Peer-reviewed article
16.1 EPIGENETIC SIGNATURES OF CHILDHOOD AND ADOLESCENT VICTIMISATION USING A GENETICALLY SENSITIVE LONGITUDINAL COHORT STUDY.
Fisher H, Marzi S, Arseneault L, Wong C, Kandaswamy R et al. ·
Summary
Written by AI, not yet AICS's view · claude-haiku-4-5-20251001This study examined whether childhood and adolescent victimisation—including abuse, neglect, bullying, and crime—leaves biological marks in DNA through changes in DNA methylation patterns. Using data from 2,232 children followed from birth to age 18 in England and Wales, researchers found that while some associations between victimisation and DNA methylation appeared in initial analyses, these were explained by other factors like smoking and did not hold up in more rigorous testing. The findings do not support the idea that victimisation causes robust, detectable changes in DNA methylation in young people.
Key points
- Multiple forms of victimisation during childhood and adolescence showed some associations with DNA methylation at age 18, but these associations were confounded by tobacco smoking
- Associations with DNA methylation did not survive co-twin control tests, suggesting they may reflect shared family factors rather than victimisation-specific effects
- Specific forms of victimisation showed sparse associations with DNA methylation that did not replicate across different measurements of the same victimisation 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
- Findings suggest that epigenetic epidemiology may not yet be well-matched to experimental models in detecting the biological effects of early-life stress
Limitations
The study measures DNA methylation at a single time point (age 18) in peripheral blood, which may not capture the full biological effect of victimisation or reflect changes in other tissues. The lack of findings may indicate that victimisation's biological effects operate through different mechanisms than DNA methylation, or that epigenetic changes may be tissue- or time-specific.
Abstract
Abstract Background Stress is a normal, adaptive response to stressors (e.g. events that make a person feel threatened or upset). However, healthy development can be derailed by excessive or prolonged exposure to stress especially during important developmental periods such as childhood and adolescence. Exposure to severe stress may have immediate as well as long-lasting damaging effects on learning, behaviour, and health, and has been implicated in the development of psychosis. One way these may occur is via changes to epigenetic processes (e.g. alterations in DNA methylation). Initial studies have shown that individuals exposed to severe psychosocial stress have different patterns of DNA methylation (epigenetic ‘signatures’) compared to individuals exposed to no/minimal stressful life events, but these studies are methodologically limited. Methods This paper describes our examination of the potential link between exposure to multiple forms of severe victimisation (poly-victimisation) during childhood adolescence and DNA methylation differences utilising data from the Environmental Risk (E-Risk) Longitudinal Twin Study, an epidemiological study of 2,232 children (1,116 twin pairs) born in 1994–1995 in England and Wales and followed to 18 years of age (with 93% retention). Multiple forms of victimisation were ascertained in childhood and adolescence (including physical, sexual and emotional abuse, neglect, exposure to intimate-partner violence, bullying, cyber- and crime victimization) by combining the best practices in survey research with comprehensive interview-based approaches. Whole blood samples were collected from participants at age 18, and the extracted DNA was used to quantify genome-wide patterns of DNA methylation. Results Epigenome-wide analyses of poly-victimisation across childhood and adolescence revealed several significant associations with DNA methylation in peripheral blood at age 18 years, but these were confounded by tobacco smoking and/or did not survive co-twin control tests. Secondary analyses of specific forms of victimisation revealed sparse associations with DNA methylation that did not replicate across different operationalisations 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. Discussion 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 victimised young people. It is possible that epigenetic epidemiology is not yet well matched to experimental, non-human models in uncovering the biological embedding of stress.
Findings the Hub has extracted
Each claim below is labelled by its type of design and links back to this report.
- Intervention
- Observational assessment of exposure to multiple forms of victimisation (physical, sexual and emotional abuse, neglect, intimate-partner violence exposure, bullying, cyber-victimisation, crime victimisation) and measurement of genome-wide DNA methylation patterns
- Population
- 2,232 children (1,116 twin pairs) born in 1994–1995 in England and Wales, followed to age 18 (93% retention)
Key finding
Epigenome-wide associations between poly-victimisation and DNA methylation were confounded by tobacco smoking and/or did not survive co-twin control tests
H et al. · PubMed Central (PMC) · 1 Apr 2018