title: Vitamin D deficiency and risk of cardiovascular disease.
abstract: BACKGROUND
  Vitamin D receptors have a broad tissue distribution that includes vascular smooth muscle, endothelium, and cardiomyocytes. A growing body of evidence suggests that vitamin D deficiency may adversely affect the cardiovascular system, but data from longitudinal studies are lacking.
  
  
  RESULTS
  We studied 1739 Framingham Offspring Study participants (mean age 59 years; 55% women; all white) without prior cardiovascular disease. Vitamin D status was assessed by measuring 25-dihydroxyvitamin D (25-OH D) levels. Prespecified thresholds were used to characterize varying degrees of 25-OH D deficiency (< 15 ng/mL, < 10 ng/mL). Multivariable Cox regression models were adjusted for conventional risk factors. Overall, 28% of individuals had levels < 15 ng/mL, and 9% had levels < 10 ng/mL. During a mean follow-up of 5.4 years, 120 individuals developed a first cardiovascular event. Individuals with 25-OH D < 15 ng/mL had a multivariable-adjusted hazard ratio of 1.62 (95% confidence interval 1.11 to 2.36, P=0.01) for incident cardiovascular events compared with those with 25-OH D > or = 15 ng/mL. This effect was evident in participants with hypertension (hazard ratio 2.13, 95% confidence interval 1.30 to 3.48) but not in those without hypertension (hazard ratio 1.04, 95% confidence interval 0.55 to 1.96). There was a graded increase in cardiovascular risk across categories of 25-OH D, with multivariable-adjusted hazard ratios of 1.53 (95% confidence interval 1.00 to 2.36) for levels 10 to < 15 ng/mL and 1.80 (95% confidence interval 1.05 to 3.08) for levels < 10 ng/mL (P for linear trend=0.01). Further adjustment for C-reactive protein, physical activity, or vitamin use did not affect the findings.
  
  
  CONCLUSIONS
  Vitamin D deficiency is associated with incident cardiovascular disease. Further clinical and experimental studies may be warranted to determine whether correction of vitamin D deficiency could contribute to the prevention of cardiovascular disease.
authors.affiliation: Framingham Heart Study, Framingham, Mass, USA. tjwang@partners.org
authors.forename: Thomas J
authors.initials: TJ
authors.lastname: Wang
authors.forename: Michael J
authors.initials: MJ
authors.lastname: Pencina
authors.forename: Sarah L
authors.initials: SL
authors.lastname: Booth
authors.forename: Paul F
authors.initials: PF
authors.lastname: Jacques
authors.forename: Erik
authors.initials: E
authors.lastname: Ingelsson
authors.forename: Katherine
authors.initials: K
authors.lastname: Lanier
authors.forename: Emelia J
authors.initials: EJ
authors.lastname: Benjamin
authors.forename: Ralph B
authors.initials: RB
authors.lastname: D'Agostino
authors.forename: Myles
authors.initials: M
authors.lastname: Wolf
authors.forename: Ramachandran S
authors.initials: RS
authors.lastname: Vasan
mesh_terms: D002318:Cardiovascular Diseases / Q000209:etiology*; D005260:Female; D006801:Humans; D006973:Hypertension / Q000150:complications; D015994:Incidence; D008137:Longitudinal Studies; D008297:Male; D008875:Middle Aged; D012307:Risk Factors; D014808:Vitamin D Deficiency / Q000150:complications* / Q000453:epidemiology*