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There were 3 presentations at the symposium, one by Ahmed El-Sohemy of the Department of Nutritional Sciences of the University of Toronto; one by George J. Brewer, Emeritus Professor, Department o...

In this review, we provide evidence based on our studies, for zinc deficiency and cell mediated immune disorders, and the effects of protein and zinc status on clinical morbidities in patients with head and neck cancer. We investigated subjects with newly diagnosed squamous cell carcinoma of the oral cavity, oropharynx, larynx, and hypopharynx. Patients with metastatic disease and with severe co-morbidity were excluded. Nutritional assessment included dietary history, body composition, and prognostic nutritional index (PNI) determination. Zinc status was determined by zinc assay in plasma, lymphocytes, and granulocytes. Pretreatment zinc status and nutritional status were correlated with clinical outcomes in 47 patients. Assessment of immune functions included production of TH1 and TH2 cytokines, T cell subpopulations and cutaneous delayed hypersensitivity reaction to common antigens. At baseline approximately 50% of our subjects were zinc-deficient based on cellular zinc criteria and had decreased production of TH1 cytokines but not TH2 cytokines, decreased NK cell lytic activity and decreased proportion of CD4+ CD45RA+ cells in the peripheral blood. The tumor size and overall stage of the disease correlated with baseline zinc status but not with PNI, alcohol intake, or smoking. Zinc deficiency was associated with increased unplanned hospitalizations. The disease-free interval was highest for the group which had both zinc sufficient and nutrition sufficient status. Zinc deficiency and cell mediated immune dysfunctions were frequently present in patients with head and neck cancer when seen initially. Zinc deficiency resulted in an imbalance of TH1 and TH2 functions. Zinc deficiency was associated with increased tumor size, overall stage of the cancer and increased unplanned hospitalizations. These observations have broad implications in the management of patients with head and neck cancer.

Objective: Leptin, the product of the ob gene, plays a key role in a feedback loop that maintains energy balance by signaling the state of energy stores to the brain and by influencing the regulation of appetite and energy metabolism. Zinc also plays an important role in appetite regulation. Thus, we evaluated the relationship between zinc status and the leptin system in humans.Methods: We studied nine healthy men with marginal zinc deficiency, induced by dietary means, before and after zinc supplementation.Results: Zinc restriction decreased leptin levels while zinc supplementation of zinc-depleted subjects increased circulating leptin levels. In addition, zinc supplementation increased IL-2 and TNF-α production that could be responsible for the observed increase in leptin concentrations.Conclusions: Zinc may influence serum leptin levels, possibly by increasing the production of IL-2 and TNF-α.

Although a great deal of attention has been given to protein and calorie malnutrition in patients with head and neck cancer, zinc status has not been assessed properly in such patients in the past.In this study we characterized zinc status by cellular zinc criteria and assessed several measures of protein and calorie malnutrition in patients with head and neck cancer. We determined prognostic nutritional index (PNI) based on serum albumin, serum transferrin, triceps skin fold measures, and delayed hypersensitivity, as proposed by Buzby et al. In this study, the baseline zinc status and PNI of 60 head and neck cancer patients were correlated with the tumor size and overall stage of the disease.Our results showed that the tumor size and overall stage correlated significantly to zinc status whereas no correlation was seen with PNI, alcohol intake, or smoking in our study subjects.We conclude that zinc status is a better indicator of tumor burden and stage of the disease in head and neck cancer patients than ...

One of the important issues in nutrition today is whether healthy people should take any vitamin and/or mineral supplements, and if so, which ones and how much? Americans spend billions of dollars ...

Zinc deficiency in humans is widespread and is more prevalent in areas where the population subsists on cereal proteins. Conditioned deficiency of zinc is seen in many diseased states. A mild deficiency of zinc in pregnancy is associated with increased maternal morbidity, abnormal taste sensation, prolonged gestation, inefficient labor, atonic bleeding, and increased risks to the fetus. Among the urban poor in the US, a marginal zinc intake during pregnancy was associated with increased risk of preterm and very preterm delivery. Factors responsible for zinc deficiency in premature infants include high fecal losses of zinc, low body stores of zinc at birth, and increased zinc requirement during rapid growth. Zinc supplemented infants demonstrated improved linear growth velocity and maximum motor development scores. Marginal and moderate growth impairment in children as a consequence of inadequate zinc intake has been reported from many developed and developing countries. In one study from Japan, 21 prepubertal children were diagnosed to have zinc deficiency. The caloric intake, growth velocity, serum zinc, and plasma insulin-like growth factor-1 increased significantly in the zinc supplemented group. The clinical manifestations of zinc deficiency include growth retardation, hypogonadism in males, neurosensory disorders, cell-mediated immunological dysfunctions, and skin changes. Approximately 300 enzymes are known to require zinc for their activities. Zinc is required for DNA synthesis, cell division and protein synthesis. Several hundreds of zinc containing nucleoproteins are probably involved in gene expression of various proteins. A deficiency of zinc also affects proliferation and maturity of lymphocytes adversely.

Since the discovery in the early sixties that zinc deficiency occurred in humans [1], it is now clear that the deficiency of zinc is very widespread throughout the world and may even be as prevalen...

Zinc status in human subjects is assessed by measurement of zinc in plasma, erythrocytes, neutrophils, lymphocytes, and hair. Available data indicate that zinc in neutrophils and the assay of activity of alkaline phosphatase in neutrophils may be the best tools for the diagnosis of zinc deficiency. Measurement of zinc in the plasma is simple and readily available in many laboratories. Plasma zinc is useful provided the plasma is unhemolyzed and conditions, such as infections, acute stress, myocardial infarction and intravascular hemolysis, are ruled out. Inasmuch as hair and erythrocytes turn over slowly, their zinc levels do not reflect recent changes with respect to zinc status. Other useful parameters for assessment of zinc status include metabolic balance studies, urinary zinc excretion. Cu:Zn ratio, zinc tolerance test, and measurement of activities of zinc-dependent enzymes in suitable biological samples.

During the past two decades, essentiality of zinc for man has been established. Deficiency of zinc in man attributable to nutritional factors and several diseased states has been recognized. High phytate content of cereal proteins decreases availability of zinc; thus the prevalence of zinc deficiency is likely to be high in the population subsisting mainly on cereal proteins. Zinc deficiency has been noted to occur in patients with malabsorption syndrome, chronic renal disease, cirrhosis of the liver, sickle cell disease, AE (acrodermatitis enteropathica), and other chronically debilitating diseases. Growth retardation, male hypogonadism, skin changes, poor appetite, mental lethargy, and delayed wound healing are some of the manifestations of chronically zinc-deficient human subjects. In severely zinc-deficient patients, dermatological manifestations, diarrhea, alopecia, mental disturbances, and intercurrent infections predominate. If untreated, the condition becomes fatal. Zinc deficiency affects testicular functions adversely in man and animals. This effect of zinc is at the end-organ level. It appears that zinc is essential for spermatogenesis. Zinc is involved in many biochemical functions. Several zinc metalloenzymes have been recognized in the past decade. Zinc is required for each step of cell cycle in microorganisms and is essential for DNA synthesis. The effect of zinc on protein synthesis may be attributable to its vital role in nucleic acid metabolism. The activities of many zinc-dependent enzymes have been shown to be affected adversely in zinc-deficient tissues.(ABSTRACT TRUNCATED AT 250 WORDS)

Growth retardation is seen in experimental animals as a result of severe dietary restriction of several essential trace elements. However, in humans, the effect of zinc deficiency is most pronounced. Growth failure and hypogonadism in males, related to a deficiency of zinc, have been recognized in many developing countries. A mild deficiency of zinc, affecting growth and development in children and adolescents, has been reported from developed countries as well. Zinc deficiency in humans may manifest as severe, moderate, or mild. The manifestations of severe zinc deficiency include bullous pustular dermatitis, alopecia, diarrhea, emotional disorder, weight loss, intercurrent infections due to cell-mediated immune dysfunctions, hypogonadism in males, neurosensory disorders, and problems with healing of ulcers. This condition can be fatal. A moderate level of zinc deficiency has been reported in a variety of conditions. Clinical manifestations include growth retardation and male hypogonadism in adolescence, rough skin, poor appetite, mental lethargy, delayed wound healing, cell-mediated immune dysfunctions, and abnormal neurosensory changes. A mild level of zinc deficiency may manifest with decreased serum testosterone level and oligospermia in males, decreased lean body mass, hyper-ammonemia, neurosensory changes, anergy, decreased serum thymulin activity, and decreased IL-2 activity. Although the clinical aspects of severe and moderate levels of zinc deficiency are well known, the recognition of mild levels of zinc deficiency has been difficult. Currently plasmas zinc appears to be the most widely used parameter for assessment of human zinc status, and it is known to be decreased in cases of severe and moderate deficiency of zinc.(ABSTRACT TRUNCATED AT 250 WORDS)

The effect of 1,25(OH)2D3 on zinc absorption was indirectly determined in hemodialysis patients using the oral zinc tolerance test. The increment in plasma zinc and the area under the curve following an oral zinc load of 25 mg were studied in seven patients, before and after 6 weeks of therapy with 1 microgram/day of 1,25(OH)2D3 [Rocaltrol(R)]. Before therapy, fasting plasma zinc, 2 hour plasma zinc, and the area under the curve (AUC) were subnormal (hemodialysis patients vs normals: 96 +/- 2 vs 105 +/- 3 micrograms/dl, p less than 0.05, 161 +/- 8 vs 222 +/- 16 micrograms/dl, p less than 0.025, and 188 +/- 25 vs 302 +/- 33 micrograms hr/dl, p less than 0.025, respectively). Following Rocaltrol, serum calcium level increased (8.9 +/- .12 to 9.8 +/- .4 mg/dl, p less than 0.05), parathyroid hormone levels decreased (20.4 +/- 8.9 to 13.6 +/- 7.2 ng/ml, p less than 0.05), but there was no significant change in fasting plasma zinc, 2 hour plasma zinc, or AUC (89 +/- 3 micrograms/dl, 149 micrograms/dl, and 176 +/- 18 micrograms hr/dl, respectively). These results suggest that short-term 1,25(OH)2D3 therapy had no significant impact on zinc absorption or plasma zinc level in uremics.