Background: Marital separation and divorce are stressful life transitions associated with increased risk for a range of poor mental and physical health outcomes. A key task for research in this area is to identify individual differences that may index risk for these adverse outcomes.
Purpose: To examine the association between DNA methylation across the serotonin transporter gene (SLC6A4) and self-reported emotional distress following marital separation.
Methods: Genomic DNA methylation (from buffy coat fractions of whole blood) was quantified in a sample of 47 adults following a recent marital separation; concurrent with the blood draw, participants completed questionnaires on their psychological adjustment to the separation experience.
Results: Relatively greater methylation of SLC6A4 was associated with less subjective separation-related psychological distress, and this association held after accounting for participants' age, length of the relationship, time since the separation, and SLC6A4 genotype, b = -211.99, SE = 94.91, p = .03, 95% CI: -402.22, -25.21. Significantly stronger negative associations were observed between methylation and psychological adjustment among participants who had more recently separated from their former partner.
Conclusions: Although results derived from small samples must be considered preliminary and hypothesis generating, the current study raises new questions about the role of DNA methylation and psychosocial adaptation to stressful life events such as divorce, and the findings can inform future studies in this research area.
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http://dx.doi.org/10.1093/abm/kaz013 | DOI Listing |
Curr Rheumatol Rev
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Department of Rheumatology, Beijing Jishuitan Hospital, Guizhou Hospital, China.
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J Pathol
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Laboratory of Pathology, Center for Cancer Research, NCI, Bethesda, MD, USA.
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View Article and Find Full Text PDFNoncoding RNA Res
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Kresge Eye Institute, Wayne State University, Detroit, MI, USA.
Diabetic retinopathy, a microvascular complication of diabetes, is the leading cause of blindness in adults, but the molecular mechanism of its development remains unclear. Retinal mitochondrial DNA is damaged and hypermethylated, and mtDNA-encoded genes are downregulated. Expression of a long noncoding RNA (larger than 200 nucleotides, which does not translate into proteins), encoded by mtDNA, cytochrome B (Lnc), is also downregulated.
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