Zinc

BACKGROUND

Zinc is a component of various enzymes that help maintain structural integrity of proteins and regulate gene expression. Zinc metalloenzymes include ribonucleic acid polymerases, alcohol dehydrogenase, carbonic anhydrase and alkaline phosphatase. The biological function of zinc can be catalytic, structural or regulatory. More than 85% of total body zinc is found in skeletal muscle and bone (King & Keen 1999).

Zinc is widely distributed in foods. Meats, fish and poultry are the major contributors to the diet but cereals and dairy foods also contribute substantial amounts. The presence of zinc in foods as a complex rather than as free ions affects its bioavailability. The environment within the gastrointestinal tract, which can be affected by other dietary constituents, markedly influences the solubility and absorptive efficiency of zinc (Cousins 1989, Lonnerdal 1989). The amount of protein in the diet is a factor contributing to the efficiency of zinc absorption as zinc binds to protein. Small changes in protein digestion may produce significant changes in zinc absorption (Sandstrom & Lonnerdal 1989). The markedly greater bioavailability of zinc from breast milk than from cow's milk is an example of how the lower protein digestibility of cow's milk influences zinc absorption (Roth & Kirchgessner 1985). In general, zinc absorption from a diet high in animal protein will be greater than from a diet rich in plant derived proteins (King & Keen 1999). The requirement for dietary zinc may be as much as 50% greater for vegetarians, particularly strict vegetarians whose major staples are grains and legumes and whose dietary phytate:zinc ratio exceeds 15:1.

Dietary intake of iron at levels found in some supplements can decrease zinc absorption, which is of particular concern in the management of pregnancy and lactation. High intakes of calcium have been shown to have a negative effect on zinc absorption in animal experiments, but human data are equivocal with calcium phosphate decreasing zinc absorption (Wood & Zheng 1997) and calcium as citrate-malate complex having no effect (McKenna et al 1997). Current data suggest that consumption of calcium-rich diets does not have a major effect on zinc absorption at an adequate intake level. There is also some evidence of potential interrelationship of zinc with copper and folate, but studies are limited. Regulation of zinc metabolism is achieved through a balance of absorption and secretion of reserves and involves adaptive mechanisms related to dietary zinc intake.

Zinc depletion in humans results in reduced endogenous zinc loss and increased efficiency of intestinal zinc absorption. While plasma zinc is only 1% of the body's total, its concentration is tightly regulated and is generally not affected by mild deficiency. Situations of stress, acute trauma and infection can lead to lower plasma zinc. Mild deficiency can result in impaired growth velocity, suboptimal pregnancy outcomes and impaired immune responses. Severe deficiency can result not only in growth impairment but also alopecia, diarrhoea, delayed sexual development and impotency, eye and skin lesions and impaired appetite.

Assessment of requirements is based on estimates of the minimal amount of absorbed zinc necessary to match total daily excretion of endogenous zinc (FNB:IOM 2001). Estimates are made using a factorial approach that involves calculation of both intestinal and non-intestinal losses (via the kidney, skin, semen and menstruation). Although urinary zinc losses decrease markedly with severe deficiency (Baer & King 1984), across a dietary intake range of 4–25 mg/day, urinary zinc (and non-intestinal losses in general) appears to be largely independent of dietary intake. Intestinal losses, however, correlate strongly to absorbed zinc.

To determine the dietary zinc requirement for a given age/gender group, it is necessary to define the relationship between absorption and intestinal losses and adjust by a constant for the non-intestinal losses in order to calculate the minimum quantity of absorbed zinc necessary to offset total endogenous losses. The factorial calculations used are based on metabolic/tracer studies in which participants are fed diets from which the bioavailability of zinc is likely to be representative of typical diets in Australia and New Zealand.