the current study were genotyped for both DAT1 (A9 vs A10) and OPRM1 (AA vs *G) genotypes after completion of the alcohol sensitivity sessions. We opted to study social drinkers rather than persons with AUD to minimize the effects of heavy alcohol exposure on outcome measures. Our apriori hypotheses were 1) DAT1 A9 carriers would show greater negative subjective effects of alcohol than A10 carriers independent of OPRM1 genotype, 2) that increased positive and stimulant subjective responses to alcohol in OPRM1 *G carriers would be dependent upon DAT1 A9 vs. A10 genotype. Since alcohol sensitivity differs depending on intensity and frequency of alcohol drinking, we also examined whether there were independent or epistatic genotype effects on self-reported measures of drinking outside the laboratory.
