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.
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