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Abstract
The expectation that dietary sodium intake might influence cardiovascular disease occurrence has been based upon its impact on blood pressure (BP). Solid experimental data confirms the ability of large (75–100 mmols/24 hours) changes in dietary sodium to reduce pressure by, on average, mid-low single digits. However, there is substantial inter-individual variation in BP response. In addition, sodium restriction generates other, sometimes undesirable effects, including increased insulin resistance, activation of the renin-angiotensin system, and increased sympathetic nerve activity. The health effects of salt restriction are, therefore, the sum of these recognized, and probably other unrecognized, intermediate effects. Ideally, salt restriction would be tested in a randomized clinical trial. In its absence, there are 9 observational studies linking baseline sodium intake, estimated by either 24 hour urine or dietary intake, to morbidity and mortality. The results have been inconsistent. The only study in hypertensive patients, there was an inverse relation of sodium to cardiovascular outcome. In a Japanese study, stroke incidence was increased among males with the highest salt intake. Two studies found a direct relation of sodium intake to cardiovascular mortality in an obese minority of the group studied. Taken together, these results suggest, not surprisingly given the genetic, behavioral, and environmental variety of humankind, that heterogeneity best describes the relation of sodium intake to cardiovascular morbidity and mortality. In short, the available data provides no support for any universal recommendation of a particular level of dietary sodium.
