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Alpha
Nutrition Health Education
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Calcium, Magnesium and Zinc Supplement
Mineral
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Sodium &
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Osteoporosis
Trace Minerals
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These discussions of
mineral nutrients and nutrition are continued in Nutrition Notes.
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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)
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