Early-life stress interactions with the epigenome

Lewis, Candace R.

doi:10.1097/fbp.0000000000000057

Cited by 42 publications

(15 citation statements)

References 123 publications

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“…Of note, we found that proximal exposures (e.g., maternal smoking and alcohol use) correlated with DNAm more strongly than more distal exposures (e.g., life events). Albeit preliminary, these findings are consistent with previous studies showing that DNAm is associated with environmental influences (e.g., Lewis & Olive, 2014), with smoking-related effects, in particular, being among the most replicated across epigenetic studies (Gao, Jia, Zhang, Breitling, & Brenner, 2015). For example, we found that prenatal smoking correlated with hypomethylation of the MGLL probe, which in turn prospectively associated with early-onset CP.…”

Section: Genetic and Prenatal Influences On Dnam Patterns Associated supporting

confidence: 92%

Neonatal DNA methylation and early-onset conduct problems: A genome-wide, prospective study

et al. 2017

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2017). Neonatal DNA methylation and early-onset conduct problems: A genome-wide, prospective study. Development and Psychopathology, 1-15. DOI: 10.1017/S095457941700092XCiting this paper Please note that where the full-text provided on King's Research Portal is the Author Accepted Manuscript or Post-Print version this may differ from the final Published version. If citing, it is advised that you check and use the publisher's definitive version for pagination, volume/issue, and date of publication details. And where the final published version is provided on the Research Portal, if citing you are again advised to check the publisher's website for any subsequent corrections. General rightsCopyright and moral rights for the publications made accessible in the Research Portal are retained by the authors and/or other copyright owners and it is a condition of accessing publications that users recognize and abide by the legal requirements associated with these rights.•Users may download and print one copy of any publication from the Research Portal for the purpose of private study or research.•You may not further distribute the material or use it for any profit-making activity or commercial gain •You may freely distribute the URL identifying the publication in the Research Portal Take down policyIf you believe that this document breaches copyright please contact librarypure@kcl.ac.uk providing details, and we will remove access to the work immediately and investigate your claim. (0)207 848 0992 Development & Psychopathology.DNA methylation and conduct problems 2 AbstractEarly-onset conduct problems (CP) are a key predictor of adult criminality and poor mental health. While previous studies suggest that both genetic and environmental risks play an important role in the development of early-onset CP, little is known about potential biological processes underlying these associations. In this study, we examined prospective associations between DNA methylation (cord blood at birth) and trajectories of CP (4-13yrs), using data drawn from the Avon Longitudinal Study of Parents and Children (ALSPAC). Methylomic variation at seven loci across the genome (FDR<0.05) differentiated children who go on to develop early-onset (n = 174) vs low (n = 86) CP, including sites in the vicinity of MGLL (involved in endocannabinoid signaling and pain perception). Sub-threshold associations in the vicinity of three candidate genes for CP (MAOA, BDNF, and FKBP5) were also identified. Within the early-onset CP group, methylation levels of the identified sites did not distinguish children who will go on to persist vs desist in CP behavior over time. Overall, we found that several of the identified sites correlated with prenatal exposures, and none were linked to known genetic mQTLs. Findings contribute to a better understanding of epigenetic patterns associated with early-onset CP.

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Section: Genetic and Prenatal Influences On Dnam Patterns Associated supporting

confidence: 92%

Neonatal DNA methylation and early-onset conduct problems: A genome-wide, prospective study

et al. 2017

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“…Inclusion criteria for studies of cellular aging. Although there have been prior reviews and meta-analyses exploring the effects of ELA on telomere length (Coimbra et al, 2017;Price et al, 2013) or DNAm age (Gershon & High, 2015;Lewis & Olive, 2014;Silberman, Acosta, & Zorrilla Zubilete, 2016;Vinkers et al, 2015;Wolf et al, 2018), none has focused on differences across distinct adversity types or restricted the focus to studies measuring ELA and cellular aging in childhood or adolescence. Telomere length and DNAm age can be assessed through both blood and saliva samples (Wren, Shirtcliff, & Drury, 2015); we have included both measures in our analyses.…”

Section: Study Inclusion Criteriamentioning

confidence: 99%

Biological Aging in Childhood and Adolescence Following Experiences of Threat and Deprivation: A Systematic Review and Meta-Analysis

Colich

Rosen

Williams³

et al. 2019

Preprint

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Life history theory argues that exposure to early-life adversity (ELA) accelerates development, although existing evidence for this varies. We present a meta-analysis and systematic review testing the hypothesis that ELA involving threat (e.g., violence exposure) will be associated with accelerated biological aging across multiple metrics, whereas exposure to deprivation (e.g., neglect, institutional rearing) and low-socioeconomic status (SES) will not. We meta-analyze 46 studies (n=64,925) examining associations of ELA with pubertal timing and cellular aging (telomere length and DNA methylation age), systematically review 19 studies (n=2276) examining ELA and neural markers of accelerated development (cortical thickness and amygdala-prefrontal cortex functional connectivity) and evaluate whether associations of ELA with biological aging vary according to the nature of adversity experienced. ELA overall was associated with accelerated pubertal timing (d=-0.12) and cellular aging (d=-0.32). Moderator analysis revealed that ELA characterized by threat (d=-0.26), but not deprivation or SES, was associated with accelerated pubertal development. Similarly, exposure to threat-related ELA was associated with accelerated cellular aging (d=-0.43), but not deprivation or SES.Systematic review revealed associations between ELA and accelerated cortical thinning, with threat-related ELA consistently associated with thinning in ventromedial prefrontal cortex, and deprivation and SES associated with thinning in frontoparietal, default, and visual networks.There was no consistent association of ELA with amygdala-PFC connectivity. These findings suggest specificity in the types of early environmental experiences associated with accelerated biological aging and highlight the importance of evaluating how accelerated aging contributes to health disparities and whether this process can be mitigated through early intervention.

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“…The long-term effects of epigenetically moderated placenta dysfunction on health and behavior of children is clearly moderated by postnatal parenting choices, and this interaction is a rich subject for additional study (39). Even broader measures of the social environment such as neighborhoods and larger social groups appear to have some influence on methylation patterns, probably by effects on stress, although to what extent these are permanent changes is still under investigation (18,34,35,41,57,67–70). …”

Section: Evidence For Social Environmental Effects On Methylationmentioning

confidence: 99%

DNA methylation, early life environment, and health outcomes

2015

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Epigenetics, and especially DNA methylation, have recently become provocative biological explanations for early-life environmental effects on later health. Despite the large increase in papers on the topic over the last few years, many questions remain with regards to the biological feasibility of this mechanism and the strength of the evidence to date. In this review, we examine the literature on early-life effects on epigenetic patterns, with special emphasis on social environmental influences. First, we review the basic biology of epigenetic modification of DNA and debate the role of early-life stressful, protective, and positive environments on gene-specific, system-specific, and whole-genome epigenetic patterns later in life. Second, we compare the epigenetic literatures of both humans and other animals and review the research linking epigenetic patterns to health in order to complete the mechanistic pathway. Third, we discuss physical environmental and social environmental effects, which have to date, generally not been jointly considered. Finally, we close with a discussion of the current state of the area’s research, its future direction, and its potential use in pediatric health.

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Early-life stress interactions with the epigenome

Cited by 42 publications

References 123 publications

Neonatal DNA methylation and early-onset conduct problems: A genome-wide, prospective study

Neonatal DNA methylation and early-onset conduct problems: A genome-wide, prospective study

Biological Aging in Childhood and Adolescence Following Experiences of Threat and Deprivation: A Systematic Review and Meta-Analysis

DNA methylation, early life environment, and health outcomes

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