Vitamin D insufficiency and skeletal development in utero

Over the last 10 years, our perception of what constitutes normal vitamin D status has undergone a substantial revision. Prior to this, suboptimal vitamin D was defined at a very basic level by the presence or absence of associated bone disease (i.e., rickets in children and osteomalacia in adults). As a consequence, vitamin D deficiency was determined by serum concentrations of 25‐hydroxyvitamin D (25‐OHD) of less than 25 nM (10 ng/mL), and anything higher was “normal.” However, this has changed with the observation that several parameters of calcium homeostasis continue to correlate with serum levels of 25‐OHD up to concentrations as high as approximately 80 nM (32 ng/mL).1, 2 The implication is that optimal vitamin D status is achieved only at 25‐OHD concentrations above this; anything less is suboptimal or “insufficient.” Based on these revised parameters, it has been concluded that vitamin D insufficiency is a global phenomenon, with an estimated 1 billion people worldwide having suboptimal levels of 25‐OHD.3 Some groups appear to be at greater risk of vitamin D insufficiency than others, notably pregnant women.4–8 In a study carried out in Pittsburgh, PA, Bodnar and colleagues showed that 74% to 95% of pregnant black women and 46% to 62% of pregnant white women were vitamin D insufficient.5 Notably, during early pregnancy, almost 45% of the African‐American mothers had 25‐OHD levels that were less than 37.5 nM.5 A key question arising from these epidemiologic data concerns the physiologic impact of vitamin D insufficiency during pregnancy. In the current issue of the Journal, Mahon and colleagues have addressed this through a prospective longitudinal study of pregnant women in which they have characterized the impact of maternal vitamin D status on in utero measures of fetal skeletal development.9