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Alcohol tolerance refers to a decreased response to the effects of ethanol in alcoholic beverages. This reduced sensitivity requires that higher quantities of alcohol be consumed in order to achieve the same effects as before tolerance began to occur.

Laws establishing maximum blood alcohol concentration (BAC) levels for legal operation of motor vehicles do not take into consideration alcohol tolerance. In one study, a group of alcoholics whose BAC was brought to .10, only 24% showed any clinical signs of impairment. Conversely, a person who drinks only rarely may be dangerously impaired even when his/her BAC is still under the legal limit.

The alcohol tolerance is connected with activity of Alcohol dehydrogenases (a group of enzymes responsible for the breakdown of alcohol) in the liver, and in the bloodstream. High level of Alcohol dehydrogenase activity results in fast transformation of ethanol to more toxic acetaldehyde. Such atypical alcohol dehydrogenase is less frequent in alcoholics than in nonalcoholics. Furthermore, among alcoholics, the carriers of this atypical enzyme consume lower ethanol doses, compared to the individuals without the allele.

Some persons of South-East Asian and near-Eastern descent have an Alcohol flush reaction, a condition where the body cannot break down ingested alcohol completely. Flushing, or blushing, is associated with the erythema (reddening caused by dilation of capillaries) of the face, neck, and shoulder, after consumption of alcohol. [1]

Heavy alcohol consumption over a period of years can lead to "reverse tolerance". A liver can be damaged by alcohol abuse leading to a buildup of fat and scar tissue. The reduced ability of such a liver to metabolize or break down alcohol means that small amounts can lead to a high BAC and resulting intoxication.

ReferencesEdit

  • Carroll, Charles R. Drugs in Modern Society. NY: McGraw-Hill, 2000 (fifth ed.).
  • Chesher, G., & Greeley, J. Tolerance to the effects of alcohol. Alcohol, Drugs and Driving, 1992, 8(2):93-106.
  • Osier M., Pakstis A.J., Kidd J.R., Lee J.F., Yin S.J., Ko H.C., Edenberg H.J., Lu R.B., Kidd K.K. Linkage disequilibrium at the ADH2 and ADH3 loci and risk of alcoholism // Am. J. Hum. Genet. 1999, 6: 1147-1157.
  • Muramatsu T., Zu-Cheng W., Yi-Ru F., Kou-Bao H., Heqin Y., Yamada K., Higuchi S., Harada S., Kono H. Alcohol and aldehyde dehydrogenase genotypes and drinking behavior of Chinese living in Shanghai // Hum. Genet. 1995,96: 151-154.
  • Neumark Y.D., Friedlander Y., Thomasson H.R., Li T.K. Association of the ADH2*2 allele with reduced ethanol consumption in Jewish men in Israel: a pilot study // J. Stud. Alcohol. 1998, 59: 133-139.
  • Osier M.V., Pakstis A.J., Soodyall H., Comas D., Goldman D., Odunsi A., Okonofua F., Parnas J., Schulz L.O., Bertranpetit J., Bonne-Tamir B., Lu R.B., Kidd J.R., Kidd K.K. A global perspective on genetic variation at the ADH genes reveals unusual patterns of linkage disequilibrium and diversity // Am. J. Hum. Genet. 2002,71: 84-99.
  • Borinskaya S. A., Gasemianrodsari F., Kalyina N. R., Sokolova M. V., Yankovsky N. K. Polymorphism of alcohol dehydrogenase gene ADH1B in eastern Slavic and Iranian-speaking populations. Genetika. 2005, 41: 1563-1566 (in Russian).

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