Hypovitaminosis A is a problem in many parts of the developing world.
Beyond the stop-gap measures of capsule distribution and food fortific
ation, increased consumption of accessible sources of vitamin A, speci
fically of the carotenoid provitamin A in yellow, orange, and green pl
ants, has been promoted as the sustainable, long-term solution. Howeve
r, a search of the available literature reveals few examples of human
studies to support the effectiveness of this solution. Evidence from f
eeding studies shows an almost universally poorer uptake of intact car
otenoids from plant sources as opposed to pure, chemical sources. With
notable exceptions, the bioconversion of plant carotenoids to preform
ed vitamin A also seems to be inefficient. Epidemiologic observations
in poor Third World populations and in vegetarians in an industrialize
d nation indicate a relatively greater potency for animal sources of v
itamin A. In developing countries, low fat intakes, intestinal roundwo
rms, recurrent diarrhea, and tropical enteropathy all may contribute t
o reduced utilization of plant provitamin A. The accepted 6:1 equivale
ncy of beta-carotene to preformed vitamin A must be challenged and ree
xamined in the context of dietary plants. The consequences of operatin
g on a miscalculation could be serious indeed for public health progra
ms designed to alleviate and eradicate hypovitaminosis A.