Journal
PSYCHOLOGICAL MEDICINE
Volume 43, Issue 9, Pages 1813-1823Publisher
CAMBRIDGE UNIV PRESS
DOI: 10.1017/S0033291712002784
Keywords
Bullying; childhood victimization; cortisol; DNA methylation; hypothalamic-pituitary-adrenal axis; SERT
Categories
Funding
- Medical Research Council [G9806489, G1002190]
- Jacobs Foundation
- British Academy
- Nuffield Foundation
- Economic and Social Research Council [RES-177-25-0013]
- National Institute of Child Health and Human Development [HD061298]
- Canadian Institutes of Health Research
- NARSAD Young Investigator Awards
- ESRC [ES/H034897/1] Funding Source: UKRI
- MRC [G108/603, G9806489, G1002190] Funding Source: UKRI
- Economic and Social Research Council [ES/H034897/1] Funding Source: researchfish
- Medical Research Council [G108/603, MR/J002739/1, G9806489, G1002190] Funding Source: researchfish
- National Institute for Health Research [CSA/01/05/001] Funding Source: researchfish
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Background. Childhood adverse experiences are known to induce persistent changes in the hypothalamic-pituitary-adrenal (HPA) axis reactivity to stress. However, the mechanisms by which these experiences shape the neuroendocrine response to stress remain unclear. Method. We tested whether bullying victimization influenced serotonin transporter gene (SERT) DNA methylation using a discordant monozygotic (MZ) twin design. A subsample of 28 MZ twin pairs discordant for bullying victimization, with data on cortisol and DNA methylation, were identified in the Environmental Risk (E-Risk) Longitudinal Twin Study, a nationally representative 1994-1995 cohort of families with twins. Results. Bullied twins had higher SERT DNA methylation at the age of 10 years compared with their non-bullied MZ co-twins. This group difference cannot be attributed to the children's genetic makeup or their shared familial environments because of the study design. Bullied twins also showed increasing methylation levels between the age of 5 years, prior to bullying victimization, and the age of 10 years whereas no such increase was detected in non-bullied twins across time. Moreover, children with higher SERT methylation levels had blunted cortisol responses to stress. Conclusions. Our study extends findings drawn from animal models, supports the hypothesis that early-life stress modifies DNA methylation at a specific cytosine-phosphate-guanine (CpG) site in the SERT promoter and HPA functioning and suggests that these two systems may be functionally associated.
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