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6
Sodium and Chloride

SUMMARY

The cation sodium and the anion chloride are normally found in most foods together as sodium chloride, also termed salt. For this reason, this report presents data on the requirements for and the effects of sodium and chloride together.1

Sodium and chloride are required to maintain extracellular volume and plamsa osmolality. Human populations have demonstrated the capacity to survive at extremes of sodium intake from less than 0.2 g (10 mmol)/day of sodium in the Yanomamo Indians of Brazil to over 10.3 g (450 mmol)/day in Northern Japan. The ability to survive at extremely low levels of sodium intake reflects the capacity of the normal human body to conserve sodium by markedly reducing losses of sodium in the urine and sweat. Under conditions of maximal adaptation and without sweating, the minimal amount of sodium required to replace losses is estimated to be no more than 0.18 g (8 mmol)/day. Still, it is unlikely that a diet providing this level of sodium intake is sufficient to meet dietary requirements for other nutrients.

1  

In view of the format of published data, this report presents intake data primarily as g (mmol)/day of sodium and of chloride, rather than g (mmol)/day of sodium chloride (salt). To convert mmol to mg of sodium, chloride, or of sodium chloride, multiply mmol by 23, 35.5, or 58.5 (the molecular weights of sodium, chloride, and sodium chloride), respectively.



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Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate 6 Sodium and Chloride SUMMARY The cation sodium and the anion chloride are normally found in most foods together as sodium chloride, also termed salt. For this reason, this report presents data on the requirements for and the effects of sodium and chloride together.1 Sodium and chloride are required to maintain extracellular volume and plamsa osmolality. Human populations have demonstrated the capacity to survive at extremes of sodium intake from less than 0.2 g (10 mmol)/day of sodium in the Yanomamo Indians of Brazil to over 10.3 g (450 mmol)/day in Northern Japan. The ability to survive at extremely low levels of sodium intake reflects the capacity of the normal human body to conserve sodium by markedly reducing losses of sodium in the urine and sweat. Under conditions of maximal adaptation and without sweating, the minimal amount of sodium required to replace losses is estimated to be no more than 0.18 g (8 mmol)/day. Still, it is unlikely that a diet providing this level of sodium intake is sufficient to meet dietary requirements for other nutrients. 1   In view of the format of published data, this report presents intake data primarily as g (mmol)/day of sodium and of chloride, rather than g (mmol)/day of sodium chloride (salt). To convert mmol to mg of sodium, chloride, or of sodium chloride, multiply mmol by 23, 35.5, or 58.5 (the molecular weights of sodium, chloride, and sodium chloride), respectively.

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Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate Because of insufficient data from dose-response trials, an Estimated Average Requirement (EAR) could not be established, and thus a Recommended Dietary Allowance could not be derived. Hence, an Adequate Intake (AI) is provided. The AI for sodium is set for young adults at 1.5 g (65 mmol)/day (3.8 g of sodium chloride) to ensure that the overall diet provides an adequate intake of other important nutrients and to cover sodium sweat losses in unacclimatized individuals who are exposed to high temperatures or who become physically active as recommended in other dietary reference intakes (DRI) reports. This AI does not apply to individuals who lose large volumes of sodium in sweat, such as competitive athletes and workers exposed to extreme heat stress (e.g., foundry workers and fire fighters). The AI for sodium for older adults and the elderly is somewhat less, based on lower energy intakes, and is set at 1.3 g (55 mmol)/day for men and women 50 through 70 years of age, and at 1.2 g (50 mmol)/day for those 71 years of age and older. Concerns have been raised that a low level of sodium intake adversely affects blood lipids, insulin resistance, and cardiovascular disease risk. However, at the level of the AI, the preponderance of evidence does not support this contention. A potential indicator of an adverse effect of inadequate sodium is an increase in plasma renin activity. However, in contrast to the well-accepted benefits of blood pressure reduction, the clinical relevance of modest rises in plasma renin activity as a result of sodium reduction is uncertain. The AI for chloride is set at a level equivalent on a molar basis to that of sodium, since almost all dietary chloride comes with the sodium added during processing or consumption of foods. Thus the AI for chloride for younger adults is 2.3 g (65 mmol)/day of chloride, which is equivalent to 3.8 g/day sodium chloride. The AIs for chloride for older adults and the elderly are 2.0 and 1.8 g of chloride per day respectively, equivalent to 3.2 g (55 mmol) and 2.9 g (50 mmol) of sodium chloride per day. The major adverse effect of increased sodium chloride intake is elevated blood pressure, which has been shown to be an etiologically related risk factor for cardiovascular and renal diseases. On average, blood pressure rises progressively with increased sodium chloride intake. The dose-dependent rise in blood pressure appears to occur throughout the spectrum of sodium intake. However, the relationship is nonlinear in that the blood pressure response to changes in sodium intake is greater at sodium intakes below 2.3 g (100 mmol)/day than above this level. The strongest

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Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate dose-response evidence comes from those clinical trials that specifically examined the effects of at least three levels of sodium intake on blood pressure. The range of sodium intake in these studies varied from 0.23 g (10 mmol)/day to 34.5 g (1,500 mmol)/day. Several trials included sodium intake levels close to 1.5 g (65 mmol) and 2.3 g (100 mmol)/day. While blood pressure, on average, rises with increased sodium intake, there is well-recognized heterogeneity in the blood pressure response to changes in sodium chloride intake. Individuals with hypertension, diabetes, and chronic kidney disease, as well as older-age persons and African Americans, tend to be more sensitive to the blood pressure-raising effects of sodium chloride intake than their counterparts.2 Genetic factors also influence the blood pressure response to sodium chloride. There is considerable evidence that salt sensitivity is modifiable. The rise in blood pressure from increased sodium chloride intake is blunted in the setting of a diet that is high in potassium or that is low in fat, and rich in minerals; nonetheless, a dose-response relationship between sodium intake and blood pressure still persists. In nonhypertensive individuals, a reduced salt intake can decrease the risk of developing hypertension (typically defined as systolic blood pressure ≥140 mm Hg or diastolic blood pressure ≥ 90 mm Hg). The adverse effects of higher levels of sodium intake on blood pressure provide the scientific rationale for setting the Tolerable Upper Intake Level (UL). Because the relationship between sodium intake and blood pressure is progressive and continuous without an apparent threshold, it is difficult to precisely set a UL, especially because other environmental factors (weight, exercise, potassium intake, dietary pattern, and alcohol intake) and genetic factors also affect blood pressure. For adults, a UL of 2.3 g (100 mmol)/day is set. In dose-response trials, this level was commonly the next level above the AI that was tested. It should be noted that the UL is not a recommended intake and, as with other ULs, there is no benefit to consuming levels above the AI. 2   In research studies, different techniques and quantitative criteria have been used to define salt sensitivity. In general terms, salt sensitivity is expressed as either the reduction in blood pressure in response to a lower salt intake or the rise in blood pressure in response to sodium loading. Salt sensitivity differs among subgroups of the population and among individuals within a subgroup. The term “salt sensitive blood pressure” applies to those individuals or subgroups who experience the greatest change in blood pressure from a given change in salt intake—that is, the greatest reduction in blood pressure when salt intake is reduced.  

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Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate Among certain groups of individuals who are most sensitive to the blood pressure effects of increased sodium intake (e.g., older persons; African Americans; and individuals with hypertension, diabetes, or chronic kidney disease), their UL may well be lower. These groups also experience an especially high incidence of blood pressure-related cardiovascular disease. In contrast, for individuals who are unacclimatized to prolonged physical activity in a hot environment, their needs may exceed the UL because of sodium sweat losses. It is well-recognized that the current intake of sodium for most individuals in the United States and Canada greatly exceeds both the AI and UL. Progress in achieving a reduced sodium intake will likely be incremental and will require changes in individual behavior towards salt consumption, replacement of high salt foods with lower salt versions, increased collaboration of the food industry with public health officials, and a broad spectrum of additional research. The latter includes research designed to develop reduced sodium food products while maintaining flavor, texture, consumer acceptability, and low cost. BACKGROUND INFORMATION Function Sodium is the principal cation of the extracellular fluid and functions as the osmotic determinant in regulating extracellular fluid volume and thus plasma volume. Approximately 95 percent of the total sodium content of the body is found in extracellular fluid. Sodium is also an important determinant of the membrane potential of cells and the active transport of molecules across cell membranes. The concentration of sodium within the cell is typically less than 10 percent of that outside cell membranes, and an active, energy-dependent process is required to maintain this concentration gradient. Chloride, in association with sodium (i.e., sodium chloride), is the principal osmotically active anion in the extracellular fluid and is also important in maintaining fluid and electrolyte balance; it also serves as an important component of gastric juice as hydrochloric acid. Physiology of Absorption and Metabolism Sodium and chloride ions are typically consumed as sodium chloride. Absorption of sodium and chloride occurs primarily in the

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Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate small intestine and is approximately 98 percent across a wide intake range. The majority of ingested sodium chloride is excreted in the urine, provided that sweating is not excessive (Holbrook et al., 1984; Pitts, 1974). In humans who are at “steady-state” conditions of sodium and fluid balance and who have minimal sweat losses, the amount of sodium excreted in urine roughly equals intake. This phenomenon occurs due to the capacity of the normal human kidney to filter some 25,000 mmol of sodium each day and to reabsorb, by extremely precise mechanisms, 99 percent or more of the filtered load (Valtin and Schafer, 1995). Absorbed sodium and chloride remain in the extracellular compartments, which include plasma (at concentrations of 140 mmol/L for sodium and 104 mmol/L for chloride), interstitial fluid (at concentrations of 145 mmol/L for sodium and 115 mmol/L for chloride), and plasma water (at concentrations of 150 mmol/L for sodium and 111 mmol/L for chloride); intracellular concentrations in tissues such as muscle are 3 mmol/L for sodium and 3 mmol/L for chloride (Oh and Uribarri, 1999). Sodium is maintained outside of the cell via the Na+/K+-ATPase pump. There are various systems and hormones that influence sodium and chloride balance, including the renin-angiotensin-aldosterone axis, the sympathetic nervous system, atrial natriuretic peptide, the kallikrein-kinin system, various intrarenal mechanisms, and other factors that regulate renal and medullary blood flow. Angiotensin II, a potent vasoconstrictor, regulates the proximal tubule of the nephron to promote sodium and chloride retention and also to stimulate the release of aldosterone from the adrenal cortex (Valtin and Schafer, 1995). Aldosterone promotes the renal reabsorption of sodium in the distal tubule of the nephron by mineralocorticoid receptor-mediated exchange for hydrogen and potassium ions. With reduced salt intake, reduced blood volume, or reduced blood pressure, the renin-angiotensin-aldosterone axis is stimulated. When the renin-angiotensin-aldosterone system is less responsive, as with advancing age, there is a greater blood pressure reduction from a reduced intake of sodium chloride (Cappuccio et al., 1985; Weinberger et al., 1993a). Atrial natriuretic peptide (ANP) is released in response to elevated blood volume and serves as a counter-regulatory system to the renin-angiotensin-aldosterone system. ANP decreases the release of renin and therefore the release of angiotensin II and aldosterone and increases the glomerular filtration rate. These actions contribute to reductions in blood volume and blood pressure. The sympathetic nervous system is another major regulatory sys-

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Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate tem for sodium and chloride excretion through at least three mechanisms: alteration in renal medullary blood flow, release of renin, and direct effects on the renal tubules. Similar to the renin-angiotensin-aldosterone system, the sympathetic nervous system is activated during sodium depletion and suppressed during sodium excess (Luft et al., 1979a). With increased extracellular fluid volume, there is increased blood flow in the medulla (the inner part of the kidney), resulting in a decreased sodium concentration of the fluid delivered to the ascending limb of Henle’s loop in the renal tubule. This decrease leads to reduced sodium reabsorption of the kidney’s nephron so that more sodium is delivered to the distal tubules for excretion. Intrarenal mechanisms are also important for sodium and chloride homeostasis. These mechanisms include locally released prostaglandins, kinins, angiotensin, endothelial relaxing factor, and other less-well defined factors. Other Forms of Sodium Sodium is consumed as sodium chloride (salt), sodium bicarbonate, and as sodium in a variety of forms provided in processed foods (e.g., monosodium glutamate and other food additives, such as sodium phosphate, sodium carbonate, and sodium benzoate). Still, the major form of dietary sodium is sodium chloride (Fregly, 1984; Mattes and Donnelly, 1991), which accounts for approximately 90 percent of the total sodium intake in the United States. Sodium bicarbonate is used as an ingredient in foods. It can also be used in the treatment of metabolic acidosis because its bicarbonate component induces an increase in plasma bicarbonate concentration, the prime “metabolic” determinant of blood pH (the numerator of the Henderson-Hasselbalch equation3), with the pCO2 concentration being determined by respiration. Normally bicarbonate is the major determinant of plasma alkalinity. Although there is strong evidence that metabolic acidosis, which occurs in chronic renal insufficiency, is an important determinant of deleterious muscle and bone catabolism (Bushinsky, 1998; Mitch, 1998), sodium bicarbonate is not widely used clinically to correct such acido- 3   where BA is the ionized salt of the acid HA; in the case of the bicarbonate-carbonic acid buffer system in blood, the pK1 = 6.1, and the concentration of carbonic acid [H2CO3] is based on the blood concentration of pCO2.

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Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate sis. This is because large volumes of sodium bicarbonate are required, leading to concern that the sodium load may induce plasma volume overload. It might be expected that sodium chloride loading rather than sodium bicarbonate loading would substantially expand plasma volume because sodium and chloride are both distributed as osmotic agents almost restrictively within the plasma-containing extracellular fluid. In contrast, bicarbonate is distributed throughout the much larger total body water. However, in a variety of clinical circumstances, sodium bicarbonate and/or sodium citrate appear to induce an expansion of plasma volume, as judged by suppression of plasma renin activity and the plasma concentration of aldosterone (Kurtz et al., 1987; Luft et al., 1990; Schorr et al., 1996; Sharma et al., 1992) and by changes in insulin space (Van Goidsenhoven et al., 1954). Yet, in these studies, sodium loading without chloride (e.g., with sodium bicarbonate) did not raise blood pressure to the same extent as sodium chloride (Luft et al., 1990; Schorr et al., 1996). INDICATORS CONSIDERED FOR ESTIMATING THE REQUIREMENTS FOR SODIUM AND CHLORIDE The following section reviews the potential markers for adverse effects resulting from insufficient sodium intake in apparently healthy individuals. Sodium Balance When substantial sweating does not occur, total obligatory sodium losses are very small, up to 0.18 g/day or 8 mmol/day (Table 6-1) (Dahl, 1958). For this reason, in a temperate climate or even a TABLE 6-1 Obligatory Losses of Sodium   g/d mmol/d Urine 0.005–0.035 0.2–1.5 Skin (nonsweating) 0.025 1.1 Feces 0.010–0.125 0.4–5.4 Total 0.040–0.185 1.7–8.0 SOURCE: Dahl (1958).

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Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate tropical climate, acclimatized persons can survive on extremely low sodium intakes (Kempner, 1948; Oliver et al., 1975). Urine and Feces In nonsweating individuals living in a temperate climate who are in a steady-state of sodium and fluid balance, urinary sodium excretion is approximately equal to sodium intake (i.e., 90 to 95 percent of total intake is excreted in urine) (Holbrook et al., 1984; Pietinen, 1982). Obligatory urinary losses of sodium in adults are approximately 23 mg (1 mmol)/day (Dole et al., 1950). This estimated level of excretion is similar to those that have been actually measured in studies of the Yanomamo Indians in Brazil: in one study sodium excretion of 26 men averaged 23.5 ± 34.7 mg (1.02 ±1.51 mmol)/day (Oliver et al., 1975), and in a subsequent study (n = 195), urinary sodium excretion was 20.7 ± 52.9 mg (0.9 ± 2.3 mmol)/day (Rose et al., 1988). Excretion of sodium in the stool is minimal. When sodium intakes ranged from 0.05 to 4.1 g/day of sodium, only about 0.01 to 0.125 g (0.4 to 5.4 mmol)/day appeared in the stool (Dahl, 1958; Dole et al., 1950; Henneman and Dempsey, 1956). In a sodium balance study with three levels of intake, 1.5, 4.0, and 8.0 g (66, 174, and 348 mmol)/day (Allsopp et al., 1998), fecal sodium excretion increased as sodium intake rose. Still, fecal excretion of sodium was less than 5 percent of intake even at the highest level of sodium intake (Table 6-2). Skin and Sweat Daily dermal losses of sodium have been reported to average less than 0.025 g (1.1 mmol)/day (Dahl, 1958; Dahl et al., 1955). In another study, estimated obligatory dermal losses of sodium ranged from 0.046 to 0.09 g (2 to 4 mmol)/day (Fregly, 1984). Sweat sodium loss depends on a number of factors, including: (1) the sweat rate, (2) sodium intake, and (3) heat acclimation (Allsopp et al., 1998). For these reasons, the sodium concentration in sweat varies widely. Most studies that measure sodium content of sweat are short-term (Table 6-3), and report sweat sodium concentrations rather than total sodium lost in sweat. Of note, in these studies intake data on dietary sodium was frequently not given. However, in the three studies where dietary sodium information was provided, dietary intakes were high (up to 8.7 g [378 mmol]/day).

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Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate TABLE 6-2 Sodium Balance at Three Levels of Sodium Intake Sodium Intake (g/d) Sodium Intake (mmol/d) Number of Men 24-h Urinary Sodium, g (mmol) 24-h Fecal Sodium, g (mmol) 12-h Sweat Sodium, g (mmol) Sodium Balance, g (mmol) 1.5 66 9 0.7 (32.4) 0.03 (1.4) 0.57 (24.8) +0.005 (0.2) 4.0 174 9 2.1 (92.3) 0.12 (5.4) 0.89 (39.1) +0.67 (29.1) 8.0 348 7 5.8 (251.3) 0.33 (14.2) 1.2 (52.6) +0.34 (14.7) NOTE: Reported values were obtained after 8 d on the assigned sodium level. Measurements were obtained at the end of the 8-d period of which the last 5 d were spent in an environmental chamber (40°C [104°F] from 8 am to 6 pm, and from 6 pm to 8 am at 25°C [77°F]). SOURCE: Allsopp et al. (1998). One study provided detailed information on sweat losses at three levels of dietary sodium intake (Allsopp et al., 1998). Men were exposed to heat in an environmental chamber at 40°C (104°F) for 10 hours/day of the last 5 days of an 8-day experimental period. Sweat sodium loss, as well as fecal and urinary sodium losses, were progressively greater across the three levels of sodium studied (1.5 g [66 mmol], 4 g [174 mmol], or 8 g [348 mmol]/day) (see Table 6-2). By the eighth day, participants on the lowest sodium level were in sodium balance. Plasma aldosterone concentrations were significantly increased during the low sodium condition and significantly decreased during the high sodium condition. Earlier studies, including a 10-day pre-post study, reported similar reductions in sodium sweat loss following exercise in the heat over time (Kirby and Convertino, 1986), as well as decreased sweat sodium concentration with heat acclimation without exercise (Allan and Wilson, 1971). This reduction in sweat sodium concentration is a protective mechanism to minimize plasma volume loss. Conn (1949) demonstrated that healthy persons sweating 5 to 9 L/day could maintain sodium chloride balance on intakes ranging from as low as 1.9 g (83 mmol)/day to 3.2 g (139 mmol)/day of sodium chloride, the maximum intake provided. In aggregate, available data indicate that healthy, free-living individuals can achieve sodium balance following acclimation under a variety of conditions, including low sodium intake and extreme heat.

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Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate TABLE 6-3 Sweat Sodium Concentration Reference Study Design Adults Consolazio et al., 1963 3 men 37.8°C (100°F) 8.7 g/d sodium (378 mmol/d), 16 d Murakami and Hirayama, 1964 16 Japanese adults Ambient temperature No dietary information Allan and Wilson, 1971 3 subjects Unacclimated and acclimated, 40°C (104°F) for 1 h/d No diet information, 3 wk Kirby and Convertino, 1986 10 men 1–2 h postexercise, 40°C (104°F), measured at 1 and 10 d of heat acclimation 3.2–3.5 g/d (141–152 mmol/d) sodium Barr et al., 1991 6 subjects Moderate exercise for 6 h, 30°C (86°F); provided water or saline at 5.8 g/L (25 mmol/L) No dietary information Meyer et al., 1992 16 men and women 42°C (107.6°F) and 40 min cycling No dietary information, 1 d Allsopp et al., 1998 25 men, each on different dietary levels 25°C (77°F) for 3 d, acclimated at 40°C (104°F) for 5 d, 3 levels of sodium intake/d 1.5 g (66 mmol) (9 men) 4.0 g (174 mmol) (9 men) 8.0 g (348 mmol) (7 men), 8 d Inoue et al., 1999 5 men Exercise 90 min/d, 43°C (109.4°F) No dietary information, 8 d Children Murakmi and Hirayama, 1964 193 Japanese children Ambient temperature No dietary information Meyer et al., 1992 18 prepubescent (PP) and 17 pubescent (P) boys and girls 42°C (107.6°F) and 40 min cycling No dietary information, 1 d

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Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate Sodium Concentration in Sweat, mmol/L (g/L) Sweat Sodium Loss, mmol/d (g/d) 49–180 (1.13–4.20) 122–265 (2.8–6.1) 21–53 (0.48–1.21) Not determined 10–58 (0.23–1.33) Not determined Day 1:75–100 (1.7–2.3) Day 10:40–45 (0.92–1.0) Not determined Water: 33 (0.76) Saline: 36 (0.83) Water: 156 (3.6) Saline: 176 (4.0) 35–55 (0.81–1.3) Not determined   50 (1.2) 78 (1.8) 105 (2.4) 45–60 (1.0–1.4) Not determined 5–55 (0.12–1.2) Not determined 25–35 (0.58–0.80) (PP) 35–40 (0.80–0.92) (P) Not determined

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Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate Mascioli S, Grimm R, Launer C, Svendsen K, Flack J, Gonzalez N, Elmer P, Neaton J. 1991. Sodium chloride raises blood pressure in normotensive subjects. Hypertension 17:I21–I26. Masugi F, Ogihara T, Hashizume K, Hasegawa T, Sakaguchi K, Kumahara Y. 1988. Changes in plasma lipids and uric acid with sodium loading and sodium depletion in patients with essential hypertension. J Hum Hypertens 1:293–298. Matkovic V, Ilich JZ, Andon MB, Hsieh LC, Tzagournis MA, Lagger BJ, Goel PK. 1995. Urinary calcium, sodium, and bone mass of young females. Am J Clin Nutr 62:417–425. Matlou SM, Isles CG, Higgs A, Milne FJ, Murray GD, Schultz E, Starke IF. 1986. Potassium supplementation in blacks with mild to moderate essential hypertension. J Hypertens 4:61–64. Mattes RD, Donnelly D. 1991. Relative contributions of dietary sodium sources. J Am Coll Nutr 10:383–393. McCarron DA, Rankin LI, Bennett WM, Krutzik S, McClung MR, Luft F. 1981. Urinary calcium excretion at extremes of sodium intake in normal man. Am J Nephrol 1:84–90. McParland BE, Goulding A, Campbell AJ. 1989. Dietary salt affect biochemical markers of resorption and formation of bone in elderly women. Br Med J 299:834–835. Meade TW, Cooper JA, Peart WS. 1993. Plasma renin activity and ischemic heart disease. N Engl J Med 329:616–619. Medici TC, Schmid AZ, Hacki M, Vetter W. 1993. Are asthmatics salt-sensitive? A preliminary controlled study. Chest 104:1138–1143. Messerli FH, Soria F. 1994. Ventricular dysrhythmias, left ventricular hypertrophy, and sudden death. Cardiovasc Drugs Ther 8:557S–5563S. Meyer F, Bar-Or O, MacDougall D, Heigenhauser GJF. 1992. Sweat electrolyte loss during exercise in the heat: Effects of gender and maturation. Med Sci Sports Exerc 24:776–781. Midgley JP, Matthew AG, Greenwood CMT, Logan AG. 1996. Effect of reduced dietary sodium on blood pressure: A meta-analysis of randomized controlled trials. J Am Med Assoc 275:1590–1597. Miller JZ, Weinberger MH. 1986. Blood pressure response to sodium restriction and potassium supplementation in healthy normotensive children. Clin Exp Hypertens 8:823–827. Miller JZ, Daughtery SA, Weinberger MH, Grim CE, Christian JC, Lang CL. 1983. Blood pressure response to dietary sodium restriction in normotensive adults. Hypertension 5:790–795. Miller JZ, Weinberger MH, Daugherty SA, Fineberg NS, Christian JC, Grim CE. 1987. Heterogeneity of blood pressure response to dietary sodium restriction in normotensive adults. J Chronic Dis 40:245–250. Miller JZ, Weinberger MH, Daugherty SA, Fineberg NS, Christian JC, Grim CE. 1988. Blood pressure response to dietary sodium restriction on healthy normotensive children. Am J Clin Nutr 47:113–119. Mitch WE. 1998. Robert H. Herman Memorial Award in Clinical Nutrition Lecture, 1997. Mechanisms causing loss of lean body mass in kidney disease. Am J Clin Nutr 67:359–366. Mizushima S, Cappuccio FP, Nichols R, Elliott P. 1998. Dietary magnesium intake and blood pressure: A qualitative overview of the observational studies. J Hum Hypertens 12:447–453.

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