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Letters to the Editor |
Center for Studies of Sensory Impairment, Aging and Metabolism (CESSIAM) Guatemala City 01011 Guatemala E-mail: cessiam{at}tikal.net.gt
Center for Human Nutrition Faculty of Medicine University of Chile Santiago Chile
Department of Human Nutrition University of Otago Dunedin New Zealand
Dear Sir:
The recent article by Kikafunda et al (1) raises several issues about oral zinc supplementation in free-living populations. In general, such an intervention might 1) determine whether zinc deficiency is extant in a population, 2) determine whether zinc is a limiting factor in growth, 3) determine to what extent zinc nutriture is related to neurophysiologic performance, and 4) investigate the antiinfective properties of zinc supplementation, or fulfill any combination of these motives. It appears that the study by Kikafunda et al embodied at least 3 of these.
Sandstead (2), in his landmark paper published in 1973, stated that whether a condition or abnormality was related to zinc deficits was best gauged by how the condition or abnormality responded (improved) to the administration of oral zinc. Several investigators, including ourselves, have followed this suggestion with oral zinc supplementation of free-living populations. Indeed, the Uganda-based researchers commented on our previous study in Guatemalan schoolchildren (3) and the study by Bates et al (4) in Gambian infants as examples of previous studies in which protracted administration of oral zinc in a randomized, placebo-controlled design led to changes in body composition but not to any increase in linear growth. That more data on zinc supplementation and body composition are not available is not because of a proven lack of effect, but rather because researchers have not looked at this association.
The critical issue, recognized by Kikafunda et al (1), is whether zinc, in the single-nutrient experimentation used, is or is not the first-limiting nutrient. Kikafunda et al found a weight-gain response in the school with the better-off student body, commenting: "The children from the school with the highest socioeconomic status, and therefore a better nutritional background, responded significantly in weight gain to zinc supplementation whereas the children from the poorer schools did not.... This indicated that zinc was the limiting nutrient in the nutrition of the children with relatively better nutritional status, whereas those with poorer nutritional status were deficient in other nutrients that limited the response in zinc supplementation." They note a feature of our study in Guatemalan schoolchildren (3), namely that it began with a pretreatment phase with supplementation of essential micronutrients (excluding zinc) so as to better expose zinc as the only remaining deficiency. In none of the other community-based zinc supplementation studies reviewed by Brown et al (5) was the need for the remaining micronutrients covered simultaneously. Perhaps even greater growth would have been seen in some of these studies if concurrent micronutrient deficiencies had not limited the responses. Recently, Sandstead et al (6) conducted a zinc supplementation trial using this approach (ie, zinc, zinc plus micronutrients, and micronutrients alone) in Chinese children. These investigators found that the knee-height increase was significantly greater in the zinc-plus-micronutrients group than in the zinc-alone group.
The comments by Kikafunda et al (1) and the aforementioned considerations suggest that it is likely that different effects will be seen when zinc is given in supplemental doses if an individual 1) is without any micronutrient deficits, 2) is uniquely zinc deficient, or 3) has multiple micronutrient deficiencies. This will lead to heterogeneous responses to zinc in free-living populations because all 3 conditions will likely coexist to different degrees.
So what do we accomplish and what might we provoke in free-living populations when we apply oral zinc as a single nutrient in a prolonged intervention? This becomes even more imposing a question with emerging evidence of the antiinfective potential of zinc in preventing and shortening diarrhea, in combating respiratory infections, and even in reducing mortality in malaria (7). We can reverse zinc deficiency if zinc is the limiting nutrient; if the situation is one of multiple micronutrient deficiencies, however, we may fail to achieve the desired effect and instead create a nutrient imbalance.
There are clearly serious programmatic and policy implications: single-nutrient interventions might be avoided in favor of balanced, multinutrient programs, even when the primary objective is to provide zinc. It is heartening that some of the agencies working to combat zinc deficiency are moving toward a similar conclusion. In this Journal, Alnwick (8) commented on the perspective of the United Nations Children's Fund (UNICEF) that intermittent combined dosing of iron, iodine, vitamin A, vitamin D, riboflavin, folic acid, and zinc is being considered for its feasibility. As more and more single-nutrient intervention research is conducted, it becomes clear that zinc-responsive deficits in body composition are widespread in developing countries. However, how clearly they are revealed in experimental trials, how efficiently they are addressed in public health nutrition, or how well-tolerated will be the chronic administration of oral zinc to prevent childhood infections may depend on the simultaneous redress of coexisting micronutrient deficiencies.
REFERENCES
This article has been cited by other articles:
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  O Muller, M Garenne, P Reitmaier, A B. van Zweeden, B Kouyate, and H Becher Effect of zinc supplementation on growth in West African children: a randomized double-blind placebo-controlled trial in rural Burkina Faso Int. J. Epidemiol., December 1, 2003; 32(6): 1098 - 1102. [Abstract] [Full Text] [PDF]
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 M. Hambidge Human Zinc Deficiency J. Nutr., May 1, 2000; 130(5): 1344S - 1349. [Abstract] [Full Text]
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