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Alcohol and coronary heart disease: the evidence for a protective effect
1Evans Department of Medicine, Boston University School of Medicine, MA, USA.
Insights
Moderate alcohol consumption may reduce coronary heart disease (CHD) risk, but heavy drinking increases cardiovascular mortality. The relationship forms a U-shaped curve, with potential protective mechanisms like increased HDL and antithrombotic effects, though caution is advised for general recommendations.
Area of Science:
- Cardiovascular Science
- Epidemiology
- Alcohol Research
Background:
- Moderate alcohol intake is linked to reduced coronary heart disease (CHD) incidence and mortality.
- Problem drinking significantly increases cardiovascular mortality.
- Harmful effects of alcohol abuse may be misattributed to CHD, including alcohol-induced cardiomyopathy and dysrhythmias.
Purpose of the Study:
- To investigate the complex relationship between alcohol consumption and cardiovascular health.
- To explore the potential protective effects of moderate alcohol intake on coronary heart disease.
- To examine the U-shaped mortality curve associated with alcohol consumption.
Main Methods:
- Review of population studies, case-control studies, prospective cohort studies, arteriographic studies, and animal experiments.
- Analysis of evidence for biologically plausible protective mechanisms, including HDL elevation and antithrombotic effects.
- Consideration of confounding factors and limitations in observational data, such as lifestyle and smoking.
Main Results:
- Consistent evidence suggests a protective effect of moderate alcohol intake against CHD and possibly atherosclerotic-thrombotic brain infarction.
- Alcohol consumption exhibits a U-shaped mortality curve, with benefits at moderate levels and harm at excessive levels.
- Red wine may show a greater protective effect, but confounding factors related to lifestyle are difficult to control.
Conclusions:
- A true protective effect of moderate alcohol intake on CHD is likely, supported by consistent findings and plausible biological mechanisms.
- Heavy alcohol consumption carries significant cardiovascular risks that cannot be ignored.
- Caution is necessary when making general recommendations to drink alcohol for cardiovascular benefit due to the risk of increased abuse.
Abstract:
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.