Following consumption, alcohol is primarily metabolized by alcohol dehydrogenase (ADH) enzymes in the liver, which oxidize ethanol into acetaldehyde. There are seven known genes that code for ADH enzymes. The majority of research has examined the class I ADH genes (ADH1A, ADH1B, ADH1C). Two of these (ADH1B and ADH1C) have been found to exhibit variants that encode for enzymes with different kinetic properties (Edenberg, 2007). Acetaldehyde is, in turn, broken down into acetate by aldehyde dehydrogenase (ALDH). There are also several molecular forms of ALDH. The gene for mitochondrial ALDH (ALDH2) has been found to have two allele variants and three variants have been identified in the promoter region of the cytosolic isoform ALDH1A1. Genes that encode for ADH enzymes that more rapidly metabolize alcohol, or for ALDH enzymes that are less efficient in the breakdown of acetaldehyde, have been found to be associated with lower risk for alcohol dependence and heavy drinking. The hypothesized mechanism for this protection is higher transient levels of acetaldehyde, which can produce a stronger response to alcohol, including a “flushing reaction” (see Wall, 2005
