A salt substitute reduces the risks of CVD, stroke, and death Original paper

Blood pressure (BP) is considered elevated between 120 and 129 mmHg systolic, and is formally classified as high when it reaches 130 mmHg systolic or 80 mmHg diastolic. Among the various factors that promote high BP (and thus the risk of CVD^[1]) is sodium chloride (table salt); there is abundant evidence that decreases in sodium intake promote decreases in BP. Sodium is delicious, however, so low-sodium diets can be difficult to stick to.

Potassium can reduce blood pressure,^[2] so potassium-containing salt substitutes (50–75% sodium chloride, 25–50% potassium chloride) can help reduce BP both by reducing sodium intake and by increasing potassium intake.

Note that sodium chloride (NaCl) is 39% sodium (Na) and 61% chloride (Cl) by weight, whereas potassium chloride (KCl) is 52% potassium (K) and 48% chloride (Cl) by weight. The graphic below shows sodium intake, and 4,600 mg of sodium is the content of 11,800 mg (11.8 grams!) of table salt.

Univariate metaregression for people with ≥131 mmHg of systolic blood pressure

Adapted from Graudal et al. Am J Clin Nutr. 2019 May^[3]

The Salt Substitute and Stroke Study (SSaSS) was a randomized controlled trial (RCT) conducted in 20,995 people (aged 65.4 on average; 49.5% female) from 600 villages in China. The participants (i) had a history of stroke or (ii) were ≥60 years old and had poorly controlled BP. Poorly controlled BP was defined as (i) systolic BP ≥160 mmHg or (ii) systolic BP ≥140 mmHg despite the use of antihypertensive medication.

The intervention group was provided with a salt substitute (75% sodium chloride, 25% potassium chloride), to be used for cooking and food preservation. The control group maintained their usual use of table salt (100% sodium chloride).

The primary outcome was the risk of stroke, both fatal and nonfatal. The two secondary outcomes were major cardiovascular events (nonfatal stroke, nonfatal acute coronary syndrome, or death from vascular causes) and all-cause mortality. Moreover, the safety of the salt substitute was determined by assessing the risks of hyperkalemia (a potentially life-threatening condition involving high levels of potassium in the blood) and sudden death.

The salt-substitute group had lower risks of stroke (2.91% vs. 3.37%, so 14% lower), cardiovascular events (4.91% vs. 5.63%, so 13% lower), and all-cause mortality (3.93% vs. 4.46%, so 12% lower). The risk of hyperkalemia did not differ between groups.

The participants were followed for 4.74 years on average. At baseline, their average sodium intake was 4,300 mg/day and their average potassium intake 1,400 mg/day. Over the course of the trial, the salt-substitute group decreased their sodium intake by 350 mg/day and increased their potassium intake by 803 mg/day. Compared to the control group, the salt-substitute group experienced a 3.34 mmHg reduction in blood pressure.

The Findings of the trial

Many of the case studies of (sometimes fatal) hyperkalemia caused by salt substitutes involved potassium intakes over 7,000 mg,^[4][5][6] so it isn’t too surprising that, in the present RCT, the increased potassium intake in the salt-substitute group (+803 mg/day) didn’t lead to an increased risk of hyperkalemia.

The present RCT did only limited kidney-function monitoring, however, and it excluded people with serious kidney disease and people who were taking potassium-sparing diuretics (two factors that can dramatically increase the risk of hyperkalemia). On the other hand, many of the participants used angiotensin-inhibiting medications — which can increase the risk of hyperkalemia by reducing potassium excretion — so the fact that even these participants didn’t suffer from hyperkalemia over the course of the trial is a good sign.

A 2011 meta-analysis of previous RCTs found that reducing sodium intake might reduce CVD risk. The included RCTs had limitations, however. One example is the use of comprehensive dietary changes to achieve sodium reductions (an imprecise method that introduces potential confounders). Another example is that some RCTs kept collecting data for years after the end of the intervention, which means that during most of the data-collection period the intervention group may have been consuming just as much salt as the control group.^[7]

The present RCT provides strong evidence that using a salt substitute to decrease sodium intake and increase potassium intake can decrease the risk of stroke and CVD in people at high risk of these diseases. Its results are consistent with those of a 2006 RCT (not included in the 2011 meta-analysis mentioned above) that observed a reduction in cardiovascular events in elderly men using a potassium-containing salt substitute.^[8]

Still, it’s important to interpret the present RCT in the proper context. At baseline, a 24-hour urine assessment showed that the participants had a high intake of sodium (4,300 mg/day, so a lot more than the DRI) and a low intake of potassium (1,400 g/day, so a lot less than the DRI). This is important because some observational evidence suggests that reducing sodium may be most beneficial in people with high sodium intakes^[9] and that, likewise, increasing potassium may be most beneficial in people with low potassium intakes.^[10] As a result, it remains difficult to say whether similar benefits would be seen in people with lower intakes of sodium or higher intakes of potassium.