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Suggested Citation:"5 Potassium." Institute of Medicine. 2005. Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate. Washington, DC: The National Academies Press. doi: 10.17226/10925.
×

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.

 

Suggested Citation:"5 Potassium." Institute of Medicine. 2005. Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate. Washington, DC: The National Academies Press. doi: 10.17226/10925.
×

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).

 

Suggested Citation:"5 Potassium." Institute of Medicine. 2005. Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate. Washington, DC: The National Academies Press. doi: 10.17226/10925.
×

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.

Suggested Citation:"5 Potassium." Institute of Medicine. 2005. Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate. Washington, DC: The National Academies Press. doi: 10.17226/10925.
×

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

Suggested Citation:"5 Potassium." Institute of Medicine. 2005. Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate. Washington, DC: The National Academies Press. doi: 10.17226/10925.
×

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

Suggested Citation:"5 Potassium." Institute of Medicine. 2005. Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate. Washington, DC: The National Academies Press. doi: 10.17226/10925.
×

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).

Suggested Citation:"5 Potassium." Institute of Medicine. 2005. Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate. Washington, DC: The National Academies Press. doi: 10.17226/10925.
×

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

Suggested Citation:"5 Potassium." Institute of Medicine. 2005. Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate. Washington, DC: The National Academies Press. doi: 10.17226/10925.
×

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.

Suggested Citation:"5 Potassium." Institute of Medicine. 2005. Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate. Washington, DC: The National Academies Press. doi: 10.17226/10925.
×

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-

Suggested Citation:"5 Potassium." Institute of Medicine. 2005. Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate. Washington, DC: The National Academies Press. doi: 10.17226/10925.
×

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

Suggested Citation:"5 Potassium." Institute of Medicine. 2005. Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate. Washington, DC: The National Academies Press. doi: 10.17226/10925.
×

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

Suggested Citation:"5 Potassium." Institute of Medicine. 2005. Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate. Washington, DC: The National Academies Press. doi: 10.17226/10925.
×

are noted for women, with non-Hispanic white women aged 19 to 30 years having higher intakes than non-Hispanic African-American women of the same age group.

Predictably, over the range of dietary potassium evaluated in the study of salt sensitivity (Figure 5-1), the serum concentration of potassium remained well within the normal range, increasing only minimally (from ≈ 3.8 to 4.0 mmol/L) when potassium bicarbonate was supplemented (Morris et al., 1999b). It has been postulated that such dose-dependent suppression of salt sensitivity might prevent or delay the occurrence of hypertension (Berenson et al., 1979; Frisancho et al., 1984; Grim et al., 1980; Morris et al., 1999b). In hypertensive individuals, potassium supplementation can mitigate the pressor effect of sodium chloride (Iimura et al., 1981; Morgan et al., 1984).

The antipressor effect of dietary potassium may in part result from its natriuretic effects (Morris et al., 1999b; Schmidlin et al., 1999). As mentioned earlier, potassium acts directly on the renal tubule to increase the urinary excretion of sodium chloride (Brandis et al., 1972; Stokes et al., 1982), an action apparently unaffected by the anion accompanying ingested potassium (van Buren et al., 1992).

Blood Pressure

Epidemiological Evidence

Numerous observational studies (Table 5-2) have examined the relationship between blood pressure and dietary potassium intakes, or urinary potassium excretion, used as a proxy of intake (Ascherio et al., 1992; Dai et al., 1984; Dyer et al., 1994; Geleijnse et al., 1996; Hajjar et al., 2001; Khaw and Barrett-Connor, 1984; Langford, 1983; Liu et al., 1988, 1996; Rose et al., 1988; Takemori et al., 1989; Tunstall-Pedoe, 1999; Walker et al., 1979). Many, but not all, studies documented an inverse association—that is, a higher intake of potassium that was associated with lower blood pressure. In the Intersalt study, a 50-mmol (2.0-g) higher excretion of urinary potassium was associated with a 2.5- and 1.5-mm Hg lower level of systolic and diastolic blood pressure, respectively (Rose et al., 1988).

While blood pressure is inversely associated with potassium intake and directly associated with sodium intake and the sodium:potassium ratio, blood pressure is typically more closely associated with the sodium:potassium ratio than intake of either electrolyte alone. This pattern was evident in Intersalt and in other observational studies (Khaw and Barrett-Connor, 1988; Morris and Sebastian, 1995;

Suggested Citation:"5 Potassium." Institute of Medicine. 2005. Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate. Washington, DC: The National Academies Press. doi: 10.17226/10925.
×

TABLE 5-2 Epidemiological Studies on Potassium Intake and Blood Pressure

Reference

Study Design

Walker et al., 1979

Cross-sectional, 574 men and women

Khaw and Barrett-Connor, 1984

Cross-sectional, 685 men and women

Kok et al., 1986

Cross-sectional, 2,291 men and women in the Netherlands, multivariate analysis

Kesteloot and Joossens, 1988

Belgian Interuniversity Research on Nutrition and Health Study, cross-sectional, 8,058 men and women

Khaw and Barrett-Connor, 1988

Cross-sectional, 1,302 men and women

Liu et al., 1988

Cross-sectional, 3,248 men and women in China

Rose et. al., 1988

Intersalt study, cross-sectional, 10,648 men and women

Takemori et al., 1989

Cross-sectional, 7,441 women in Japan

Witteman et al., 1989

Nurses Health Study, prospective, 4-yr follow up, 58,218 women, multivariate analysis

Khaw and Barrett-Connor, 1990

Cross-sectional, 2,046 men and women

Ascherio et al., 1992

Health Professionals Follow-Up Study, prospective 4-yr follow-up, 30,681 men, multivariate analysis

Suggested Citation:"5 Potassium." Institute of Medicine. 2005. Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate. Washington, DC: The National Academies Press. doi: 10.17226/10925.
×

Resultsa

Urinary K was inversely correlated with DBP

Dietary K intake inversely correlated with age-adjusted SBP in men and women and age-adjusted DBP in men

No significant association between blood pressure and potassium intake

No independent effects of dietary K intake on BP

Blood pressure varied directly with dietary Na:K ratio, age-adjusted SBP and DBP significantly and inversely correlated with potassium intake

Urinary potassium was inversely correlated with DBP and SBP only in the 20- to 29-yr-old age group

Urinary K was inversely correlated with blood pressure

Urinary potassium inversely correlated with blood pressure

Potassium intake

g/d (mmol/d)

RR of hypertension

Q1 < 2.0 (51)

1.0

Q2 2.0–2.39 (51–61)

0.93

Q3 2.4–2.79 (61–71)

1.02

Q4 2.8–3.19 (72–82)

1.05

Q5 > 3.2 (82)

1.05

 

p = 0.26

No independent association with potassium intake and risk of hypertension

Age-adjusted SBP and DBP correlated significantly and directly with Na:K ratio

Potassium intake

g/d (mmol/d)

RR of hypertension

Q1 < 2.4 (61)

1.2

Q2 2.4–2.79 (61–71)

1.1

Q3 2.8–3.19 (72–82)

1.0

Q4 3.2–3.59 (82–92)

1.1

Q5 > 3.6 (92)

1.0

 

p = 0.41

No independent association with potassium intake and risk of hypertension

Suggested Citation:"5 Potassium." Institute of Medicine. 2005. Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate. Washington, DC: The National Academies Press. doi: 10.17226/10925.
×

Reference

Study Design

Dyer et al., 1994

Intersalt study, cross-sectional, 10,079 men and women

Zhou et al., 1994

Cross-sectional, 705 men and women in China

Geleijnse et al., 1996

Rotterdam Study, cross-sectional, 3,239 men and women

Liu et al., 1996

CARDIA Study, cross-sectional, 4,146 men and women

Tunstall-Pedoe, 1999

Scottish Heart Health Study, cross-sectional, 11,629 men and women

Hajjar et al., 2001

NHANES III, cross-sectional, 17,030 men and women, multivariate analysis

a DBP = diastolic blood pressure, SBP = systolic blood pressure, K = potassium, Na = sodium, BP = blood pressure, RR = relative risk, Q = quintile of potassium intake.

Zhou et al., 1994). Still, because of high colinearity of nutrient intake (Rose et al., 1988), it is difficult to tease apart the effects of potassium from the effects of other nutrients closely associated with potassium in foods.

Evidence from Intervention Studies

Results from intervention studies demonstrate that potassium can reduce blood pressure in nonhypertensive (Tables 5-3 and 5-4) as well as hypertensive individuals (Tables 5-3 and 5-5). Table 5-3 provides corresponding results for studies in which potassium was increased through diet, while Tables 5-4 and 5-5 provide corresponding results for studies in which potassium was increased by use of potassium supplements. Although the trials in Tables 5-4 and 5-5 tested the effect of supplemental potassium, their findings are assumed to apply to potassium from foods as well. A few studies have tested the effects of diets rich in potassium (Appel et al., 1997; Sacks et al., 2001). One other trial documented that increased fruit and vegetable intake can reduce blood pressure, but it did not

Suggested Citation:"5 Potassium." Institute of Medicine. 2005. Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate. Washington, DC: The National Academies Press. doi: 10.17226/10925.
×

Resultsa

A 0.6 g (15 mmol) increase in potassium intake was associated with an estimated mean change in SBP of −1.0 mm Hg

A positive association with SBP and sodium:potassium ratio in the setting of low calcium intakes

An increase in K intake of 1 g/d (26 mmol/d) was associated with a 0.9 mm Hg lower SBP and 0.8 mm Hg lower DBP

Potassium intake was significantly and inversely related to blood pressure in white women and African-American men

Potassium excretion was significantly and inversely associated with blood pressure, especially SBP in men

SBP and DBP were inversely associated with K intake

specify the amount of dietary potassium provided by the increased fruit and vegetable diet (John et al., 2002). Because of the potential for confounding from concomitant changes in other nutrients (e.g., fiber and magnesium), evidence from Table 5-3 should be interpreted with caution.

A number of the supplemental studies gave potassium supplements (e.g., potassium chloride) without documenting the amount of potassium in the diet (Tables 5-4 and 5-5). Hence, total intake of potassium from diet and supplements in some of the studies is unknown. It should also be recognized that none of the studies listed in Tables 5-3, 5-4, or 5-5 provide more than two levels of potassium; thus a dose-response assessment within the same study is unavailable.

In the absence of large-scale trials, pooling of the results of small clinical trials provides a more statistically precise estimate of intervention effects and allows for the exploration of the basis for heterogeneity in outcome effects. At least three major meta-analyses of the effects of oral potassium in the treatment and prevention of human hypertension have been conducted (Cappuccio and MacGregor, 1991; Geleijnse et al., 2003; Whelton et al., 1997). The meta-

Suggested Citation:"5 Potassium." Institute of Medicine. 2005. Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate. Washington, DC: The National Academies Press. doi: 10.17226/10925.
×

TABLE 5-3 Intervention Studies Evaluating the Effect of Changes in Dietary Potassium Intake from Foods on Blood Pressure

Reference

Study Design

Potassium Intake, g/d (mmol/d) by Group

Nonhypertensive individuals

 

Lawton et al., 1990b

6-d crossover, 10 men; formula diet + foods

1.2 (29)

3.9 (92)

Appel et al., 1997d,e

8-wk parallel, 326 men and women

1.8 (45) = control diet

4.1 (105) = fruit/veg

4.4 (113) = DASH

Hypertensive individuals

 

Lawton et al., 1990

6-d crossover, 11 men; formula diet + foods

1.2 (29)

3.9 (92)

Appel et al., 1997d,e

8-wk parallel, 133 men and women

1.8 (45) = control diet

4.1 (105) = fruit/veg

4.4 (113) = DASH

a At end of dietary period.

b As determined by random analysis of sample diets.

c Difference in response to diet intervention pre- and post- between control and experimental group; SBP = systolic blood pressure, DBP = diastolic blood pressure.

analysis by Whelton and colleagues (1997) and the one by Geleijnse and coworkers (2003) were confined to randomized controlled trials in which the only difference between the intervention and control groups was potassium intake. Both assessed the potential input of confounders, while the analysis by Whelton presented data from individual trials, including estimates of potassium intake.

Of the 33 trials included in the meta-analysis by Whelton and coworkers (1997) (see studies marked in Tables 5-3 and 5-5), there were 2,609 African-American and white participants (18 to 79 years of age). Twelve trials were conducted in nonhypertensive individu-

Suggested Citation:"5 Potassium." Institute of Medicine. 2005. Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate. Washington, DC: The National Academies Press. doi: 10.17226/10925.
×

Sodium Intake, g/d (mmol/d)

Urinary Potassium,a mmol/d, During Follow-up

Urinary Sodium,a mmol/d, During Follow-up

Blood Pressure (mm Hg) Changes

Statistical Significance

 

n = 7

 

Δ SBP significant at p < 0.01

8.5 (371)

27

302

123/69

8.5 (368)

62

343

116/72

 

 

SBPc

DBPc

3.0 (132)

39

138

2.8 (122)

71

130

↓ 0.8

↓ 0.3

2.9 (124)

75

134

↓ 3.5

↓ 2.1

 

n = 8

 

 

Δ SBP significant at p < 0.001

8.5 (371)

30

322

134/79

8.5 (368)

76

324

124/76

 

 

SBPc

DBPc

3.0 (132)

39

138

2.8 (122)

71

130

↓ 7.2

↓ 2.8

2.9 (124)

75

134

↓ 11.4

↓ 5.5

d Estimate of nutrient intake based on chemical analysis of 2,100 kcal menu; three food-based diets: control diet, fruit/veg diet (higher in fruits and vegetables), and DASH diet (higher in fruits, vegetables, and dairy, lower in meats, fats, and sweets).

e Urinary excretion averaged over both nonhypertensive and hypertensive subjects.

NOTE: Difference in response to diet intervention significant at p ≤ 0.01.

als (1,005 participants) and 21 trials were conducted in individuals with hypertension (1,560 participants). Hypertensive patients received antihypertensive medications concurrently in 4 of the 21 trials. All but six of the trials provided potassium in the form of potassium chloride. As such, there was little capacity to compare the efficacy of different potassium salts. Just one trial tested potassium citrate as well as potassium chloride (Mullen and O’Conner, 1990). In this small, placebo-controlled trial, neither form of potassium significantly affected blood pressure.

Average net change in urinary potassium excretion for the inter-

Suggested Citation:"5 Potassium." Institute of Medicine. 2005. Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate. Washington, DC: The National Academies Press. doi: 10.17226/10925.
×

TABLE 5-4 Clinical Trials on the Effects of Potassium Supplements on Blood Pressure in Nonhypertensive Individuals in Order of Increasing Duration of Intervention

Reference

Subjects

Study Design

Potassium Intake,b g/d (mmol/d)

Barden et al., 1991a

37 women

4-d crossover

Placebo

3.1 (80) KCl supplement

Gallen et al., 1998

10 men, 11 women

9-d crossover; K restriction; 4.1 g (180 mmol) Na

0.78 (20) diet plus placebo

3.1 (80) KCl supplement

Krishna et al., 1989a

10 men

10-d crossover; 2.8–4.6 (120–200 mmol) Na

0.4 (10) diet plus placebo

3.5 (90) [80 KCl supplement]

Skrabal et al., 1981a

20 men

2-wk crossover

3.1 (80) KCl supplement [4.6 (200) Na]

3.1 (80) KCl supplement [1.2 (50) Na]

7.8 (200) KCl supplement [4.6 (200) Na]

7.8 (200) KCl supplement [1.2 (50) Na]

Khaw and Thom, 1982a

20 men

2-wk crossover

1.6 (41) diet

2.5 (64) KCl supplement

Poulter and Sever, 1986a

19 men

2-wk crossover

Placebo

2.5 (64) KCl supplement

Mullen and O’Connor, 1990a

24 men

2-wk crossover

Placebo

2.9 (75) KCl supplement

2.9 (75) K citrate supplement

Brancati et al., 1996a

31 men, 56 women

3-wk parallel, 2.9–4.0g (127–175 mmol) Na

Placebo plus 1.3-1.4 (32-35) K from diet

3.1 (80) KCl supplement plus 1.3-1.4 (32-35) K from diet

Suggested Citation:"5 Potassium." Institute of Medicine. 2005. Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate. Washington, DC: The National Academies Press. doi: 10.17226/10925.
×

Urinary Electrolytes,c g/d (mmol/d) During Follow-up

Mean Blood Pressure (mm Hg) on Placebo or Control Dietd

Mean Net Change in Blood Pressuree (mm Hg)

Comments

Potassium (K)

Sodium (Na)

SBP

DBP

2.1 (53)

2.4 (105)

105.9/64.1

 

4.9 (125)

2.8 (120)

 

−1.7

−0.6

 

2.5 (64)

3.2 (140)

MAP

MAP

 

No significant difference between African-American and white participants

 

82.7

7.8 (20)

2.5 (109)

 

+3.7

1.1 (28)

2.3 (100)

120.0/73.1

 

2.9 (75)

3.3 (144)

 

−5.5

−7.4

2.8 (71)

4.8 (210)

125.0/73.1

2.5 (65)

0.9 (40)

 

−2.7

−3.0

4.5 (116)

3.6 (155)

−1.7

−4.5

6.7 (172)

0.6 (28)

−2.3

−3.5

3.0 (78)

3.6 (155)

155.7/72.1

5.1 (130)

3.8 (164)

 

−1.1

−2.4

1.6 (41)

2.6 (113)

109.6/64.6

3.1 (79)

2.6 (114)

 

−1.2

+2.0

3.0 (77)

3.5 (153)

117/69

3.9 (100)

3.2 (141)

 

0

+3.0

4.3 (111)

3.2 (138)

−2.0

+2.0

0.9 (25)

2.9 (130)

127/77

3.5 (89)

3.3 (143)

 

−6.9

−2.5

Suggested Citation:"5 Potassium." Institute of Medicine. 2005. Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate. Washington, DC: The National Academies Press. doi: 10.17226/10925.
×

Reference

Subjects

Study Design

Potassium Intake,b g/d (mmol/d)

Barden et al., 1986a

44 women

4-wk crossover

Placebo

3.1 (80) KCl supplement

Naismith and Braschi, 2003

33 men, 26 women

6-wk parallel

Placebo plus 3.3 (84) diet

0.9 (24) KCl supplement plus 3.3 (84) diet

Whelton et al., 1995a

255 men, 98 women

24-wk parallel

Placebo

2.3 (60) KCl supplement

Hypertension Prevention Trial Research Group, 1990a

247 men, 144 women

3-yr parallel

3.9 (100) diet

a Included in meta analysis by Whelton et al. (1997).

b Potassium intake from diet unless otherwise indicated.

c Surrogate marker for electrolyte intake. CI = confidence interval.

vention versus the control (21 trials) in the meta-analysis (Whelton et al., 1997) varied from 0 to 129 mmol (5.0 g)/24 hours (median = 50 mmol [1.9 g]/24 hours) and was greater than or equal to 40 mmol (1.6 g)/24 hours in 21 (68 percent) trials. The weighted net change in urinary potassium was 53 mmol (2.1 g)/24 hours. Average net change in urinary sodium excretion for the intervention versus control ranged from −55 to +44 mmol (−1.3 g to +1.0 g)/24 hours, with a median of 7 mmol (0.3g)/24 hours. There was an intervention-related trend toward a reduction in systolic blood pressure in 26 of the 32 trials (81 percent), and in 11 trials (34 percent) the reduction in blood pressure was statistically significant. For diastolic blood pressure, an intervention-related trend toward reduction in blood pressure was noted in 24 of 33 trials (73 percent), and in 11 trials (30 percent) the reduction was statistically significant. Overall pooled estimates of the effects of potassium supplementation on systolic and diastolic blood pressure were −4.4 and −2.4 mm Hg, respectively (p < 0.001 for both values). Exclusion of an outlier

Suggested Citation:"5 Potassium." Institute of Medicine. 2005. Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate. Washington, DC: The National Academies Press. doi: 10.17226/10925.
×

Urinary Electrolytes,c g/d (mmol/d) During Follow-up

Mean Blood Pressure (mm Hg) on Placebo or Control Dietd

Mean Net Change in Blood Pressuree (mm Hg)

Comments

Potassium (K)

Sodium (Na)

SBP

DBP

1.9 (51)

2.9 (126)

118/71

 

4.6 (118)

3.1 (136)

 

−1.4

−1.4

 

3.5 (151)

116/71

3.8 (166)

 

−7.6

−6.5

2.1 (54)

3.3 (144)

121.6/81.1

3.8 (97)

3.3 (144)

 

−0.13

−0.26

2.5 (65)

3.5 (154)

124.1/82.3

−1.3

−0.9

d MAP = mean arterial pressure.

e If potassium supplement, then change in blood pressure compared to placebo. SBP = systolic blood pressure, DBP = diastolic blood pressure.

trial (Obel, 1989) reduced the overall pooled effect size estimates to −3.1 mm Hg for systolic blood pressure and −2.0 mm Hg for diastolic blood pressure (p < 0.001 for both values) (Whelton et al., 1997).

When the analysis was restricted to the 29 trials with a documented intervention-related net change in urinary potassium greater than or equal to 20 mmol (0.8 g)/24 hours, the effect size estimates were −4.9 mm Hg for systolic and −2.7 mm Hg for diastolic blood pressure. These effect size estimates were also higher when analyses were restricted to the 29 trials in nonhypertensive and hypertensive individuals in whom no antihypertensive medications were administered (Whelton et al., 1997).

In subgroup analyses, there was a trend toward greater treatment-related reductions in systolic and diastolic blood pressure at higher levels of urinary sodium excretion during follow-up (p < 0.001). Linear regression analysis also identified a significant, independent positive relationship between average 24-hour urinary sodium ex-

Suggested Citation:"5 Potassium." Institute of Medicine. 2005. Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate. Washington, DC: The National Academies Press. doi: 10.17226/10925.
×

TABLE 5-5 Clinical Trials on the Effects of Potassium Supplements on Blood Pressure in Hypertensive Individuals in Order of Increasing Duration of Intervention

Reference

Subjects

Study Design

Potassium Intake,b g/d (mmol/d)

Smith et al., 1992a

12 men

9 women

4-d crossover

4.6 g (200 mmol) Na

Placebo

4.7 (120) KCl

Krishna and Kapoor, 1991

10 men

2 women

10-d parallel; K restriction

2.8 g (120 mmol) Na

3.8 (96) [80 mmol KCl supplement]

0.62 (16) diet

Zoccali et al., 1985a

10 men

9 women

2-wk crossover

Placebo

3.9 (100) KCl supplement

MacGregor et al., 1982a

12 men

11 women

4-wk crossover

Placebo

2.5 (64) KCl supplement

Richards et al., 1984a

8 men

4 women

4- to 6-wk crossover; 4.1g (180 mmol) Na

2.3 (60)

7.8 (200)

Smith et al., 1985a

11 men

9 women

4-wk crossover; 1.6 g (70 mmol) Na

Placebo

2.5 (64) KCl supplement

Valdes et al., 1991a

13 men

11 women

4-wk crossover

Placebo

2.5 (64) KCl supplement

Fotherby and Potter, 1992a

5 men

13 women

4-wk crossover

Placebo

2.3 (60) KCl supplement

Kaplan et al., 1985a

6 men

10 women

6-wk crossover

Placebo

2.3 (60) KCl supplement

Matlou et al., 1986a

32 women

6-wk crossover

Placebo

2.5 (65) KCl supplement

Grobbee et al., 1987a

34 men

6 women

6-wk crossover

Placebo

2.8 (72) KCl supplement

Svetkey et al., 1987a

75 men

26 women

8-wk parallel

Placebo

4.7 (120) KCl supplement

Patki et al., 1990a

8 men

29 women

8-wk crossover

Placebo

2.3 (60) KCl supplement

Suggested Citation:"5 Potassium." Institute of Medicine. 2005. Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate. Washington, DC: The National Academies Press. doi: 10.17226/10925.
×

Urinary Electrolytes,c g/d (mmol/d)

Mean Blood Pressure (mm Hg) Placebo or Control Diet

Mean Net Change in Blood Pressured (mm Hg)

Comments

Potassium (K) g (mmol)

Sodium (Na) g (mmol)

SBP

DBP

2.7 (70)

4.4 (192)

150.5/85.9

 

7.0 (179)

5.1 (221)

 

−4.3

−1.7

1.1 (27)

1.9 (83)

141/96

Isocaloric diets

2.8 (72)

2.5 (110)

 

+7

+6

 

2.3 (58)

4.2 (182)

147/92

−1.0

−3.0

Lying BP

5.4 (139)

4.5 (195)

 

 

2.4 (62)

3.2 (140)

155/99

4.6 (118)

3.9 (169)

 

−7.0

−4.0

2.4 (61)

4.6 (200)

149.9/92.4

7.4 (190)

4.7 (205)

 

−1.9

−1.0

2.6 (67)

1.7 (73)

162/103

4.6 (117)

1.8 (80)

 

−2.0

0

2.2 (55)

3.4 (147)

145/92

4.8 (123)

3.8 (166)

 

−7.0

−3.0

2.3 (60)

2.8 (123)

186/100

3.9 (99)

3.1 (136)

 

−10.0

−6.0

1.4 (36)

3.9 (168)

133.2/97.7

Subjects treated with antihypertensive medication

3.2 (82)

3.9 (169)

 

−5.6

−5.8

2.0 (52)

2.9 (130)

151/103

 

4.5 (114)

3.8 (165)

 

−7.0

−3.0

2.9 (74)

1.3 (57)

135.7/72.5

5.1 (131)

1.6 (69)

 

−2.5

−0.6

Not given

Not given

142/92.4

 

−0.9

−1.3

2.3 (60)

4.6 (198)

155.7/97.6

3.2 (82)

4.2 (184)

 

−12.1

−13.1

Suggested Citation:"5 Potassium." Institute of Medicine. 2005. Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate. Washington, DC: The National Academies Press. doi: 10.17226/10925.
×

Reference

Subjects

Study Design

Potassium Intake,b g/d (mmol/d)

Overlack et al., 1991a

8 men

4 women

8-wk crossover

Placebo

4.7 (120) K citrate and bicarbonate

Cushman and Langford, 1988a

58 men

10-wk parallel

Placebo

3.1 (80) KCl supplement

Bulpitt et al., 1985a

15 men

18 women

12-wk parallel

Placebo

2.5 (64) KCl supplement

Chalmers et al., 1986a

91 men

16 women

12-wk parallel

Normal diet

High K 3.9 (100)

 

90 men

15 women

12-wk parallel

Low Na 1.2–1.7 (50–75)

High K 3.9 (100)

Grimm et al., 1988a

298 men

12-wk parallel

Placebo

3.8 (96) KCl supplement

Gu et al., 2001

60 men

90 women

12-wk parallel

Placebo

2.3 (60) KCL supplement

Siani et al., 1987a

23 men

14 women

15-wk parallel

Placebo

1.9 (48) KCl supplement

Obel, 1989a

21 men

27 women

16-wk parallel

Placebo

2.5 (64) potassium supplement

Peart et al., 1987a

269 men

215 women

24-wk parallel

Placebo

0.7–1.3 (17–34) KCl supplement

a Included in meta-analysis by Whelton et al. (1997).

b Potassium intake from diet unless otherwise indicated.

c Surrogate marker for electrolyte intake.

d If potassium supplement, then change in blood pressure compared to placebo. SBP = systolic blood pressure, DBP = diastolic blood pressure.

Suggested Citation:"5 Potassium." Institute of Medicine. 2005. Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate. Washington, DC: The National Academies Press. doi: 10.17226/10925.
×

Urinary Electrolytes,c g/d (mmol/d)

Mean Blood Pressure (mm Hg) Placebo or Control Diet

Mean Net Change in Blood Pressured (mm Hg)

Comments

Potassium (K) g (mmol)

Sodium (Na) g (mmol)

SBP

DBP

2.4 (62)

3.9 (169)

150/100

+2.8

+3.0

 

6.5 (167)

3.6 (156)

 

1.9 (45)

Not given

Not given/91.2

Not given

−0.1

4.4 (113)

Not given

 

2.2 (55)

3.2 (139)

182/129

Subjects treated with antihypertensive medication

3.7 (95)

3.4 (149)

 

+2.3

+4.8

2.9 (75)

3.6 (156)

146.2/93.4

 

3.8 (96)

3.3 (145)

 

−3.9

−3.1

2.9 (75)

1.9 (86)

143.1/89.2

3.4 (87)

1.7 (72)

 

+1.0

+1.6

2.9 (76)

2.6 (114)

121.8/79.5

−0.2

−0.6

Subjects treated with antihypertensive medication

5.9 (150)

2.7 (116)

 

1.3 (34)

3.8 (164)

134/83

 

2.1 (54)

4.3 (185)

 

−3.7

−0.16

2.2 (57)

4.2 (183)

145.8/92.5

3.4 (87)

4.3 (189)

 

−14.0

−10.5

2.4 (62)

 

172/100

4.0 (102)

Not given

 

−39.0

−17.0

 

133.5/84.9

Subjects treated with antihypertensive medication

Not given

Not given

 

−0.8

−0.7

Suggested Citation:"5 Potassium." Institute of Medicine. 2005. Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate. Washington, DC: The National Academies Press. doi: 10.17226/10925.
×

cretion in each trial during follow-up and the corresponding net reduction in systolic (p = 0.004) and diastolic (p = 0.003) blood pressure. At higher levels of baseline 24-hour urinary sodium and of change in 24-hour urinary sodium, change in 24-hour urinary potassium showed a dose-response relationship with effect size for both systolic and diastolic blood pressure (p < 0.01). A similar graded response between change in 24-hour urinary potassium and effect size was observed at higher levels of 24-hour urinary sodium as follow-up for systolic (p < 0.01) but not for diastolic (p = 0.2) blood pressure (Whelton et al., 1997). This finding in the meta-analysis was evident in two 2 × 2 factorial trials (Chalmers et al., 1986; Skrabel et al., 1981). In both trials, supplemented potassium lowered blood pressure when sodium intake was high, but not when sodium intake was low.

The role of urinary sodium excretion as an effect modifier for the relationship between potassium consumption and blood pressure is consistent with results from observational investigations where blood pressure is more closely related to the ratio of urinary sodium:potassium excretion than to either urinary sodium or potassium excretion alone (Khaw and Barrett-Connor, 1988, 1990).

Treatment-related systolic blood pressure effect size estimates were significantly (p = 0.03) greater for the six trials with greater than 80 percent African-American participants compared with the 25 trials with greater than 80 percent white participants (Whelton et al., 1997). Also, there was some evidence for a dose-response relationship between potassium dose and blood pressure and some evidence for greater blood pressure reduction in African-American compared with white participants. In the two trials included that enrolled exclusively African-American individuals, potassium significantly lowered both systolic and diastolic blood pressure (Brancati et al., 1996; Obel, 1989). The blood pressure reductions in the study by Obel (1989) were particularly striking.

Overall, available evidence from observational studies, clinical trials, and meta-analyses of trials documents that higher intakes of potassium lower blood pressure. Blood pressure reductions from supplemental potassium occurred when baseline intake was low (e.g., 32 to 35 mmol/day in Brancati et al., 1996) and when baseline intake was much higher (> 80 mmol/day in Naismith and Braschi, 2003). Because virtually all trials used potassium chloride supplements, while observational studies assessed dietary potassium intake from foods (paired with nonchloride anions), the effects of potassium on blood pressure appear to result from potassium rather than its conjugate anion.

Suggested Citation:"5 Potassium." Institute of Medicine. 2005. Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate. Washington, DC: The National Academies Press. doi: 10.17226/10925.
×

Prevention of Cardiovascular Disease

In addition to its blood pressure-reducing effects, increased potassium intake may have independent vascular protective properties. This possibility has been evaluated in experimental studies conducted in rodents over the last four decades. In a series of animal models, including both stroke-prone spontaneously hypertensive (SHRSP) and Dahl salt-sensitive rats, the addition of either potassium chloride or potassium citrate markedly reduced the mortality from stroke, a reduction that was unrelated to any measured attenuation of hypertension (Tobian, 1986; Tobian et al., 1984). In a more recent study with SHRSP rats in which aortic blood pressure was measured by continuous radiotelemetry, dietary potassium supplemented as either potassium bicarbonate or potassium citrate attenuated hypertension and prevented stroke (Tanaka et al., 1997). However, supplemental potassium chloride exacerbated hypertension, increased risk of stroke (Tanaka et al., 1997), and amplified renal microangiopathy (Tanaka et al., 2001), in comparison with potassium bicarbonate or citrate.

Hence, at least in this animal model, the anion accompanying potassium had a major qualitative effect on outcomes such that potassium citrate or bicarbonate was beneficial, while potassium chloride appeared to be harmful. Still, the discordant results between this study and the cited study of Tobian and coworkers (1984) are difficult to reconcile and therefore preclude firm conclusions.

An inverse relationship between dietary potassium intake at baseline and subsequent stroke-associated morbidity and mortality has also been noted in several, but not all, cross-sectional and cohort studies (Table 5-6). In a 12-year follow-up of 859 men and women enrolled in the Rancho Bernardo Study and who were 50 to 79 years of age at baseline, a significant (p = 0.01) inverse relationship between potassium intake and subsequent risk of stroke-related mortality was noted (Khaw and Barrett-Connor, 1987). Each standard deviation increase in potassium intake (0.4 g [10 mmol]/day) at baseline was associated with a 40 percent reduction in risk of stroke-related mortality relative risk (RR) = 0.6; 95 percent confidence interval (CI) = 0.44 to 0.81 after adjustment for age, gender, systolic blood pressure, caloric intake, and other potential confounders. Limitations of the study included the restricted characteristics of the cohort and the fact that the findings were based on only 24 stroke deaths. No significant relationship with coronary heart disease was detected.

Over a 16-year follow-up in the Honolulu Heart Study (n = 7,591

Suggested Citation:"5 Potassium." Institute of Medicine. 2005. Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate. Washington, DC: The National Academies Press. doi: 10.17226/10925.
×

TABLE 5-6 Epidemiological Studies on Potassium Intake: Stroke and Heart Disease

Reference

Study Design

Stroke

Khaw and Barrett-Connor, 1987

Rancho Bernardo Study, 12-yr follow-up

n = 859 men and women, not energy adjusted

Lee et al., 1988

Honolulu Heart Study, 16-yr follow-up

n = 7,591 Japanese men

Sasaki et al., 1995

Pearson correlation and multiple regression analysis

n = 17 countries

Ascherio et al., 1998

Health Professionals Follow-up Study

n = 43,738 men, multivariate analysis

Iso et al., 1999

Nurses’ Health Study, prospective cohort

n = 85,764 women, multivariate analysis

Suggested Citation:"5 Potassium." Institute of Medicine. 2005. Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate. Washington, DC: The National Academies Press. doi: 10.17226/10925.
×

Potassium Intake,a g/d (mmol/d)

Resultsb

Other Results and Comments

Men

Rate of stroke/100

Multivariate regression analysis showed that a 0.39-g increase in daily potassium intake was associated with a 40 percent reduction in the risk of stroke-associated mortality.

T1

< 2.3 (59)

3.4

 

T2

2.3–2.96 (59–76)

2.4

T3

> 2.96 (76)

0.0

 

p trend = 0.16

RR T1 vs T3 = 2.6

Women

 

T1

< 1.9 (49)

5.3

 

T2

1.9–2.57 (49–66)

2.1

T3

> 2.6 (67)

0.0

 

p trend = 0.01

RR T1 vs T3 = 4.8

 

Incidence rate of fatal thromboembolic stroke

No significant correlation for nonfatal thromboembolic and fatal and nonfatal hemorrhagic

Q1

< 1.47 (38)

6.9

 

Q2

1.47–1.86 (38–48)

5.3

Q3

1.86–2.27 (48–58)

4.1

Q4

2.27–2.77 (58–71)

2.4

Q5

> 2.77 (71)

2.0

 

p = 0.002 strokes.

Potassium intake not reported

Urinary potassium correlated inversely with incidence of stroke mortality (p < 0.05)

 

 

RR of stroke

Risk for ischemic stroke alone was similar to risk for total strokes.

Q1

2.4 (61)

1.0

 

Q2

3.0 (77)

0.85

Q3

3.3 (85)

0.78

Q4

3.6 (92)

0.76

Q5

4.3 (110)

0.62

 

p trend = 0.007

 

RR of all strokes

RR of ischemic stroke

 

Q1

2.02 (52)

1.0

1.0

 

Q2

2.41 (62)

0.75

0.68

Q3

2.71 (69)

0.90

0.85

Q4

3.03 (78)

0.80

0.73

Q5

3.55 (91)

0.83

0.71

 

p trend = 0.19

p trend = 0.07

Suggested Citation:"5 Potassium." Institute of Medicine. 2005. Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate. Washington, DC: The National Academies Press. doi: 10.17226/10925.
×

Reference

Study Design

Fang et al., 2000

NHANES I study, 17-yr follow-up

n = 9,866 men and women, not energy adjusted

Bazzano et al., 2001

NHANES I 19-yr follow-up

n = 9,805 men and women, multivariate analysis

Green et al., 2002

4–8 yr follow-up

3,595 men and women, > 65 yr

Coronary heart disease

Tunstall-Pedoe et al., 1997

Scottish Heart Health Study, prospective

n = 11,629 men and women, 7.6 yr of follow-up

a T = tertile of intake, Q = quartile or quintile of intake.

b RR = relative risk, HR = hazard ratio, CHD = coronary heart disease.

Suggested Citation:"5 Potassium." Institute of Medicine. 2005. Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate. Washington, DC: The National Academies Press. doi: 10.17226/10925.
×

Potassium Intake,a g/d (mmol/d)

Resultsb

Other Results and Comments

 

RR of stroke mortality (T1 vs. T3)

Only among African-American men was lower dietary potassium intake a predictor of stroke mortality.

White men n = 3,169

 

T1

< 2.0 (51)

T2

2.0–2.88 (51–74)

T3

> 2.88 (74)

1.66, p = 0.42

African-American men n = 595

 

T1

< 1.3 (33)

T2

1.3–2.2 (33–56)

T3

> 2.2 (56)

4.27, p = 0.0016

African-American women n = 1,029

 

 

T1

< 1.0 (26)

T2

1.0–1.64 (26–42)

T3

> 1.64 (42)

1.13, p = 0.53

Nonhypertensive n = 7,632

 

Males

1.23, p = 0.458

Females

1.11, p = 0.415

 

HR of stroke

HR of CHD

Q1

< 1.35 (35)

1.0

1.0

Q2

1.35–1.94 (35–50)

0.75

1.04

Q3

1.94–2.67 (50–68)

0.85

0.95

Q4

> 2.67 (68)

0.76

1.01

 

p trend = 0.14

p trend = 0.93

 

HR = 1.28 when comparing Q1 to Q4, p < 0.0001

 

RR for stroke

Q1

< 2.34 (59.8)

1.76

 

Q2

2.35–2.92 (60–75)

1.22

Q3

2.93–3.47 (75–89)

1.11

Q4

3.48–4.16 (89–106)

1.37

Q5

> 4.17 (107)

1.0

Potassium intake not reported

 

Potassium excretion was inversely correlated with incidence of CHD and all deaths

Suggested Citation:"5 Potassium." Institute of Medicine. 2005. Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate. Washington, DC: The National Academies Press. doi: 10.17226/10925.
×

Japanese-American participants), there was a significant inverse relationship (p = 0.002) between potassium intake and mortality from thromboembolic stroke (Lee et al., 1988). No significant association was noted for nonfatal thromboembolic stroke or for fatal or nonfatal hemorrhagic strokes. Additionally, inverse relationships between potassium intake and stroke mortality were noted in several cohort studies (Sasaki et al., 1995; Xie et al., 1992; Yamori et al., 1994) but these findings were not adjusted for caloric intake and/or were based on an ecologic analysis (Xie et al., 1992). In a 7-year follow-up report of 5,754 men and 5,875 women who were participants in the Scottish Heart Health Study, an inverse relationship between potassium intake and subsequent death, both from all causes and from coronary heart disease, was found (Tunstall-Pedoe et al., 1997).

Similarly, over the course of 8 years of follow-up in 43,738 U.S. men in the Health Professionals Study, there was a significant inverse relationship between baseline potassium intake and stroke (p = 0.007 for trend across quintiles of potassium intake) after adjustment for established cardiovascular disease risk factors, including blood pressure and caloric intake (Ascherio et al., 1998). The multivariate RR of stroke for men in the highest versus lowest quintile of potassium intake was 0.62 (95 percent CI = 0.43−0.88). The association was similar for both ischemic (n = 210) and all (n = 328) strokes. Use of potassium supplements was also inversely associated with the risk of stroke.

In a 14-year study of 85,764 U.S. women who participated in the Nurses Health Study, there was an inverse relationship between potassium intake and ischemic stroke (RR = 0.72; 95 percent CI = 0.51 to 1.01 for comparison of upper and lower quintiles of potassium intake; 347 strokes occurred during this time period), but much of the association was lost following adjustment for calcium intake (Iso et al., 1999). Two analyses of NHANES I follow-up study have been reported. In a 17-year analysis of subsequent stroke mortality in approximately 10,000 men and women (during which there were 304 strokes), there was a significant inverse relationship between potassium intake and stroke mortality in hypertensive and African-American men, but not in other subgroups (Fang et al., 2000). In a 19-year follow-up of the same cohort, the relationships of potassium intake with fatal and nonfatal strokes (total n = 927) and coronary heart disease (n = 1847) events were assessed (Bazzano et al., 2001). Overall, stroke hazard was significantly different among quartiles of potassium intake (p = 0.03), but the relationship was nonlinear. Participants in the lowest quartile of potassium intake at baseline

Suggested Citation:"5 Potassium." Institute of Medicine. 2005. Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate. Washington, DC: The National Academies Press. doi: 10.17226/10925.
×

(< 1.4 g [34.6 mmol]/day) experienced a 28 percent higher risk of stroke (95 percent CI = 1.11 to 1.47; e.g., p < 0.0001) compared with the remainder of the cohort after adjustment for established cardiovascular disease risk factors.

Prevention of Bone Demineralization

Epidemiological Studies

Observational studies suggest that increased fruit and potassium consumption is associated with increased bone mineral density (BMD) (see Table 5-7). Pyridinoline excretion, a marker of bone resorption, was negatively associated with energy-adjusted potassium intakes (New et al., 2000). Longitudinal studies have documented that potassium intake was positively associated with BMD at various sites (Macdonald et al., 2004; Tucker et al., 1999).

Given that net endogenous acid production (NEAP) can be closely estimated by the dietary protein-to-potassium ratio (Frassetto et al., 1998), these observations are those predicted if sustained high rates of diet-induced endogenous acid act over time to demineralize bone. The association of NEAP with several indices of skeletal status in 1,056 pre- and perimenopausal women was recently reported (New et al., 2004). Lower estimates of energy-adjusted NEAP were correlated with higher BMD at the spine and hip, as assessed by dual X-ray absorptiometry. Hip and forearm bone mass decreased significantly across increasing quartiles of NEAP. These differences remained significant when adjusted for age, weight, height, and menstrual status. Lower estimates of NEAP were correlated with lower urinary excretion of deoxypyridinoline, a marker of bone resorption, and were significant predictors of spine and forearm bone mass (New et al., 2004).

Intervention Studies

Two studies have been reported in which supplemental potassium was provided and subsequent measures of calcium and phosphorus balance were evaluated. In a study of 18 healthy postmenopausal women (Sebastian et al., 1994), supplemental potassium bicarbonate provided for 18 days induced a slight but sustained and near immediate increase in the plasma bicarbonate concentration and blood pH and virtually abolished net renal acid excretion. Calcium and phosphorus balance improved (as measured by the difference between dietary intake and fecal/urine excretion). There was also

Suggested Citation:"5 Potassium." Institute of Medicine. 2005. Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate. Washington, DC: The National Academies Press. doi: 10.17226/10925.
×

TABLE 5-7 Epidemiological Studies on the Effect of Potassium Intake on Bone Mineral Density (BMD)

Reference

Study Design

Effect

Findings

New et al., 1997

Cross-sectional

944 women

+

Potassium intake was significantly (p < 0.05) correlated with BMD for lumbar spine, femoral neck, trochanter, and Ward’s area in premenopausal women

Tucker et al., 1999

Cross-sectional and longitudinal

907 men and women

+

Potassium intake was significantly (p < 0.05) associated with BMD for the femoral neck, trochanter, Ward’s area, and radius in men (cross-sectional)

In women potassium intake was significantly (p < 0.05) associated with bone mineral density for the trochanter, Ward’s area, and radius (cross-sectional)

In a 4-yr analysis of change in BMD, potassium intake was significantly (p < 0.05) associated with less decline in BMD for femoral neck and trochanter in men

New et al., 2000

Cross-sectional

62 women

+

Potassium intake was significantly (p < 0.01) associated with higher total bone mass (p < 0.05 to p < 0.005)

Potassium intake was significantly (p < 0.02) and negatively associated with pyridinoline excretion and deoxypyridinoline excretion

Jones et al., 2001

Cross-sectional

330 children

+

Significant (p < 0.001) association between urinary potassium, femoral neck, lumbar spine, and total body BMD in prepubertal children

Macdonald et al., 2004

Longitudinal

891 women

+

Significant (p < 0.05) and positive correlation between potassium intake and femoral neck BMD in premenopausal and perimenopausal women

Suggested Citation:"5 Potassium." Institute of Medicine. 2005. Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate. Washington, DC: The National Academies Press. doi: 10.17226/10925.
×

Reference

Study Design

Effect

Findings

New et al., 2004

Cross-sectional

1,056 women

+

Diets with lower estimates of net endogenous acid production (NEAP) (higher dietary intake of potassium and lower dietary protein) were significantly (p < 0.02−0.05) correlated with BMD in the hip and spine and greater forearm mass

A significant (p < 0.05) correlation was found between lower estimates of NEAP and lower excretion of deoxypyridinoline

NOTE: + means potassium had a significant impact on BMD.

a reduction in the urinary excretion of hydroxyproline, a marker of bone breakdown, and an increase in the serum concentration of osteocalcin, a marker of bone formation. When supplemental potassium bicarbonate was discontinued, the levels of plasma bicarbonate and arterial pH, like those of all other measured variables that had changed with the supplement, returned almost immediately to levels nearly identical to those occurring before the potassium bicarbonate was supplemented. This pattern of results suggests that a state of low-grade metabolic acidosis existed immediately before and after potassium bicarbonate was supplemented; that the acidosis resulted from the endogenous generation of noncarbonic acid at a rate greater than that at which the kidney could excrete it; that the acidosis induced increased bone resorption and reduced bone formation; that the acidosis induced increased renal loss of calcium and phosphate and thereby negative balances of both; and that supplemental potassium bicarbonate reversed each of these metabolic derangements by fully correcting the low-grade metabolic acidosis by titrating endogenously produced noncarbonic acid. Similar results were seen and conclusions drawn in metabolic studies of nonhypertensive young men and women in whom dietary potassium chloride was replaced with potassium bicarbonate, where-upon the urinary excretion of deoxypyridinoline, pyridinoline, and n-telopeptide (markers of bone resorption) promptly decreased (Maurer et al., 2003).

In a pre- and poststudy in which 21 adult patients with calcium urolithiasis were treated with potassium citrate for 11 to 120 months,

Suggested Citation:"5 Potassium." Institute of Medicine. 2005. Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate. Washington, DC: The National Academies Press. doi: 10.17226/10925.
×

spinal BMD substantially increased over a period of time (which varied from approximately 1 to 10 years) in which an age-related decrease might otherwise have occurred (Pak et al., 2002). In normal adults, potassium bicarbonate has been demonstrated to be hypocalciuric, whereas potassium chloride has not (Lemann et al., 1991). This reflects not only the direct acidosis-countering effect of the bicarbonate component of potassium bicarbonate, but also the capacity of potassium (Brunette et al., 1992) and bicarbonate (Peraino and Suki, 1980) to jointly enhance the renal reclamation of calcium.

Relationship with Sodium

The dietary intake of sodium chloride is an important determinant of urinary calcium excretion and calcium balance. The urinary excretion of calcium is well documented to vary directly with that of sodium (see Table 6-19 in Chapter 6). There is evidence that reducing dietary sodium chloride can induce beneficial effects on bone by reducing the renal loss of calcium and increasing its retention (Devine et al., 1995; Matkovic et al., 1995). However, on a mole-for-mole basis, the hypocalciuric effect of orally administered potassium overrides the hypercalciuric effect of dietary sodium (Morris et al., 1999b; Sellmeyer et al., 2002). In a metabolically controlled outpatient study of normal men fed a diet deficient in potassium (1.2 g [30 mmol]/day), increasing dietary sodium chloride from 1.8 g (30 mmol)/day to 14.6 g (250 mmol)/day induced a 50 percent increase in urinary calcium that supplemental potassium bicarbonate either reversed or abolished, depending on whether dietary potassium was increased to 2.7 or 4.7 g (70 or 120 mmol)/day (Morris et al., 1999b). In an outpatient study of postmenopausal women, the hypercalciuric effects of sodium loading with 5.2 g (225 mmol)/day sodium and a concomitant increase in bone resorption, as indicated by biochemical markers, was abolished by supplying 3.5 g (90 mmol)/day of dietary potassium as potassium citrate, a supplement that increased urinary potassium to 141 mmol (5.5 g)/day (Sellmeyer et al., 2002).

Prevention of Kidney Stones

Epidemiological Evidence

In several studies, an increased dietary intake of potassium has been associated with a reduced risk of kidney stones. The occur-

Suggested Citation:"5 Potassium." Institute of Medicine. 2005. Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate. Washington, DC: The National Academies Press. doi: 10.17226/10925.
×

rence of kidney stones in both sexes is directly related to the urinary sodium:potassium ratio (Cirillo et al., 1994). In a pre-post, uncontrolled study of children with idiopathic hypercalciuria, reducing the dietary sodium:potassium ratio greatly reduced urinary calcium excretion (Alon and Berenbom, 2000). Hypercalciuria is generally accepted as a major risk factor for calcium-containing kidney stones (Coe et al., 1992). The incidence of kidney stones has been shown to increase with an increased sodium:potassium ratio (Stamler and Cirillo, 1997).

In a longitudinal study of 51,529 men conducted prospectively over 4 years, the incidence of symptomatic kidney stones, while not correlating with dietary sodium, did correlate strongly and negatively with dietary potassium as measured by a food-frequency questionnaire over a broad range of intake (2.9 to 4.0 g [74 to 102 mmol]/day) (Curhan et al., 1993) (see Table 5-8). The absence of a relationship between dietary sodium and kidney stones should be

TABLE 5-8 Epidemiological Studies on Potassium Intake and Risk of Kidney Stone Formation

Reference

Study Design

Potassium Intake,a g/d (mmol/d)

Relative Risk for Kidney Stones

Curhan et al., 1993

Health Professionals Study, 45,619 men, 4-yr follow-up

Q1

< 2.9 (74)

1.0

Q2

3.1 (79)

0.88

 

Q3

3.4 (87)

0.74

Q4

3.8 (97)

0.69

Q5

> 4.0 (102)

0.49

 

p trend < 0.001

Curhan et al., 1997

Nurses’ Health Study, 91,731 women, 12-yr follow-up

Q1

2.0 (52)

1.0

Q2

2.7 (69)

0.86

 

Q3

3.2 (81)

0.75

Q4

3.7 (95)

0.67

Q5

4.7 (119)

0.65

 

p trend < 0.001

Hirvonen et al., 1999

Prospective cohort, n = 27,001 Finnish male smokers

Q1

3.8 (97)

1.0

Q2

4.6 (118)

0.76

Q3

5.1 (131)

0.85

 

Q4

5.7 (146)

0.79

 

p trend = 0.34

a Q = quartile or quintile of intake.

Suggested Citation:"5 Potassium." Institute of Medicine. 2005. Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate. Washington, DC: The National Academies Press. doi: 10.17226/10925.
×

interpreted cautiously because the food-frequency questionnaire used in these studies did not measure sodium intake either accurately or precisely (Subar et al., 2001). In this study (Curhan et al., 1993), the incidence of kidney stones correlated directly with meat intake. In a 12-year prospective study of an even larger number of female nurses, the incidence of stone formation was inversely associated with dietary potassium (2.0 to 4.7 g [52 to 119 mmol]/day) (Curhan et al., 1997). In a study conducted in Finland where the dietary potassium intake is greater than in the United States, risk for kidney stones appeared to decrease with an increased intake of potassium (3.8 compared with 4.6 g [97 to 118 mmol]/day) (Hirvonen et al., 1999). However, higher intakes of potassium did not appear to further reduce risk, and the relationship between potassium intake and kidney stones, overall, was nonsignificant.

Role of Acid-Base Balance, Urinary Citrate, and Relationship with Sodium

An increased intake of meat has long been recognized as a risk factor for kidney stones, presumably because of the resultant acid load and the well-documented impact of that load on urinary calcium excretion (Lemann, 1999; Lemann et al., 2003). By increasing the acid load and slightly reducing the plasma bicarbonate concentration, an increased intake of animal protein also induces a decrease in the urinary excretion of citrate (Breslau et al., 1988), a major risk factor for the formation of kidney stones (Coe et al., 1992; Pak, 1987). Urinary citrate chelates urinary calcium in a soluble form (Bisaz et al., 1978; Meyer and Smith, 1975; Pak, 1987). Both hypocitraturia and hypercalciuria occur with even modest potassium deficiencies (Hamm, 1990; Simpson, 1983). Administration of either potassium bicarbonate or potassium citrate induces an increase in the urinary excretion of citrate (Pak, 1987; Sakhaee et al., 1991; Simpson, 1983), as well as a reduction in the urinary excretion of calcium (Lemann et al., 1989, 1991). Neither the citraturic effect of potassium citrate nor its hypocalciuric effect is greater than that of potassium bicarbonate, presumably because these salts induce similarly small increases in the plasma concentration of bicarbonate (Sakhaee et al., 1991).

One clinical trial tested the effects of potassium citrate in preventing recurrent kidney stones (Barcelo et al., 1993). In a double-blind, placebo-controlled trial of 57 patients (25 men and 32 women) with kidney stones and hypocitraturia conducted over 3 years, 1.2 to 2.3 g (30 to 60 mmol) of potassium citrate were administered in addition

Suggested Citation:"5 Potassium." Institute of Medicine. 2005. Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate. Washington, DC: The National Academies Press. doi: 10.17226/10925.
×

to the usual diet. This regimen induced a highly significant reduction in the occurrence of kidney stones. The stone formation rate was significantly lower in the potassium citrate group than in the control group (0.1 stone/patient-year versus 1.1 stones/patient-year, p < 0.001). Total urinary excretion of potassium in the 18 subjects in the potassium citrate group averaged 105 mmol (4.1 g)/day after 36 months, compared with their baseline average of 61 mmol (2.4 g)/day (Barcelo et al., 1993). While not directly measured, it is thus assumed that 2.4 g (61 mmol) would have been present in the diets consumed, for a total intake with the supplement of around 3.6 to 4.7 g (90 to 120 mmol). Similar results have been recorded in uncontrolled studies of potassium citrate (Pak and Fuller, 1986; Pak et al., 1985, 1986; Preminger et al., 1985).

Overall, evidence from several prospective observational studies and one clinical trial supports the use of kidney stones as an outcome criterion to establish dietary adequacy of potassium. However, additional trials are clearly warranted.

Prevention of Impaired Pulmonary Function

Changes in the extracellular and intracellular concentration of electrolytes, including potassium, can influence the contraction and relaxation of bronchial smooth muscles (Souhrada and Souhrada, 1983, 1984). The limited studies on potassium intakes and pulmonary function in adults have yielded mixed results, with one study showing increased airway responsiveness to chemicals that induce constriction of the airways (e.g., histamine) with decreasing urinary potassium excretion (Tribe et al., 1994), while no relationship was found between potassium intake and bronchial responsiveness or respiratory symptoms in adults in a second study (Zoia et al., 1995).

As in adults, data on children are limited. Increased bronchial responsiveness with higher levels of potassium excretion was observed in the children studied (Pistelli et al., 1993), while in another study, low potassium intakes were associated in children with lower pulmonary function (e.g., expiratory volume, flow, and capacity) (Gilliland et al., 2002).

FACTORS AFFECTING POTASSIUM REQUIREMENTS

Climate and Physical Activity

Increased losses of potassium, primarily via sweat, can occur with heat exposure and exercise. Thus the requirement for potassium

Suggested Citation:"5 Potassium." Institute of Medicine. 2005. Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate. Washington, DC: The National Academies Press. doi: 10.17226/10925.
×

will increase in both situations. The potassium concentration in sweat is approximately 4 to 5 mmol (0.2 g)/L. This concentration can increase up to 14 mmol (0.5 g)/L upon thermal exposure (Fukumoto et al., 1988). The sweat potassium concentration in heat-acclimatized individuals exposed to heat stress (40°C [104°F]) was approximately 5.4 mmol (0.2 g)/L, and total sweat loss was approximately 11 L/day, yielding a total potassium sweat loss of approximately 60 mmol (2.3 g)/day while consuming a diet providing 3.8 g (97 mmol)/day (Malhotra et al., 1976). When total estimated losses (sweat + urine) were summed (estimating sweat volume of 8 L/ day), the maximum loss was equivalent to 116 mmol (4.5 g)/day, which exceeded the potassium intake. Average sweat potassium daily losses of three men who were exposed to 37.8°C (100°F) heat for 7.5 hours per day for 16 days fell from 79 mmol (3.1 g) measured on day 2 to 14 mmol (0.55 g) by day 11. Hence, there was a decline in sweat loss over time, demonstrating that acclimation occurred and suggesting that potassium balance might be achieved over a short period of time.

The effects of 90 minutes of heat exposure (46°C [117°F]) without exercise during low (0.78 to 1.2 g [20 to 30 mmol]/day) and high (7.8 g [200 mmol]/day) sodium intakes on a number of parameters, including plasma potassium concentrations, were studied in eight healthy volunteers (20 to 28 years of age) (Follenius et al., 1979). There were significant changes in plasma potassium concentrations whether the subjects were on a low or high sodium diet. Plasma potassium concentrations ranged from about 3.97 to 4.15 mmol/L.

Seven healthy men, 18 to 23 years of age, were exposed to 40°C (104°F) heat in a controlled heat chamber and to exercise (Fukumoto et al., 1988). Sweat potassium concentration was 11.3 ± 3.1 mmol/L during the running exercise compared with 14.2 ± 4.6 mmol/L during thermal exposure (40°C). Conversely, sweat sodium losses were greater during the running exercise (123.1 ± 33.6 mmol/ L) compared with the heat exposure (84.3 ± 31.5 mmol/L).

Approximately 1.2 g (32 mmol)/day of potassium losses from sweat were observed during 6 hours of intermittent treadmill activity in a 40°C environment in 12 unacclimatized men (Armstrong et al., 1985). No significant changes in serum potassium concentrations in 10 experienced male marathon runners were seen after they completed three 20-mile runs under three different fluid replacement treatments (water, electrolyte-glucose solution, or a caffeine solution [5 mg of caffeine/kg of body weight]) (Wells et al., 1985). Pre-exercise serum potassium concentrations were about 4.4

Suggested Citation:"5 Potassium." Institute of Medicine. 2005. Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate. Washington, DC: The National Academies Press. doi: 10.17226/10925.
×

mmol/L for all three trials, and averaged about 4.9 mmol/L for all three trials postexercise (Wells et al., 1985). Hence, under these three conditions, a potassium deficit was not evident.

The effects of two diets and exercise on potassium losses were evaluated in eight men during two 4-day exercise-dietary regimens (Costill et al., 1982). The control diet contained 3.1 g (80 mmol)/day of potassium, while the experimental diet contained only 0.98 g (25 mmol)/day of potassium. Urinary potassium excretion was significantly lower with the low potassium diet (2.6 versus 1.2 g [67 versus 31 mmol]/day) on day 5 of the study for each dietary period. Sweat potassium also significantly decreased from 12.3 to 10.9 mmol/day (measured on day 1 of the study for each dietary period). When fed 3.1 g (80 mmol)/day, the individuals were in balance, whereas a negative potassium balance was observed (−0.5 g [−14 mmol]/day) when fed the low potassium diet. Still, the authors did not detect diminished total body potassium content with a combination of heavy exercise and the lower potassium diet. However, this dietary and exercise regimen was brief; the long-term effects are uncertain.

Diuretics

Diuretics, which are often prescribed for the treatment of hypertension and congestive heart failure, result in increased urinary excretion of potassium and can lead to hypokalemia. However, the response is highly dose-dependent. Continual loss of potassium, if sustained, can result in clinical signs and symptoms of potassium deficiency, including arrhythmias (Robertson, 1984). For this reason, potassium supplements are often prescribed. In a recently completed trial (Furberg et al., 2002), approximately 8 percent of individuals assigned to the thiazide diuretic, chlorthalidone (12.5 to 25 mg/day), required a potassium supplement as treatment for diuretic-induced hypokalemia. Alternatively, potassium-sparing diuretics (e.g., amiloride, triamterene, and spirolactones) are frequently used concurrently with thiazide-type diuretics, which increase urinary potassium excretion. Triamterene has been shown to prevent diuretic-induced potassium loss comparable to 3.1 to 4.7 g (80 to 120 mmol)/day of supplemental potassium. While diuretics can cause hypokalemia, the amount of additional potassium required to prevent hypokalemia is uncertain and highly variable. Accordingly, in individuals taking diuretics, serum potassium should be regularly checked by their health care provider.

Suggested Citation:"5 Potassium." Institute of Medicine. 2005. Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate. Washington, DC: The National Academies Press. doi: 10.17226/10925.
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Forms of Potassium

The anions that accompany potassium have metabolic and physiologic properties that influence health. Plant foods rich in potassium, like fruits and nongrain vegetables, are also rich in bicarbonate-yielding precursors like citrate. In contrast, plants contain little chloride. In fact, chloride, like sodium, is ingested almost entirely as sodium chloride, primarily in processed foods and in discretionary use during cooking for seasoning. In the present Western diet, which dates from the Industrial Revolution some 200 years ago, the content of sodium and chloride is not only much higher than that of previous diets, but the contents of both potassium and bicarbonate-yielding substances are also much lower (Eaton et al., 1999; Morris RC et al., 2001; Sebastian et al., 2002). Thus most dietary deficiencies of potassium are accompanied by a relative lack of bicarbonate precursors. With the advent of the Western diet, both the potassium:sodium ratio and the bicarbonate:chloride ratio have become reversed.

Potassium is also consumed as potassium chloride as a food additive ingredient, a salt substitute, or as pills used therapeutically to treat diuretic-induced hypokalemia. While potassium chloride can correct hypokalemia and reduce blood pressure (see Tables 5-4 and 5-5), it cannot correct the low-grade metabolic acidosis induced by modern diets because chloride, in contrast to bicarbonate precursors, does not titrate diet-derived acids.

In healthy adults, potassium bicarbonate increased excretion of citrate and decreased calcium, whereas potassium chloride did not (Lemann et al., 1991; Sakhaee et al., 1991), suggesting that potassium bicarbonate or citrate is the form most conducive to a reduced risk of kidney stones. Because diet-derived acid can result in bone demineralization (Bushinsky and Frick, 2000; Lemann et al., 1966; New et al., 2000) as illustrated in Figure 5-2, the nonalkaline potassium chloride would not be expected to promote bone health as would be predicted with potassium bicarbonate (Lemann et al., 1991, 1993).

Interactions with Other Electrolytes

The effects of potassium intake depend, in part, on the level of sodium chloride intake (and vice versa). Previous sections have documented that potassium blunts the effect of sodium chloride on blood pressure—that an increased intake of potassium bicarbonate or other bicarbonate-yielding potassium salts mitigates salt sensitiv-

Suggested Citation:"5 Potassium." Institute of Medicine. 2005. Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate. Washington, DC: The National Academies Press. doi: 10.17226/10925.
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FIGURE 5-2 Hypothesized relationships between certain dietary inorganic electrolytes and bicarbonate, the kidney, essential hypertension, kidney stones, and osteoporosis: the modern diet’s excessive dietary sodium and chloride and deficient dietary potassium and bicarbonate precursors as determinants of both low-grade metabolic acidosis and hypercalciuria and thereby osteoporosis and kidney stones. As formulated, the acidosis can be amplified by impaired renal acidification that occurs as part of the “incomplete syndrome of renal tubular acidosis” (IRTA), an age-related decline in renal function (“age”), or both. The underlined dietary determinants and pathogenic events are those originally hypothesized and depicted. In this scheme, the word “osteoporosis” replaces the term “bone mineralization” specified in the depiction of the original formulation (Modified from MacGregor and Cappuccio [1993] by Morris RC et al. [2001]). Reprinted with permission from Morris RC et al. (2001). Copyright 2001 by Elsevier.

Suggested Citation:"5 Potassium." Institute of Medicine. 2005. Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate. Washington, DC: The National Academies Press. doi: 10.17226/10925.
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ity and lowers urinary calcium excretion. At higher levels of sodium chloride intake, potassium reduces blood pressure to a greater extent than at lower levels of sodium chloride intake (Whelton et al., 1997). While the relationship of kidney stones with urinary potassium excretion was weak and nonsignificant, the relationship of kidney stones to the urinary sodium: potassium ratio was direct and highly significant (Cirillo et al., 1994). Finally, the hypocalciuric effect of supplemental dietary potassium bicarbonate is also dampened by dietary sodium chloride (Sellmeyer et al., 2002).

Given the interrelatedness of sodium and potassium, the requirement for potassium may well depend on the level of dietary sodium, and the deleterious effects of sodium may be attenuated by higher dietary intakes of potassium. However, data are presently insufficient to set different potassium intake recommendations according to the level of sodium intake, and vice versa. Likewise, data are insufficient to set requirements based on the sodium: potassium ratio.

Race

As previously discussed, sodium chloride raises blood pressure to a greater extent in African-American men than in white men (Morris et al., 1999b; Weinberger, 1996) and the expression of salt sensitivity is modulated by dietary potassium (Morris et al., 1999b; Weinberger et al., 1982). In one trial (Morris et al., 1999b; Figure 5-1), salt sensitivity continued among some of the nonhypertensive African-American men who consumed a high-normal level of potassium (4.7 g [120 mmol]/day). In another study of African Americans, most of whom were nonhypertensive, a higher dietary intake of potassium (6.6 g [170 mmol]/day) as potassium bicarbonate abolished salt sensitivity (Schmidlin et al., 1999).

Available data also suggest that African Americans, compared with their white counterparts, are more sensitive to the blood pressure-reducing effects of increased dietary potassium. A significant reduction in systolic and diastolic blood pressure was seen when African-American individuals, most of whom were nonhypertensive, increased dietary potassium from a level of 1.3 to a level of 3.1 g (33 to 80 mmol)/day (Brancati et al., 1996). In another study that enrolled African-American hypertensive subjects, supplementation with 2.5 g (64 mmol)/day of potassium chloride significantly reduced systolic and diastolic blood pressure (Obel, 1989). However, neither of these trials enrolled white participants, so the extent of blood pressure reduction in African Americans from increased po-

Suggested Citation:"5 Potassium." Institute of Medicine. 2005. Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate. Washington, DC: The National Academies Press. doi: 10.17226/10925.
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tassium intake cannot be directly compared with that of non-African Americans. The Dietary Approaches to Stop Hypertension (DASH) trial tested the effects of a diet high in fruits and vegetables (and thus also higher levels of potassium, magnesium, and fiber) in both African Americans and non-African Americans (Appel et al., 1997; see Table 5-4). While blood pressure was reduced in both groups, only the reductions in African Americans achieved statistical significance. Such evidence must be interpreted cautiously because the diet emphasized several nutrients besides potassium. The potential for race or ethnicity to modify the effects of potassium on kidney stone formation and metabolic bone disease has not been well studied. Overall, there is insufficient evidence at this time to set different potassium recommendations based on race or ethnicity.

FINDINGS BY LIFE STAGE AND GENDER GROUP

Infants Ages 0 Through 12 Months

Evidence Considered in Setting the AI

The health effects of potassium intake in infants are uncertain. Thus recommended intakes of potassium are based on an Adequate Intake (AI) that reflects a calculated mean potassium intake of infants principally fed human milk, or a combination of human milk and complementary foods.

Ages 0 Through 6 Months. Using the method described in Chapter 2, the AI for potassium for infants ages 0 though 6 months is based on the average amount of potassium in human milk that is consumed. A mean intake of 0.39 g/day of potassium is estimated based on the average volume of milk intake of 0.78 L/day (see Chapter 2) and an average concentration of potassium in human milk of 0.5 g/L during the first 6 months of lactation (see Table 5-9). An AI of 0.4 g/day of potassium is set for infants 0 through 6 months of age, after rounding.

Ages 7 Through 12 Months. The potassium intake for older infants can be determined by estimating the intake from human milk (concentration × 0.6 L/day) and complementary foods (see Chapter 2). Potassium intake (n = 51) from complementary foods was estimated to average 0.44 g/day based on data from the Continuing Survey of Food Intakes of Individuals (CSFII) (see Appendix Table E-4). The average intake from human milk is approximately 0.3 g/

Suggested Citation:"5 Potassium." Institute of Medicine. 2005. Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate. Washington, DC: The National Academies Press. doi: 10.17226/10925.
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TABLE 5-9 Potassium Content in Human Milk

Reference

Study

Stage of Lactationa

Potassium Concentration (g/L)b

Gross et al., 1980

18 women

1 mo pp

0.59

Picciano et al., 1981

26 women

1 mo pp

2 mo pp

3 mo pp

0.46

0.42

0.41

Keenan et al., 1982

14 women

3.5–6 wk pp

8.5–18 wk pp

20–32 wk pp

0.59

0.54

0.52

Lemons et al., 1982

7 women

1 mo pp

1.5 mo pp

> 2 mo pp

0.53

0.56 preterm

0.53 preterm

Dewey and Lonnerdal, 1983

20 women

1 mo pp

2 mo pp

3 mo pp

4 mo pp

5 mo pp

6 mo pp

0.53

0.48

0.47

0.46

0.46

0.43

a pp = postpartum.

b All values except those from mothers with preterm infants were averaged together to derive average potassium content of human milk = 0.5 g/L.

day (0.5 g/L × 0.6 L/day). Thus the total potassium intake is estimated to be 0.74 g/day (0.3 g/day + 0.44 g/day). Therefore, the AI is 0.7 g (18 mmol)/day of potassium, after rounding.

Potassium AI Summary, Ages 0 Through 12 Months

AI for Infants

0–6 months

0.4 g (10 mmol)/day of potassium

7–12 months

0.7 g (18 mmol)/day of potassium

Children and Adolescents Ages 1 Through 18 Years

Evidence Considered in Setting the AI

Direct evidence on the potassium requirements of children is lacking. Blood pressure is one potential indicator; however, few studies

Suggested Citation:"5 Potassium." Institute of Medicine. 2005. Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate. Washington, DC: The National Academies Press. doi: 10.17226/10925.
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have assessed the relationship of potassium intake with blood pressure or its rise during childhood and adolescence. In one prospective observational study of 233 Dutch children aged 5 to 17 years, the rise in blood pressure over 7 years was significantly and inversely associated with dietary potassium intake and the dietary sodium:potassium ratio, as estimated from multiple overnight urine collections (Geleijnse et al., 1990). Two small trials tested the effects of potassium supplementation in children (Miller et al., 1987; Sinaiko et al., 1993). In both trials, potassium had no significant effect on blood pressure; however, statistical power may have been inadequate.

Because the conditions resulting from potassium deficiency (i.e., elevated blood pressure, bone demineralization, and kidney stones) are chronic and likely result from inadequate intake over an extended period of time, including childhood, it is appropriate to extrapolate recommended intakes of potassium in adults to children. However, the optimal approach to extrapolation is uncertain (e.g., adjustment based on weight, energy intake, or another method). Adjustment based on energy intake was deemed most appropriate because of concern that adjustment based on weight might lead to a relatively low and potentially inadequate intake of potassium. Furthermore, given the high energy intake of children relative to their weight and the potential for a high sodium intake as a result of their high energy intake, a greater intake of dietary potassium would be appropriate as a means to mitigate the adverse effects of sodium.

The AI is thus derived by extrapolating from the adult AI on the basis of the average of median energy intake levels. Based on data from CSFII, the median energy intake for 1- to 3- and 4- to 8-year-old children is 1,372 and 1,759 kcal/day, respectively (IOM, 2002). Median energy intakes for preadolescent (9 to 13 years of age) and adolescent (14 to 18) boys and girls range from 1,877 to 2,226 and 1,872 to 2,758 kcal/day, respectively.

Potassium AI Summary, Ages 1 Through 18 Years

AI for Children

1–3 years

3.0 g (77 mmol)/day of potassium

4–8 years

3.8 g (97 mmol)/day of potassium

AI for Boys

9–13 years

4.5 g (115 mmol)/day of potassium

14–18 years

4.7 g (120 mmol)/day of potassium

Suggested Citation:"5 Potassium." Institute of Medicine. 2005. Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate. Washington, DC: The National Academies Press. doi: 10.17226/10925.
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AI for Girls

9–13 years

4.5 g (115 mmol)/day of potassium

14–18 years

4.7 g (120 mmol)/day of potassium

Adults Ages 19 Through 50 Years

Evidence Considered in Setting the AI

In clinical trials, potassium chloride has been shown to reduce blood pressure (Cappuccio and MacGregor, 1991; Geleijnse et al., 2003; Whelton et al., 1997); potassium bicarbonate has been shown to reduce the rise in blood pressure in response to increased sodium chloride intake (salt sensitivity) (Morris et al., 1999b); and potassium citrate has been shown to reduce the risk of kidney stones (Barcelo et al., 1993) (see earlier section, “Indicators Considered for Estimating the Requirement for Potassium”). Observational studies suggest that diets rich in potassium may also prevent bone disease and cardiovascular disease, particularly stroke.

Dose-response trials that test the effect of at least three levels of potassium are not available. While such studies would be useful in trying to estimate an average requirement (an EAR) based on blood pressure, substantial reductions in blood pressure in nonhypertensive individuals were observed at total dietary potassium intakes ranging from around 3.1 to 4.7 g (80 to 120 mmol)/day (Table 5-4). One dose-response trial tested the effect of potassium on salt sensitivity; in this study, an intake of 4.7 g (120 mmol)/day of potassium as potassium bicarbonate abolished severe sodium sensitivity in most nonhypertensive African-American men, a degree of salt sensitivity not observed in white men also tested (Morris et al., 1999b) (see Figure 5-1). In white men enrolled in this trial, salt sensitivity was reduced at a potassium intake of 2.7 g (70 mmol)/day compared with a potassium intake of 1.2 g (30 mmol)/day. Finally, three epidemiological studies suggest that increasing potassium intakes may reduce the risk of kidney stones (Table 5-8) (Curhan et al., 1993, 1997; Hirvonen et al., 1999). At the highest quintile of potassium intake in two studies conducted in the United States (4.0 and 4.7 g [102 and 120 mmol]/day), the lowest relative risk of kidney stones was observed (RR 0.49 and 0.65) (Curhan et al., 1993, 1997). In Finland where potassium intakes are greater than in the United States or Canada (Rose et al., 1988), at the second quartile of intake (4.6 g [118 mmol]/day), there was a reduced relative risk of kidney stones (0.76) that was not further reduced at higher potassium intakes (Hirvonen et al., 1999).

Suggested Citation:"5 Potassium." Institute of Medicine. 2005. Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate. Washington, DC: The National Academies Press. doi: 10.17226/10925.
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The trial data are nonetheless insufficient for setting an EAR, which would require data at multiple intake levels so that a level could be derived that would reduce blood pressure, mitigate salt sensitivity, or decrease the risk of kidney stones in 50 percent of individuals evaluated. Still, it is possible to set an AI at 4.7 g (120 mmol)/day using available data.

While the AI is set at the same intake level for men and women, it is recognized that differences in body size, body composition, and caloric intake may affect requirements. However, presently available data are insufficient to set gender-specific requirements. Since most of the studies used to derive the AI included both men and women and did not report findings on the basis of these characteristics, it is thus appropriate at this point to set the recommended intake at the same level of intake for both.

It should be recognized that the studies used to set the AI were conducted in the setting of a high sodium intake (2.7 to 5.7 g [117 to 13 mmol]/day), which greatly exceeds the AI of 1.5 g (65 mmol)/ day of sodium. While it is plausible that the AI for potassium might be lower in the setting of a reduced sodium intake, data are insufficient to set this level.

Summary. The AI for potassium is set at 4.7 g (120 mmol)/day based on blunting the severe salt sensitivity prevalent in African-American men and decreasing the risk of kidney stones, as demonstrated in a 3-year double-blind controlled study. Blood pressure studies in nonhypertensive individuals (Table 5-3) are supportive of this level of intake as a means to lower blood pressure. Epidemiological studies also suggest that higher levels of potassium intake from foods are associated with decreased bone loss. It is important to note that the beneficial effects of potassium in these studies appears to be mainly from the forms of potassium that are associated with bicarbonate precursors—the forms found naturally in foods such as fruits and vegetables.

Potassium AI Summary, Ages 19 Through 50 Years

AI for Men

19–30 years

4.7 g (120 mmol)/day of potassium

31–50 years

4.7 g (120 mmol)/day of potassium

AI for Women

19–30 years

4.7 g (120 mmol)/day of potassium

31–50 years

4.7 g (120 mmol)/day of potassium

Suggested Citation:"5 Potassium." Institute of Medicine. 2005. Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate. Washington, DC: The National Academies Press. doi: 10.17226/10925.
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Older Adults and the Elderly Ages 50+ Years

Evidence Considered in Setting the AI

Few humans studies are available that examine the effects of aging on renal and extrarenal adaptation to high potassium loads or dietary potassium deprivation. However, in two studies age-related decreases in both total body potassium and total exchangeable potassium, found in both men and women, were more evident in women (Davis et al., 1989; Rowe et al., 1992). Decreases in total body potassium may be due in part to the decrease in muscle mass that occurs with age (Rowe et al., 1992). In turn, the decrease in muscle mass with age may be, in part, a result of an inadequate intake of dietary potassium and its accompanying base (Frassetto et al., 1997).

In potassium adaptation studies in rats, the kaliuretic response to intravenous infusion of potassium chloride and the rise in plasma potassium have been shown not to be influenced by age (Friedman and Friedman, 1957; Rowe et al., 1992). However, when potassium intake was high, the efficiency of kaliuretic response to intravenous potassium chloride was impaired in the aging rat; a significantly greater plasma potassium concentration also occurred (Friedman and Friedman, 1957; Rowe et al., 1992). Following bilateral nephrectomy, the rise in plasma potassium concentration was also higher in the aged rats that were on a high potassium, but not normal potassium, intake. The renal and extrarenal impairment in potassium adaptation was associated with significant decreases in renal and colon Na+/K+-ATPase activity (Friedman and Friedman, 1957; Rowe et al., 1992). The applicablity of these findings to humans is still unclear.

Over the past several years there has been substantial attention paid to extrarenal potassium disposal. Beta-adrenergic mechanisms have been found to be responsible for potassium disposal during potassium infusion in healthy individuals across the adult age range (aged 23 to 85 years) (Rosa et al., 1980; Rowe et al., 1992). No observed effects of age on the extrarenal potassium disposal or the effect of β-adrenergic blockade was found. The effects of insulin concentration, β-adrenergic blockage, and age on potassium homeostasis during hyperinsulinemia was evaluated in 16 younger (22 to 37 years of age) and 10 older (63 to 77 years of age) men (Minaker and Rowe, 1982; Rowe et al., 1992). Increasing steady-state concentrations of insulin were associated with dose-dependent declines in plasma potassium concentration during the first hour of

Suggested Citation:"5 Potassium." Institute of Medicine. 2005. Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate. Washington, DC: The National Academies Press. doi: 10.17226/10925.
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insulin infusion, but during the second hour of insulin infusion, plasma potassium concentration continued to decline at the lowest insulin doses but began to rise at the highest insulin dose levels. This finding suggests the presence of a regulatory mechanism that influences insulin-mediated alterations in plasma potassium. The effect was not influenced by β-adrenergic blockade or aging (Minaker and Rowe, 1982; Rowe et al., 1992). These studies suggest that during aging, hormonal regulation of extrarenal potassium homeostasis remains normal.

Summary. In summary, for children, the AI was extrapolated from the adult AI based on energy intake. Older adults consume less energy than younger adults; however, because of the increased risk of elevated blood pressure with aging, the potassium need may be greater, and is thus not adjusted down for older adults. Because of the lack of evidence to suggest that the requirement for potassium differs in apparently normal, healthy older adults and the elderly compared with that of younger individuals, the AI is set at the same level of intake as for young adults.

Still, the AI does not apply to individuals with medical conditions or who are taking drugs that impair potassium excretion because of the potential for serious adverse effects on the heart from hyperkalemia (see later section, “Special Considerations”). Older individuals more commonly have such conditions or take such drugs and hence are at greater risk of hyperkalemia.

Potassium AI Summary, Ages 51+ Years

AI for Men

51–70 years

4.7 g (120 mmol) /day of potassium

> 70 years

4.7 g (120 mmol)/day of potassium

AI for Women

51–70 years

4.7 g (120 mmol)/day of potassium

> 70 years

4.7 g (120 mmol)/day of potassium

Pregnancy

Evidence Considered in Setting the AI

Accretion. There is little information on body potassium stores during pregnancy. The few available estimates range from cumula-

Suggested Citation:"5 Potassium." Institute of Medicine. 2005. Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate. Washington, DC: The National Academies Press. doi: 10.17226/10925.
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tive gains of 3.9 to 12.5 g (100 to 320 mmol), of which about 7.8 g (200 mmol) is destined for the products of conception (Forsum et al., 1988; Hytten and Leitch, 1971; Lindheimer and Katz, 2000). The latter value comes from a review of the literature by Hytten and Leitch (1971), including one serial study that measured total exchangeable potassium (MacGillivray and Buchanan, 1958). Additionally, one report provided estimates of potassium accretion as measured by the 40K naturally present in human tissues (Godfrey and Wordsworth, 1970). The accumulation at birth was 12 g of potassium (307 mmol), while at 1 month of age the total estimated potassium had decreased to 7 g (179 mmol) (Godfrey and Wordsworth, 1970).

A subsequent study, however, suggests that body potassium stores decrease early in gestation and then increase to only 3.9 g (100 mmol) above those present prior to conception (Forsum et al., 1988). Hormonal changes may affect potassium balance and deposition (Ehrlich and Lindheimer, 1972; Lindheimer and Katz, 1985). It has also been noted that pregnant women develop bicarbonaturia at substantially lower plasma bicarbonate levels than do nonpregnant women (Lindheimer and Katz, 2000).

Serum and Plasma Potassium Concentrations. Plasma and serum concentrations of potassium decrease about 0.2 to 0.3 mmol/L, which may not indicate hypokalemia until values decrease by 0.5 mmol, or to below 3 mmol/L. The reason for the decrement in circulating potassium concentrations during gestation is obscure, but could relate to the mild physiologic alkalemia of gestation in which blood concentrations of hydrogen ions have been shown to decrease about 2 to 4 nmol/L (Lindheimer and Katz, 1985).

Urinary Potassium Excretion. Of further interest and in striking contrast to nonpregnant women, pregnant women are resistant to the kaliuresis provoked by a combination of exogenous mineralocorticoids and a high sodium diet (Ehrlich and Lindheimer, 1972). This ability to conserve potassium in the face of high concentrations of potent mineralocorticoids, such as aldosterone or desoxycorticosterone, and the delivery to the distal nephron of substantial quantities of sodium, may be due to the increased concentrations of progesterone, also characteristic of gestation—a view supported by some (Ehrlich and Lindheimer, 1972; Lindheimer et al., 1987; Mujais et al., 1993), but not others (Brown et al., 1986). Of importance, this resistance to the kaliuretic effects may benefit women with certain potassium-losing diseases, such as primary aldoster-

Suggested Citation:"5 Potassium." Institute of Medicine. 2005. Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate. Washington, DC: The National Academies Press. doi: 10.17226/10925.
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onism and Bartter’s syndrome (August and Lindheimer, 1999; Lindheimer et al., 1987). On the other hand, if the kidneys of pregnant women resist kaliuretic stimuli, one might speculate that women with underlying disorders that impair their ability to excrete potassium may be jeopardized by gestation. In this respect, there have been isolated descriptions of abnormally high potassium concentrations in pregnant women with sickle cell anemia and normal serum creatinine concentrations (Lindheimer et al., 1987), and at least one instance where a woman believed to have renal tubular acidosis developed hyperkalemia when treated with a potassium sparing diuretic (Szwed and Clarke, 1982).

Blood Pressure. Intervention trials that tested the effects of potassium intake on blood pressure during pregnancy are lacking. In one observational study, maternal potassium intake was not associated with pregnancy-associated hypertension or pre-eclampsia (Morris CD et al., 2001). One observational study showed that maternal prenatal potassium intake was inversely related to the infant’s diastolic blood pressure at 6 and 12 months of age (McGarvey et al., 1991).

Summary. Overall, potassium accretion during pregnancy is very small and there is an absence of data to suggest that the requirement for potassium is different during pregnancy. Therefore, the AI is set at 4.7 g (120 mmol)/day, the same as for nonpregnant women.

Potassium AI Summary, Pregnancy

AI for Pregnancy

14–18 years

4.7 g (120 mmol)/day of potassium

19–30 years

4.7 g (120 mmol)/day of potassium

31–50 years

4.7 g (120 mmol)/day of potassium

Lactation

Evidence Considered in Setting the AI

The potassium content of human milk averages around 0.5 g/L (13 mmol/L) during the first 6 months of lactation (see Table 5-9). Average milk production during the first 6 months of lactation is ≈ 0.78 L/d. Thus approximately 0.4 g (10 mmol)/day of potassium is needed for lactation during this period (0.5 g/L × 0.78 L/day =

Suggested Citation:"5 Potassium." Institute of Medicine. 2005. Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate. Washington, DC: The National Academies Press. doi: 10.17226/10925.
×

0.4 g/day). In the absence of information to the contrary, it is assumed that the efficiency of conversion of dietary potassium to milk produced is almost 100 percent. Therefore, the AI for potassium during lactation is set at 5.1 g (130 mmol)/day (4.7 g + 0.4 g/day).

Potassium AI Summary, Lactation

14–18 years

5.1 g (130 mmol)/day of potassium

19–30 years

5.1 g (130 mmol)/day of potassium

31–50 years

5.1 g (130 mmol)/day of potassium

Special Considerations

Very Low Carbohydrate, High Protein Diets

Low-grade metabolic acidosis occurs with very low carbohydrate, high protein diets consumed by some individuals to promote and maintain weight loss. These diets, which may be adequate in potassium due to the high protein content, are inadequate as a source of alkali, because fruits are often excluded in these diets.

Over a 6-month period in which the metabolic consequences of such a diet were investigated in 51 overweight or obese volunteers, weight loss occurred, but the concomitant and intended ketosis led to an ongoing low-grade, metabolic acidosis, as judged by decreases in serum bicarbonate of 2 to 3 mmol/L (still in the normal range), as well as a persistent increase in urinary excretion of calcium of approximately 80 mg/day (Westman et al., 2002).

In a 6-week study of the metabolic effects of a low carbohydrate/high protein diet ingested by 10 adult subjects, a doubling of urinary net acid excretion was attended by a 50 percent increase in urinary excretion of calcium, which was not compensated by a commensurate increase in fractional intestinal calcium absorption (Reddy et al., 2002). Failure of intestinal compensation has been consistently demonstrated for acidosis-induced urine calcium losses (Breslau et al., 1988; Lemann et al., 1966).

Urinary excretion of citrate and serum osteocalcin also concurrently decreased with the increase in urinary excretion of calcium (Reddy et al., 2002). It was concluded that the diet delivered a marked acid load to the kidney, increased the risk of stone formation, led to negative calcium balance, and may have increased bone loss. Those diets that concomitantly restrict the intake of fruits like oranges, bananas, and grapes also restrict the intake of bicarbonate precursors like citrate, a restriction which would amplify the

Suggested Citation:"5 Potassium." Institute of Medicine. 2005. Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate. Washington, DC: The National Academies Press. doi: 10.17226/10925.
×

acidogenic effect of the intended ketosis due to the lack of carbohydrate. There are no published studies of the long-term metabolic effects of this kind of diet in any group of individuals.

Replacement of Diuretic-Induced Potassium Losses

Substantial numbers of individuals receive treatment with diuretic therapies for medical conditions, primarily high blood pressure, but also congestive heart failure and chronic kidney disease. Thiazide diuretics (e.g., hydrochlorothiazide and chlorthalidone) and loop diuretics (e.g., furosemide) increase urinary potassium excretion, which in some instances leads to overt hypokalemia—that is, a serum potassium concentration of 3.5 mmol/L or less. Accordingly, many individuals on diuretic therapy are given a potassium supplement. In a recently completed trial (Furberg et al., 2002), approximately 8 percent of individuals assigned to low-dose chlorthalidone (12.5 to 25 mg/day) required a potassium supplement. Because of diuretic-induced urinary potassium losses, it is plausible that individuals on diuretic therapy should have an AI greater than 4.7 g (120 mmol)/day. However, available evidence is insufficient to confirm the need for a higher AI in such individuals.

Predisposition to Hyperkalemia

Several relatively common clinical conditions can predispose individuals to hyperkalemia, even at levels of potassium intake that are below the AI. The most common of these conditions are chronic kidney disease, heart failure, and type 1 diabetes, each of which can impair renal excretion of potassium. Angiotensin converting enzyme (ACE) inhibitor drug therapy, which is a recommended therapy for each of these conditions, increases the risk of hyperkalemia (Schoolwerth et al., 2001).

The risk for hyperkalemia during ACE inhibitor therapy increases as kidney function declines. The conclusion from a case series of 33 hypertensive patients in which serum potassium levels were measured before and after ACE inhibitor therapy was that serum potassium levels rarely rose to greater than 5.0 mmol/dL unless the estimated glomerular filtration rate (GFR) was less than 40 mL/minute (Textor et al., 1982). In this study, patients consumed between 2.7 and 3.1 g (70 and 80 mmol)/day of potassium. Whether a higher dietary intake of potassium would precipitate hyperkalemia is uncertain. In a case-control study of 1,818 medical outpatients on ACE inhibitor therapy, severe hyperkalemia (defined as serum potassium

Suggested Citation:"5 Potassium." Institute of Medicine. 2005. Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate. Washington, DC: The National Academies Press. doi: 10.17226/10925.
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> 6.0 mmol/day) was uncommon in patients less than 70 years old with normal renal function (Reardon and Macpherson, 1998); however, data on dietary potassium intake was not collected in this study. Since the 95th percentile estimates of potassium intake for men and women in the United States range from 4.3 to 5.1 g and 2.9 to 3.7 g/day, respectively (Appendix Table D-5), it can be assumed that many of these outpatients had intakes below the AI of 4.7 g (120 mmol)/day.

In case reports additional factors appear to precipitate hyperkalemia in ACE inhibitor-treated patients. These factors include use of potassium supplements, potassium-sparing diuretics, nonsteroidal anti-inflammatory agents, cyclo-oxygenase-2 (COX-2) inhibitors, and heparin (see Box 5-1). Although most case reports relating hyperkalemia and ACE inhibitor treatment occurred in individuals with diabetes, chronic kidney disease, and/or heart failure, there have been a few case reports in other settings. Two cases of hyperkalemia in older men were reported to be due to the use of a potassium-containing salt substitute while taking ACE inhibitor therapy (Ray et al., 1999). One case report documented fatal hyperkalemia in a 77-year-old woman after addition of COX-2 inhibitor therapy to a medical regimen that included an ACE inhibitor and a diet that included a banana each day (Hay et al., 2002). Her serum creatinine had been 0.9 mg/dL, which in retrospect might reflect subtle evidence of chronic kidney disease (Hay et al., 2002). This case illustrates the difficulty of using serum creatinine levels to diagnose early chronic kidney disease. Among older individuals, women who are non-African American often have serum creatinine values that appear to be “normal” (0.9 to 1.2 mg/dL) despite an underlying reduction in kidney function (Culleton et al., 1999).

Overall, because of the concern for hyperkalemia and resultant arrhythmias that might be life-threatening, the proposed AI should not be applied to individuals with chronic kidney disease, heart failure, or type 1 diabetes, especially those who concomitantly use ACE inhibitor therapy. Among otherwise healthy individuals with hypertension on ACE inhibitor therapy, the AI should apply as long as renal function is unimpaired.

INTAKE OF POTASSIUM

Sources

Good sources of potassium, as well as bicarbonate precursors, are fruits and vegetables (see Table 5-10). Foods that contain relatively

Suggested Citation:"5 Potassium." Institute of Medicine. 2005. Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate. Washington, DC: The National Academies Press. doi: 10.17226/10925.
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BOX 5-1 Clinical Circumstances That May Result in Hyperkalemia

  • Impaired renal excretion of potassium

    • Severe reduction in glomerular filtration rate

      • Chronic kidney disease

      • Subacute-reversible

        • Volume depletion

        • Pharmacological inhibition by angiotensin converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs)

    • Effective hypoaldosteronism

      • Reduced synthesis due to

        • Addison’s disease

        • Heparin administration

      • Reduced secretion of aldosterone

        • Hyporeninemia

          • Diabetic nephropathy

          • Obstructive nephropathy

          • Nonsteroidal anti-inflammatory drugs (e.g., indomethacin)

          • Cyclo-oxygenase-2 inhibitors (COX-2, e.g., Vioxx, Celebrex)

        • Reduced activity of angiotensin-converting enzyme

      • Reduced renal tubular response to aldosterone

        • Aldosterone-receptor blockers (e.g., spironolactone)

        • Type 4 renal tubular acidosis

    • Pharmacological inhibitors of distal renal tubular Na+-K+ exchange (e.g., amilioride, triamterene)

  • Impaired systemic cellular accumulation of potassium

    • Hypoinsulinemia (type 1 diabetes)

    • Metabolic acidosis

    • β-andrenergic blockers (e.g., propanolol)

    • α-andrenergic agonists (e.g., phenylephrine)

  • Excessive cellular release of potassium

    • Rhabdomyolosis

    • Tumor lysis

    • Leukemia

Clinical conditions that commonly occur together and that amplify their hyperkalemic effects

  • Hyporeninemia/hypoaldosteronism and diabetic nephropathy

  • Chronic kidney disease with either ACE or ARB therapy

SOURCE: Fisch et al. (1966); Gennari and Segal (2002); Kamel et al. (1996); Oster et al. (1995); Schoolwerth et al. (2001); Tannen (1986); Textor et al. (1982).

Suggested Citation:"5 Potassium." Institute of Medicine. 2005. Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate. Washington, DC: The National Academies Press. doi: 10.17226/10925.
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TABLE 5-10 Comparative Amounts of Approximate Potassium Content in Various Food Groups

Food Group

Potassium mg (mmol)/100 kcal

Examples

Leafy greens

1,500 (38)

Spinach, lettuce, romaine, cabbage, kale

Fruit of vine-based plants

1,200 (30)

Tomatoes, cucumbers, zucchini, eggplant, pumpkin

Root vegetables

975 (25)

Carrots, radishes, turnips, rutabaga, onions

Beans and peas

500 (13)

Kidney beans, peas, green beans, chick peas, soybeans

Tree fruits

430 (11)

Apples, oranges, bananas, apricots, grapes, strawberries

Tubers

400 (10)

Potatoes, sweet potatoes, yams

Milk and yogurt

350 (9)

Skimmed milk, whole milk, yogurt

Meats

230 (6)

Beef, lamb, pork, poultry, fish, rabbit

Nuts

110 (3)

Walnuts, cashews, almonds, brazil, hazelnuts

Eggs

90 (2.3)

Chicken eggs

Cereal grains

90 (2.3)

Wheat, rice, oats, rye

Cheese

150 (1.1)

Edam, stilton, cottage, cheddar

high amounts of potassium include spinach (≈ 840 mg [22 mmol] per cup), cantaloupe (315 mg [8 mmol] per 1/6 large), dry roasted almonds (210 [5 mmol] per oz.), brussels sprouts (250 mg [6 mmol] per 1/2 cup), mushrooms (550 mg [14 mmol] per 1 cup), bananas (470 mg [12 mmol] per 1 medium), oranges (200 mg [5 mmol] per 1 small), grapefruit (230 mg [6 mmol] per 1/2 large), and potatoes (600 mg [15 mmol] per potato without skin). The Adequate Intake (AI) for adults of 4.7 g (120 mmol)/day of potassium can be achieved by consuming a diet that contains generous amounts of potassium-rich fruits and vegetables.

While meat, milk, and cereal products contain potassium, their content of bicarbonate precursors does not sufficiently balance the amount of acid-forming precursors, such as sulfur amino acids, found in higher protein foods (Lemann et al., 2003). Tables of citrate and bicarbonate content of foods are lacking, making it difficult to estimate the amount consumed of these other food components.

On a calorie basis, the comparative amounts of potassium in various food groups, expressed in mg/100 kcal, are shown in Table 5-10. As for many other nutrients, from a nutrient density perspec

Suggested Citation:"5 Potassium." Institute of Medicine. 2005. Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate. Washington, DC: The National Academies Press. doi: 10.17226/10925.
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tive, the richest sources of potassium are leafy green vegetables, fruit from vines, and root vegetables.

Salt substitutes currently available in the marketplace range from 440 mg to 2,800 mg (11 to 72 mmol)/tsp of potassium, all as potassium chloride (Pennington, 1998; Riccardella and Dwyer, 1985). In the Third National Health and Nutrition Examination Survey (NHANES III), less than 10 percent of respondents reported that they used a reduced-sodium salt or a salt substitute (Loria et al., 2001). The maximum amount of potassium in over-the-counter supplements is 0.099 g (2.5 mmol) (Medical Economics, 2001).

Table 5-11 provides an estimate of the potassium intake from foods when consuming approximately 2,200 kcal/day, the combined average energy intake of young men and women (IOM, 2002), while meeting recommended intakes for other nutrients. This table illustrates that potassium intake at levels in the range of the AI (4.7 g/day or 120 mmol/day) can be achieved by consuming a diet rich in fruits and vegetables.

Intake

Based on intake data from the NHANES III (Appendix Table D-5), the median intake of potassium in the United States 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. The median potassium intakes of white respondents exceeded that of African-American respondents. The median intakes of potassium by adults obtained from Canadian surveys conducted between 1990 and 1999 in 10 provinces 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), indicating that on average, Canadian intake of potassium was somewhat greater than that of adults in the United States. The percentage of men and women who consumed equal to or greater than the AI was less than 10 and 1 percent, respectively, in the United States.

These dietary intake surveys do not include estimates of the usage of salt substitutes. Less than 10 percent of those surveyed in NHANES III reported using salt substitutes or a reduced-sodium salt (Loria et al., 2001). No other data were found that estimate the intake of potassium from various salt substitutes on the market.

While there are very few data regarding potassium intake during pregnancy, the Calcium for Prevention of Preeclampsia trial (CPEP) estimated intake using dietary recalls in 4,589 participants at recruitment, during weeks 13 to 20 of gestation (Morris CD et al., 2001). Daily potassium intake of the 3,125 women who remained

Suggested Citation:"5 Potassium." Institute of Medicine. 2005. Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate. Washington, DC: The National Academies Press. doi: 10.17226/10925.
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TABLE 5-11 Daily Potassium Intake from a Diet Providing 2,200 kcal

Meal

Food/Beverage Consumed

Calories (kcal)

Potassium (mg)

Breakfast

Shredded wheat miniatures (1 cup)

183

248

 

Cantaloupe, cubed (1/2 cup)

27

214

Milk, 1% (8 oz)

102

290

Orange juice (6 oz)

82

355

White toast (1 slice) with unsalted margarine vegetable oil spread (1 tsp)

89

30

Coffee, black, unsweetened (12 oz)

13

171

Total for meal

496

1,278

Snack

Banana (1 medium)

105

422

 

Water (1 cup)

0

0

Total for meal

105

422

Lunch

Sandwich with turkey (2 oz), swiss cheese (1 oz), lettuce (2 leaves), tomato (1/4″ slice), mayonnaise (1 tbsp) and whole wheat bread (2 slices)

395

499

 

Baby carrots (8)

28

190

Fig bar cookies (2)

111

66

Iced tea, brewed, decaffeinated (16 oz)

5

176

Total for meal

539

857

Snack

Almonds, dry roasted, unsalted (1/4 cup)

206

257

 

Raisins (1/4 cup)

108

272

Milk, 1% (8 oz)

102

290

Water (12 oz)

0

0

Total for Meal

416

819

Dinner

Baked salmon (3 oz)

151

257

 

Long-grain brown rice (1/2 cup cooked)

108

42

Tossed salad (1 1/2 cups) with safflower oil and vinegar dressing (2 tbsp)

155

371

Asparagus (6 spears)

20

202

Wheat roll, (1 medium) with unsalted margarine vegetable oil spread (1 tsp)

101

34

Angel food cake (1 slice) with sliced strawberries (1/2 cup) and whipped cream topping (2 tbsp)

114

162

Iced tea, brewed, decaffeinated (16 oz)

5

176

Coffee, black, unsweetened, decaffeinated (8 oz)

9

114

Total for meal

663

1,492

Suggested Citation:"5 Potassium." Institute of Medicine. 2005. Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate. Washington, DC: The National Academies Press. doi: 10.17226/10925.
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Meal

Food/Beverage Consumed

Calories (kcal)

Potassium (mg)

 

Daily total

2,219 kcal

4,868 mg

(124 mmol)

NOTE: This diet meets the Adequate Intake or Recommended Dietary Allowance for adult men and women for all nutrients for which one has been established (for fiber, it meets the ratio of 14 g/1,000 kcal) and provides energy nutrients within the acceptable macronutrient distribution ranges. Nutrient totals may not equal the sum of the parts due to rounding. Vegetables and rice were prepared without salt.

FOOD COMPOSITION DATA: U.S. Department of Agriculture Agricultural Research Service, Nutrient Database for Standard Reference, Release 16.

DATA SOURCE: Environ International.

nonhypertensive throughout pregnancy averaged 3.1 g (79 mmol)/day. While this population group had over-representation by African-American and Hispanic pregnant women, in two other studies in which potassium excretion was measured serially throughout gestation, 24-hour urinary excretion averaged 2.0 to 2.3 g (50 to 60 mmol)/day of potassium (Brown and et al., 1986; Wilson et al., 1980). While there were few (n = 83) pregnant women in NHANES III, and even fewer (n = 19) lactating women (Appendix Table D-6), their intake of potassium intake was substantially greater than their nonpregnant counterparts, with median intakes of 2.8 g (72 mmol)/day and 3.8 g (97 mmol)/day, respectively.

ADVERSE EFFECTS OF OVERCONSUMPTION

Hazard Identification

Gastrointestinal Discomfort

Gastrointestinal discomfort has been reported with some forms of potassium supplements, but not with potassium from diet. When healthy individuals were provided 2.3 g (60 mmol)/day of potassium chloride for 18 days in the form of a wax/polymer matrix tablet, a powder-in-liquid formulation, or a microencapsulated gelatin capsule, there was a significant increase in gastrointestinal distress reported for the wax/polymer matrix as compared with the other two (Sinar et al., 1986). Gastrointestinal discomfort was also

Suggested Citation:"5 Potassium." Institute of Medicine. 2005. Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate. Washington, DC: The National Academies Press. doi: 10.17226/10925.
×

reported by some patients receiving 0.8 to 1.6 g (20 to 40 mmol)/ day of potassium chloride either as a wax-matrix tablet (5 of the 17 receiving the treatment) or as a microencapsulated tablet (6 of the 17) (Pietro and Davidson, 1990).

Ulceration of gastrointestinal tract mucosa and perforation of the small bowel have been reported in patients using various potassium chloride supplements (Lambert and Newman, 1980; Leijonmarck and Raf, 1985). In a placebo-controlled trial that provided 2.3 g (60 mmol)/day of microencapsulated potassium to 175 prehypertensive subjects for 6 months, high pill compliance but no serious gastrointestinal effect was reported (Whelton et al., 1995). Overall, the specific product/vehicle appears to be a critical determinant of the risk of gastrointestinal side effects from supplemental potassium.

Arrhythmia from Hyperkalemia

Cardiac arrhythmias from hyperkalemia are the most serious consequence of excessive potassium intake. The typical sequence of findings is hyperkalemia, followed by conduction abnormalities on electrocardiogram (ECG) and then cardiac arrhythmias, which can be life-threatening. Such consequences result from either a high plasma concentration of potassium or from rapid and extreme changes in its concentration (Kallen et al., 1976). At typical dietary intakes of potassium, the normal range of plasma concentration of potassium is 3.5 to 5.0 mmol/L. The actual level at which hyperkalemia increases the risk of serious arrhythmias is uncertain, but is likely at a level greater than 5.5 mmol/L.

Acute toxicity from accidental or intentional consumption of large quantities of potassium chloride or potassium-containing salt substitutes by apparently healthy individuals has been reported (Kallen et al., 1976; Su et al., 2001; Wetli and Davis, 1978). However, such evidence of acute toxicity is of limited value in assessing the potential hazards from chronic ingestion of high levels of potassium. In clinical trials that assessed the effects of potassium supplementation as high as 15.6 g (400 mmol)/day over a period of at least 5 days in apparently healthy individuals, plasma levels of potassium increased but remained within the normal range (see Table 5-12). Importantly, there were no instances of hyperkalemia reported in these studies.

However, in individuals whose urinary potassium excretion is impaired by a medical condition, drug therapy, or both, instances of life-threatening hyperkalemia have been reported. There have been several case reports of hyperkalemia in individuals who reported

Suggested Citation:"5 Potassium." Institute of Medicine. 2005. Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate. Washington, DC: The National Academies Press. doi: 10.17226/10925.
×

use of a potassium-containing salt substitute while under treatment for chronic diseases (Haddad and Strong, 1975; Ray et al., 1999; Snyder et al., 1975) (see Table 5-13). These individuals had some type of heart or renal disease and therefore were taking other medications, including ACE inhibitors. The potassium-containing salt substitute might have been prescribed to reduce sodium chloride intake, to replace diuretic-induced potassium losses, or both. Such patients are at risk both for hypokalemia and hyperkalemia and therefore require close medical supervision.

Dose-Response Assessment

In otherwise healthy individuals (that is, individuals without impaired urinary potassium excretion from a medical condition or drug therapy), there have been no reports of hyperkalemia resulting from acute or chronic ingestion of potassium naturally occurring in food. Hyperkalemia might theoretically occur if the capacity of the normal kidney to excrete a potassium load is exceeded. The maximum excretion rate of normal kidneys after adaptation to high levels of intake has been estimated to be approximately 31.3 g (800 mmol)/day for adults (Berliner, 1961), a level that would be difficult to achieve from food alone. Gastrointestinal discomfort has been reported with some forms of potassium supplements, but not with potassium from foods.

UL Summary

Adults. In otherwise healthy individuals (i.e., individuals without impaired urinary potassium excretion from a medical condition or drug therapy), there is no evidence that a high level of potassium from foods has adverse effects. Therefore, a Tolerable Upper Intake Level (UL) for potassium from foods is not set for healthy adults.

In contrast, supplemental potassium can lead to acute toxicity in healthy individuals. Also, chronic consumption of a high level of potassium can lead to hyperkalemia in individuals with impaired urinary potassium excretion (see later section, “Special Considerations”). Hence, supplemental potassium should only be provided under medical supervision because of the well-documented potential for toxicity.

Infants and Children. Almost all of the potassium that appears in urine is secreted by the last half of the distal tubule (Schultze, 1973).

Suggested Citation:"5 Potassium." Institute of Medicine. 2005. Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate. Washington, DC: The National Academies Press. doi: 10.17226/10925.
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TABLE 5-12 Effects of Chronic Intake of High Levels of Potassium

Reference

Study Design

Diet

Nonhypertensive individuals

Hene et al., 1986

6 men, 24 ± 2 yr

2-wk crossover

Control diet: 3.1 g (80 mmol) potassium (K), 3.4 g (150 mmol) sodium (Na)

High-K diet: 8.6 g (220 mmol) K, 3.4 g (150 mmol) Na (additional potassium as K citrate)

Witzgall and Behr, 1986

16 men, 27 ± 6 yr, control diet 2 wk prior to loading

Control diet: 2.3 g (60 mmol) K, 4.6 g (200 mmol) Na

High K diet: control diet + 7.8 g (200 mmol) as K citrate and K hydrogen carbonate = 10.1 g (260 mmol) K total

Rabelink et al., 1990

3 men, 3 women, 22–26 yr

5-d control diet: 3.9 g (100 mmol) K, 2.3 g (100 mmol) Na

20-d high K diet: 15.6 g (400 mmol)K, 2.3 g (100 mmol) Na

Deriaz et al., 1991

8 men, 26 ± 2 yr

5-d crossover

Baseline diet: 2.7 g (69 mmol) K

High K diet: 6.4 g (163 mmol) K

Dluhy et al., 1972

8 women, 2 men

Crossover

5 subjects: 0.23 g (10 mmol) Na

1.6 g (40 mmol) K, 6–7 d

7.8 g (200 mmol) K, 3 d

5 subjects: 4.6 g (200 mmol) Na

1.6 g (40 mmol) K, 6–7 d

7.8 g (200 mmol) K, 3 d

Zoccali et al., 1985

10 men, 20–29 yr

5-d crossover

Baseline diet: 3.0 g (76 mmol) K, 3.4 g (145 mmol) Na

High K diet: 6.9 g (176 mmol) K, 3.4 g (145 mmol) Na

Hypertensive individuals

Zoccali et al., 1985

10 men, 9 women, 26–53 yr

2-wk crossover

Baseline diet: Normal diet + placebo

Higher K diet: + 3.9 g (100 mmol) K

a SBP = systolic blood pressure, DBP = diastolic blood pressure.

Suggested Citation:"5 Potassium." Institute of Medicine. 2005. Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate. Washington, DC: The National Academies Press. doi: 10.17226/10925.
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Urinary Potassium (mmol/24 h)

Effectsa

50 ± 12

233 ± 45

Serum K within normal limits but 10% higher (p < 0.05) with K load

≈ 60

↑ Plasma K (p < 0.01) (from 4.3 to 4.6 mmol/L)

↓ SBP (p < 0.01); ↓ DBP (p < 0.01)

≈ 220

↑ Plasma renin in 13 of 16 subjects; no adverse effects identified

82

With high K diet, ↑ plasma K (p < 0.05); plasma renin and aldosterone, while increased significantly (p < 0.01) after

385

2 d, were back to baseline levels by 20 d

50

119

Serum K was within normal limits

 

Fasting plasma aldosterone levels ↑ with increased K regardless of Na intake; no other effects noted

59

Serum K was 10% higher (p < 0.05) on high K diet, but still within normal range

161

No other changes noted

58

139

4 patients withdrew from the study: 1 due to diarrhea from the K supplement; 1 due to ↑ BP when receiving placebo; 2 due to taste of K supplement

Suggested Citation:"5 Potassium." Institute of Medicine. 2005. Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate. Washington, DC: The National Academies Press. doi: 10.17226/10925.
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TABLE 5-13 Studies and Case Reports of Adverse Effects Due to Chronic Intake of High Levels of Potassium

Case Report

Description of Patient

Haddad and Strong, 1975

39-yr-old woman, Lupus Erythematosus, w/chronic renal failure (creatinine clearance = 30 mL/min)

Snyder et al., 1975

75-yr-old woman, history of myocardial infarction, on a low sodium diet

Ray et al., 1999

67-yr-old man; hypertensive, previous coronary artery bypass surgery and left ventricular dysfunction

Ray et al., 1999

64-yr-old man; 24-yr history of diabetes mellitus and recent systolic hypertension, retinopathy, and renal impairment; on a low sodium diet

While an infant’s renal secreting capacity is initially less than adults, renal function rapidly reaches the normal adult level in early childhood, so little concern exists for consumption of high levels of potassium from foods. Because the renal secreting ability of normal infants is not fully developed, potassium intake should be limited to that contained in formula and complementary foods.

Pregnancy. Other than occasional gastrointestinal discomfort as noted above from the use of certain forms of supplemental potassium, adverse effects from high intakes of potassium have not been noted in apparently healthy individuals, which would include pregnant women who are not identified as having hypertension or preeclampsia. Therefore, a UL for potassium is not set for healthy women during normal pregnancy.

Lactation. As with other adults, there is little reason to restrict the potassium intake of healthy lactating women due solely to lac-

Suggested Citation:"5 Potassium." Institute of Medicine. 2005. Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate. Washington, DC: The National Academies Press. doi: 10.17226/10925.
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Potassium Amount Ingested

Adverse Effect

Medications

Ad lib use of salt substitute

Serum potassium = 7.4 mmol/L

Spironolactone, a potassium-sparing diuretic

Ad lib use of a “lite” salt substitute

Edema, shortness of breath, right-sided and left-sided congestive heart failure

None reported

Estimate of 2.7 g (70 mmol)/d of potassium as “LoSalt” for previous week; diet high in fruits and vegetables

Serum potassium = 7.6 mmol/L; loss of consciousness, dizziness, intermittent vomiting

Atenolol, furosemide, aspirin, and lisinopril (an angiotensin converting enzyme inhibitor)

Estimate of 5.2 g (133 mmol)/d of potassium as “Lo Salt” previously; diet estimated to also provide 2.7 g (70 mmol)/d

Serum potassium = 7 mmol/L

Enalapril (an angiotensin converting enzyme inhibitor)

tation. Therefore, a UL is not set for healthy women during this period.

Special Considerations

Problem Pregnancy. It is suggested that high potassium levels be consumed with care in women with problem pregnancies, such as preeclampsia. High concentrations of the antikaliuretic hormone progesterone (which circulate during gestation) may make women with undetected renal dysfunction or with a sudden decrease in glomerular filtration rate (as occurs with preeclampsia) more likely to develop hyperkalemia when potassium intake is high.

Other Situations. Clinical settings in which high intakes of potassium could pose a serious risk include type 1 diabetes, chronic renal insufficiency (e.g., GFR < 40 mL/minute), end-stage renal disease, severe heart failure, and adrenal insufficiency (see Box 5-1). In these

Suggested Citation:"5 Potassium." Institute of Medicine. 2005. Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate. Washington, DC: The National Academies Press. doi: 10.17226/10925.
×

situations, medical supervision is typically provided, including individualized diet instruction (IOM, 2000), and a potassium intake below the AI is often appropriate. For individuals with these diseases or clinical conditions, salt substitutes (containing potassium chloride) should be used cautiously. While adverse events following high potassium consumption usually do not occur in these special populations, there are case studies cited in the literature indicating that these groups are vulnerable (see Table 5-13).

RESEARCH RECOMMENDATIONS

  • Dose-response trials testing the effects of different levels of potassium intake on blood pressure at different levels of sodium intake.

  • Additional dose-response trials evaluating the effect of potassium on salt sensitivity in subgroups of the population that are salt sensitive (e.g., African Americans, older persons, and persons with hypertension, chronic kidney disease, or diabetes).

  • Randomized clinical trials to compare the effect of different potassium salts on blood pressure and other outcomes at different levels of sodium intake.

  • Development of improved measurements and instruments that assess total potassium intake and total body potassium.

  • Trials that test the efficacy of increased potassium intake on preventing stroke.

  • Trials that test the main and interactive effects of potassium and sodium intake on bone mineral density and, if feasible, bone fractures.

  • Trials testing the main and interactive effects of sodium and potassium intake on the risk of kidney stones.

  • Studies to assess the main and interactive effects of potassium and sodium intake on glucose intolerance and insulin resistance.

  • Studies on the role of potassium intake during infancy and childhood on blood pressure later in life.

  • Potassium balance studies during pregnancy.

  • Better estimates of potassium losses in sweat with various dietary, activity, and environmental conditions in diverse populations.

  • Development of food tables for citrate and bicarbonate.

  • Studies on the effects of chronic, low-grade metabolic acidosis on clinical outcomes, particularly kidney stones and osteoporosis.

  • Trials to assess the effects of high potassium intake on serum potassium levels and blood pressure in the setting of early stages of renal insufficiency (with and without ACE inhibitor therapy).

Suggested Citation:"5 Potassium." Institute of Medicine. 2005. Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate. Washington, DC: The National Academies Press. doi: 10.17226/10925.
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Alpern RJ. 1995. Trade-offs in the adaptation to acidosis. Kidney Int 47:1205–1215.

Appel LJ, Moore TJ, Obarzanek E, Vollmer WM, Svetkey LP, Sacks FM, Bray GA, Vogt TM, Cutler JA, Windhauser MM, Lin PH, Karanja N. 1997. A clinical trial of the effects of dietary patterns on blood pressure. N Engl J Med 336:1117–1124.

Armstrong LE, Hubbard RW, Szlyk PC, Matthew WT, Sils IV. 1985. Voluntary dehydration and electrolyte losses during prolonged exercise in the heat. Aviat Space Environ Med 56:765–770.

Ascherio A, Rimm EB, Giovannucci EL, Colditz GA, Rosner B, Willet WC, Sacks F, Stampfer MJ. 1992. A prospective study of nutritional factors and hypertension among US men. Circulation 86:1475–1484.

Ascherio A, Rimm EB, Hernan MA, Giovannucci EL, Kawachi I, Stampfer MJ, Willett WC. 1998. Intake of potassium, magnesium, calcium, and fiber and risk of stroke among US men. Circulation 98:1198–1204.

August P, Lindheimer MD. 1999. Chronic hypertension and pregnancy. In: Lindheimer MD, Roberts JM, Cunningham FG, eds. Hypertensive Disorders in Pregnancy, 2nd ed. Stamford, CT: Appleton & Lange. Pp. 605–633.


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Suggested Citation:"5 Potassium." Institute of Medicine. 2005. Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate. Washington, DC: The National Academies Press. doi: 10.17226/10925.
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Next: 6 Sodium and Chloride »
Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate Get This Book
×

Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate The Dietary Reference Intakes (DRIs) are quantitative estimates of nutrient intakes to be used for planning and assessing diets for healthy people. This new report, the sixth in a series of reports presenting dietary reference values for the intakes of nutrients by Americans and Canadians, establishes nutrient recommendations on water, potassium, and salt for health maintenance and the reduction of chronic disease risk. Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate discusses in detail the role of water, potassium, salt, chloride, and sulfate in human physiology and health. The major findings in this book include the establishment of Adequate Intakes for total water (drinking water, beverages, and food), potassium, sodium, and chloride and the establishment of Tolerable Upper Intake levels for sodium and chloride. The book makes research recommendations for information needed to advance the understanding of human requirements for water and electrolytes, as well as adverse effects associated with the intake of excessive amounts of water, sodium, chloride, potassium, and sulfate. This book will be an invaluable reference for nutritionists, nutrition researchers, and food manufacturers.

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