COMMENTARY

Is Cutting Salt Ever Harmful?

Nayan Arora, MD

Disclosures

April 12, 2021

Sodium restriction is one of the most common dietary recommendations made by US physicians. But there is lack of consensus on how low to go and whether cutting salt can ever be harmful.

Nayan Arora, MD

When our evolutionary ancestors left the salty environment of the sea for dry land, the burden of salt and water conservation fell to the kidneys. "The tenacious conservation of salt is one of the most primitive — if not the most primitive — of functions in the vertebrate kidney," wrote Homer W. Smith in From Fish to Philosopher.

Over time, dietary habits changed, and in the current US environment there is no shortage of salt. One nationally representative survey reported a dietary sodium intake of over 3600 mg daily in US adults. While major scientific societies are united in asking us to cut our salt intake, they generally differ regarding sodium thresholds. For example, the CDC advises a daily limit of 2300 mg of sodium, the AHA goes lower with 1500 mg, and the WHO sits in the middle at 2000 mg/day.

Sodium Intake and Hypertension

It is clear that sodium-restricted diets lower blood pressure. A Cochrane review of 185 studies demonstrated that a mean reduction in dietary sodium from a whopping 11.5 g/day to 3.8 g/day was associated with an average decrease of 5.5 mm Hg systolic and 2.9 mm Hg diastolic blood pressure in hypertensive individuals.

The effect of reduced sodium intake on systolic and diastolic blood pressure.

A low-sodium diet is associated with near linear improvement in blood pressure as compared with an intermediate- or high-sodium diet (see figure).

A low-sodium diet is associated with near linear improvement in blood pressure as compared with an intermediate- or high-sodium diet. A recent meta-analysis of 85 high-quality trials confirmed this linear relationship between reductions in dietary sodium and decreases in both systolic and diastolic blood pressure.

But does sodium restriction lead to improved cardiovascular outcomes? The data here are not quite as clear.

Dietary Sodium Intake and Cardiovascular Risk

One observational study in JAMA assessed the effects of sodium restriction on cardiovascular events in two cohorts at high risk for cardiovascular disease. They identified a J-shaped curve with sodium intake below 3 g/day associated with an increase in cardiovascular events.

The PURE study similarly found an association between sodium intake under 3 g and an increase in cardiovascular events. The majority of participants in this observational trial had no underlying cardiovascular disease.

More than 90% of dietary sodium is excreted in the urine, making urine sampling ideal to define sodium intake. The problem with these two observational studies is their use of a single spot urine collection to estimate 24-hour sodium excretion via the Kawasaki formula, a method that has been criticized and one that is not widely used clinically.

The Trials of Hypertension Prevention study, which used an average of three to seven carefully collected 24-hour urine collections to assess sodium intake, did not observe a J-shaped curve and instead found a significant decrease in cardiovascular events, even at the lower end of sodium intake (1500 mg/day).

In the Cochrane review, dietary sodium restriction was associated with neurohumoral activation, as defined by increased levels of renin, aldosterone, noradrenaline, and adrenaline, which in theory could lead to clinical harm. The Yanomami tribe of South America have been shown to consume < 1g (!) of sodium daily, associated with some of the highest renin and aldosterone levels ever recorded. However, they did not appear to be at increased risk for cardiovascular disease, a finding that may be confounded by their overall reduced life expectancy.

Sodium Restriction and Chronic Heart Failure

Patients with heart failure may be particularly vulnerable to neurohumoral activation. The advice to restrict salt in heart failure has been called into question.

A study from Italy randomly assigned 232 patients with heart failure with reduced ejection fraction to a diet with 2.7 g/day of sodium or a more restrictive 1.8 g. Both groups were limited to a liter of water per day and given diuretics and other guideline-recommended heart failure medications. The more liberal sodium group had lower BNP levels, as well as decreased rates of hospital readmissions and mortality, compared with the tighter sodium-restricted group.

In a similar trial by the same research group, patients with heart failure on a sodium-restricted diet had higher levels of renin, aldosterone, and inflammatory cytokines, as well as an increased frequency of hospital readmissions compared with the groups randomly assigned to usual sodium intake.

These Italian studies have several flaws. Some have suggested that there is duplication of data between the two studies. Additionally, they involved rigid diuretic protocols which may have influenced results. If patients on the stricter sodium diet were given the same dose of diuretics as those consuming more sodium, that would put them at greater risk for hypovolemia and hence secondary neurohumoral activation.

That said, it is theoretically possible that salt restriction (to a degree) leads to neurohumoral activation, which is initially compensatory in patients with heart failure to maintain organ perfusion; but over time, this neurohumoral activation becomes maladaptive and is a driver of poor prognosis and end organ damage.

Sodium can clearly have detrimental effects in the body, including myocardial hypertrophy, glomerular fibrosis, increased VEGF, and decreased nitric oxide.

Blame the Anion?

But what if our focus on sodium is shortsighted? When we restrict sodium intake, we're actually talking about both sodium and chloride.

Although sodium can be consumed in various forms, table salt, or sodium chloride (NaCl) — much of which is hidden in processed foods — provides 90% of dietary sodium consumption.

Decreased chloride levels in patients with congestive heart failure are independently associated with diuretic resistance, neurohumoral activation, and increased mortality. It is therefore possible that a significant degree of salt restriction can lead to poor outcomes in patients with heart failure because of chloride depletion.

While I am not ready to advocate for my patients with heart failure to liberally use their salt shaker, it's at least food for thought.

Nayan Arora, MD, is an academic nephrologist in Seattle, Washington. His practice focuses on the care of patients with cardiorenal syndrome. He is also interested in using social media to advance ideas in academic medicine. Outside of medicine he enjoys spending time with his wife and children, skiing, hiking, playing golf, and finding fantastic cups of coffee. You can follow him on Twitter @captainchloride

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