Veterinary nutritional science has embraced the study of copper for decades, but copper has languished as an orphan among human nutritionists because of the obscurity of clinical copper-deficiency states in man. As medical investigators, we may have gone down a long road, missing the forest for the trees. Indeed, overt copper-deficiency syndromes in humans have been recognized since the 1960s, and the list of contributing factors is expanding. Unwise self-medication with megadoses of zinc, for instance, might produce a mini-epidemic of copper deficiency. Moreover, induced copper deficiency may someday prove to be a legitimate therapeutic intervention in some disease states. But, the influence of subtle differences in dietary intakes of copper on human health may be much more important than frank copper depletion. Moreover, the recognition of disordered copper metabolism simulating a deficiency state--as occurs in Menkes' KHS and in variant Elhers-Danlos syndrome--has important implications. The full description of the relationship that thionein and other intracellular proteins might have in the etiology of these alterations has yet to be written. The elegance of the interplay of biochemical defects, physiological dysfunction, and clinical manifestations in copper metabolism is virtually unmatched in nutritional biology; yet, our present abilities to determine human copper status are limited. Now that it is clear that intracellular redistribution as well as total-body depletion can effect the disruption of copper-dependent functions, a concerted effort to improve status assessment through the use of functional indices should become a high priority. Finally, the pursuit of the bases of copper's involvement in host defenses, antiotoxidant protection and carbohydrate metabolism--functions in which clear links to established mammalian cuproenzyme are at present elusive--should provide exciting substrate for investigators for years to come.