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Zinc in Human Biology pp 281–296Cite as

Mild Zinc Deficiency in Human Subjects

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Part of the book series: ILSI Human Nutrition Reviews ((ILSI HUMAN))

Abstract

The controversies and uncertainties associated with “mild” zinc deficiency in human subjects are as evident today as at any time in the 30-year interval since the possibility that alcoholic cirrhosis may be associated with a secondary zinc deficiency state was first suggested (Vallee et al. 1957). Incidentally, continuing uncertainties about the interrelationship between alcoholic cirrhosis and zinc nutritional status can serve very effectively to illustrate the extraordinary difficulties still encountered by investigators in this field. That profound alterations in zinc metabolism occur in alcoholic liver disease and other hepatic disorders (Hambidge et al. 1987) is not in question. However, whether or not these changes in metabolism are associated with, or lead to, impaired zinc nutriture remains controversial. On the one hand, it has been reported that the characteristic hyperzincuria is not associated with negative zinc balance because of a corresponding increase in zinc absorption from the gastrointestinal tract (Milman et al. 1983). On the other hand, there have been case reports of zinc-responsive “acrodermatitis enteropathica syndromes” with severe hypozincaemia in association with alcoholic cirrhosis (Ilchyshyn and Mendelsohn 1982); these extreme examples of acute, severe zinc deficiency occur only in very special circumstances and are considered to represent indisputable proof of clinically significant zinc deficiency.

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  1. Rowett Research Institute, AB2 9SB, Bucksburn, Aberdeen, Scotland, UK

    Colin F. Mills MSc, PhD, CChem, FRSC, FRSE (Director of Postgraduate Studies) (Director of Postgraduate Studies)

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Hambidge, K.M. (1989). Mild Zinc Deficiency in Human Subjects. In: Mills, C.F. (eds) Zinc in Human Biology. ILSI Human Nutrition Reviews. Springer, London. https://doi.org/10.1007/978-1-4471-3879-2_18

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