Alcohol tolerance

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Beer Street and Gin Lane by William Hogarth, 1751, detailing the Gin Craze in UK cities during the early Industrial Revolution.

Alcohol tolerance refers to the bodily responses to the functional effects of ethanol in alcoholic beverages. This includes direct tolerance, speed of recovery from insobriety and resistance to the development of alcoholism.

Consumption-induced tolerance[edit]

Alcohol tolerance is increased by regular drinking.[1] This reduced sensitivity requires that higher quantities of alcohol be consumed in order to achieve the same effects as before tolerance was established. Alcohol tolerance may lead to (or be a sign of) alcohol dependency.[1]

Heavy alcohol consumption over a period of years can lead to "reverse tolerance". A liver can be damaged by chronic alcohol use, 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 blood alcohol concentration (BAC) and more rapid intoxication.

Physiology of alcohol tolerance[edit]

Alcohol dehydrogenase is a dimeric zinc metalloenzyme that catalyzes the reversible oxidation of alcohols to aldehydes

Direct alcohol tolerance is largely dependent on body size. Large-bodied people will require more alcohol to reach insobriety than lightly built people.[citation needed] Thus men, being larger than women on average, will have a higher alcohol tolerance. The alcohol tolerance is also 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 levels are less frequent in alcoholics than in nonalcoholics and, alongside other symptoms, can indicate various forms of liver disease.[citation needed] Furthermore, among alcoholics, the carriers of this atypical enzyme consume lower ethanol doses, compared to the individuals without the allele.

Alcohol tolerance in different ethnic groups[edit]

The tolerance to alcohol is not equally distributed throughout the world's population, and genetics of alcohol dehydrogenase indicate resistance has arisen independently in different cultures.[2] In North America, Native Americans have the highest probability of developing alcoholism compared to Europeans and Asians.[3][4][5][6] The high legal drinking age has been cited as a causal factor for alcohol abuse.[7]

Higher body masses and the prevalence of high levels of alcohol dehydrogenase in an individual increase alcohol tolerance.[8][9]

Not all differences in tolerance can be traced to biochemistry.[10] Differences in tolerance levels are also influenced by socio-economic and cultural difference including diet, average body weight and patterns of consumption.[11][12]

An estimated one out of twenty people have an alcohol flush reaction. It is not in any way an indicator for the drunkenness of an individual.[13][14] It is colloquially known as "Face Flush", a condition where the body metabolizes alcohol nearly 100-times more efficiently into acetaldehyde, a toxic metabolite.[15][16] Flushing, or blushing, is associated with the erythema (reddening caused by dilation of capillaries) of the face, neck, and shoulder, after consumption of alcohol.[17]


  1. ^ a b "Alcohol and Tolerance". National Institute on Alcohol Abuse and Alcoholism (NIAAA), Alcohol Alert (28). April 1995. Retrieved 2009-08-13. 
  2. ^ Osier, Michael V.; Pakstis, Andrew J.; Soodyall, Himla; Comas, David; Goldman, David; Odunsi, Adekunle; Okonofua, Friday; Parnas, Josef; et al. (2002). "A Global Perspective on Genetic Variation at the ADH Genes Reveals Unusual Patterns of Linkage Disequilibrium and Diversity". American Journal of Human Genetics 71 (1): 84–99. doi:10.1086/341290. PMC 384995. PMID 12050823. 
  3. ^
  4. ^ Mail & al. (eds., 2002): Alcohol Use Among American Indians and Alaska Natives: Multiple Perspectives on a Complex Problem. NIAAA Research Monograph No. 37. Bethesda, MD: National Institute on Alcohol Abuse and Alcoholism[page needed]
  5. ^ Caetano, Raul; Clark, Catherine L (1998). "Trends in Alcohol-Related Problems among Whites, Blacks, and Hispanics: 1984-1995". Alcoholism: Clinical and Experimental Research 22 (2): 534. doi:10.1111/j.1530-0277.1998.tb03685.x. 
  6. ^ "Ethnicity and Health Disparities in Alcohol Research". 
  7. ^
  8. ^ Yin, S. -J.; Cheng, T. -C.; Chang, C. -P.; Chen, Y. -J.; Chao, Y. -C.; Tang, H. -S.; Chang, T. -M.; Wu, C. -W. (1988). "Human stomach alcohol and aldehyde dehydrogenases (ALDH): A genetic model proposed for ALDH III isozymes". Biochemical Genetics 26 (5–6): 343–60. doi:10.1007/BF00554070. PMID 3214414. 
  9. ^ Fenna, D; Schaefer, O; Mix, L; Gilbert, JA (1971). "Ethanol metabolism in various racial groups". Canadian Medical Association journal 105 (5): 472–5. PMC 1931291. PMID 5112118. 
  10. ^ Bennion L., Li T. K. (1976). "Alcohol metabolism in american indian and whites". New England Journal of Medicine 294: 9–13. doi:10.1056/nejm197601012940103. 
  11. ^ Waldram, J. B., Herring, A., & Young, K. (1995). Aboriginal Health in Canada: Historical, Cultural, and Epidemiological Perspectives. Toronto: University of Toronto Press Book online
  12. ^ Saggers, S. & Gray, D. (1998b). Dealing with Alcohol: Indigenous Usage in Australia, New Zealand and Canada. Cambridge: Cambridge University Press[page needed]
  13. ^
  14. ^
  15. ^ Eng, MY; Luczak, SE; Wall, TL (2007). "ALDH2, ADH1B, and ADH1C genotypes: A literature review". Alcohol research & health 30 (1): 22–7. PMID 17718397. 
  16. ^ Peng, Yi; Shi, Hong; Qi, Xue-bin; Xiao, Chun-jie; Zhong, Hua; Ma, Run-lin Z; Su, Bing (2010). "The ADH1B Arg47His polymorphism in farming populations and expansion of rice domestication in history". BMC Evolutionary Biology 10: 15. doi:10.1186/1471-2148-10-15. PMC 2823730. PMID 20089146. Lay summaryScienceNow (January 20, 2010). 
  17. ^ Ohta, Shigeo; Ohsawa, Ikuroh; Kamino, Kouzin; Ando, Fujiko; Shimokata, Hiroshi (2004). "Mitochondrial ALDH2 Deficiency as an Oxidative Stress". Annals of the New York Academy of Sciences 1011: 36–44. doi:10.1196/annals.1293.004. PMID 15126281. 


Further reading[edit]