can contribute to meeting the adequate intake, no one source is essential for normal physiological function and health.

The major intracellular cation in the body, potassium 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,² 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 organic anions, such as citrate, that are converted in the body to bicarbonate. Acting as a buffer, bicarbonate neutralizes diet-derived 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 excess acid and in the process bone becomes demineralized. Increased bone turnover and calcium-containing kidney stones are the resulting adverse consequences.

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 evaluation focuses on research pertaining to non-