Salt substitutes may reduce the risk of clinical outcomes of cardiovascular diseases

Cardiovascular diseases are the leading cause of death worldwide, and high blood pressure is a major risk for premature death. Excess dietary sodium and insufficient dietary potassium are both well-established causes of high blood pressure. Randomised trials demonstrate that reduced dietary sodium consumption or potassium supplementation lowers blood pressure. Sodium-reduced, potassium-enriched salt substitutes, in which a proportion of the sodium chloride (NaCl) in regular salt is replaced with potassium chloride (KCl), combine these blood pressure-lowering effects.

The recently reported Salt Substitute and Stroke Study (SSaSS), the largest ever trial of a potassium-enriched salt substitute, showed clear blood pressure-mediated protective effects for stroke, major cardiovascular events and premature death. The trial also addressed concerns about possible adverse effects of dietary potassium supplementation, with no evidence of any harmful effect on hyperkalaemia risk among the 20 995 trial participants. Prior systematic reviews of salt substitutes have reported clear beneficial effects on blood pressure levels, but effects on clinical outcomes and the risk of premature death have been ill-defined due to sparse data.

This systematic review summarised the effects of salt substitute on blood pressure and clinical outcomes for all available trials. There were 21 trials and 31 949 participants included, with 19 reporting effects on blood pressure and 5 reporting effects on clinical outcomes. Overall reduction of systolic blood pressure (SBP) was −4.61 mm Hg (95% CI −6.07 to −3.14) and of diastolic blood pressure (DBP) was −1.61 mm Hg (95% CI −2.42 to −0.79). Reductions in blood pressure appeared to be consistent across geographical regions and population subgroups defined by age, sex, history of hypertension, body mass index, baseline blood pressure, baseline 24-hour urinary sodium and baseline 24-hour urinary potassium (all p homogeneity >0.05). Metaregression showed that each 10% lower proportion of sodium choloride in the salt substitute was associated with a −1.53 mm Hg (95% CI −3.02 to −0.03, p=0.045) greater reduction in SBP and a −0.95 mm Hg (95% CI −1.78 to −0.12, p=0.025) greater reduction in DBP. There were clear protective effects of salt substitute on total mortality (risk ratio (RR) 0.89, 95% CI 0.85 to 0.94), cardiovascular mortality (RR 0.87, 95% CI 0. 81 to 0.94) and cardiovascular events (RR 0.89, 95% CI 0.85 to 0.94).

The effects of salt substitutes on blood pressure were largely consistent across trial subsets divided by population characteristics, as well as across the predefined SSaSS participant subgroups. Since blood pressure lowering is the mechanism by which salt substitutes confer their cardiovascular protection, the observed consistent blood pressure reductions make a strong case for generalisability of the cardiovascular protective effect observed in SSaSS both outside of China and beyond the SSaSS population.

Further investigation of the potential for population-wide salt substitution is warranted since the available data indicate that salt substitutes are likely to offer large benefits across diverse communities with a very low likelihood of causing harm.



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