Vitamin A Deficiency and Postnatal Asthma

Researchers have long wondered what makes some people more susceptible than others to developing asthma symptoms when exposed to the same stimulus. A new study suggests that the presence of structural and functional abnormalities in the lungs due to vitamin A deficiency during development is an important and under appreciated factor in this susceptibility.

Previous studies had shown that retinoic acid (RA)—the active metabolite of vitamin A—is essential for normal lung development. Until now, however, little was known about the impact of prenatal RA deficiency on postnatal airway function.

The researchers used a mouse model in which they could control when and in what amount vitamin A would reach the developing fetus through maternal diet. They timed the vitamin A deficiency to the middle of gestation, coinciding with the period of formation of the airway tree in the fetus. Fetuses that were deprived of vitamin A were found to have excess smooth muscle in the airways, compared with controls. 

In a subsequent experiment, the mice were again deprived of vitamin A during the same developmental stage, but returned to a normal diet after that stage and until adulthood. When the animals reached adulthood, pulmonary function tests showed that their lungs were clearly not normal. When the mice were challenged with methacholine, a chemical that causes the airway to contract, their response was significantly more severe than that of controls. 

The findings underscore the importance of sufficient vitamin A in the diet, which remains a significant challenge in developing countries. The study also has potential clinical implications in the developed world.