Sodium is normally present in food and in the body in its ionic (charged) form rather than as metallic sodium. Sodium is a positively charged ion or cation (Na+), and it forms salts with a variety of negatively charged ions (anions). Table salt or sodium chloride (NaCl) is an example of a sodium salt. In solution, NaCl dissociates into its ions, Na+ and Cl-. Other sodium salts include those of both inorganic (e.g., nitrite or bicarbonate) and organic anions (e.g., citrate or glutamate) in aqueous solution, these salts also dissociate into Na+ and the respective anion.
Types and Amounts of Common Foods That Contain the Recommended Levels of Sodium
Only small amounts of salt or sodium occur naturally in foods, but sodium salts are added to foods during food processing or during preparation as well as at the table. Most sodium is added to foods as sodium chloride (ordinary table salt), but small amounts of other salts such as sodium bicarbonate (baking soda and baking powder), monosodium glutamate, sodium sulfide, sodium nitrate, and sodium citrate are also added. Studies in a British population found that 75 percent of sodium intake came from salts added during manufacturing and processing, 15 percent from table salt added during cooking and at the table, and only 10 percent from natural foods (Sanchez-Castillo et al., 1987). Most sources of drinking water are low in sodium. However, the use of home water softening systems may greatly increase the sodium content of water; the system should be installed so that water for cooking and drinking bypasses the water softening system.
The estimated minimum safe daily intake of sodium for an adult (0.5 grams) can be obtained from ¼ teaspoon of salt, ¼ of a large dill pickle, ⅕ can of condensed tomato soup, one frankfurter, or fifteen potato chips. The effect of salt added in processing is noted by the calculation that, whereas one would need to consume 333 cups of fresh green peas (with no salt added during cooking or at the table) in order to consume 0.5 grams of sodium, the estimated minimum safe daily intake of sodium is provided by only 1.4 cups of canned or 2.9 cups of frozen green peas.
Whereas the estimated minimum safe intake for an adult is 0.5 g/day of sodium (1.3 g/day of sodium chloride), average Americans consume between 2 and 5 g/day of sodium (between 5 and 13 g/day of sodium chloride) (National Research Council, 1989). Sodium chloride, or salt, intake varies widely among cultures and among individuals. In Japan, where consumption of salt-preserved fish and the use of salt for seasoning are customary, salt intake is high, ranging from 14 to 20 g/day (Kono et al., 1983). On the other hand, the unacculturated Yanomamo Indians, who inhabit the tropical rain forest of northern Brazil and southern Venezuela, do not use salt in their diet and have an estimated sodium chloride intake of less than 0.3 g/day (Oliver et al., 1975). In the United States, individuals who consume diets high in processed foods tend to have high sodium chloride intakes, whereas vegetarians consuming unprocessed food may ingest less than 1 g/day of salt. Individuals with salt intakes less than 0.5 g/day do not normally exhibit chronic deficiencies, but appear to be able to regulate sodium chloride retention adequately.
Recommended Intake of Sodium
The daily minimum requirement of sodium for an adult is the amount needed to replace the obligatory loss of sodium. The minimum obligatory loss of sodium by an adult in the absence of profuse sweating or gastrointestinal or renal disease has been estimated to be approximately 115 mg/day, which is due to loss of about 23 mg/day in the urine and feces and of 46 to 92 mg/day through the skin (National Research Council, 1989). Because of large variations in the degrees of physical activity and in environmental conditions, the estimated level of safe minimum intake for a 70-kg adult was set at 500 mg/day of sodium (equivalent to 1,300 mg/day of sodium chloride) by the National Research Council (1989). Although there is no established optimal range of intake of sodium chloride, it is recommended that daily salt intake should not exceed 6 grams because of the association of high intake with hypertension (National Research Council, 1989). The Dietary Guidelines for Americans, published in 2000, include a recommendation to choose and prepare foods with less salt.
Individuals who wish to lower their sodium or salt intakes should use less salt at the table and during cooking, avoid salty foods such as potato chips, soy sauce, pickled foods, and cured meat, and avoid processed foods such as canned pasta sauces, canned vegetables, canned soups, crackers, bologna, and sausages. Individuals should also become aware of and avoid "hidden" sources of sodium such as softened water, products made with baking soda, and foods containing additives in the form of sodium salts.
The need for sodium chloride is increased during pregnancy and lactation, with the estimated safe minimum intake being increased by 69 mg/day and 135 mg/day, respectively, for women during pregnancy and lactation. The estimated minimum requirement for sodium is 120 mg/day for infants between birth and 5 months of age and 200 mg/day for infants 6 to 11 months of age (National Research Council, 1989); these intakes are easily met by human milk or infant formulas. The estimated minimum requirements of sodium for children range from 225 mg/day at one year of age to 500 mg/day at 10 to 18 years of age.
General Overview of Role of Sodium in Normal Physiology
Total body sodium has been estimated at 100 grams (4.3 moles) for a 70-kg adult. In general, the cytoplasm of cells is relatively rich in potassium (K>) and poor in sodium (Na>) and chloride (Cl<) ions. The concentrations of sodium (and potassium and chloride) ions in cells and the circulating fluids are held remarkably constant, and small deviations from normal levels in humans are associated with malfunction or disease. Na+, K+, and Cl- are referred to as electrolytes because of their role in the generation of gradients and electrical potential differences across cell membranes. Sodium and sodium gradients across cell membranes play several important roles in the body. First, sodium gradients are important in many transport processes. Sodium tends to enter cells down its electrochemical gradient (toward the intracellular compartment that has a lower Na+ concentration and a more negative charge compared to the extracellular fluid compartment). This provides a secondary driving force for absorption of Cl- in the same direction as Na+ movement or for the secretion of K+ or hydrogen ions (H+) in the opposite direction in exchange for Na+. The sodium gradient is also used to drive the coupled transport of Na+ and glucose, galactose, and amino acids by certain carrier proteins in cell membranes; because as Na+ enters down its electrochemical gradient, uptake of glucose/galactose or amino acids can occur against their concentration gradient. Second, sodium ions, along with potassium ions, play important roles in generating resting membrane potentials and in generating action potentials in nerve and muscle cells. Nerve and muscle cell membranes contain gated channels through which Na+ or K+ can flow. In the resting state, these cell membranes are highly impermeable to Na+ and permeable to K+ (i.e., Na+ channels are closed and K+ channels are open). These gated channels open or close in response to chemical messengers or to the traveling current (applied voltage). Action potentials are generated in nerve and muscle due to opening of Na+ channels followed by their closing and the re-opening of K+ channels.
A third important function of sodium is its osmotic role as a major determinant of extracellular fluid volume. The volume of the extracellular fluid compartment is determined primarily by the total amount of osmotic particles present. Because Na+, along with Cl-, is the major determinant of osmolarity of extracellular fluid, disturbances in Na+ balance will change the volume of the extracellular fluid compartment. Finally, because Na+ is a fixed cation, it also plays a role in acid-base balance in the body. An excess of fixed cations (versus fixed anions) requires an increase in the concentration of bicarbonate ions.
Consequences of Deficiency or Excessive Intake Levels
Sodium balance in the body is well controlled via regulation of Na+ excretion by the kidneys. The kidneys respond to a deficiency of Na+ in the diet by decreasing its excretion, and they respond to an excess of Na+ by increasing its excretion in the urine. Physiological regulatory mechanisms for conservation of Na+ seem to be better developed in humans than mechanisms for excretion of Na+, and pathological states characterized by inappropriate retention of Na+ are more common than those characterized by Na+ deficiency.
Retention of Na+ occurs when Na+ intake exceeds the renal excretory capacity. This can occur with rapid ingestion of large amounts of salt (for example, ingestion of seawater) or with too-rapid intravenous infusion of saline. Hypernatremia (abnormally high plasma concentration of Na+) and hypervolemia (abnormally increased volume of blood), resulting in acute hypertension, usually occur in these situations, and the Na+ regulatory mechanisms will cause natriuresis (urinary excretion of Na+) and water retention.
The body may be depleted of Na+ under extreme conditions of heavy and persistent sweating or when conditions such as trauma, chronic vomiting or diarrhea, or renal disease produce an inability to retain Na+. Sodium depletion produces hyponatremia (abnormally low plasma concentration of Na+) and hypovolemia (abnormally decreased volume of blood) which place the individual at risk of shock. Medical treatment includes replacement of Na+ and water to restore the circulatory volume. If the loss of Na+ is not due to renal disease, mechanisms to conserve Na+ and water are activated. Loss of Na+ can also be caused by the administration of diuretics, which inhibit Na+ and Cl- reabsorption, or by untreated diabetes mellitus, which causes diuresis.
Regulatory Processes That Govern the Uptake and Excretion of Sodium
The kidneys are the main site of regulation of Na+ balance. The intestines play a relatively minor role. Under normal circumstances, about 99 percent of dietary Na+ and Cl- are absorbed, and the remainder is excreted in the feces. Absorption of Na+ and Cl- occurs along the entire length of the intestines; 90 to 95 percent is absorbed in the small intestine and the rest in the colon. Intestinal absorption of Na+ and Cl- is subject to regulation by the nervous system, hormones, and paracrine agonists released from neurons in the enteric nervous system in the wall of the intestines. The most important of these factors is aldosterone, a steroid hormone produced and secreted by the zona glomerulosa cells of the adrenal cortex. Aldosterone stimulates absorption of Na+ and secretion of K+, mainly by the colon and, to a lesser extent, by the ileum.
The kidneys respond to a deficiency of Na+ in the diet by decreasing its excretion, and they respond to an excess by increasing its excretion in the urine. Urinary loss of Na+ is controlled by varying the rate of Na+ reabsorption from the filtrate by renal tubular cells. Individuals consuming diets that are low in Na+ efficiently reabsorb Na+ from the renal filtrate and have low rates of excretion of Na+. When there is an excess of Na+ from high dietary intake, little Na+ is reabsorbed by renal tubular cells, resulting in the excretion of the excess Na+ in the urine. As much as 13 g/day of Na+ can be excreted in the urine.
The most important regulator of renal excretion of Na+ and Cl- is the renin-angiotensin-aldosterone system (Laragh, 1985). Sensors in the nephrons of the kidney respond to changes in Na+ load by influencing the synthesis and secretion of renin (Levens et al., 1981). A decrease in renal perfusion or Na+ load will increase the release of renin. In the circulation, renin acts to initiate the formation of active angiotensin II from angiotensinogen, a protein produced by the liver. Angiotensin II conserves body Na+ by stimulating Na+ reabsorption by the renal tubules and indirectly via stimulating secretion of aldosterone. Secretion of aldosterone by the adrenal cortex is stimulated by a low plasma Na+ concentration and by angiotensin II. Aldosterone stimulates cells of the renal tubules to reabsorb Na+.
Because of the close association of Na+ and Cl- concentrations with effective circulating volume, Na+ (and Cl-) retention results in proportionate water retention, and Na+ (and Cl-) loss results in proportionate water loss. Expansion or contraction of the extracellular volume affects the activation of vascular pressure receptors, as well as the release of natriuretic peptides by certain tissues, and result in changes, mediated largely by antidiuretic hormone (ADH), in renal excretion of Na+, Cl-, and water. A deficiency of sodium chloride and hypovolemia have also been shown to produce an increase in appetite for salt, which will increase sodium chloride intake.
Evidence That Sodium Intake May Be Related to Risk of Hypertension
Both epidemiological and experimental studies implicate habitual high dietary salt intake in the development of hypertension (Weinberger, 1996). Primary hypertension, or abnormally high blood pressure, is a significant risk factor for cardiovascular disease, stroke, and renal failure in industrialized societies. Diets that are high in fat, high in sodium, low in potassium, low in calcium, and low in magnesium may contribute to the development of hypertension (Reusser and McCarron, 1994).
Although epidemiological and experimental evidence suggest a positive correlation between habitual high-salt consumption and hypertension, controversy remains regarding the importance of sodium salts in the regulation of blood pressure and the mechanisms by which salt influences blood pressure. This is not surprising, because the response of blood pressure depends on an interplay of various factors, such as genetic susceptibility, body mass, cardiovascular factors, regulatory mechanisms mediated through the neural and hormonal systems, and renal function.
A large comprehensive study on the role of sodium in hypertension was carried out in fifty-two geographically separate centers in thirty-two countries by the INTERSALT Cooperative Research Group (Stamler, 1997). Four centers included in the study had median values for Na+ excretion that were under 1.3 g/day. Subjects in these four unacculturated centers had low blood pressure, rare or absent hypertension, and no age-related rise in blood pressure as occurred in populations in the other forty-eight centers in which mean values for Na+ excretion were between 2.4 and 5.6 grams Na+ per day. Although blood pressure and sodium intake appeared to be associated when all fifty-two centers were included, the correlation between systolic blood pressure and excretion of sodium was not significant when the four centers with the lowest median values of sodium excretion were excluded from the analysis.
Intervention studies of dietary salt restriction to lower blood pressure have produced mixed results. This may be explained by the facts that not all hypertensive patients are salt-sensitive and that many cases of hypertension are due to other causes. Nevertheless, various clinical trials indicate some beneficial effects of dietary restriction of sodium on blood pressure (Cutler et al., 1997; Reusser and McCarron, 1994) with response being greater in older patients, patients with the highest degree of restriction, and in nonoverweight, mildly hypertensive patients.
Researchers are currently attempting to identify the genetic basis of salt-sensitive hypertension and to identify polymorphisms associated with salt-sensitive hypertensive individuals. More than thirty different gene variations could be responsible for essential hypertension, and hypertension is considered to have a complex genetic basis. Further insight into the basis of hypertension may help to determine individuals for whom lowering salt intake would be beneficial and to facilitate the prescription of appropriate drugs.
Brief Outline of the History of Salt
Common salt is the chemical compound NaCl. Salt makes up nearly 80 percent of the dissolved material in seawater and is also widely distributed in solid deposits. It is found in many evaporative deposits, where it crystallizes out of evaporating brine lakes, and in ancient bedrock, where large extinct salt lakes and seas evaporated millions of years ago. Salt was in general use long before history began to be recorded. Salt has been used widely for the curing, seasoning, and preserving of foods.
Bibliography
Church, Charles F., and Helen N.Church. Food Values of Portions Commonly Used: Bowes and Church. Philadelphia: J. B. Lippincott, 1970.
Cutler, Jeffrey A., Dean Follmann, and P. Scott Allender. "Randomized Trials of Sodium Reduction: An Overview." American Journal of Clinical Nutrition 65 (1997, Supp.): 643S–651S.
Kono, Suminori, Masato Ikeda, and Michiharu Ogata. "Salt and Geographical Mortality of Gastric Cancer and Stroke in Japan." Journal of Epidemiology and Community Health 37 (1983): 43–46.
Laragh, John H. "Atrial Natriuretic Hormone, the Renin-Aldosterone Axis, and Blood Pressure—Electrolyte Homeostasis." New England Journal of Medicine 313 (1985): 1330–1340.
Levens, Nigel R., Michael J. Peach, and Robert M. Carey. "Role of Intrarenal Renin-Angiotensin System in the Control of Renal Function." Circulation Research 48 (1981):157–167.
National Research Council. Recommended Dietary Allowances. 10th ed. Washington, D.C.: National Academy Press, 1989, pp. 247–261.
Oliver, Walter J., Erik L. Cohen, and James V. Neel. "Blood Pressure, Sodium Intake and Sodium-Related Hormones in the Yanomamo Indians, a 'No-Salt' Culture." Circulation 52 (1975): 146–151.
Reusser, Molly E., and David A. McCarron. "Micronutrient Effects on Blood Pressure Regulation." Nutrition Reviews 52 (1994): 367–375.
Sanchez-Castillo, C. P., S. Warrender, T. P. Whitehead, and W. P. James. "An Assessment of the Sources of Dietary Salt in a British Population." Clinical Science 72 (1987): 95–102.
Sheng, Hwai-Ping. "Sodium, Chloride, and Potassium." In Biochemical and Physiological Aspects of Human Nutrition, edited by Martha H. Stipanuk, pp. 686–710. Philadelphia: W. B. Saunders Co., 2000.
Stamler, Jeremiah. "The INTERSALT Study: Background, Methods, Findings, and Implications." American Journal of Clinical Nutrition 65 (1997, Supp.): 626S–642S.
United States Department of Agriculture. Nutrition and Your Health: Dietary Guidelines for Americans. 5th ed.. Washington, D.C.: U. S. Government Printing Office, 2000.
Weinberger, Myron H. "Salt Sensitivity of Blood Pressure in Humans." Hypertension 27 (1996): 481–490.
—Martha H. Stipanuk