This study was supported by Merck, Sharpe, and Dohme Medical Research Foundation. L.J.B. and I.B.P. are recipients of a Programme Grant from the National Health and Medical Research Committee of Australia.
Oxidative Susceptibility of Low-Density Lipoproteins—Influence of Regular Alcohol Use
Article first published online: 11 APR 2006
Alcoholism: Clinical and Experimental Research
Volume 20, Issue 6, pages 980–984, September 1996
How to Cite
Croft, K. D., Puddey, I. B., Rakic, V., Abu-Amsha, R., Dimmitt, S. B. and Beilin, L. J. (1996), Oxidative Susceptibility of Low-Density Lipoproteins—Influence of Regular Alcohol Use. Alcoholism: Clinical and Experimental Research, 20: 980–984. doi: 10.1111/j.1530-0277.1996.tb01934.x
- Issue published online: 11 APR 2006
- Article first published online: 11 APR 2006
- Received for publication December 5, 1995; accepted April 2, 1996
- Low-Density Lipoprotein;
- Intervention Study
In population studies, a low-to-moderate intake of alcohol has been consistently linked to a lower risk of coronary artery disease. The recent suggestion that alcoholic beverages may be conferring this decrease in risk because they contain antioxidant phenolic compounds that reduce the oxidizability of low-density lipoprotein (LDL) has to be reconciled with the possible counteracting influence of a pro-oxidant effect of alcohol. In a controlled crossover study, we have now measured the oxidizability of LDL in 27 regular beer drinkers during consecutive 4-week periods, wherein they consumed a high versus low alcohol beer (4.9 vs. 0.9% alcohol v/v, respectively), with the two beers being similar in phenolic content. This resulted in a decrease in alcohol consumption by ˜80% (408 ± 25 ml/week vs. 75 ± 11 ml/week). During the low alcohol period, there was no change in LDL vitamin E or its cholesterol or protein content. Analysis of LDL oxidation kinetics revealed an increase in oxidizability during the high alcohol phase. This was despite a decrease in arachidonic acid content of LDL and a corresponding increase in palmitic acid during high alcohol intake—a change in fatty acid composition that has the potential to favor a decrease in oxidizability. Our results suggest that alcohol ingestion increases LDL oxidation, despite reducing the polyunsaturated fatty acid composition. The overall effect of alcoholic beverages on LDL oxidation may be a balance between the pro-oxidant and antioxidant activity of its various constituents. The predominant pro-oxidant effect demonstrated in these beer drinkers, although not relevant to any potential decrease in coronary artery disease, may be important in the pathogenesis of alcohol-related disease in other organ systems.