Identification, prevention and treatment of iron deficiency during the first 1000 days

Abstract

Iron deficiency is a global problem across the life course, but infants and their mothers are especially vulnerable to both the development and the consequences of iron deficiency. Maternal iron deficiency during pregnancy can predispose offspring to the development of iron deficiency during infancy, with potentially lifelong sequelae. This review explores iron status throughout these "first 1000 days" from pregnancy through two years of age, covering the role of iron and the epidemiology of iron deficiency, as well as its consequences, identification, interventions and remaining research gaps.

Figure 1

Simplified representation of iron metabolism. Adapted from [12]. Iron is absorbed in the intestine, with non-heme iron being imported by divalent metal transporter 1 (DMT1). Ferrous iron is reduced to ferric iron and then exported by ferroportin. Within an aqueous solution, iron is stored within transferrin. Transferrin-bound iron is imported with the help of the transferrin receptor into the liver, heart and other storage areas, where it is stored within ferritin. Hepcidin, produced by the liver, helps to regulate iron metabolism by binding to ferroportin and, thus, inhibiting iron export. Within the bone marrow, iron is incorporated into hemoglobin for incorporation into erythrocytes. Macrophages recycle iron from erythrocytes, largely in the spleen. There is no mechanism for iron excretion by the kidneys or liver, though small amounts are lost via feces. Menstruation, pregnancy and lactation result in iron loss in women.