STANFORD, Calif. — Does your face turn red while drinking alcohol? For millions of Asians, a genetic variant that inhibits their ability to metabolize alcohol. Commonly referred to as the “Asian flush,” a new study warns that this somewhat embarrassing condition can have deadly consequences. Researchers at Stanford say this genetic variant puts the 540 million people who carry it at a significantly higher risk for coronary artery disease.

Luckily, study author Dr. Joseph Wu says there may be a treatment that lowers the risk of heart disease tied to the Asian flush. The study finds that the common diabetes drug empagliflozin, which is available under the brand name Jardiance, is capable of improving vascular function in mice genetically engineered to carry the variant.

“Empagliflozin targets the downstream pathways of ALDH2*2 rather than directly stimulating ALDH2 activity, so it won’t reduce alcohol flush. However, it may be used as a preventive measure against vascular diseases, especially in high-risk patients such as ALDH2*2 carriers who drink excessively,” Wu says in a university release.

Why do these drinkers look flushed?

Researchers say the gene variant reduces dilation of blood vessels which can cause cardiovascular disease – the world’s number one killer. It stops the protein ALDH2 from working in the body.

The findings are based on an analysis of thousands of participants from BioBank Japan. Those with the mutation causing ALDH2 deficiency produce a slightly different enzyme, ALDH2*2.

The enzyme fuels inflammation and harmful chemicals called free radicals — which can also trigger diabetes and cancer.

“If you’re drinking, drink less. If you’re not drinking, don’t start.” Dr. Wu says.

Alcohol intolerance can cause immediate and uncomfortable reactions, including a stuffy nose, sneezing, and flushing or rash. An efficient ALDH2 destroys toxic chemicals from alcohol and mops up free radicals that damage DNA. The flushing is caused by the release of immune system chemicals called histamines.

“In addition, the ALDH2 variant is linked to an increased risk of atrial fibrillation in habitual drinkers, which is one of the most common types of cardiac arrhythmias,” Wu adds. “We are looking into the role of alcohol-induced arrhythmias in ALDH2 carriers using patient-specific induced pluripotent stem cell models.”

How does the diabetes drug fix this?

Mice medicated with empagliflozin displayed improved vascular response, healthier endothelial cells, and improved circulation overall. Study authors found that the drug reduces the amount of oxidative damage and inflammation in the cells. It also increases the production of nitric oxide, which compensates for the drinker’s ALDH2 deficiency.

Wu’s team is hoping to see future clinical trials look at whether the combination of having an ALDH2 deficiency and drinking alcohol exacerbates blood cell dysfunction in diabetics and those already dealing with heart disease.

“If confirmed, this should better inform patients on cutting down alcohol consumption in general, and especially for ALDH2 carriers (those who show the alcoholic flush) to avoid drinking alcohol if possible,” Wu concludes.

South West News Service writer Mark Waghorn contributed to this report.

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