Cobalamin, the stomach, and aging

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Abstract
Low cobalamin concentrations are common in the elderly. Although only a minority of such persons display clinically obvious symptoms or signs, metabolic data clearly show cellular deficiency of cobalamin in most cases. The evidence suggests that this is not a normal physiologic expression of the aging process. Rather, the elderly seem at increased risk for mild, preclinical cobalamin deficiency. Classical disorders such as pernicious anemia are the cause of this deficiency in only a small proportion of the elderly. A more frequent problem is food-cobalamin malabsorption, which usually arises from atrophic gastritis and hypochlorhydria but other mechanisms seem to be involved in some patients. The diminished absorption should not be viewed as a natural consequence of aging. The partial nature of this form of malabsorption produces a more slowly progressive depletion of cobalamin than does the more complete malabsorption engendered by disruption of intrinsic factor-mediated absorption. The slower progression of depletion probably explains why mild, preclinical deficiency is associated with food-cobalamin malabsorption more often than with pernicious anemia. Decisions about the optimal management of the very common problem of mild, preclinical cobalamin deficiency in the elderly await further clarification of the processes and the complex issues involved, including the possibility that routine nitrous oxide use during surgery, proposed dietary changes, and other practices may further stress the marginal cobalamin status of many elderly people.