Does reducing salt intake increase cardiovascular mortality?

Overwhelming evidence shows that reducing salt intake from 9-12 to 5-6  g/d lowers blood pressure, thereby preventing cardiovascular disease. A recent paper claims that lower salt intake is associated with higher cardiovascular mortality despite lower blood pressure. The study is flawed and cannot refute the evidence for the benefits of salt reduction.

Sodium: a wolf in sheep's clothing.

High blood pressure is the main cause of disease-related morbidity and mortality worldwide. It is virtually absent in populations that consume natural foods low in sodium. In other countries, however, where the individual intake of sodium is at least 10 times greater, the prevalence of arterial hypertension is about 40%.

Plasma sodium stiffens vascular endothelium and reduces nitric oxide release.

Dietary salt plays a major role in the regulation of blood pressure, and the mineralocorticoid hormone aldosterone controls salt homeostasis and extracellular volume. Recent observations suggest that a small increase in plasma sodium concentration may contribute to the pressor response of dietary salt. Because endothelial cells are (i) sensitive to aldosterone, (ii) in physical contact with plasma sodium, and (iii) crucial regulators of vascular tone, we tested whether acute changes in plasma sodium concentration, within the physiological range, can alter the physical properties of endothelial cells.

Links between dietary salt intake, renal salt handling, blood pressure, and cardiovascular diseases.

Epidemiological, migration, intervention, and genetic studies in humans and animals provide very strong evidence of a causal link between high salt intake and high blood pressure. The mechanisms by which dietary salt increases arterial pressure are not fully understood, but they seem related to the inability of the kidneys to excrete large amounts of salt. From an evolutionary viewpoint, the human species is adapted to ingest and excrete <1 g of salt per day, at least 10 times less than the average values currently observed in industrialized and urbanized countries.

Plasma sodium and hypertension.

Dietary salt is the major cause of the rise in the blood pressure with age and the development of high blood pressure in populations. However, the mechanisms whereby salt intake raises the blood pressure are not clear. Existing concepts focus on the tendency for an increase in extracellular fluid volume (ECV), but an increased salt intake also induces a small rise in plasma sodium, which increases a transfer of fluid from the intracellular to the extracellular space, and stimulates the thirst center.

Plasma sodium: ignored and underestimated.

Salt intake is a major regulator of blood pressure. There is evidence that those who develop high blood pressure have an underlying defect in the ability of the kidney to excrete salt. It has been suggested that this results in a greater tendency to retain sodium and an increased compensatory response that is responsible for the rise in blood pressure.

Sodium and blood pressure.

The human race is genetically programmed to consume less than 1 g of salt per day. In most human populations, the diet contains 6 to 12 g of salt per day and, in contrast to populations that consume less than 3 g of salt per day, their blood pressure rises with age. Independent of the rise in blood pressure, a high-salt diet also increases left ventricular mass, incidence of strokes, stiffness of conduit arteries, and activity of resistance arteries.