Alcohol inhibits the progression as well as the initiation of atherosclerotic lesions in C57Bl/6 hyperlipidemic mice

Background: Evidence that a moderate consumption of alcohol is associated w ith a reduced incidence of and mortality due to coronary artery disease con tinues to accumulate. Despite recent evidence that substances in red wine c onfer resistance to coronary artery disease, it is clear that at least a su bstantial proportion of the protective effect is due to the alcohol content of the beverage. We have previously shown that the chronic ingestion of al cohol incorporated into a total liquid diet during a 24-week period inhibit s the development of fatty streak lesions in hyperlipidemic C57Bl/6 mice. W e have now repeated this study and demonstrated that alcohol continues to m arkedly inhibit atherogenesis during a 48-week period. Methods: Mice were fed a high fat atherogenic liquid diet with 0% or 6% alc ohol or a high fat atherogenic pelleted diet with 0% or 15% alcohol in thei r drinking water. After 24 and 48 weeks on these diets, subgroups of mice w ere euthanized and the aortas were studied for extent of atherosclerosis. P lasma lipid levels were also measured and flow cytometry studies performed to characterize their T and B lymphocyte populations. Additional groups of mice were given the high fat atherogenic diets for 24 weeks to allow lesion s to develop and were then treated with alcohol diets to determine whether they inhibit the progression of the lesions. Results: The alcohol diets suppressed the development of atherosclerotic le sions at both 24 and 48 weeks in both the liquid and pelleted diet models. The addition of the alcohol diets after allowing lesions to form for 24 wee ks halted the further progression of the lesions. The alcohol treatments al so decreased the plasma levels of total cholesterol and high density lipopr otein (HDL) cholesterol at almost all time intervals. Conclusions: We conclude that alcohol not only inhibits the initial develop ment of atherosclerotic lesions but also inhibits the progression of existi ng atherosclerotic lesions. The alcohol-mediated decrease in HDL cholestero l in these experiments suggests that HDL plays little or no role in amelior ation of atherogenesis in this model.