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Infants are at risk for iron deficiency as breast milk or formula is replaced by semisolid foods during weaning. The scope of this article is to briefly review new findings on developmental iron deficiency and the persistence of deficiency effects into adulthood. A lack of sufficient iron intake may significantly delay the development of the central nervous system because of alterations in morphology, neurochemistry, and bioenergics. Depending on the stage of development at the time of iron deficiency, there may be an opportunity to reverse adverse effects, but the success of repletion efforts may be time dependent. The program project on “Brain and Behavior in Early Iron Deficiency” (B. Lozoff, P.I.) undertook preclinical and clinical studies to identify the regions of the brain and behaviors affected, and perhaps irreversibly altered, by early-life iron deficiency. Multiple outcomes are being measured in humans, nonhuman primates, and rodents. Data in monkeys show significant effects on neurodevelopment with dietary iron deficiency. Findings in human infants are consistent with altered myelination and changes in monoamine functioning. Rodent studies show that effects of iron deficiency during gestation and lactation persist despite restoration of iron status at weaning. These cross-species studies indicate a vulnerable period in early development that may result in long-lasting damage. J. Nutr. 137: 524S-530S, 2007.