The Effect of 2 Different Single Injections of High Dose of Vitamin D on Improving the Depression in Depressed Patients With Vitamin D Deficiency

2013 ◽  
Vol 33 (3) ◽  
pp. 378-385 ◽  
Author(s):  
Hassan Mozaffari-Khosravi ◽  
Lale Nabizade ◽  
Seyed Mojtaba Yassini-Ardakani ◽  
Hossein Hadinedoushan ◽  
Kazem Barzegar
2016 ◽  
Vol 101 (2) ◽  
pp. 533-538 ◽  
Author(s):  
Gauree Gupta Konijeti ◽  
Pankaj Arora ◽  
Matthew R. Boylan ◽  
Yanna Song ◽  
Shi Huang ◽  
...  

Abstract Context: Although studies have linked vitamin D deficiency with immune-mediated diseases, data demonstrating a direct effect on T-cell function are sparse. Objective: Our objective was to determine whether oral vitamin D3 influences T-cell activation in humans with vitamin D deficiency. Design: This was a single-center ancillary study within Vitamin D Therapy in Individuals at High Risk of Hypertension, a double-blind, multicenter, randomized controlled trial. Setting: This study was undertaken in a single academic medical center. Participants: Adults with vitamin D deficiency and untreated pre- or early stage I hypertension were included. Intervention: In Vitamin D Therapy in Individuals at High Risk of Hypertension, participants were randomized to either low- (400 IU daily) or high- (4000 IU daily) dose oral vitamin D3 for 6 months. In this ancillary study of 38 patients, we measured CD4+ T-cell activation estimated by intracellular ATP release after stimulation of whole blood with plant lectin phytohemagglutinin collected at baseline (pretreatment) and 2-month follow-up. Main Outcome Measure: Determining whether ATP level changes were significantly different between treatment groups was the main outcome measure. Results: Treatment with 4000 IU of vitamin D3 decreased intracellular CD4+ ATP release by 95.5 ng/ml (interquartile range, −219.5 to 105.8). In contrast, 400 IU of vitamin D3 decreased intracellular CD4+ ATP release by 0.5 ng/ml (interquartile range, −69.2 to 148.5). In a proportional odds model, high-dose vitamin D3 was more likely than low-dose vitamin D3 to decrease CD4+ ATP release (odds ratio, 3.43; 95% confidence interval, 1.06–1.11). Conclusions: In this ancillary study of a randomized controlled trial, we found that high-dose vitamin D3 significantly reduced CD4+ T-cell activation compared to low-dose vitamin D3, providing human evidence that vitamin D can influence cell-mediated immunity.


2013 ◽  
Vol 2013 ◽  
pp. 1-7 ◽  
Author(s):  
Rolf Jorde ◽  
Moira Strand Hutchinson ◽  
Marie Kjærgaard ◽  
Monica Sneve ◽  
Guri Grimnes

Data were pooled from four randomized clinical trials with vitamin D performed in Tromsø with weight reduction, insulin sensitivity, bone density, and depression scores as endpoints. Serum lipids, glycated hemoglobin (HbA1c), and high sensitivity C-Reactive Protein, (HS-CRP) were measured at baseline and after 6–12 months of supplementation with vitamin D 20 000 IU–40 000 IU per week versus placebo. A total of 928 subjects who completed the interventions were included. At baseline the mean serum 25-hydroxyvitamin D (25(OH)D) level in those given vitamin D was 55.9 (20.9) nmol/L and the mean increase was 82.4 (40.1) nmol/L. Compared with the placebo group there was in the vitamin D group at the end of the studies a slight, but significant, increase in HbA1c of 0.04%, an increase in HS-CRP of 0.07 mg/L in those with serum 25(OH)D < 50 nmol/L, and in those with low baseline HDL-C and serum 25(OH)D < 50 nmol/L a slight decrease serum HDL-C of 0.08 mmol/L (P<0.05). No serious side-effects were seen. In conclusion, in subjects without vitamin D deficiency, there is no improvement in serum lipids, HbA1c, or HS-CRP with high dose vitamin D supplementation. If anything, the effect is negative.


2015 ◽  
Vol 18 (02) ◽  
pp. 1550008 ◽  
Author(s):  
Negin Masoudi Alavi ◽  
Mahla Madani ◽  
Mohsen Taghizadeh ◽  
Mohammad Reza Sharif

Purpose: To investigate the effect of weekly single high dose vitamin D supplementation on serum 25-hydroxyvitamin D [25(OH)D], and non-specific musculoskeletal pain in female nurses. Methods: In this prospective study in Kashan/Iran, from April 1, 2014, through September 30, 2014, the 150 nurses with vitamin D deficiency received the weekly pearls of 50,000 units of vitamin D3 for 10 weeks. The serum level of 25(OH)D was measured before and after supplement therapy. The subjects were also asked to complete the Extended Nordic Musculoskeletal Questionnaire. All analyses were conducted with SPSS version 16. Results: After 10 weeks of intervention there was [Formula: see text][Formula: see text]ng/mL increase in 25(OH)D. The 82 nurses (54.7%) had 25(OH)D in normal range, while the 68 nurses (45.3%) were still vitamin D deficient. Weight could explain 15.4% increase in 25(OH)D. Before intervention 135 (90%), of nurses reported musculoskeletal pain in at least one region, after intervention this number decreased to 72.7%. There was a statistically significant improvement in musculoskeletal pain in neck, shoulders, upper back, lower back, hips/tights, knees, and ankles/feet after intervention. Conclusions: The weekly single high dose of vitamin D for 10 weeks could resolve vitamin D deficiency in about half of the patients. Patients with non-specific musculoskeletal pain might benefit from vitamin D supplementation.


2019 ◽  
Vol 104 (9) ◽  
pp. 4033-4050 ◽  
Author(s):  
Thomas F Hiemstra ◽  
Kenneth Lim ◽  
Ravi Thadhani ◽  
JoAnn E Manson

Abstract Context A large body of experimental and observational data has implicated vitamin D deficiency in the development of cardiovascular disease. However, evidence to support routine vitamin D supplementation to prevent or treat cardiovascular disease is lacking. Design and Results A comprehensive literature review was performed using PubMed and other literature search engines. Mounting epidemiological evidence and data from Mendelian randomization studies support a link between vitamin D deficiency and adverse cardiovascular health outcomes, but randomized trial evidence to support vitamin D supplementation is sparse. Current public health guidelines restrict vitamin D intake recommendations to the maintenance of bone health and prevention of fractures. Two recently published large trials (VITAL and ViDA) that assessed the role of moderate- to high-dose vitamin D supplementation as primary prevention for cardiovascular outcomes in the general population had null results, and previous randomized trials have also been generally negative. These findings from general population cohorts that are largely replete in vitamin D may not be applicable to chronic kidney disease (CKD) populations, in which the use of active (1α-hydroxylated) vitamin D compounds is prevalent, or to other high-risk populations. Additionally, recent trials in the CKD population, as well as trials using vitamin D analogs, have been limited. Conclusions Current randomized trials of vitamin D supplementation do not support benefits for cardiovascular health, but the evidence remains inconclusive. Additional randomized trials assessing larger numbers of participants with low baseline vitamin D levels, having longer follow-up periods, and testing higher vitamin D dosages are needed to guide clinical practice.


2018 ◽  
Vol 103 (2) ◽  
pp. e1.9-e1
Author(s):  
Christiansen Nanna ◽  
Ashraf Saleha

AimsPatients with cystic fibrosis (CF) require supplementation of fat-soluble vitamins due to the effects of the disease on the pancreas and the resulting inability of absorb fat effectively.1The study aimed to assess the effectiveness of current of vitamin D supplementation to achieve adequate serum Vitamin D (25OHD) levels in paediatric CF patients.2 Secondly, this study assessed the effectiveness of ‘Stoss’ therapy (a high dose vitamin D therapy administered every three months) as an alternative to daily vitamin D supplementation for patients with known poor compliance.3MethodsVitamin D doses and serum 25OHD levels between January and December 2016 were reviewed for paediatric CF patients at a UK centre. Data was collected for 138 paediatric patients. The ‘clinical record summary’ system was used to extract the data which included age, hospital number, weight in 2015 and 2016, 25OHD levels from 2015 and 2016, vitamin D dose before each level and pancreatic status.Data was entered onto Statistical Package for the Social Sciences (SPSS) system for analysis. A paired T-test was conducted to ascertain if there was a significant difference in weekly/kg doses between patients that were sufficient (25OHD>50 nmol/L) and insufficient (25OHD<50 nmol/L).ResultsData was collected for a total of 138 patients. The data from only 70 patients was analysed when investigating the first objective, as all other patients did not have 25OHD levels available for both 2015 and 2016. A further five patients wereexcluded and analysed seperately due to receiving Stoss therapy. The weekly Vitamin D dose range was very wide for both years with 43% (n=40) of patients requiring additional vitamin D in addition to Aquadeks (CF multivitamin preparation). There was no significant difference in Vitamin D doses between patients with sufficient and insufficient 25OHD levels. This was thecase for both 2015 (p=0.432) and 2016 (p=0.192). The daily supplementation doses were successful at maintaining vitamin D sufficiency for 83% of patients in 2015 and 93% in 2016.Out of the 5 patients who received ‘Stoss’ therapy, 3 had an increase in 25OHD levels. However, only one of the patients had a significant increase leading to sufficient 25OHD levels. In 2 cases there was actually a 60%–68% decrease in 25OHD levels, which lead to these patients developing vitamin D deficiency.ConclusionThis study was useful in determining the effectiveness of current Vitamin D dosing. The results suggest that patients having insufficient 25OHD levels may not be due to an inadequacy of doses provided in the current guideline, as there was no significant difference in dose between patients with sufficient and insufficient 25OHD levels. Given the patient group, the difference could be attributable to a lack of compliance to daily therapies in the patients with insufficient 25OHD levels or even differences in individual responses to therapy.In this sample, ‘Stoss’ therapy is not effective in maintaining sufficient 25OHD levels. Although the data for this part of the study was very limited, it identifies a need to investigate the effectiveness of ‘Stoss’ therapy further.ReferencesFerguson JH, Chang AB. Vitamin D supplementation for cystic fibrosis. Cochrane Database of Syst Rev [Internet] 2014. http://onlinelibrary.wiley.com/ & doi:10.1002/14651858.CD007298.pub3/pdf [Available: 2017April 12].Green D, Carson K, Leonard A, et al. Current treatment recommendations for correcting vitamin D deficiency in paediatric patients with cystic fibrosis is inadequate. J Pediatr2008;4:554–559.Shepherd D, Belessis Y, Katz, et al. Single high-dose oral vitamin D3 (stoss) therapy: A solution to vitamin D deficiency in children with cystic fibrosis?J Cyst Fibros2013;2:177–182.


2020 ◽  
Vol 45 (10) ◽  
pp. 1092-1098
Author(s):  
Soodabeh Aliashrafi ◽  
Mehrangiz Ebrahimi-Mameghani ◽  
Mohammad Asghari Jafarabadi ◽  
Lida Lotfi-Dizaji ◽  
Elnaz Vaghef-Mehrabany ◽  
...  

As there is limited and inconsistent evidence in potential role of vitamin D on insulin resistance and matrix metalloproteinases, this study aimed to examine the effect of vitamin D supplementation on glucose homeostasis, insulin resistance, and matrix metalloproteinases in obese subjects with vitamin D deficiency. A total of 44 participants with serum 25-hydroxyvitamin D (25(OH)D) level ≤ 50 nmol/L and body mass index (BMI) 30–40 kg/m2 were randomly allocated into receiving weight reduction diet with either 50 000 IU vitamin D3 pearl (n = 22) or placebo (n = 22) once weekly for 12 weeks. Primary outcomes were changes in fasting serum glucose (FSG), homeostasis model assessment of insulin resistance (HOMA-IR), quantitative insulin sensitivity check index (QUICKI), and matrix metalloproteinases (MMPs). Secondary outcomes were changes in weight, BMI, 25(OH)D, calcium, phosphorous and parathyroid hormone (PTH). Sun exposure and dietary intakes were also assessed. Serum levels of 25(OH)D3 increased significantly with a simultaneous decrease in serum concentration of PTH in the vitamin D group. Weight, BMI, FSG, and MMP-9 decreased significantly in both groups, and there were significant differences in changes in weight, serum 25(OH)D3, PTH, and MMP-9 levels between the groups. Within- and between-groups analysis revealed no significant differences in serum calcium, phosphorous, serum insulin, HOMA-IR, QUICKI, and MMP-2 after intervention. Our results indicated that improvement in vitamin D status resulted in greater reductions in weight and MMP-9 during weight loss. These preliminary results are sufficient to warrant a bigger study group.


2015 ◽  
Vol 2015 ◽  
pp. 1-7 ◽  
Author(s):  
Amanda Zaleski ◽  
Gregory Panza ◽  
Heather Swales ◽  
Pankaj Arora ◽  
Christopher Newton-Cheh ◽  
...  

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 (allp>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).


Sign in / Sign up

Export Citation Format

Share Document