Vitamin D, the autonomic nervous system, and cardiovascular risk

Cardiovascular disease (CVD) and vitamin D deficiency are extremely prevalent worldwide (Holick 2007; World Health Organization 2011). The potential link between vitamin D deficiency and CVD-related death in both healthy and diseased populations is a growing area of translational research. Historically, the traditional role of vitamin D in maintaining calcium homeostasis and mineral metabolism has been extensively studied (Lieben and Carmeliet 2013). Vitamin D, via its classical genomic transcriptional activity, is known to affect the physiological function of a number of target organs such as the heart, bone, and kidneys (Lieben et al. 2011). Furthermore, as highlighted in a paper published recently in Physiological Resports (Foong et al. 2014), there appears to be a link between vitamin D deficiency and respiratory symptoms in chronic lung disease. In addition, a number of nongenomic, rapid action roles of vitamin D are now known to affect tissue function, which fall outside the traditional role of regulating mineral metabolism (Gniadecki 1998; Brown et al. 1999; Norman et al. 2002; Haussler et al. 2011). While calcium and phosphate have long been regarded as the major players in the interactions observed between mineral metabolism dysfunction and CVDrelated deaths, (Peacock 2010; Bolland et al. 2011; Brini et al. 2013), these newer nongenomic roles outside of the traditional target organs suggest that vitamin D itself may have intrinsic actions outside the realm of mineral metabolism (Gniadecki 1998; Brown et al. 1999; Norman et al. 2002; Haussler et al. 2011).