Hypertension is a leading risk of death in the world. It is widely believed that high dietary salt contributes to increased blood pressure. There has been a continuing debate as to the importance of sodium in the causation and control of hypertension. On one side of the spectrum, various salt studies have led to overwhelming evidence for a causal relationship between dietary salt intake and blood pressure levels in adult humans. On the other side of the spectrum, salt-BP association was generally found to not be very strong.
The main evidence for the association between high intakes of salt and blood pressure relates to sodium. The major source of sodium in the diet is from salt (NaCl); the terms salt and sodium are often used interchangeably. Sodium is a major cation in the extracellular fluid, with a key role in maintaining fluid balance in the body. The kidneys regulate sodium and water homeostasis, and the sodium composition is regulated largely by renal excretion and conservation. Most functions of sodium are interdependent with potassium (Campbell, N., & Mohan, S. 2009). Albeit any decrease in extracellular fluid volume due to decrease in plasma volume, lowers blood pressure and any rise in extracellular fluid volume increase blood pressure by increasing plasma volume.
Even though sodium intake and the bodily processes that it triggers is fairly complex in terms of development of hypertension, many studies have been done on animals to illustrate the causal effect between dietary sodium and blood pressure increase. Many animal species, such as rats, rabbits, dogs, pigs and monkeys, have an increase in blood pressure when high amounts of sodium is provided (Campbell, N., & Mohan, S. 2009). The inability of human kidneys to fully excrete excess sodium is one of the major mechanisms in the association between sodium intake and blood pressure. The process of aging can deter the ability of a human to excrete, this in turn can cause an increase in blood pressure when only even a small amount of sodium is consumed. Sodium has played a major role in the evolution of human; it was used as a major tool for food preservation. Until recently, there was limited access to sodium and hence, diets typically contained a low amount of sodium (<0.25 g) per day (Campbell, N., & Mohan, S. 2009). However, with widespread inexpensive commercial access to sodium, most diets now have almost 10 g daily (Campbell, N., & Mohan, S. 2009). It is likely that the rapid increase in the consumption of dietary sodium will directly influence the presently dominance of high blood pressure in all type of individuals.
Different animal models have been used to test for sodium-BP relationship; they have been developed to be more or less sensitive to dietary sodium. Many clinical trials of sodium reduction were done on humans; they gave results that were very convincing in the direct relationship between dietary sodium and blood pressure increase. Various clinical trials have presented solid evidence that sodium reduction decreases blood pressure. There have been studies where sodium was either withdrawn or supplemented (Hollenberg, N. 2006). The result of these studies were converging and fairly consistent in terms of sodium-BP association in certain population. The response to a reduction in sodium of approximately 100 mmol/day led to a reduction in systolic BP of 4 – 5 mmHg, and a decrease in diastolic blood pressure of 1 – 3 mmHg (Hollenberg, N. 2006).
The results presented were very consistent with individual blood pressures fluctuating widely in response to high or low sodium intakes. McCarron (2000) showed this heterogeneity (the fluctuation of blood pressures in response to varying sodium intakes) by showing that ~18% of 163 participants with a high sodium intake had blood pressure increases >5 mm Hg, whereas ~15% had blood pressure decreases >5 mm Hg,…