Pankaj Arora1, Yanna Song1, Jeffery Dusek1, Gregory Plotnikoff1, Marc S Sabatine1, Susan Cheng1, Andre Valcour1, Heather Swales1, Beth Taylor1, Erin Carney1, Derek Guanaga1, Joseph R Young1, Courtney Karol1, Michael Torre1, Atum Azzahir1, Semerit M Strachan1, Dillon C O'Neill1, Myles Wolf1, Frank Harrell1, Christopher Newton-Cheh1, Thomas J Wang2. 1. From the Cardiology Division, Department of Medicine, University of Alabama at Birmingham, Birmingham (P.A.); Department of Biostatistics (Y.S., F.H.) and Division of Cardiovascular Medicine, Department of Medicine (D.C.O., T.J.W.), Vanderbilt University, Nashville, TN; Integrative Health Research Center, Abbott Northwestern Hospital, Minneapolis, MN (J.D., G.P.); Division of Cardiology, Department of Medicine, Brigham & Women's Hospital, Harvard Medical School, Boston, MA (M.S.S., S.C.); Esoterix Clinical Lab Services, LabCorp, Research Triangle Park, NC (A.V.); Division of Cardiology, Department of Medicine, Hartford Hospital, Hartford, CT (H.S., B.T.); Division of Cardiology, Department of Medicine, Massachusetts General Hospital, Harvard Medical School, Boston (E.C., D.G., J.R.Y., C.K., M.T., C.N.-C.); Division of Cardiology, Cultural Wellness Center, Minneapolis, MN (A.A., S.M.S.); and Division of Nephrology, Department of Medicine, Feinberg School of Medicine, Northwestern University, Chicago, IL (M.W.). 2. From the Cardiology Division, Department of Medicine, University of Alabama at Birmingham, Birmingham (P.A.); Department of Biostatistics (Y.S., F.H.) and Division of Cardiovascular Medicine, Department of Medicine (D.C.O., T.J.W.), Vanderbilt University, Nashville, TN; Integrative Health Research Center, Abbott Northwestern Hospital, Minneapolis, MN (J.D., G.P.); Division of Cardiology, Department of Medicine, Brigham & Women's Hospital, Harvard Medical School, Boston, MA (M.S.S., S.C.); Esoterix Clinical Lab Services, LabCorp, Research Triangle Park, NC (A.V.); Division of Cardiology, Department of Medicine, Hartford Hospital, Hartford, CT (H.S., B.T.); Division of Cardiology, Department of Medicine, Massachusetts General Hospital, Harvard Medical School, Boston (E.C., D.G., J.R.Y., C.K., M.T., C.N.-C.); Division of Cardiology, Cultural Wellness Center, Minneapolis, MN (A.A., S.M.S.); and Division of Nephrology, Department of Medicine, Feinberg School of Medicine, Northwestern University, Chicago, IL (M.W.). thomas.j.wang@vanderbilt.edu.
Abstract
BACKGROUND: A large body of epidemiological and experimental evidence suggests that vitamin D deficiency may promote hypertension. This raises the possibility that vitamin D supplementation could be a simple intervention to reduce blood pressure, but data from prospective, randomized trials are limited. METHODS AND RESULTS: A double-blind, randomized, controlled trial was conducted at 4 sites in the United States. We enrolled 534 individuals 18 to 50 years of age with low vitamin D status (25-hydroxyvitamin D levels ≤25 ng/mL) and systolic blood pressure of 120 to 159 mm Hg. Participants were randomized to high-dose (4000 IU/d) versus low-dose (400 IU/d) oral vitamin D3 for 6 months. The primary end point was change in mean 24-hour systolic blood pressure. Secondary end points included change in ambulatory diastolic blood pressure and clinic systolic and diastolic blood pressures. The median age was 38 years, and 62% of participants were men. Forty-six percent of participants were white, and 48% were black. The median 25-hydroxyvitamin D level at baseline was 15.3 ng/mL. Four-hundred fifty-five participants (85%) had at least 1 follow-up blood pressure measurement; 383 participants (72%) completed the full 6-month study. At the end of the study, there was no significant difference in the primary end point (change in mean 24-hour systolic blood pressure, -0.8 versus -1.6 mm Hg in the high-dose and low-dose arms; P=0.71) or in any of the secondary end points. Furthermore, there was no evidence of association between change in 25-hydroxyvitamin D and change in 24-hour systolic blood pressure at 6 months (Spearman correlation coefficient, -0.05, P=0.34). Results were consistent across prespecified subgroups. CONCLUSIONS:Vitamin D supplementation did not reduce blood pressure in individuals with prehypertension or stage I hypertension and vitamin D deficiency. Our findings suggest that the association between vitamin D status and elevated blood pressure noted in observational studies is not causal. CLINICAL TRIAL REGISTRATION URL: http://www.clinicaltrials.gov. Unique identifier: NCT01240512.
RCT Entities:
BACKGROUND: A large body of epidemiological and experimental evidence suggests that vitamin D deficiency may promote hypertension. This raises the possibility that vitamin D supplementation could be a simple intervention to reduce blood pressure, but data from prospective, randomized trials are limited. METHODS AND RESULTS: A double-blind, randomized, controlled trial was conducted at 4 sites in the United States. We enrolled 534 individuals 18 to 50 years of age with low vitamin D status (25-hydroxyvitamin D levels ≤25 ng/mL) and systolic blood pressure of 120 to 159 mm Hg. Participants were randomized to high-dose (4000 IU/d) versus low-dose (400 IU/d) oral vitamin D3 for 6 months. The primary end point was change in mean 24-hour systolic blood pressure. Secondary end points included change in ambulatory diastolic blood pressure and clinic systolic and diastolic blood pressures. The median age was 38 years, and 62% of participants were men. Forty-six percent of participants were white, and 48% were black. The median 25-hydroxyvitamin D level at baseline was 15.3 ng/mL. Four-hundred fifty-five participants (85%) had at least 1 follow-up blood pressure measurement; 383 participants (72%) completed the full 6-month study. At the end of the study, there was no significant difference in the primary end point (change in mean 24-hour systolic blood pressure, -0.8 versus -1.6 mm Hg in the high-dose and low-dose arms; P=0.71) or in any of the secondary end points. Furthermore, there was no evidence of association between change in 25-hydroxyvitamin D and change in 24-hour systolic blood pressure at 6 months (Spearman correlation coefficient, -0.05, P=0.34). Results were consistent across prespecified subgroups. CONCLUSIONS:Vitamin D supplementation did not reduce blood pressure in individuals with prehypertension or stage I hypertension and vitamin D deficiency. Our findings suggest that the association between vitamin D status and elevated blood pressure noted in observational studies is not causal. CLINICAL TRIAL REGISTRATION URL: http://www.clinicaltrials.gov. Unique identifier: NCT01240512.
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