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home:diseases:ms [01.28.2019] – [Recent Research] sallieqhome:diseases:ms [09.14.2022] (current) – external edit 127.0.0.1
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-[[http://www.mayoclinic.org/diseases-conditions/multiple-sclerosis/home/ovc-20131882|Mayo Clinic overview]]+[[https://www.mayoclinic.org/diseases-conditions/multiple-sclerosis/home/ovc-20131882|Mayo Clinic overview]]
  
  
 ==== Triggers and associations ==== ==== Triggers and associations ====
  
-- Exposure of the eyes to near-horizon sunshine may be a trigger for multiple sclerosis.(({{pubmed>long:19906495}}))+- Exposure of the eyes to near-horizon sunshine may be a trigger for multiple sclerosis.(({{pmid>long:19906495}}))
  
 BACKGROUND: Multiple sclerosis (MS) incidence is higher among those who live at high latitudes before adulthood. This is usually attributed to lower levels of Vitamin D, caused by lower UV levels. However direct damage of the optic nerve by near-horizon sunshine is a possible alternative explanation.  BACKGROUND: Multiple sclerosis (MS) incidence is higher among those who live at high latitudes before adulthood. This is usually attributed to lower levels of Vitamin D, caused by lower UV levels. However direct damage of the optic nerve by near-horizon sunshine is a possible alternative explanation. 
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 Multiple sclerosis etiology – an Epstein Barr hypothesis.  Multiple sclerosis etiology – an Epstein Barr hypothesis. 
-(({{pubmed>long:2833683}})) +(({{pmid>long:2833683}})) 
  
 The pathogenesis of multiple sclerosis: reconsideration of  The pathogenesis of multiple sclerosis: reconsideration of 
-the role of viral agents and defence mechanisms. (({{pubmed>long:8803938}})) +the role of viral agents and defence mechanisms. (({{pmid>long:8803938}})) 
  
  
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 Anti-tumor necrosis factor Anti-tumor necrosis factor
-treatment restores the gut barrier in Crohn’s disease.   (({{pubmed>long:12190167}})) +treatment restores the gut barrier in Crohn’s disease.   (({{pmid>long:12190167}})) 
  
-Changes in gastrointestinal permeability in celiac disease.   (({{pubmed>long:10207217}})) +Changes in gastrointestinal permeability in celiac disease.   (({{pmid>long:10207217}})) 
  
 Increased intestinal permeability as a cause of fluctuating postprandial Increased intestinal permeability as a cause of fluctuating postprandial
-blood glucose levels in Type 1 diabetic patients.   (({{pubmed>long:12713453}}))+blood glucose levels in Type 1 diabetic patients.   (({{pmid>long:12713453}}))
  
 Role of the intestinal tight junction modulator zonulin in the Role of the intestinal tight junction modulator zonulin in the
-pathogenesis of type I diabetes in BB diabetic-prone rats.   (({{pubmed>long:15710870}})) +pathogenesis of type I diabetes in BB diabetic-prone rats.   (({{pmid>long:15710870}})) 
  
  
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-Multiple sclerosis or Lyme disease? a diagnosis problem of exclusion.(({{pubmed>long:2388492}}))+Multiple sclerosis or Lyme disease? a diagnosis problem of exclusion.(({{pmid>long:2388492}}))
  
-Non-MS autoimmune demyelination.(({{pubmed>long:18928881}}))+Non-MS autoimmune demyelination.(({{pmid>long:18928881}}))
  
-Multiple sclerosis: an infectious syndrome involving Chlamydophila pneumoniae. (({{pubmed>long:16996738}}))+Multiple sclerosis: an infectious syndrome involving Chlamydophila pneumoniae. (({{pmid>long:16996738}}))
  
-Multiple sclerosis associated with Chlamydia pneumoniae infection of the CNS.(({{pubmed>long:9484408}}))+Multiple sclerosis associated with Chlamydia pneumoniae infection of the CNS.(({{pmid>long:9484408}}))
  
-Chlamydia pneumoniae infection of the central nervous system in multiple sclerosis.(({{pubmed>long:10401775}}))+Chlamydia pneumoniae infection of the central nervous system in multiple sclerosis.(({{pmid>long:10401775}}))
  
-Chlamydia pneumoniae infection of microglial cells in vitro: a model of microbial infection for neurological disease.(({{pubmed>long:16772424}}))+Chlamydia pneumoniae infection of microglial cells in vitro: a model of microbial infection for neurological disease.(({{pmid>long:16772424}}))
  
-Association between Multiple Sclerosis and Cystic Structures in Cerebrospinal Fluid (({{pubmed>long:11787831}}))+Association between Multiple Sclerosis and Cystic Structures in Cerebrospinal Fluid (({{pmid>long:11787831}}))
  
-Multifocal central nervous system lesions --multiple sclerosis or neuroborreliosis?(({{pubmed>long:16909774}}))+Multifocal central nervous system lesions --multiple sclerosis or neuroborreliosis?(({{pmid>long:16909774}}))
  
-MR imaging assessment of brain and cervical cord damage in patients with neuroborreliosis.(({{pubmed>long:16611786}}))+MR imaging assessment of brain and cervical cord damage in patients with neuroborreliosis.(({{pmid>long:16611786}}))
  
  
  
  
-Multiple sclerosis: infectious hypothesis.   (({{pubmed>long:11603624}}))  +Multiple sclerosis: infectious hypothesis.   (({{pmid>long:11603624}}))  
-Role of viruses in etiology and pathogenesis of multiple sclerosis.  (({{pubmed>long:11450311}}))  +Role of viruses in etiology and pathogenesis of multiple sclerosis.  (({{pmid>long:11450311}}))  
-Infection and the etiology and pathogenesis of multiple sclerosis. (({{pubmed>long:11898529}}))  +Infection and the etiology and pathogenesis of multiple sclerosis. (({{pmid>long:11898529}}))  
  
  
 Part I: the role of infection. Part I: the role of infection.
-Although genetic susceptibility explains the clustering of multiple sclerosis (MS) cases within families and the sharp decline in risk with increasing genetic distance, it cannot fully explain the geographic variations in MS frequency and the changes in risk that occur with migration. Epidemiological data provide some support for the "hygiene hypothesis," but with the additional proviso for a key role of Epstein-Barr virus (EBV) in determining MS risk. We show that whereas EBV stands out as the only infectious agent that can explain many of the key features of MS epidemiology, by itself the link between EBV and MS cannot explain the decline in risk among migrants from high to low MS prevalence areas. This decline implies that either EBV strains in low-risk areas have less propensity to cause MS, or that other infectious or noninfectious factors modify the host response to EBV or otherwise contribute to determine MS risk. (({{pubmed>long:17444504}}))+Although genetic susceptibility explains the clustering of multiple sclerosis (MS) cases within families and the sharp decline in risk with increasing genetic distance, it cannot fully explain the geographic variations in MS frequency and the changes in risk that occur with migration. Epidemiological data provide some support for the "hygiene hypothesis," but with the additional proviso for a key role of Epstein-Barr virus (EBV) in determining MS risk. We show that whereas EBV stands out as the only infectious agent that can explain many of the key features of MS epidemiology, by itself the link between EBV and MS cannot explain the decline in risk among migrants from high to low MS prevalence areas. This decline implies that either EBV strains in low-risk areas have less propensity to cause MS, or that other infectious or noninfectious factors modify the host response to EBV or otherwise contribute to determine MS risk. (({{pmid>long:17444504}}))
  
-**Correlation of mollicutes and their viruses with multiple sclerosis and other demyelinating diseases.**(({{pubmed>long:12606251}}))+**Correlation of mollicutes and their viruses with multiple sclerosis and other demyelinating diseases.**(({{pmid>long:12606251}}))
  
-**The MSMV hypothesis: measles virus and multiple sclerosis, etiology and treatment.**   (({{pubmed>long:18703291}})) +**The MSMV hypothesis: measles virus and multiple sclerosis, etiology and treatment.**   (({{pmid>long:18703291}})) 
  
-**Epidemiology and etiology of multiple sclerosis.**(({{pubmed>long:15893675}}))+**Epidemiology and etiology of multiple sclerosis.**(({{pmid>long:15893675}}))
  
  
 Detection of EBV-infected B-cells in patients' brain raises the possibility that intrathecal B-cell abnormalities and T-cell-mediated immunopathology in MS are the consequence of a persistently dysregulated EBV infection. Detection of EBV-infected B-cells in patients' brain raises the possibility that intrathecal B-cell abnormalities and T-cell-mediated immunopathology in MS are the consequence of a persistently dysregulated EBV infection.
-(({{pubmed>long:19359987}}))+(({{pmid>long:19359987}}))
  
  
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 This review encompasses the clinical and pathological findings that pertain to the CNS infection in humans and includes experimental data from animal models that illuminate how these microbes enter the CNS. Recent experimental data showing that L. monocytogenes can invade the CNS by more than one mechanism make it a useful model for discussing the various routes for neuroinvasion used by intracellular bacterial pathogens. This review encompasses the clinical and pathological findings that pertain to the CNS infection in humans and includes experimental data from animal models that illuminate how these microbes enter the CNS. Recent experimental data showing that L. monocytogenes can invade the CNS by more than one mechanism make it a useful model for discussing the various routes for neuroinvasion used by intracellular bacterial pathogens.
-(({{pubmed>long:15084504}}))+(({{pmid>long:15084504}}))
  
 ===== Of further interest ===== ===== Of further interest =====
  
 By shedding light on the involvement of EBV in MS, these findings will pave the way to disease prevention and increase the therapeutic index of future treatments. By shedding light on the involvement of EBV in MS, these findings will pave the way to disease prevention and increase the therapeutic index of future treatments.
-(({{pubmed>long:19359987}}))+(({{pmid>long:19359987}}))
  
-[[https://www.marshallprotocol.com/view_topic.php?id=14494&forum_id=39&highlight=+Antibiotic+use+increases+the+risk+of+Multiple+Sclerosis|Antibiotic Use]]+ In a collaborative GWAS involving 9772 cases of European descent collected by 23 research groups working in 15 different countries, we have replicated almost all of the previously suggested associations and identified at least a further 29 novel susceptibility loci. Within the MHC we have refined the identity of the DRB1 risk alleles and confirmed that variation in the HLA-A gene underlies the independent protective effect attributable to the Class I region. Immunologically relevant genes are significantly over-represented amongst those mapping close to the identified loci and particularly implicate T helper cell differentiation in the pathogenesis of multiple sclerosis.  (({{pmid>long:21833088}}))
  
-<blockquote> +Antibiotic Use (({{pmid>long:21920946}})) 
- +
-From: edj2001 +
-Date: 2011-12-30 20:49:17 +
-Reply: http://www.marshallprotocol.com/reply.php?topic_id=14494+
  
  
 +<blockquote>
 Add vitamin D to Scotland's food – experts, Dosing whole population would help cut levels of multiple sclerosis, say scientists  Sarah      Boseley, health editor guardian.co.uk, Friday       23 December 2011      15.30 EST Article      history   The following is a letter from Professor Stewart Fleming, University  of Dundee to the Guardian in regard to above article: Add vitamin D to Scotland's food – experts, Dosing whole population would help cut levels of multiple sclerosis, say scientists  Sarah      Boseley, health editor guardian.co.uk, Friday       23 December 2011      15.30 EST Article      history   The following is a letter from Professor Stewart Fleming, University  of Dundee to the Guardian in regard to above article:
  
  
-{{http://www.guardian.co.uk/science/2011/dec/28/vitamin-d-ms-medical-research?newsfeed=true|bureaucratic blight on medical research}} +{{https://www.guardian.co.uk/science/2011/dec/28/vitamin-d-ms-medical-research?newsfeed=true|bureaucratic blight on medical research}}
  
  
 Your report  (24 December) on the proposal that there should be artificial supplementation of Scotland's food by vitamin D to reduce the frequency of multiple sclerosis did not address the two main questions of whole-population interventions. Is it effective? Is it safe? Your report  (24 December) on the proposal that there should be artificial supplementation of Scotland's food by vitamin D to reduce the frequency of multiple sclerosis did not address the two main questions of whole-population interventions. Is it effective? Is it safe?
- 
  
  
 Current evidence strongly supports a role for low levels of vitamin D in the development of MS, as your article says. However, other factors are also involved. There are no population-based clinical trials supporting the effectiveness of artificial dietary supplementation by vitamin D in lowering the frequency of MS. Current evidence strongly supports a role for low levels of vitamin D in the development of MS, as your article says. However, other factors are also involved. There are no population-based clinical trials supporting the effectiveness of artificial dietary supplementation by vitamin D in lowering the frequency of MS.
- 
  
  
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 How common are these conditions? In Scotland hyperparathyroidism alone affects 6 per 1,000 of the population – it is several times more frequent than MS. So while we need to examine this issue carefully, mass medication with no published evidence of benefit, and with the risk that more people could be harmed than are likely to benefit, would be irresponsible.” How common are these conditions? In Scotland hyperparathyroidism alone affects 6 per 1,000 of the population – it is several times more frequent than MS. So while we need to examine this issue carefully, mass medication with no published evidence of benefit, and with the risk that more people could be harmed than are likely to benefit, would be irresponsible.”
  
- +//Professor  Stewart Fleming, University of Dundee//
-Professor  Stewart Fleming +
- +
-University of Dundee+
 </blockquote> </blockquote>
  
  
-**Occupational exposure to UV light and mortality from multiple sclerosis**(({{pubmed>long:19197935}}))+**Occupational exposure to UV light and mortality from multiple sclerosis**(({{pmid>long:19197935}}))
  
 <blockquote> <blockquote>
  
-"Cholecalciferol plus calcium suppresses abnormal PBMC reactivity in patients with multiple sclerosis."(({{pubmed>long:21697250}}))+"Cholecalciferol plus calcium suppresses abnormal PBMC reactivity in patients with multiple sclerosis."(({{pmid>long:21697250}}))
  
 Forty-nine patients were matched (for age, sex, disease duration, disease-modifying drug, and disability) and enrolled (treated n = 25; control n = 24). Four patients were lost to follow-up (n = 2 from each group).  Forty-nine patients were matched (for age, sex, disease duration, disease-modifying drug, and disability) and enrolled (treated n = 25; control n = 24). Four patients were lost to follow-up (n = 2 from each group). 
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 </blockquote> </blockquote>
  
-{{https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3182531/|Genetic risk and a primary role for cell-mediated immune mechanisms in multiple sclerosis}} 
  
  
-==== Myelin sheath ====+[{{home:diseases:multiple_sclerosis_incidence_world_map.jpg|MS is rare in China. 
 +Low prevalence in Russia, although it varies by ethnic region.}}] **map from msrc.co.uk** 
 + 
 + 
 + 
 + 
 + 
 + 
 +===== Myelin sheath =====
  
  
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-2018 This review focuses on four main themes influencing current understanding of thermoregulatory dysfunction in MS   (({{pubmed>long:30459034}})) +2018 This review focuses on four main themes influencing current understanding of thermoregulatory dysfunction in MS   (({{pmid>long:30459034}})) 
  
 2019 [[https://www.cell.com/neuron/fulltext/S0896-6273(18)31123-1?_returnURL=https%3A%2F%2Flinkinghub.elsevier.com%2Fretrieve%2Fpii%2FS0896627318311231%3Fshowall%3Dtrue|from Misgeld, Kerschensteiner. et al]] 2019 [[https://www.cell.com/neuron/fulltext/S0896-6273(18)31123-1?_returnURL=https%3A%2F%2Flinkinghub.elsevier.com%2Fretrieve%2Fpii%2FS0896627318311231%3Fshowall%3Dtrue|from Misgeld, Kerschensteiner. et al]]
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     •    Calcium influx from the extracellular space drives axon degeneration     •    Calcium influx from the extracellular space drives axon degeneration
     •    Nanoscale ruptures allow entry of calcium across the axonal plasma membrane     •    Nanoscale ruptures allow entry of calcium across the axonal plasma membrane
 +    
 ===== Member experience ===== ===== Member experience =====
  
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 First: Greg Blaney some years ago...   First: Greg Blaney some years ago...  
-[[http://AutoimmunityResearch.org/transcripts/ICA2008_Transcript_GregBlaney.pdf|Two MS cases]]+[[https://AutoimmunityResearch.org/transcripts/ICA2008_Transcript_GregBlaney.pdf|Two MS cases]]
  
 Next: Dr Roswitha Goetze-Pelka,  on MS patient in 2011: Next: Dr Roswitha Goetze-Pelka,  on MS patient in 2011:
-[[http://autoimmunityresearch.org/transcripts/Singapore_ACA2011_Goetze-Pelka.pdf|Case history by neurologist]]+[[https://autoimmunityresearch.org/transcripts/Singapore_ACA2011_Goetze-Pelka.pdf|Case history by neurologist]]
  
-Our simplified article in [[http://autoimmunityresearch.org/preprints/Proal_2013_CurrentOpinion-Preprint.pdf|Current Opinion in Rheumatology 2013]]+Our simplified article in [[https://autoimmunityresearch.org/preprints/Proal_2013_CurrentOpinion-Preprint.pdf|Current Opinion in Rheumatology 2013]]
  
 {{tag>disease }} {{tag>disease }}
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 +<nodisp>
 ===== Notes and comments ===== ===== Notes and comments =====
  
 removed FAILED LINK  --- //Sallie Q 01.18.2019// removed FAILED LINK  --- //Sallie Q 01.18.2019//
-{{http://www.wired.com/wiredscience/2010/04/multiple-sclerosis-twinmystery/|MS study deepens twin mystery}}+{{https://www.wired.com/wiredscience/2010/04/multiple-sclerosis-twinmystery/|MS study deepens twin mystery}}
  
  
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 <blockquote>High-dose vitamin D also was not associated with a significant difference in change in total volume of T2 lesions, with median changes of −330 mm3 compared with a change of −95 mm3 for low-dose vitamin D (P=0.6), the investigators reported in the October 25 issue of Neurology. <blockquote>High-dose vitamin D also was not associated with a significant difference in change in total volume of T2 lesions, with median changes of −330 mm3 compared with a change of −95 mm3 for low-dose vitamin D (P=0.6), the investigators reported in the October 25 issue of Neurology.
  
-[[http://www.medpagetoday.com/clinical-context/MultipleSclerosis/29235|High-Dose Vitamin D No Help in MS]]+[[https://www.medpagetoday.com/clinical-context/MultipleSclerosis/29235|High-Dose Vitamin D No Help in MS]]
  
 2011. "A randomized trial of high-dose vitamin D2 in relapsing-remitting multiple sclerosis."  2011. "A randomized trial of high-dose vitamin D2 in relapsing-remitting multiple sclerosis." 
  
- OBJECTIVE: Higher latitude, lower ultraviolet exposure, and lower serum 25-hydroxyvitamin D (25OHD) correlate with higher multiple sclerosis (MS) prevalence, relapse rate, and mortality. We therefore evaluated the effects of high-dose vitamin D2 (D2) in MS. METHODS: Adults with clinically active relapsing-remitting MS (RRMS) were randomized to 6 months' double-blind placebo-controlled high-dose vitamin D2, 6,000 IU capsules, dose adjusted empirically aiming for a serum 25OHD 130-175 nM. All received daily low-dose (1,000 IU) D2 to prevent deficiency. Brain MRIs were performed at baseline, 4, 5, and 6 months. Primary endpoints were the cumulative number of new gadolinium-enhancing lesions and change in the total volume of T2 lesions. Secondary endpoints were Expanded Disability Status Scale (EDSS) score and relapses. RESULTS: Twenty-three people were randomized, of whom 19 were on established interferon or glatiramer acetate (Copaxone) treatment. Median 25OHD rose from 54 to 69 nM (low-dose D2) vs 59 to 120 nM (high-dose D2) (p = 0.002). No significant treatment differences were detected in the primary MRI endpoints. Exit EDSS, after adjustment for entry EDSS, was higher following high-dose D2 than following low-dose D2 (p = 0.05). There were 4 relapses with high-dose D2 vs none with low-dose D2 (p = 0.04). CONCLUSION: We did not find a therapeutic advantage in RRMS for high-dose D2 over low-dose D2 supplementation. Classification of evidence: This study provides Class I evidence that high-dose vitamin D2 (targeting 25OHD 130-175 nM), compared to low-dose supplementation (1,000 IU/d), was not effective in reducing MRI lesions in patients with RRMS. (({{pubmed>long:22025459}}))+ OBJECTIVE: Higher latitude, lower ultraviolet exposure, and lower serum 25-hydroxyvitamin D (25OHD) correlate with higher multiple sclerosis (MS) prevalence, relapse rate, and mortality. We therefore evaluated the effects of high-dose vitamin D2 (D2) in MS. METHODS: Adults with clinically active relapsing-remitting MS (RRMS) were randomized to 6 months' double-blind placebo-controlled high-dose vitamin D2, 6,000 IU capsules, dose adjusted empirically aiming for a serum 25OHD 130-175 nM. All received daily low-dose (1,000 IU) D2 to prevent deficiency. Brain MRIs were performed at baseline, 4, 5, and 6 months. Primary endpoints were the cumulative number of new gadolinium-enhancing lesions and change in the total volume of T2 lesions. Secondary endpoints were Expanded Disability Status Scale (EDSS) score and relapses. RESULTS: Twenty-three people were randomized, of whom 19 were on established interferon or glatiramer acetate (Copaxone) treatment. Median 25OHD rose from 54 to 69 nM (low-dose D2) vs 59 to 120 nM (high-dose D2) (p = 0.002). No significant treatment differences were detected in the primary MRI endpoints. Exit EDSS, after adjustment for entry EDSS, was higher following high-dose D2 than following low-dose D2 (p = 0.05). There were 4 relapses with high-dose D2 vs none with low-dose D2 (p = 0.04). CONCLUSION: We did not find a therapeutic advantage in RRMS for high-dose D2 over low-dose D2 supplementation. Classification of evidence: This study provides Class I evidence that high-dose vitamin D2 (targeting 25OHD 130-175 nM), compared to low-dose supplementation (1,000 IU/d), was not effective in reducing MRI lesions in patients with RRMS. (({{pmid>long:22025459}}))
  
  
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-May 2005: Interesting new abstract about MS as an infection (({{pubmed>long:15893675}}))+May 2005: Interesting new abstract about MS as an infection (({{pmid>long:15893675}}))
  
  
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 Here is an example of the type of study which had initially side-tracked me into thinking viruses might play a part in MS Here is an example of the type of study which had initially side-tracked me into thinking viruses might play a part in MS
-http://www.primezone.com/newsroom/news.html?d=87395+https://www.primezone.com/newsroom/news.html?d=87395
  
 But what these scientists are forgetting is that a monkey is not a human. Animal models have failed to predict human autoimmune disease time after time. So, while this study sounds very persuasive, it will fail to be replicated in man. But what these scientists are forgetting is that a monkey is not a human. Animal models have failed to predict human autoimmune disease time after time. So, while this study sounds very persuasive, it will fail to be replicated in man.
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 Here is a paper on cytokine profiles in MS Here is a paper on cytokine profiles in MS
-http://tinyurl.com/5pa9n+https://tinyurl.com/5pa9n
  
 They concluded that the Th1 profile is predominant, except during pregnancy. That conclusion was erroneous, in my opinion, for the reasons I stated here They concluded that the Th1 profile is predominant, except during pregnancy. That conclusion was erroneous, in my opinion, for the reasons I stated here
-http://tinyurl.com/6f6qr+https://tinyurl.com/6f6qr
  
 however their raw data seem reliable, and it indicates Th1 is dominant. however their raw data seem reliable, and it indicates Th1 is dominant.
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 Proc Natl Acad Sci U S A. 2010 Apr 6;107(14):6418-23. Epub 2010 Mar 22. Proc Natl Acad Sci U S A. 2010 Apr 6;107(14):6418-23. Epub 2010 Mar 22.
-UV radiation suppresses experimental autoimmune encephalomyelitis independent of vitamin D production.(({{pubmed>long:20308557}}))+UV radiation suppresses experimental autoimmune encephalomyelitis independent of vitamin D production.(({{pmid>long:20308557}}))
 Becklund BR, Severson KS, Vang SV, DeLuca HF. Becklund BR, Severson KS, Vang SV, DeLuca HF.
 Department of Biochemistry, University of Wisconsin, Madison, WI 53706, USA. Department of Biochemistry, University of Wisconsin, Madison, WI 53706, USA.
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 Abstract Abstract
 Although the exact cause of multiple sclerosis (MS) is unknown, a number of genetic and environmental factors are thought to influence MS susceptibility. One potential environmental factor is sunlight and the subsequent production of vitamin D. A number of studies have correlated decreased exposure to UV radiation (UVR) and low serum 25-hydroxyvitamin D(3) [25(OH)D(3)] levels with an increased risk for developing MS. Furthermore, both UVR and the active form of vitamin D, 1alpha,25-dihydroxyvitamin D(3), suppress disease in the experimental autoimmune encephalomyelitis (EAE) animal model of MS. These observations led to the hypothesis that UVR likely suppresses disease through the increased production of vitamin D. However, UVR can suppress the immune system independent of vitamin D. Therefore, it is unclear whether UVR, vitamin D, or both are necessary for the putative decrease in MS susceptibility. We have probed the ability of UVR to suppress disease in the EAE model of MS and assessed the effect of UVR on serum 25(OH)D(3) and calcium levels. Our results indicate that continuous treatment with UVR dramatically suppresses clinical signs of EAE. Interestingly, disease suppression occurs with only a modest, transient increase in serum 25(OH)D(3) levels. Further analysis demonstrated that the levels of 25(OH)D(3) obtained upon UVR treatment were insufficient to suppress EAE independent of UVR treatment. These results suggest that UVR is likely suppressing disease independent of vitamin D production, and that vitamin D supplementation alone may not replace the ability of sunlight to reduce MS susceptibility. Although the exact cause of multiple sclerosis (MS) is unknown, a number of genetic and environmental factors are thought to influence MS susceptibility. One potential environmental factor is sunlight and the subsequent production of vitamin D. A number of studies have correlated decreased exposure to UV radiation (UVR) and low serum 25-hydroxyvitamin D(3) [25(OH)D(3)] levels with an increased risk for developing MS. Furthermore, both UVR and the active form of vitamin D, 1alpha,25-dihydroxyvitamin D(3), suppress disease in the experimental autoimmune encephalomyelitis (EAE) animal model of MS. These observations led to the hypothesis that UVR likely suppresses disease through the increased production of vitamin D. However, UVR can suppress the immune system independent of vitamin D. Therefore, it is unclear whether UVR, vitamin D, or both are necessary for the putative decrease in MS susceptibility. We have probed the ability of UVR to suppress disease in the EAE model of MS and assessed the effect of UVR on serum 25(OH)D(3) and calcium levels. Our results indicate that continuous treatment with UVR dramatically suppresses clinical signs of EAE. Interestingly, disease suppression occurs with only a modest, transient increase in serum 25(OH)D(3) levels. Further analysis demonstrated that the levels of 25(OH)D(3) obtained upon UVR treatment were insufficient to suppress EAE independent of UVR treatment. These results suggest that UVR is likely suppressing disease independent of vitamin D production, and that vitamin D supplementation alone may not replace the ability of sunlight to reduce MS susceptibility.
-PMID: 20308557  (({{pubmed>long:11111111}}))+PMID: 20308557  (({{pmid>long:11111111}}))
 </blockquote> </blockquote>
  
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 From: Varia From: Varia
 Date: 2010-07-07 15:47:41 Date: 2010-07-07 15:47:41
-Reply: http://www.curemyth1.org/reply.php?topic_id=2490+Reply: https://www.curemyth1.org/reply.php?topic_id=2490
  
  
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 Phillyguy: Probably explains one of the reasons why the incidence of autoimmune disease is lower in developing countries and infectious disease is higher.  Interestingly, VDR generally increases the expression ofTregs, IL-10 and TGFbeta and represses IFNg and IL-12. Phillyguy: Probably explains one of the reasons why the incidence of autoimmune disease is lower in developing countries and infectious disease is higher.  Interestingly, VDR generally increases the expression ofTregs, IL-10 and TGFbeta and represses IFNg and IL-12.
  
-(({{pubmed>long:11111111}}))+(({{pmid>long:11111111}}))
 PMID: 21277637 </blockquote> PMID: 21277637 </blockquote>
  
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 Abstract Abstract
 It has recently been suggested that, rather than being an autoimmune disease, multiple sclerosis (MS) is an example of a neurocristopathy, a pathological process resulting from a faulty development of the neural crest. Whilst several characteristics of the disease suggest a neurocristopathy, other aetiological factors require consideration, including hygiene-related factors that alter the immune responses to common pathogens resulting in an eclipse of immune reactivity that could protect against MS, the possible role of human endogenous retroviruses (HERVs) in pathogenesis and autoimmune phenomena, HLA polymorphism, vitamin D levels before and after birth and immune repair mechanisms. A postulated aetiological factor in MS, associated with altered vitamin D metabolism and abnormal HERV expression, is a long-lasting disturbed redox regulation in the biosynthesis of a melanoma-like melanin pigment. Although intensive further studies on melanin pigments in nerve tissue in MS are required, the known properties of a pathological form of such pigments in melanoma could explain a number of observations in MS, including the impact of light, UV-light, and vitamin D, and could explain the clinical manifestations of MS on the basis of an oscillating process of oxidative charge and discharge of the pigments and a threshold phenomenon with a change of the quasi-catalytic function of the pigment from destroying reactive oxygen radicals or species to transforming them to more harmful long-persisting highly reactive species. Taken together with the consequences of an adaptive process in partly demyelinated neurons, resulting in an increase in number of mitochondria, and the impact of stressful life events, these conditions are necessary and sufficient to explain the disease process of MS with its spatial (plaques) and temporal (attacks and remissions) characteristics. This suggested unifying concept of the pathogenesis of MS may open perspectives for prevention, diagnosis and therapy. In particular, prevention may be achieved by vaccinating against Epstein-Barr virus in early childhood. It has recently been suggested that, rather than being an autoimmune disease, multiple sclerosis (MS) is an example of a neurocristopathy, a pathological process resulting from a faulty development of the neural crest. Whilst several characteristics of the disease suggest a neurocristopathy, other aetiological factors require consideration, including hygiene-related factors that alter the immune responses to common pathogens resulting in an eclipse of immune reactivity that could protect against MS, the possible role of human endogenous retroviruses (HERVs) in pathogenesis and autoimmune phenomena, HLA polymorphism, vitamin D levels before and after birth and immune repair mechanisms. A postulated aetiological factor in MS, associated with altered vitamin D metabolism and abnormal HERV expression, is a long-lasting disturbed redox regulation in the biosynthesis of a melanoma-like melanin pigment. Although intensive further studies on melanin pigments in nerve tissue in MS are required, the known properties of a pathological form of such pigments in melanoma could explain a number of observations in MS, including the impact of light, UV-light, and vitamin D, and could explain the clinical manifestations of MS on the basis of an oscillating process of oxidative charge and discharge of the pigments and a threshold phenomenon with a change of the quasi-catalytic function of the pigment from destroying reactive oxygen radicals or species to transforming them to more harmful long-persisting highly reactive species. Taken together with the consequences of an adaptive process in partly demyelinated neurons, resulting in an increase in number of mitochondria, and the impact of stressful life events, these conditions are necessary and sufficient to explain the disease process of MS with its spatial (plaques) and temporal (attacks and remissions) characteristics. This suggested unifying concept of the pathogenesis of MS may open perspectives for prevention, diagnosis and therapy. In particular, prevention may be achieved by vaccinating against Epstein-Barr virus in early childhood.
-(({{pubmed>long:11111111}}))+(({{pmid>long:11111111}}))
 PMID: 21547536 [</blockquote> PMID: 21547536 [</blockquote>
  
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 In an astonishing new study published in Nature today, researchers at the Max Planck Institute of Neurobiology in Martinsried in Munich, Germany say they have found evidence that suggests multiple sclerosis (MS) is triggered by natural intestinal flora, the so-called friendly bacteria that reside in the gut. They found genetically engineered mice with normal gut bacteria developed brain inflammation similar to MS in humans. They say the bacteria first activated the immune T-cells, then the B-cells, which resulted in an attack on the myelin layer in the brain. The same could happen in humans with a corresponding genetic predisposition, they say. In an astonishing new study published in Nature today, researchers at the Max Planck Institute of Neurobiology in Martinsried in Munich, Germany say they have found evidence that suggests multiple sclerosis (MS) is triggered by natural intestinal flora, the so-called friendly bacteria that reside in the gut. They found genetically engineered mice with normal gut bacteria developed brain inflammation similar to MS in humans. They say the bacteria first activated the immune T-cells, then the B-cells, which resulted in an attack on the myelin layer in the brain. The same could happen in humans with a corresponding genetic predisposition, they say.
  
-http://www.medicalnewstoday.com/articles/236776.php+https://www.medicalnewstoday.com/articles/236776.php
  
  
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 Department of Neuroimmunology, Max Planck Institute of Neurobiology, 82152 Martinsried, Germany. Department of Neuroimmunology, Max Planck Institute of Neurobiology, 82152 Martinsried, Germany.
 Abstract Abstract
-Active multiple sclerosis lesions show inflammatory changes suggestive of a combined attack by autoreactive T and B lymphocytes against brain white matter. These pathogenic immune cells derive from progenitors that are normal, innocuous components of the healthy immune repertoire but become autoaggressive upon pathological activation. The stimuli triggering this autoimmune conversion have been commonly attributed to environmental factors, in particular microbial infection. However, using the relapsing-remitting mouse model of spontaneously developing experimental autoimmune encephalomyelitis, here we show that the commensal gut flora-in the absence of pathogenic agents-is essential in triggering immune processes, leading to a relapsing-remitting autoimmune disease driven by myelin-specific CD4(+) T cells. We show further that recruitment and activation of autoantibody-producing B cells from the endogenous immune repertoire depends on availability of the target autoantigen, myelin oligodendrocyte glycoprotein (MOG), and commensal microbiota. Our observations identify a sequence of events triggering organ-specific autoimmune disease and these processes may offer novel therapeutic targets. (({{pubmed>long:11111111}}))+Active multiple sclerosis lesions show inflammatory changes suggestive of a combined attack by autoreactive T and B lymphocytes against brain white matter. These pathogenic immune cells derive from progenitors that are normal, innocuous components of the healthy immune repertoire but become autoaggressive upon pathological activation. The stimuli triggering this autoimmune conversion have been commonly attributed to environmental factors, in particular microbial infection. However, using the relapsing-remitting mouse model of spontaneously developing experimental autoimmune encephalomyelitis, here we show that the commensal gut flora-in the absence of pathogenic agents-is essential in triggering immune processes, leading to a relapsing-remitting autoimmune disease driven by myelin-specific CD4(+) T cells. We show further that recruitment and activation of autoantibody-producing B cells from the endogenous immune repertoire depends on availability of the target autoantigen, myelin oligodendrocyte glycoprotein (MOG), and commensal microbiota. Our observations identify a sequence of events triggering organ-specific autoimmune disease and these processes may offer novel therapeutic targets. (({{pmid>long:11111111}}))
 PMID: 22031325 PMID: 22031325
 </blockquote></blockquote> </blockquote></blockquote>
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 <blockquote>New autoantibody found in MS <blockquote>New autoantibody found in MS
  
-http://www.sciencedaily.com/releases/2012/07/120712101549.htm?utm_source=feedburner&utm_medium=email&utm_campaign=Feed%3A+sciencedaily%2Fmind_brain%2Fmultiple_sclerosis+%28ScienceDaily%3A+Mind+%26+Brain+News+--+Multiple+Sclerosis%29+https://www.sciencedaily.com/releases/2012/07/120712101549.htm?utm_source=feedburner&utm_medium=email&utm_campaign=Feed%3A+sciencedaily%2Fmind_brain%2Fmultiple_sclerosis+%28ScienceDaily%3A+Mind+%26+Brain+News+--+Multiple+Sclerosis%29
  
 </blockquote> </blockquote>
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-- Review Finds Marijuana May Help MS Patients - http://bit.ly/7ksqMT+- Review Finds Marijuana May Help MS Patients - https://bit.ly/7ksqMT
  
 <blockquote> <blockquote>
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-===== References =====+===== References =====</nodisp> 
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