Increased dietary iron intake

A. Role of Iron Iron is the essential metaDic component of heme, the molecule responsible for the bulk of oxygen transport in the blood. Although most of the iron in the body is present in hemoglobin, an important fraction is bound to transferrin, a transport protein, and to ferritin, a storage protein. Deficiency of iron occurs most often in women because of menstmal blood loss and in vegetarians or malnourished individuals because of inadequate dietary iron intake. Children and pregnant women have increased requirements for iron. 

Homeostatic mechanisms are very important for the prevention of accumulation of excess Fe that is believed to generate oxidative stress by catalysis of variety of chemical reactions involving free radicals, which could result in cell damage (Pietrangelo, 2002 Puntarulo, 2005). Excess Fe accumulation may promote cancer and increase the cardiovascular risk (Martmez-Navarrete et ah, 2002). Iron overload can be observed in some cases including an excessive dietary iron intake, inherited diseases, for example, idiopathic hemochromatosis, congenital atransferrinemia, or the medical treatment of thalassemia (Fontecave and Pierre, 1993). 

Absorption/Dlstrlbutlon - The average dietary intake of iron is 12 to 20 mg/day for males and 8 to 15 mg/day for females however, only about 10% of this iron is absorbed (1 to 2 mg/day) in individuals with adequate iron stores. Absorption is enhanced (20% to 30%) when storage iron is depleted or when erythropoiesis occurs at an increased rate. Iron is primarily absorbed from the duodenum and jejunum. The ferrous salt form is absorbed 3 times more readily than the ferric form. The common ferrous salts (ie, sulfate, gluconate, fumarate) are absorbed almost on a milligram-for-milligram basis but differ in the content of elemental iron. Sustained-release... 

At normal levels of iron intake, absorption requires uptake from the intestinal lumen by the mucosa and transfer from the mucosa to the portal blood. Both events are inversely affected by the state of body iron stores. In iron deficiency states, nonferrous metals such as cobalt and manganese, which have an ionic radius similar to that of iron and form octahedral complexes with six-coordinate covalent bonds, also are absorbed at an increased rate. Oral administration of a large dose of iron reduces (or temporarily inhibits) the absorption of a second dose of iron by the absorptive enterocytes even in the presence of systemic iron deficiency. The mechanism of mucosal block, which resists acquiring additional iron by the en-teroeytes with high amounts of intracellular iron, is not yet understood. It probably involves set points established in the enterocytes for iron recently consumed in the diet (dietary regulator). 

Nonpharmacologic therapy for anemia of CKD includes maintaining adequate dietary intake of iron. A relatively small amount of dietary iron, approximately 1 to 2 mg (or approximately 10%), is absorbed each day, primarily in the duodenum. While there is some debate as to whether GI absorption of iron is significantly altered in patients with severe CKD, it is clear that oral intake from dietary sources alone is generally not sufficient to meet the increased iron requirements that are necessitated by the initiation of erythropoietic therapy. ... 

Interaction between iron and manganese occurs only between nonheme iron and manganese. Davis et al. (1992a) demonstrated that increasing dietary intakes of nonheme iron, but not heme iron, depressed biomarkers of manganese status, i.e., serum manganese concentrations and lymphocyte manganese-dependent superoxide dismutase activity. 

Iron-deficiency anemia can be caused by inadequate dietary intake, inadequate GI absorption, increased iron demand (e.g., pregnancy), blood loss, and chronic diseases. 

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