A similar pharmacogenetic effect of OPRD1^4 was observed for alcohol craving (Figure 4). In this model, there was no significant effect of OPRD1^4 (β = 0.36, SE = 0.32, t = 1.1, p > .01), but an effect of medication (β = 0.29, SE = 0.14, t = 2.11, p < 0.05), and a significant OPRD1^4 × medication interaction (β = −0.76, SE = 0.16, t = −4.76, p < 0.0001). Finally, there was an effect of BrAC (β = 0.27, SE = 0.045, t = 5.95, p < 0.001). There was no BrAC × medication interaction (p > 0.1), and thus this interaction term was not included in the above model. For this tSNP, A-allele carriers showed greater naltrexone-induced blunting of alcohol craving as compared to G-allele homozygotes. Controlling for the OPRM1 A118G SNP or restricting the sample to Whites only did not alter the significance of the OPRD1^4 pharmacogenetic effect. For OPRD1^4, there was no significant pharmacogenetic effect on sedation (β = 0.39, SE = 0.212, t = 1.84, p = 0.066). Models testing the other OPRD1 tSNPs (^1, ^2, ^3, ^5) yielded no significant pharmacogenetic effects on either subjective intoxication measure or craving (all ps > 0.01).
