Ethanol, essential fatty acids and prostaglandins.

In the body the essential fatty acid (EFA) linoleic acid (18:2, omega-6) is desaturated and chain elongated to form homo-gamma-linoleic acid (20:3, omega-6) and arachidonic acid (20:4, omega-6). Apart from their structural function in cell membranes, the EFAs serve as precursors to the prostaglandins and related substances. The prostaglandins can, in general terms, be described as a defensive regulatory system of importance for cardiovascular, gastrointestinal and urogenital function. Acute intake of ethanol gives facial flushing, inhibition of platelet aggregation and elevation of tissue c-AMP. These effects are consistent with release of vasodilatory and antiaggregating PGs. In epidemiological studies, moderate ethanol intake offers some protection against coronary heart disease. Chronic intake high doses of ethanol is associated with damage to, e.g., liver, heart, brain, immunoregulation and various hormonal systems. Decreased tissue levels of 18:2, 20:4 and PGs have been observed both in animals and man. The conversion of 18:2 to 20:4 is inhibited by chronic ethanol exposure. It is suggested that ethanol depletes the PG precursor pool by a dual mechanism of releasing precursor acids and by inhibiting their synthesis. This would lead to a functional EFA-deficiency, manifested by a hypoactive PG system.