Maternal Mineral and Bone Metabolism During Pregnancy, Lactation, and Post-Weaning Recovery

Abstract

During pregnancy and lactation, female physiology adapts to meet the added nutritional demands of fetuses and neonates. An average full-term fetus contains ϳ30 g calcium, 20 g phosphorus, and 0.8 g magnesium. About 80% of mineral is accreted during the third trimester; calcium transfers at 300-350 mg/day during the final 6 wk. The neonate requires 200 mg calcium daily from milk during the first 6 mo, and 120 mg calcium from milk during the second 6 mo (additional calcium comes from solid foods). Calcium transfers can be more than double and triple these values, respectively, in women who nurse twins and triplets. About 25% of dietary calcium is normally absorbed in healthy adults. Average maternal calcium intakes in American and Canadian women are insufficient to meet the fetal and neonatal calcium requirements if normal efficiency of intestinal calcium absorption is relied upon. However, several adaptations are invoked to meet the fetal and neonatal demands for mineral without requiring increased intakes by the mother. During pregnancy the efficiency of intestinal calcium absorption doubles, whereas during lactation the maternal skeleton is resorbed to provide calcium for milk. This review addresses our current knowledge regarding maternal adaptations in mineral and skeletal homeostasis that occur during pregnancy, lactation, and post-weaning recovery. Also considered are the impacts that these adaptations have on biochemical and hormonal parameters of mineral homeostasis, the consequences for long-term skeletal health, and the presentation and management of disorders of mineral and bone metabolism.

Irreversible Deterioration of Cortical and Trabecular Microstructure Associated With Breastfeeding

“…The newly deposited smaller volume of osteoid undergoes rapid primary mineralisation reaching $80% of its peak mineralisation density within days to weeks but secondary mineralisation, the enlargement of crystals deposited during primary mineralisation takes months if not years to complete so that even after return of menses, a residual deficit in matrix mineralisation density was present. (7,39) Bone loss also occurs by peri-osteocytic osteolysis -focal osteocytic perilacunar resorption of bone is documented during lactation in rodents. (40) After cessation of lactation, periosteocytic lacunar matrix remineralisation may also occur by rapid primary, but slower secondary mineralisation contributing to the persisting deficits in the mean degree of mineralisation of matrix.…”

“…(7,(19)(20)(21)(22)(23)(24)(25)(26)(27)(28) The reasons for the reversibility at the central skeleton are not clear.…”

“…Epidemiological studies report that lactation is neutral or protective against fracture; no long term deleterious effects on fracture risk are reported. (7,41,42) Further studies are needed to establish whether the deterioration in microarchitecture of the appendicular skeleton contributes to fracture risk later in life.…”

“…(4)(5)(6) Breastfeeding is an estrogen-deficient state associated with bone loss. (6)(7)(8)(9) Bone remodeling accelerates and may also become unbalanced. Studies in rodent and other animal models demonstrate that trabeculae perforate, their numbers decrease, and cortical porosity increases.…”

“…(10)(11)(12)(13)(14)(15)(16)(17)(18) This structural deterioration has been reported to be reversible in some animal models. (7,17,18) Bone loss during breastfeeding in humans is reported, but whether the microstructural deterioration is reversible after cessation of breastfeeding in human subjects is uncertain. (19)(20)(21)(22)(23)(24)(25)(26)(27)(28)(29) As trabecular bone loss, trabecular thinning, and perforation proceed rapidly after estrogen deficiency, the resulting bone fragility is attributed to deterioration in trabecular bone.…”