Your body needs vitamin D to maintain proper levels of calcium and phosphorus, which help build your baby's bones and teeth. A vitamin D deficiency during pregnancy can cause growth retardation and skeletal deformities. It may also have an impact on birth weight.
If you're lacking vitamin D during pregnancy, your baby may be short on the vitamin at birth. This can put her at risk for rickets (which can lead to fractures and deformity), abnormal bone growth, and delayed physical development. And the results can be long lasting: Researchers believe that a vitamin D deficiency during pregnancy can affect bone development and immune function from birth through adulthood.
The importance of vitamin D in pregnancy and childhood
Lack of vitamin D in childhood is associated with rickets, characterized by aches and pains, muscular weakness and bone deformity. This is commonest in infancy, and was thought to have been eradicated in the west in the 20th century. However, with the migtermration of dark-skinned populations to the Northern 
hemisphere, there is now a resurgence of this condition. The higher levels of cutaneous melatonin in dark-skinned peoples mean that the levels of sunshine available in Northern hemisphere countries are often not sufficient to allow synthesis of adequate levels of vitamin D in the skin. In the absence of vitamin D supplementation, growth may be affected permanently. In children not showing signs of rickets, there is now evidence from randomized placebo-controlled trials that supplementation with vitamin D may lead to increased accrual of bone mineral over 1 year. It is not known whether these improvements are maintained longer term.
It is becoming apparent that vitamin D may play a crucial and persisting role in bone development well before it is implicated in childhood rickets. During pregnancy, the fetus accrues bone mineral most rapidly in the last trimester and then after delivery the childs skeleton grows until a peak is reached in 3rd or 4th decade. Acquisition of bone mineral appears to track such that a child remains in the same ranking relative to peers throughout life. Recent work has suggested that the magnitude of peak bone mass reached is as important a determinant of osteoporosis risk in older age as is rate of subsequent bone loss. Poor childhood growth is associated with lower bone mineral and greater risk of hip fracture in later life. Observational data suggest that vitamin D may be implicated in mechanisms underlying these epidemiological observations.
A retrospective study of 8 year old children demonstrated higher bone mineral density at the femoral neck in those who had been supplemented with vitamin D in the first year of life compared with those who had not. This was one of the first suggestions that modulation of bone health in early life might have long lasting effects, and recent work has demonstrated the importance of adequate exposure to vitamin D at an even earlier point in the life-course: the intrauterine period. In a white-Caucasian mother-offspring cohort in Southampton, in which 18% mothers had levels of 25(OH)-vitamin D less than 10 ng/ml, we found that low levels of maternal vitamin D in pregnancy were associated with children having lower bone mineral density at nine years old. Similar results were found in a later cohort, the Southampton Womens Survey (SWS), with babies at birth. Thus there is epidemiological evidence that low maternal vitamin D status may have a persisting influence on bone development in the offspring. The initial cohort study also suggested a role for placental calcium transport: to try to understand this further, we measured levels of gene expression of active placental calcium transporters in SWS deliveries and related this to bone mineral in the offspring at birth. We found that greater expression of an active calcium transporter, PMCA3, was positively associated the size and calcium content of the babys skeleton at birth. Animal studies suggest that some PMCA transporters may be regulated by vitamin D, although there are no data in humans.
