Either diminished absorbable dietary iron or excessive loss of body iron can cause iron deficiency. Diminished absorption usually is due to an insufficient intake of dietary iron in an absorbable form. Hemorrhage is the most common cause of excessive loss of body iron, but it can occur with hemoglobinuria from intravascular hemolysis. These are the heme pathway and separate pathways for ferric and ferrous iron. In North America and Europe, one third of dietary iron is heme iron, but two thirds of body iron is derived from dietary myoglobin and hemoglobin.
Examples are phytates, phosphates, tannates, oxalates, and carbonates.
Heme is maintained soluble and available for absorption by globin degradation products produced by pancreatic enzymes. Heme iron and nonheme iron are absorbed into the enterocyte noncompetitively. Heme enters the cell as an intact metalloporphyrin, presumably by a vesicular mechanism. Heme is degraded within the enterocyte by heme oxygenase with release of iron so that it traverses the basolateral cell membrane in competition with nonheme iron to bind transferrin in the plasma. Ferric iron utilizes a different pathway to enter cells than ferrous iron.