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HEMOCHROMATOSIS

Hemochromatosis is the excessive buildup of iron in the body, especially noted in the liver. It appears to me that hemochromatosis is the result of a copper deficiency.

 

While there appears to be a hereditary form of the disease, there may also be a dietary form. While many people think that there is some genetic damage which causes the hereditary form, I think that it is most likely a genetic adaptation which enables the offspring of persons eating a high copper diet to increase copper excretion to maintain normal levels. When these offspring then have a diet low in copper, they develop a copper deficiency and this can lead to hemochromatosis for those eating a high iron diet (high red meat or fruit diet).

It is my belief that persons with high iron from hemochromatosis should supplement with copper and reduce their high iron intake to get these two minerals balanced. Increased zinc might also be appropriate in individuals with adequate copper, since zinc will reduce iron levels also.

The following study indicates that excessive vitamin C intake may be a contributing factor in hemochromatosis. Vitamin C increases iron absorption while at the same time it seems to have an effect in decreasing copper. This copper decreasing effect could be the direct result of increasing iron absorption or it could be an independent effect.

Int J Vitam Nutr Res 1999 Mar;69(2):67-82

High-dose vitamin C: a risk for persons with high iron stores?

Gerster H.

Vitamin Research Department, F. Hoffmann-La Roche Ltd, Basel, Switzerland.

The contribution of vitamin C (ascorbic acid) to the prevention of iron deficiency anemia by promoting the absorption of dietary non-heme iron-especially in persons with low iron stores--is well established. But the question has been raised whether high-dose intakes of vitamin C might unduly enhance the absorption of dietary iron in persons with high iron stores or in patients with iron overload, possibly increasing the potential risk of iron toxicity. Extensive studies have shown that overall the uptake and storage of iron in humans is efficiently controlled by a network of regulatory mechanisms. Even high vitamin C intakes do not cause iron imbalance in healthy persons and probably in persons who are heterozygous for hemochromatosis. The uptake, renal tubular reabsorption and storage of vitamin C itself are also strictly limited after high-dose intake so that no excessive plasma and tissue concentrations of vitamin C are produced. The effect of high-dose vitamin C on iron absorption in patients with iron overload due to homozygous hemochromatosis has not been studied. Of special importance is the early identification of hemochromatosis patients, which is assisted by the newly developed PCR test for hereditary hemochromatosis. Specific treatment consists of regular phlebotomy and possibly iron-chelating therapy. These patients should moreover avoid any possibility of facilitated absorption of iron and need to limit their intake of iron. Patients with beta-thalassemia major and sickle cell anemia who suffer from iron overload due to regular blood transfusions or excessive destruction of red blood cells need specialized medical treatment with iron chelators and should also control their intake of iron. The serum of patients with pathological iron overload can contain non-transferrin-bound iron inducing lipid peroxidation with subsequent consumption of antioxidants such as vitamin E and vitamin C. The role of iron in coronary heart disease and cancer is controversial. Early suggestions that moderately elevated iron stores are associated with an increased risk of CHD have not been confirmed by later studies. In vitro, ascorbic acid can act as a prooxidant in the presence of transition metals such as iron or copper, but in the living organism its major functions are as an antioxidant. High intakes of vitamin C have thus not been found to increase oxidative damage in humans. Accordingly, the risk of CHD or cancer is not elevated. On the contrary, most studies have shown that diets rich in vitamin C are inversely related to the incidence of these diseases.