Vitamin D Therapy in Individuals with Pre-Hypertension or Hypertension: The DAYLIGHT Trial
Pankaj Arora1; Yanna Song2; Jeffery Dusek3; Gregory Plotnikoff3; Marc Sabatine4; Susan Cheng4; Andre Valcour5; Heather Swales6; Beth Taylor6; Erin Carney7; Derek Guanaga7; Joseph R. Young7; Courtney Karol7; Michael Torre7; Atum Azzahir8; Semerit M. Strachan8; Dillon C. O'Neill2; Myles Wolf9; Frank Harrell2; Christopher Newton-Cheh7; Thomas J. Wang2*
1University of Alabama at Birmingham, Birmingham, AL
2Vanderbilt University, Nashville, TN
3Abbott Northwestern Hospital, Minneapolis, MN
4Brigham & Women's Hospital, Harvard Medical School, Boston, MA
5Esoterix Clinical Lab Services, LabCorp, NC
6Hartford Hospital, Hartford, CT
7Massachusetts General Hospital, Harvard Medical School, Boston, MA
8Cultural Wellness Centre, Minneapolis, MN
9Feinberg School of Medicine, Northwestern University, Chicago, IL
↵* Division of Cardiovascular Medicine, Vanderbilt University Medical Center, 2220 Pierce Avenue, 383 PRB, Nashville, TN 37232 thomas.j.wang at vanderbilt.edu
Options for reduction in hypertension include
- Loading dose - to get good level of vitamin D in days, not months (see chart below)
- Use more than 4,000 IU
- Run trial for longer than 6 months
Example chart (click on it for details)
See also VitaminDWiki
- Overview Hypertension and Vitamin D
- Blood pressure in diabetics reduced by 12 weekly doses of 50,000 IU vitamin D – RCT Jan 2014
- Hypertension (both systolic and diastolic) reduced with 2,000 IU of vitamin D – RCT June 2014
Also only 6 months - but the Chinese had a lower level of vitamin D to start with
and concurrently used an anti-hypertension drug
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 aged 18 to 50 years with low vitamin D status (25-hydroxyvitamin D levels ≤ 25 ng/ml) and systolic blood pressure 120-159 mm Hg. Participants were randomized to high-dose (4,000 IU/day) versus low-dose (400 IU/day) oral vitamin D3 for 6 months. The primary endpoint was change in mean 24-hour systolic blood pressure. Secondary endpoints 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 one 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 endpoint (change in mean 24-hour systolic blood pressure, -0.8 mm Hg versus -1.6 mm Hg in the high-dose and low-dose arms, p=0.71) or in any of the secondary endpoints. Further, 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 pre-specified subgroups.
Conclusions—Vitamin D supplementation did not reduce blood pressure in individuals with pre- 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 Information—ClinicalTrials.gov. Identifier: NCT01240512.
Received June 17, 2014. Revision received September 28, 2014. Accepted October 22, 2014.
Subsequent article on same trial by similar authors
High-Dose versus Low-Dose Vitamin D Supplementation and Arterial Stiffness among Individuals with Prehypertension and Vitamin D Deficiency
Hindawi Publishing Corporation Disease Markers, Volume 2015, Article ID 918968, 7 pages http://dx.doi.org/10.1155/2015/918968
Amanda Zaleski,1,2 Gregory Panza,1,2 Heather Swales,1 Pankaj Arora,3 Christopher Newton-Cheh,4 Thomas Wang,5 Paul D. Thompson,1 and Beth Taylor1,2
1 Division of Cardiology, Hartford Hospital, Hartford, CT 06102, USA
2Department of Kinesiology, University of Connecticut, Storrs, CT 06069, USA
3Cardiology Division, Department of Medicine, University of Alabama, Birmingham, AL16686, USA
4Cardiovascular Research Center and Center for Human Genetic Research, Massachusetts General Hospital,
Harvard Medical School, Boston, MA 02115, USA
5Division of Cardiovascular Medicine, Vanderbilt University Medical Center, Nashville, TN 37201
USA Correspondence should be addressed to Amanda Zaleski; amanda.zaleski at hhchealth.org Received 26 June 2015; Accepted 2 September 2015
Augmentation Pressure
Introduction. Vitamin D deficiency is associated with the onset and progression of hypertension and cardiovascular disease (CVD). However, mechanisms underlying vitamin D deficiency-mediated increased risk of CVD remain unknown. We sought to examine the differential effect of high-dose versus low-dose vitamin D supplementation on markers of arterial stiffness among ~40 vitamin D deficient adults with prehypertension.
Methods. Participants were randomized to high-dose (4000 IU/d) versus low-dose (400 IU/d) oral vitamin D3 for 6 months. 24 hr ambulatory blood pressure (BP), carotid-femoral pulse wave velocity, and pulse wave analyses were obtained at baseline and after 6 months of vitamin D supplementation.
Results. There were no changes in resting BP or pulse wave velocity over 6 mo regardless of vitamin D dose (all p > 0.202). High-dose vitamin D decreased augmentation index and pressure by 12.3 ± 5.3% (p = 0.047) and 4.0 ± 1.5 mmHg (p = 0.02), respectively. However, these decreases in arterial stiffness were not associated with increases in serum 25-hydroxyvitamin D over 6 mo (p = 0.425).
Conclusion. High-dose vitamin D supplementation appears to lower surrogate measures of arterial stiffness but not indices of central pulse wave velocity. Clinical Trial Registration. This trial is registered with www.clinicaltrials.gov (Unique Identifier: NCT01240512).