Croft K D, Puddey I B, Rakic V, Abu-Amsha R, Dimmitt S B, Beilin L J
Department of Medicine, Royal Perth Hospital, University of Western Australia.
Alcohol Clin Exp Res. 1996 Sep;20(6):980-4. doi: 10.1111/j.1530-0277.1996.tb01934.x.
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 approximately 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.
在人群研究中,低至中度饮酒一直与较低的冠状动脉疾病风险相关。最近有观点认为,酒精饮料可能会降低风险,因为它们含有抗氧化酚类化合物,可降低低密度脂蛋白(LDL)的氧化能力,但这一观点必须与酒精的促氧化作用可能产生的抵消影响相协调。在一项对照交叉研究中,我们现在测量了27名经常饮用啤酒者在连续4周内LDL的氧化能力,在此期间他们分别饮用高酒精度啤酒和低酒精度啤酒(酒精体积分数分别为4.9%和0.9%),两种啤酒的酚类含量相似。这导致酒精摄入量减少了约80%(从每周408±25毫升降至每周75±11毫升)。在低酒精摄入期,LDL维生素E及其胆固醇或蛋白质含量没有变化。对LDL氧化动力学的分析显示,在高酒精摄入阶段氧化能力增加。尽管在高酒精摄入期间LDL的花生四烯酸含量降低,棕榈酸含量相应增加——这种脂肪酸组成的变化有可能有利于氧化能力的降低。我们的结果表明,尽管酒精摄入会降低多不饱和脂肪酸组成,但仍会增加LDL的氧化。酒精饮料对LDL氧化的总体影响可能是其各种成分的促氧化和抗氧化活性之间的平衡。在这些啤酒饮用者中表现出的主要促氧化作用,虽然与冠状动脉疾病的任何潜在降低无关,但可能在其他器官系统中与酒精相关疾病的发病机制中起重要作用。