this is especially important with regard to our findings on peer affiliation. Such associations could have important implications. For example, it may be that adolescent carriers of the G allele are more susceptible to developing an AUD when parental monitoring is low compared to youth who are homozygous for the A allele. Alternatively, carriers of the G allele may evoke lower levels of parental monitoring, which in turn set the stage for these youth to develop an AUD. The first example suggests that carriers of the G allele might benefit disproportionately from interventions aimed at increasing parental monitoring. In the second example, however, the key mechanism of risk involves parental monitoring and not direct genetic effects on alcohol outcomes, and therefore interventions would be appropriately aimed at all youth with low levels of parental monitoring, regardless of genotype. While our findings provide initial evidence of interplay between OPRM1 genotypes and environmental variables, elucidating the precise nature of these relationships is an important area for future research.
