Iron absorption in adults is regulated by homeostatic mechanisms that decrease absorption when iron status is high. There are few data, however, regarding the existence of a similar homeostatic regulation in infants. We studied 2 groups of human milk-fed infants using 57Fe (given as ferrous sulfate without any milk) and 58Fe (given at the time of a breast-milk feeding) stable isotopes to determine whether healthy infants at risk for iron deficiency would regulate their iron absorption based on their iron status. We studied 20 Peruvian infants at 5–6 mo of age and 18 infants at 9–10 mo of age. We found no effect of infant hemoglobin concentration on iron absorption with 5–6 mo–old infants absorbing 19.2 ± 2.1% and 9- to 10-mo–old infants absorbing 25.8 ± 2.6% of the 57Fe dose. For 58Fe, 5- to 6-mo–old infants absorbed 42.6 ± 5.0% and 9 to 10-mo–old infants absorbed 51.9 ± 10.3%. Following log transformation, iron absorption from 57Fe (r = -0.61, P = < 0.001) and 58Fe (r = -0.61, P = < 0.001) were inversely correlated to serum ferritin (S-Ft). For both the 57Fe and 58Fe doses, infants with S-Ft <12 mg/L (n = 11) had significantly higher iron absorption than those with S-Ft >12 mg/L. We concluded that iron absorption in infants is related to iron status as assessed by serum ferritin but not hemoglobin concentration. Infants with low iron status upregulate iron absorption from breast milk at both 5–6 and 9–10 mo of age.