Asian flush

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Alcohol flush reaction is a condition in which the body cannot break down ingested alcohol completely, due to a missense polymorphism that encodes the enzyme, acetaldehyde dehydrogenase (ALDH2) 1, normally responsible for breaking down acetaldehyde, a product of the metabolism of alcohol.2 Flushing, or blushing, is associated with the erythema (reddening caused by dilation of capillaries) of the face, neck, shoulder, and in some cases, the entire body after consumption of alcohol.

Contents

Mechanism/Symptoms

Ordinarily, alcohol dehydrogenase (ADH) is responsible for conversion of primary alcohols to aldehydes; aldehydes are then converted to carboxylic acids by aldehyde dehydrogenase (ALDH). In the case of ethanol, the alcohol found in alcoholic beverages, ethanol is converted first into acetaldehyde and then into acetic acid. Acetaldehyde is the most toxic of these three compounds, and is both a possible carcinogen and a major cause of hangovers; ethanol's toxicity is lower, and acetic acid is relatively harmless.

The result is the accumulation of acetaldehyde. Approximately half of people of Asian descent are considered to be sensitive to alcohol due to this condition. 3 Flushing, after consuming one or two alcoholic beverages, includes a range of symptoms: nausea, headaches, light-headedness, an increased pulse, occasional extreme drowsiness, and occasional skin swelling and itchiness. These unpleasant side effects often prevent further drinking that may lead to further inebriation, but the symptoms can lead to mistaken assumption that the people affected are more easily inebriated than others.

Mitigating the effects

Much anecdotal evidence suggests that ingestions of low doses of heartburn medicine, containing ranitidine or famotidine (such as Zantac or Pepcid AC), may be able to relieve the body of the symptoms if taken an hour before drinking.4

It is not known definitively why ranitidine and famotidine may, in some cases, but not all, help reduce the symptoms of the alcohol flush reaction.

One possible theory that may explain the effects of famotidine (and similar classed drugs) on the skin erythema or redness secondary to alcohol consumption is because the drugs are H2-antagonists or H2 antihistamines, which are used to treat peptic/gastric ulcers. In essence, if the "Asian flush" is an allergic reaction to the alcohol, then the mechanism of action of H2-antagonists can explain its effects on curtailing or decreasing the redness. However, H2-antagonists do not actually reduce blood concentrations of histamine, but rather works by reversing the effect of histamine on the H2 receptor, and so this theory is disputed.

Another theory, is that acetaldehyde causes the redness and vasodialation, and because the H2-antagonist class of medicine inhibits the ADH enzyme(the conversion from ethanol to acetaldehyde) both in the GI tract and in the liver5, the conversion happens at a much slower pace, reducing the effects acetaldehyde has on the drinker. The idea that acetaldehyde is the cause of the flush is also shown by the clinical use of Antabuse, which blocks the removal of acetaldehyde from the body via ALDH inhibition. The high acetaldehyde concentrations described share similarity to symptoms of the flush(flushing of the skin, accelerated heart rate, shortness of breath, throbbing headache, mental confusion).

Although many people with this condition view it as a lifetime inconvenience, some people have suggested that they can condition their body to be more tolerant of alcohol with repeated, moderate drinking, perhaps increasing the concentration of ALDH2 to metabolize acetaldehyde. Unfortunately, acetaldehyde is a known carcinogen; recent research suggests that alcohol flush-afflicted individuals consuming alcohol continually may be at a higher risk for alcohol-related diseases, such as liver and esophageal cancers and digestive tract cancer.3

Studies in rats have also shown that consumption of carbohydrates (glucose & fructose) significantly increase the metabolism of ethanol through a yet unknown pathway, and without affecting alcohol dehydrogenase activity.6

Other effects

Individuals who experience the alcohol flushing reaction may be less prone to alcoholism. Antabuse, a drug sometimes given as treatment alcoholism, works by inhibiting acetaldehyde dehydrogenase, causing a five to tenfold increase in the concentration of acetaldehyde in the body. The resulting irritating flushing reaction is intended to discourage alcoholics from drinking.7 8


Other similar conditions

  • Rosacea, also known as gin blossoms, is a chronic facial skin condition in which capillaries are excessively reactive, leading to redness from flushing or telangiectasia. Rosacea has been mistakenly attributed to alcoholism because of its similar appearance to the temporary flushing of the face that often accompanies the ingestion of alcohol.
  • Degreaser's flush -- a flushing condition arising from consuming alcohol shortly before or during inhalation of trichloroethylene (TCE), an organic solvent with suspected carcinogenic properties.
  • Carcinoid syndrome -- episodes of severe flushing precipitated by alcohol, stress and certain foods. May also be associated with diarrhea, wheezing and weight loss.

References

  1. ^ Xiao Q, Weiner H, Crabb DW (1996). "The mutation in the mitochondrial aldehyde dehydrogenase (ALDH2) gene responsible for alcohol-induced flushing increases turnover of the enzyme tetramers in a dominant fashion". J. Clin. Invest. 98 (9): 2027–32. doi:10.1172/JCI119007. PMID 8903321. 
  2. ^ Ohta S, Ohsawa I, Kamino K, Ando F, Shimokata H (2004). "Mitochondrial ALDH2 deficiency as an oxidative stress". Ann. N. Y. Acad. Sci. 1011: 36–44. PMID 15126281, http://www.annalsnyas.org/cgi/content/abstract/1011/1/36. 
  3. ^ a b "Can heavy alcohol use lead to some kinds of cancer?". Science Blog.
  4. ^ Haynie D. "Asian party-goers strive to get rid of that 'glow' often caused by the first drink".
  5. ^ Joan Caballería, et al. (1991). "Effects of H2-receptor antagonists on gastric alcohol dehydrogenase activity". Digestive Diseases and Sciences 36 (12): 1673-1679. doi:10.1007/BF01296608. 
  6. ^ Keegan A, Batey R (1993). "Dietary carbohydrate accelerates ethanol elimination, but does not alter hepatic alcohol dehydrogenase". Alcohol. Clin. Exp. Res. 17 (2): 431–3. PMID 8488989, http://www.blackwell-synergy.com/openurl?genre=article&sid=nlm:pubmed&issn=0145-6008&date=1993&volume=17&issue=2&spage=431. 
  7. ^ "Disulfiram". MedlinePlus Drug Information.
  8. ^ Toxicity, Disulfiram at eMedicine

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  • This page was last modified on 20 November 2008, at 07:52.

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