The relationship between alcohol use and cardiovascular disease is repeatedly investigated in epidemiological
studies, and mostly described as J-shaped or U-shaped with a higher risk for non-drinkers and
heavy drinkers, and a lower risk for moderate drinkers (1). However, there is still a scientific debate on
the apparent protective effects of alcohol use on coronary heart disease, which is not ready to be closed
down (2, 3). Several possible biological mechanisms have been brought forward to explain the apparent
beneficial effects of moderate alcohol use (4, 5). Alcohol use has been found to increase high-density
lipoprotein cholesterol, to reduce blood clotting and platelet aggregation, to decrease insulin resistance
and increase insulin sensitivity, to reduce plasma homocysteine levels, to increase paraoxonase activity,
and to raise oestrogen levels. Negative effects of increased alcohol use are an increase in blood pressure
and damage to myocardial tissue. The question remains whether alcohol use is really beneficial, there
might be other explanations, such as psychological mechanisms or methodological pitfalls, relevant in
explaining the J-shaped curve in addition to these potential biological explanations.
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