Alcohol is interesting because despite its unhealthy reputation within the mainstream, even relatively high intakes are protective of disease. In particular, alcohol appears to protect from cardiovascular disease, and a number of mechanisms have been put forward to explain this effect. Attention to date has focussed mainly on the ability to affect blood lipids, with alcohol able to favourably modify a number of steps in the metabolism of lipoproteins. These include the changes to apolipoproteins synthesis, to the activity of hepatic and lipoprotein lipase, and to the function of the cholesterol transfer protein. As a result alcohol causes favourable changes to lipoprotein concentrations that include an increase in high density lipoprotein (HDL). However, an often overlooked effect of alcohol is the ability to raise plasma levels of n-3 fatty acids. Because n-3 plasma levels are associated with protection from cardiovascular disease, this aspect of alcohol metabolism is of considerable interest.
For example, researchers1 have investigated the association between alcohol and n-3 long-chain fatty acids (marine fatty acids) in the plasma and red blood cells of 1604 subjects aged 26 to 65 years. The n-3 content of the diet was determined by food frequency questionnaires over a 1 year duration, and the n-3 fatty acid content of plasma and red blood cells was determined through biochemical analysis of a blood sample. Following adjustment for known confounding variables, alcohol intake was found to be associated with eicosapentanoic acid (EPA, C20:5 (n-3)) and docosahexanoic acid (DHA, C22:6 (n-3)) concentrations in the plasma of women, and with EPA concentrations in the plasma and red blood cells of men. Further analysis showed that alcohol was associated with plasma EPA and DHA and with red blood cell EPA and DHA concentrations in wine drinkers, but not in those who drank beer or spirits.
Alcoholic drinks do not contain the long-chain n-3 fatty acids EPA or DHA and so this cannot be the source of the increased blood concentrations of these fatty acids. It is possible that consumption of alcohol increases ingestion of n-3 fatty acid containing foods, as might be the case with those who consume the Mediterranean diet rich in both red wine and n-3 fatty acid from fish. However, in this study it was reported that there was an inverse association between plasma α-linolenic acid (ALA, C18:3 (n-3)) concentrations and alcohol consumption in men that remained even after adjustment for known confounding variables. This might suggest that the low levels of ALA in heavy drinkers are caused by an increased conversion of ALA to its metabolites EPA and DHA. If alcohol could increase flux through the essential fatty acid pathway, this would explain the increased plasma concentrations of both EPA and DHA and the lower levels of ALA.
Conversion of ALA to EPA and DHA in humans is inefficient due to genetic deficiency of the Δ6-desatuarse enzyme (here) that limits pathway flux. Ingested ALA is preferentially oxidised for energy in humans, which is surprising because EPA and DHA have important health effects and use of the parent compound as a source of energy has never been suitably explained. High intakes of ALA from plant foods do not provide the same health benefits as consumption of the long chain n-3 metabolites EPA and DHA from fish oils. If alcohol is able to increase the conversion of ALA to EPA it could be the key that unlocks the health benefits of ALA ingestion and might explain the cardioprotective effects of ethanol. Alcohol could therefore increase flux through the essential fatty acid pathway by activating the elongation and desaturation enzymes required for the conversion of ALA to EPA and DHA.
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