Of the two OPRK1 tSNPs examined, one marker (OPRK1^2, rs997917) showed a significant effect on alcohol-induced sedation. Specifically, there was no significant effect of OPRK1^2 genotype (β = −0.36, SE = 0.21, t = −1.62, p > .05), an effect of medication (β = −0.39, SE = 0.13, t = −2.90, p < .01), and an OPRK1^2 × medication interaction (β = 0.63, SE = 0.182, t = 3.43, p < .001). There was also an effect of rising BrAC (β = 0.52, SE = 0.08, t = 6.46, p < 0.0001). There was no interaction between BrAC and medication (p > 0.1) and this interaction term was not included in the model reported above. As shown in Figure 2, individuals who were homozygous for TT reported reduced feelings of alcohol sedation on naltrexone versus placebo, and as compared to C allele carriers. Controlling for the OPRM1 A118G SNP did not alter the significance of the pharmacogenetic effect reported above. However, when the model was reexamined among Whites only, the OPRK1^2 × medication interaction was reduced to a trend level of significance (β = 0.26, SE = 0.5, t = 1.74, p =0.083).
