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Keywords:

  • Adolescents;
  • OPRM1 ;
  • Alcohol;
  • Parental Monitoring;
  • Deviant Peer Affiliation

Background

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.

Methods

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.

Results

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).

Conclusions

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.