Study questions salt, hypertension link

Lower urinary sodium excretion was not associated with less cardiovascular mortality or improved survival, new study findings indicate, raising questions about the true health benefits of current recommendations that favor cutting sodium intake population wide.

European researchers found that although systolic BP increases as urinary sodium excretion levels increase, diastolic BP does not, and neither do a patient's risks for hypertension and cardiovascular disease complications. In fact, patients with the lowest levels of sodium secretion had the greatest risk for CVD death, according to data published in the May 4 issue of the Journal of the American Medical Association.

“Taken together, our current findings refute the estimates of computer models of lives saved and health care costs reduced with lower salt intake,” Katarzyna Stolarz-Skryzpek, MD, PhD, of the University of Leuven in Belgium and the Jagiellonian University Medical College in Krakow, Poland, and colleagues from several other sites wrote.

They conducted a prospective population-based study involving 3,681 people without CVD to determine the relationship between sodium excretion, BP changes, mortality and morbidity over a median of 7.9 years.

The researchers analyzed 24-hour urinary sodium secretions and changes in BP for a median 6.1 years among 1,429 participants that had complete and accurate urine collection and who were not taking antihypertensive medications.

In a separate subsection of the cohort that involved 2,096 patients free of hypertension at baseline, the researchers studied incidence of the condition during a median 6.5-year follow-up.

Patients were stratified into low (average 107 mmol), medium (168 mmol) and high (260 mmol) sodium secretion groups. Average patient age at baseline ranged from 40.9 in the low tertile to 38.6 in the medium tertile and 38.6 in the high group.

The researchers found an inverse association between cardiovascular deaths and increasing 24-hour urinary sodium excretion, with deaths decreasing across tertiles — 50 deaths in the lowest tertile, 24 in the medium tertile and 10 in the highest tertile (P<0.001). Risk for cardiovascular death was significantly elevated among participants in the lowest tertile (HR=1.56; 95% CI: 1.02-2.36; P=0.04).

Furthermore, data indicated that urinary sodium secretion was not associated with hypertension incidence, with patients in the lowest tertile experiencing 187 new cases of hypertension vs. 175 in the highest tertile and 190 in the medium tertile.

Multivariate analyses revealed that although systolic BP increased by 1.71 mm of mercury with each 100-mmol increase in sodium secretion (P<0.001), no changes were noted in diastolic BP.

The researchers acknowledged several study limitations, including: a young study population and a short follow-up, which may underestimate cardiovascular death rates; inability to measure individual sodium sensitivity; and a cohort made up exclusively of white Europeans.

“[F]indings can not be extrapolated to Asian or in particular black individuals, who might be more salt sensitive than white people,” the researchers wrote.

They also emphasized that the findings do not negate the BP-lowering effects of salt intake in patients that are already hypertensive.

The average American consumes about 3,500 mg of sodium a day, according to the American Heart Association, which has set a goal to limit population-wide salt intake to 1,500 mg a day by 2020.

Skryzpek KS. JAMA. 2011;205:1777-1785.

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