Posttraumatic stress disorder is associated with reduced vitamin D levels and functional polymorphisms of the vitamin D binding-protein in a population-based sample

2020 ◽  
Vol 96 ◽  
pp. 109760 ◽  
Author(s):  
Jan Terock ◽  
Anke Hannemann ◽  
Sandra Van der Auwera ◽  
Deborah Janowitz ◽  
Carsten Spitzer ◽  
...  
Keyword(s):  
Vitamin D ◽  
Posttraumatic Stress Disorder ◽  
Posttraumatic Stress ◽  
Stress Disorder ◽  
Binding Protein ◽  
Population Based ◽  
Vitamin D Binding Protein ◽  
Functional Polymorphisms ◽  
Vitamin D Levels

scholarly journals Reduction in circulating vitamin D binding protein in patients with multiple sclerosis

BMC Neurology ◽  
2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Zhila Maghbooli ◽  
Abolfazl Omidifar ◽  
Tarlan Varzandi ◽  
Tayebeh Salehnezhad ◽  
Mohammad Ali Sahraian
Keyword(s):  
Multiple Sclerosis ◽  
Vitamin D ◽  
Binding Protein ◽  
Serum Levels ◽  
Causative Role ◽  
Vitamin D Binding Protein ◽  
Control Groups ◽  
Current Case ◽  
Vitamin D Levels ◽  
And Control

Abstract Background In this study, we aimed to determine the risk association between vitamin D binding protein (VDBP) polymorphism in patients with multiple sclerosis (MS) in a MS biobank and the difference in VDBP serum levels in MS patients who were recently diagnosed. Method The current case-control study was performed on 296 MS patients and 313 controls. Thereafter, two common missense VDBP polymorphisms, named rs7041and rs4588, were evaluated in all the participants. Serum levels of vitamin D and vitamin D binding protein were assessed in 77 MS patients who were diagnosed since one year ago and in 67 healthy people who were matched in terms of age and sex. Result The frequency distributions of VDBP genotypes and alleles of SNP rs7041 and rs4588 were observed to be similar in both the MS and control groups (p > 0.05). The VDBP haplotypes, as Gc2/Gc2, Gc1/Gc1, and Gc1/Gc2, were found to be similar in the MS and control groups (p > 0.05). In subgroup analysis, circulating VDBP was lower in MS patients (Ln-VDBP (μgr/ml): 3.64 ± 0.91 vs. 5.31 ± 0.77, p = 0.0001) even after adjusting for vitamin D levels, body mass index, and taking vitamin D supplement. There was no significant association between VDBP haplotypes and vitamin D levels in the two groups. Conclusion The present study suggested an association between lower levels of circulating VDBP and multiple sclerosis in newly diagnosed patients. However, the VDBP causative role in the development of MS is still unclear, so it needs more studies.

scholarly journals P431 Vitamin D binding protein in the limelight: IBD-related inflammation and circulating levels of vitamin D binding protein, total, free and bioavailable 25-hydroxyvitamin D

2020 ◽  
Vol 14 (Supplement_1) ◽  
pp. S393-S393
Author(s):  
A Aksan ◽  
K Böttger ◽  
N Hein ◽  
Y Caicedo-Zea ◽  
I Diehl ◽  
...  
Keyword(s):  
Vitamin D ◽  
Binding Protein ◽  
Transferrin Saturation ◽  
Simultaneous Detection ◽  
Full Blood Count ◽  
Vitamin D Binding Protein ◽  
Vitamin D Metabolism ◽  
Hydroxyvitamin D ◽  
Vitamin D Levels ◽  
25 Hydroxyvitamin D

Abstract Background Vitamin D deficiency occurs frequently in patients with Crohn’s disease (CD) and ulcerative colitis (UC). While recent cohort studies support an association of vitamin D with important clinical parameters and outcomes in IBD, the complex interplay of inflammation with vitamin D metabolism in IBD poses a viscious circle. We sought to further illucidate the relation between inflammation and different vitamin D parameters. To the best our knowledge, this was the first study to focus on the relationship between vitamin D binding protein (VDBP), circulating total, free, and bioavailable 25-hydroxyvitamin D (25(OH)D), and inflammation, in adult IBD patients. Methods This was a comparative, single-centred, cross-sectional study in patients with IBD aged 18–65 years. Full blood count, transferrin, albumin and hsCRP were determined by standard methods. The presence/absence of inflammation was assessed based on serum hsCRP levels (cutoff <5mg/l). VDBP levels were determined by ELISA, and 25(OH)D by LCMS. Free and bioavailable vitamin D levels were calculated using the validated formula. IBM SPSS version 25.0 was used for statistical analysis. Results In total, 129 subjects with IBD (70 male/59 female; 82 CD/47 UC; mean age 41.7 ± 12.6 years) were enrolled. Of these, 38/129 had inflammation (19 m/19 f; 26 CD/12 UC; 39.6 ± 12.9 years) while 91/129 had no inflammation (40 m/51 f; 56 CD/35 UC; 42.5 ± 12.5 years). Subjects with disease activity had significantly higher leukocyte, erythrocyte sedimentation rate (ESR) and hsCRP, but lower transferrin, transferrin saturation (TSAT) and albumin levels than those without inflammation (p < 0.05). Average serum levels of 25(OH)D (24.6[6.8–54.8] vs. 26.4[5.0–74.4]ng/ml), free 25(OH)D (5.9[1.3–13.3] vs. 1.0[1.0–21.4]ng/ml) and bioavailable 25(OH)D(2.3 [0.1–4.7] vs. 2.4[0.5–19.5]ng/ml) were similar in patients with vs. without inflammation (p > 0.05). However, VDBP levels were significantly higher in inflammatory conditions (359.6[252.2–530.6] mg/l vs. 327.4[183.5–560.3]mg/l; p < 0.05) and showed a positive correlation with CRP levels (0.293, p < 0.001). Ratio of free/total 25(OH)D correlated negatively with CRP levels (−0.282, p = 0.002). Conclusion High levels of circulating VDBP were associated with inflammatory activity. Moreover, free/total 25(OH)D ratio was inversely associated with inflammation. Other vitamin D parameters including total, free and bioavailable 25(OH)D showed no association with inflammation. These findings suggest that VDBP may play a bigger role than thought as a modulator of vitamin D and inflammation, and that simultaneous detection and investigation of plasma VDBP may provide additional insights into this complex interaction.

Response of vitamin D binding protein and free vitamin D concentrations to vitamin D supplementation in hospitalized premature infants

2015 ◽  
Vol 28 (9-10) ◽  
Author(s):  
Corrine Hanson ◽  
Elizabeth Lyden ◽  
Amy Nelson ◽  
Melissa Thoene ◽  
Julie Wagner ◽  
...  
Keyword(s):  
Vitamin D ◽  
Bone Mineral Content ◽  
Bone Mineral ◽  
Premature Infants ◽  
Vitamin D3 ◽  
Mineral Content ◽  
Binding Protein ◽  
Vitamin D Binding Protein ◽  
Vitamin D Levels ◽  
Free Vitamin D

AbstractThe objective of this study was to evaluate the relationship between 25(OH)D, Vitamin D Binding Protein (DBP), and free vitamin D in premature infants.Thirty-two infants <32 weeks’ gestation were randomized to two different levels of vitamin D3 supplementation (400 vs. 800 IU/day). 25(OH)D levels were measured by LC-MS/MS; DBP was measured by validated ELISA. Free vitamin D was calculated using molar ratios of 25(OH)D and DBP. The Wilcoxon signed rank test was used to compare DBP, free D and 25(OH)D levels; Spearman’s correlation coefficients were used to assess correlations.The mean gestational age at birth was 30.5 weeks; mean birth weight was 1405 g. Mean 25(OH)D levels at birth were 17.3 ng/mL; DBP levels were 297 mg/L, and estimated free vitamin D levels were 18.9. There was a statistically significant change in 25(OH)D levels after 8 weeks (24.6 vs. 39.1 ng/mL in the 400 vs. 800 group, respectively, p=0.02). DBP levels from birth to 8 weeks showed a statistically significant decrease (267 vs. 208, p=0.04). Estimated free 25(OH)D concentrations increased over the study period, from 18.9 at birth to 64.7 at 8 weeks of age (p=0.0001). Free vitamin D levels at birth were associated with global DEXA bone mineral content at discharge from the NICU (r=0.58, p=0.05).Supplementation with vitamin D3 increased the free portion of the vitamin D metabolite, providing increased bioavailable substrate. Improved free vitamin D levels may improve measurable outcomes such as bone mineral content and deserve further evaluation.

Vitamin D homeostasis is compromised due to increased urinary excretion of the 25-hydroxycholecalciferol-vitamin D-binding protein complex in the Zucker diabetic fatty rat

2010 ◽  
Vol 299 (6) ◽  
pp. E959-E967 ◽  
Author(s):  
R. L. Anderson ◽  
S. B. Ternes ◽  
K. A. Strand ◽  
M. J. Rowling
Keyword(s):  
Vitamin D ◽  
Urinary Excretion ◽  
Binding Protein ◽  
Serum Vitamin ◽  
Vitamin D Status ◽  
Vitamin D Binding Protein ◽  
Renal Reabsorption ◽  
Vitamin D Levels ◽  
Zucker Diabetic Fatty Rats ◽  
25 Hydroxycholecalciferol

Altered serum concentrations of the major circulating form of vitamin D [25-hydroxycholecalciferol (25D3)] and its active hormone derivative [1,25-dihydroxycholecalciferol (1,25D3)] have been linked to non-insulin-dependent diabetes mellitus (NIDDM). However, a mechanistic basis for this occurrence has not been fully elucidated. Normally, renal reabsorption of vitamin D-binding protein-bound 25D3 absolutely requires receptor-mediated endocytosis via a receptor complex containing megalin, cubilin, and disabled-2 (Dab2), whereas an absence of megalin or its endocytic partners can lead to a marked urinary loss of 25D and severe vitamin D deficiency. Therefore, we hypothesized that reduced serum vitamin D status in NIDDM may be due to reduced expression of megalin and/or its endocytic partners and increased urinary excretion of protein-complexed 25D3. In the present study, we utilized Zucker diabetic fatty Rats (ZDF) to demonstrate that renal reuptake of the 25D3-DBP complex was compromised in ZDF animals, which was reflected by a reduction in expression of megalin and Dab2. Moreover, serum levels of both 25D3 and 1,25D3 were reduced, and urinary 25D3, 1,25D3, and DBP excretion were elevated in the ZDF animals compared with their lean controls regardless of vitamin D levels in the diet. Taken together, these are the first reports to our knowledge that associate compromised renal reabsorption of the 25D3-DBP complex with expression of megalin and its endocytic partners in NIDDM, which in turn can lead to compromised vitamin D status.

Serum levels of interleukins IL-6 and IL-10 in individuals with posttraumatic stress disorder in a population-based sample

2018 ◽  
Vol 260 ◽  
pp. 111-115 ◽  
Author(s):  
Jacqueline Flores de Oliveira ◽  
Carolina David Wiener ◽  
Karen Jansen ◽  
Luis Valmor Portela ◽  
Diogo R. Lara ◽  
...  
Keyword(s):  
Posttraumatic Stress Disorder ◽  
Posttraumatic Stress ◽  
Stress Disorder ◽  
Serum Levels ◽  
Population Based

scholarly journals A Population-Based Study of Familial and Individual-Specific Environmental Contributions to Traumatic Event Exposure and Posttraumatic Stress Disorder Symptoms in a Norwegian Twin Sample

2012 ◽  
Vol 15 (5) ◽  
pp. 656-662 ◽  
Author(s):  
Ananda B. Amstadter ◽  
Steven H. Aggen ◽  
Gun Peggy Knudsen ◽  
Ted Reichborn-Kjennerud ◽  
Kenneth S. Kendler
Keyword(s):  
Posttraumatic Stress Disorder ◽  
Posttraumatic Stress ◽  
Stress Disorder ◽  
Traumatic Event ◽  
Trauma Exposure ◽  
Population Based ◽  
Ptsd Symptoms ◽  
Familial Factors ◽  
Best Fitting ◽  
Traumatic Event Exposure

Objective: Posttraumatic stress disorder (PTSD) is one of the only disorders in the Diagnostic and Statistical Manual of Mental Disorders that requires an environmental exposure. The relationship between liability factors for trauma exposure and those for PTSD symptoms following exposure are unclear. Methods: Exposure to a trauma and resulting PTSD symptoms were assessed in a sample of 2,794 members of the Norwegian Institute of Public Health Twin Panel. Results: In the full sample, 737 twins experienced a trauma. A modified causal, contingent, common pathway model was used to examine trauma exposure and liability for PTSD. Genetic and common environmental factors could not be distinguished, so a model that included only familial and individual specific components was fit. The best-fitting model suggested that familial factors played an important role in liability for trauma exposure and for resulting PTSD symptoms, and that there was a modest transmission between trauma exposure and subsequent PTSD symptoms. Conclusions: One third of the variance in liability of PTSD symptoms is due to familial factors, and of this, approximately one fifth overlaps with the familial liability for trauma exposure while the other four fifths of the variance is specific to the risk of PTSD symptoms following exposure. The hypothesis that PTSD is etiologically similar to exposures to a traumatic event is not supported, suggesting that the factors that confer risk for trauma do not overlap completely with those that confer risk for PTSD.

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