期刊
AMERICAN JOURNAL OF PSYCHIATRY
卷 175, 期 6, 页码 517-529出版社
AMER PSYCHIATRIC PUBLISHING, INC
DOI: 10.1176/appi.ajp.2017.17060693
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资金
- Medical Research Council [G1002190, MR/P005918/1]
- National Institute of Child Health and Human Development [HD077482]
- New Zealand Health Research Council
- New Zealand Ministry of Business, Innovation, and Employment
- National Institute on Aging [AG032282]
- American Asthma Foundation
- Jacobs Foundation
- Avielle Foundation
- EU-FP7 Marie Curie ITN EpiTrain (REA) [316758]
- North Carolina Biotechnology Center [2016-IDG-1013]
- Johnson Johnson
- Wellcome-ledconsortium
- GlaxoSmithKline
- Pfizer
- Lundbeck
- [MQ14F40]
- MRC [MR/P005918/1, G1002190, G108/603] Funding Source: UKRI
- Medical Research Council [G108/603] Funding Source: researchfish
- National Institute for Health Research [NF-SI-0616-10074] Funding Source: researchfish
- MQ: Transforming Mental Health [MQ14F40] Funding Source: researchfish
- EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT [R01HD077482, P2CHD065563] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON AGING [R01AG032282, P30AG034424] Funding Source: NIH RePORTER
- OFFICE OF THE DIRECTOR, NATIONAL INSTITUTES OF HEALTH [S10OD018164] Funding Source: NIH RePORTER
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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