The regulation of fetal mineral and bone metabolism is quite different from the well-known system in children and adults. The placenta actively transports calcium, phosphorus, and magnesium from the maternal circulation, and is capable of extracting sufficient mineral even when maternal blood levels are reduced. The fetal kidneys, intestines, and skeleton are not important sources of mineral for the fetus and play comparatively minor roles in mineral metabolism. The fetus maintains serum mineral concentrations at higher values than in the mother and normal adult; these high levels appear necessary for normal mineral accretion to be achieved by the fetal skeleton. Fetal bone development and the regulation of serum minerals are critically dependent upon parathyroid hormone (PTH) and PTH-related protein (PTHrP), but not vitamin D/calcitriol, fibroblast growth factor-23, calcitonin, or the sex steroids. PTH and calcitriol circulate at very low concentrations even though the fetus is quite capable of producing much higher levels in response to maternal hypocalcemia. After birth, mineral and skeletal metabolism rapidly changes. The intestines become the main source of mineral for the neonate, the kidneys reabsorb mineral, and bone turnover contributes mineral to the circulation. This changeover in the regulation of mineral homeostasis is triggered by loss of placental hormones, the mineral infusion, and the onset of breathing. Serum calcium falls and phosphorus rises before gradually reverting to adult values over the subsequent 24-48 hours. The postnatal fall in serum calcium and rise in phosphorus is followed in turn by increasing PTH and then an increase in calcitriol. Intestinal calcium absorption is initially a passive process facilitated by lactose, but later becomes active and calcitriol-dependent. However, calcitriol’s role can be bypassed by increasing the calcium content of the diet, or by parenteral administration of calcium.