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Copper intake of 2-3 mg / day is usually suggested for adults. Copper is actively transported through the intestinal wall, carried in a special protein, ceruloplasmin, in the blood, and stored in the liver. Vitamin C and zinc in excess interfere with copper availability. Copper deficiency results anemia, that may be indistinguishable from iron deficiency. Copper plays a role in iron absorption and mobilization. Copper, deficiency impairs the formation of connective tissue proteins, collagen and elastin. Weak bone (osteoporosis) and defective arterial walls are the more obvious manifestations.
In animals, copper deficiency may result in dramatic death from rupture of a major blood vessel, or the heart itself. Cooper intake should be carefully evaluated in patients with cardiovascular disease. Copper deficiency also contributes to increased blood cholesterol. Deficiency also results in growth disturbances of the brain. Infants with blocked copper utilization develop severe brain dysfunction due to defective myelinization of nerve fibers (Menke's disease).
Irving et al reported a case of sideroblastic anemia and neutropenia in a 19-year-old woman who was fed by gastrojejunal tube and received supplemental vitamin E, vitamin C, riboflavin and zinc (50 mg twice daily). Her hemoglobin level dropped to 49 g/L with associated severe neutropenia. The peripheral blood film revealed macrocytic anemia. Her zinc intake was estimated at 120 mg per day over a five year period. Zinc toxicity was confirmed by elevated serum zinc, low serum copper and low serum ceruloplasmin levels.
Irving stated: “Copper deficiency secondary to zinc excess arises from an indirect interaction between the 2 metals in the intestine. When exposed to excess dietary zinc, the absorptive duodenal cells upregulate metallothionein, an intracellular metal-binding ligand. Metallothionein binds both zinc and copper ions but has a much greater affinity for copper. Dietary copper that is bound to metallothionein becomes sequestered within the duodenal enterocytes, which are sloughed into the intestinal lumen. Increased oral copper intake is ineffective in restoring the zinc–copper balance in the presence of excess dietary zinc, as the induced metallothionein continues to intercept the copper and reduce its absorption.”
Conversely, copper accumulates in the brains of children with Wilson's disease and produces mental retardation.
Copper may be supplied in drinking water from leaching of copper water pipes, especially if the drinking water is acidic. Copper supplementation levels are best calculated when the copper content of the water supply is known, since copper excess may be as damaging as copper deficiency. It is clear that supplementation of zinc and vitamin C should not be attempted without an awareness of copper requirements. Zinc supplements in the range of 5-15 mg per day may be desirable. Check the copper content of your water before taking a copper supplement. If water copper is low or absent then add 1 mg copper per day.
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