Clinical:Sodium

Sodium is the major extracellular cation. The body of an adult stores approximately 100 g of sodium; more than half is in the extracellular space, and much of the remainder is in bone.

Sodium functions to regulate the distribution of water in the body, regulate acid–base balance, and maintain transmembrane potential. Sodium deficiency, which results in hyponatremia, causes weakness, fatigue, anorexia, and confusion; if severe, hyponatremia can cause seizures and be life threatening.

There is no RDA for sodium, but a daily intake of at least 115 mg is thought to be essential, and an intake of at least 500 mg is advised. Excess intake may play a role in hypertension and osteoporosis. Intake should be limited to not more than 2,400 mg per day; typical daily intake in the United States is nearly 4,000 mg. Paleolithic intake of sodium is estimated to have been less than 1,000 mg per day. Of note, potassium intake exceeded sodium intake by a factor of more than 10 in the prehistoric diet of humans, whereas in the modern diet of developed countries, sodium intake exceeds that of potassium by a factor of 2. Sodium is abundant in foods of animal origin, but it is present in the food supply principally as a seasoning or preservative added to processed foods.

Sodium is almost certainly the most extensively studied nutrient influencing blood pressure. Evidence from a variety of sources, including epidemiologic studies as well as intervention trials, indicates rather conclusively at this point that sodium contributes to blood pressure elevations on a population and individual basis.^{[1] [2]} Such a conclusion is supported by results of the INTERSALT study, which examined the association between sodium intake and blood pressure in multiple cohorts around the globe. ^[3] Generally, each incremental increase in sodium intake of 100 mEq/day increases mean systolic blood pressure in a population by 3 to 6 mm Hg.

Although there is decisive evidence that sodium contributes to blood pressure elevation, the causal role of sodium in hypertension is less well established. Studies suggest that roughly 50% of hypertensives in the United States are responsive to sodium, demonstrating blood pressure variation with change in sodium intake; this figure was previously set at about 10%.^[4] A substantial, but smaller percentage of normotensives are salt-sensitive. Salt sensitivity is more prevalent among African Americans; up to 75% of hypertensive African Americans are responsive to dietary sodium.

The efficacy of sodium restriction in the management of hypertension has been demonstrated in the context of clinical trials, but establishing real-world effectiveness is a greater challenge. Adherence to a low-sodium diet is difficult for most patients,^[5] and such diets inevitably introduce other changes that may account in part for blood pressure reduction. Cook and colleagues ^[6] assert that the effect of salt restriction on blood pressure has generally been underestimated. In 2005, the Center for Science in the Public Interest filed suite against the US FDA for according sodium the designation “generally recognized as safe” (GRAS). CSPI alleges that excess dietary salt is responsible for as many as 150,000 premature deaths each year in the US (http://www.cspinet.org/new/pdf/salt_lawsuit.pdf). Kumanyika has suggested that to achieve recommended sodium intake levels in the US with any consistency will require appreciable changes to the food supply.^[7]

Despite the uncertainties, recommendations for sodium restriction below prevailing levels in the United States can be made with considerable confidence. Intake in the United States generally exceeds the recommended limit of 2,400 mg per day. Ancestral intake, which may indicate optimal levels, was approximately 700 to 800 mg per day, less than one fourth the average intake today. ^[8] Advocacy of a health-promoting diet will result in sodium restriction by reducing the intake of fast and highly processed foods.

Patients should be advised of the importance of reading food labels. The sodium content of many commercial breakfast cereals is comparable to that of potato chips and pretzels, although the taste of salt in such products is masked by the sugar. In attempting to limit sodium intake, many patients will report not using a salt shaker. However, the salt added to food during preparation is less readily tasted than the salt shaken on just as the food is eaten. Therefore, selection and preparation of relatively low-salt foods and continued, albeit controlled, use of a salt shaker may be a preferred approach. As with other dietary changes, salt restriction becomes less objectionable as it becomes familiar. Whereas the salt content of many processed foods goes unnoticed by most consumers, those acclimated to a lower-sodium diet begin to taste salt more readily and to prefer lower intake levels.^{[9] [10]} Acclimation to a high-salt diet has the opposite effect. ^[11]

Source: Katz DL. Clinically Relevant Micronutrient Metabolism. In: Katz DL with Friedman RSC. Nutrition in Clinical Practice, 2nd Edition. Lippincott Williams & Wilkins. Philadelphia, PA. 2008. pp. 29-40

References

1. ↑ Cutler JA. The effects of reducing sodium and increasing potassium intake for control of hypertension and improving health. Clin Exp Hypertens 1999;21:769
2. ↑ He J, Whelton PK. Role of sodium reduction in the treatment and prevention of hypertension. Curr Opin Cardiol 1997;12:202
3. ↑ Stamler J. The INTERSALT Study: background, methods, findings, and implications. Am J Clin Nutr 1997;65:626S-642S
4. ↑ Chrysant GS, Bakir S, Oparil S. Dietary salt reduction in hypertension–what is the evidence and why is it still controversial? Prog Cardiovasc Dis 1999;42:23
5. ↑ Kumanyika S. Behavioral aspects of intervention strategies to reduce dietary sodium. Hypertension 1991;17:I190
6. ↑ Cook NR, Kumanyika SK, Cutler JA. Effect of change in sodium excretion on change in blood pressure corrected for measurement error. The Trials of Hypertension Prevention, phase I. Am J Epidemiol 1998;148:431
7. ↑ Kumanyika S. Behavioral aspects of intervention strategies to reduce dietary sodium. Hypertension 1991;17:I190
8. ↑ Eaton SB, Eaton SB III, Konner MJ. Paleolithic nutrition revisited: a twelve-year retrospective on its nature and implications. Eur J Clin Nutr 1997;51:207
9. ↑ Bertino M, Beauchamp GK, Engelman K. Long-term reduction in dietary sodium alters the taste of salt. Am J Clin Nutr 1982;36:1134
10. ↑ Rogers PJ. Eating habits and appetite control: a psychobiological perspective. Proc Nutr Soc 1999;58:59
11. ↑ Bertino M, Beauchamp GK, Engelman K. Increasing dietary salt alters salt taste preference. Physiol Behav 1986;38:203