The consumption of ethanol has been shown to exert profound effects on cellular membranes which result in damage and/or adaptation. Both membrane lipids and proteins are affected, but because of the physicochemical properties of ethanol, many of the membrane effects are directly related to the interaction of ethanol with the lipid component of the membrane. In addition to the direct lipid-ethanol interaction, ethanol has been shown to dramatically alter lipid metabolism. Triacylglycerol accumulates dramatically in the liver, and biosynthesis of the polyunsaturated fatty acids seems to be altered via effects upon the acyl-CoA desaturases. Because precursors of both families of unsaturated fatty acids, i.eΩ3 andΩ6 families, cannot be synthesizedde novo, they must be supplied from dietary sources. Thus, the unsaturated membrane fatty acid composition depends upon these dietary fats and their metabolism via the desaturases. Further, the level of dietary fat seems to play a very important role in ethanol-induced damage to various cellular membranes. Diets with high levels of fat greatly enhance liver steatosis as well as liver membrane damage and liver fibrosis. By altering the composition of dietary fat to include either more saturated fatty acids, higher levels of a specificΩ6 fatty acid,α-linolenic acid, or higher levels of theΩ3 fatty acids, biochemical, physiological and neurobehavioral effects of ethanol have been shown to be modulated. Therefore, it appears that dietary fatty acids may play an important role in altering some of the deleterious effects of eth
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