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Should we now abandon the low-salt diet?

A.J. Drake-Holland, M.I.M. Noble
DOI: http://dx.doi.org/10.1093/qjmed/hcr124 1103-1106 First published online: 10 August 2011

Introduction—controversy triggered by paper in JAMA

The publication in the May 2011 issue of JAMA of the paper by Stolarz-Skrzypek et al.1 once again raises previous opinions that low-salt diet in normal people can be harmful. The conclusions of that paper,1 that low-salt diet is associated with increased mortality has been heavily criticized in the US press, and the Lancet,2 and has been impressively rebutted by the leader of the research team.3 Interestingly, in the same study,1 there was no increased mortality in those with high salt intake. The JAMA study1 was large; 3681 subjects, normal European Caucasians, daily urinary sodium excretion rates were measured as an indication of sodium intake, as recommended by He and MacGregor4 (excess sodium is excreted in the urine5). We can expect protracted debate on the rights and wrongs, for and against the ‘salt causes hypertension’ hypothesis.

The issue that should be considered now is: Is there evidence to suggest that salt deprivation causes harm? The recommendation to the general public to restrict its sodium intake [mainly as ‘salt’—sodium chloride (the terms salt and sodium are often used synonymously. However, on a weight basis, salt comprises 40% sodium and 60% chloride. 1 g salt = 0.4 g sodium; 100 MEq = 2.9 g sodium = 5.8 g salt/sodium chloride = 100 mmol)] is based on a large body of opinion. Official bodies such as NICE6 and the Institute of Medicine7 repeat this recommendation in press releases, which do not include the evidence on which the advice is based and do not mention the contrary evidence. In an extreme form this is expressed as ‘a reduction in population salt intake worldwide will result in a major improvement in public health’,4 based on the fact that arterial blood pressure (BP) can be reduced in normals and hypertensives by salt restriction. The coronary heart disease policy model was used to make similar recommendations,8 even though the recommendations were challenged in the same journal.9

The extensive review of He and MacGregor4 (164 references) has been a major influence in producing the call for salt reduction in the normal population. The review covers evidence from experimental animals as well as studies in humans. However, most of the epidemiological studies correlate cardiovascular death with sodium excretion rate. This ignores the possibility of non-cardiovascular death and morbidity (particularly brain morbidity) due to salt deprivation. Moreover, the supposedly independent variable (salt) is used ‘after correction of confounding factors’,4 a kind of statistical cleaning-up process. Correlation does not mean cause and effect. There is much scatter in the results; more of the variance is not due to salt, than is attributable to salt. Indeed, not all these epidemiological studies give significance for the cardiovascular mortality vs. salt correlation, e.g. Scottish men;10 other population studies have mixed ethnic groups and the data may not apply to normal Caucasians. Other causes of our unease about accepting the conclusions of this review4 are: (i) the harmful effects of salt deprivation are not adequately addressed; (ii) the authors do not consider studies on salt loading, only deprivation; and (iii) there is no consideration of studies that measure total body sodium. We conclude that, in spite of considerable evidence compatible with the ‘salt causes hypertension’ hypothesis, it is not overwhelming, and implementation of salt deprivation of the normal Caucasian population with normal renal function is premature.

Primary prevention should not cause harm

Our recommendation for treatment in primary prevention (preventing normal people contracting disease) has always been, ‘Do not give a normal person a drug with side effects’. By the same token, we recommend, ‘Do not change a normal person's diet if it can cause harm’. Salt restriction can cause harm. Sodium is the essential ion for nerve conduction, muscle activation and cell signaling. Low urine sodium indicates inadequate intake,11 and a low-salt diet causes changes in brain function.12–14 The conclusions of Stolarz-Skrzypek et al.1 are in line with previous reports.15,16 There are other indications that caution should be deployed in this regard. Some elderly people and pregnant women have an inability of the kidneys to retain Na+; hyponatremia is an increasingly common problem in the elderly.17 Low salt intake can lead to hyponatremia,18 swelling of the brain and consequent damage, possibly associated with Alzheimer's amyloid plaque formation.19 Low salt intake combined with high water intake (‘detox diet’) caused 5259 hospital admissions in England in 2006–07. (One such patient with brain damage after ‘detox’ was awarded £800 000 as compensation.) Low-salt diet is associated with increased body mass index and alcoholism.20 Salt restriction elevates renin, angiotensin, aldosterone and the sympatho-adrenergic system. Are these effects desirable in the normal population?

Others agree on the dangers of sodium restriction.

‘Sodium restriction generates other, sometimes undesirable effects, including increased insulin resistance, activation of the renin–angiotensin system, and increased sympathetic nerve activity’.21 ‘Prognosis in hypertension is improved substantially by the array of antihypertensive drugs available today; we probably do not have to deprive even hypertensive patients of sodium if we have effective drugs with fewer dangers than salt restriction’.22

Salt restriction and BP

Solid experimental data confirms the ability of large (75–100 mmol/24 h) reductions in dietary sodium to reduce pressure by, on average, mid-low single digits.21 We accept the fact that, as summarized by a Cochrane Review,23 BP can be reduced a little by salt restriction, but the conclusion in that review that ‘a modest and long-term reduction in population salt intake could reduce strokes, heart attacks, and heart failure’23 seems us to express uncertainty, i.e. ‘could’ not ‘does’. Why subject the entire population to the possible risk of harm before there is certainty? Another Cochrane Review states, ‘the magnitude of the effect in Caucasians with normal blood pressure does not warrant a general recommendation to reduce sodium intake’.24 Evidence from salt restriction in hypertensive patients is applicable only to hypertensive patients, whose kidneys may have been affected by the disease, i.e. as a secondary effect,15 and not to normal people.

Salt and hypertension

As early as 1979, the whole subject was reviewed and discussed with the conclusion that convincing evidence that salt restriction should apply to normal people was lacking.16 The same skepticism has continued ever since. Another Cochrane review18 on this subject reported on patients with hypertension, not on normal people; it nevertheless concluded that solid evidence in favor of salt restriction was lacking: ‘Whether dietary sodium reduction should be recommended for the general population remains questionable because of marginal benefit and the suggestion of possible deleterious effects on cardiovascular outcomes independent of blood pressure’25; ‘Despite studies involving many thousands of subjects and patients, performed in many hundreds of centers, the issue (salt restriction for hypertension) remains controversial’22; and ‘The available data provides no support for any universal recommendation of a particular level of dietary sodium’.26. Nicolaysen and Iversen27 have come out against salt restriction for the normal Scandinavian population.

What evidence is not consistent with the ‘sodium causes hypertension’ hypothesis?

  1. When normal people with normal renal function ingest sodium, any excess is excreted in the urine,19 and total body sodium remains normal.5

  2. A salt-loading study28 has been used to support the ‘salt causes hypertension’ hypothesis. Reanalysis of the relationship, of systolic BP to salt loading of 7 days, in that study showed no significance (Spearman's rank correlation), until doses of >50 g/day (Caucasian subjects, n = 7). The other group of Afro-Caribbean subjects (n = 7) started to show a small increase in BP at 20 g/day, showing that ethnicity is important.24 Studies with longer periods of salt loading and more subjects (4 weeks, Kirkendal et al.29), 9 weeks (Gros et al.30) found no increase in BP in normotensive and hypertensive subjects, respectively.

  3. If too much sodium causes hypertension, hypertensive patients would have higher than normal sodium in the body. They do not; total exchangeable sodium (Na+) is not increased in Caucasian subjects with hypertension, even in the developmental stages of the disease15 or in patients with Type II diabetes mellitus.31

  4. Long-term sodium loading studies on normal people would be our preferred way of advancing this subject because it would greatly reduce ‘confounding factors’. As such studies are not likely to be possible, the most feasible studies now, and in the future, would be in normal subjects in whom BP is measured as a function of average daily urinary sodium excretion. Some such studies have been performed and show no consistent correlation.15,16 Correlation does not prove cause and effect, but lack of correlation could be argued to disprove cause and effect! There should be a focus in such studies on non-cardiovascular, particularly central nervous system, morbidity and mortality, and there must be distinction between ethnic groups.


Low-salt diets have been shown to be harmful in many cases. It should be recognized that salt restriction is a valid method of therapy for physicians treating patients with hypertension, renal disease and other sodium retaining clinical conditions (although we think pharmacological control is preferable). However, it does not follow logically from this that normal people can benefit from sodium restriction. The supposedly ‘overwhelming evidence’ in favor of depriving the normal population of sodium is not actually overwhelming and can be criticized. The evidence to the contrary, that normal salt intake is harmless also lacks certainty. The question remains open. In the meantime, there is concern about the harmful effects of sodium deprivation, including the recent report of increased mortality recorded with low-salt diet in a large cohort of normal subjects.1 If salt deprivation causes harm, and its benefits are uncertain, we suggest that a moratorium on dietary advice to the population to reduce salt ingestion would be wise, at least until the question of harm vs. benefit is clarified.


The authors would like to thank Michelle Elliot (The Robert Gordon University) for a literature review on the topic of Caucasian vs. Afro-Carribean hypertensive effects of salt, January 2010.

Conflict of interest: None declared.