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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.


Disordered potassium metabolism that is expressed as hypokalemia (that is, a serum potassium level below 3.5 mmol/L) can result in cardiac arrhythmias, muscle weakness, hypercalciuria, and glucose intolerance. Such disorders, which are correctable by potassium administration, can be induced by diuretics, chloride-depletion associated forms of metabolic alkalosis, and increased aldosterone production (Knochel, 1984).

Hypokalemia reduces the capacity of the pancreas to secrete insulin and therefore is a recognized reversible cause of glucose intolerance (Helderman et al., 1983). There is some limited evidence that hypokalemia can also confer insulin resistance (Helderman et al., 1983; Pollare et al., 1989). A low potassium diet (0.58 g [15 mmol]/day), which did not induce frank hypokalemia, resulted in a decrease in plasma insulin concentration and a resistance to insulin action, which were reversed when dietary potassium was supplemented with 4.8 g (64 mmol)/day of potassium chloride (Norbiato et al., 1984). Decreased erythrocyte and plasma potassium concentrations have been associated with glucose intolerance (Modan et al., 1987). Diuretic-induced hypokalemia leads to insulin resistance (hyperglycemia and hyperinsulinemia) and glucose intolerance (Helderman et al., 1983; Plavinik et al., 1992). In one trial, individu-

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