https://immattersacp.org/weekly/archives/2011/05/10/1.htm

Higher-salt diets didn't increase mortality in European study

Higher sodium consumption was associated with increased systolic blood pressure, but not greater mortality or cardiovascular events, in a new prospective analysis of Europeans' sodium excretion.


Higher sodium consumption was associated with increased systolic blood pressure, but not greater mortality or cardiovascular events, in a new prospective analysis of Europeans' sodium excretion.

The study included 3,681 people without cardiovascular disease (CVD) at the start of the trial who were followed for a median of 7.9 years. They were divided into tertiles by their 24-hour urinary sodium excretion, and cardiovascular-related death rates were compared among the tertiles. The results were published in the May 4 Journal of the American Medical Association.

Over the entire course of the study, the patients with the lowest sodium excretion (mean, 107 mmol) had the highest death rate (4.1%), compared to 1.9% in the middle group (mean, 168 mmol) and 0.8% in the highest sodium group (mean, 260 mmol). The inverse association maintained significance, at a P value of 0.02, even when adjusted for multiple variables. The study also found no relationship between baseline sodium excretion and mortality or CVD events. Incident hypertension didn't vary significantly among the tertiles either.

A subset of 1,499 participants also had their blood pressure measured during the study. On average, their systolic blood pressure increased by 0.37 mm Hg per year, but their sodium excretion did not change. However, an adjusted analysis found that every 100-mmol increase in sodium excretion was associated with a 1.71-mm Hg increase in systolic blood pressure, but no change in diastolic blood pressure.

The study authors noted that other studies have analyzed the relationship between salt intake and hypertension and CVD, but few have used 24-hour urinary sodium excretion, which is the most accurate measure. They also noted that the inverse association between sodium intake and mortality found in this study is unlikely to result from reverse causality, because patients with existing CVD were excluded. The authors speculated instead that low salt intake may increase mortality because it can negatively impact sympathetic nerve activity, insulin sensitivity, the renin-angiotensin system and aldosterone secretion.

The study was limited by its inclusion of only relatively young, white Europeans, so the results may not apply to other races or to hypertensive patients. However, the authors believe that their results refute commonly publicized estimates of avoidable morbidity and mortality resulting from the general population's salt intake.

“[The results] do also not support the current recommendations of a generalized and indiscriminate reduction of salt intake at the population level,” the authors wrote.