on the descending limb. DAT1 A9 and OPRM1*G carriers, who showed higher SHAS scores and greater negative effects of alcohol when compared to other genotype subgroups, would be at lower risk for AUD based on both the LLR and DM models. We did not, however, detect genotype differences for stimulation or positive subjective effects of alcohol, as would be predicted by the DM. This may reflect the quantitative and qualitative differences in stimulation and positive subjective effects in light/moderate drinkers vs. heavy drinkers as proposed by Holdstock and colleagues (2000). Following administration of 0.6 or 0.8 g/kg alcohol, light/moderate drinkers report greater negative effects and more sedation when compared to heavy drinkers, despite similar BAC (peak 0.06 and 0.08 g/dL). In this group of light/moderate social drinkers, the OPRM1 A118G SNP interacts with the DAT1 A9 vs. A10 allele to determine the sedative and negative effects of alcohol and drinking.
