Vitamin A in Nutritional Anemia

Vitamin A deficiency (VAD) affects ~30% of preschoolers and 15% of pregnant women in low- and middle-income countries. Known to cause xerophthalmia and increase risk of mortality in children, clinical and experimental studies have also long revealed disturbed hematopoiesis and an anemia of vitamin A deficiency (VAD) that responds to vitamin A repletion, irrespective of iron sufficiency. VAD and anemia are common and often coexist in undernourished populations. In children and pregnant women, hemoglobin (Hb) concentration has been shown to be 0.2–0.8 g/L higher for each 1 μg per deciliter increase in serum retinol, underlying an increased risk of anemia in VAD versus vitamin A adequate individuals. Vitamin A interventions for varying durations in anemic and at least mildly VAD populations have found Hb to increase by 2–10 g/L in children, and 3–24 g/L in women of reproductive age, over controls. While the metabolic effects of vitamin A on iron metabolism remain under-researched, available evidence suggests that vitamin A may affect hemoglobin concentration by regulating (a) storage, mobilization, and release of tissue iron into circulation, (b) erythropoiesis via effects on cell differentiation, (c) sequestration and release of tissue iron in response to infection, or (d) mechanisms of iron absorption. Disruption of any of these pathways due to VAD can cause a preventable anemia, offering an often unrecognized, additional public health benefit of assuring an adequate vitamin A intake and status in nutritionally at-risk populations.