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There are two distinct mechanisms for intestinal vitamin B12 absorption; receptor-mediated absorption and passive diffusion.  In the first, vitamin B12 attaches to a salivary “R-binder” protein, which transports it into the small intestine, where vitamin B12 is released.  The vitamin then binds to “Intrinsic Factor” (IF), a glycoprotein normally produced by the gastric parietal cells.  This vitamin B12-IF complex is carried down to the ileum, where it binds to mucosal receptors.  Finally, the complex is absorbed and bound to serum vitamin B12-binding proteins.  The second absorption mechanism, passive diffusion, does not require any carriers, such as B-binder or IF.  Only about 1% of free vitamin B12 is passively absorbed, but this can be nutritionally significant with higher dietary vitamin B12 intakes.*

Almost 40% of the population is suggested to have “low normal” plasma B12 levels. Strict vegetarians, the elderly, and HIV/AIDS patients are often at risk for vitamin B12 deficiency, either due to low intake or impaired absorption. In the elderly, hypo- or achlorhydria maintains binding of the vitamin with dietary proteins, leading to malabsorption. Vitamin B12 deficiency can lead to CNS impairment, including cognition. The elderly, HIV/AIDS patients, and strict vegetarians are often at risk for vitamin B12 deficiency, either due to low dietary intake or impaired absorption.*

The receptor-mediated absorption pathway is subject to numerous genetic and pathologic defects which can severely impair normal vitamin B12 absorption. These defects include hereditary absence of IF production, gastric atrophy, gastrectomy, and small intestinal disorders affecting the ileum, such as gluten-induced enteropathy, regional enteritis, chronic diarrhea, and intestinal resection.  Affected individuals depend almost exclusively on the passive diffusion pathway, which requires high dietary vitamin B12 intakes.*