In pigs, iron deficiency anemia (IDA) is the most prevalent deficiency disorder during the early postnatal period frequently developing into a critical illness. Meanwhile, in humans, only low-birth-weight infants, including premature infants are especially susceptible to developing IDA. In both human and pig neonates, the initial cause of IDA is low birth iron stores. In piglets this shortage of stored iron results mainly from genetic selection over the past few decades for large litter size and high birth weight. In consequence, pregnant sows cannot provide sufficient amount of iron to the increasing number of developing fetuses. Supplementation with iron is a common practice for the treatment of IDA in piglets. For decades, the preferred procedure for delivering iron supplements during early life stages has been through the intramuscular injection of large amount of iron dextran. However, this relatively simple therapy, which in general, efficiently corrects IDA, may generate toxic effects, and by inducing hepcidin expression, may decrease bioavailability of supplemental iron. New iron supplements are considered now with the aim to combine improvement of hematological status, blunting hepcidin expression, and minimizing toxicity of the administered iron. We propose that iron-deficient piglets constitute a convenient animal model for performing pre-clinical studies with iron supplements.