Copper deficiency and excess have been recognized as potential health problems for infants and children worldwide. Clinical manifestations of copper deficiency and excess are well characterized but the precise sequence by which high copper intake interacts with genetic control systems, leading to liver damage in infants, is unknown. The possibility that genetic mutations or epigenetic factors related to the functional development of copper homeostasis, could make otherwise normal infants on normal copper intake more susceptible to copper toxicity has been an issue of concern. In January 2001 a group of pediatricians and researchers interested in this area met at Tegernsee, Bavaria, Germany, to reviewing the state of knowledge on the topic. They addressed six main issues: 1) The relevance of copper deficit and excess as health problems. 2) The appropriate biomarkers to identify and characterize copper status 3) The genetic variability in copper metabolism 4) The mechanisms of whole body copper homeostasis in early life and their changes with age 5) The development of experimental and animal models to address research questions on copper homeostasis in infants. 6) The safe upper and lower limits of copper intake/exposure from water and food. We present here the highlights of the discussions and the main conclusions of the meeting.