A poor
vitamin D status, i.e. low serum levels of
25-hydroxyvitamin D [25(
OH)D], is common in the general population. This finding is of concern not only because of the classic
vitamin D effects on musculoskeletal outcomes, but also because expression of the
vitamin D receptor (VDR) and
vitamin D metabolizing
enzymes in the heart and blood vessels suggests a role of
vitamin D in the cardiovascular system. VDR-knockout mice suffer from
cardiovascular disease (CVD), and various experimental studies suggest cardiovascular protection by
vitamin D, including antiatherosclerotic, anti-inflammatory and direct cardio-protective actions, beneficial effects on classic cardiovascular risk factors as well as suppression of
parathyroid hormone (PTH) levels. In epidemiological studies, low levels of 25(
OH)D are associated with increased risk of CVD and mortality. Data from randomized controlled trials (RCTs) are sparse and have partially, but not consistently, shown some beneficial effects of
vitamin D supplementation on cardiovascular risk factors (e.g. arterial
hypertension). We have insufficient data on
vitamin D effects on cardiovascular events, but meta-analyses of RCTs indicate that
vitamin D may modestly reduce all-cause mortality. Despite accumulating data suggesting that a sufficient
vitamin D status may protect against CVD, we still must wait for results of large-scale RCTs before raising general recommendations for
vitamin D in the prevention and treatment of CVD. In current clinical practice, the overall risks and costs of
vitamin D supplementation should be weighed against the potential adverse consequences of untreated
vitamin D deficiency.