Abstract
Iron is an essential micronutrient and is important not only in carrying oxygen but also to the catalytic activity of a variety of enzymes. In the fetus, it is vital to the synthesis of hemoglobin and in brain development. Iron deficiency (ID) anemia in pregnancy is a common problem, even in high-income country settings. Around 50% of pregnant women worldwide are anemic, with at least half of this burden due to ID. Iron supplements are widely recommended and used during pregnancy globally. However, the evidence on the extent of benefit they contribute to the offspring's health is not well established, and their routine use has its side effects and drawbacks. Dietary iron intake is difficult to assess accurately and it is unlikely to be sufficient to meet the demands of pregnancy if women start with inadequate body iron stores at conception. Evidence from experimental animal models suggests that maternal ID during pregnancy is associated with fetal growth restriction, as well as offspring obesity and high blood pressure later in life. The possible biological mechanisms for this observed association may be due to ID-induced changes in placental structure and function, enzyme expression, nutrient absorption, and fetal organ development. However, such evidence is limited in human studies. Prenatal ID in experimental animal models also adversely affected the developing brain structures, neurotransmitter systems, and myelination resulting in acute brain dysfunction during the period of deficiency and persistence of various postnatal neurobehavioral abnormalities as well as persistent dysregulation of some genes into adult life after iron repletion pointing to the possibility of gene expression changes. The evidence from human population studies is limited and heterogeneous and more research is needed in the future, investigating the effects of ID in pregnancy on future offspring health outcomes.
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