Adequate intake of dietary zinc is necessary for the absorption and utilization of vitamin A. Zinc deficiency is thought to interfere with vitamin A metabolism in several ways:

1. zinc deficiency results in decreased synthesis of retinol binding protein (RBP), which transports retinol through the circulation to tissues (e.g., the retina) and also protects the organism against potential toxicity of retinol;
2. zinc deficiency results in decreased activity of the enzyme that releases retinol from its storage form, retinyl palmitate, in the liver; and
3. zinc is required for the enzyme that converts retinol into retinal

At present, the health consequences of zinc deficiency on vitamin A nutritional status in humans are unclear.

Vitamin A deficiency may worsen iron deficiency anemia. Vitamin A supplementation has beneficial effects on iron deficiency anemia and improves iron nutritional status among children and pregnant women. The combination of supplemental vitamin A and iron seems to reduce anemia more effectively than either supplemental iron or vitamin A alone. Moreover, studies in rats have shown that iron deficiency alters plasma and liver levels of vitamin A.

Several animal studies have shown that liver reserves of vitamin A are depleted by a high dietary intake of protein, while vitamin A increases in non-liver tissues. One explanation for this is that adequate protein is necessary for vitamin A transport. Morever, protein synthesis requires adequate amounts of Vitamin A.

A study revealed that copper deficiency results in higher liver concentrations of vitamin A (retinol) and lower blood levels of vitamin A, suggesting that a copper-deficient diet may cause defective transport of vitamin A from liver to blood.

Excess vitamin A interferes with the absorption of vitamin K, a fat-soluble vitamin necessary for blood clotting.

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