Subjective Response to Alcohol Among Alcohol-Dependent Individuals: Effects of the Mu-Opioid Receptor (OPRM1) Gene and Alcoholism Severity
Article first published online: 14 DEC 2012
Copyright © 2012 by the Research Society on Alcoholism
Alcoholism: Clinical and Experimental Research
Volume 37, Issue Supplement s1, pages E116–E124, January 2013
How to Cite
Ray, L. A., Bujarski, S., MacKillop, J., Courtney, K. E., Monti, P. M. and Miotto, K. (2013), Subjective Response to Alcohol Among Alcohol-Dependent Individuals: Effects of the Mu-Opioid Receptor (OPRM1) Gene and Alcoholism Severity. Alcoholism: Clinical and Experimental Research, 37: E116–E124. doi: 10.1111/j.1530-0277.2012.01916.x
- Issue published online: 15 JAN 2013
- Article first published online: 14 DEC 2012
- Manuscript Accepted: 10 JUN 2012
- Manuscript Received: 2 MAR 2012
- Foundation for Alcohol Research
- UCLA Clinical and Translational Science Institute
- National Institutes of Health. Grant Numbers: M01-RR00865, K23 AA016936
- Alcohol Dependence;
- Responses to Alcohol;
- A118G SNP;
Subjective response to alcohol has been examined as a marker of alcoholism risk. The A118G single-nucleotide polymorphism (SNP) of the mu-opioid receptor (OPRM1) gene has been previously associated with subjective response to alcohol in heavy drinkers. This study seeks to extend the literature by examining the effect of OPRM1 genotype on responses to alcohol in a sample of alcohol-dependent individuals. A secondary aim of this study is to examine alcoholism severity as a predictor of subjective responses to alcohol.
Nontreatment seeking problem drinkers (n = 295) were assessed in the laboratory for clinical dimensions of alcohol dependence. Following prospective genotyping, 43 alcohol-dependent individuals across the 2 genotype conditions (AA, n = 23 and AG/GG, n = 20) were randomized to 2 intravenous infusion sessions: 1 of alcohol (target breath alcohol concentration = 0.06 g/dl) and 1 of saline. Measures of subjective responses to alcohol were administered in both infusion sessions.
Alcohol-dependent G-allele carriers reported greater alcohol-induced stimulation, vigor, and positive mood, as compared to A-allele homozygotes. There was no genotype effect on alcohol-induced sedation or craving. There was a statistical trend-level severity × alcohol interaction such that individuals at higher levels of severity reported greater alcohol-induced tension reduction.
These results support the hypothesis that OPRM1 genotype moderates the hedonic effects of alcohol, but not the sedative and unpleasant effects of alcohol, in a sample of alcohol-dependent patients. Results are discussed in light of a clinical neuroscience framework to alcoholism.