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BMJ No 7106 Volume 315 Letters Saturday 23 August 1997 Intersalt dataData linking sodium intake to subsequent morbid and fatal outcomes must be studiedEditor,Papers and editorials in the issue of 18 May 1996 addressed the relation of dietary sodium intake and blood pressure. The heart of the matter is whether a low sodium diet reduces blood pressure in populations. The BMJ printed a more and JAMA a less enthusiastic view of the magnitude of this relation.(1) Several commentators in the BMJ then made the unjustified leap of converting what is a scientific controversy about a physiological mechanism into a public health issue. Public health recommendations must be based on proof of safety and benefit. Even if a low sodium diet could lower the blood pressure of most people (probably not true) and both the diet and the change in blood pressure could be sustained (not established), this alone would not justify a recommendation to reduce sodium intake. For such advice to be responsibly given there must be evidence that the change will improve and not impair health. While the advantage of a lower blood pressure, at any level, is well established,(2) it is not true that every method to lower blood pressure would necessarily improve health. Some techniques to lower blood pressure, like giving short acting calcium antagonists,(3) may not be safe. All interventions aimed at enhancing or extending life by manipulating a single mechanism inevitably produce a variety of effects, some of which may not be advantageous. Extrapolation from mechanistic thinking demands evidence that the sum total of all the effects of the intervention - and not just one, such as lowering blood pressure - will help and not harm; and particularly here since the target is the whole population. A low sodium intake produces many effects, not all of which are salutary.(4) The integrated impact of these effects remains to be established. The scanty evidence directly linking sodium intake to morbidity and mortality is not encouraging.(5) Unfortunately, we simply do not know whether a universal change in sodium consumption will cause benefit or harm. Insufficient evidence - for good or ill - is not a sturdy basis for making health policy. Gratuitous exhortation, reflecting the hopes of even the most well meaning authorities, is no substitute for data. Toward this end, a good start would be to collect and analyse further observational data linking sodium intake to subsequent morbid and fatal outcomes. Michael Alderman President, American Society of Hypertension Department of Epidemiology and Social Medicine, References 1 Midagley J P, Matthew A G, Greenwood C M T, Logan A G. Effect of reduced dietary sodium on blood pressure. JAMA 1996;275:1590-7. 2 MacMahon S, Peto R, Cutler J, Collins R, Sorlie P, Neaton J, et al. Blood pressure, stroke and coronary heart disease. Part 1. Prolonged differences in blood pressure: prospective observational studies corrected for the regression dilution bias. Lancet 1990;335:765-74. 3 Psaty B M, Heckbert S R, Koepsell T D, Siscovick D S, Raghunathan T E, Weiss N S, et al. The risk of myocardial infarction associated with anti-hypertensive drug therapies. JAMA 1995;274:620-5. 4 Alderman M H, Madhavan S, Ooi W L, Cohen H, Sealey J E, Laragh J H. Association of the renin-sodium profile with the risk of myocardial infarction in patients with hypertension. N Engl J Med 1991;324:1098-104. 5 Alderman M H, Madhavan S, Cohen H, Sealey J E, Laragh J H. Low urinary sodium is associated with greater risk of myocardial infarction among treated hypertensive men. Hypertension 1995;25:1144-52.
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