Numerous studies have shown a link between moderate alcohol consumption, versus abstinence or heavy consumption, and decreased mortality from cardiovascular disease. Conversely, the rapid consumption of large amounts of alcohol within a short period of time also known as binge drinking is associated with increased mortality from all causes, including cardiovascular ones. Alcohol’s effects on platelet adhesion and aggregation may provide part of the answer to this riddle, as shown by findings published in the October issue of Alcoholism: Clinical & Experimental Research.
For this study, healthy volunteers (n=20) were asked to drink either three glasses of alcohol (Bacardi Breezer®) or red wine during a 45-minute period of time, after which 45 minutes were allowed for alcohol absorption. Ninety minutes after the start of the experiment, blood was collected from all participants. This entire cycle was then repeated once, resulting in consumption of six alcoholic drinks in three hours. Researchers then measured levels of platelet aggregation, induced by a modest stimulatory substance called adenosine-diphosphate (ADP), platelet adhesion to fibrinogen, and collagen.
Binge consumption of alcohol both increased platelet aggregation and inhibited platelet adhesion to fibrinogen-coated surface under flow. In contrast, binge consumption of red wine did not increase platelet aggregation.
Simplistically speaking, excess platelet aggregation is bad whereas inhibited platelet adhesion tends to be good. “Platelet adhesion, rolling platelets that stick to a vessel wall, is the first step to repairing a damaged vessel wall,” said de Lange. “This is then followed by platelet aggregation, platelets sticking to each other, to form a plug that clogs the hole in a vessel. Thus, adhesion and aggregation of platelets are very important for the repair of vessels. However, clog formation in vessels can also prevent delivery of blood and oxygen to tissues beyond the clog, which will die as a result of oxygen and energy shortage. This is called ‘infarction,’ which can be life threatening if it occurs in your heart or brain.”
De Lange and his co-authors speculate it is doubtful, at these binge-consumption levels, that alcohol’s beneficial effects of diminished adhesion completely compensate for the increase in platelet aggregation.
“Maybe drinking regularly two to five glasses a day results in inhibition of platelets,” said de Lange, “but drinking large quantities of alcohol in a short period of time, like in our binge-drinking volunteers, actually agitates platelets. This might explain why more people die from heart attacks after a night of binge drinking.”
De Lange said there are two take-home messages from his study. First, “for the modest daily consumption of an alcohol-containing beverage, perhaps red wine is superior to other beverages because of its high polyphenol count , it might be beneficial to cardiovascular diseases. However, it appears that drinking large quantities in a short period can have detrimental effects through agitation of platelets. This might explain the increased cardiovascular mortality associated with binge drinking...
Second, we showed that alcohol was able to inhibit platelets adhering to fibrinogen at high-flowing speed. This might prevent occlusion of damaged vessels, thus preventing infarction. In short, we did find opposing results, one beneficial and one detrimental to ‘atherosclerosed vessels. We cannot predict which of these prevails in the human body; this must be explored in further studies”.
Source: October issue of Alcoholism: Clinical & Experimental Research (abstracts available via http://www.alcoholism-cer.com/pt/re/alcoholism/currenttoc.htm)