Barbara A. Underwood2
Institute of Medicine, National Academies, 2101 Constitution Ave., NW, Washington, D.C. 20418
2To whom correspondence should be addressed. E-mail: e-mail: email@example.com.
Visual symptoms (night blindness) of vitamin A deficiency (VAD) were among the earliest diet-related deficiencies documented. Knowledge of vitamin A chemistry, metabolism and deficiency consequences accrued rapidly during the first eight decades of the 20th century. A series of disorders were described in animals, including impaired growth, reproduction, epithelial integrity, and disease resistance that were relieved by consumption of both animal and plant sources of the vitamin.
Identification of the intestinal beta-carotene cleavage enzyme in the laboratory of James Allen Olson was seminal to understanding the mechanism for formation of vitamin A from ingested carotenoids. WHO’s 1990 estimate of about 40 million children annually with clinical eye signs of VAD was revised upward to 140–250 million at risk of vitamin A deficiency disorders (VADD) when epidemiological and clinical trials demonstrated morbidity and mortality risk even in the absence of ocular signs. Alternative methods for VAD status assessment and more reliable analytical techniques were developed, several in Dr. Olson’s laboratory. The last decade has seen global progress in VADD control by expanding distribution of medicinal supplements, fortification of foods and dietary diversification through horticulture and education programs.
Experience shows that achievements gained through narrowly focused interventions are fragile and vulnerable to national political and economic instability. Contextually relevant, community-centered strategies that improve household food and nutrition security and self-reliance are critical to sustaining international efforts to control the VADD “pox.”