Commentary: Alcohol and coronary heart disease—laying the foundation for future work

E Rimm

Harvard School of Public Health, 181 Longwood Ave, Boston, MA 02115, USA. E-mail: eric.rimm{at}channing.harvard.edu

In the epidemiology of modifiable risk factors for chronic disease, evidence is first gathered from relatively simple cross-cultural studies and then from more rigorous and time-consuming studies of observational and experimental design. With a sufficient body of evidence, a general consensus about the strength of the association can be established and reviews, book chapters and meta-analyses soon follow. For the association between alcohol and coronary heart disease (CHD), the evidence as far back as the late 1970s suggested an inverse association between moderate alcohol consumption and lower risk of CHD. Professor Marmot provided the first real comprehensive review1 to cover the range of health risks associated with light, moderate and heavy alcohol consumption. In just seven pages the review covered the most controversial areas and highlighted the strengths and weaknesses of the available evidence. Maybe as important, it created a framework or foundation from which all future work in this area could be based. For over a decade after its publication, research articles in the field cited Marmot's review even though excellent updated reviews were published.2,3 Marmot's review was quite insightful and has survived the test of time.

Many of the scientific issues he discussed are still not resolved in the literature, although public health guidelines for moderate alcohol consumption have come a long way in the last decade. Recent guidelines for the moderate consumption of alcohol in the United Kingdom and the United States most certainly were based on Marmot's early insights.4,5 Below I summarize several of the key areas he highlighted and the advances we have made since 1984.

Does heavy alcohol consumption increase CHD risk?

Evidence at the time of the review as well as newer evidence have shown that heavy drinkers have equal or lower risk of CHD than abstainers. Any discussion of the effects of heavy alcohol consumption is merely academic because benefits from heavy consumption are far outweighed by increased risks from other causes of mortality.6

Does moderate alcohol consumption protect against CHD?

Even in 1984 there was substantial literature to suggest that moderate alcohol consumption lowered risk of CHD. Professor Marmot wrestled with the issue of ‘sick quitters’, an idea later carefully examined in detail.7 In most prospective studies, non-drinkers include a percentage of individuals who were sick and subsequently stopped drinking alcohol; however, this potential bias still cannot explain the strong inverse association between moderate alcohol consumption and CHD.8,9

Inaccuracy in reporting of alcohol consumption has and always will be a problem with observational studies. However, if the goal is to assess moderate alcohol consumption, then many of our current assessment tools are adequate and can differentiate moderate drinkers at lowest risk of CHD from those who abstain. A recent review in this area concluded that methods that inquire about both the frequency and amount consumed for beer, wine, and liquor separately yield the most realistic levels of intake.10 Marmot also postulated that non-drinkers may differ in other ways that put them at higher risk. As with the explanation for the sick quitters, this surely is the case, as many studies have now shown that non-drinkers and moderate drinkers differ in many important lifestyle characteristics (e.g. physical activity, diet and smoking). Over the last 17 years, better methods for assessing these characteristics have become available. With time, we have gained better insight into the independent inverse association for moderate alcohol consumption and as a consequence gained a keener insight into other factors which co-vary with alcohol, namely, the more deadly effects of cigarette smoking. Unable to document adequately an alternative explanation for the apparent inverse association for moderate alcohol consumption and CHD, Marmot simply concludes that moderate drinking is protective (i.e. causal). Although the definition of ‘moderate’ was yet not well defined and not universally accepted, the overall conclusion of this statement, though basic in nature, is now accepted by almost all scientists familiar with this field.

How might alcohol protect against CHD?

Professor Marmot used the published associations between moderate alcohol consumption and a better lipid and haemostatic profile as support for a negative causal association between moderate alcohol consumption and CHD. We have learned much since this time and now know alcohol from any source can have a significant benefit on many biological parameters.11 Evidence for beneficial effects of ethanol may go beyond just effects on high density lipoprotein cholesterol and fibrinogen levels since these factors may only explain 50–80% of the risk-lowering effect. Other factors such as insulin sensitivity, platelet aggregation, endothelial function and inflammation also may be beneficially affected by moderate alcohol consumption.

What recommendations should be made?

Marmot ends his review on a conservative note citing a WHO expert committee on the prevention of CHD: ‘Increased alcohol intake is not recommended as a preventive measure in CHD, either in populations or in individuals.' More recent national and international guidelines have refined this statement and generally conclude that, on an individual basis, if you do drink alcoholic beverages, then do so in moderation. Moderation is generally described as less than 30 g of alcohol a day (in the US, this equals two drinks, and in the UK, this equals three units). Although the evidence is much more substantial now than it was 17 years ago, we still have much to learn in this important area of research. Whether drinking patterns, dietary constituents or genetic predisposition to ethanol metabolism modify the basic underlying association which Marmot described is still yet to be thoroughly explained.

References

1 Marmot MG. Alcohol and coronary heart disease. Int J Epidemiol 1984;13:160–67.[Abstract]

2 Moore RD, Pearson TA. Moderate alcohol consumption and coronary artery disease: a review. Medicine 1986;65:242–67.[ISI][Medline]

3 National Institute on Alcohol Abuse and Alcoholism. Alcohol and the Cardiovascular System, Research Monograph—31, Zakhari S, Wassef M (eds). Bethesda, MD: National Institutes of Health, 1996.

4 Inter-Departmental Working Group. Sensible Drinking. Wetherby, UK: Department of Health, 1995.

5 US Department of Agriculture, US Department of Health and Human Services. Nutrition and Your Health: Dietary Guidelines for Americans, 5th edn. Washington, DC: US Government Printing Office, 2000.

6 Thun MJ, Peto R, Lopez AD et al. Alcohol consumption and mortality among middle-aged and elderly US adults. N Engl J Med 1997;337: 1705–14.[Abstract/Free Full Text]

7 Shaper AG, Wannamethee G, Walker M. Alcohol and mortality in British men: explaining the U-shaped curve. Lancet 1988;ii:1267–73.

8 Rimm EB, Giovannucci EL, Willett WC et al. Prospective study of alcohol consumption and risk of coronary disease in men. Lancet 1991;338:464–68.[ISI][Medline]

9 Klatsky AL, Armstrong MA, Friedman GD. Risk of cardiovascular mortality in alcohol drinkers, ex-drinkers, and nondrinkers. Am J Cardiol 1990;66:1237–42.[ISI][Medline]

10 Feunekes GIJ, van't Veer P, van Staveren WA, Kok FJ. Alcohol intake assessment: the sober facts. Am J Epidemiol 1999;150:105–12.[Abstract]

11 Rimm EB, Williams P, Fosher K, Criqui M, Stampfer MJ. A biologic basis for moderate alcohol consumption and lower coronary heart disease risk: a meta-analysis of effects on lipids and hemostatic factors. Br Med J 1999;319:1523–28.[Abstract/Free Full Text]