a good clinical outcome to naltrexone + MM, as compared to 55% of homozygotes for the A allele; and the groups did not differ in their response to MM plus placebo (Anton et al., 2008). And overall, naltrexone was superior to placebo in the COMBINE Study when delivered in combination with MM (Anton et al., 2006). However, one recent study did not find support for the moderating role of OPRM1 genotype on clinical response to naltrexone in a sample of male veterans (Gelernter et al., 2007). Moreover, a placebo-controlled laboratory study of naltrexone suggested that individuals who were carriers of the G allele of the OPRM1 gene showed significantly greater naltrexone-induced blunting of alcohol “high,” as compared to individuals who were homozygote for the A allele (Ray & Hutchison, 2007). These findings suggest that the differential clinical response to naltrexone, discussed above, may be due to differential blunting of the subjective experience of alcohol reward as a function of genotype, which in turn suggests a biobehavioral mechanism for this important pharmacogenetic relationship. Future studies are certainly needed to probe for this relationship before individualized treatment approaches may be implemented, including consideration of issues such as the differential allele frequencies of
