Vitamin D insufficiency and skeletal development in utero

Abstract

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)