The Durk Pearson & Sandy Shaw®
Life Extension NewsTM
Volume 13 No. 4 • August 2010


Patients on a Low Salt Diet Have Increased Mortality

A 2010 paper1 reports on the “controversial clinical finding that reduced sodium intake or reduced urine output inversely correlates with cardiac mortality in patients.” This is not something being widely discussed in public media.

The authors of this new paper say that “… an interesting series of clinical studies by Alderman over the past 20 years call into question the wisdom of this approach [following a low salt diet], lacking a strong mechanistic scientific basis such as reduced NO bioavailability in the heart. For instance, patients on a LS [low salt] diet have an increase in coronary events compared to those on normal salt (NS) intake.” “The controversy around the potential detrimental effects of a LS diet has been discussed by Aviv, proposing the hypothesis that there is a U-shaped function curve governing salt intake. Furthermore, the effect responsible for mortality at both high and LS intake is proposed to be NO-superoxide.”

The authors cite a paper supporting their statement that “during restriction of salt intake, it is already established that there is an increase in plasma angiotensin II.” “The ability of NO [nitric oxide] to reduce oxygen consumption in vitro in the normal mouse heart is almost abolished during incubation with angiotensin II via an AT1 [angiotensin II type 1] receptor-dependent mechanism.” Increased superoxide production stimulated by angiotensin II results in decreased availability of NO due to the interaction of superoxide and NO that creates the potent oxidant peroxynitrite. Interestingly, gamma tocopherol is a potent scavenger of peroxynitrite (more effective than alpha tocopherol) and protects against peroxynitrite-induced lipid oxidation.2

The researchers performed experiments on adult male mongrel dogs that were placed on a low salt (LS) diet (0.05% sodium chloride) for two weeks. They found that NO-mediated vasodilation was inhibited by 44% in the LS as compared to controls. However, importantly they found that intravenous infusion of ascorbic acid or apocynin at the same time as the LS diet “acutely and completely reversed this inhibition.” As apocynin is a powerful inhibitor of NADPH oxidase, which generates superoxide, it shows how important superoxide is to the inhibitory effect of LS on NO-mediated vasodilation.

Moreover, LS induced increases in two subunits of NADPH oxidase, p47phox (121% increase) and gp91phox (44% increase) and also increased gene expression in the LS heart tissue of p47phox by 1.6 fold and gp91phox by 2.0 fold. The authors conclude: “LS diet induces the activation of the renin-angiotensin system, which increases oxidative stress via the NADPH oxidase and attenuates NO bioavailability in the heart.”

“… our studies have defined a potential mechanism, the reduction in NO bioactivity, which may contribute to the detrimental effects of LS in patients.”1 The authors caution, however, that “[t]he clinical relevance of our study still remains to be determined.”1

Lower Ratio of Potassium/Sodium in Modern Diet As Compared to Paleolithic Diet

Evidence indicates that it is not high sodium that is the basic problem in hypertension, but the low ratio of potassium to sodium in the modern diet.3 In a study of patients selected for essential hypertension, potassium bicarbonate significantly reduced high blood pressure by 8 weeks compared with placebo, while potassium chloride did not,3 suggesting the possibility that excess chloride rather than sodium may be the pathogenic agent in salt-induced hypertension. In another study, this one performed by the authors of paper #3, they showed in 41 metabolically controlled studies of 38 healthy normotensive men (24 black men and 14 white men) “that in most of the blacks but not the whites, salt sensitivity occurred when dietary potassium was even marginally deficient, 30 mmol/day, but not attended by hypokalemia [clinically apparent potassium deficiency], as judged by a fasting serum concentration of potassium of 4.0 mmol/L. However, the pressor [blood pressure increasing] effect of NaCl loading was dose-dependently suppressed when dietary potassium was increased to 70 and 120 mmol/L per day by supplemental KHCO3 [potassium bicarbonate].” Moreover, the authors3 report that with aging, plasma bicarbonate decreases, while the serum concentration of chloride increases. Hence, if excess chloride is a problem and decreasing bicarbonate certainly is, it gets worse with age.

We each take a potassium bicarbonate supplement (Potassium Basics™) for reduced blood pressure, as well as reduced dietary acid load, increased muscle mass, decreased bone loss, reduced risk of stroke, and improved endothelial function. [See “Potassium Bicarbonate Supplementation” and “Potassium Bicarbonate for Reduced Blood Pressure and Increased Muscle Mass” in the April 2009 issue.]

References

  1. 1. Suematsu et al. Potential mechanisms of low sodium diet induced cardiac disease: superoxide-NO in the heart,” Circ Res 106:593-600 (2010).
  2. 2. Christen et al. Gamma tocopherol traps mutagenic electrophiles such as [reactive nitrogen oxide species] and complements alpha-tocopherol: physiological implications. Proc Natl Acad Sci USA 94:3217-22 (1997).
  3. 3. Morris et al. Differing effects of supplemental KCl and KHCO3: pathophysiological and clinical implications. Semin Nephrol 19(5):487-93 (1999).

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