Vitamin D is produced in the skin when ultraviolet B light catalyses the conversion of 7-dehydrocholesterol to previtamin D3, which is spontaneously converted to vitamin D3 (cholecalciferol) through the action of heat. Once formed vitamin D binds to the vitamin D binding protein, a transport protein that allows the fat soluble vitamin D to be transported in the aqueous environment of the blood. Vitamin D is transported to cells where it acts on the vitamin D receptor in the nucleus of cells. The structure, transport and cellular uptake of vitamin D is similar to the steroid hormones because vitamin D is a steroid hormone. Its ability to be produced in the skin, and the lack of a requirement of a dietary source precludes vitamin D from vitamin status. For decades vitamin D was associated only with the traditional diseases of osteomalacia and rickets. However, the realisation that vitamin D plays a wide ranging steroid hormonal role in mammals has opened a pandora’s box of diseases that respond to vitamin D therapy.
Being a hormone, it is not surprising that the maternal vitamin D status has been shown to influence the growth and development of the foetus. The placenta contains enzymes capable of converting 25-hydroxyvitamin D (a metabolite of cholecalciferol) to its biologically active 1,25-dihydroxycholecalciferol form, and it is known that poor maternal vitamin D status can cause foetal growth restriction. One reason for restricted growth might be restrictions to the foetal vasculature under conditions of poor maternal vitamin D status. For example, one group of researchers measured maternal serum 25-hydroxyvitamin D over 26 weeks of gestation and monitored pathologies in the infants born to these mothers1. The results showed a correlation between the vitamin D status of the maternal serum and the vascular pathology of the infant but this association was only present in boys. A maternal 25-hydroxyvitamin D concentrations of over 80 nmol/L was associated with a 49 % lower risk of pathology compared to a serum level of less than 50 nmol/L.
It is interesting that the association between maternal vitamin D status and infant vasculature was present only in boys. This suggest that the sex hormones in the foetus are able to modify the effects of vitamin D. In female offspring, and association between vascular pathology and a reduced birthweight was observed, if the maternal 25-hydroxyvitamin D level was below 30 nmol/L, but this association was not present if the maternal serum 25-hydroxyvitamin D level was above 30 nmol/L or if the offspring was male. Restricted growth in a foetus is generally considered detrimental because it exposes the individual to a lifelong increased risk of disease and increased risk of mortality. A number of vitamins and minerals are firmly established as growth restrictors in foetal growth, and the role played by vitamin D may also be significant. The CYP27B1 enzyme which converts 25-hydroxyvitamin D to 1,25-dihydroxyvitamin D is present in the placenta, which suggests that the latter plays an important role in foetal growth. One such role may be that of vascular development.
Dr Robert Barrington’s Nutritional Recommendation: The wealth of information linking poor vitamin D status to ill health is growing at a rapid rate. Optimising vitamin D status is not only important for an individual’s health but for that of any future offspring.
RdB
