Preliminary Evidence for a Gene–Environment Interaction in Predicting Alcohol Use Disorders in Adolescents
Article first published online: 8 NOV 2012
Copyright © 2012 by the Research Society on Alcoholism
Alcoholism: Clinical and Experimental Research
Volume 37, Issue 2, pages 325–331, February 2013
How to Cite
Miranda, R., Reynolds, E., Ray, L., Justus, A., Knopik, V. S., McGeary, J. and Meyerson, L. A. (2013), Preliminary Evidence for a Gene–Environment Interaction in Predicting Alcohol Use Disorders in Adolescents. Alcoholism: Clinical and Experimental Research, 37: 325–331. doi: 10.1111/j.1530-0277.2012.01897.x
- Issue published online: 1 FEB 2013
- Article first published online: 8 NOV 2012
- Manuscript Accepted: 22 MAY 2012
- Manuscript Received: 24 OCT 2011
- National Institute on Drug Abuse. Grant Number: DA016904
- National Institute on Alcohol Abuse and Alcoholism. Grant Numbers: K23 AA014966, T32 AA07459
- Medical Research Service
- OPRM1 ;
- Parental Monitoring;
- Deviant Peer Affiliation
Emerging research suggests that genetic influences on adolescent drinking are moderated by environmental factors. The present study builds on molecular-genetic findings by conducting the first analysis of gene–environment interactions in the association between a functional single nucleotide polymorphism (SNP) of the μ-opioid receptor (OPRM1) gene (A118G) and risk of developing an alcohol use disorder (AUD) during adolescence. Specifically, we tested whether variation in parenting practices or affiliation with deviant peers moderated the link between the OPRM1 gene and risk of an AUD.
Adolescents reporting European ancestry (N = 104), ages 12 to 19 years (M = 15.60, SD = 1.77), were interviewed to ascertain AUD diagnoses, provided a DNA sample for genetic analyses, and completed measures of parental monitoring and deviant peer affiliation. Logistic regression was used to test the effects of environmental variables and their interactions with OPRM1 genotype as predictors of AUD diagnosis while controlling for age and sex.
Case–control comparisons showed that the proportion of youth with an AUD (n = 18) significantly differed by genotype such that 33.3% of G allele carriers met criteria for an AUD compared to 10.8% of youth who were homozygous for the A allele (p = 0.006). The OPRM1 × parental monitoring (odds ratio = 0.16) and OPRM1 × deviant peer affiliation (odds ratio = 7.64) interactions were significant predictors of AUD risk, such that G allele carriers with high levels of deviant peer affiliation or lower levels of parental monitoring had the greatest likelihood of developing an AUD (p-values <0.01).
This study provides initial evidence that the association between the A118G SNP of the OPRM1 gene and risk of AUDs is moderated by modifiable factors. These results are limited, however, by the small sample size and require replication.