Alcohol’s mechanism of action includes its effects on the brain’s “reward centers” in the ventral tegmental area (VTA) and nucleus accumbens via interactions with numerous neurotransmitter systems. As it relates to a person’s subjective response to alcohol, the endogenous opioid system is thought to partially mediate the reinforcing effects of alcohol in these brain regions (Gianoulakis, 2004; Koob and Kreek, 2007; Mague and Blendy, 2010). Specifically, acute alcohol administration acts on μ-opioid receptors in the VTA and nucleus accumbens, thereby increasing extracellular levels of dopamine in the mesolimbic pathway. The gene encoding the μ-opioid receptor (OPRM1) has received considerable attention as a neurological target for exogenous opioid and non-opioid substances. Studies have identified a nonsynonymous single nucleotide polymorphism (SNP) in OPRM1 (rs1799971; A118G) that causes the Asn40Asp substitution from asparagine to aspartic acid at a N-glycosylation site (Ray et al., 2012). Though findings from in vitro studies have been mixed (for a review, see Ray et al., 2012), the amino acid change brought on by the presence of the minor (Asp) G allele has been shown to triple the mu-opioid
