The long-standing debate on the impact of salt on health has been characterized by claims that salt reduction would improve cardiovascular health. In contrast, there is a considerable body of documented knowledge that asserts this claim as being without scientific merit. Despite this, the FDA has been asked to revise the regulatory status of salt and establish restrictive food labeling regarding salt. The outcome of restrictive sodium labeling may induce the food industry and consumers to significantly cut back on salt consumption. The reverse side of this issue, that is, the negative health impacts of a population-wide reduction in sodium intake is a subject of great significance and one that is seldom discussed.

In an analysis of 219 patients with essential hypertension in the early 1970s, heart attacks and strokes were observed when plasma rennin was elevated. It was concluded that renin may be a risk factor for heart attacks (1). In 1991, Alderman et al reported on the relationship of reduced-salt related high rennin levels with increased myocardial infarction rates (2). This relationship was again confirmed in 1997 (3).

In 58 trials of hypertensive persons, reducing sodium intake to 118 mmol/24 h (urinary sodium excretion) lowered systolic blood pressure (SBP) by 3.9 mm Hg and diastolic blood pressure (DBP) by 1.9 mm Hg. In 56 trials of normotensive persons, reducing sodium intake to 160 mmol/24 h resulted in a reduction of 1.2 mm Hg on SBP and 0.26 mm Hg on DBP. However, another consequence of this drop in sodium consumption was a significant 3.6-fold increase in the levels of plasma renin and a 3.2-fold increase in the level of aldosterone. These increases were proportional to the degree of sodium reduction and were accompanied by a significant decrease in body weight, and an increase in noradrenaline, cholesterol, and low-density lipoprotein cholesterol levels (4).

In his introduction of Dr. Michael H. Alderman as Editor-in-Chief of the American Journal of Hypertension, renowned hypertension researcher, Dr. John Laragh stated that Dr Alderman rightly "questioned the popular wisdom of unselectively advising salt avoidance for all hypertensives, and for all normotensive people, - a popular public health strategy which will surely chronically raise all of their plasma renin values and may have other unintended adverse consequences. (5)"

The primitive Yanomamo Indians of Brazil do not use added salt in their diet. As a consequence, this group provides an opportunity to study the hormonal regulation of sodium metabolism in a culture with a life-long restriction of dietary sodium. Results indicate that urinary excretion of sodium is very low, however, plasma renin activities were elevated when compared to other societies. The findings suggest that the hormonal adjustments to life-long low sodium intakes are similar to those achieved in acute sodium restriction of civilized man. In other words, there is a constant struggle to retain salt through the employment of the renin-angiotensin-aldosterone system, together with all its other consequences. Yanomamo Indians have a life expectancy of 48.5 years.

While there is little doubt that increased plasma rennin and aldosterone have a potential to result in increased myocardial infarction, a recent publication may reveal the mechanism of this action.

Aldosterone might affect arterial stiffening, in both the short and long term. Shapiro, Boaz, Matas, Fux, and Shargorodsky investigated the association between excess aldosterone, reflected by an increased aldosterone-renin ratio (ARR) and pulse wave velocity (PWV) in young healthy adults. In a single-center study, 60 subjects were evaluated for lipid profile, glucose, hs-CRP, renin and aldosterone (6). PWV was performed as a simple noninvasive recording and computer analysis of the two artery sites pressure waveform . The ARR was significantly and positively associated with PWV and had the potential to exhibit the direct effects of aldosterone on the vascular wall. Most significantly, the participants received instructions to consume intermediate levels of sodium proportional to energy intake, corresponding to 2,300 mg/day sodium per 2,100 kcal and to avoid foods notably high in sodium due to processing or foods with salt topically added - in other word to comply with the upper limit DV recommendations of the Institute of Medicine (7). This level of intake resulted in increased aldosterone and increased arterial stiffness.

There are a number of reasonable conclusions that can be derived from the above data. In the first instance, there is a strong possibility that a reduction in salt intake will elicit increased plasma aldosterone-renin output, thereby placing normotensive people at a greater risk for myocardial infarction. It appears likely that the arbitrarily derived IOM upper limit of sodium may not be sufficient to protect the majority of the population from arterial stiffening.

Finally, we must tread very carefully during any consideration of a change in the regulatory status of salt to ensure that we do not do the population more harm than good.

At this point in time, there is no justification to change the GRAS status of salt and there is sufficient information to reconsider increasing the IOM's DV of salt.

(1) Brunner, H. R., Laragh, J.H., Baer, L., et al, "Essential hypertension: renin and aldosterone, heart attack and stroke," N Engl J Med, 286, 441-449, (1972). (2) Alderman, M. H., Madhavan, S., Ooi, W. L., et al, "Association of the renin-sodium profile with the risk of myocardial infarction in patients with hypertension," N Engl J Med, 324, 1098-1104, (1991). (3) Alderman, M. H., Ooi, W. L., Cohen, H., et al, "Plasma renin activity: a risk factor for myocardial infarction in hypertensive patients," Am J Hypertens, 10, 1-8, (1997). (4) Graudal, N. A.., Galløe, A. M., abd P. Garred, "Effects of Sodium Restriction on Blood Pressure, Renin, Aldosterone, Catecholamines, Cholesterols, and Triglyceride - A Meta-analysis," JAMA, 279,1383-1391, (1998). (5) Laragh,J. H., "Dr. Michael H. Alderman Takes the Helm as Editor-in-Chief of the American Journal of Hypertension, Am J Hypertens 19, 1197-1198, (2006). (6) Shapiro, Y., Boaz, M., Matas, Z., Fux, A., & M. Shargorodsky, "The association between the renin-angiotensin-aldosterone system and arterial stiffness in young healthy subjects," Clinical Endocrinology (OnlineAccepted Articles). doi:10.1111/j.1365-2265.2008.03176.x. (7) Dietary Reference Intakes For Water, Potassium, Sodium, Chloride, and Sulfate, Institute of Medicine of The National Academies, The National Academies Press, Washington, D.C. (2005).