It is clearly established that adequate supplies of zinc are essential to the development and maintenance of a healthy immune system and that aging is associated with immune impairment that can be partially repaired with zinc supplementation.
There are many groups in our population at increase risk of at least marginal zinc deficiency. We now know that the elderly may be getting insufficient zinc in their diets.
Another problem related to zinc is macular degeneration. "Because this disorder affect parts of the eyes in which zinc is known to have an important impact on the metabolic function of enzymes crucial in vision, investigators hypothesized that zinc deficiencies might play a role in the disease. to test this idea they constructed a double-blind, placebo-controlled trial involving 151 patients afflicted by this condition. In a 12 to 24 month follow-up they found that the patients given zinc supplements had significantly less visual loss than the group that got placebos. The zinc was given in 100 mg tablets, twice a day with meals. Side effects were minimal." (Sheldon Saul Hendler, Md, Phd, The Doctors’ Vitamin & Mineral Encyclopedia, Simon & Shuster)
The following study provides another cause for concern about adequate zinc levels:
Zinc deficiency may increase arterial oxidative stress
The starting point of this study was the observation that zinc deficiency severely impairs endothelial cell function, an effect reversed by zinc supplementation. To determine how zinc affects cytokine production, the activation of a nuclear transcription factor (NF-kB)was examined in endothelial cell cultures. NF-kB was chosen because this transcription factor activates genes directing the synthesis of proinflammatory cytokines and to increased oxidative stress. Cells deprived of zinc were triggered by tumor necrosis factor (TNF). TNF signals a cascade of events leading to the synthesis of proteins that regulate oxidative stress and promote free radicals. Zinc supplementation reversed the activation by TNF in these cells: zinc inhibited activation of oxidative stress transcription factors and the synthesis of Interleukin 8 and promoted a return to homoeostatic balance.
Comment: Arteries are vulnerable to ongoing oxidative stress due to exposure to oxidizing agents such as drugs and free radicals, including superoxide and lipid peroxyl radicals. Blood contains an elaborate array of antioxidants, including ascorbic acid, uric acid and defensive serum proteins to limit this damage. However, antioxidant defenses are not 100% efficient. Zinc participates in these defenses by serving as a cofactor for the antioxidant enzyme, superoxide dismutase. Other aspects of zinc Metabolism must be involved, since zinc deficiency causes profound oxidative damage to proteins, lipids and DNA. As one example of a nonenzymatic function, zinc is a cell membrane stabilizer. In addition, this paper shows that zinc deficiency seems to regulate cytokine-mediated activation of transcription factors, especially those triggering inflammation and oxidative stress. If zinc deficiency promotes activation of oxidative stress and inflammatory cytokines by endothelial cells, then zinc status may be important in the development of atherosclerosis. Zinc is removed by food processing and subclinical deficiencies are-likely with compromised diets.
Connell P et al. Zinc attenuates tumor necrosis factor-mediated activation of transcription factors in endothelial cells. J Am College Nutr 1997; 16: 41