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The Vitamin C/Ferritin/Iron Connection Vitamin C (ascorbic acid) is an essential chemical our body needs to function normally. It is necessary for the body to make connective tissue. It is also essential for the absorption of iron from our foods and plays a role in iron metabolism. Deficiency of ascorbic acid leads to scurvy, which is characterized by easy bruising, mucous membrane bleeding and anemia. It has been known since the 1960's that vitamin C is intimately involved in iron metabolism when it was noted that when given to treat scurvy, vitamin C increased serum iron levels. In 1962, desferrioxamine (Desferal) began to be used to treat iron overload in thalassemic children in Great Britain. Not long after Desferal was introduced, it was found that vitamin C could double the amount of iron removed during its administration. By 1979 optimum doses of Desferal and vitamin C were still not known. During trials it was discovered that the administration of intramuscular desferrioxamine with daily doses of vitamin C (500 mg per day) was followed by a decrease in cardiac function. Function was returned to normal when the vitamin C was discontinued. Since these trials, lower doses of vitamin C (100 to 250 mg) have been given to individuals who use Desferal, and it has been recommended that the vitamin C be given after Desferal administration has begun. The above experience and knowledge lead to the rational use of vitamin C during chelation therapy. When Desferal is given in low doses, such as with daily intramuscular injections, high doses of vitamin C makes available more iron from the tissues than the medication can chelate. There has been no cardiac dysfunction reported when vitamin C and Desferal are used appropriately. Vitamin C should never be taken in large doses by individuals who have large total body iron burden. In the past there has been speculation that ascorbic acid administration could lead to a redistribution of iron from the spleen (the reticuloendothelial cells) to the liver (parenchymal cells). This has not been substantiated by studies in humans, though it may occur in some animals during treatment for ascorbic acid deficiency (guinea pigs). <page 1> <page 2> References: 'Ascorbic Acid and Ferritin Catabolism,' Nutr Rev, 47:218-219, 1989. Cohen A, Cohen IJ, Schwartz E. 'Scruvy and altered iron stores in thalassemia major.' NEJM, 304:158-160, 1981. Hoffman, KE, Yanelli K, Bridges KR. 'Ascorbic acid and iron metabolism: alterations in lysosomal function.' Am J Clin Nutr, 54:1188S-92S, 1991. Nienhuis AW. 'Vitamin C and Iron.' NEJM, 304:170-71, 1981. |
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