How binge drinking increases heart risk

U.S. researchers say they have identified the precise mechanisms by which binge drinking contributes to increased risk of heart attack and stroke.

John Cullen of the University of Rochester Medical Center said that alcoholic beverages contain ethanol, which is mostly converted into acetaldehyde once in the human system at binge levels, with the levels of acetaldehyde remaining high for many hours after the binge has ended.

The current study, published in the journal Atherosclerosis, clarified for the first time that binge levels of acetaldehyde cause an important type of immune cell -- the monocyte -- to become better able to stick to blood vessel walls.

In the past, experts believed that atherosclerosis developed when too much cholesterol clogged arteries with fatty deposits called plaques and when blood vessels became completely blocked, heart attacks occurred, Cullen explained.

Cullen said that today, most believe that the reaction of the body's immune system, more than the build-up itself, creates heart attack risk. Vessel walls mistake fatty deposits for intruders, akin to bacteria and call for help from the immune system. Monocytes arrive with the goal of preventing infection, but end up causing inflammation that drives blood vessel blockage.

Binge-drinking has been linked to increased risk for heart disease, and the newer inflammatory model is beginning to explain how, Cullen said in a statement. We found acetaldehyde, at levels found in the blood after binge drinking, increased the number of monocytes by 700 percent.

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