Kannel W B, Ellison R C
Evans Department of Medicine, Boston University School of Medicine, MA, USA.
Clin Chim Acta. 1996 Mar 15;246(1-2):59-76. doi: 10.1016/0009-8981(96)06227-4.
There is a considerable body of evidence indicating that moderate alcohol intake is associated with a reduced incidence of, and mortality from, coronary heart disease (CHD). There is also substantial evidence that problem drinking (well beyond two drinks per day) is associated with increased cardiovascular mortality. However, the frequently reported harmful effect of alcohol abuse on CHD mortality rates could be a result of mislabelling as CHD conditions such as alcohol-induced dilated cardiomyopathy, dysrhythmias, and hypertensive cardiovascular disease. The combination of protective and harmful influences of alcohol consumption results in a U-shaped mortality curve. A true protective effect of moderate intake of alcohol is likely, because of consistent findings in many large, well-conducted studies of diverse population samples and the apparent specificity of the protective effect for CHD and possibly atherosclerotic-thrombotic brain infarction. There are also biologically plausible mechanisms whereby the protection might be conferred. Alcohol has been shown convincingly to raise HDL subfractions which have been found to be protective against CHD, and it may also provide protection by an antithrombotic effect. There is a suggestion that wine, and red wine in particular, may be more protective than other alcoholic beverages. However, it is difficult to control adequately for confounding factors, since persons who prefer wine have been found to have a more advantageous lifestyle, a better cardiovascular risk profile, are better educated, and smoke less. The evidence for a protective effect of moderate alcohol intake includes population studies of alcohol and CHD mortality in 20 countries, case-control studies, prospective cohort studies, arteriographic studies, and animal experiments. Nevertheless, because there are no controlled trial data, it is possible that some other factor may be responsible for the apparent protective effect of alcohol. The inclusion of former drinkers or sick individuals in the non-drinker category, and lack of control for cigarette smoking and other risk factors, have been excluded as reasons for higher CHD rates among individuals who do not consume alcohol. No alternative explanation for the protective effect has surfaced after two decades of investigation of the alcohol-CHD relationship, yet, the penalties of heavy alcohol consumption are too large to ignore. Until we can be sure that advice that encourages the public to drink to avoid coronary heart disease does not increase abuse, we must be cautious in making general recommendations.
有大量证据表明，适度饮酒与冠心病（CHD）发病率和死亡率的降低有关。也有大量证据表明，问题饮酒（远超每天两杯）与心血管死亡率增加有关。然而，经常报道的酒精滥用对冠心病死亡率的有害影响可能是由于将诸如酒精性扩张型心肌病、心律失常和高血压性心血管疾病等病症误列为冠心病所致。酒精消费的保护和有害影响相结合导致了U型死亡率曲线。适度饮酒可能具有真正的保护作用，这是因为在许多针对不同人群样本的大型、精心开展的研究中都有一致的发现，而且这种保护作用对冠心病以及可能的动脉粥样硬化性血栓性脑梗死具有明显的特异性。也存在可能赋予这种保护作用的生物学上合理的机制。酒精已被确凿地证明能提高高密度脂蛋白亚组分，而这些亚组分已被发现对冠心病具有保护作用，并且它还可能通过抗血栓作用提供保护。有人认为葡萄酒，尤其是红酒，可能比其他酒精饮料更具保护作用。然而，由于发现偏好葡萄酒的人具有更有利的生活方式、更好的心血管风险状况、受教育程度更高且吸烟较少，因此很难充分控制混杂因素。适度饮酒具有保护作用的证据包括对20个国家酒精与冠心病死亡率的人群研究、病例对照研究、前瞻性队列研究、血管造影研究以及动物实验。然而，由于没有对照试验数据，可能是其他一些因素导致了酒精明显的保护作用。将以前饮酒者或患病个体纳入不饮酒类别，以及未对吸烟和其他风险因素进行控制，已被排除为不饮酒个体中冠心病发病率较高的原因。在对酒精与冠心病关系进行了二十年的调查之后，尚未出现对这种保护作用的其他解释，然而，大量饮酒的危害太大，不容忽视。在我们能够确定鼓励公众饮酒以预防冠心病的建议不会增加酒精滥用之前，我们在提出一般性建议时必须谨慎。
