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.[citation needed]

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.[2] 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.[3] Furthermore, among alcoholics, the carriers of this atypical enzyme consume lower ethanol doses, compared to the individuals without the allele.

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.[4][5] A mild flushing reaction occurs when the body metabolizes alcohol more quickly into acetaldehyde, a toxic metabolite.[3][6] A more severe flushing reaction occurs when the body metabolizes the acetaldehyde more slowly, generally due to an inactive aldehyde dehydrogenase enzyme. Both of those conditions -- faster conversion of alcohol to acetaldehyde and slower removal of acetaldehyde -- reduce the risk for excessive drinking and alcohol dependence.[3]

Alcohol tolerance in different ethnic groups[edit]

To engage in alcohol consumption and development of alcoholism appear to be common to primates, and is not a specific human phenomenon.[7] Humans have access to alcohol on far greater quantity than non-human primates, and the availability increased particularly with the development of agriculture.[8] The tolerance to alcohol is not equally distributed throughout the world's population.[9] Genetics of alcohol dehydrogenase indicate resistance has arisen independently in different cultures.[10] In North America, Native Americans have the highest probability of developing alcoholism compared to Europeans and Asians.[11][12][13][14] Different alcohol tolerance also exists within Asian groups, such as between Chinese and Koreans.[15] The health benefit of a modest alcohol consumption reported in people of European descent appear not to exist among people of African descent.[16]

Higher body masses and the prevalence of high levels of alcohol dehydrogenase in an individual increase alcohol tolerance, and both adult weight and enzymes vary with ethnicity.[17][18] Not all differences in tolerance can be traced to biochemistry however.[19] Differences in tolerance levels are also influenced by socio-economic and cultural difference including diet, average body weight and patterns of consumption.[20][21]

Footnotes[edit]

  1. ^ a b "Alcohol and Tolerance". National Institute on Alcohol Abuse and Alcoholism (NIAAA), Alcohol Alert (28). April 1995. Retrieved 2009-08-13.
  2. ^ "Factors That Affect How Alcohol is Absorbed & Metabolized". Student affairs - Office of Alcohol Policy and Education. Stanford University. Retrieved 26 May 2018.
  3. ^ a b c Hurley TD, Edenberg HJ. (2012) Genes encoding enzymes involved in ethanol metabolism. Alcohol Res. 34(3): 339-344. PMID 23134050
  4. ^ "Myth or reality? The Asian alcohol 'gene' explained". Difford's Guide. September 10, 2013. Archived from the original on 2013-10-22. Retrieved 2013-10-22.
  5. ^ "Identifying the Signs of Intoxication" (PDF). Government of Western Australia. December 2010. Archived from the original (PDF) on March 27, 2011.
  6. ^ Eng, MY; Luczak, SE; Wall, TL (2007). "ALDH2, ADH1B, and ADH1C genotypes: A literature review". Alcohol Research & Health. 30 (1): 22–7. PMC 3860439. PMID 17718397.
  7. ^ Juarez, J; Guzman-Flores, C; Ervin, FR; Palmour, RM (December 1993). "Voluntary alcohol consumption in vervet monkeys: individual, sex, and age differences". Pharmacology Biochemistry and Behavior. 46 (4): 985–8. PMID 8309979.
  8. ^ Curry, A. "Our 9,000-Year Love Affair With Booze". National Geographic. Retrieved 26 May 2018.
  9. ^ Chan, AW (1986). "Racial differences in alcohol sensitivity". Alcohol and alcoholism (Oxford, Oxfordshire). 21 (1): 93–104. PMID 2937417.
  10. ^ 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.
  11. ^ "Alcohol Use Disorder". NY Times. 2013. Retrieved July 21, 2016.
  12. ^ 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]
  13. ^ 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): 534–538. doi:10.1111/j.1530-0277.1998.tb03685.x.
  14. ^ Karen Chartier; Raul Caetano. "Ethnicity and Health Disparities in Alcohol Research".
  15. ^ Duranceaux & al. (2008). "Ethnic differences in level of response to alcohol between Chinese Americans and Korean Americans". J Stud Alcohol Drugs. 69 (2): 227–234. PMID 18299763.
  16. ^ Jackson, Chandra L.; Hu, Frank B.; Kawachi, Ichiro; Williams, David R.; Mukamal, Kenneth J.; Rimm, Eric B. (July 2015). "Black–White Differences in the Relationship Between Alcohol Drinking Patterns and Mortality Among US Men and Women". American Journal of Public Health. 105 (S3): S534–S543. doi:10.2105/AJPH.2015.302615. PMC 4455501. Retrieved 26 May 2018.
  17. ^ 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.
  18. ^ 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.
  19. ^ Bennion L.; Li T. K. (1976). "Alcohol metabolism in American Indians and whites". New England Journal of Medicine. 294 (1): 9–13. doi:10.1056/nejm197601012940103. PMID 1244489.
  20. ^ Waldram, J. B.; Herring, A. & Young, K. (1995). Aboriginal Health in Canada: Historical, Cultural, and Epidemiological Perspectives. Toronto: University of Toronto Press.
  21. ^ Saggers, S. & Gray, D. (1998b). Dealing with Alcohol: Indigenous Usage in Australia, New Zealand and Canada. Cambridge: Cambridge University Press[page needed]

References[edit]

Further reading[edit]