The occurrence of zinc deficiency in man remained unsuspected until the 1960s. Since then, however, our understanding of the clinical importance of human zinc deficiency has grown rapidly. Zinc depletion has been demonstrated or suggested to be responsible for a variety of clinical features, ranging from minor aberrations of normal growth patterns and subtle impairments of taste perception to life-threatening disease states. The latter have been observed most frequently as a result of an inherited defect in zinc absorption and from feeding intravenously without adding zinc to the infusates. Notable clinical features of severe zinc deficiency states include a florid acro-orificial rash, behavioural changes, poor appetite, severe disturbance of normal growth and development, impaired reproductive performance, and frequent infections associated with abnormalities of the immune system. In general, the biochemical correlates of these clinical features remain poorly defined. While the clinical and laboratory diagnosis of severe zinc deficiency states is quite straightforward, existing techniques are inadequate for the detection of sub-optimal zinc nutrition. This difficulty presents a major challenge as there is evidence that mild or moderate zinc deficiency states are quite common in certain population groups. Though there is reason for particular concern about the zinc status of some socially deprived groups, inadequate zinc intake is also a potential problem in more affluent population groups. The occurrence of zinc deficiency is frequently associated with dietary factors that have an unfavourable effect on zinc absorption, for example phytate, and with a variety of special circumstances including premature delivery. There is evidence that the absorption of zinc from human milk is especially favourable. There is an outstanding need for further research to achieve a clearer understanding of the origins, incidence and effects of human zinc deficiency.