Vitamin D in pregnancy and lactation: maternal, fetal, and neonatal outcomes from human and animal studies

Abstract

During pregnancy and lactation, mothers require significant amounts of calcium to pass on to the developing fetus and suckling neonate, respectively. Given the dependence of adult calcium concentrations and bone metabolism on vitamin D, one might anticipate that vitamin D sufficiency would be even more critical during pregnancy and lactation. However, maternal adaptations during pregnancy and lactation and fetal adaptations provide the necessary calcium relatively independently of vitamin D status. It is the vitamin D-deficient or insufficient neonate who is at risk of problems, including hypocalcemia and rickets. Due to poor penetrance of vitamin D and 25-hydroxyvitamin D [25(OH)D] into milk, exclusively breastfed infants are at higher risk of vitamin D deficiency than are formula-fed infants. Dosing recommendations for women during pregnancy and lactation might be best directed toward ensuring that the neonate is vitamin D-sufficient and that this sufficiency is maintained during infancy and beyond. A dose of vitamin D that provides 25(OH)D sufficiency in the mother during pregnancy should provide normal cord blood concentrations of 25(OH)D. Research has shown that during lactation, supplements administered directly to the infant can easily achieve vitamin D sufficiency; the mother needs much higher doses (100 g or 4000 IU per day) to achieve adultnormal 25(OH)D concentrations in her exclusively breastfed infant. In addition, the relation (if any) of vitamin D insufficiency in the fetus or neonate to long-term nonskeletal outcomes such as type 1 diabetes and other chronic diseases needs to be investigated. Am J Clin Nutr 2008;88(suppl):520S-8S.

Human skin pigmentation, migration and disease susceptibility

“…region (and colour zone in figure 1 expressing the vitamin D receptor [48] The importance of vitamin D was first recognized because of its association with bone health and the development of rickets in children. Nutritional rickets is a short-latency disease that results from impaired bone mineralization in children because of calcium malabsorption arising from vitamin D deficiency or, less frequently, from calcium or phosphate deficiency [49,50]. Rickets became more common after industrialization led to increases in UVB-quenching pollutants [51,52], but is not a disease of industrialization.…”

Vitamin D and Human Pregnancy

“…As a consequence, many maternal adaptations are observed in pregnancy that supports the need for this extra calcium. In contrast to the situation in adult, the regulation of mineral homeostasis during pregnancy appears to be less dependent on vitamin D 33 .…”

“…Calcium is actively transported across the placenta 34,35 and human fetuses typically accrete 21g-30g of calcium by term, and 80% of this is accumulated in the third trimester, indicating a daily transfer requirement of approximately 200mg of calcium 33,36 . To attain the required amount of calcium and regulate the fetal calcium level, the fetus makes use of the placenta, kidneys, bone and intestine.…”

“…This was initially thought to be mediated by 1,25(OH) 2 D, as it is known that serum levels of 1,25(OH) 2 D increase early in pregnancy and peak at twice the non-pregnant range 33,43,[48][49][50][51][52][53] . However, free concentrations of 1,25(OH) 2 D appear to increase only during the third trimester, and the peak in intestinal calcium absorption occurs well before this 54,55 .…”

“…Inadequate accumulation of calcium early in pregnancy may lead to a net loss of maternal skeletal calcium in later pregnancy. Maternal vitamin D deficiency has been found to cause maternal skeletal demineralization by the end of pregnancy 33 . The markers of bone formation and reabsorption in humans indicate that bone turnover is probably low in the first half of pregnancy, but maybe increased in the third trimester.…”