New Research Reveals How Binge Drinking Could Drive Atherosclerosis

December 02, 2008

December 2, 2008 (Rochester, New York) — An in vitro experiment has enabled US researchers to put their finger on a precise mechanism by which binge drinking might contribute to atherosclerosis [1]. Dr John P Cullen (University of Rochester Medical Center, Rochester, NY) and colleagues report their findings online October 18, 2008 in Atherosclerosis.

Although epidemiological data have suggested an association between irregular bouts of heavy drinking, cardiovascular disease, and stroke, "this is the first study to examine the effects of acetaldehyde [the primary metabolite of alcohol] on the mechanisms of atherosclerosis," Cullen told heartwire .

"This helps generate some data as to how we tie these things in," he added. "Most people look at volume of alcohol consumed rather than the pattern. This is a whole new niche: we're trying to provide scientific data to say, 'This is what happens when you binge drink, you are at [cardiovascular] risk.' "

Acetaldehyde Involved in Initiation of Atherosclerosis

In their study, Cullen et al used human umbilical venous endothelial cells and monocytes and exposed them to acetaldehyde for six hours. They looked at the effects of the alcohol metabolite on the monocytes alone, the endothelial cells alone, and both together.

We're trying to provide scientific data to say, 'This is what happens when you binge drink, you are at [cardiovascular] risk.'

"At physiologically relevant concentrations of acetaldehyde that you would find in the blood of binge drinkers, we found this caused an increase of 700% in the adherence of monocytes to endothelial cells," Cullen told heartwire . "Also, we saw increased expression of adhesion molecules on the endothelial cells and the release of tumor necrosis factor [TNF-{:alpha:}], which is implicated in the progression of the atherosclerotic plaque."

"This study demonstrates for the first time that physiologically relevant concentrations of acetaldehyde can initiate several key steps involved in monocyte recruitment," the researchers say. Previous published work on acetaldehyde has examined its effects only on the nervous system and the liver, they note.

Cullen says this work "ties in nicely" with previous work his team has done in mouse models of atherosclerotic plaques, where some animals were given the equivalent of two alcoholic drinks per day (moderate drinkers), some were given seven drinks on two days per week and none on the others--to approximate binge drinking--and some animals were given no alcohol at all (controls).

"After two weeks, we saw that there was much more plaque formation within the binge model, and the lumen in these animals was totally occluded. In contrast, in the moderate-drinking mice models, there was a lot less plaque formation and more open lumens than in the controls, so this did show the opposing effects of alcohol, based on the pattern of drinking.

"If someone is binge drinking, you get a rise in pure alcohol levels and a rise in acetaldehyde levels, but then the alcohol levels fall off and you are left with circulating levels of the metabolite, with no pure alcohol there to counteract these vascular effects of acetaldehyde."

A Delicate Equilibrium: When Does Drinking Become Harmful?

The key to when drinking becomes harmful is the point at which the balance is tipped, a "delicate equilibrium" between pure alcohol and acetaldehyde and their effects on the vasculature, Cullen believes.

In the future, he and his team hope to examine this issue in vivo in animals and will look at not only atherosclerotic plaque formation in the presence of alcohol and acetaldehyde but also at plaque stability.

"You can have a plaque present for years; as long as it's stable, you'llbe fine. But we want to see at what point does the plaque rupture, which is the key to a heart attack," he observes. "We hope to confirm that the actions of acetaldehyde underlie, in part, the detrimental effects of binge drinking on cardiovascular disease."

Pattern of Drinking Important for Cardiovascular Health

Cullen says this new work adds to a growing body of epidemiological evidence that drinking patterns matter as much, if not more, to risk for cardiovascular disease than the total amount consumed.

A lot of people think they can save up their units until the weekend--we are all guilty of that. . . . That's where the problem lies.

"We know that light to moderate drinking every day--around two drinks for a man and about one for a woman--is protective in cardiovascular terms, reducing risk of events by about 30% to 50%. But it's very difficult to do; not many people have one to two drinks per day. A lot of people think they can save up their units until the weekend--we are all guilty of that. We say, 'I'm allowed 14 to 21 drinks per week so that's fine, I can have seven or eight on a Friday and seven or eight on a Saturday.' That's where the problem lies."

Another issue, he says, "is that a lot of people now drink at home, so the measures become important."

According to the US National Institute on Alcohol Abuse and Alcoholism, going on a "binge" means having five or more drinks for men and four or more for women in two hours, and around 15% of drinkers in the US report this kind of pattern in national surveys. And some countries suffer even more from the effects of binge drinking, Cullen notes, citing his native Ireland and the UK as examples of heavy "binge-drinking" cultures.

Cullen also acknowledges that it is one thing to provide evidence that binge drinking is harmful in cardiovascular terms but quite another to get this message across. He hopes the results of this new study will help empower public-health campaigns that discourage binge drinking.

"This is for healthcare professionals, so they can see and counsel patients and say, 'There is proof that binge drinking is harmful for your cardiovascular health.' It's a bit like smoking--until there was proof out there that smoking was actually bad for you, it was hard to get the message across."

  1. Redmond EM, Morrow D, Kundimi S, et al. Acetaldehyde stimulates monocyte adhesion in a P-selectin- and TNFalpha-dependent manner. Atherosclerosis 2008; DOI:10.1016/j.atherosclerosis.2008.10.008. Available at: http://atherosclerosis-journal.com. Abstract



The complete contents of Heartwire , a professional news service of WebMD, can be found at www.theheart.org, a Web site for cardiovascular healthcare professionals.

Comments

3090D553-9492-4563-8681-AD288FA52ACE
Comments on Medscape are moderated and should be professional in tone and on topic. You must declare any conflicts of interest related to your comments and responses. Please see our Commenting Guide for further information. We reserve the right to remove posts at our sole discretion.
Post as:

processing....