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The absorption of vitamin B12 in humans is complex (1, 2). Vitamin B12 in food is bound to proteins and is released from the proteins by the action of a high concentration of hydrochloric acid present in the stomach. This process results in the free form of the vitamin, which is immediately bound to a mixture of glycoproteins secreted by the stomach and salivary glands. These glycoproteins, called R-binders (or haptocorrins), protect vitamin B12 from chemical denaturation in the stomach. The stomach’s parietal cells, which secrete hydrochloric acid, also secrete a glycoprotein called intrinsic factor. Intrinsic factor binds vitamin B12 and ultimately enables its active absorption. Although the formation of the vitamin B12 – intrinsic factor complex was initially thought to happen in the stomach, it is now clear that this is not the case. At an acidic pH the affinity of the intrinsic factor for vitamin B12 is low whereas its affinity for the R-binders is high. When the contents of the stomach enter the duodenum, the R-binders become partly digested by the pancreatic proteases, which causes them to release their vitamin B12. Because the pH in the duodenum is more neutral than that in the stomach, the intrinsic factor has a high binding affinity to vitamin B12, and it quickly binds the vitamin as it is released from the R-binders. The vitamin B12-intrinsic factor complex then proceeds to the lower end of the small intestine, where it is absorbed by phagocytosis by specific ileal receptors (1, 2).