Context

Numerous studies have shown that a high dietary salt intake increases blood pressure (BP) and the risk of cardiovascular events.1 ,2 Conversely, a moderate and even low-level salt intake lowers BP in a dose-dependent way.

Findings

The present study corroborates the findings showing that a ‘modest’ reduction in salt intake from 9.4 to 4.4 g/day caused a significant fall in BP in hypertensive as well as normotensive individuals (systolic change −4.18 mm Hg (95% CI −5.18 to −3.18; p<0.0001)). This fall in BP was associated with a ‘small physiological increase in plasma renin, aldosterone and norepinephrine’. The authors stated that the current recommendations to reduce salt intake to 5–6 g/day are not ideal. A further reduction to 3 g will have a greater effect and should become the long-term target for population salt intake.

Commentary

Most hypertension guidelines are consistent in recommending a salt intake of below 5–6 g/day. Since the initial report in 1977, the US Joint National Committee guidelines3 have been remarkably consistent in recommending a sodium intake of <4 g in hypertensive patients. Stubbornly, the salt intake in the US population has remained almost unchanged (between 7 and 11 g/day), despite these strong recommendations. In spite of consistently high salt intake, the stroke rate has fallen over 65% in the US population during the same period. This would indicate that the guideline recommendations have had remarkably little effect on changing dietary habits and, importantly, that it is possible to drastically reduce stroke risk despite the high sodium intake. The recent European guidelines4 recommend a daily intake of 5–6 g of salt for the general population. They cautiously state that ‘there is no evidence that reducing sodium from high to moderate intakes causes harm’. Vigorous efforts in the UK have reduced salt intake by only 10% over the past 20 years.

Surprisingly, most guidelines do not give a lower limit for recommended salt intake. This seems to indicate that it is not possible to ingest sodium levels so low that they actually cause harm or that there are no unsafe lower limits of sodium intake. This assumption is largely based on studies in Yanomamo Indians who consumed exceedingly little salt and have a very low prevalence of hypertension. Not surprisingly, plasma renin activity and aldosterone levels were found to be drastically elevated in these tribes. In fact these physiological aldosterone levels were in the range observed only with primary aldosteronism in Westernised populations. Thus, there is little doubt that low dietary salt intake will stimulate the rennin–angiotensin cascade, sympathetic nervous system and cause insulin resistance and possibly dyslipidaemia. Indeed, in the present meta-analysis, there was a 0.26 ng/mL/h increase in plasma renin activity, 31.67 pg/mL increase in norepinephrine and 73.20 pmol/L increase in aldosterone. The authors interpreted these changes as ‘small and physiological’. Obviously, a more drastic dietary salt reduction to 3 g/day might trigger changes that are neither small nor physiological. This may be one reason why cardiovascular outcomes are exceedingly controversial in patients on a low salt diet, and a J-shaped relationship between sodium intake and cardiovascular death has been shown in a few studies. In the ONTARGET study,5 there was a J-shaped association for cardiovascular death and congestive heart failure, but not for myocardial infarction or stroke. Epidemiological associations are never free of confounding despite extensive adjustments; therefore, these findings are difficult to interpret.

However, it is important to remember that BP is a surrogate endpoint that often (but not always) moves parallel with the real endpoints: heart attack, stroke, heart failure and death. The metaregression analysis by He and colleagues predicted that a reduction of 6 g/day in salt intake would decrease systolic BP by 5.8 mL of mercury. As acknowledged, this is exploratory and is prone to confounding; however, the dose relationship between salt intake and BP has been established in RCTs. When focusing on BP only, the recommendations to reduce salt intake from the current level of 9–12 g/day to 5–6 g/day is not ideal and that a further reduction to 3 g/day will have a greater effect. However, the compensatory, not so small ‘physiological’ increases in neurohumoural findings may well override the potential benefits and, paradoxically, increase the risk of stroke, heart attack and death.

The controversy regarding the lower limit of salt intake is prone to remain unresolved until an RCT will give us an answer. A compromise on a modest salt reduction will lower BP and very likely reduce the risk of cardiovascular disease although salt intake below 4–5 g/day seems to confer no further risk reduction. Thus, efforts to moderate dietary salt intake in individual patients and possibly in populations from the current high intake are probably sensible and achievable. However, a very low salt intake seems to confer no benefit, may even be harmful and is unlikely to be practically attainable.