ZINC INTAKE AND RESISTANCE TO H1N1 INFLUENZA

Abstract

Stevenson, et al1 summarized the needs of children at risk for H1N1 influenza and noted the poverty of 14.5 million child recipients of free school meals every day in the United States. Such children are at risk for dietary zinc deficiency, a condition likely to afflict at least 1 in 5 persons worldwide,2 in part because of low intakes of foods derived from animal flesh, especially red meat (the richest common dietary source of zinc), and high intakes of whole grain cereal products and legumes rich in phytate and other indigestible zinc-binding ligands.3 Zinc deficiency is relevant to H1N1 influenza because it decreases cell-mediated immunity.4 At the practical level, zinc treatment has been found to be efficacious for a variety of infections4; in low-income Mexican Americans aged 6 to 7 years who are not visibly ill but have mild zinc deficiency (normal plasma zinc), a randomized trial showed that the administration of zinc and other micronutrients together were significantly more efficacious for cell-mediated immunity than was administration of other micronutrients alone.5 The presence of zinc in the diet affects various aspects of cell-mediated immunity, including expression of interleukin-2 and interferon-γ.4 Interleukin-2 stimulates generation of natural killer and cytolytic T cells that kill viruses, bacteria, and tumor cells. Interferon-γ and interleukin-2 together activate macrophage monocytes that kill parasites. Zinc also suppresses ICAM-1, which serves as a receptor for viruses, and inhibits the protease from HIV type 1.6 Pertinent to bacterial pneumonia–complicating influenza, a 1-year study of 420 nursing home patients who daily were administered 50% of the United States Department of Agriculture Recommended Daily Allowance for vitamins and minerals found that participants with plasma concentrations of zinc greater than 70 μg/dL had a significantly lower risk of pneumonia requiring antibiotics than did participants with plasma zinc levels of less than 70 μg/dL.7 Zinc treatment is likely to be most efficacious when administered with a mixture of other micronutrients.8 In nature, micronutrient deficiencies seldom occur alone, and micronutrients act in concert. For example, the methionine cycle–transsulfuration pathway requires folate, riboflavin, pyridoxine, cobalamine, choline/betaine, methionine, and zinc for several reactions.9 Food fortification is an effective method for prevention of nutrient deficiencies. Groups at high risk for zinc deficiency could be specifically targeted by the introduction of inexpensive, culturally acceptable fortified foods into their diets, thus avoiding treatment of groups at low risk. We believe it would be appropriate to use such an approach to ascertain if zinc given with other micronutrients is at least as efficacious for preventing H1N1 influenza as zinc administered with oral rehydration fluids is for treatment of diarrhea.10