CHAMPAIGN, Ill. -- Efforts to battle vitamin A deficiency have been thrown a curve: Carotenoids that promote vitamin A production -- and are often consumed in mass quantities when available -- are not sufficiently stored and converted to vitamin A, according to new research.
Vitamin A deficiency causes blindness and has been linked with poor growth in children, immunity problems and death. The World Health Organization estimates that 2.8 million preschool children are at risk of blindness, and the health of 251 million people is compromised.
"In many countries, either because of lack of access or because of religious preference, vitamin A is not in the diet or is consumed in very small amounts," said John Erdman, director of the University of Illinois Division of Nutritional Sciences. "You only get pre-formed vitamin A from animal foods such as liver, dairy products and fish oil. Millions of people don't get these highly bioavailable sources."
In the absence of animal-based sources, vitamin A supplements or an infusion of carotenoid-rich vegetables can be substituted. Some carotenoids, particularly beta carotene, act as precursors to vitamin A. The carotenoids convert into retinol, which is the active form of the vitamin.
The new research, involving two studies, was performed on Mongolian gerbils and reported in the July issue of the Journal of Nutrition. Implications of the work for humans is not completely clear. However, since gerbils convert beta carotene to vitamin A at a ratio similar to humans (a discovery reported earlier this year in the same journal by Erdman and colleagues), the new findings are worthy of a closer look, Erdman said. A followup study with the same animal model begins this month.
"We found that stored carotenoids from a previously consumed diet were not converted to vitamin A when the vitamin was removed from the diet," Erdman said. "This is the first scientific evidence that questions the utility of this vitamin A precursor."
There was a rapid loss of beta carotene from the two pools in the gerbils' liver. One pool was lost slowly; the second, which included the most beta carotene, was lost rapidly. High levels of beta carotene absorbed in tissues failed to improve vitamin A status, and feeding pre-formed vitamin A without beta carotene failed to slow the loss of stores of previously fed beta carotene.
"Without continual feeding of beta carotene in the diet, most of the tissue beta carotene is eventually depleted," Erdman said. "If stored or accumulated beta carotene is not converted to vitamin A when initially absorbed, beta carotene provides no vitamin A value.
"A popular public health approach in some countries with rampant vitamin A deficiency is to promote consumption of fruits and vegetables high in beta carotene as they are available. It was assumed this would offer protection for much of the year. This approach will have to be revisited."
Coauthors were Erdman, technician Christine M. Lee and former graduate student Angela J. Thatcher. Funding came from the National Research Initiative of the U.S. Department of Agriculture.