Zinc status influences several aspects of vitamin A metabolism, including its absorption, transport, and utilization. Two common mechanisms postulated to explain this dependence relate to 1) the regulatory role of zinc in vitamin A transport mediated through protein synthesis, and 2) the oxidative conversion of retinol to retinal that requires the action of a zinc-dependent retinol dehydrogenase enzyme. However, evidence of an effect of zinc intake on vitamin A status from animal experiments is inconclusive, mainly because of the use of inadequate control groups. The higher weight gain of control animals as compared with the zinc-deficient ones in these experiments, even though pair fed, makes it difficult to isolate effects of zinc deficiency per se from those of generalized protein-energy malnutrition. A curvilinear relation has been suggested to describe an effect of plasma zinc on vitamin A transport. In humans, cross-sectional studies have more often than not shown a weak linkage between vitamin A and zinc status. Randomized trials have failed to show a consistent effect of zinc supplementation on vitamin A status. In disease states in which liver function is severely compromised and both zinc and vitamin A metabolism and transport are impaired, serum zinc and vitamin A concentrations tend to be positively correlated. In conclusion, clear evidence of synergy between these 2 micronutrients and its public health significance in humans is lacking. Research should focus on understanding this interaction in the context of coexisting moderate-to-severe zinc and vitamin A deficiencies in the population.