Vitamin D Supplementation as Add-on Therapy in Multiple Sclerosis—Balance between Benefit and Risk?: A Commentary on Vitamin D Supplementation in Central Nervous System Demyelinating Disease—Enough Is Enough

Goischke, Hans-Klaus

doi:10.3390/ijms20061513

Cited by 3 publications

(2 citation statements)

References 21 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The highest prevalence of relapses was observed at a value of 17.2 ng/ mL 25(OH)D3 [7]. It is to be demanded that studies on the effect of vitD with determination of the sNfL values with a daily supplementation with 4,000 IU/die to a maximum of 10,000 IU/die vitD (not high doses weekly or monthly) be carried out [8]. At higher doses (up to 14,000 IU/die), no improvement was registered, although there were signs of a protective effect on new MRI lesions [9].…”

Section: Dear Editormentioning

confidence: 99%

Neurofilament Light Chain Determination: Referee for Future Vitamin D3 Supplementation in Multiple Sclerosis?

Goischke¹

2022

Neuroimmunomodulation

View full text Add to dashboard Cite

Section: Dear Editormentioning

confidence: 99%

Neurofilament Light Chain Determination: Referee for Future Vitamin D3 Supplementation in Multiple Sclerosis?

Goischke¹

2022

Neuroimmunomodulation

View full text Add to dashboard Cite

“…The role of circadian dysregulation in multiple sclerosis (MS) is indicated by the modulation of its course by circadian gene alleles [1], and the increased risk associated with single nucleotide polymorphisms (SNPs) in the circadian genes Aryl Hydrocarbon Receptor Nuclear Translocator Like (ARNTL) and Circadian Locomotor Output Cycles Kaput (CLOCK) [2]. The heightened MS risk linked with latitudes further from the equator has classically been seen as indicative of a role for decreased vitamin D in the etiology and course of MS [3,4,5,6]. However, such data may also be attributed to an irregularity in the circadian rhythm, as supported by an increased risk of MS in shift-workers [7].…”

Section: Introductionmentioning

confidence: 99%

Multiple Sclerosis: Melatonin, Orexin, and Ceramide Interact with Platelet Activation Coagulation Factors and Gut-Microbiome-Derived Butyrate in the Circadian Dysregulation of Mitochondria in Glia and Immune Cells

Anderson¹,

Rodriguez

Reíter

2019

IJMS

View full text Add to dashboard Cite

Recent data highlight the important roles of the gut microbiome, gut permeability, and alterations in mitochondria functioning in the pathophysiology of multiple sclerosis (MS). This article reviews such data, indicating two important aspects of alterations in the gut in the modulation of mitochondria: (1) Gut permeability increases toll-like receptor (TLR) activators, viz circulating lipopolysaccharide (LPS), and exosomal high-mobility group box (HMGB)1. LPS and HMGB1 increase inducible nitric oxide synthase and superoxide, leading to peroxynitrite-driven acidic sphingomyelinase and ceramide. Ceramide is a major driver of MS pathophysiology via its impacts on glia mitochondria functioning; (2) Gut dysbiosis lowers production of the short-chain fatty acid, butyrate. Butyrate is a significant positive regulator of mitochondrial function, as well as suppressing the levels and effects of ceramide. Ceramide acts to suppress the circadian optimizers of mitochondria functioning, viz daytime orexin and night-time melatonin. Orexin, melatonin, and butyrate increase mitochondria oxidative phosphorylation partly via the disinhibition of the pyruvate dehydrogenase complex, leading to an increase in acetyl-coenzyme A (CoA). Acetyl-CoA is a necessary co-substrate for activation of the mitochondria melatonergic pathway, allowing melatonin to optimize mitochondrial function. Data would indicate that gut-driven alterations in ceramide and mitochondrial function, particularly in glia and immune cells, underpin MS pathophysiology. Aryl hydrocarbon receptor (AhR) activators, such as stress-induced kynurenine and air pollutants, may interact with the mitochondrial melatonergic pathway via AhR-induced cytochrome P450 (CYP)1b1, which backward converts melatonin to N-acetylserotonin (NAS). The loss of mitochnodria melatonin coupled with increased NAS has implications for altered mitochondrial function in many cell types that are relevant to MS pathophysiology. NAS is increased in secondary progressive MS, indicating a role for changes in the mitochondria melatonergic pathway in the progression of MS symptomatology. This provides a framework for the integration of diverse bodies of data on MS pathophysiology, with a number of readily applicable treatment interventions, including the utilization of sodium butyrate.

show abstract

Vitamin D supplementation in multiple sclerosis – Can be done something more?

Tutor

2019

Medical Hypotheses

View full text Add to dashboard Cite

Vitamin D Supplementation as Add-on Therapy in Multiple Sclerosis—Balance between Benefit and Risk?: A Commentary on Vitamin D Supplementation in Central Nervous System Demyelinating Disease—Enough Is Enough

Abstract: The excellent publication by Häusler and Weber [...]

Cited by 3 publications

References 21 publications

Neurofilament Light Chain Determination: Referee for Future Vitamin D3 Supplementation in Multiple Sclerosis?

Neurofilament Light Chain Determination: Referee for Future Vitamin D3 Supplementation in Multiple Sclerosis?

Multiple Sclerosis: Melatonin, Orexin, and Ceramide Interact with Platelet Activation Coagulation Factors and Gut-Microbiome-Derived Butyrate in the Circadian Dysregulation of Mitochondria in Glia and Immune Cells

Vitamin D supplementation in multiple sclerosis – Can be done something more?

Contact Info

Product

Resources

About