December 04, 2008
Binge Drinking Clogs Arteries With Plaque
THURSDAY, Dec. 4 (HealthDay News) -- The specific pathway through which binge drinking contributes to clogged arteries has been identified by University of Rochester Medical Center researchers.
Alcoholic beverages contain ethanol, which is mostly converted into acetaldehyde. The Rochester team found that binge drinking-related levels of acetaldehyde make immune cells called monocyctes more likely to stick to blood vessel walls and cause inflammation that contributes to blood vessel blockage -- atherosclerosis.
The study contributes to a growing body of evidence that drinking patterns have as much, or more, impact on cardiovascular disease risk than the total amount of alcohol consumed. The findings also may help efforts to develop new treatments to counter atherosclerosis, which can lead to heart attack and stroke, the researchers said.
"Factors like binge drinking have been linked to increased risk for heart disease, and the newer inflammatory model is beginning to explain how," study leader John Cullen, an assistant professor in the department of surgery, said in a medical center news release. "One of our experiments found that acetaldehyde, at levels found in the blood after binge drinking, increased the number of monocytes that can adhere to cells lining blood vessels by 700 percent."
The study was published in the current issue of the journal Atherosclerosis.
Binge drinking means having five or more drinks for men and four or more drinks for women in two hours, according to the U.S. National Institute on Alcohol Abuse and Alcoholism. Some studies have suggested that an irregular pattern of heavy drinking increases the risk of heart attack about two-fold.
An estimated 65 percent of Americans drink alcohol, and 15 percent reporting binge patterns, the researchers said.
More information
The U.S. Centers for Disease Control and Prevention has more about alcohol and health.
-- Robert Preidt
SOURCE: University of Rochester Medical Center, news release, Nov. 26, 2008
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