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Calcium metabolism in pregnancy is a complex process involving calcium, phosphorus, vitamin D, parathyroid hormone (PTH), and calcitonin (CT). Calcium absorption is enhanced in pregnancy, and increased storage in the maternal skeleton probably occurs as well. Adequate amounts are provided by the current Recommended Dietary Allowance of 1,200 mg. daily which can be met readily by natural foods, specifically milk. If supplemental calcium is given, a nonphosphate salt is probably advisable, since some evidence suggests that excessive phosphate intake may be related to leg cramps in pregnancy. Vitamin D is necessary for optimal calcium utilization in pregnancy, although the possibility of fetal toxicity with overdosage has been suggested. From a review of available information with respect to maternal-perinatal calcium interrelationships, I propose the following hypothesis: While total maternal serum calcium declines during pregnancy because of the physiologic hypoalbuminemia, the level of ionic calcium remains constant, in part, at least, because of increasing maternal PTH output. The placenta plays a primary role in fetal calcium metabolism by transporting calcium ions from the mother to the fetus against a concentration gradient. Relatively high fetal ionic calcium levels cause suppression of PTH and stimulation of CT in the fetus, facilitating growth of the fetal skeleton. With sudden loss of the placental source of calcium at birth, the newborn infant becomes functionally hypoparathyroid and/or hypercalcitonemic, and the serum calcium level declines until 3 to 4 days of life when PTH rises and CT falls with a resultant slight rise in calcium.