Alcohol dependence (AD) is extremely costly to individuals and to society in the United States and throughout the world, contributing to morbidity and mortality and a host of economic, interpersonal, and societal problems. Although until recently the only genes established to affect risk for AD were those encoding several alcohol metabolizing enzymes, there are now several other genes that can be regarded as confirmed risk loci (GABRA2; Edenberg et al. 2004; Covault et al. 2004; Lappalainen et al. 2005; Fehr et al. 2006), or strong candidates based on published data (e.g., CHRM2, Wang et al. 2004; Luo et al. 2005a, b, c, GABRG1, Covault et al. 2008; Enoch et al. 2009). Although the mechanism of action of the effects of alcohol-metabolizing enzymes on AD risk is thought to be well understood, we are still in the early stages of understanding the physiology of other risk loci. Further, it is clear that only a small number of the many genes that influence risk for AD have been identified. However, genomewide association and other new methodologies hold the promise of identifying a greater set of AD susceptibility loci, as for many other complex traits.
