Stressful life events (SLEs) are associated with hyper(re-)activity of the HPA-axis. HPA-axis hyper(re-)activity is thought to be a major risk factor for depression development. SLEs may induce changes in an organism’s stress system via epigenetic mechanisms. The neuropeptide oxytocin (OT) is able to attenuate the stress response, and OT pathways are dysregulated in individuals suffering from Major Depressive Disorder (MDD). Therefore, the gene coding for oxytocin (OXT) is a possible target for the investigation of depression development.
We collected data on SLEs, OXT promoter methylation (Sequenom Epityper MassArray) and depression severity from 90 MDD inpatients and 90 matched healthy controls.
We found MDD inpatients to have a significantly lower OXT methylation than healthy controls. Methylation status was significantly negatively associated with SLEs but only in the group of MDD inpatients. There were no associations between methylation status and depression severity.
Methylation in blood samples is only a proxy for epigenetic profiles in brain tissue. We did not assess mRNA or protein levels and cannot draw conclusions regarding the functionality or specificity of differences in OXT methylation between groups.
SLEs leave their traces in the epigenetic profiles of the OT system of MDD inpatients. Alterations in epigenetic profiles of the OXT system could constitute a vulnerability factor predisposing individuals for depression development. Better understanding of DNA methylation profiles of depression-associated genes could serve as basis for a personalized medicine, in which pharmacological or psychotherapeutic treatment of depression is tailored to the patient’s individual characteristics.

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