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Objectives: The effect of vitamin D supplementation on the disease course of multiple sclerosis (MS) is not established. Neurofilament light chain (NFL) is a sensitive marker of axonal degeneration. The aim of this study was to establish whether high-dose vitamin D supplementation reduces serum levels of NFL., Materials and Methods: We have performed a 96 weeks placebo-controlled randomized study of weekly supplementation with 20 000 IU vitamin D3 in 71 patients with relapsing remitting MS (RRMS). Serum levels of NFL were measured at baseline, week 48 and week 96 with a single molecule (Simoa) assay in 69 of these patients., Results: Serum levels of 25-hydroxyvitamin D more than doubled in the vitamin D group. Compared to placebo, vitamin D supplementation had no overall effect on the change in serum levels of NFL from baseline (P = 0.93 at week 48 and P = 0.56 at week 96). In the subgroup of patients not receiving disease-modifying therapy, NFL decreased by 30.9% to week 48% and 32.6% to week 96 from baseline in the vitamin D group as compared to the placebo group (P = 0.06 for both time points)., Conclusion: With a possible exception for patients not treated with disease-modifying drugs, weekly supplementation with 20 000 IU vitamin D3 did not affect NFL levels in these RRMS patients., (© 2018 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

Background: People with multiple sclerosis have high risk of osteoporosis and fractures. A poor vitamin D status is a risk factor for MS, and vitamin D supplementation has been recommended both to prevent MS progression and to maintain bone health., Methods: We assessed the effect of 20,000 IU vitamin D 3 weekly compared to placebo on biochemical markers of bone metabolism in 68 persons with relapsing remitting multiple sclerosis., Results: Serum levels of 25-hydroxyvitamin D more than doubled in the vitamin D group, and parathyroid hormone decreased in the vitamin D group compared to the placebo group at week 48 and week 96. There was however no effect on bone formation as measured by procollagen type I N propeptide (PINP), or on bone resorption as measured by C-terminal cross-linking telopeptide of type I collagen (CTX1). Neither PINP nor CTX1 predicted bone loss from baseline to week 96., Conclusions: These findings corroborate the previously reported lack of effect of weekly high dose vitamin D supplementation on bone mass density in the same patients, and suggest that such vitamin D supplementation does not prevent bone loss in persons with MS who are not vitamin D deficient., Trial Registration: The trial was registered at ClinicalTrials.gov on April 4 2008, registration number NCT00785473 .

Background: Several recent studies have found a higher risk of multiple sclerosis (MS) among people with a low level of education. This has been suggested to reflect an effect of smoking and lower vitamin D status in the social class associated with lower levels of education., Objective: The objective of this paper is to investigate the association between level of education and MS risk adjusting for the known risk factors smoking, infectious mononucleosis, indicators of vitamin D levels and body size., Methods: Within the case-control study on Environmental Factors In MS (EnvIMS), 953 MS patients and 1717 healthy controls from Norway reported educational level and history of exposure to putative environmental risk factors., Results: Higher level of education were associated with decreased MS risk (p trend = 0.001) with an OR of 0.53 (95% CI 0.41-0.68) when comparing those with the highest and lowest level of education. This association was only moderately reduced after adjusting for known risk factors (OR 0.61, 95% CI 0.44-0.83). The estimates remained similar when cases with disease onset before age 28 were excluded., Conclusion: These findings suggest that factors related to lower socioeconomic status other than established risk factors are associated with MS risk., (© The Author(s), 2015.)

Observational studies have suggested that vitamin D may reduce inflammation in relapsing-remitting multiple sclerosis (RRMS), but this has not been clearly confirmed in randomized controlled trials. To further explore the possible anti-inflammatory effects of vitamin D in RRMS, we examined the effect of high-dose oral vitamin D3 on eleven markers of systemic inflammation in 68 RRMS patients enrolled in a double-blinded randomized placebo-controlled trial of vitamin D3 supplementation (20,000 IU/week) (NCT00785473). Serum inflammation markers and 25-hydroxyvitamin D (25(OH)D) were measured at baseline and week 96, and no restrictions were set on additional standard immunomodulatory treatment for RRMS. The mean 25(OH)D level rose from 56 ± 29 to 123 ± 34 nmol/L among patients receiving vitamin D3 supplementation, whereas only a minor increase from 57 ± 22 to 63 ± 24 nmol/L was seen in the placebo group. However, no significant differences appeared between the vitamin D group and the placebo group for any of the inflammation markers. Patients on immunomodulatory therapy had significantly higher levels of interleukin-1 receptor antagonist and chemokine (C-X-C motif) ligand 16 than patients without immunomodulatory treatment, but there were no clear synergistic effects between immunomodulatory therapy and vitamin D3 supplementation on any of the inflammation markers. The rise in 25(OH)D levels after vitamin D3 supplementation was unaffected by immunomodulatory treatment. We conclude that in this study of RRMS patients, high-dose oral vitamin D3 supplementation prominently increased serum 25(OH)D levels without affecting markers of systemic inflammation, while a more anti-inflammatory phenotype was found among patients on immunomodulatory treatment.

Vitamin D sufficiency has been associated with lower risk of multiple sclerosis and may also have a favorable effect on the course of the disease. The aim of this work was to identify predictors of serum 25-hydroxy vitamin D (25[OH]D) levels in persons with multiple sclerosis (MS) and to assess the effect of high-dose vitamin D(3) supplementation on vitamin D status. A 96-week randomized controlled trial was performed to assess the effect of supplementation with 20,000 IU of vitamin D(3) weekly on bone mineral density in 68 patients. We collected data on vitamin D intake and UV-exposure and repeatedly measured serum 25(OH)D levels. Half of the participants had sufficient winter vitamin D levels at baseline (≥ 50 nmol/l). Vitamin D status was predicted by sun exposure during the last 3 months and by ingested vitamin D from diet and supplements. In the placebo group, the proportion of the participants with sufficient levels increased from 55 % in winter to 92 % during the summer. In the intervention group, all participants had winter 25(OH)D levels above 50 nmol/l at the end of the study. MS patients who have no sun exposure and low dietary vitamin D intake during the winter months should be recommended to take vitamin D supplements to achieve serum 25(OH)D levels of at least 50 nmol/l.

Epidemiological and experimental evidence suggest that a poor vitamin D status is associated with an increased risk of developing multiple sclerosis (MS), and also an unfavorable disease course. Vitamin D may exert relevant effects both on the immune system and on resident cells within the CNS. The data from clinical trials is, however, restricted, and does not allow any conclusion on the effect of high-dose vitamin D supplementation on disease course. The results from sufficiently powered studies will not be available for at least 2 years. MS patients are, however, prone to develop osteoporosis and have increased risk of fractures. Therefore, the authors advise that the serum concentration of 25-hydroxyvitamin D is monitored in order to prevent bone deficit, and that a serum level of 75-125 nmol/l is targeted. This level is sufficient for maintenance of bone health, is not known to be associated with adverse events, and is in the range that has been associated with low risk of developing MS and low disease activity.

Multiple sclerosis (MS) risk is determined by environmental influences acting on the individual genetic background. Recent epidemiologic and experimental evidence supports a role of low environmental supplies of vitamin D in mediating an increased susceptibility to MS. We review available evidence suggesting that vitamin D status may influence MS risk and even modulate clinical disease activity. The level of serum 25-hydroxyvitamin D providing these effects remains to be determined., (Copyright © 2010 Elsevier B.V. All rights reserved.)

Multiple sclerosis (MS) is a chronic disease of the central nervous system, pathologically characterized by inflammation, demyelination, and axonal damage, presumably auto-immune in nature. Complex interactions between genetic susceptibility and environmental factors, such as vitamin D status and primary Epstein-Barr virus infection in adolescence or later in life, probably determine the MS risk. Norway at a latitude 58-71 degrees N is a discrete exception to the hypothesis that solar UV radiation exposure, mediated by vitamin D, coheres with the latitude gradient seen for MS prevalence. Where UV radiation exposure is low in Norway,vitamin D sufficiency is maintained through a traditional diet providing vitamin D as well as marine omega-3 polyunsaturated fatty acids. This observation supports an environmental interaction between diet and latitude, with vitamin D as the common mediator. The potential roles of vitamin D, other environmental exposures, and genes in the complex aetiology of MS are discussed in this review., ((c) 2008 S. Karger AG, Basel)

Background: Elevated antibody levels against Epstein–Barr virus (EBV) and a poor vitamin D status are environmental factors that may interact in relapsing-remitting multiple sclerosis (RRMS) aetiology. Objectives: To examine effects of high-dose oral vitamin D3 supplementation on antibody levels against EBV nuclear antigen 1 (EBNA1) in RRMS. Methods: Serum 25-hydroxyvitamin D3 (25(OH)D) and immunoglobulin G antibody levels against EBNA1 (whole protein and amino acid 385–420 fragment), EBV viral capsid antigen (VCA), cytomegalovirus (CMV) and varicella zoster virus (VZV) were measured in 68 RRMS patients enrolled in a 96-week randomised double-blinded placebo-controlled clinical trial of oral vitamin D3 supplementation (20,000 IU/week) (NCT00785473). Results: The mean 25(OH)D level more than doubled in the vitamin D group and was significantly higher than in the placebo group at study conclusion (123.2 versus 61.8 nmol/L, p < 0.001). Compared to the placebo group, both anti-EBNA1 protein and fragment antibody levels decreased in the vitamin D group from baseline to week 48 (p = 0.038 and p = 0.004, respectively), but not from baseline to week 96. Vitamin D3 supplementation did not affect antibodies against VCA, CMV or VZV. Conclusion: The results indicate that high-dose oral vitamin D3 supplementation can affect humoral immune responses against the latent EBV antigen EBNA1 in RRMS. [ABSTRACT FROM AUTHOR]

Background: Low vitamin D levels have been associated with an increased risk of multiple sclerosis (MS), although it remains unknown whether this relationship varies by age. Objective: The objective of this paper is to investigate the association between vitamin D3 supplementation through cod liver oil at different postnatal ages and MS risk. Methods: In the Norwegian component of the multinational case-control study Environmental Factors In Multiple Sclerosis (EnvIMS), a total of 953 MS patients with maximum disease duration of 10 years and 1717 controls reported their cod liver oil use from childhood to adulthood. Results: Self-reported supplement use at ages 13-18 was associated with a reduced risk of MS (OR 0.67, 95% CI 0.52-0.86), whereas supplementation during childhood was not found to alter MS risk (OR 1.01, 95% CI 0.81-1.26), each compared to non-use during the respective period. An inverse association was found between MS risk and the dose of cod liver oil during adolescence, suggesting a dose-response relationship (p trend = 0.001) with the strongest effect for an estimated vitamin D3 intake of 600-800 IU/d (OR 0.46, 95% CI 0.31-0.70). Conclusions: These findings not only support the hypothesis relating to low vitamin D as a risk factor for MS, but further point to adolescence as an important susceptibility period for adult-onset MS. [ABSTRACT FROM AUTHOR]

The article presents research which examines if body size influences the risk of multiple sclerosis (MS) in a population-based, case control study in Norway and Italy. It notes the definition of body size-related MS risk by odds ratios (ORs) in logistic regression analyses adjusting for age, smoking and outdoor activity. It reveals the possibility of obesity from childhood until young adulthood to be a risk factor for MS with a seemingly stronger effect in countries mentioned.

The article examines the association between multiple sclerosis (MS) and measures of sun exposure in specific age periods in Norway and Italy. The multinational case-control study (EnvIMS) study included 1660 MS patients and 3050 controls from Italy and Norway. It found converging evidence that underlines the beneficial effect of sun exposure on MS risk.

The article focuses on the research which shows the association between infectious mononucleosis (IM) and multiple sclerosis (MS) in Norway. The research was conducted on 1660 MS patients and 3050 control groups from Norway and Italy .It states that IM occurs frequently in Norway but was linked with MS to a similar degree in the country. It mentions that IM is linked with MS independently of season, while its association with IM during spring is not stronger.

The article discusses a randomised controlled trial on the effect of supplementing vitamin D3 on relapses, disease progression, and measures of functions in multiple sclerosis. The study investigates the effect on Expanded Disability Status Scale (EDSS), exploratory outcomes annualised relapse rate (ARR), and multiple sclerosis functional composite (MSFC) components, grip strength, and fatigue. The study concludes that the supplementation was not beneficial on the related outcomes.