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Clinical Studies (Return to Clinical
Studies page)
IRON IS ESSENTIAL FOR
OXYGEN TRANSPORT IN BLOOD
Koury MJ, Ponka P (2004). New
insights into erythropoiesis: the roles of folate, vitamin B12, and iron. Annu Rev Nutr. 24:105-31.
Erythropoiesis is the process
in which new erythrocytes are produced. These new erythrocytes replace the oldest erythrocytes
(normally about one percent) that are phagocytosed and destroyed each day. Folate, vitamin B12,
and iron have crucial roles in erythropoiesis. Erythroblasts require folate and vitamin B12 for
proliferation during their differentiation. Deficiency of folate or vitamin B12 inhibits purine
and thymidylate syntheses, impairs DNA synthesis, and causes erythroblast apoptosis, resulting
in anemia from ineffective erythropoiesis. Erythroblasts require large amounts of iron for
hemoglobin synthesis. Large amounts of iron are recycled daily with hemoglobin breakdown from
destroyed old erythrocytes. Many recently identified proteins are involved in absorption,
storage, and cellular export of nonheme iron and in erythroblast uptake and utilization of iron.
Erythroblast heme levels regulate uptake of iron and globin synthesis such that iron deficiency
causes anemia by retarded production rates with smaller, less hemoglobinized
erythrocytes.
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Newhouse IJ, Clement DB.
(1988). Iron status in athletes. An update. Sports
Med. 5(6):337-52.
As more studies are done on
the iron status of athletes, the significance of apparent iron deficiency remains controversial.
Do observed changes in iron status in athletes indicate an actual iron deficiency or a
physiological response to exercise? Iron replacement would clearly be indicated if an iron
deficiency was present but would not be necessary or effective if the observed changes were
simply a physiological response. There is agreement that serum ferritin and haemoglobin decrease
with some exercise conditions and that some indicators of haemolysis, such as serum haptoglobin
and bilirubin, change in response to exercise. Expansion of plasma volume and the shift of iron
storage from bone marrow to the liver could support the claim that the apparent reduced iron
status parameters occurring with exercise are misleading. Countering this concept are studies in
athletes which demonstrate dietary iron intake deficiencies and blood loss in the
gastrointestinal and urinary tract. Iron deficiency is common in the general population,
particularly in women. Therefore, continued monitoring of iron status in athletes appears
justified in the face of present knowledge. Replacement therapy, when iron deficiency is
apparent, is recommended.
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