Several studies have suggested that the mu receptor may also mediate some of the hedonic and/or addictive effects of non-opioid drugs, such as alcohol [23,24]. Indirect support for this hypothesis is provided by studies demonstrating the efficacy of naltrexone for the treatment of alcohol dependence [25-31]. Further support is provided by studies evaluating associations between response to naltrexone pharmacotherapy for alcohol dependence and the presence of the A118G variant. In a study that combined data from three different clinical trials, Oslin and colleagues [32] demonstrated that carriers of the 118G allele had a significantly lower rate of relapse and a longer time to a return to heavy drinking when compared to those individuals who were homozygous for the 118A allele. This finding was not supported in the Veterans Affairs (VA) Cooperative Study where no significant interactions were found between naltrexone treatment response and any polymorphic variants at each of the three opioid receptor genes [33]. More recently, data from the Study for the Combined Pharmacotherapies and Behavioral Interventions for Alcohol Dependence (COMBINE) study demonstrated that treatment with naltrexone produced a
