March 24 (HealthDay News) -- People who experience facial flushing when they drink alcohol are much more likely to develop alcohol-related esophageal cancer, say American and Japanese experts.
Facial flushing, nausea and increased heart rate when drinking alcohol occurs in about a third of East Asians (Chinese, Japanese and Koreans), mainly due to an inherited deficiency in an enzyme called aldehyde dehydrogenase 2 (ALDH2). There is increasing evidence that people with this deficiency are at much higher risk for alcohol-related esophageal cancer (specifically squamous cell carcinoma) than people with fully active ALDH2, the experts wrote in an article in this week's issue of PLoS Medicine.
However, many doctors and people with alcohol flushing response aren't aware of this increased risk. This lack of awareness is "unfortunate as esophageal cancer is one of the deadliest cancers worldwide, with five-year survival rates of 15.6 percent in the United States, 12.3 percent in Europe, and 31.6 percent in Japan," noted Dr. Philip Brooks and colleagues at the U.S. National Institute on Alcohol Abuse and Alcoholism, and Dr. Akira Yokoyama of the Kurihama Alcohol Center in Japan.
"Our goal in writing this article is to inform doctors firstly that their ALDH2-deficient patients have an increased risk for esophageal cancer if they drink moderate amounts of alcohol, and secondly that the alcohol flushing response is a biomarker for the ALDH2 deficiency," the researchers said in a news release from the journal.
ALDH2 deficiency can be determined by asking patients about previous episodes of alcohol-induced flushing, the experts said.
"As a result, ALDH2-deficient patients can then be counseled to reduce alcohol consumption, and high-risk patients can be assessed for endoscopic cancer screening," Brooks and colleagues said.
There are about 540 million ALDH2-deficient people worldwide, which means even a minor reduction in the rate of alcohol-related esophageal cancers would save a large number of lives.
SOURCE: PLoS Medicine, news release, March 23, 2009