reabsorbed, the average loss of biliary B₁₂ in the stool would be 0.5 nmol/day (0.7 µg/day). Research with baboons (Green et al., 1982) suggests that the form of B₁₂ present in bile may be absorbed more readily than is cyanocobalamin, but the absorption of both forms was enhanced by intrinsic factor. Both Green and colleagues (1982) and Teo and coworkers (1980) reported data suggesting that bile enhances B₁₂ absorption. However, in the absence of intrinsic factor, essentially all the B₁₂ from the bile is excreted in the stool rather than recirculated. Thus, B₁₂ deficiency develops more rapidly in individuals who have no intrinsic factor or who malabsorb B₁₂ for other reasons than it does in those who become complete vegetarians and thus ingest no B₁₂.

If the circulating B₁₂ exceeds the B₁₂ binding capacity of the blood, the excess is excreted in the urine. This typically occurs only after injection of B₁₂. The highest losses of B₁₂ ordinarily occur through the feces. Sources of fecal B₁₂ include unabsorbed B₁₂ from food or bile, desquamated cells, gastric and intestinal secretions, and B₁₂ synthesized by bacteria in the colon. Other losses occur through the skin and metabolic reactions. Fecal (Reizenstein, 1959) and urinary losses (Adams, 1970; Heinrich, 1964; Mollin and Ross, 1952) decrease when B₁₂ stores decrease. Various studies have indicated losses of 0.1 to 0.2 percent of the B₁₂ pool per day (Amin et al., 1980; Boddy and Adams, 1972; Bozian et al., 1963; Heinrich, 1964; Heyssel et al., 1966; Reizenstein et al., 1966) regardless of the size of the store, with the 0.2 percent value generally applicable to those with pernicious anemia.