Iron is an essential micronutrient, integral to understanding the relationship between nutrition, inflammation, and immunity. It is also vital for promoting health during pregnancy and in infants. Our research has shown that obesity, stress, and illness, in addition to poor nutrition, compromise the placental transfer of maternal iron to the fetus. This reduction reflects iron sequestration, similar to the universal response to bacterial infection. Decreased iron absorption and transfer of systemic iron to storage is an acute phase reaction induced by IL-6 and hepcidin. Leukocytes are also critically involved in postnatal iron homeostasis. Macrophages scavenge iron from dying red blood cells in young infants, and recycle it to the liver. Therefore, we investigated if delayed cord clamping, expanding neonatal blood volume by 15–50mL, reduced the risk for iron deficiency. In addition, stable iron isotopes, administered to the gravid female before term, were employed to track iron recycling and conservation. Finally, we tested a novel remedial strategy using the storage form of iron, ferritin, for treating anemia, instead of free iron. The goal was to reduce iron bioavailability to pathogenic bacteria in the gut. We demonstrated that consumable yeast, genetically modified to express human ferritin, provides an effective therapeutic modality for the prevalent anemia of infancy. This finding has worldwide significance for population health, especially in regions where iron-responsive enteric pathogens and malaria, are endemic.
