Psychosocial adversity and socioeconomic position during childhood and epigenetic age: Analysis of two prospective cohort studies

Rebecca B. Lawn*, Emma L. Anderson, Matthew Suderman, Andrew J. Simpkin, Tom R. Gaunt, Andrew E. Teschendorff, Martin Widschwendter, Rebecca Hardy, Diana Kuh, Caroline L. Relton, Laura D. Howe

*Corresponding author for this work

Research output: Contribution to journalArticle (Academic Journal)peer-review

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Psychosocial adversity in childhood (e.g. abuse) and low socioeconomic position (SEP) can have significant lasting effects on social and health outcomes. DNA methylation-based biomarkers are highly correlated with chronological age; departures of methylation-predicted age from chronological age can be used to define a measure of age acceleration, which may represent a potential biological mechanism linking environmental exposures to later health outcomes. Using data from two cohorts of women Avon Longitudinal Study of Parents and Children, (ALSPAC), N=989 and MRC National Survey of Health and Development, NSHD, N=773), we assessed associations of SEP, psychosocial adversity in childhood (parental physical or mental illness or death, parental separation, parental absence, sub-optimal maternal bonding, sexual, emotional and physical abuse and neglect) and a cumulative score of these psychosocial adversity measures, with DNA methylation age acceleration in adulthood (measured in peripheral blood at mean chronological ages 29 and 47 in ALSPAC and buccal cells at age 53 in NSHD). Sexual abuse was strongly associated with age acceleration in ALSPAC (sexual abuse data were not available in NSHD), e.g. at the 47-year time point sexual abuse associated with a 3.41 years higher DNA methylation age (95% CI 1.53 to 5.29) after adjusting for childhood and adulthood SEP. No associations were observed between low SEP, any other psychosocial adversity measure or the cumulative psychosocial adversity score and age acceleration. DNA methylation age acceleration is associated with sexual abuse, suggesting a potential mechanism linking sexual abuse with adverse outcomes. Replication studies with larger sample sizes are warranted.

Original languageEnglish
Pages (from-to)1301-1308
Number of pages8
JournalHuman Molecular Genetics
Issue number7
Early online date22 Jan 2018
Publication statusPublished - 1 Apr 2018


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