a A disorder in which lack of intrinsic factor severely limits the absorption of vitamin B12.
b Heyssel et al. (1966).
c Berlin et al. (1968).
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.