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Relationship of alcohol consumption and type of alcoholic beverage consumed with plasma lipid levels: Differences between whites and African-Americans

The authors state that alcohol consumption has been shown to contribute to a favorable lipid profile, and most studies have reported a reduction in coronary heart disease risk with low-to-moderate consumption of alcohol that is generally attributed to the beneficial effects of alcohol on lipids. The influence of different types of alcoholic beverages on plasma lipid levels has been investigated to a lesser extent and in limited populations. The investigators investigated the effect of overall alcohol consumption, as well as the type of alcoholic beverage consumed, on multiple lipid measures in the large bi-ethnic population of the Atherosclerosis Risk in Communities study.

Results showed that both low-to-moderate and heavy alcohol consumption, regardless of the type of alcoholic beverage consumed, was associated significantly with greater levels of high-density lipoprotein (HDL) cholesterol, HDL3 cholesterol, and apolipoprotein A-I in both white and African-American males and females. Associations with other lipid measures contrasted between whites and African Americans, with greater levels of alcohol consumption resulting in significantly greater triglyceride levels in African Americans. The authors conclude that their results confirm previous studies associating alcohol consumption, regardless of beverage type, with greater HDL cholesterol levels, with additional consistent associations detected for the major HDL cholesterol density subfraction, HDL3 cholesterol, and the major HDL cholesterol structural apolipoprotein, apolipoprotein A-I.

R. Curtis Ellison comments: While some studies have suggested that wine drinkers may have greater increase in HDL after alcohol consumption, most previous research has shown that all types of alcoholic beverages – beer, wine, and spirits – increase HDL cholesterol and its associated lipids similarly.

The current study excluded subjects who stated they were former drinkers or those who stated they were drinkers but reported zero grams/week of alcohol consumed (those reporting less than one drink/week). Thus, the paper is based on current consumers versus what were considered to be lifetime abstainers.

This study confirms the finding that all types of alcohol were associated strongly with HDL cholesterol; among the white subjects, the highest category of alcohol intake was associated with 11 - 13 mg/dL higher levels of HDL; for African-Americans it was 9 - 10 mg/dL higher. In epidemiologic studies, such increases are generally associated with a 20% or greater reduction in rates of coronary heart disease.

As for differences according to type of beverage, there were too few drinkers to have good estimates among African-Americans. Among whites, subjects who consumed at least two-thirds of their alcohol intake from wine consistently showed higher levels of HDL than subjects preferring other beverages, although the numbers in some cells were very small. Further, the average amount of alcohol in each amount/type cell was not reported (and the total alcohol for subjects in the “heavy” consumption categories for different beverages may have differed). Thus, it is difficult to determine if there were any real differences in HDL by type of beverage.

All other lipids (e.g., sub-classes of HDL, LDL, Apolipoproteins) showed generally similar “beneficial” effects of alcohol, effects that have been associated with less coronary disease. For African-Americans, however, blood triglycerides showed an increase with heavy alcohol intake, which was not seen in whites. Whether due to genetic differences, different drinking patterns, or other causes is not known; whether alcohol intake was regular or episodic (as in binge drinking) was not recorded in this study.

Source: Relationship of alcohol consumption and type of alcoholic beverage consumed with plasma lipid levels: Differences between whites and African-Americans of the ARIC Study. Volcik KA, Ballantyne CM, Fuchs FD, Sharrett AR, Boerwinkle E. Ann Epidemiol 2008;18:101–107.

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