Researchers identify how binge drinking may drive hea...( As the holidays arrive a group of re...),Health

As the holidays arrive, a group of researchers has identified the precise mechanisms by which binge drinking contributes to clogs in arteries that lead to heart attack and stroke, according to a study published today in the journal Atherosclerosis. The works adds to a growing body of evidence that drinking patterns matter as much, if not more, to risk for cardiovascular disease than the total amount consumed.

According to the National Institute on Alcohol Abuse and Alcoholism (NIAAA), going on a 'binge' means having five or more drinks for men, and four or more drinks for women, in two hours. Many studies suggest that an irregular pattern of heavy drinking brings about a two-fold increase in risk for a fatal heart attack, even as moderate drinking has been shown to reduce risk (the red wine effect). About 65 percent of Americans drink alcohol, with 15 percent reporting binge patterns in a national survey of problem drinkers.

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 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, an important step in initiating atherosclerotic disease. Clarifying these mechanisms promises to empower the design of new treatments to counter the effects when combined with lifestyle change, researchers said.

In the past, experts believed that atherosclerosis developed when too much cholesterol clogged arteries with fatty deposits called plaques. When blood vessels became completely blocked, heart attacks occurred. Now 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
'/>"/>