Main content

Home

Menu

Loading wiki pages...

View
Wiki Version:
**PLEASE READ** ---------- **Article title**: Analysis of DNA methylation in young people reveals limited evidence for an association between victimization stress and epigenetic variation in blood. ---------- **Authors**: Sarah J. Marzi, Karen Sugden, Louise Arseneault, Daniel W. Belsky, Joe Burrage, David Corcoran, Andrea Danese, Helen L. Fisher, Eilis Hannon, Terrie E. Moffitt, Candice L. Odgers, Carmine Pariante, Richie Poulton, Benjamin S. Williams, Chloe C.Y. Wong, Jonathan Mill, Avshalom Caspi. ---------- **Article link**: https://ajp.psychiatryonline.org/doi/10.1176/appi.ajp.2017.17060693 ---------- **Abstract:** Objective: To test if victimization stress is associated with genome-wide DNA methylation. 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. Method: We 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 2232 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- and crime victimization). Results: Epigenome-wide analyses of polyvictimization across childhood and adolescence revealed few 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 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. Conclusion: 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, non-human models in uncovering the biological embedding of stress. ---------- **Supplemental file:** Within the ‘Files’ section is a supplemental results file named ‘Caspi_Victimization_and_Methylation_AJP_Online_data_supplement.xlsx’. This file is not available with the published article and must be accessed from here. The file lists the results of analyses of DNA methylation and various measures of polyvictimization. Summary statistics across all ~430,000 methylation probes under 5 different models are included (including estimates after adjustment for smoking behavior). To interact with the file effectively, we recommend downloading and opening in Microsoft Excel (WARNING: file size is ~210MB and might take a long time to download on slow internet connections). Once open in excel, we have included filter/sort options for each column; the option is available via the filter button included in each column header. To apply a filter option, select the button in the appropriate column and select a filter or sort criterion from the drop-down menu (e.g. increasing P-value sort, text string filter for gene name). To deselect a currently applied filter, select ‘clear filter’ option from the drop-down menu.
OSF does not support the use of Internet Explorer. For optimal performance, please switch to another browser.
Accept
This website relies on cookies to help provide a better user experience. By clicking Accept or continuing to use the site, you agree. For more information, see our Privacy Policy and information on cookie use.
Accept
×

Start managing your projects on the OSF today.

Free and easy to use, the Open Science Framework supports the entire research lifecycle: planning, execution, reporting, archiving, and discovery.