Alcohol and Facial Flushing

Genetic variations in ADH and ALDH may explain why particular individuals develop some of the pathologies of alcoholism and others do not. For example, up to 50% of Orientals have a genetically determined reduction in ALDH2 activity ('flushing' phenotype). As a result, acetaldehyde accumulates after ethanol administration, with plasma levels up to 20 times higher in people with ALDH2 deficiency. Even small amounts of alcohol produce a rapid facial flush, tachycardia, headache, and nausea. Acetaldehyde partly acts through cate-cholamines, although other mediators have been implicated, including histamine, bradykinin, prostaglandin, and endogenous opioids.

This is similar to the disulfiram reaction due to the rise of acetaldehyde after inhibition of ALDH. Disulfiram is used therapeutically to encourage abstinence in alcohol rehabilitation programs. The aversive effects of acetaldehyde may reduce the development of alcoholism and the incidence of cirrhosis in 'flushers.' However, some alcoholics with ALDH2 deficiency and, presumably, higher hepatic acetaldehyde levels develop alcoholic liver disease at a lower intake of ethanol than controls.

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