The behavioral and subjective consequences of possession of genetic variants that affect ADH enzymatic activity to increase the presence of acetaldehyde are acutely aversive in nature, including flushing, headache, tachycardia, and nausea. As a result, possession of the ADH1B-2 allele has been demonstrated to reduce the risk of AUDs in populations where the frequency of this allele is high, such as East Asians (Luczak et al. 2006; Thomasson et al. 1991; Whitfield 2002). In addition, even in populations where the allele frequency is lower, a protective effect has been demonstrated for individuals of European and African ancestry (Whitfield, 2002) and individuals of Jewish descent (Luczak et al., 2002; Hasin et al., 2002). Similarly, Edenberg et al. (2006) found that possession of the ADH1B-3 allele reduces the risk of alcoholism in African-Americans, although not in Europeans. Wall et al. (2003) found the ADH1B-3 allele had a protective effect among Southwest American Indians. With regard to ADH1C, there is evidence that the faster metabolism of alcohol (i.e., greater accumulation of acetaldehyde), mediated by the possession of the ADH1C-1 allele, has protective effects
