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Martin Bobak 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 martinb{at}public-health.ucl.ac.uk
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.
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 infarction2 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 elsewhere3).
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 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.
Table 1.
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
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Participants, methods, and results
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9 l (325 g of alcohol).
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Acknowledgments |
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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.
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Footnotes |
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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.
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References |
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| 1. |
Rimm EB, Klatsky A, Grobbee D, Stampfer MJ.
Review of moderate alcohol consumption and reduced risk of coronary heart disease: is the effect due to beer, wine, or spirits?
BMJ
1996;
312:
731-736 |
| 2. |
World Health Organization.
Multinational monitoring of trends and determinants of cardiovascular diseases "MONICA project." Manual of operations. Version 1.1. CDV/MNC. December 1986.
Geneva: WHO, 1987.
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| 3. |
Bobak M, Skodova Z, Hertzman C, Marmot M.
Own education, current conditions, parental material circumstances and risk of myocardial infarction in a former communist country.
J Epidemiol Community Health
2000;
54:
91-96 |
| 4. |
Rehm J, Greenfield TK, Walsh G, Xie X, Robson L, Single E.
Assessment methods for alcohol consumption, prevalence of high risk drinking and harm: a sensitivity analysis.
Int J Epidemiol
1999;
28:
219-224 |
| 5. | Keil U, Chambless LE, Doering A, Filipiak B, Stieber J. The relation of alcohol intake to coronary heart disease and all-cause mortality in a beer-drinking population. Epidemiology 1997; 8: 150-156[Medline]. |
(Accepted 16 March 2000)
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