Variation in Mu-Opioid Receptor Gene (OPRM1) as a Moderator of Naltrexone Treatment to Reduce Heavy Drinking in a High Functioning Cohort
Andrew CH Chen1,2*, Jon Morgenstern1, Christine M Davis2, Alexis N Kuerbis2, Jonathan Covault3 and Henry R Kranzler4
1Department of Psychiatry, College of Physicians and Surgeons, Columbia University, New York, USA
2Research Foundation for Mental Hygiene, Inc., New York State Psychiatric Institute, New York, USA
3Department of Psychiatry, University of Connecticut Health Center, Farmington, CT, USA
4Treatment Research Center, Department of Psychiatry, Perelman School of Medicine of the University of Pennsylvania and VISN4 MIRECC, Philadelphia VAMC Philadelphia, USA
- *Corresponding Author:
- Andrew C. Chen
Department of Psychiatry
College of Physicians and Surgeons of the Columbia University
1775 Broadway, Suite 1404, New York, USA
E-mail: [email protected]
Received date: November 05, 2012; Accepted date: November 23, 2012; Published date: November 26, 2012
Citation: Chen ACH, Morgenstern J, Davis CM, Kuerbis AN, Covault J, et al. (2013) Variation in Mu-Opioid Receptor Gene (OPRM1) as a Moderator of Naltrexone Treatment to Reduce Heavy Drinking in a High Functioning Cohort. J Alcoholism Drug Depend 1:101 doi:10.4172/2329-6488.1000101
Copyright: © 2013 Chen ACH et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Background: It is well known that naltrexone
, an FDA-approved medication for treatment of alcohol dependence, is effective for only a subset of individuals. Recent studies have examined the utility of a functional A118G single nucleotide polymorphism (SNP) of the mu-opioid receptor gene (OPRM1) as a predictor of naltrexone treatment response. Although the findings to date have generally been consistent with a moderating effect of the SNP, further evaluation of this hypothesis is warranted.
Objective: To evaluate whether problem drinkers with one or two copies of the 118G allele
respond better to naltrexone treatment. The treatment goal in this cohort of high functioning men who have sex with men (MSM) was to reduce heavy drinking, rather than to promote abstinence.
Method: 112 subjects of European ancestry from a randomized clinical trial of naltrexone and behavioral therapy for problem drinking MSM were included in the analysis. Subjects were treated for 12 weeks with 100 mg/day of oral naltrexone hydrochloride. All participants received medical management with a modified version of the Brief Behavioral Compliance Enhancement Treatment (BBCET), alone or in combination with Modified Behavioral Selfcontrol Therapy (MBSCT).
Results: Naltrexone-treated subjects with one or two 118G alleles had a significantly greater percentage of nonhazardous drinking (NoH) (p<0.01) than those treated with placebo or A118 homozygotes in either medication group.
Conclusions: These results are consistent with a modest moderating effect of the OPRM1 118G allele on the reduction of heavy drinking by naltrexone treatment.