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This pathway probably evolved as a detoxification mechanism for environmental alcohols. However, with the consumption of large amounts of ethanol, the oxidation of ethanol can become a major energy source and, particularly in the liver, interferes with the metabolism of other nutrients. Polymorphic variants of the genes for these enzymes encode enzymes with altered kinetic properties. The pathophysiological effects of these variants may be mediated by accumulation of acetaldehyde; high-activity ADH variants are predicted to increase the rate of acetaldehyde generation, while the low-activity ALDH2 variant is associated with an inability to metabolize this compound. The effects of acetaldehyde may be expressed either in the cells generating it, or by delivery of acetaldehyde to various tissues by the bloodstream or even saliva. Inheritance of the high-activity ADH \u03b22, encoded by the<jats:italic>ADH2*2<\/jats:italic>gene, and the inactive<jats:italic>ALDH2*2<\/jats:italic>gene product have been conclusively associated with reduced risk of alcoholism. This association is influenced by gene\u2013environment interactions, such as religion and national origin. The variants have also been studied for association with alcoholic liver disease, cancer, fetal alcohol syndrome, CVD, gout, asthma and clearance of xenobiotics. The strongest correlations found to date have been those between the<jats:italic>ALDH2*2<\/jats:italic>allele and cancers of the oro-pharynx and oesophagus. It will be important to replicate other interesting associations between these variants and other cancers and heart disease, and to determine the biochemical mechanisms underlying the associations.<\/jats:p>","DOI":"10.1079\/pns2003327","type":"journal-article","created":{"date-parts":[[2006,5,9]],"date-time":"2006-05-09T12:07:47Z","timestamp":1147176467000},"page":"49-63","source":"Crossref","is-referenced-by-count":438,"title":["Overview of the role of alcohol dehydrogenase and aldehyde dehydrogenase and their variants in the genesis of alcohol-related pathology"],"prefix":"10.1017","volume":"63","author":[{"given":"David 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