Zinc deficiency

a relationship often overlooked in clinical practice.

Research published in the American Journal of Clinical Nutrition demonstrates that zinc deficiency impairs the synthesis of retinol-binding protein , the transport mechanism that carries vitamin A from hepatic stores to peripheral tissues.

Without sufficient zinc, vitamin A remains sequestered in the liver despite apparently adequate dietary intake, effectively creating a functional vitamin A deficiency.

Key takeaways Zinc is essential for synthesizing retinol-binding protein, the primary transport mechanism for vitamin A. Zinc deficiency impairs this synthesis regardless of dietary vitamin A intake, The Recommended Dietary Allowance for adult zinc is 11 mg per day.

For vitamin A, 700-900 mg Retinol Activity Equivalents per day.

But these must be interpreted in the context of each other.

Second, zinc is required for the hepatic enzymes that mobilize stored retinal esters from the liver.

Third, the World Health Organization's assessment of micronutrient interactions notes that zinc facilitates the conversion of dietary carotenoids, provitamin A compounds, into active retinol, a process involving multiple zinc-dependent enzymatic steps.