Twin and adoption studies have shown that the heritability of alcohol dependence (AD) may be as high as 50–60% (Kendler et al., 1997; Prescott and Kendler, 1999). However, the genetic architecture of AD is complex and remains largely elusive. In recent years, risk gene identification has progressed through the use of intermediate phenotypes for alcohol use disorders (Ducci and Goldman, 2008; Hines et al., 2005), including the subjective effects of alcohol (Ray et al., 2010b). To that end, the endogenous opioid system has been implicated in the pathophysiology of alcoholism as it modulates the reinforcing effects of alcohol via activation of mu opioid receptors in the ventral tegmental area and nucleus accumbens, which in turn enhances extracellular concentrations of dopamine in the mesolimbic pathway (Gianoulakis, 2009; Koob and Kreek, 2007).
