Defending the JAMA Study on Salt: A Talk With Jan Staessen, MD, PhD

Linda Brookes, MSc


June 14, 2011

In This Article

Background to the Interview

A study by Dr. Staessen and colleagues in Belgium, Poland, the Czech Republic, Italy, The Netherlands, and the Russian Federation published recently in JAMA[1,2] has reignited the debate about the benefits of reducing salt in the diet (if it had ever died down). The results appeared to challenge the recommendations of current guidelines that population-wide reductions in sodium consumption will lower blood pressure and reduce cardiovascular risk.[3,4,5,6] Extrapolations from observational studies such as INTERSALT[7]and short-term intervention trials in hypertensive patients and normotensive individuals[8,9] led to the idea that a generalized reduction of sodium consumption in the general population must be beneficial. In contrast to these assumptions, the study by European investigators found that only systolic blood pressure increased slightly over time with increasing sodium excretion, but that this association did not translate into a higher risk for hypertension or cardiovascular disease complications.[1] In addition, lower sodium excretion was associated with higher cardiovascular disease mortality.

In what they believe to be the first longitudinal and comprehensive population-based study of the association between sodium consumption and various cardiovascular outcomes (blood pressure, hypertension, and events), Dr. Staessen and coinvestigators examined the incidence of mortality and morbidity and hypertension in relation to baseline 24-hour urinary sodium excretion. The study involved 3681 people without cardiovascular disease, all white Europeans, who were members of families randomly enrolled in the Flemish Study on Genes, Environment, and Health Outcomes (FLEMENGHO; 1985-2004) or in the European Project on Genes in Hypertension (EPOGH; 1999-2001). During a median follow-up of 7.9 years, cardiovascular deaths decreased across increasing tertiles of 24-hour sodium excretion, from 50 deaths in the low (mean, 107 mmol; 2.5 g sodium), 24 in the medium (mean, 168 mmol; 3.9 g), and 10 in the high excretion group (mean, 260 mmol; 6.0 g; P < .001), resulting in death rates of 4.1% 1.9%, and 0.8%, respectively. This significant inverse association between cardiovascular mortality and tertile of sodium excretion was retained in multivariate analyses (P = .02), with a hazard ratio of 1.56 in the low tertile (P = .04). Baseline sodium excretion did not predict either total mortality or fatal combined with nonfatal cardiovascular events.

In the 2096 participants who were normotensive at baseline, who were followed for a median of 6.5 years, increasing tertiles of 24-hour urinary sodium were not associated with increased risk for hypertension. Another subgroup of 1499 participants who had blood pressure and sodium excretion measured at baseline and at last follow-up and who were followed for a median of 6.1 years showed average annual increases in blood pressure of 0.37 mm Hg systolic and 0.47 mm Hg diastolic blood pressure (P < .001) but no changes in sodium excretion. However, in multivariable analyses, a 100-mmol increase in sodium excretion was associated with a significant 1.71-mm Hg increase in systolic blood pressure (P < .001) but no significant change in diastolic blood pressure.

The authors concluded, "The associations between systolic pressure and sodium excretion did not translate into less morbidity or improved survival. On the contrary, low sodium excretion predicted higher cardiovascular mortality. Taken together, our current findings refute the estimates of computer models of lives saved and health care costs reduced with lower salt intake. They do also not support the current recommendations of a generalized and indiscriminate reduction of salt intake at the population level. However, they do not negate the blood pressure-lowering effects of a dietary salt reduction in hypertensive patients."

Publication of the study elicited many comments in the news media, including spokespersons for US national organizations such as the American Heart Association.[10,11,12,13] A special editorial published later in The Lancet called the study “disappointingly weak,” saying that it “contributes little to our understanding of salt and disease.”[14]

In an interview with Linda Brookes, MSc, for Medscape Cardiology, Dr. Staessen gave his reaction to these comments.


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