The phosphorus supply of children and adults is adequate, and usually in excess. Therefore, it is surprising that in breast-fed infants phosphorus intake is very low. This is very rare among mammals. In infants three pathophysiological mechanisms argue in favour of a low, but adequate phosphorus intake in the presence of a balanced ratio of calcium to phosphorus. A low intestinal phosphorus concentration is an essential condition of an acid pH of the faeces, inhibiting the growth of potentially pathogenic germs. Owing to the characteristic renal physiology of the newborn, a small metabolic phosphorus surplus results in a high serum phosphorus level, a well-known risk factor for several disorders, e.g. hypocalcaemic tetany. During infections, impairment of intestinal calcium but not of phosphorus absorption results in an increased phosphorus and renal net acid excretion. Considering the low renal capacity for acid excretion in newborns, a high intake of calcium and phosphorus is a risk factor for the development of metabolic acidosis. It is thought that all three pathophysiologic mechanisms were effective in the biochemical evolution of humans, selecting women with a low phosphorus milk and infants with a constant high intestinal absorption rate of phosphorus.