| Abstract: | For the past 50 years laboratory animals have been used to ascertain the metabolic bases for signs of zinc deficiency such as sharply reduced food intake, severe dermatitis, slow wound healing, delayed sexual development and function, reduced immunocompetence, severe teratogenic abnormalities, and abnormal metabolism of carbohydrate, lipid, and protein. Current evidence indicates that many of these symptoms may be consequences of inhibition of early steps in nucleic acid metabolism that lead to problems with cellular replication and growth and also that zinc plays an important role in membrane structure and function. Bioavailability of zinc to experimental animals was early shown to be reduced by plant protein diets and to be further reduced by feeding excess calcium. Current evidence indicates phytic acid in plant proteins to be a major inhibitor of zinc absorption, although food-processing methods can either increase or decrease zinc bioavailability. The inhibitory effect of phytic acid is very dependent on dietary calcium in association with phytate and zinc. Usual calcium intakes by humans are much below those demonstrated in animals to cause phytate inhibition of dietary zinc availability. |
