Authors' reply

BMJ 1996; 313 doi: https://doi.org/10.1136/bmj.313.7053.366 (Published 10 August 1996) Cite this as: BMJ 1996;313:366
  1. H O Hein,
  2. P Suadicani,
  3. F Gyntelberg
  1. Associate professor Senior researcher Professor Copenhagen Male Study, Epidemiological Research Unit, 7122 Rigshospitalet, DK-2200 Copenhagen N, Denmark

    EDITOR,—The proposal that alcohol has a protective effect on the risk of ischaemic heart disease no longer has the charm of novelty. Frontline research should now attempt to identify those people who benefit from drinking alcohol and those who do not.

    We investigated the interplay between alcohol consumption, serum low density lipoprotein cholesterol concentration, and risk of ischaemic heart disease. The strength of the association between alcohol and risk was highly dependent on the low density lipoprotein cholesterol concentration: the higher the concentration the stronger the inverse association. There was no association among men with a low low density lipoprotein cholesterol concentration (defined as those with concentrations in the lowest fifth, < 3.63 mmol/l).

    For obvious reasons, studies on alcohol and risk must be natural experiments. Accordingly, it is not possible to conclude whether associations are causal. Suggestive of causality are a set of criteria accounted for in our study, such as temporality, strength of association, and biological plausibility.1 2

    The possibility of bias also has to be considered. Non-drinkers were older than drinkers. In regression analyses we took into account the possibility of a non-linear relation between age and risk. Including age as a continuous variable, a dichotomous variable, or several five year age group dummy variables had no influence on the results. Non-drinking was not simply a proxy for old age, suggesting increased risk. A bias caused by “sick non-starters” seems unlikely. We excluded all men with overt cardiovascular disease at the baseline, and relevant electrocardiographic changes were equally distributed among drinkers and abstainers. We discussed other potentially biasing factors in our paper and a previous one.3

    The BMJ is not a health magazine for the public. In our paper we did not attempt to deviate from the hypothesis advanced. We did not discuss the well known potential risks and side effects of alcohol consumption since public health advice was not the issue. In a liberal society with a free press it is generally not possible to prevent the public from misinterpreting scientific results.

    In his editorial Ian R White claims that our hypothesis has been tested before.4 No previous study has analysed the interaction of alcohol, low density lipoprotein cholesterol concentration, and risk, presenting data on the association between alcohol and risk stratified by different levels of lipid concentrations. Another claim is that our findings could be the result of chance. That is possible. We agree that the results of one epidemiological study can never stand alone.


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