Zinc

Essential Knowledge in Nutrition

 

 

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Zinc is a co-factor for at least 70 critical enzyme pathways. Deficiency can therefore result in diverse, profound problems; impaired synthesis of DNA, RNA, and protein underlie the clinical manifestations. Zinc deficiency may be more common than is diagnosed.

The RDA for zinc is 5 mg/day for infants, 10 mg for children and 15 mg for adults. Zinc requirements increase in pregnant women to 20 mg/day. Zinc, deficiency.

Any child with growth retardation, poor hair growth, impaired immunity or skin problems should be considered for zinc deficiency, particularly if there are gastrointestinal absorption problems. Zinc absorption is impaired by phytates in cereal grains, and by the concurrent ingestion of other minerals, especially calcium, iron, cadium and copper. The best body zinc evaluation is the measurement of zinc concentrations in white blood cells. Hair zinc levels may be increased when zinc is markedly deficient.

Zinc deficiency produces: impaired senses of taste and smell, slow wound healing, white spots in the fingernails, night blindness (interacts with Vitamin A deficiency), low sperm count, hair loss, behavior or sleep problems; mental lethargy, impaired immune function, cyclic feeding and loss of appetite, dermatitis.

Zinc is depleted by the following drugs: Penicillamine, steroids, ethanol, diuretics, and oral contraceptives. Zinc is often promoted to "enhance immunity". It is an essential mineral for immune function. Perhaps because of its immune promoting role, deficiencies in zinc may be helpful in autoimmune diseases. Zinc concentrations are referred to copper, and the minerals tend to have a reciprocal relationship. A low tissue concentration of copper may result from zinc supplements. A suggested optimal zinc to copper ratio is 8:1.

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. It is not clear that these events in human pathology are related to copper deficiency, but suggests that 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  [i] reported a case of severe 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 toxicitywas 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 upregulatemetallothionein, an intracellular metal-binding ligand. Metallothioneinbinds both zinc and copper ions but has a much greater affinityfor copper. Dietary copper that is bound to metallothioneinbecomes sequestered within the duodenal enterocytes, which aresloughed into the intestinal lumen. Increased oral copperintake is ineffective in restoring the zinc–copper balancein the presence of excess dietary zinc, as the induced metallothioneincontinues 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.


 

[i]  Julie A. Irving, Andre Mattman, Gillian Lockitch, Kevin Farrell and Louis D. Wadsworth. A case of reversible cytopenias associated with excessive zinc supplementation. CMAJ • July 22, 2003; 169 (2)