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5
Potassium

SUMMARY

Potassium, the major intracellular cation in the body, is required for normal cellular function. Severe potassium deficiency is characterized by hypokalemia—a serum potassium concentration of less than 3.5 mmol/L. The adverse consequences of hypokalemia include cardiac arrhythmias, muscle weakness, and glucose intolerance. Moderate potassium deficiency, which typically occurs without hypokalemia, is characterized by increased blood pressure, increased salt sensitivity,1 an increased risk of kidney stones, and increased bone turnover (as indicated by greater urinary calcium excretion and biochemical evidence of reduced bone formation and increased bone resorption). An inadequate intake of dietary potassium may also increase the risk of cardiovascular disease, particularly stroke.

The adverse effects of inadequate potassium intake can result from a deficiency of potassium per se, a deficiency of its conjugate anion, or both. In unprocessed foods, the conjugate anions of potassium are mainly organic anions, such as citrate, that are converted in the body to bicarbonate. Hence an inadequate intake of potassium is also associated with reduced intake of bicarbonate precursors. Acting as a buffer, bicarbonate neutralizes diet-derived noncarbonic

1  

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.

 



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Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate 5 Potassium SUMMARY Potassium, the major intracellular cation in the body, is required for normal cellular function. Severe potassium deficiency is characterized by hypokalemia—a serum potassium concentration of less than 3.5 mmol/L. The adverse consequences of hypokalemia include cardiac arrhythmias, muscle weakness, and glucose intolerance. Moderate potassium deficiency, which typically occurs without hypokalemia, is characterized by increased blood pressure, increased salt sensitivity,1 an increased risk of kidney stones, and increased bone turnover (as indicated by greater urinary calcium excretion and biochemical evidence of reduced bone formation and increased bone resorption). An inadequate intake of dietary potassium may also increase the risk of cardiovascular disease, particularly stroke. The adverse effects of inadequate potassium intake can result from a deficiency of potassium per se, a deficiency of its conjugate anion, or both. In unprocessed foods, the conjugate anions of potassium are mainly organic anions, such as citrate, that are converted in the body to bicarbonate. Hence an inadequate intake of potassium is also associated with reduced intake of bicarbonate precursors. Acting as a buffer, bicarbonate neutralizes diet-derived noncarbonic 1   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.  

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Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate acids, such as sulfuric acid generated from sulfur-containing amino acids commonly found in meats and other high protein foods. In the setting of an inadequate intake of bicarbonate precursors, buffers in the bone matrix neutralize the excess diet-derived acid, and in the process, bone becomes demineralized. Excess diet-derived acid titrates bone and leads to increased urinary calcium and reduced urinary citrate excretion. The resultant adverse clinical consequences are possibly increased bone demineralization and increased risk of calcium-containing kidney stones. In processed foods to which potassium has been added and in supplements, the conjugate anion is typically chloride, which does not act as a buffer. Because the demonstrated effects of potassium often depend on the accompanying anion and because it is difficult to separate the effects of potassium from the effects of its accompanying anion, this report primarily focuses on research pertaining to nonchloride forms of potassium—the forms found naturally in fruits, vegetables, and other potassium-rich foods. On the basis of available data, an Adequate Intake (AI) for potassium is set at 4.7 g (120 mmol)/day for all adults. This level of dietary intake (i.e., from foods) should maintain lower blood pressure levels, reduce the adverse effects of sodium chloride intake on blood pressure, reduce the risk of recurrent kidney stones, and possibly decrease bone loss. Because of insufficient data from dose-response trials demonstrating these effects, an Estimated Average Requirement (EAR) could not be established, and thus a Recommended Dietary Allowance (RDA) could not be derived. At present, dietary intake of potassium by all groups in the United States and Canada is considerably lower than the AI. In recent surveys, the median intake of potassium by adults in the United States was approximately 2.8 to 3.3 g (72 to 84 mmol)/day2 for men and 2.2 to 2.4 g (56 to 61 mmol)/day for women; in Canada, the median intakes ranged from 3.2 to 3.4 g (82 to 87 mmol)/day for men and 2.4 to 2.6 g (62 to 67 mmol)/day for women (Appendix Tables D-5 and F-3). Because African Americans have a relatively low intake of potassium and a high prevalence of elevated blood pressure and salt sensitivity, this subgroup of the population would especially benefit from an increased intake of potassium. In the generally healthy population with normal kidney function, a potassium intake from foods above the AI poses no potential for 2   To convert millimoles (mmol) of potassium to milligrams (mg) of potassium, multiply mmol by 39.1 (the molecular weight of potassium).  

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Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate increased risk because excess potassium is readily excreted in the urine. Therefore, a Tolerable Upper Intake Level (UL) was not set. However, in individuals in whom urinary excretion of potassium is impaired, a potassium intake below 4.7 g (120 mmol)/day is appropriate because of adverse cardiac effects (arrhythmias) from the resulting hyperkalemia (a markedly elevated serum potassium concentration). Such individuals are typically under medical supervision. Common drugs that can substantially impair potassium excretion are angiotensin converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARB), and potassium-sparing diuretics. Medical conditions associated with impaired urinary potassium excretion include diabetes, chronic renal insufficiency, end-stage renal disease, severe heart failure, and adrenal insufficiency. Elderly individuals are at increased risk of hyperkalemia because they often have one or more of these conditions or are treated with one of these medications. BACKGROUND INFORMATION Function The major intracellular cation in the body is potassium, which is maintained at a concentration of about 145 mmol/L of intracellular fluid, but at much lower concentrations in the plasma and interstitial fluid (3.8 to 5 mmol/L of extracellular fluid). Relatively small changes in the concentration of extracellular potassium greatly affect the extracellular:intracellular potassium ratio and thereby affect neural transmission, muscle contraction, and vascular tone. Physiology of Absorption and Metabolism In unprocessed foods, potassium occurs mainly in association with bicarbonate-generating precursors like citrate, and to a lesser extent with phosphate. In foods to which potassium is added in processing and in supplements, the form of potassium is potassium chloride. In healthy persons, approximately 85 percent of dietary potassium is absorbed (Holbrook et al., 1984). The high intracellular concentration of potassium is maintained via the activity of the Na+/K+-ATPase pump. Because this enzyme is stimulated by insulin, alterations in the plasma concentration of insulin can affect cellular influx of potassium and thus plasma concentration of potassium.

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Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate The preponderance of dietary potassium (approximately 77 to 90 percent) is excreted in urine, while the remainder is excreted mainly in feces, with much smaller amounts being lost in sweat (Agarwal et al., 1994; Holbrook et al., 1984; Pietinen, 1982). The correlation between dietary potassium intake and urinary potassium content is high (r = 0.82) (Holbrook et al., 1984). The great majority of potassium that is filtered by the glomerulus of the kidney is reabsorbed (70 to 80 percent) in the proximal tubule such that only a small amount of filtered potassium reaches the distal tubule. The majority of potassium in urine results from secretion of potassium into the cortical collecting duct, a secretion regulated by a number of factors, including the hormone aldosterone. An elevated plasma concentration of potassium stimulates the adrenal cortex to release aldosterone, which in turn increases secretion of potassium in the cortical collecting duct and hence into urine. Potassium and Acid-Base Considerations A diet rich in potassium from fruits and vegetables favorably affects acid-base metabolism because these foods are rich in precursors of bicarbonate, which neutralizes diet-induced acid in vivo (Sebastian et al., 1994, 2002). The net quantitative outcome of this acid-base interaction is termed “the net endogenous acid production” (NEAP). Because most endogenous noncarbonic acid is derived from protein, and because most endogenous bicarbonate (base) is derived from organic anions present in potassium-rich fruits and vegetables, the dietary protein-to-potassium ratio closely estimates NEAP and thus predicts urinary net acid excretion, which in turn predicts calcium excretion. For many years it has been hypothesized that the modern Western diet could induce a low-grade metabolic acidosis that in turn could induce bone demineralization, osteoporosis, and kidney stones (Barzel, 1995; Barzel and Jowsey, 1969; Lemann et al., 1966; Wachman and Bernstein, 1968). The results of several recent epidemiological (New et al., 1997, 2000; Tucker et al., 1999) and metabolic (Maurer et al., 2003; Morris RC et al., 2001; Sebastian et al., 1994) studies support this hypothesis. Noncarbonic acids are generated from metabolism of both plant and animal proteins (e.g., in both, sulfuric acid is generated from the metabolism of sulfur-containing amino acids found in meats, fish, dairy products, grains, and to a lesser extent, in fruits and vegetables). Unlike fruits and vegetables, meats and other animal foods contain few precursors of bicarbonate. The only plant food group that consistently yields noncarbonic acid precursors in excess

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Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate of bicarbonate precursors is cereal grains (e.g., wheat, rice, and barley). Thus the typical Western diet is usually a net producer of noncarbonic acids not only because of its large content of acid-generating animal proteins, but also because of large amounts of cereal grain products and relatively lower amounts of bicarbonate-generating plant foods (Kurtz et al., 1983; Lemann et al., 1966; Lennon et al., 1966; Sebastian et al., 2002). Although the premodern diet contained considerable amounts of meat (Sebastian et al., 2002), it was a net producer of bicarbonate because it also contained large amounts of fruits and vegetables that generated substantial amounts of bicarbonate via metabolism (Eaton et al., 1999; Sebastian et al., 2002). Accordingly, humans evolved to excrete large loads of bicarbonate and potassium, not the large net acid loads chronically generated by the current Western dietary patterns. The renal acidification process in humans does not completely excrete the modern acid load (Frassetto et al., 1996; Kurtz et al., 1983; Lennon et al., 1966; Sebastian et al., 1994). The unexcreted acid does not titrate plasma bicarbonate to ever lower concentrations, but rather to sustained concentrations only slightly lower than those that otherwise occur. This is because the unexcreted hydrogen ion not only exchanges with bone sodium and potassium, but also titrates and is neutralized by basic salts of bone (Bushinsky, 1998; Lemann et al., 1966, 2003). Although preventing the occurrence of frank metabolic acidosis, the acid titration of calciumcontaining carbonates and hydroxyapatite mobilizes bone calcium and over time dissolves bone matrix (Barzel, 1995; Bushinsky, 1998; Bushinsky and Frick, 2000; Lemann et al., 1966, 2003). The buffering by bone of diet-derived acid may be regarded as a biological tradeoff (Alpern, 1995; Morris RC et al., 2001). At the cost of bone demineralization, arterial pH and plasma bicarbonate concentration are only modestly reduced by an acidogenic diet, such as the Western-type diet (Morris RC et al., 2001), and not to values below their “normal” range. These normal reduced values, however, reflect a state of low-grade metabolic acidosis. INDICATORS CONSIDERED FOR ESTIMATING THE REQUIREMENT FOR POTASSIUM This section reviews potential physiological indices and pathologic endpoints for adverse effects of insufficient dietary intake of potassium in apparently healthy individuals. Because the demonstrated effects of potassium often depend on the accompanying anion and

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Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate because it is difficult to separate the effects of potassium from the effects of its accompanying anion, this report focuses primarily on research pertaining to nonchloride forms of potassium—the forms found naturally in foods. Potassium Balance As previously mentioned, urinary potassium excretion reflects dietary potassium intake. The effects on potassium balance of two levels of potassium intake (3.1 g [80 mmol]/day and 11.7 g [300 mmol]/day) were examined in six healthy men about 24 years of age (Hene et al., 1986). After 18 days on the high potassium diet, urinary potassium excretion increased from 2.0 to 9.1 g (50 to 233 mmol)/day. In a separate study, daily fecal potassium loss ranged from 0.11 to 0.85 g (2.8 to 22 mmol)/day on dietary intakes approximating 2.6 to 2.9 g (66 to 74 mmol)/day (Holbrook et al., 1984). Losses of potassium in sweat vary; under conditions in which sweat volume is minimal, the reported values range from 2.3 to 16 mmol (90 to 626 mg)/L (Consolazio et al., 1963). A number of dietary factors, including dietary fiber and sodium, can affect potassium balance. The effects of increased wheat fiber intake on fecal potassium loss were examined in six healthy men, 21 to 25 years of age, who consumed 45 g/day of wheat fiber for 3 weeks; their previous average intake was 17 g/day. Potassium intake was held constant at 3.1 g (80 mmol)/day (Cummings et al., 1976). Fecal weight increased significantly from about 79 g/day to about 228 g/day with the increased fiber intake. Fecal potassium loss also significantly increased from a prestudy level of 0.3 g to a final value of 1.1 g (8.6 to 28.5 mmol)/day (Cummings et al., 1976). The level of sodium intake does not appear to influence potassium excretion (Bruun et al., 1990; Castenmiller et al., 1985; Overlack et al., 1993; Sharma et al., 1990; Sullivan et al., 1980) except at levels of sodium intake above 6.9 g (300 mmol)/day, at which point net loss of potassium has been demonstrated (Kirkendall et al., 1976; Luft et al., 1982). At dietary sodium intakes greater than 6.9 g (300 mmol)/day, there was a net loss of potassium—urinary potassium excretion exceeded dietary intake, at least during the 3-day periods in this trial (Luft et al., 1982). Over the long term, net potassium losses do not occur at lower levels of sodium intake. At three levels of dietary sodium, 1.5, 2.4, and 3.2 g (65, 104, and 140 mmol)/day, each provided for 28 days, urinary potassium excretion did not exceed intake and urinary potassium excretion was similar at each sodium level (Sacks et al., 2001).

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Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate In nonhypertensive individuals who maintained potassium balance while consuming at least 1.6 g (40 mmol)/day of potassium, serum potassium concentrations were at the lower end of the clinically accepted normal range (Sebastian et al., 1971). As discussed subsequently, while potassium balance can be maintained at this lower level of dietary intake, if such levels are consumed chronically, clinically important adverse effects may result (Morris RC et al., 2001). Serum Potassium Concentration Serum potassium concentration, as well as body potassium content, is determined jointly by the amount of potassium consumed and the amount excreted since the gastrointestinal tract normally absorbs 85 percent of dietary intake and because the kidney excretes most of the potassium absorbed (Young, 1985, 2001; Young and McCabe, 2000). Humans evolved from ancestors who habitually consumed large amounts of uncultivated plant foods that provided substantial amounts of potassium. In this setting, the human kidney developed a highly efficient capacity to excrete excess potassium. The normal human kidney efficiently excretes potassium when dietary intake is high enough to increase serum concentration even slightly, but inefficiently conserves potassium when dietary intake and thus serum concentration is reduced (Young, 2001). While normal renal function protects against the occurrence of hyperkalemia when dietary potassium is increased, it does not prevent the occurrence of potassium deficiency when dietary intake of potassium is reduced (Squires and Huth, 1959), even marginally, relative to the usual potassium intake in the Western diet. Based on recent diet surveys, the estimated median potassium intakes for adult age groups in the United States (Appendix Table D-5) ranged from 2.8 to 3.3 g (72 to 84 mmol)/day for men and 2.2 to 2.4 g (56 to 61 mmol)/day for women, while median intakes in Canada from surveys conducted between 1990 and 1999 ranged from 3.2 to 3.4 g (82 to 87 mmol)/day for men and 2.4 to 2.6 g (62 to 67 mmol)/day for women (Appendix Table F-2). Signs and symptoms of potassium deficiency can occur without frank hypokalemia (i.e., they occur while the serum potassium concentration remains at or somewhat above 3.5 mmol/L, an accepted minimum of the range for normal serum potassium levels) (Table 5-1). In generally healthy people, frank hypokalemia is not a necessary or usual expression of a subtle dietary potassium deficiency. As

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Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate TABLE 5-1 Dietary Potassium and Serum Potassium Concentrations Reference Subjects Dietary Potassium (K),a g/d (mmol/d) Serum Potassium (mmol/L) ± standard deviation Dluhy et al., 1972 8 women, 2 men, crossover 5 subjects, 6–7 d, 0.23 g (10 mmol) sodium (Na)/d 5 subjects, 3 d, 4.6 g (200 mmol) Na/d 1.6 (40) 7.8 (200) 1.6 (40) 7.8 (200) 4.1 ± 0.1b 4.3 ± 0.1b 4.0 ± 0.1b 4.2 ± 0.1b Zoccali et al., 1985 5-d crossover, 10 men 3.0 (76) 6.9 (176) 3.9 ± 0.1b 4.3 ± 0.1b Hene et al., 1986 18-d parallel, 6 men 3.1 (80) 11.7 (300) 4.26 ± 0.28b 4.39 ± 0.32b Witzgall and Behr, 1986 6 d on high K diet, 16 men 2.3 g (60) 10.1 g (260) 4.2 ± 0.3b 4.6 ± 0.3c Grimm et al., 1990 2.2 yr supplement/placebo intervention, 287 men, 45–68 yr, baseline urinary K = 2.2 g/d + 3.8 (96) + 0 4.2b 4.5c The difference averaged 0.26 mmol/L over the 2-yr period Rabelink et al., 1990 20 d, 6 men 3.9 (100) 15.6 (400) 3.75 ± 0.16b 4.22 ± 0.12b Clinkingbeard et al., 1991 3-d crossover, 8 men 0.39 (10) 7.8 (200) 3.8 ± 0.1b 4.3 ± 0.2c Deriaz et al., 1991 5-d crossover, 8 men 2.7 (69) 6.4 (163) 4.1 ± 0.2b 3.8 ± 0.1c Valdes et al., 1991 4-wk crossover, 24 men and women, provided placebo or supplement + 0 + 2.5 (64) 3.8 ± 0.1b 4.1 ± 0.1c Smith et al., 1992 4-d crossover, 22 men and women 2.7 (70) 4.7 (120) 3.9 ± 0.1b 4.3 ± 0.1c Sebastian et al., 1994 18 d, 18 postmenopausal women 2.3 (60) + 4.7 (120) 3.9 ± 0.15b 4.0 ± 0.2b Morris et al., 1999b 38 men, parallel + 1.17 (30) 4.7 (120) 3.7 ± 0.2b 4.0 ± 0.2c Coruzzi et al., 2001 10-d isocaloric crossover, 8 men, 3 women 0.70 (18) 3.1 (80) 3.2 ± 0.1 (standard error)b 4.1 ± 0.05c a “+” means amount of potassium provided as a supplement. b,c Values with different superscripts differed significantly at p < 0.05 or less.

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Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate will be discussed in subsequent sections, a typical dietary intake of potassium that gives rise to a serum potassium concentration somewhat greater than 3.5 mmol/L would still be considered inadequate if a higher intake of potassium prevents, reduces, or delays expression of certain chronic diseases or conditions, such as elevated blood pressure, salt sensitivity, kidney stones, bone loss, or stroke (Morris et al., 1999a, 1999b; Morris RC et al., 2001; Schmidlin et al., 1999; Sudhir et al., 1997). The Western diet gives rise not only to low-grade potassium deficiency, but also to low-grade bicarbonate deficiency that is expressed as low-grade metabolic acidosis (Morris et al., 1999a, 1999b; Morris RC et al., 2001; Sebastian et al., 2002). Because plasma concentrations of potassium and other electrolytes (bicarbonate, sodium, and chloride) are highly regulated, their plasma concentrations remain normal or little changed despite substantial increases in dietary potassium intake (Lemann et al., 1989, 1991; Morris RC et al., 2001; Schmidlin et al., 1999). Thus serum potassium is not a sensitive indicator of potassium adequacy related to mitigating chronic disease. Hypokalemia Disordered potassium metabolism that is expressed as hypokalemia (that is, a serum potassium level below 3.5 mmol/L) can result in cardiac arrhythmias, muscle weakness, hypercalciuria, and glucose intolerance. Such disorders, which are correctable by potassium administration, can be induced by diuretics, chloride-depletion associated forms of metabolic alkalosis, and increased aldosterone production (Knochel, 1984). Hypokalemia reduces the capacity of the pancreas to secrete insulin and therefore is a recognized reversible cause of glucose intolerance (Helderman et al., 1983). There is some limited evidence that hypokalemia can also confer insulin resistance (Helderman et al., 1983; Pollare et al., 1989). A low potassium diet (0.58 g [15 mmol]/day), which did not induce frank hypokalemia, resulted in a decrease in plasma insulin concentration and a resistance to insulin action, which were reversed when dietary potassium was supplemented with 4.8 g (64 mmol)/day of potassium chloride (Norbiato et al., 1984). Decreased erythrocyte and plasma potassium concentrations have been associated with glucose intolerance (Modan et al., 1987). Diuretic-induced hypokalemia leads to insulin resistance (hyperglycemia and hyperinsulinemia) and glucose intolerance (Helderman et al., 1983; Plavinik et al., 1992). In one trial, individu-

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Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate als with diuretic-induced hypokalemia did not achieve reduction in cardiovascular events compared with diuretic-treated individuals without hypokalemia (Franse et al., 2000). Because moderate potassium deficiency and its adverse side effects occur without hypokalemia, hypokalemia is not a sensitive indicator appropriate for use to establish adequacy. Salt-Sensitive Blood Pressure The extent to which blood pressure responds to changes in sodium chloride intake varies among individuals. “Salt-sensitive” blood pressure is that which varies directly with the intake of sodium chloride (Morris et al., 1999b; Weinberger, 1996). Salt sensitivity, even in those who are nonhypertensive, has been found to confer its own cardiovascular risks, including incident hypertension and cardiovascular death (Morimoto et al., 1997; Weinberger et al., 2001). Salt sensitivity occurs with greater frequency and severity in nonhypertensive African Americans than in nonhypertensive whites (Morris et al., 1999b; Price et al., 2002; Weinberger, 1996). The expression of salt sensitivity is strongly modulated by dietary potassium intake (Morris et al., 1999b; Schmidlin et al., 1999; Luft et al., 1979). In a metabolic study of 38 healthy, nonhypertensive men (24 African Americans and 14 whites) fed a basal diet with low levels of potassium (1.2 g [30 mmol]/day) and sodium (0.7 g [30 mmol]/day), the modulating effect of potassium supplementation on the pressor effect of dietary sodium chloride loading (14.6 g [250 mmol]/day) was investigated (Morris et al., 1999b) (Figure 5-1). Before potassium was supplemented, 79 percent of the African-American men and 26 percent of the white men were termed salt sensitive, as defined by a sodium chloride-induced increase in mean arterial pressure of at least 3 mm Hg. Salt sensitivity was defined as “severe” if sodium chloride induced an increase in mean arterial pressure of 10 mm Hg or more, an increase observed only in African-American men. When dietary potassium was increased with potassium bicarbonate from 1.2 g (30 mmol)/day to 2.7 g (70 mmol)/day, over half of the African-American men, but only one-fifth of the white men, remained salt sensitive. In the African Americans with severe salt sensitivity, increasing dietary potassium to a high-normal intake of 4.7 g (120 mmol)/day reduced the frequency of salt sensitivity to 20 percent, the same percentage as that observed in white subjects when their potassium intake was increased to only 2.7 g (70 mmol)/day. In another metabolic study of 16 mostly nonhypertensive African-American subjects loaded with 14.6 g (250 mmol) of

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Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate FIGURE 5-1 Effect of potassium intake on frequency of salt sensitivity in nonhypertensive African-American men (solid bar) and white men (gray bar). No white men were tested with 4.7 g (120 mmol)/day of potassium. Throughout an initial 7-day period of salt loading in all study subjects, potassium intake as potassium bicarbonate was set at 1.2 g (30 mmol)/day, then increased to a total of either 2.7 or 4.7 g (70 or 120 mmol)/day for a subsequent 7-day period of salt loading. Reprinted with permission from Morris et al. (1999b). Copyright 1999 by W.B. Saunders Co. sodium chloride per day, increasing dietary potassium as potassium bicarbonate to an intake of 6.6 g (170 mmol)/day abolished the salt sensitivity of all subjects (Schmidlin et al., 1999). In aggregate, these trials document that supplemental potassium bicarbonate mitigates the pressor effect of dietary sodium chloride in a dose-dependent fashion. Furthermore, these trials highlight the potential benefit of increased potassium intake in African Americans, who have a higher prevalence of hypertension and of salt sensitivity and a lower intake of potassium than non-African Americans. Survey data from the Third National Health and Nutrition Examination Survey (NHANES III) in the United States (Appendix Tables D-6 and D-7) estimated that the median intake of potassium of non-Hispanic African-American men (aged 19 to 30 years) was 3.0 g (78 mmol)/day, while that for non-Hispanic white men (aged 19 to 30 years) was 3.4 g (87 mmol)/day, approximately 10 percent lower than their white counterparts. Similar differences

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