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Alcohol Dependence Candidate Gene Studies

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Influence of genetic polymorphism at some loci encoding the acetaldehyde dehydrogenases and ADHs on risk of AD in some populations is well established. The mechanism for these effects is very clear. Ethanol is metabolized to acetaldehyde by ADHs, with the most important loci for AD research being ADH1B (previously known as ADH2) and ADH1C (previously known as ADH3). Acetaldehyde is metabolized primarily by acetaldehyde dehydrogenases, the relevant locus for which is ALDH2. Acetaldehyde, a toxic intermediate in the metabolic pathway, produces a "flushing reaction" characterized by a set of uncomfortable symptoms including flushing, lightheadedness, palpitations, and nausea. Thus, deviation from the normal metabolism of ethanol that results in increased exposure to acetaldehyde, such as that produced by the medication disulfiram or that which occurs due to genetic variation, produces an aversive effect of ethanol consumption, which might decrease the behavior and thereby the risk of AD (Goedde et al. 1979). A genetic variant that greatly reduces or eliminates acetaldehyde dehydrogenase function, thereby decreasing the elimination of acetaldehyde (which occurs mostly in Asian populations), has long been known to be protective against AD; ADH variants that increase function, yielding elevated acetaldehyde concentrations, may also be protective (e.g., see Hasin et al. 2002; Konishi et al. 2003; Thomasson et al. 1991).

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