Pharmacogenetic studies of the A118G SNP have found that G-allele carriers exhibit greater naltrexone-induced blunting of alcohol high (Ray and Hutchison, 2007) and lower relapse rates in clinical trials of naltrexone for alcoholism (Anton et al., 2008, Oslin et al., 2003). A recent study in Asian Americans found that G-allele carriers reported greater alcohol-induced sedation, subjective intoxication, and lower alcohol craving while on naltrexone versus placebo, and as compared to A-allele homozygotes (Ray et al., 2012b). Some studies, however, have failed to support this pharmacogenetic effect (Coller et al., 2011, Gelernter et al., 2007, Tidey et al., 2008). These null findings may be due, in part, to the relatively small effect size of naltrexone and its interaction with OPMR1 genotype compared to more robust psychosocial interventions, high type II error, and study design limitations as several did not prospectively genotype participants prior to medication randomization (for review see Ray et. al, 2012a).
