Effect of beer drinking on risk of myocardial infarction: population based case-control studyBMJ 2000; 320 doi: https://doi.org/10.1136/bmj.320.7246.1378 (Published 20 May 2000) Cite this as: BMJ 2000;320:1378
- a International Centre for Health and Society, Department of Epidemiology and Public Health, University College London, London WC1E 6BT
- b Department of Preventive Cardiology, Institute of Clinical and Experimental Medicine, 140 00 Prague, Czech Republic
- Correspondence to: M Bobak
- Accepted 16 March 2000
Many studies have shown an inverse association between alcohol consumption and coronary heart disease, with a possible flattening at higher consumption levels.1 It remains unclear, however, whether the protective effect is confined to specific beverages (such as red wine) or relates to ethanol. This question is complicated because wine drinkers may differ from people drinking other beverages or have a different drinking pattern. We addressed this issue by conducting a study in the Czech Republic, a predominantly beer drinking country, and by restricting the analyses to people who did not drink wine or spirits.
Participants, methods, and results
We conducted a population based case-control study in five Czech districts. All men aged 25–64 who had a first non-fatal myocardial infarction that fulfilled the World Health Organization MONICA (monitoring trends and determinants in cardiovascular disease) criteria of definite or probable infarction 2 over 18 months were considered eligible. All cases agreed to participate in the study. An age stratified random sample of the population (response rate 77%) served as controls. Data on cases and controls were collected by identical protocols (details are available elsewhere 3).
Participants reported the frequency of drinking any alcohol (never; less than once a month; once or twice a month; several times a week; almost daily or daily; and twice a day or more often). They also reported how much wine, spirits, and beer they consumed during a typical week. The average consumption of pure alcohol was 148 g a week, 87% of which was consumed as beer. The analyses were restricted to non-drinkers and “exclusive” beer drinkers (men who typically do not drink wine or spirits). Participants were categorised into four groups according to their average weekly intake of beer: <0.5 l (about 18 g of alcohol), including non-drinkers; 0.5-3.9 l (18-144 g of alcohol); 4-8.9 l (145-324 g of alcohol); and ≥9 l (325 g of alcohol).
The lowest risk was found among men who drank almost daily or daily (adjusted odds ratio 0.38, 95% confidence interval 0.19 to 0.75) and among men who drank 4-8.9 l of beer a week (0.34, 0.19 to 0.61) (table 1). When beer intake was analysed in narrower categories, the lowest risk was found for weekly consumption of 5–6 l, but because of the small numbers of subjects in each category the confidence intervals were wide (not shown). The results did not change when men with a history of heart disease, stroke, diabetes, or cancer were excluded.
In this study of beer drinkers, the lowest risk of myocardial infarction was found among men who drank almost daily or daily and who drank 4–9 l of beer a week. There was a suggestion that the protective effect was lost in men who drank twice a day or more. This is similar to results of studies of other beverages.
It is unlikely that our results are due to bias or confounding. This was a population based study with highly complete recruitment of incident cases through a myocardial infarction register in a well defined population and with good response rate in controls randomly selected from the population register.3 Questions on average consumption usually lead to underestimation of the real intake, but the ranking of subjects in terms of long term average intake is reasonably reliable.4 Restricting the analysis to exclusive beer drinkers eliminated potential confounding by other beverages. It is unlikely that cases and controls answered questions differently; a cohort study in Bavaria, another beer drinking region, produced similar findings.5 These results support the view that the protective effect of alcohol intake is due to ethanol rather than to specific substances present in different types of beverages.1
We thank local cardiologists in the participating districts.
Contributors: MB, ZS, and MM jointly designed the case-control extension of the Czech MONICA project. MB analysed the data and drafted the paper. ZS coordinated the data collection and participated in the interpretation of the data and writing of the paper. MM initiated the project and participated in data interpretation and writing of the paper. MB will act as guarantor.
Funding The study was funded by a grant from the Wellcome Trust and by the Czech Ministry of Health. MB was supported by the Wellcome Trust fellowship in clinical epidemiology. MM is supported by an MRC research professorship.
Competing interests None declared.