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Arterial stiffness reduced by vitamin D


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Arterial stiffness reduced by monthly 120,000 IU Vitamin D (overweight African-Americans) – RCT Dec 2017

Dose responses of vitamin D3 supplementation on arterial stiffness in overweight African Americans with vitamin D deficiency: A placebo controlled randomized trial.
PLoS One. 2017 Dec 7;12(12):e0188424. doi: 10.1371/journal.pone.0188424. eCollection 2017.
Raed A1,2, Bhagatwala J1,2, Zhu H1,3, Pollock NK1,3, Parikh SJ1,2, Huang Y1, Havens R1, Kotak I1, Guo DH1, Dong Y1,3.
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BACKGROUND:
Clinical trials are scant and equivocal on whether vitamin D can ameliorate arterial stiffness, particularly in populations at high risk for vitamin D deficiency and cardiovascular disease (CVD). This study determined the dose-response effects of vitamin D3 supplementation on arterial stiffness in overweight African Americans with vitamin D deficiency.

METHODS:
Seventy overweight African Americans (aged 13-45 years) with serum 25-hydroxyvitamin D 25(OH)D levels ≤ 20 ng/mL were randomized to monthly oral supplementation of 18,000 IU (~600 IU/day, n = 17), 60,000 IU (~2000 IU/day, n = 18), or 120,000 IU (~4000 IU/day, n = 18) of vitamin D3 or placebo (n = 17) for 16-weeks. The arterial stiffness measurements, carotid-femoral pulse wave velocity (PWV) and carotid-radial PWV, were assessed by applanation tonometry at baseline and 16 weeks.

RESULTS:
Vitamin D3 supplementation demonstrated a dose-response increase in serum 25(OH)D concentrations between groups (P<0.01). A significant downward linear trend was observed for carotid-femoral PWV (P<0.01), as the mean changes in carotid-femoral PWV across the four treatment groups were 0.13 m/s (95% CI: -0.24, 0.51 m/s) for placebo, 0.02 m/s (95% CI: -0.34, 0.38 m/s) for 600 IU/day group, -0.11 m/s (95% CI: -0.50, 0.27 m/s) for the 2,000 IU/day group, and -0.70 m/s (95% CI: -1.07, -0.32 m/s) for the 4,000 IU/day group. Findings were similar for carotid-radial PWV (P = 0.03), as the mean changes in carotid-radial PWV across the four treatment groups were 0.24 m/s (95% CI: -0.45, 0.92 m/s) for placebo, 0.09 m/s (95% CI: -0.54, 0.73 m/s) for 600 IU/day group, -0.57 m/s (95% CI: -1.20, 0.07 m/s) for the 2,000 IU/day group, and -0.61 m/s (95% CI: -1.25, 0.02 m/s) for the 4,000 IU/day group.

CONCLUSION:
Arterial stiffness was improved by vitamin D3 supplementation in a dose-response manner in overweight African Americans with vitamin D deficiency.

Less arterial stiffness if take enough Vitamin D and Calcium – Sept 2014

Association between dietary calcium intake and arterial stiffness according to dietary vitamin D intake in men.
Br J Nutr. 2014 Sep 5:1-8. [Epub ahead of print]
Uemura H1, Katsuura-Kamano S1, Yamaguchi M1, Nakamoto M2, Hiyoshi M1, Arisawa K1.

Studies on the associations of dietary Ca and vitamin D intakes with arterial stiffness are scarce. In the present study, these associations were evaluated in Japanese men. Data from a total of 535 eligible men, aged 35-69 years, who participated in the baseline survey of a cohort study in Tokushima Prefecture, Japan, and underwent brachial-ankle pulse wave velocity (ba-PWV) measurements were analysed. ba-PWV is a measure of arterial stiffness and is recognised as a marker of atherosclerotic vascular damage. Information regarding the cohort's lifestyle characteristics including dietary behaviour over the past year was obtained from a structured self-administered questionnaire. Dietary Ca and vitamin D intakes were adjusted for total energy intake using the residual method and divided into quartiles; the highest quartile was used as the reference. General linear models were used to evaluate the associations between dietary Ca and vitamin D intakes and ba-PWV values adjusted for probable covariates. The association between dietary Ca intake and ba-PWV was further evaluated using similar general linear models stratified by dietary vitamin D intake (median or below/above median). Dietary Ca intake was found to be significantly inversely associated with ba-PWV after adjusting for probable covariates (P for trend = 0·020). However, no such association was observed between dietary vitamin D intake and ba-PWV. The inverse association between dietary Ca intake and ba-PWV was striking in subjects with higher dietary vitamin D intake. However, no association was found in subjects with lower dietary vitamin D intake. These results indicate that adequate dietary Ca and vitamin D intakes may be protective against the development of arterial stiffness in Japanese men.

PMID: 25192171
This study is described by the Vitamin C Council - behind a $5/month paywall
Publisher wants $45 for the PDF


Arterial stiffness reduced with vitamin D intervention – June 2011

__Vitamin D Status Is Associated With Arterial Stiffness and Vascular Dysfunction in Healthy Humans
J Am Coll Cardiol, 2011; 58:186-192, doi:10.1016/j.jacc.2011.02.051
© 2011 by the American College of Cardiology Foundation
CLINICAL RESEARCH: VASCULAR DISEASE
Ibhar Al Mheid, MD*, Riyaz Patel, MD*,{dagger}, Jonathan Murrow, MD{ddagger}, Alanna Morris, MD*, Ayaz Rahman, MD*, Lucy Fike, MPH*, Nino Kavtaradze, MD*, Irina Uphoff*, Craig Hooper, PhD§, Vin Tangpricha, MD, PhD¶, R. Wayne Alexander, MD, PhD*, Kenneth Brigham, MD*, and Arshed A. Quyyumi, MD*, aquyyum at emory.edu
* Emory University School of Medicine, Atlanta, Georgia
{dagger} Cardiff University, Cardiff, Wales, United Kingdom
{ddagger} Medical College of Georgia-The University of Georgia Medical Partnership, Athens, Georgia
§ Centers for Disease Control and Prevention, Atlanta, Georgia
|| Emory-Georgia Institute of Technology Predictive Health Institute, Atlanta, Georgia
¶ Atlanta VA Medical Center, Atlanta, Georgia

Manuscript received November 3, 2010; revised manuscript received January 31, 2011, accepted February 15, 2011.

Objectives: The primary objective of this study was to elucidate mechanisms underlying the link between vitamin D status and cardiovascular disease by exploring the relationship between 25-hydroxyvitamin D (25-OH D), an established marker of vitamin D status, and vascular function in healthy adults.

Background: Mechanisms underlying vitamin D deficiency-mediated increased risk of cardiovascular disease remain unknown. Vitamin D influences endothelial and smooth muscle cell function, mediates inflammation, and modulates the renin-angiotensin-aldosterone axis. We investigated the relationship between vitamin D status and vascular function in humans, with the hypothesis that vitamin D insufficiency will be associated with increased arterial stiffness and abnormal vascular function.

Methods: We measured serum 25-OH D in 554 subjects. Endothelial function was assessed as brachial artery flow-mediated dilation, and microvascular function was assessed as digital reactive hyperemia index. Carotid-femoral pulse wave velocity and radial tonometry-derived central augmentation index and subendocardial viability ratio were measured to assess arterial stiffness.

Results: Mean 25-OH D was 31.8 ± 14 ng/ml.
After adjustment for age, sex, race, body mass index, total cholesterol, low-density lipoprotein, triglycerides, C-reactive protein, and medication use,
25-OH D remained independently associated with

  • flow-mediated vasodilation (? = 0.1, p = 0.03),
  • reactive hyperemia index (? = 0.23, p < 0.001),
  • pulse wave velocity (? = –0.09, p = 0.04),
  • augmentation index (? = –0.11, p = 0.03), and
  • subendocardial viability ratio (? = 0.18, p = 0.001).

In 42 subjects with vitamin D insufficiency, normalization of 25-OH D at 6 months was associated with
increases in

  • reactive hyperemia index (0.38 ± 0.14, p = 0.009) and
  • subendocardial viability ratio (7.7 ± 3.1, p = 0.04), and a
  • decrease in mean arterial pressure (4.6 ± 2.3 mm Hg, p = 0.02).


Conclusions: Vitamin D insufficiency is associated with increased arterial stiffness and endothelial dysfunction in the conductance and resistance blood vessels in humans, irrespective of traditional risk burden. Our findings provide impetus for larger trials to assess the effects of vitamin D therapy in cardiovascular disease.

Abbreviations and Acronyms
25-OH D = 25-hydroxyvitamin D; AIX = augmentation index; CRP = C-reactive protein; FMD = (brachial artery) flow-mediated dilation;
PWV = pulse wave velocity; RHI = reactive hyperemia index; SEVR = subendocardial viability ratio


Aortic stiffness 9 for <20 ng vitamin D vs 7.7 for highest level of vitamin D - Oct 2011

The association between low 25-hydroxyvitamin D and increased aortic stiffness.
J Hum Hypertens. 2011 Oct 20. doi: 10.1038/jhh.2011.94.
Mayer O Jr, Filipovský J, Seidlerová J, Van?k J, Dolejšová M, Vrzalová J, Cífková R.
2nd Department of Internal Medicine, Charles University, Medical Faculty, Pilsen, Czech Republic.

There is accumulating evidence that vitamin D exerts important pathophysiological effects on cardiovascular system. Low vitamin D was associated with increased cardiovascular risk in several reports. We studied the association between vitamin D and arterial stiffness in a random sample of 560 subjects selected from general population. Arterial stiffness was measured as aortic pulse-wave velocity (PWV) using Sphygmocor device. Serum 25-hydroxyvitamin D OH)D) was measured using commercial kits. We found a clear negative trend in aortic PWV among 25(OH)D quartiles. Subjects in the bottom 25(OH)D quartile (<20?ng?ml(-1 showed the highest aortic PWV (9.04?m?s(-1)), compared with 2nd-4th quartile (8.07?m?s(-1), 7.93?m?s(-1) and 7.70?m?s(-1), respectively; P for trend <0.0001). The association between 25(OH)D and aortic PWV remained significant after adjustment for age, gender and other potential confounders; subjects in the first 25(OH)D quartile had adjusted odds ratio 2.04 (1.26-3.30) for having aortic PWV ?9?m?s(-1) (top quartile) in multiple regression.

In conclusion, we found a clear significant and independent negative association between 25(OH)D and aortic PWV. Subjects with lowest vitamin D status showed the highest arterial stiffness.Journal of Human Hypertension advance online publication, 20 October 2011; doi:10.1038/jhh.2011.94.
PMID: 22011876

Attached files

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