Adversity exposure during sensitive periods predicts accelerated epigenetic aging in children.
ALSPAC
Adversity
Aging
Epigenetic clock
Sensitive periods
Journal
Psychoneuroendocrinology
ISSN: 1873-3360
Titre abrégé: Psychoneuroendocrinology
Pays: England
ID NLM: 7612148
Informations de publication
Date de publication:
03 2020
03 2020
Historique:
received:
22
05
2019
revised:
11
10
2019
accepted:
11
10
2019
pubmed:
10
1
2020
medline:
20
1
2021
entrez:
10
1
2020
Statut:
ppublish
Résumé
Exposure to adversity has been linked to accelerated biological aging, which in turn has been shown to predict numerous physical and mental health problems. In recent years, measures of DNA methylation-based epigenetic age--known as "epigenetic clocks"--have been used to estimate accelerated epigenetic aging. Although a small number of studies have found an effect of adversity exposure on epigenetic age in children, none have investigated if there are "sensitive periods" when adversity is most impactful. Using data from the Avon Longitudinal Study of Parents and Children (ALSPAC; n = 973), we tested the prospective association between repeated measures of childhood exposure to seven types of adversity on epigenetic age assessed at age 7.5 using the Horvath and Hannum epigenetic clocks. With a Least Angle Regression variable selection procedure, we evaluated potential sensitive period effects. We found that exposure to abuse, financial hardship, or neighborhood disadvantage during sensitive periods in early and middle childhood best explained variability in the deviation of Hannum-based epigenetic age from chronological age, even after considering the role of adversity accumulation and recency. Secondary sex-stratified analyses identified particularly strong sensitive period effects. These effects were undetected in analyses comparing children "exposed" versus "unexposed" to adversity. We did not identify any associations between adversity and epigenetic age using the Horvath epigenetic clock. Our results suggest that adversity may alter methylation processes in ways that either directly or indirectly perturb normal cellular aging and that these effects may be heightened during specific life stages.
Identifiants
pubmed: 31918390
pii: S0306-4530(19)30475-5
doi: 10.1016/j.psyneuen.2019.104484
pmc: PMC7832214
mid: NIHMS1553530
pii:
doi:
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
104484Subventions
Organisme : NIA NIH HHS
ID : R03 AG051877
Pays : United States
Organisme : Medical Research Council
ID : MC_PC_19009
Pays : United Kingdom
Organisme : Medical Research Council
ID : MC_PC_15018
Pays : United Kingdom
Organisme : NIMH NIH HHS
ID : K01 MH102403
Pays : United States
Organisme : Medical Research Council
ID : G9815508
Pays : United Kingdom
Organisme : NIMH NIH HHS
ID : R01 MH113930
Pays : United States
Organisme : Wellcome Trust
ID : 102215/2/13/2
Pays : United Kingdom
Organisme : Medical Research Council
ID : MC_UU_12013/2
Pays : United Kingdom
Organisme : Medical Research Council
ID : MC_UU_00011/5
Pays : United Kingdom
Organisme : Wellcome Trust
Pays : United Kingdom
Organisme : CSRD VA
ID : I01 CX001276
Pays : United States
Commentaires et corrections
Type : ErratumIn
Informations de copyright
Copyright © 2019. Published by Elsevier Ltd.
Déclaration de conflit d'intérêts
Declarations of Competing Interest None.
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