Epigenetic regulation of the glucocorticoid receptor in human brain associates with childhood abuse. McGowan PO, Sasaki A, D'Alessio AC, Dymov S, Labonte B, Szyf M et al. J Am Acad Child Adolesc Psychiatry 2010 49: 752–771. Epigenetics and the biological basis of gene x environment interactions. Working class matters: Socioeconomic disadvantage, race/ethnicity, gender, and smoking in NHIS 2000. Soc Psychiatry Psychiatr Epidemiol 2003 38: 229–237.īarbeau EM, Krieger N, Soobader M. Social inequalities and the common mental disorders: a systematic review of the evidence. Ann NY Acad Sci 2010 1186: 37–55.įryers T, Melzer D, Jenkins R. Childhood socioeconomic status and adult health. Am J Public Health 2003 93: 1844–1850.Ĭohen S, Janicki-Deverts D, Chen E, Matthews KA. The public health impact of socioeconomic status on adolescent depresssion and obesity. Adverse childhood experiences and the risk of depressive disorders in adulthood. If replicated, this prospective pathway may represent a novel target biomarker for intervention and prevention among high-risk individuals.Ĭhapman DP, Whitfield CL, Felitti VJ, Dube SR, Edwards VJ, Anda RF. These initial results suggest a specific biological mechanism through which adversity contributes to altered brain function, which in turn moderates the emergence of general liability as individual risk for mental illness. We subsequently demonstrate that greater increases in amygdala reactivity moderate the association between a positive family history for depression and the later manifestation of depressive symptoms. Specifically, we find that lower SES during adolescence is associated with an increase in methylation of the proximal promoter of the serotonin transporter gene, which predicts greater increases in threat-related amygdala reactivity. Using prospective longitudinal epigenetic, neuroimaging and behavioral data from 132 adolescents, we demonstrate that changes in gene methylation associated with lower socioeconomic status (SES) predict changes in risk-related brain function. However, it is not yet clear whether differential gene methylation as a function of adversity contributes to the emergence of individual risk for mental illness. Recent clinical studies have suggested that epigenetic modification, particularly methylation of gene regulatory regions, also acts to shape human brain function associated with risk for mental illness. Preclinical studies have identified epigenetic modification of gene expression as one such mechanism. Identifying biological mechanisms through which the experience of adversity emerges as individual risk for mental illness is an important step toward developing strategies for personalized treatment and, ultimately, prevention.
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