, H., Parent, C., Diorio, J., McEwen, L.M., MacIsaac, J.L., Kobor, M.S., Beijers, R., Weerth, C. de, Silveira, P.P., Karama, S., Meaney, M.J., O'Donnell, K.J., and MAVAN Study Team

Subjects
child development, polygenic risk score, ADHD, perinatal mental health, gene by environment (GxE)
Abstract

Maternal antenatal depression strongly influences child mental health but with considerable inter-individual variation that is, in part, linked to genotype. The challenge is to effectively capture the genotypic influence. We outline a novel approach to describe genomic susceptibility to maternal antenatal depression focusing on child emotional/behavioral difficulties. Two cohorts provided measures of maternal depression, child genetic variation, and child mental health symptoms. We constructed a conventional polygenic risk score (PRS) for attention-deficit/hyperactivity disorder (ADHD) (PRSADHD) that significantly moderated the association between maternal antenatal depression and internalizing problems at 60 months (p = 2.94 x 10(-4), R-2 = .18). We then constructed an interaction PRS (xPRS) based on a subset of those single nucleotide polymorphisms from the PRSADHD that most accounted for the moderation of the association between maternal antenatal depression and child outcome. The interaction between maternal antenatal depression and this xPRS accounted for a larger proportion of the variance in child emotional/behavioral problems than models based on any PRSADHD (p = 5.50 x 10(-9), R-2 = .27), with similar findings in the replication cohort. The xPRS was significantly enriched for genes involved in neuronal development and synaptic function. Our study illustrates a novel approach to the study of genotypic moderation on the impact of maternal antenatal depression on child mental health and highlights the utility of the xPRS approach. These findings advance our understanding of individual differences in the developmental origins of mental health.

Published
2020

9. Internalizing symptoms associate with the pace of epigenetic aging in childhood

Author

Tollenaar, M.S., Beijers, R., Garg, E., Nguyen, T.T.T., Lin, D.T.S., MacIsaac, J.L., Shalev, I., Kobor, M.S., Meaney, M.J., O'Donnell, K.J., Weerth, C. de, Tollenaar, M.S., Beijers, R., Garg, E., Nguyen, T.T.T., Lin, D.T.S., MacIsaac, J.L., Shalev, I., Kobor, M.S., Meaney, M.J., O'Donnell, K.J., and Weerth, C. de

Abstract

Contains fulltext : 228771.pdf (publisher's version ) (Open Access), Childhood psychiatric symptoms may be associated with advanced biological aging. This study examined whether epigenetic age acceleration (EAA) associates with internalizing and externalizing symptoms that were prospectively collected across childhood in a longitudinal cohort study. At age 6 buccal epithelial cells from 148 children (69 girls) were collected to survey genome-wide DNA methylation. EAA was estimated using the Horvath clock. Internalizing symptoms at ages 2.5 and 4 years significantly predicted higher EAA at age 6, which in turn was significantly associated with internalizing symptoms at ages 6-10 years. Similar trends for externalizing symptoms did not reach statistical significance. These findings indicate advanced biological aging in relation to child mental health and may help better identify those at risk for lasting impairments associated with internalizing disorders.

Published
2021

10. DCC gene network in the prefrontal cortex is associated with total brain volume in childhood

Author

Wadhwa, P., O'Donnell, K.J., Pokhvisneva, I., Nolvi, S., Gilmore, J., Styner, M., Flores, C.A., Sassi, R.B., Entringer, S., Meaney, M.J., Buss, C., Morgunova, A., Hall, G.B.C., and Silveira, P.P.

Abstract

BACKGROUND: Genetic variation in the guidance cue DCC gene is linked to psychopathologies involving dysfunction in the prefrontal cortex. We created an expression-based polygenic risk score (ePRS) based on the DCC coexpression gene network in the prefrontal cortex, hypothesizing that it would be associated with individual differences in total brain volume. METHODS: We filtered single nucleotide polymorphisms (SNPs) from genes coexpressed with DCC in the prefrontal cortex obtained from an adult postmortem donors database (BrainEAC) for genes enriched in children 1.5 to 11 years old (BrainSpan). The SNPs were weighted by their effect size in predicting gene expression in the prefrontal cortex, multiplied by their allele number based on an individual's genotype data, and then summarized into an ePRS. We evaluated associations between the DCC ePRS and total brain volume in children in 2 community-based cohorts: the Maternal Adversity, Vulnerability and Neurodevelopment (MAVAN) and University of California, Irvine (UCI) projects. For comparison, we calculated a conventional PRS based on a genome-wide association study of total brain volume. RESULTS: Higher ePRS was associated with higher total brain volume in children 8 to 10 years old (β = 0.212, p = 0.043; n = 88). The conventional PRS at several different thresholds did not predict total brain volume in this cohort. A replication analysis in an independent cohort of newborns from the UCI study showed an association between the ePRS and newborn total brain volume (β = 0.101, p = 0.048; n = 80). The genes included in the ePRS demonstrated high levels of coexpression throughout the lifespan and are primarily involved in regulating cellular function. LIMITATIONS: The relatively small sample size and age differences between the main and replication cohorts were limitations. CONCLUSION: Our findings suggest that the DCC coexpression network in the prefrontal cortex is critically involved in whole brain development during the first decade of life. Genes comprising the ePRS are involved in gene translation control and cell adhesion, and their expression in the prefrontal cortex at different stages of life provides a snapshot of their dynamic recruitment.

Published
2020
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11. Maternal antenatal depression and child mental health: Moderation by genomic risk for attention-deficit/hyperactivity disorder

Author

Chen, L.M., Tollenaar, M.S., Hari Dass, S.A., Bouvette-Turcot, A.A., Pokhvisneva, I., Gaudreau, H., Parent, C., Diorio, J., McEwen, L.M., MacIsaac, J.L., Kobor, M.S., Beijers, R., Weerth, C. de, Silveira, P.P., Karama, S., Meaney, M.J., O'Donnell, K.J., Chen, L.M., Tollenaar, M.S., Hari Dass, S.A., Bouvette-Turcot, A.A., Pokhvisneva, I., Gaudreau, H., Parent, C., Diorio, J., McEwen, L.M., MacIsaac, J.L., Kobor, M.S., Beijers, R., Weerth, C. de, Silveira, P.P., Karama, S., Meaney, M.J., and O'Donnell, K.J.

Abstract

Contains fulltext : 228341.pdf (Publisher’s version ) (Closed access), Maternal antenatal depression strongly influences child mental health but with considerable inter-individual variation that is, in part, linked to genotype. The challenge is to effectively capture the genotypic influence. We outline a novel approach to describe genomic susceptibility to maternal antenatal depression focusing on child emotional/behavioral difficulties. Two cohorts provided measures of maternal depression, child genetic variation, and child mental health symptoms. We constructed a conventional polygenic risk score (PRS) for attention-deficit/hyperactivity disorder (ADHD) (PRSADHD) that significantly moderated the association between maternal antenatal depression and internalizing problems at 60 months (p = 2.94 × 10-4, R2 = .18). We then constructed an interaction PRS (xPRS) based on a subset of those single nucleotide polymorphisms from the PRSADHD that most accounted for the moderation of the association between maternal antenatal depression and child outcome. The interaction between maternal antenatal depression and this xPRS accounted for a larger proportion of the variance in child emotional/behavioral problems than models based on any PRSADHD (p = 5.50 × 10-9, R2 = .27), with similar findings in the replication cohort. The xPRS was significantly enriched for genes involved in neuronal development and synaptic function. Our study illustrates a novel approach to the study of genotypic moderation on the impact of maternal antenatal depression on child mental health and highlights the utility of the xPRS approach. These findings advance our understanding of individual differences in the developmental origins of mental health.

Published
2020

12. The PedBE clock accurately estimates DNA methylation age in pediatric buccal cells

Author

McEwen, L.M., O'Donnell, K.J., McGill, M.G., Edgar, R.D., Jones, M.J., MacIsaac, J.L., Weerth, C. de, Beijers, R., Horvath, S., Kobor, M.S., McEwen, L.M., O'Donnell, K.J., McGill, M.G., Edgar, R.D., Jones, M.J., MacIsaac, J.L., Weerth, C. de, Beijers, R., Horvath, S., and Kobor, M.S.

Abstract

Contains fulltext : 219496.pdf (Publisher’s version ) (Closed access), DNA methylation is the most studied modification in human population epigenetics. Its information content can be explored in 2 principal ways - epigenome-wide association studies and epigenetic age. The latter likely reflects cellular/biological age and works with impressive accuracy across most tissues. In adults, it associates with various environments and health. However, current epigenetic clocks are not very accurate in the pediatric age range perhaps because DNA methylation changes much faster in children. Addressing this crucial gap, we created a precise tool to estimate DNA methylation age specific to pediatric buccal epithelial cells. This tool has the potential to become the standard reference for epigenetic studies broadly relevant to child development across the spectrum from health to disease.The development of biological markers of aging has primarily focused on adult samples. Epigenetic clocks are a promising tool for measuring biological age that show impressive accuracy across most tissues and age ranges. In adults, deviations from the DNA methylation (DNAm) age prediction are correlated with several age-related phenotypes, such as mortality and frailty. In children, however, fewer such associations have been made, possibly because DNAm changes are more dynamic in pediatric populations as compared to adults. To address this gap, we aimed to develop a highly accurate, noninvasive, biological measure of age specific to pediatric samples using buccal epithelial cell DNAm. We gathered 1,721 genome-wide DNAm profiles from 11 different cohorts of typically developing individuals aged 0 to 20 y old. Elastic net penalized regression was used to select 94 CpG sites from a training dataset (n = 1,032), with performance assessed in a separate test dataset (n = 689). DNAm at these 94 CpG sites was highly predictive of age in the test cohort (median absolute error = 0.35 y). The Pediatric-Buccal-Epigenetic (PedBE) clock was characterized in additional cohorts, s

Published
2020

13. Childhood internalizing symptoms and epigenetic aging

Author

Tollenaar, M.S., Beijers, R., Garg, E., Nguyen, T., Lin, D.T.S., MacIsaac, J.L., Shalev, I., Kobor, M.S., Meaney, M.J., O'Donnell, K.J., and Weerth, C. de

Subjects
Social Development
Abstract

Contains fulltext : 203547.pdf (Publisher’s version ) (Closed access) 1 p.

Published
2019

14. Integrated analysis of environmental and genetic influences on cord blood DNA methylation in new-borns

Author

Czamara, D. (Darina), Eraslan, G. (Gökçen), Page, C.M. (Christian M.), Lahti, J. (Jari), Lahti-Pulkkinen, M. (Marius), Hämäläinen, E. (Esa), Kajantie, E. (Eero), Laivuori, H. (Hannele), Villa, P.M. (Pia M.), Reynolds, R.M. (Rebecca M.), Nystad, W. (Wenche), Håberg, S.E. (Siri E), London, S.J. (Stephanie J.), O’Donnell, K.J. (Kieran J.), Garg, E. (Elika), Meaney, M.J., Entringer, S., Wadhwa, P.D. (Pathik D.), Buss, C. (Claudia), Jones, M.J. (Meaghan J.), Lin, D.T.S. (David T. S.), MacIsaac, J.L. (Julie L.), Kobor, M.S. (Michael S.), Koen, N. (Nastassja), Zar, H.J., Koenen, M.E. (Marjorie), Dalvie, S. (Shareefa), Stein, D.J. (Dan), Kondofersky, I. (Ivan), Müller, N.S. (Nikola S.), Theis, F. (Fabian), Wray, N.R. (Naomi), Ripke, S. (Stephan), Mattheisen, M. (Manuel), Trzaskowski, M. (Maciej), Byrne, E.M. (Enda), Abdellaoui, A. (Abdel), Adams, M.J. (Mark J.), Agerbo, E. (Esben), Air, T.M. (Tracy M.), Andlauer, T.F.M. (Till F. M.), Bacanu, S.A. (Silviu), Bækvad-Hansen, M. (Marie), Beekman, A.T.F. (Aartjan), Bigdeli, T.B. (Tim B.), Blackwood, D.H.R. (Douglas), Bryois, J. (Julien), Buttenschøn, H.N. (Henriette N.), Bybjerg-Grauholm, J. (Jonas), Cai, N. (Na), Castelao, E. (Enrique), Christensen, J.H. (Jane Hvarregaard), Clarke, T.-K., Coleman, J.R.I. (Jonathan R. I.), Colodro-Conde, L. (Lucía), Couvy-Duchesne, B. (Baptiste), Craddock, N.J. (Nick), Crawford, G.E. (Gregory E.), Davies, G. (Gail), Deary, I.J. (Ian), Degenhardt, F., Derks, E.M. (Eske), Direk, N. (Nese), Dolan, C.V. (Conor), Dunn, E.C. (Erin C.), Eley, T.C. (T.), Escott-Price, V. (Valentina), Kiadeh, F.F.H. (Farnush Farhadi Hassan), Finucane, H.K. (Hilary K.), Forstner, A.J. (Andreas J.), Frank, J. (Josef), Gaspar, H.A. (Héléna A.), Gill, M. (Michael), Goes, F.S. (Fernando S.), Gordon, S.D. (Scott D.), Grove, J. (Jakob), Hall, L.S. (Lynsey S.), Hansen, C.S. (Christine Søholm), Hansen, T.F. (Thomas F.), Herms, S. (Stefan), Hickie, I.B. (Ian), Hoffmann, P. (Per), Homuth, G. (Georg), Horn, C. (Carsten), Hottenga, J.J. (Jouke Jan), Hougaard, D.M. (David M.), Ising, M. (Marcus), Jansen, R. (Rick), Jorgenson, E. (Eric), Knowles, J.A. (James A), Kohane, I.S., Kraft, J. (Julia), Kretzschmar, W.W. (Warren W.), Krogh, J. (Jesper), Kutalik, Z. (Zoltán), Li, Y. (Yihan), Lind, P.A. (Penelope), Macintyre, D.J. (Donald J), MacKinnon, D.F. (Dean F.), Maier, R.M. (Robert M.), Maier, W. (Wolfgang), Marchini, J. (Jonathan), Mbarek, H., McGrath, P. (Patrick), McGuffin, P. (Peter), Medland, S.E. (Sarah), Mehta, D. (Divya), Middeldorp, C.M. (Christel), Mihailov, E. (Evelin), Milaneschi, Y. (Yuri), Milani, L. (Lili), Mondimore, F.M. (Francis M.), Montgomery, G.W. (Grant), Mostafavi, S. (Sara), Mullins, N. (Niamh), Nauck, M. (Matthias), Ng, B. (Bernard), Nivard, M. (Michel), Nyholt, D.R. (Dale), O’Reilly, P.F. (Paul F.), Oskarsson, H. (Hogni), Owen, M.J. (Michael J.), Painter, J.N. (Jodie N.), Pedersen, C.B. (C.), Pedersen, M.G. (Marianne Giørtz), Peterson, R.E. (Roseann E.), Pettersson, E. (Erik), Peyrot, W.J. (Wouter ), Pistis, G. (Giorgio), Posthuma, D. (Danielle), Quiroz, J.A. (Jorge A.), Qvist, P. (Per), Rice, J.P. (John), Riley, B.P. (Brien P.), Rivera, M. (Margarita), Mirza, S.S. (Saira), Schoevers, R. (Robert), Schulte, E.C. (Eva C.), Shen, L. (Ling), Shi, J. (Jianxin), Shyn, S.I. (Stanley I), Sigurdsson, E. (Engilbert), Sinnamon, G.C.B. (Grant C. B.), Smith, A.V. (Davey), Smith, D.J. (Daniel J.), Stefansson, H. (Hreinn), Steinberg, S. (Stacy), Streit, F. (Fabian), Strohmaier, J. (Jana), Tansey, K.E., Teismann, H. (Henning), Teumer, A. (Alexander), Thompson, W.K. (Wesley K.), Thomson, P.A. (Pippa A.), Thorgeirsson, T.E. (Thorgeir E.), Traylor, M. (Matthew), Treutlein, J. (Jens), Trubetskoy, V. (Vassily), Uitterlinden, A.G. (André), Umbricht, D. (Daniel), Van der Auwera, S. (Sandra), van Hemert, A.M. (Albert M.), Viktorin, A. (Alexander), Visscher, P.M. (Peter M.), Wang, Y. (Yunpeng), Webb, B.T. (Bradley T.), Weinsheimer, S.M. (Shantel Marie), Wellmann, J. (Jürgen), Willemsen, G.A.H.M. (Gonneke), Witt, S.H. (Stephanie H), Wu, Y. (Yang), Xi, H.S. (Hualin S.), Yang, J. (Jian), Zhang, F. (Futao), Arolt, V. (Volker), Baune, B.T., Berger, K. (Klaus), Boomsma, D.I. (Dorret), Cichon, S. (Sven), Dannlowski, U. (Udo), Geus, E.J.C. (Eco) de, DePaulo, J.R. (J. Raymond), Domenici, E. (Enrico), Domschke, K. (Katharina), Esko, T. (Tõnu), Grabe, H.J. (Hans Jörgen), Hamilton, S.P. (Steven P), Hayward, C. (Caroline), Heath, A.C. (Andrew), Jablensky, A. (Assen), Kloiber, S. (Stefan), Lewis, G., Li, Q.S. (Qingqin S.), Lucae, S. (Susanne), Madden, P.A. (Pamela), Magnusson, P.K. (Patrik K.), Martin, N.G. (Nicholas), McIntosh, A.M. (Andrew M.), Metspalu, A. (Andres), Mors, O. (Ole), Mortensen, P.B. (Preben Bo), Müller-Myhsok, B. (B.), Nordentoft, M. (Merete), Nöthen, M.M. (Markus), O’Donovan, M.C. (Michael C.), Paciga, S.A. (Sara A.), Pedersen, N.L. (Nancy), Penninx, B.W.J.H. (Brenda), Perlis, R.H. (Roy H), Porteous, D.J. (David J.), Potash, J.B. 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(Christel), Mihailov, E. (Evelin), Milaneschi, Y. (Yuri), Milani, L. (Lili), Mondimore, F.M. (Francis M.), Montgomery, G.W. (Grant), Mostafavi, S. (Sara), Mullins, N. (Niamh), Nauck, M. (Matthias), Ng, B. (Bernard), Nivard, M. (Michel), Nyholt, D.R. (Dale), O’Reilly, P.F. (Paul F.), Oskarsson, H. (Hogni), Owen, M.J. (Michael J.), Painter, J.N. (Jodie N.), Pedersen, C.B. (C.), Pedersen, M.G. (Marianne Giørtz), Peterson, R.E. (Roseann E.), Pettersson, E. (Erik), Peyrot, W.J. (Wouter ), Pistis, G. (Giorgio), Posthuma, D. (Danielle), Quiroz, J.A. (Jorge A.), Qvist, P. (Per), Rice, J.P. (John), Riley, B.P. (Brien P.), Rivera, M. (Margarita), Mirza, S.S. (Saira), Schoevers, R. (Robert), Schulte, E.C. (Eva C.), Shen, L. (Ling), Shi, J. (Jianxin), Shyn, S.I. (Stanley I), Sigurdsson, E. (Engilbert), Sinnamon, G.C.B. (Grant C. B.), Smith, A.V. (Davey), Smith, D.J. (Daniel J.), Stefansson, H. (Hreinn), Steinberg, S. (Stacy), Streit, F. (Fabian), Strohmaier, J. (Jana), Tansey, K.E., Teismann, H. 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Abstract

Epigenetic processes, including DNA methylation (DNAm), are among the mechanisms allowing integration of genetic and environmental factors to shape cellular function. While many studies have investigated either environmental or genetic contributions to DNAm, few have assessed their integrated effects. Here we examine the relative contributions of prenatal environmental factors and genotype on DNA methylation in neonatal blood at variably methylated regions (VMRs) in 4 independent cohorts (overall n = 2365). We use Akaike’s information criterion to test which factors best explain variability of methylation in the cohort-specific VMRs: several prenatal environmental factors (E), genotypes in cis (G), or their additive (G + E) or interaction (GxE) effects. Genetic and environmental factors in combination best explain DNAm at the majority of VMRs. The CpGs best explained by either G, G + E or GxE are functionally distinct. The enrichment of genetic variants from GxE models in GWAS for complex disorders supports their importance for disease risk.

Published
2019
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16. Intergenerational Transmission of Well Being–Genetic and Epigenetic Mechanisms

Author

Unternaehrer, E., primary, Greenlaw, K., additional, Hari Dass, S., additional, Chen, L.M., additional, Bouvette-Turcot, A.A., additional, Cost, K., additional, O’Donnell, K.J., additional, Gaudreau, H., additional, McEwen, L., additional, MacIsaac, J., additional, Kobor, M.S., additional, Fleming, A.S., additional, Atkinson, L., additional, Lydon, J.E., additional, Steiner, M., additional, Ciampi, A., additional, Greenwood, C.M.T., additional, and Meaney, M.J., additional

Published
2017
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