controlling for multiple testing using the Bonferroni correction (adjusted α = 0.025). As hypothesized, decomposition of theOPRM1 × parental monitoring interaction indicated that carriers of the G allele who reported relatively high levels parental monitoring were least likely to develop an AUD. Conversely, youth with a copy of the G allele and relatively high levels of deviant peer affiliation were more likely to develop an AUD than G allele carriers with relatively low levels of deviant peer affiliation. Decomposition of the effect of sex showed that more girls (26%) meet diagnostic criteria for an AUD than boys (9%).
