Sodium homeostasis is maintained over a wide range of environmental and dietary circumstances, primarily through the action of the hormone aldosterone on the renal tubules of the kidney. When sodium intake is high, the aldosterone level decreases and urinary sodium increases. When dietary sodium intake is low, the aldosterone level increases and urinary excretion of sodium rapidly falls almost to zero. Although the kidney can thus conserve sodium, there is some obligatory loss via feces and sweat. Sodium deficiency resulting from low dietary intake thus does not normally occur, even among those existing on very low sodium diets (Page, 1976, 1979). Even relatively heavy sweating does not normally create a need to provide salt supplements (Conn, 1949). The body may be depleted of sodium under extreme conditions of heavy and persistent sweating, or where trauma, chronic diarrhea, or renal disease produce an inability to retain sodium (Gothberg et al., 1983). These latter conditions require medical attention.