Salt, Blood Pressure, and Public Policy by David A. Freedman and Diana B. Petitti 1 August 2001 The "salt hypothesis" is that higher levels of salt in the diet lead to higher levels of blood pressure, increasing the risk of cardiovascular disease. The corollary is a public-health recommendation for a drastic cut in the level of dietary salt, by a factor of two or more. The salt hypothesis and its public health corollary have a number of highly visible advocates, both individual and corporate. Alderman [1] provides an incisive review of the evidence from epidemiologic studies, as well as experiments on humans and animals. He concludes that existing data do not support draconian restrictions on salt intake. He even cites some studies showing that a marked reduction in salt levels will do more harm than good, while properly noting the limitations in such data. Results depend on making the proper adjustments, but statistical science offers only the most general guidelines as to which adjustments should be made and which should not. Alderman also mentions two remarkable and little-known natural experiments-- the San Blas Indians and the Italian nuns-- which demonstrate that the link between dietary salt and blood pressure is weak at best. The San Blas study is cross-sectional rather than longitudinal, which perhaps weakens the force of the data. What would be the health effects of cutting salt intake in half? To settle the question, Alderman points out, long-term clinical trials would be needed, measuring primary endpoints of mortality and morbidity rather than intermediate endpoints like blood pressure. Others have reached similar conclusions about the state of the evidence and its policy implications [2,3], as does our own review [4]. We examined [4] the summary data published by INTERSALT [5]; if anything, these data contradict the salt hypothesis. The data cover 52 centers scattered around the world-- ranging from two Indian tribes in Brazil, through Chicago and Warsaw to Kenya and Beijing. As Alderman notes, however, such ecologic comparisons are especially prone to confounding. Alderman does not address the recent DASH-sodium trial which measured the effects of diet and salt on blood pressure [6]. This trial randomized subjects to two diets-- a control diet like a typical American diet, and a modified "Mediterranean" diet. Subjects were rotated through three levels of salt. The protocol for this trial [7]-- published two years after the trial was underway-- states that one of the two primary research questions was the effect of the DASH diet at various levels of salt intake. Additivity and linearity of effects of diet and salt were protocol-specified secondary questions. Such questions are given short shrift in the final report, which stresses the impact of reducing salt intake [6]. The accompanying news release is even more one-sided [7]. Published data summaries, sketchy as they are, indicate that adopting the DASH diet will lead to a marked reduction in systolic blood pressure, at ordinary levels of salt intake; but there are striking nonlinear interactions between salt and diet [6]. Indeed, one way to read the data is this: with a good diet, salt has almost no impact on systolic pressure. Practically no attention is given to the effect of salt on diastolic pressure, which is independently associated with cardiovascular mortality, and is the benchmark for estimating the public-health benefits from blood-pressure reduction [6,9]. Moreover, the study population substantially over-represents salt-sensitive demographic groups; extrapolating to the general population is therefore unwarranted [4,9], despite sweeping claims [6]. The response of the DASH investigators to these points is unconvincing [9]. The INTERSALT investigators refuse to make their data public [4]. So do the DASH investigators, who even decline requests for data on diastolic pressure [9]. The take- home message from the DASH trials [6,10], despite the NHLBI spinmeisters, is that diet matters more than salt. The effect of diet has been confirmed by a clinical trial on secondary prevention, with endpoints defined in terms of mortality and morbidity [11]. Funding agencies and medical journals have taken a stronger position favoring the salt hypothesis than is warranted, raising questions about the interaction between the policy process and science. Dietary advice on salt is presented to the public with rhetorical force that is not in any reasonable balance with the evidence. How did this come about? As we see it, public-policy programs, once in place, rapidly develop a life of their own. The possibility of benefits becomes probability, and probability becomes certainty. Ambiguity must be suppressed-- just as data must be hidden-- because the public is too easily confused. Only professionals can be trusted to weigh the evidence, and not all professionals at that. Besides, where is the harm in salt reduction? The harm is to rational discourse. The appearance of scientific unanimity is a powerful political tool, especially when the evidence is weak. Dissent becomes a threat, which must be marginalized. There soon comes about the pretense of public policy based on science, without the substance. Salt is only one example of this phenomenon. References 1. Alderman MH. Salt, blood pressure, and health: A cautionary tale. International Journal of Epidemiology. 2. Ebrahim S, Davey-Smith G. Lowering blood pressure: A systematic review of sustained effects of non-pharmacological interventions. Journal of Public Health Medicine 1998; 20; 441--8. 3. Graudal NA, Galloe AM, Garred P. Effects of sodium restriction on blood pressure, renin, aldosterone, catecholamines, cholesterols, and triglyceride. A meta-analysis. Journal of the American Medical Association 1998; 279; 1383-91. 4. Freedman DA, Petitti DB. Salt and Blood Pressure: Conventional wisdom reconsidered. Evaluation Review 2001; 25; 267-87. 5. Intersalt Cooperative Research Group. 1988. Intersalt: an international study of electrolyte excretion and blood pressure. Results for 24 hour urinary sodium and potassium excretion. British Journal of Medicine 297:319--28. 6. Sacks FM, Svetkey LP, Vollmer WM, et al. Effects on blood pressure of reduced dietary sodium and the dietary approaches to stop hypertension (DASH) diet. New England Journal of Medicine 2001; 344; 3--10. 7. Svetkey LP, Sacks FM, Obarzanek E, et al. The DASH diet, sodium intake and blood pressure trial (DASH-sodium): rationale and design. Journal of the American Dietetic Association 99 Suppl; 96-104. 8. NHLBI press release, May 17, 2000. http://www.nhlbi.nih.gov. 9. Correspondence. Dietary Sodium and Blood Pressure. NEJM 2001; 344; 1716-19. 10. Appel LJ, Moore TJ, Obarzanek E, et al. 1997. A clinical trial of the effects of dietary patterns on blood pressure. DASH Collaborative Research Group. New England Journal of Medicine 1997; 336; 1117-24. 11. de Lorgeril M, Salen P, Martin JL, et al. Mediterranean diet, traditional risk factors, and the rate of cardiovascular complications after myocardial infarction: final report of the Lyon Diet Heart Study [with comments]. Circulation 1999; 99; 779-85. Copyright by International Journal of Epidemiology http://www.ije.oupjournals.org