Oxytocin receptor gene methylation and substance use problems among young African American men

• Type of Material: Article
• Authors: Steven M. Kogan, University of Georgia; Junhan Cho, University of Southern California; Steven R. H. Beach, University of Georgia; Alicia Smith, Emory University; Shota Nishitani, Emory University
• Language: English
• Date: 2018-11-01
• Publisher: Elsevier: 12 months
• Publication Version: Author Accepted Manuscript (After Peer Review)
• Copyright Statement: © 2018 Elsevier B.V.
• License: Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International
• Final Published Version (URL): http://dx.doi.org/10.1016/j.drugalcdep.2018.08.022
• Title of Journal or Parent Work: Drug and Alcohol Dependence
• ISSN: 0376-8716
• Volume: 192
• Start Page: 309
• End Page: 315
• Grant/Funding Information: Funding for this study was provided by Grants R01 DA029488 and P30 DA027827 from the National Institute on Drug Abuse.
• Keywords: Psychiatry; OXTR METHYLATION; Substance Abuse; DNA METHYLATION; STRESS; African American men; UNITED-STATES; Life Sciences & Biomedicine; Oxytocin; DRUG-USE; ALCOHOL; Social environment; DNA; Life stress; Substance abuse; Science & Technology; PROTECTIVE FACTORS; BLACK-MEN; ADDICTION; HIDDEN POPULATIONS
• Research Categories: Psychology, Behavioral; Psychology, Psychobiology

Abstract

Background: Stressful or supportive social environments promote biological changes with regulatory implications for future relationships and substance abuse. Recent research suggests links between adverse social environments, prosocial relationships, methylation at the oxytocin receptor gene (OXTR), and substance abuse. The potential for OXTR methylation to act as the mechanism linking social environments to substance abuse has yet to be investigated. We hypothesized that, for young African American men, childhood adversity increases, and supportive, prosocial bonds with parents, peers, partners, and community mentors decrease OXTR methylation levels, which in turn predict increases in substance-related symptoms. Methods: A sample of 358 rural African American men (age 19 at baseline) provided self-report data at three time points separated by 18 months and a genetic specimen at Time 2. Results: Early adversity was associated with OXTR methylation indirectly via contemporary prosocial relationships. OXTR methylation was a proximal predictor of changes in substance-related symptoms. We found no evidence for a direct association of self-reported childhood trauma with OXTR methylation status. Conclusions: Findings suggest that OXTR methylation is linked to substance use symptomatology, ostensibly resulting in increased expression of oxytocin (OT) in peripheral and central nervous systems. OXTR may act as a mechanism to explain how prosocial ties deter substance abuse and related problems. Despite conjectures in the literature that early adversity may become physiologically embedded via methylation in the OT system, direct effects were not evident. Rather, early adversity may affect OXTR methylation via influence on contemporary prosocial relationships.