The Journal of Clinical Endocrinology & Metabolism August 3, 2012 jc.2012-2126 Adrian D. Wood, Karen R. Secombes, Frank Thies, Lorna Aucott, Alison J. Black, Alexandra Mavroeidi, William G. Simpson, William D. Fraser, David M. Reid and Helen M. Macdonald
School of Medicine and Dentistry (A.D.W., K.R.S., F.T., L.A., D.M.R., H.M.M.), Medical Sciences (A.M.), University of Aberdeen, Foresterhill, Aberdeen AB252ZD, United Kingdom; Grampian Osteoporosis Service (A.J.B.), Woolmanhill Hospital, Aberdeen AB251LD, United Kingdom; Department of Clinical Biochemistry (W.G.S.), Aberdeen Royal Infirmary, Foresterhill AB252ZD, United Kingdom; and Norwich Medical School (W.D.F.), University of East Anglia, Norwich NR47TJ, United Kingdom
Address all correspondence and requests for reprints to: Helen M. Macdonald, Ph.D., Health Sciences Building, University of Aberdeen, Foresterhill, Aberdeen AB25 2ZD, United Kingdom. E-mail: h.macdonald at abdn.ac.uk.
Context: Observational studies show an association between low vitamin D status assessed by circulating 25-hydroxyvitamin D and cardiovascular events and mortality. Data from randomized controlled trials are limited.
Objective: The aim of this study was to test whether daily doses of vitamin D3 at 400 or 1000 IU/d for 1 yr affected conventional markers of cardiovascular disease (CVD) risk.
Design: We conducted a parallel-group, double-blind, placebo-controlled randomized controlled trial.
Randomization was computer generated.
Participants and study investigators were blinded to intervention groupings throughout the trial.
Setting: The study was conducted at the Clinical Research Facility, University of Aberdeen, United Kingdom.
Participants: A total of 305 healthy postmenopausal women aged 60–70 yr were recruited for the study.
Intervention: Each woman received a daily capsule of 400 or 1000 IU vitamin D3 or placebo randomly allocated.
Main Outcome Measures: Primary outcomes were
- serum lipid profile [total, high-density lipoprotein, and low-density lipoprotein cholesterol; triglycerides; and apolipoproteins A-1 and B100],
- insulin resistance (homeostatic model assessment),
- inflammatory biomarkers (high-sensitivity C-reactive protein, IL-6, soluble intracellular adhesion molecule-1), and
- blood pressure.
Results: A total of 265 (87%) participants completed all study visits.
Small differences between groups for serum apolipoprotein B100 change [repeated measures ANOVA, P = 0.04; mean (SD), ?1.0 (10.0) mg/dl (400 IU); ?1.0 (10.0) mg/dl (1000 IU); and +0.02 (10.0) mg/dl (placebo)] were not considered clinically significant. Other systemic markers for CVD risk remained unchanged. There was significant seasonal variation in systolic and diastolic blood pressure independent of vitamin D dose (P < 0.001, linear mixed model). Mean (SD) reduction in systolic blood pressure from winter to summer was ?6.6 (10.8) mm Hg.
Conclusions: Improving vitamin D status through dietary supplementation is unlikely to reduce CVD risk factors.
Confounding of seasonality should be recognized and addressed in future studies of vitamin D.
Received May 2, 2012, Accepted July 6, 2012, Copyright © 2012 by The Endocrine Society
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- Overview Cardiovascular and vitamin D
Many previous studies have shown that at least 2,000 IU of vitamin D is needed