Alcohol Flush Reaction & Genetics

How it works

When we drink alcohol, a toxin called acetaldehyde is produced as the body breaks down the alcohol. The body then clears out this harmful toxin by breaking it down further. In people who experience the alcohol flush reaction, their bodies have a harder time clearing out the acetaldehyde, so it builds up.

The genetic link

A variant in the ALDH2 gene can cause the alcohol flush reaction. This gene contains instructions for making a protein that helps the body process alcohol. In people with the ALDH2 genetic variant, this enzyme is less efficient at clearing away acetaldehyde than in people without the variant, which can result in the alcohol flush reaction.

The alcohol flush variant is most common in Eastern Asia (43%), South-Eastern Asia (18%), and Central Asia (2.7%)

Did you know?

Scientists believe that the alcohol flush variant in the 23andMe Alcohol Flush Reaction report first appeared in ancient China due to a random genetic mutation, and spread to neighboring regions as people migrated. It’s very rare for people who don’t have East Asian ancestry to carry the variant, though it does happen.

Explore more

Does your favorite craft beer or cocktail make you blush? 23andMe’s Health + Ancestry Service can help you uncover more. Order a kit to learn whether you have a genetic variant that makes you more likely to flush after drinking alcohol.

Health + Ancestry Service Kit

Health + Ancestry Service

Learn more

References

Brooks PJ et al. (2009). “The alcohol flushing response: an unrecognized risk factor for esophageal cancer from alcohol consumption.” PLoS Med. 6(3):e50.

Crabb DW et al. (1989). “Genotypes for aldehyde dehydrogenase deficiency and alcohol sensitivity. The inactive ALDH2(2) allele is dominant.” J Clin Invest. 83(1):314-6.

Kim JS et al. (2005). “Association of ALDH2 polymorphism with sensitivity to acetaldehyde-induced micronuclei and facial flushing after alcohol intake.” Toxicology. 210(2-3):169-74.

Li H et al. (2009). “Refined geographic distribution of the oriental ALDH2*504Lys (nee 487Lys) variant.” Ann Hum Genet. 73(Pt 3):335-45.

Luczak SE et al. (2011). “ALDH2 and ADH1B interactions in retrospective reports of low-dose reactions and initial sensitivity to alcohol in Asian American college students.” Alcohol Clin Exp Res. 35(7):1238–1245.

Peng GS et al. (2002). “Alcohol sensitivity in Taiwanese men with different alcohol and aldehyde dehydrogenase genotypes.” J Formos Med Assoc. 101(11):769-74.

Tanaka F et al. (2010). “Strong interaction between the effects of alcohol consumption and smoking on oesophageal squamous cell carcinoma among individuals with ADH1B and/or ALDH2 risk alleles.” Gut. 59(11):1457-64.

U.S. National Library of Medicine. (2018). “ALDH2 gene.” Genetics Home Reference.

Yokoyama T et al. (2003). “Alcohol flushing, alcohol and aldehyde dehydrogenase genotypes, and risk for esophageal squamous cell carcinoma in Japanese men.” Cancer Epidemiol Biomarkers Prev. 12(11 Pt 1):1227-33.


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