Alcohol taken in moderation may prevent
atherosclerosis, whereas heavy drinking has the opposite effect, in part by promoting oxidation of
low density lipoproteins (
LDL), a pathogenetic factor in
atherogenesis. We assess here: 1 ) whether similar alterations can be reproduced in baboons fed 50% of energy as
ethanol (the average intake of alcoholics) for 7- 8 years, and 2 ) whether such alterations are affected by supplementation with
polyenylphosphatidylcholine (PPC), a mixture of polyunsaturated
phosphatidylcholines, shown to prevent
alcoholic fatty liver,
fibrosis, and
cirrhosis. Ten animals were given the
ethanol-containing diet and ten were pair-fed isocaloric control diets. In half of the pairs, the diets were supplemented with 2.8 g of
polyenylphosphatidylcholine/1000 kcal. Alcohol feeding increased
LDL-
lipoperoxides and made
LDL-
proteins more negatively charged, changes that were attenuated or prevented by PPC. The oxidizability of
LDL was determined in vitro by the formation of conjugated dienes after oxidation with
copper. Alcohol shortened the lag time (which measures
LDL antioxidant capacity); this effect was normalized by PPC supplementation. By contrast, PPC produced no changes in the controls. Thus
polyenylphosphatidylcholine, by markedly attenuating the
ethanol-induced increase in
LDL oxidation, opposes one of the effects whereby alcohol promotes
atherosclerosis.