- Moderate alcohol consumption is believed to reduce mortality from cardiovascular disease.
- Binge drinking, on the other hand, is known to increase mortality from all causes.
- Recent findings indicate the differences in consequences may be due, in part, to the different effects that alcohol can have on platelet adhesion and aggregation.
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.
"In large studies containing thousands of healthy people, it was observed that people who drank alcohol on a regular basis appeared to have less cardiovascular disease," said Dylan W. de Lange, a researcher at the Thrombosis and Haemostasis Laboratory of the University Medical Center in Utrecht, the Netherlands and corresponding author for the study. "In these large studies, overall mortality was lowest among people who drank two to five glasses daily, compared to people who abstained from alcohol or drank excessively.
This became known as the 'U-shaped curve.' The French adopted this concept, trying to prove that drinking red wine was beneficial for one's health. This became known as the 'French Paradox,' that consumers of red wine had a low mortality from cardiovascular diseases despite smoking and consuming dietary fat."
De Lange said that the "French Paradox" does not actually exist, because consumption of dietary fat takes years before it leads to a heart attack, a realization that has led to creation of the "time-lag hypothesis."
"Perhaps the French paradoxical bubble has been burst," he said, "but the interest it has generated is enormous. We have learned, for example, to take into account differences in socioeconomic factors. To put it bluntly, rich people drink red wine and are healthier than poor whiskey-addicted bums, which might account for some of the beneficial effects of red wine consumption. However, even when these confounders are accounted for, some of the differences in beneficial effects of alcohol and red wine still stand."
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, modest daily consumption of an alcohol-containing beverage – perhaps red wine is superior to other beverages because of its high polyphenol count – 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," he said.
"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," he added, "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 scientific studies."
Alcoholism: Clinical & Experimental Research (ACER) is the official journal of the Research Society on Alcoholism and the International Society for Biomedical Research on Alcoholism. Co-authors of the ACER paper, "Rapid Intake of Alcohol (Binge Drinking) Inhibits Platelet Adhesion to Fibrinogen Under Flow," were: Michel L. Hijmering, Anouk Lorsheyd and Albert van de Wiel of the Department of Internal Medicine at Meander Medical Center in Amersfoort; Wilco L.G. Scholman and Jan-Willem N. Akkerman of the Thrombosis and Haemostasis Laboratory at the University Medical Center, as well as the Institute for Biomembranes at the University, both in Utrecht; and Rob J. Kraaijenhagen of the Department of Clinical Chemistry at the Meander Medical Center in Amersfoort; all of the Netherlands. The study was funded by the Netherlands Thrombosis Foundation.