Concerns that consumption of whole cow milk (WCM) by older infants may result in excessive gastrointestinal blood loss and subsequent iron deficiency led us to perform a prospective, randomized study in 104 infants. Infants were assigned to receive WCM beginning at 6 months or one of three formulas beginning at 4–6 months of age and followed until 12 months of age. Gastrointestinal blood loss was similar for all groups, as determined by both qualitative (Hemoccult II) and quantitative testing (HemoQuant). There was no association between concentration of fecal hemoglobin and volume of WCM consumed or iron status by 12 months of age. Of eight infants (seven WCM, one formula) who became iron-depleted, none had excessive fecal hemoglobin excretion. When pooled and analyzed regardless of feeding group, fecal hemoglobin increased with age and was greater at 11 and 12 months than at younger ages. We conclude that although infants fed WCM are at increased risk of developing iron depletion, the iron insufficiency is not due to gastrointestinal blood loss. We further conclude, based on our sample of normal infants age 4–12 months, that fecal hemoglobin concentrations of 0.5–0.8 mg/g stool correspond to the upper limits of normal, values much lower than in adults.We undertook a study of hepatic concentrations of vitamin K (vitamin K1 or phylloquinone, vitamin K1-epoxide, and menaquinones) in 18 infants, ages 1–8 days, with or without vitamin K1 supplementation. The infants who had no supplementation had a total hepatic storage ranging between 0.1 and 0.9 μg. Also, hepatic storage of phylloquinone was poor (< 1μg) when compared with daily requirements. Moreover, we did not detect any menaquinone in the livers of these infants in our study. The prophylaxis applied to the other infants was very efficient. Hepatic vitamin K1 concentrations, obtained <24 h after administration, were very high (62.8–93.5 μg/g). Vitamin K1-epoxide concentrations were high, which proved the efficiency of the vitamin K cycle. In contrast, the decrease in vitamin K1 concentrations was also very rapid, since the median value after 48 h was 8.4 (μg/g and only 2.9μg /g 5 days after administration. However, hepatic total storage after 5 days in one infant with vitamin K1 supplementation was much higher (112 μg) than in infants who had not received supplementation. In conclusion, hepatic phylloquinone storage at birth was poor (<1 μg). The newborn infant might be in a situation of potential deficiency. After prophylactic oral administration of phylloquinone, uptake by the liver was quite satisfactory, but concentrations dropped quickly. However, phylloquinone hepatic storage remained elevated (112 μg) after 5 days.