Biological mechanisms that might underlie iron's effects on fetal growth and preterm birth

A negative association between anemia and duration of gestation and low bir th weight has been reported in the majority of studies, although a causal l ink remains to be proven. This paper explores potential biological mechanis ms that might explain how anemia, iron deficiency or both could cause low b irth weight and preterm delivery. The risk factors for preterm delivery and intrauterine growth retardation are quite similar, although relatively lit tle is understood about the influence of maternal nutritional status on ris k of preterm delivery. Several potential biological mechanisms were identif ied through which anemia or iron deficiency could affect pregnancy outcome. Anemia (by causing hypoxia) and iron deficiency (by increasing serum norep inephrine concentrations) can induce maternal and fetal stress, which stimu lates 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 al so increases fetal cortisol production, and cortisol may inhibit longitudin al growth of the fetus. An alternative mechanism could be that iron deficie ncy increases oxidative damage to erythrocytes and the fetoplacental unit. Iron deficiency may also increase the risk of maternal infections, which ca n stimulate the production of CRH and are a major risk factor for preterm d elivery. It would be useful to explore these potential biological mechanism s in randomized, controlled iron supplementation trials in anemic and iron- deficient pregnant women.