all things vitamin D

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NHE
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Re: all things vitamin D

Post by NHE » Fri Nov 16, 2018 8:22 pm

jimmylegs wrote:Life-threatening vitamin D intoxication due to intake of ultra-high doses in multiple sclerosis: A note of caution (2018)

"Knowledge about complications of chronic ultra-high dose vitamin D supplementation is limited. We report a patient with primary progressive multiple sclerosis (MS) who presented with generalized weakness caused by hypercalcemia after uncontrolled intake of more than 50,000 IU of cholecalciferol per day over several months. Various treatment strategies were required to achieve normocalcemia. However, renal function improved only partly and further progression of MS was observed. We conclude that patients need to be informed about the risks of uncontrolled vitamin D intake and neurologists need to be alert of biochemical alterations and symptoms of vitamin D toxicity."
https://www.ncbi.nlm.nih.gov/pubmed/30358476

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Re: all things vitamin D

Post by jimmylegs » Fri Dec 28, 2018 7:30 am

Vitamin D and remyelination in multiple sclerosis (2018)

Abstract
Introduction

Several studies have found an association between multiple sclerosis and vitamin D (VD) deficiency, which suggests that VD may play a role in the immune response. However, few studies have addressed its role in remyelination.

Development
The VD receptor and the enzymes transforming VD into metabolites which activate the VD receptor are expressed in central nervous system (CNS) cells, which suggests a potential effect of VD on the CNS. Both in vitro and animal model studies have shown that VD may play a role in myelination by acting on factors that influence the microenvironment which promotes both proliferation and differentiation of neural stem cells into oligodendrocyte progenitor cells and oligodendrocytes. It remains unknown whether the mechanisms of internalisation of VD in the CNS are synergistic with or antagonistic to the mechanisms that facilitate the entry of VD metabolites into immune cells.

Conclusions
VD seems to play a role in the CNS and our hypothesis is that VD is involved in remyelination. Understanding the basic mechanisms of VD in myelination is necessary to manage multiple sclerosis patients with VD deficiency.
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Re: all things vitamin D

Post by Petr75 » Fri Dec 28, 2018 11:33 am

2018 Nov 14
Medical Sciences; Department of Biochemistry and Diet, School of Nutrition and Food Sciences, Tabriz University of Medical Sciences, Iran
Anti-inflammatory effects of dietary vitamin D3 in patients with multiple sclerosis.

PMC https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6244020/

Abstract
Objective:
To assess the effects of dietary vitamin D3 on proinflammatory (interleukin-17A [IL-17A] and IL-6) and anti-inflammatory (IL-10) cytokines.
Methods:
Our study was conducted on 75 participants who were divided into 3 groups: multiple sclerosis participants (MSPs, n = 25), first-degree relative participants (FDRPs, n = 25), and healthy participants (HPs, n = 25). All groups received 50,000 IU vitamin D3/wk for 8 weeks. Serum 25-(OH) vitamin D3 levels and messenger RNA (mRNA) expression levels of ILs were determined using electrochemiluminescence assay and real-time PCR, respectively.
Results:
Vitamin D3 affected the levels of IL-17A, IL-10, and IL-6 among the 3 groups (p < 0.001 for all). Levels of IL-17A (MSPs: fold change [FC] = 5.9, p = 0.014; FDRPs: FC = 5.2, p = 0.006; HPs: FC = 4.2, p = 0.012) and IL-6 (MSPs: FC = 5.6, p = 0.003; FDRPs: FC = 5.5, p = 0.002; HPs: FC = 5.1, p < 0.001) were downregulated after vitamin D3 treatment. In addition, levels of IL-10 (MSPs: FC = 6.2, p = 0.005; FDRPs: FC = 4.6, p < 0.001; HPs: FC = 5.2, p < 0.001) were upregulated after 8 weeks.
Conclusions:
Although supplementation with vitamin D3 reduced the mRNA expression levels of IL-17A and IL-6, it increased the mRNA expression level of IL-10 in all groups. However, these effects were more considerable in the MSP group than in the other groups. Of interest, in a deficiency state of serum vitamin D3, IL-17A expression had a positive feedback effect on the expression of IL-6. Conversely, in the sufficient state, IL-10 expression had a negative feedback effect on the expression of IL-17A and IL-6.

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Re: all things vitamin D

Post by jimmylegs » Fri Dec 28, 2018 12:14 pm

Vitamin D3 potentiates myelination and recovery after facial nerve injury (2015)
https://www.ncbi.nlm.nih.gov/pubmed/25261104

Roles of vitamin D on the immune and nervous systems are increasingly recognized. Two previous studies demonstrated that ergocalciferol (vitamin D2) or cholecalciferol (vitamin D3) induced functional recovery and increased myelination in a rat model of peroneal nerve transection. The current report assessed whether cholecalciferol was efficient in repairing transected rabbit facial nerves. Animals were randomized into two groups of rabbits with an unilateral facial nerve surgery: the vitamin D group included animals receiving a weekly oral bolus of vitamin D3 (200 IU/kg/day), from day 1 post-surgery; the control group included animals receiving a weekly oral bolus of vehicle (triglycerides). Contralateral unsectioned facial nerves from all experimental animals were used as controls for the histological study. The facial functional index was measured every week while the inner diameter of myelin sheath and the G ratio were quantified at the end of the 3 month experiment. The current report indicates that cholecalciferol significantly increases functional recovery and myelination, after 12 weeks of treatment. To the best of our knowledge, this is the first study investigating the therapeutic benefit of vitamin D supplementation in an animal model of facial paralysis. It paves further the way for clinical trials based on the administration of this steroid in individuals with injured facial nerves.
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Re: all things vitamin D

Post by lyndacarol » Fri Dec 28, 2018 2:01 pm

jimmylegs wrote:Vitamin D and remyelination in multiple sclerosis (2018)

Abstract
Introduction

Several studies have found an association between multiple sclerosis and vitamin D (VD) deficiency, which suggests that VD may play a role in the immune response. However, few studies have addressed its role in remyelination.

Development
The VD receptor and the enzymes transforming VD into metabolites which activate the VD receptor are expressed in central nervous system (CNS) cells, which suggests a potential effect of VD on the CNS. Both in vitro and animal model studies have shown that VD may play a role in myelination by acting on factors that influence the microenvironment which promotes both proliferation and differentiation of neural stem cells into oligodendrocyte progenitor cells and oligodendrocytes. It remains unknown whether the mechanisms of internalisation of VD in the CNS are synergistic with or antagonistic to the mechanisms that facilitate the entry of VD metabolites into immune cells.

Conclusions
VD seems to play a role in the CNS and our hypothesis is that VD is involved in remyelination. Understanding the basic mechanisms of VD in myelination is necessary to manage multiple sclerosis patients with VD deficiency.
Here is the URL to this article, Vitamin D and remyelinationIn multiple sclerosis, written by Matias-Guiu J, Oreja-Guevara C, Matias-Guiu JA, Gomez-Pinedo U.:

https://www.ncbi.nlm.nih.gov/pubmed/27321170

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Re: all things vitamin D

Post by jimmylegs » Mon Dec 31, 2018 11:06 am

re http://www.thisisms.com/forum/natural-a ... ml#p256137
i am interested in the range within which vit d3 could be helpful vs harmful to myelin processes. as with any essential, i expect d3's interaction with myelin is a u-shaped phenomenon.
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Re: all things vitamin D

Post by Petr75 » Tue Jan 01, 2019 1:17 pm

2018 Dec
Academic MS Center Limburg, Zuyderland Medical Center, Sittard, the Netherlands; School for Mental Health and Neuroscience, Maastricht University Medical Center, Maastricht, the Netherlands
Correlation of different cellular assays to analyze T cell-related cytokine profiles in vitamin D3-supplemented patients with multiple sclerosis.
https://www.ncbi.nlm.nih.gov/pubmed/30550982

Abstract
Different laboratory approaches have been exploited to analyze an effect of vitamin D3 supplements on T cell cytokine profiles in multiple sclerosis, with poorly reproducible results. We assessed the correlation between intra-cellular flowcytometry analysis of CD4 T cell-enriched CD3+CD8- lymphocytes after PMA/ionomycin stimulation directly ex-vivo or after 72 h pre-stimulation with anti-CD3, and cytokine levels excreted in culture supernatants. Pre-stimulation with anti-CD3 resulted in higher proportions of cells positive for IFN-γ, IL-17 A, IL-4, IL-10 and GM-CSF (all P < 0.001), but not TNF-α. Positive correlation between approaches was highly variable, but most eminent for IFN- γ and IL-4 (R = 0.608-0.612 and R = 0.677-0.777, resp., all P < 0.001). No effect of 16-weeks vitamin D3 supplements on any outcome was found except for a decreased TNF-α concentration in culture supernatants. Choice of immune-assay is, apparently, a relevant confounder for the reproducibility of individual studies.

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2019: Vitamin D - Enough is Enough

Post by jimmylegs » Mon Jan 28, 2019 5:54 am

once again, a disappointing absence of cofactor info other than calcium.
as for level, i'd probably go with 100-150 nmol/l but ok.
pretty sure the diet only idea is terrible advice, but for those who can demonstrably achieve that range with diet, power to them.
personally, i definitely need to do a better job on plain old UV exposure when i have the opportunity.

Vitamin D Supplementation in Central Nervous System Demyelinating Disease—Enough Is Enough (2019)
https://www.mdpi.com/1422-0067/20/1/218/htm

Therefore, we recommend a vitamin D serum level between 75–125 nmol/L, as proposed by other clinicians [126]. This range of vitamin D has been associated with low risk of developing MS and low disease activity and can be easily reached with adequate sun exposure and vitamin D balanced diet without any additional vitamin D supplementation.

3. Conclusions
There is little doubt that a low vitamin D status is a risk factor for development and progression of MS. In part, this may reflect a true deficit in vitamin D itself, on the other hand, low vitamin D levels may be indicative of a lack of sun exposure, which appears to mediate beneficial effects independent or in addition to raising the vitamin D levels. Although, controlled supplementation studies in patients with MS suggest that therapeutically raising vitamin D in affected patients may positively influence the course of disease, conclusive evidence is unfortunately still lacking. Emerging studies caution that higher dose vitamin D supplementation may have the opposite clinical effect via secondary hypercalcemia having a T cell-stimulating effect. This novel concept of a relatively narrow therapeutic window for vitamin D, may also shed light on the question of why clinical trials often using higher doses of vitamin D failed or yielded conflicting results. In conclusion, vitamin D should be supplemented at moderate doses in a serum level-controlled manner. Patients should be also assessed for hypercalcemia, which should be strictly avoided. In the big picture, moderate sun exposure, combined with a diverse diet including vitamin D precursors, in conjunction with a regular assessment of vitamin D serum levels, might be the best balanced and advisable strategy for patients with MS.
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2018 study: vitamin D3, axonal damage, de-/remyelination

Post by jimmylegs » Tue Feb 05, 2019 1:40 pm

good to know:
  • Effects of vitamin D on axonal damage during de- and remyelination in the cuprizone model (2018)
    https://www.sciencedirect.com/science/a ... 2818301826

    Highlights
    • Cuprizone mice fed high dose vs. low dose cholecalciferol had significantly less axonal damage.
    • High dose calcitriol, given after the demyelination phase, did not influence axonal loss or regeneration.
    •To protect against axonal loss high dose vitamin D had to be given before and during demyelination.
free full text is out there for anyone interested in the nitty gritty. at first glance, i'm not 100% clear on how to interpret the high dose regimen.
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2016: vit D & b-cell immunoreactivity in MS

Post by jimmylegs » Wed Feb 06, 2019 4:56 am

  • Hypovitaminosis D upscales B-cell immunoreactivity in multiple sclerosis (2016)
    https://www.sciencedirect.com/science/a ... 2816300455

    Highlights
    •B cells from MS patients with hypovitaminosis D exhibit enhanced immune responses ex vivo.
    •Hypovitaminosis D coincides with low vitamin D levels and increased frequencies of mature B-cell subtypes in the cerebrospinal fluid.
    •Vitamin D-supplementation attenuates B-cell immunoreactivities.

    Results
    B cells from MS patients with 25(OH)D serum levels < 20 ng/ml, displayed enhanced immunoreactivity ex vivo as a consequence of more vigorous responses of CD27+ memory phenotypes. Immune responses decreased when B cells from either source were co-cultured in the presence of vitamin D or when retesting B cells from MS patients after prolonged supplementation with vitamin D. Hypovitaminosis D was detectable in the serum of 40/95 MS patients, correlated with decreased vitamin D concentrations in CSF and with higher disease activity, and was paralleled by intrathecal accumulation of CD27+ B-cell subtypes and plasma cells.
if you're wondering, per the line of best fit, b-cell proliferation and il-6 release continued to drop as serum d3 levels increased

mean (range) for all participants: 25(OH)D [ng/ml] Serum 31.1 (4.7–92.4)
and for supplemented participants 38.8 (15.3–92.4)

"Dosage for vitamin D supplementation ranged from 1000 IU per day to 20,000 IU per week"

(interesting, since in other research 20K IU/wk couldn't reliably get all participants above 100 nmol/l ie 40 ng/ml. not sure if i could check whether anyone in that other work attained or came close to 90 ng/ml via 20K IU/wk)
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Re: all things vitamin D

Post by Petr75 » Sun Mar 03, 2019 2:54 am

2019 Jan 23
Neurology Department, College of Medicine, Prince Sattam bin Abdulaziz University, Saudi Arabia
Neurology Department, Faculty of Medicine, Minia University, Minia, Egypt
Effect of vitamin D replacement on depression in multiple sclerosis patients.
https://www.ncbi.nlm.nih.gov/pubmed/30708308

Abstract
BACKGROUND:
Multiple sclerosis (MS) is a chronic demyelinating disease of the central nervous system. Depression is common among MS patients. In patients without MS, lower vitamin D levels were associated with higher depression scores and severity. Supplementation of vitamin D was associated with significant improvement of depressive symptoms.
OBJECTIVE:
to evaluate the relation between vitamin D levels and depression scores, and the effect of vitamin D replacement on the depressive symptoms in patients with MS.
METHODS:
The study included 35 patients with relapsing remitting multiple sclerosis. Neurological, psychiatric, and radiological evaluations were done. Participants received 10,000 IU of cholecalciferol daily for 12 months.
RESULTS:
Vitamin D level was low at baseline. Depressive symptoms were high at baseline and improved with vitamin D replacement although, Expanded Disability Status Scale (EDSS) score was not improving. Vitamin D levels correlated negatively with depressive symptoms at baseline and follow up periods.
CONCLUSION:
Lower vitamin D levels are associated with higher depressive scores, and vitamin D replacement could improve depressive symptoms in patients with relapsing remitting multiple sclerosis.

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Re: all things vitamin D

Post by jimmylegs » Sun Mar 03, 2019 5:54 am

thx for posting :)
as for the content.. let me guess, didn't test the effect of teaming up anything important to go *with* the d3 - le sigh!
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Re: all things vitamin D

Post by jimmylegs » Sun Mar 03, 2019 6:21 am

most if not all of the below has been previously posted, but in review:
  • Magnesium, vitamin D status and mortality: results from US National Health and Nutrition Examination Survey (NHANES) 2001 to 2006 and NHANES III (2013)
    fft: https://bmcmedicine.biomedcentral.com/a ... 015-11-187

    Abstract
    Background
    Magnesium plays an essential role in the synthesis and metabolism of vitamin D and magnesium supplementation substantially reversed the resistance to vitamin D treatment in patients with magnesium-dependent vitamin-D-resistant rickets. We hypothesized that dietary magnesium alone, particularly its interaction with vitamin D intake, contributes to serum 25-hydroxyvitamin D (25(OH)D) levels, and the associations between serum 25(OH)D and risk of mortality may be modified by magnesium intake level.

    Methods
    We tested these novel hypotheses utilizing data from the National Health and Nutrition Examination Survey (NHANES) 2001 to 2006, a population-based cross-sectional study, and the NHANES III cohort, a population-based cohort study. Serum 25(OH)D was used to define vitamin D status. Mortality outcomes in the NHANES III cohort were determined by using probabilistic linkage with the National Death Index (NDI).

    Results
    High intake of total, dietary or supplemental magnesium was independently associated with significantly reduced risks of vitamin D deficiency and insufficiency respectively. Intake of magnesium significantly interacted with intake of vitamin D in relation to risk of both vitamin D deficiency and insufficiency. Additionally, the inverse association between total magnesium intake and vitamin D insufficiency primarily appeared among populations at high risk of vitamin D insufficiency. Furthermore, the associations of serum 25(OH)D with mortality, particularly due to cardiovascular disease (CVD) and colorectal cancer, were modified by magnesium intake, and the inverse associations were primarily present among those with magnesium intake above the median.

    Conclusions
    Our preliminary findings indicate it is possible that magnesium intake alone or its interaction with vitamin D intake may contribute to vitamin D status. The associations between serum 25(OH)D and risk of mortality may be modified by the intake level of magnesium. Future studies, including cohort studies and clinical trials, are necessary to confirm the findings.
checking citing articles... i enjoyed it when this one came out
  • Essential Nutrient Interactions: Does Low or Suboptimal Magnesium Status Interact with Vitamin D and/or Calcium Status? (2016)
    https://academic.oup.com/advances/artic ... 25/4524034

    Although much is known about magnesium, its interactions with calcium and vitamin D are less well studied. Magnesium intake is low in populations who consume modern processed-food diets. Low magnesium intake is associated with chronic diseases of global concern [e.g., cardiovascular disease (CVD), type 2 diabetes, metabolic syndrome, and skeletal disorders], as is low vitamin D status. No simple, reliable biomarker for whole-body magnesium status is currently available, which makes clinical assessment and interpretation of human magnesium research difficult. Between 1977 and 2012, US calcium intakes increased at a rate 2–2.5 times that of magnesium intakes, resulting in a dietary calcium to magnesium intake ratio of >3.0. Calcium to magnesium ratios <1.7 and >2.8 can be detrimental, and optimal ratios may be ∼2.0. Background calcium to magnesium ratios can affect studies of either mineral alone. For example, US studies (background Ca:Mg >3.0) showed benefits of high dietary or supplemental magnesium for CVD, whereas similar Chinese studies (background Ca:Mg <1.7) showed increased risks of CVD. Oral vitamin D is widely recommended in US age-sex groups with low dietary magnesium. Magnesium is a cofactor for vitamin D biosynthesis, transport, and activation; and vitamin D and magnesium studies both showed associations with several of the same chronic diseases. Research on possible magnesium and vitamin D interactions in these human diseases is currently rare. Increasing calcium to magnesium intake ratios, coupled with calcium and vitamin D supplementation coincident with suboptimal magnesium intakes, may have unknown health implications. Interactions of low magnesium status with calcium and vitamin D, especially during supplementation, require further study.
looks like i don't have full text access to this one (yet). pretty interesting dynamics. i don't think i had time to fully absorb what the abstract was saying first time i encountered this one.
  • Magnesium status and supplementation influence vitamin D status and metabolism: results from a randomized trial (2018)
    https://academic.oup.com/ajcn/article-a ... 49/5239886

    ABSTRACT
    Background
    Previous in vitro and in vivo studies indicate that enzymes that synthesize and metabolize vitamin D are magnesium dependent. Recent observational studies found that magnesium intake significantly interacted with vitamin D in relation to vitamin D status and risk of mortality. According to NHANES, 79% of US adults do not meet their Recommended Dietary Allowance of magnesium.

    Objectives
    The aim of this study was to test the hypothesis that magnesium supplementation differentially affects vitamin D metabolism dependent on baseline 25-hydroxyvitamin D [25(OH)D] concentration.

    Methods
    The study included 180 participants aged 40–85 y and is a National Cancer Institute independently funded ancillary study, nested within the Personalized Prevention of Colorectal Cancer Trial (PPCCT), which enrolled 250 participants. The PPCCT is a double-blind 2 × 2 factorial randomized controlled trial conducted in the Vanderbilt University Medical Center. Doses for both magnesium and placebo were customized based on baseline dietary intakes. Subjects were randomly assigned to treatments using a permuted-block randomization algorithm. Changes in plasma 25-hydroxyvitamin D3 [25(OH)D3], 25-hydroxyvitamin D2 [25(OH)D2], 1,25-dihydroxyvitamin D3, 1,25-dihydroxyvitamin D2, and 24,25-dihydroxyvitamin D3 [24,25(OH)2D3] were measured by liquid chromatography–mass spectrometry.

    Results
    The relations between magnesium treatment and plasma concentrations of 25(OH)D3, 25(OH)D2, and 24,25(OH)2D3 were significantly different dependent on the baseline concentrations of 25(OH)D, and significant interactions persisted after Bonferroni corrections. Magnesium supplementation increased the 25(OH)D3 concentration when baseline 25(OH)D concentrations were close to 30 ng/mL, but decreased it when baseline 25(OH)D was higher (from ∼30 to 50 ng/mL). Magnesium treatment significantly affected 24,25(OH)2D3 concentration when baseline 25(OH)D concentration was 50 ng/mL but not 30 ng/mL. On the other hand, magnesium treatment increased 25(OH)D2 as baseline 25(OH)D increased.

    Conclusion
    Our findings suggest that optimal magnesium status may be important for optimizing 25(OH)D status. This trial was registered at clinicaltrials.gov as NCT03265483.
which brings us to this recent editorial:
  • Personalized magnesium intervention to improve vitamin D metabolism: applying a systems approach for precision nutrition in large randomized trials of diverse populations (2018)
    https://academic.oup.com/ajcn/article-a ... 59/5239922
    fft: https://bit.ly/2SG3Qxr

    Greater intakes of micronutrients and minerals such as vitamin D, calcium, and magnesium have long been associated with decreased incidence of many late-onset disorders in observational studies (1–5), although large randomized intervention trials that directly evaluate their clinical efficacies have generated inconsistent results (6–8). Nevertheless, some observations have been well recognized, including high prevalence of vitamin D and magnesium insufficiency in westernized populations (9, 10) and the large interpersonal variations of vitamin D and magnesium metabolisms in the general population (11). Studies have shown that magnesium plays a critically important role in the synthesis and metabolism of vitamin D, raising the possibility that magnesium should be included in any vitamin D regimen for optimal biological functioning.
and nobody's had time to cite that last one yet. we're getting there. slowly lol.
take control of your own health
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ask for referrals to preventive health care specialists eg dietitians
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Re: all things vitamin D

Post by Petr75 » Tue Apr 02, 2019 11:37 am

February 2019
Multiple Sclerosis and Vitamin D – Caviar or a Dog’s Dinner?
https://www.msard-journal.com/article/S ... 9/fulltext

Evidence going back several decades suggests that vitamin D deficiency is somewhere in the causal pathway of MS. Vitamin D insufficiency might stem from decreased dietary intake, genes that control the vitamin D pathway, or sun exposure. It is usually estimated by serum 25-hydroxyvitamin D level. Of note, serum vitamin D levels are an indirect measure of sun exposure that in turn has an effect on MS risk but recent evidence suggests that sun exposure and vitamin D status are independent risk factors for MS (Langer-Gould et al., 2018).

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Re: all things vitamin D

Post by Petr75 » Mon Apr 29, 2019 10:16 am

2019 Apr;9
Department of Neurology, Institute of Neurosciences, IdISSC, Hospital Clínico San Carlos, Universidad Complutense de Madrid, Spain
Exonic variants of genes related to the vitamin D signaling pathway in the families of familial multiple sclerosis using whole-exome next generation sequencing.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6456803/

Abstract
INTRODUCTION:
Vitamin D (VD) deficiency has been associated with multiple sclerosis (MS) and other autoimmune diseases (AIDs). However, the effect of the genetics of VD on the risk of MS is subject to debate. This study focuses on genes linked to the VD signaling pathway in families with MS. The evaluation of gene variants in all the members of families could contribute to an additional knowledge on the information obtained from case-control studies that use nonrelated healthy people.
MATERIAL AND METHODS:
We studied 94 individuals from 15 families including at least two patients with MS. We performed whole-exome next generation sequencing on all individuals and analyzed variants of the DHCR7, CYP2R1, CYP3A4, CYP27A1, GC, CYP27B1, LRP2, CUBN, DAB2, FCGR, RXR, VDR, CYP24A1, and PDIA3 genes. We also studied PTH, FGF23, METTL1, METTL21B, and the role of the linkage disequilibrium block on the long arm of chromosome 12, through analysis of the CDK4, TSFM, AGAP2, and AVIL genes. We compared patients with MS, other AIDs and unaffected members from different family types.
RESULTS:
The study described the variants in the VD signaling pathway that appear in families with at least two patients with MS. Some infrequent variants were detected in these families, but no significant difference was observed between patients with MS and/or other AIDs and unaffected family members in the frequency of these variants. Variants previously associated with MS in the literature were not observed in these families or were distributed similarly in patients and unaffected family members.
CONCLUSION:
The study of genes involved in the VD signaling pathway in families that include more than one patient with MS did not identify any variants that could explain the presence of the disease, suggesting that VD metabolism could probably play a role in MS more as an environmental factor rather than as a genetic factor. Our study also supports the analysis of cases and unaffected individuals within families in order to determine the influence of genetic factors.

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