Commentary: Reflections on sick individuals and sick populations

James McCormick

Trinity College, University of Dublin, Department of Community Health and General Practice, 199 Pearse Street, Dublin 2, Ireland. E-mail: mccrmckj{at}tcd.ie

Since Geoffrey Rose published his paper there has been virtually no progress in reducing the incidence of disease by population change, with the exception of reduced cigarette smoking. This is not surprising.

In order for a population strategy to be effective two requirements need to be satisfied. The first is good evidence of a causal relationship between factors prevalent in populations and disease. The second, a strategy to alter the prevalence of such factors.

Good evidence of causal relationships must come from the study of individuals. Associations within populations are subject to the ecological fallacy, that is the error of imputing causality to such observations. For example, an association between saturated fat intake and the prevalence of breast cancer does not justify dietary advice to reduce the risk of this disease. In the examples cited by Geoffrey Rose, an association between diet and coronary heart disease and an association between salt intake and hypertension, there is no good evidence of a causal relationship based upon the study of individuals. Dietary manipulation has very small effects upon cholesterol levels and no randomized trial has shown unequivocal evidence that alteration in diet can reduce mortality from coronary heart disease. Similarily even stringent control of salt intake has very limited effects on blood pressure and no trial has demonstrated that such restriction reduces mortality from stroke.

Lack of awareness of the ecological fallacy has led to a plethora of unjustified advice and, it could be argued, to the growth of national hypochondriasis and the numbers of the worried well.

Cholesterol is a good risk marker for coronary heart disease. However, it may be that cholesterol is nothing more than a risk marker and not a cause of myocardial ischaemia. Individual cholesterol levels are largely independent of diet. In addition there is the surprising finding in the 4S Scandinavian Study that the use of statins had the same good effects in those whose cholesterol was 5 mmol/l as those whose cholesterol was 8 mmol/l.1

Geoffrey Rose’s optimism was based upon observations which assumed knowledge which we did not, and do not, have. It is at least arguable that public health strategies, as distinct from advice in the consultation, require something approaching certainty and that the ‘abominable no-men’ are important guardians of the public weal.

The best population strategies for reducing disease are those which involve no input from individuals, for instance, provision of clean water or fluoridation. When the cause of misfortune is manifest, car accidents or such like, the enforcement of law governing speed or the wearing of seat belts may become a justifiable interference with individual liberty.

It is too early to tell what the effect of our knowledge of the human genome will have. There can be no doubt that the environment will still be a major determinant of disease incidence and prevalence but it may be possible to identify differences in personal risk which may benefit individuals. Perhaps the study of those who do not get diseases will become as important as the study of the afflicted.

‘Sick individuals and sick populations’ is still an important paper and Geoffrey Rose’s comments upon the failure of case-control and cohort studies to detect necessary agents which are homogenous within a population remain entirely valid. However, altering population risk will, for the most part, remain an unreal aspiration.

References

1 Baseline serum cholesterol and treatment effect in the Scandinavian Simvastatin Survival Study(4S). Scandinavian Simvastatin Survival Study Group. Lancet 1995;345:1274–75.[ISI][Medline]





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