Alcohol tolerance
Alcohol tolerance refers to the bodily responses to the functional effects of
Consumption-induced tolerance
Alcohol tolerance is increased by regular drinking.
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.
Physiology of alcohol tolerance
Direct alcohol tolerance is largely dependent on body size. Large-bodied people will require more alcohol to reach insobriety than lightly built people.[4] Thus, men, being larger than women on average, will typically 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 non-alcoholics.[5] Furthermore, among alcoholics, the carriers of this atypical enzyme consume lower ethanol doses, compared to the individuals without the allele.[citation needed]
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.[6][7] A mild flushing reaction occurs when the body metabolizes alcohol more quickly into acetaldehyde, a toxic metabolite.[5][8] 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.[5]
Alcohol tolerance in different ethnic groups
To engage in alcohol consumption and the development of an alcohol use disorder appear to be common to
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.[19][20] Not all differences in tolerance can be traced to biochemistry, however.[21] Differences in tolerance levels are also influenced by socio-economic and cultural difference including diet, average body weight and patterns of consumption.[22][23]
Footnotes
- ^ a b "Alcohol and Tolerance". National Institute on Alcohol Abuse and Alcoholism (NIAAA), Alcohol Alert (28). April 1995. Retrieved 2009-08-13.
- ^ "Alcohol-Induced Liver Disease". UC San Diego Health. Retrieved 4 October 2020.
- PMID 20840199.
- ^ "Factors That Affect How Alcohol is Absorbed & Metabolized". Student affairs - Office of Alcohol Policy and Education. Stanford University. Retrieved 26 May 2018.
- ^ PMID 23134050.
- ^ "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.
- ^ "Identifying the Signs of Intoxication" (PDF). Government of Western Australia. December 2010. Archived from the original (PDF) on March 27, 2011.
- PMID 17718397.
- S2CID 33697201.
- ISSN 1464-3502.
- PMID 2937417.
- PMID 12050823.
- ^ "Alcohol Use Disorder". NY Times. 2013. Retrieved July 21, 2016.
- ^ 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]
- PMID 9581665.
- ^ Karen Chartier; Raul Caetano. "Ethnicity and Health Disparities in Alcohol Research".
- PMID 18299763.
- PMID 25905819.
- S2CID 9315241.
- PMID 5112118.
- PMID 1244489.
- ISBN 9780802085795.
- ^ Saggers, S. & Gray, D. (1998b). Dealing with Alcohol: Indigenous Usage in Australia, New Zealand and Canada. Cambridge: Cambridge University Press[page needed]
References
- Carroll, Charles R. Drugs in Modern Society . NY: McGraw-Hill, 2000 (fifth ed.).
- Chesher, G.; Greeley, J. (1992). "Tolerance to the effects of alcohol". Alcohol, Drugs and Driving. 8 (2): 93–106.
- Osier, M; Pakstis, AJ; Kidd, JR; Lee, JF; Yin, SJ; Ko, HC; Edenberg, HJ; Lu, RB; Kidd, KK (1999). "Linkage disequilibrium at the ADH2 and ADH3 loci and risk of alcoholism". American Journal of Human Genetics. 64 (4): 1147–57. PMID 10090900.
- Muramatsu, T; Wang, ZC; Fang, YR; Hu, KB; Yan, H; Yamada, K; Higuchi, S; Harada, S; Kono, H (1995). "Alcohol and aldehyde dehydrogenase genotypes and drinking behavior of Chinese living in Shanghai". Human Genetics. 96 (2): 151–4. S2CID 1624596.
- Neumark, YD; Friedlander, Y; Thomasson, HR; Li, TK (1998). "Association of the ADH2*2 allele with reduced ethanol consumption in Jewish men in Israel: A pilot study". Journal of Studies on Alcohol. 59 (2): 133–9. PMID 9500299.
- Borinskaya, S. A.; Gasemianrodsari, F.; Kalyina, N. R.; Sokolova, M. V.; Yankovsky, N. K. (2005). "Polymorphism of Alcohol Dehydrogenase Gene ADH1B in Eastern Slavic and Iranian-Speaking Populations". Russian Journal of Genetics. 41 (11): 1291–4. PMID 16358724.
- Borinskaya, Svetlana; Kal'Ina, Nina; Marusin, Andrey; Faskhutdinova, Gulnaz; Morozova, Irina; Kutuev, Ildus; Koshechkin, Vladimir; Khusnutdinova, Elza; et al. (2009). "Distribution of the Alcohol Dehydrogenase ADH1B∗47His Allele in Eurasia". American Journal of Human Genetics. 84 (1): 89–92, author reply 92–4. PMID 19124091.
- Li, Hui; Borinskaya, Svetlana; Yoshimura, Kimio; Kal’Ina, Nina; Marusin, Andrey; Stepanov, Vadim A.; Qin, Zhendong; Khaliq, Shagufta; et al. (2009). "Refined Geographic Distribution of the Oriental ALDH2*504Lys (nee 487Lys) Variant". Annals of Human Genetics. 73 (3): 335–45. PMID 19456322.
Further reading
- Caetano R, Clark CL, Tam T (1998). "Alcohol consumption among racial/ethnic minorities: theory and research" (PDF). Alcohol Health Res World. 22 (4): 233–41. PMID 15706749. Archived from the original(PDF) on June 16, 2015.