Zinc balance is maintained by a homeostatic mechanism which regulates its absorption and excretion. When dietary zinc intake is low, zinc absorption can increase to nearly 100%, while urinary and faecal excretion fall to low levels. This adaptation allows zinc balance to be maintained even with low Zn intakes. Since a wide range of foods including meat, fish, shellfish, nuts, seeds, legumes and whole-grain cereals are rich in zinc, deficiency does not occur in people who consume a balanced diet and have normal gastrointestinal function. Vegetarians may be theoretically more likely to become zinc deficient because zinc from plant sources is less bioavailable due to the presence of phytate which inhibits its absorption. However in practice plasma zinc levels are similar in vegetarians and nonvegetarians, and adverse effects from zinc deficiency have not been demonstrated in vegetarians in developed countries. In a survey of risk of zinc deficiency at the population level, New Zealand is classified as a low risk country .
Zinc deficiency will only occur with a prolonged and severe decrease in zinc intake (as in malnutrition or eating disorders), in malabsorption, or if zinc losses are increased (e.g. chronic diarrhoea, chelation therapy). Patients on total parenteral nutrition (TPN) or who have had gastric bypass surgery are at risk and require zinc supplements . Zinc deficiency is associated with stunted growth, decreased immunity, skin lesions and poor wound healing .
While zinc deficiency is uncommon and only occurs in malabsorption and malnutrition, mildly low plasma zinc levels are common.
As plasma zinc is 98% protein-bound, zinc levels are low in hypoproteinaemic (low albumin) patients, without indicating zinc deficiency. In addition, the proteins to which zinc is bound (albumin and alpha-2 macroglobulin) are negative acute phase reactants: their concentrations decrease in response to inflammation. For this reason low plasma zinc is a non-specific finding in a variety of disease states including infections, trauma, cancer, and haematological disorders.
An increase in the copper/zinc ratio has been reported in many disease states. This increase in the copper/zinc ratio in many diseases occurs because plasma copper has a positive acute phase response (increases) and plasma zinc has a negative acute phase response (decreases) in inflammatory states. The copper/zinc ratio is a non-specific marker of disease and has no diagnostic value.
The belief that biochemical imbalances including trace metals are the cause of autism, and that their correction by means of supplements or chelation therapy can be used to treat the disorder, is known as the "biomedical approach" to autism. This approach has been thoroughly discredited, and the measurement of zinc or other trace metals is of no value in the management of patients with autism spectrum disorder [5, 6].
This is a very rare inherited defect in zinc absorption. The features include skin lesions on the hands, feet, face and buttocks, usually appearing in early infancy.
Occupational or environmental exposure is a rare cause of zinc toxicity. Excessive zinc supplementation may cause copper deficiency because zinc and copper compete for absorption.
Zinc levels are mildly low in some patients with depression, but this difference is not diagnostically useful . Inflammation is known to be associated with depression as shown by raised levels of inflammation markers, and this may be the cause of the decreased zinc levels in depression. A causal link between zinc and depression is not supported by convincing evidence. Measurement of plasma zinc has no value in chronic fatigue syndrome [9, 10].
Plasma zinc levels should only be tested in patients at risk for deficiency because of malnutrition, gastrointestinal disease, or for investigating toxic exposure. There is no value in measuring plasma zinc in patients with depression, chronic fatigue syndrome or autism spectrum disorder.
Compiled by: Dr. Stephen du Toit, Health Waikato Laboratory, Hamilton, and Assoc. Prof. James Davidson, Labplus, Auckland City Hospital. August 2010.
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