Correspondence
Dietary Sodium and Blood Pressure
N Engl J Med 2001; 344:1716-1719May 31, 2001
- Article
To the Editor:
The DASH–Sodium Trial (Jan. 4 issue)1 has demonstrated that a reduction in sodium intake over a period of 30 days lowers blood pressure. This finding is consistent with what more than 100 previous short-term, randomized trials have convincingly shown. What is remarkable — and disappointing, given this demanding and costly undertaking — is that the report was limited to the single selected favorable effect of salt on blood pressure, to the exclusion of other important physiological effects. For example, reducing the consumption of sodium also increases the plasma renin level by a factor of 3.6 and the aldosterone level by a factor of 3.2 — effects proportional to the degree of sodium reduction.2
The relation between sodium intake and all physiological phenomena is of great scientific interest. By contrast, patients, physicians, and public health advocates need to know how salt intake affects the quality and duration of life. The scanty published data available are not encouraging to those who preach salt restraint. An exception is the finding in a subgroup of obese subjects (28 percent) in the National Health and Nutrition Examination Survey Epidemiologic Follow-up Study of a direct relation between salt intake and cardiovascular outcome. No such relation appeared in the nonobese majority (72 percent).3 Moreover, in the entire survey population, there was an inverse relation between sodium intake and cardiovascular morbidity.4
Perhaps in some people the hemodynamic benefits of salt restriction will outweigh its hormonal and metabolic hazards. However, at this point, in the absence of strong evidence of a consistent health effect, a single universal recommendation for a reduction in dietary sodium reflects faith more than science.
4 ReferencesMichael Alderman, M.D.
Albert Einstein College of Medicine, Bronx, NY 10461-16021
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. N Engl J Med 2001;344:3-10
Full Text | Web of Science | Medline2
Graudal NA ,Galloe AM ,Garred P . Effects of sodium restriction on blood pressure, renin, aldosterone, catecholamines, cholesterols, and triglyceride: a meta-analysis. JAMA 1998;279:1388-1391
CrossRef | Web of Science3
He J ,Ogden LG ,Vupputuri S ,Bazzano LA ,Loria C ,Whelton PK . Dietary sodium intake and subsequent risk of cardiovascular disease in overweight adults. JAMA 1999;282:2027-2034
CrossRef | Web of Science | Medline4
Alderman MH ,Cohen H ,Madhavan S . Dietary sodium intake and mortality: the National Health and Nutrition Examination Survey (NHANES I). Lancet 1998;351:781-785
CrossRef | Web of Science | Medline
To the Editor:
Sacks et al. concluded that their results in the DASH–Sodium Trial “provide support for a more aggressive target for reduced sodium intake, in combination with the use of the DASH (Dietary Approaches to Stop Hypertension) diet, for the prevention and treatment of elevated blood-pressure levels.” That conclusion is misleading at best.
Given the characteristics of the study cohort, which are greatly skewed toward the expression of salt sensitivity, the failure to provide the Journal 's readers with all the available data must be addressed. Even the very limited data provided in Figure 1 and Figure 2 of the article indicate that from the standpoint of clinical application, any effect of salt restriction on blood pressure was limited to black women with hypertension. Thus, the authors' statement that these findings are broadly applicable to the entire population is not true. To prove otherwise, the authors are obligated to report, in a format similar to that of Figure 1, the analyses of subgroups defined according to race, presence or absence of hypertension, sex, age, and body-mass index.
Those data are necessary to document the principal finding of the study: for the vast majority of people, overall dietary improvements eliminate the effects of salt on blood pressure. Earlier reports1,2 that adequate mineral intake from dairy products, fruits, and vegetables is far more important than salt in determining blood pressure have been confirmed by this study. If the authors had provided graphs that told the whole story, that conclusion would have been readily apparent.
Unfortunately, as currently presented, these data only provide further justification to the 70 percent of recently surveyed Americans who said they do not trust the government's dietary recommendations.3 As others have put it, the salt-restriction advocates want to protect the public not only from salt but also from the data.4
4 ReferencesDavid A. McCarron, M.D.
Oregon Health Sciences University, Portland, OR 97201-29401
McCarron DA ,Morris CD ,Cole C . Dietary calcium in human hypertension. Science 1982;217:267-269
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McCarron DA ,Morris CD ,Henry HJ ,Stanton JL . Blood pressure and nutrient intake in the United States. Science 1984;224:1392-1398
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Patterson RE ,Satia JA ,Kristal AR ,Neuhouser ML ,Drewnowski A . Is there a consumer backlash against the diet and health message? J Am Diet Assoc 2001;101:37-41
CrossRef | Web of Science | Medline4
Freedman DA, Petitti DB. Salt and blood pressure: conventional wisdom reconsidered. Evaluation Review (in press).
To the Editor:
The continuing controversy about general advice to reduce dietary sodium has arisen in part because the effect of sodium may be limited to subgroups of the population who are salt-sensitive. In their discussion of the effect of sodium reduction in persons without hypertension, Sacks et al. highlight the reductions in systolic blood pressure that occurred in subjects on the control diet. Figure 2 of the article shows that the reduction in sodium intake in subjects on the DASH diet had a significant effect on systolic blood pressure in persons without hypertension only if they were black and only when they switched from the high-sodium to the low-sodium diet.
The risk of coronary disease increases as the diastolic blood pressure increases within quintiles of systolic blood pressure.1 A meta-analysis of observational studies of blood pressure, stroke, and coronary disease2 presents data according to diastolic but not systolic blood pressure. A meta-analysis of randomized trials of antihypertensive-drug therapy shows a reduction in the risks of stroke and coronary heart disease in relation to reductions in diastolic but not systolic blood pressure.3 To arrive at the best estimates of the expected reductions in disease events that would result from changes in the diets of various subgroups — especially persons without hypertension — information is required about the effect on diastolic blood pressure of lowering dietary sodium in the DASH and control diets for subgroups defined by ethnic background, presence or absence of hypertension, and sex.
The most recent meta-analysis of clinical trials of sodium reduction reported no significant effect of sodium reduction on diastolic blood pressure in persons without hypertension.4
4 ReferencesDiana B. Petitti, M.D.
Kaiser Permanente Southern California, Pasadena, CA 91188David Freedman, Ph.D.
University of California at Berkeley, Berkeley, CA 94720-38601
Stamler J ,Stamler R ,Neaton JD . Blood pressure, systolic and diastolic, and cardiovascular risks. Arch Intern Med 1993;153:598-615
CrossRef | Web of Science | Medline2
MacMahon S ,Peto R ,Cutler J , et al. Blood pressure, stroke, and coronary heart disease. I. Prolonged differences in blood pressure: prospective observational studies corrected for the regression dilution bias. Lancet 1990;335:765-774
CrossRef | Web of Science | Medline3
Collins R, Peto R. Antihypertensive drug therapy: effects on stroke and coronary heart disease. In: Swales JE, ed. Textbook of hypertension. Oxford, England: Blackwell Scientific, 1994:1156-64.
4
Graudal NA ,Galloe AM ,Garred P . Effects of sodium restriction on blood pressure, renin, aldosterone, catecholamines, cholesterols, and triglyceride: a meta-analysis. JAMA 1998;279:1388-1391
CrossRef | Web of Science
To the Editor:
In their report of the 90-day DASH–Sodium Trial, Sacks et al. do not set their findings in the context of longer-term trials in which sodium intake has been manipulated to reduce blood pressure. We have identified 10 randomized, controlled trials that lasted six months or longer. Four trials, all conducted in the United States, were similar in size to the DASH–Sodium Trial, having at least 200 participants (Table 1Table 1
Results of Large Randomized, Controlled Trials in Which Sodium Intake Was Lowered to Reduce Blood Pressure.).In three of these trials, involving adults not receiving medication who had high-normal blood pressure,1-3 the difference between the mean reduction in systolic blood pressure in the experimental group and that in the control group was modest after 6 months of intervention and became minimal after 12 months. In the fourth trial, the Trial of Nonpharmacologic Interventions in the Elderly,4 however, there was observable but limited success in weaning seniors off antihypertensive medication by means of a low-sodium diet.
In all four trials, there was difficulty in maintaining sodium reduction at the targeted level over the long term, even though the interventions were intensive. This may explain the minimal efficacy, although an alternative hypothesis is that baroreceptor and renal homeostasis through renin–angiotensin mechanisms restored blood pressure to its preintervention level, despite the reduction in sodium.5 Thus, it is improbable that the reductions in blood pressure ascribed by Sacks and colleagues to the manipulation of sodium intake (as distinct from the reductions that were due to the DASH diet) could be sustained over the long term in adults not receiving medication, either in a clinical situation or in the general population. Nevertheless, the issue of whether low sodium intake from childhood promotes life-long normotension remains to be resolved.
5 ReferencesChristopher Bartlett, Ph.D.
University of Bristol, Bristol BS8 2PR, United KingdomLee Hooper, B.Sc.
University Dental Hospital of Manchester, Manchester M15 6FH, United KingdomShah Ebrahim, M.D.
University of Bristol, Bristol BS8 2PR, United Kingdom1
The Hypertension Prevention Trial Research Group
CrossRef | Web of Science | Medline2
The effects of nonpharmacologic interventions on blood pressure of persons with high normal levels: results of the Trials of Hypertension Prevention, Phase I. JAMA 1992;267:1213-1220[Erratum, JAMA 1992;267:2330.]
CrossRef | Web of Science3
The Trials of Hypertension Prevention Collaborative Research Group
CrossRef | Web of Science | Medline4
Whelton PK ,Appel LJ ,Espeland MA , et al. Sodium reduction and weight loss in the treatment of hypertension in older persons: a randomized controlled trial of nonpharmacologic interventions in the elderly (TONE). JAMA 1998;279:839-846
CrossRef | Web of Science | Medline5
Navar LG . The kidney in blood pressure regulation and development of hypertension. Med Clin North Am 1997;81:1165-1198
CrossRef | Web of Science | Medline
Author/Editor Response
The authors reply:
To the Editor: The contribution of the DASH–Sodium Trial to the salt issue is data on the magnitude of the reduction in blood pressure related to a reduction in sodium. In our view, the magnitude is greater in the DASH–Sodium feeding study than has been reported in meta-analyses because people have serious difficulty finding enough low-sodium foods to enable them to adhere fully to reduced-sodium diets. We hope that the food industry will respond to the DASH–Sodium findings as a business opportunity.
We are surprised by Alderman's assertion that reduced sodium intake, especially to 65 mmol per day, is harmful. Reduced sodium does raise the plasma renin level, but so does diuretic therapy, which prevents cardiovascular disease. Moreover, in a large sample of the general population, the plasma renin level was not associated with cardiovascular disease.1 Experience with antihypertensive drugs shows that any reduction in blood pressure reduces cardiovascular disease. Mortality trials are not required for drug approval. Should sodium reduction be different? Finally, the epidemiologic study by Alderman et al.2 shows an increase in the rate of death from cardiovascular disease with higher salt intake when the analysis is appropriately adjusted for the total caloric intake of the subjects.
We assure McCarron and readers that the DASH–Sodium findings are qualitatively the same among all subgroups but differ quantitatively, as we showed in representative examples. We plan to publish the full subgroup results soon. The substantial reductions in blood pressure give additional strength to the long-standing dietary guidelines of public and private health organizations.
Petitti and Freedman focus on a subgroup effect that did not attain statistical significance, while ignoring the consistency of the direction of the results for all subgroups, which vary only in magnitude. Moreover, a substantial proportion of white and normotensive persons are indeed sensitive to salt.3 Systolic blood pressure was prespecified as the trial's primary outcome because it is more closely linked than diastolic blood pressure to cardiovascular disease.4
We agree with the view of Bartlett et al. that difficulty in achieving long-term adherence to low-sodium diets limits the long-term reduction in blood pressure. In the outstanding trial of MacGregor et al.,5 the reduction of sodium intake from 200 to 50 mmol per day in a highly motivated group of subjects with hypertension reduced systolic blood pressure by 18 mm Hg after one year — the same as the reduction after one month. There is no indication in the literature of an adaptation effect.
5 ReferencesFrank M. Sacks, M.D.
Harvard School of Public Health, Boston, MA 02115Michael A. Proschan, Ph.D.
National Heart, Lung, and Blood Institute, Bethesda, MD 20892Laura P. Svetkey, M.D.
Duke University School of Medicine, Durham, NC 27710for the DASH–Sodium Collaborative Research Group
1
Meade TW ,Cooper JA ,Peart WS . Plasma renin activity and ischemic heart disease. N Engl J Med 1993;329:616-619
Full Text | Web of Science | Medline2
Alderman MH ,Cohen H ,Madhavan S . Dietary sodium intake and mortality: the National Health and Nutrition Examination Survey (NHANES I). Lancet 1998;351:781-785
CrossRef | Web of Science | Medline3
Stamler J ,Neaton JD ,Wentworth DN . Blood pressure (systolic and diastolic) and risk of fatal coronary heart disease. Hypertension 1989;13:Suppl I:I-24
Weinberger MH ,Miller JZ ,Luft FC ,Grim CE ,Fineberg NS . Definitions and characteristics of sodium sensitivity and blood pressure resistance. Hypertension 1986;8:Suppl II:II-1275
MacGregor GA ,Markandu ND ,Sagnella GA ,Singer DR ,Cappuccio FP . Double-blind study of three sodium intakes and long-term effects of sodium restriction in essential hypertension. Lancet 1989;2:1244-1247
CrossRef | Web of Science | Medline
- Citing Articles (3)
Citing Articles
1
D. A. McCarron. (2008) Dietary sodium and cardiovascular and renal disease risk factors: dark horse or phantom entry?. Nephrology Dialysis Transplantation 23:7, 2133-2137
CrossRef2
J. Ian S. Robertson. (2003) Dietary salt and hypertension: a scientific issue or a matter of faith?. Journal of Evaluation in Clinical Practice 9:1, 1-22
CrossRef3
Abraham Aviv. (2002) Salt consumption, reactive oxygen species and cardiovascular ageing: a hypothetical link. Journal of Hypertension 20:4, 555-559
CrossRef
