New Controversy on Salt, Blood Pressure, and Cardiovascular Risk

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Lowering salt intake may not reduce population rates of hypertension and cardiovascular disease (CVD) and may even lead to an elevated risk of CVD death, suggests a report in the Journal of the American Medical Association.

The researchers analyzed prospective data on 3681 participants in two European population-based studies, all free of CVD at baseline. Data on blood pressure and sodium excretion at baseline and follow-up were available for 1499 participants. The effects of changes in blood pressure and sodium excretion on the incidence of mortality and morbidity were assessed.

At a median follow-up time of 7.9 years, the risk of CVD mortality was highest for participants at the lowest level of 24-hour sodium excretion. Cardiovascular mortality was 4.1 percent in the lowest tertile (mean, 107 mmol) versus 1.9 percent in the middle tertile (mean, 168 mmol) and 0.8 percent in the highest tertile (mean, 260 mmol). On multivariate analysis, the hazard ratio for death in the lowest tertile was 1.56.

In 2096 participants who were followed up for 6.5 years, the risk of hypertension was about the same—between 25.4 percent and 27.0 percent—across tertiles of urinary sodium excretion. Data on 1499 participants who were followed up for 6.1 years showed an increase of 0.37 mm Hg per year in systolic blood pressure. An increase of 100 mmol in sodium excretion was associated with an increase of 1.71 mm Hg in systolic blood pressure but no change in diastolic pressure.

The results pose questions about the recommendation to reduce population salt intake to lower the overall rate of CVD events. Changes in sodium excretion are linked to increased systolic blood pressure but not to increases in diastolic blood pressure or the risk of hypertension. The study also suggests a link between lower sodium excretion and higher CVD mortality in healthy individuals [Stolarz-Skrzypek K, et al. Fatal and nonfatal outcomes, incidence of hypertension, and blood pressure changes in relation to urinary sodium excretion. JAMA 2011; 305:1777–1785].