A growing body of observational evidence had suggested that low 25-hydroxyvitamin D (25[OH]D)
concentrations may be a key biological predictor of increased rates of coronary heart disease
(CHD).1 Because low serum 25(OH)D concentrations are more
common and more severe among racial/ethnic minority groups, which are also affected by higher rates
of CHD and CHD risk factors, low vitamin D was being heralded as a potential modifiable contributor
to racial/ethnic disparities in cardiovascular health.2
However, the causal link between 25(OH)D concentrations and CHD remains uncertain.3,4 Additionally, the potential clinical implications of
low serum 25(OH)D concentrations, the pathological mechanisms through which vitamin D may modulate
CHD, and whether these factors differ across racial/ethnic groups are unclear.
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