Biological Mechanisms That Might Underlie Iron's Effects on Fetal Growth and Preterm Birth

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Abstract
A negative association between anemia and duration of gestation and low birth weight has been reported in the majority of studies, although a causal link remains to be proven. This paper explores potential biological mechanisms that might explain how anemia, iron deficiency or both could cause low birth weight and preterm delivery. The risk factors for preterm delivery and intrauterine growth retardation are quite similar, although relatively little is understood about the influence of maternal nutritional status on risk of preterm delivery. Several potential biological mechanisms were identified through which anemia or iron deficiency could affect pregnancy outcome. Anemia (by causing hypoxia) and iron deficiency (by increasing serum norepinephrine concentrations) can induce maternal and fetal stress, which stimulates the synthesis of corticotropin-releasing hormone (CRH). Elevated CRH concentrations are a major risk factor for preterm labor, pregnancy-induced hypertension and eclampsia, and premature rupture of the membranes. CRH also increases fetal cortisol production, and cortisol may inhibit longitudinal growth of the fetus. An alternative mechanism could be that iron deficiency increases oxidative damage to erythrocytes and the fetoplacental unit. Iron deficiency may also increase the risk of maternal infections, which can stimulate the production of CRH and are a major risk factor for preterm delivery. It would be useful to explore these potential biological mechanisms in randomized, controlled iron supplementation trials in anemic and iron-deficient pregnant women.