Alcohol shows favourable effects on lipoprotein concentrations because it is associated with an increase in high density lipoprotein (HDL). This has been suggested to be the reason for its beneficial effects on cardiovascular disease. However, consumption of ethanol has been shown to decrease platelet aggregation, and this cannot be explained by the modifications to the lipoprotein subfractions. Instead it points to a mechanisms by which the eicosanoid and docosanoid pathways are modified to decrease production of proinflammatory compounds. Evidence that alcohol modifies the essential fatty acid pathways in humans such that more α-linolenic acid (ALA, C18:3 (n-3)) is converted to eicosapentanoic acid (EPA, C20:5 (n-3)) and docosahexanoic acid (DHA, C22:6 (n-3)) would explain this mechanisms of action and result in significant cardioprotective effects. Recent research suggests that increased blood concentrations of EPA and DHA are one of the effects of regular wine consumption.
For example, researchers1 have investigated the association between ethanol consumption and plasma levels of long-chain n-3 fatty acids. Subjects at risk of coronary heart disease had their intakes of plant and marine n-3 fatty acids, as well as alcohol (mainly wine) assessed from their diets and blood lipids were assessed using biochemical tests. The results showed that as alcohol intakes increased through quartiles of consumption, there was a significant increase in the plasma n-3 fatty acid concentrations. Those subjects with high intakes of ALA had a 37 % increase in plasma levels of EPA, whereas those with low intakes of ALA had a 50 % increase in EPA. The researchers then adjusted the data to take account of dietary intakes of EPA, but the results remained significant in both groups, suggesting that alcohol increases plasma concentrations of EPA. As with other studies, drinkers had higher concentrations of high density lipoprotein (HDL).
These results therefore suggests that alcohol favourably affects the plasma concentrations of n-3 long-chain fatty acids. Ethanol is protective of cardiovascular disease because it decreases platelet aggregation and reduces the risk of myocardial infarction for around 24 hours following drinking. This physiological effects cannot be explained by the modifications it causes to plasma lipoproteins. Alcohol does raise levels of HDL cholesterol, and high HDL plasma levels are protective of cardiovascular disease. However, the mechanisms by which this is said to be protective involves the transport of cholesterol from peripheral tissues back to the liver for excretion. This does not fit with the known protective effect of alcohol that are short-term and last around 24 hours following drinking. Therefore while raised HDL levels from drinking alcohol might be associated with protection from cardiovascular disease, the cause is likely the increased plasma levels of n-3 fatty acids.
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