Effect of vitamin D supplementation on carotid intima media thickness in overweight and obese schoolchildren: A single blind randomized clinical trial

Author(s):  
Golaleh Asghari ◽  
Emad Yuzbashian ◽  
Carol Wagner ◽  
Parvin Mirmiran ◽  
Farhad Hosseinpanah
2020 ◽  
Vol 52 (05) ◽  
pp. 305-315
Author(s):  
Nasim Säidifard ◽  
Hadith Tangestani ◽  
Kurosh Djafarian ◽  
Sakineh Shab-Bidar

AbstractIt is reported that vitamin D deficiency is associated with carotid intima-media thickness (CIMT). In addition, several randomized clinical trials (RCTs) have studied the influence of vitamin D supplement on CIMT. However, results are inconclusive. This review aimed to systematically explore the potential link of the serum vitamin D level with CIMT pooling together observational studies and RCTs. PubMed and Scopus were searched for studies published until February 13, 2018. The Fisher’s z (SE) correlation coefficient, odds ratio (OR), and mean (SD) of changes in CIMT from baseline were used to perform meta-analysis in observational studies and RCTs, respectively. To pool data, both a fixed-effects model and a random-effects model (in case of heterogeneity) were used. Heterogeneity was assessed using Cochran’s Q and I2 tests. Nineteen observational studies and 3 RCTs met inclusion criteria. The pooled correlation coefficients of 17 observational studies showed [(Fisher’s z=− 0.41, 95% CI: –0.63 to –0.19, p<0.001), I2=96.9%, p < 0.001] a significant inverse association between serum vitamin D and risk of CIMT. Pooling three risk estimates of three studies [(OR = 1.69, 95% CI: 0.74 to 3.86, p=0.209); I2=085.1%, p<0.001)] indicated no significant association between serum vitamin D status and risk of CIMT. Combining data of RCTs showed vitamin D supplementation significantly reduced CIMT [(MD: –0.034, 95% CI: –0.62 to –0.05, p=0.012), I2=16.6%, p = 0.301]. Our findings show that serum vitamin D is inversely associated with CIMT and vitamin D supplementation may reduce CMIT.


Virulence ◽  
2017 ◽  
Vol 9 (1) ◽  
pp. 294-305 ◽  
Author(s):  
Allison Ross Eckard ◽  
Paolo Raggi ◽  
Mary Ann O'Riordan ◽  
Julia C. Rosebush ◽  
Danielle Labbato ◽  
...  

2021 ◽  
Vol 39 (Supplement 1) ◽  
pp. e52
Author(s):  
Atsushi Tanaka ◽  
Isao Taguchi ◽  
Hiroki Teragawa ◽  
Nobukazu Ishizaka ◽  
Toyoaki Murohara ◽  
...  

2020 ◽  
Vol 75 (11) ◽  
pp. 1903
Author(s):  
Atsushi Tanaka ◽  
Isao Taguchi ◽  
Nobukazu Ishizaka ◽  
Hirofumi Tomiyama ◽  
Masataka Sata ◽  
...  

Background and aim Deficiency of vitamin D is known as a health problem all over the world and a recognized clinical complication of beta thalassemia patients. Vitamin D acts as a hormone at the nuclear receptor rendering it a beneficial medication for a number of diseases. It is believed that vitamin D is important in the modulation of the inflammation system by regulating the formation of inflammatory cytokines and immune cells. This study aimed to investigate the effect of vitamin D supplementation on the red cell indices and cytokines levels in patients with beta thalassemia major, in an open label randomized clinical trial. Patients and Methods: this study performed an open-label randomized clinical trial in patients with beta thalassemia major. Forty-six patients completed the eight weeks clinical trial and were allocated to administer oral vitamin D3 supplement of 100,000 IU every two weeks as an add-on treatment. During the study, hematological indices, serum iron, ferritin, vitamin D, calcium and inflammatory markers (interleukin-6, interleukin-2 and interleukin-10) were evaluated before (at baseline) and after vitamin D supplementation for 8 weeks. Results: Vitamin D3 supplements significantly decreases interleukin-6 levels and elevates the serum levels of anti-inflammatory cytokines IL-2 and IL-10, it also significantly reduced serum ferritin level, but it did not alter the hematological indices. Conclusion: Our results suggest that administration of vitamin D has a potential anti-inflammatory role in beta thalassemia patients and reduces serum ferritin levels, which may reduce the burdens of iron overload in thalassemia patients.


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