AUDs are heterogeneous in etiology, pathophysiology, and response to treatment. In addition to environmental factors, AUDs are genetically complex, without an obvious pattern of Mendelian inheritance, and are moderately heritable as observed from family-based twin studies (~49%) (Kendler, Heath, Neale, Kessler, & Eaves, 1992; McGue, Pickens, & Svikis, 1992; Reed, Page, Viken, & Christian, 1996; Heath et al., 1997; Prescott & Kendler, 1999; True et al., 1999; Verhulst, Neale, & Kendler, 2015). It is likely that a combination of genetic variants and environment, each responsible for a small effect, are involved. Genome-wide association studies (GWAS) have identified several risk loci for AUDs (Dick et al., 2006; Edenberg, 2007; Hart & Kranzler, 2015). One variant associated with AUDs is a non-synonymous single nucleotide polymorphism (SNP) in OPRM1, which encodes the μ-opioid receptor (MOR), A118G (rs1799971; Asn40Asp or N40D), although this remains controversial (LaForge, Yuferov, & Kreek, 2000; Mague & Blendy, 2010; Sloan et al., 2018). The A118 OPRM1 major allele that codes for the MOR (N40) is found at the highest frequency in individuals of all ethnic backgrounds, and the minor
