<P> The human body's rate of iron absorption appears to respond to a variety of interdependent factors, including total iron stores, the extent to which the bone marrow is producing new red blood cells, the concentration of hemoglobin in the blood, and the oxygen content of the blood . The body also absorbs less iron during times of inflammation, in order to deprive bacteria of iron . Recent discoveries demonstrate that hepcidin regulation of ferroportin is responsible for the syndrome of anemia of chronic disease . </P> <P> Most of the iron in the body is hoarded and recycled by the reticuloendothelial system, which breaks down aged red blood cells . In contrast to iron uptake and recycling, there is no physiologic regulatory mechanism for excreting iron . People lose a small but steady amount by gastrointestinal blood loss, sweating and by shedding cells of the skin and the mucosal lining of the gastrointestinal tract . The total amount of loss for healthy people in the developed world amounts to an estimated average of 6994100000000000000 ♠ 1 mg a day for men, and 1.5--2 mg a day for women with regular menstrual periods . People with gastrointestinal parasitic infections, more commonly found in developing countries, often lose more . Those who cannot regulate absorption well enough get disorders of iron overload . In these diseases, the toxicity of iron starts overwhelming the body's ability to bind and store it . </P> <P> Most cell types take up iron primarily through receptor - mediated endocytosis via transferrin receptor 1 (TFR1), transferrin receptor 2 (TFR2) and GAPDH . TFR1 has a 30-fold higher affinity for transferrin - bound iron than TFR2 and thus is the main player in this process . The higher order multifunctional glycolytic enzyme glyceraldehyde - 3 - phosphate dehydrogenase (GAPDH) also acts as a transferrin receptor . Transferrin - bound ferric iron is recognized by these transferrin receptors, triggering a conformational change that causes endocytosis . Iron then enters the cytoplasm from the endosome via importer DMT1 after being reduced to its ferrous state by a STEAP family reductase . </P> <P> Alternatively, iron can enter the cell directly via plasma membrane divalent cation importers such as DMT1 and ZIP14 (Zrt - Irt - like protein 14). Again, iron enters the cytoplasm in the ferrous state after being reduced in the extracellular space by a reductase such as STEAP2, STEAP3 (in erythrocytes), Dcytb (in enterocytes) and SDR2 . </P>

Where does the iron in your blood come from