Monday, 1 June 2015

Unrelated Blogger Comments June 2015

If you want to say something unrelated to the threads this is the place for you.

Summer Solstice Stonehenge

203 comments:

  1. The researchers associated with this blog have suggested that treatment with HAART may explain the low prevalence of MS among people with HIV. This association is repeatedly cited in the justification for the Charcot and Artemis projects. I would like to suggest four alternative explanations of the low prevalence of MS in HIV patients:
    1. The initial stages of HIV infection may act as an induction therapy. There will typically be a delay between HIV infection and diagnosis (and therefore between infection and HAART initiation), and in that time, there may be enough immune destruction to eliminate autoreactive immune cells (or do whatever anti-CD52/CD20/etc drugs are doing).
    2. Tenofovir, one of the most widely prescribed reverse transcriptase inhibitors, is a fumarate. It may therefore share a mechanism of action with dimethyl fumarate. (Someone with a better biochemistry background could judge whether this is plausible.)
    3. Most HAART drugs have poor CNS penetration; the CNS is actually referred to as an HIV reservoir under HAART treatment. HIV may therefore suppress immune activity in the CNS, and decrease the probability of immune-driven damage to the CNS.
    4. This is closely related to 3. The poor CNS penetration of HAART means that there are often still neurological problems associated with HIV infection, e.g. as discussed in this interesting journal issue [1]. As a result, there may be a high rate of missed MS diagnoses in HIV patients. Lack of response of neurological symptoms to HAART will not necessarily indicate to a neurologist that the symptoms have a non-HIV origin.

    I've previously expressed my skepticism about the use of raltegravir to target EBV, or treat MS more generally. I'm raising these new issues because I don't understand the justification for testing *any* HAART drugs in MS. The justifications that I have been able to find seem quite weak. Perhaps there is data that I've missed, or that hasn't been published. But in the absence of such data, we should focus on developing new treatments for EBV, or at the very least exploring other classes of drugs for anti-EBV efficacy, not chasing phantoms.

    [1] http://journals.lww.com/co-hivandaids/toc/2014/11000

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    Replies
    1. Please remind me where your last series of question were, I tried to find them when I mentioned them to ProfG. I have posed question 3 before so I know an answer to that one.

      Delete
    2. ProfG believes EBV is the culprit in MS. ProfG down under slightly different views.
      Are these drugs the right ones? Unlikely..if they were so good would they not be used in treating infectious mono?

      Do nothing, Do something and fail, Do something, fail and kill the greater idea, Do something and succeed.

      Delete
    3. What about this in relation to EBV
      http://scienceblog.cancerresearchuk.org/2014/04/09/epstein-barr-virus-and-the-immune-system-are-cures-in-sight/

      Delete
    4. There are certainly a number of biologically plausible explanations for our epidemiological observations, but the four hypotheses proposed by this anonymous blogger are not strong. Given the possible link between MS and retro-elements and HERVs, testing HAART is quite reasonable. It may be that the blogger will be correct, but there are not enough data to either support or refute their contentions. If chasing phantoms were not a motivation for much of medical science we would not have x-rays, treatment for helicobacter and a 1000 other advances.

      There are certainly a number of biologically plausible explanations for our epidemiological observations, but the four hypotheses proposed by this anonymous blogger are not strong. Given the possible link between MS and retro-elements and HERVs, testing HAART is quite reasonable. It may be that the blogger will be correct, but there are not enough data to either support or refute their contentions. If chasing phantoms were not a motivation for much of medical science we would not have x-rays, treatment for helicobacter and a 1000 other advances.



      The question remains open and that’s why we do this research.

      Professor Julian Gold MD FRSPH

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    5. MD: My previous comments were here: http://multiple-sclerosis-research.blogspot.com/2015/05/unrelated-blogger-comments-may-2015.html?showComment=1430715731734#c7801105819771576580

      Professor Gold: Thank you for your response. Could you elaborate on why these hypotheses are not strong? Regarding HERVs, I don't see a relevant mechanism of action for reverse transcription or integrase inhibitors, e.g. raltegravir. So I didn't realize that your plan was to directly target HERVs rather than EBV. Are you planning to test a protease inhibitor in Artemis?

      Delete
    6. MD: What's the answer to question 3?

      "Do nothing, Do something and fail, Do something, fail and kill the greater idea, Do something and succeed."
      The problem with this slogan is that it can be used to justify nearly anything. Surely there are scientific ideas that are not worth pursuing with our limited resources. I'm not saying that this idea falls in that category, but it has prima facie problems and the full rationale for pursuing it doesn't seem to be spelled out anywhere. There are also other things to do before running a clinical trial, e.g. testing the effect of these drugs on HERV/EBV expression in culture, which I haven't seen reported anywhere, though perhaps they've been done.

      I also appreciate that your group goes public with its hypotheses at an early stage of research. This is a service to the community and something that is done too infrequently.

      Delete
    7. Q3 and other questions I'll leave it for ProfGs and the answers .

      However, I will say knowing how a drug works has seldom been a hamper to trying treatments in MS, beta interferon, copaxone (we still have no idea how it works), daclizumab to name a few

      Delete
    8. It's unfortunate that nobody has responded to these questions, especially because (to the best of my knowledge) they have never been addressed in the literature.

      Delete
  2. It's June already , any idea when the Ocrelizumab study report ?

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    1. Ive no idea profG will but it it is not positive i will be very very surprised.
      if it is not positive serious questions need to be asked about previous trials

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    2. Do you suspect that it will be not so positive?

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    3. No. I said if it not positive, I will be very very surprised

      Delete
  3. Where do you guys stand on supplementation on in particular the mssential supplement currently marketed which claims to have all the nutrients needed for Ms
    Is such a radical change and dietary change possibly detrimental to ms ?

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    Replies
    1. We normally stand on the fence. Without proper evidence we recomend avoiding until proper evidence is found. I dont know about the "Essential MS supplement" have you got a link-which i wont post.
      Deterimental to health possible but generally they don't do much but usually detromental to your wallet.

      Delete
    2. It's a trick minefield to negotiate in my opinion. When I was first diagnosed many many years ago, there were no DMDs for MS, so I did a post grad in herbal medicine. This helped me to be alert to the many charlatans that prey on the natural fears of people with MS, especially in the early stages after diagnosis. I also cross reference everything and do not rely on hearsay or insubstantial claims. I'm also very aware of the placebo effect, which isn't always a bad thing but as MD says, one thing for sure is a great deal of herbal supplements are detrimental to your wallet/purse.

      Some herbal medicine can work but it is unlikely to ever be as effective as a DMD and you can target specific actions with some effect. On the whole but not always, they are more benign than DMDs but that doesn't mean they don't have side affects!

      I find it interesting that quite a few things I've been taking for years are now being discovered by pharma for MS, but as I absolutely do not give advice or recommendations, I don't tend to mention what they are. Even so I now take a DMD but after 30 plus years to be still RRMS with an almost zero EDSS, it may have something to do with what I do but who knows, it could just be just luck of the draw.

      Delete
    3. Dear Kris
      Thanks for the link now deleted.

      The bit I read is
      THESE STATEMENTS HAVE NOT BEEN EVALUATED BY THE FDA. THIS PRODUCT IS NOT INTENDED TO DIAGNOSE, TREAT, CURE, OR PREVENT ANY DISEASE.

      However it does relieve you of $50 for multi-vitamins and anything else I mention that that is claimed to control MS, version II will be arriving with a lot more biotin no doubt.

      However i guess you knew I going to say this and dear anon 5.33 a nice post

      Delete
  4. What do you think of Viagra as a treatment for Ms? I've read a couple of things before showing possible efficacy of Viagra and then this article
    http://www.ncbi.nlm.nih.gov/m/pubmed/24211383/?i=3&from=/26025060/related

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    Replies
    1. To be honest I don't think....I can stop EAE with saline if I want....viagra is PDE5 inhibitor currently PDE-4 inhibitors are being tested hope they prove to be safe. Without real evidence I don't wish to speculate

      There must be enough people taking viagra and maybe they have experiences but mention viagra on the blog and all we get is a stream of robot posts trying to sell you bluepills

      Delete
  5. Picture of Anvil of Darkness Iris removed.......MD2 will be disappointed as he did want to show you if you look at flower related comments over last months lupins

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  6. nivolumab and ipilimumab: the news is getting excited about these as cancer drugs. Given the successes of past cancer drugs in MS I wonder if these might be a new treatment to be explored....

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    Replies
    1. Here you go:
      "Severe Relapse in a Multiple Sclerosis Patient Associated with Ipilimumab Treatment for Metastatic Melanoma"

      http://www.neurology.org/content/82/10_Supplement/P2.231

      Delete
  7. Hi UK readers, I just heard that the Andrew Dillon, big cheese from NICE, will be interviews on BBC radio 4 PM programme, this Wednesday. I can't find a link to this yet, but they are also asking listeners to email questions they might want to put to him. Oh my I can certainly think of quite a few:)

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    Replies
    1. I can't seem to find it on the Radio 4 website maybe it is shipping news and he is going to tell us that the NHS has sunk.

      What is your source or are you someone from radio 4 with insider knowledge, because how do you now they are asking for questions, no tweets on from NICE

      Is NICE against the re-purposing agenda as they only exist because drugs are too expensive?

      Why don't NICE include the full costs of care when assessing cost-effectiveness, as taking a carer out of the work force relevant just as drug costs to the NHS are important.

      Delete
    2. My source was listening to PM with Eddie Mair about an hour ago (i also heard it mentioned on Saturday)when they mentioned this and to email questions. I couldn't find a link either. But you could use listen again on r4 website for PM to check.http://www.bbc.co.uk/programmes/b006qskw

      I definitely like your questions, so hope you can ask them. I'll do a version of them too, as the more people ask similar questions, the more likely these will be used.

      Delete
    3. Should we do a post on the offchance you are right to gets peoples thought processes going

      Delete
    4. Cant someone tweet him and ask him to give us the time and the portal for the questions

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    5. Aaargh, I'm not imagining it. I've just put put my Mac back on to listen again and it's mentioned a few times as they're doing a section each day on NICE. But look at 40 mins in specifically. Email is PM@bbc.co.uk. So yes, I do think it is worth putting a post up.

      Delete
    6. I should also add that it says to send the questions before Wednesday's programme, which starts at 5pm. There is a section on NICE all week but it seems this is a first with an interview with Dillon.

      Delete
  8. http://www.cell.com/cell-host-microbe/abstract/S1931-3128(15)00163-8
    This study suggests IFN-beta contributes to chronic viral expression (LCMV) while blocking IFN-beta may be preventative. The use of IFN-beta in MS is supposedly anti-inflammatory although the exact mechanism is not understood. Expression of HERV elements are decreased with IFN-beta treatment. This seems contradictory.?

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  9. Some people on other MS blogs and a Facebook group are swearing by biotin and are ordering "pure biotin powder" from US suppliers plus electronic scales to weigh out the amounts. I have seen at least one claim that a neurologist has recommended taking biotin. What are your opinions on this?

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    Replies
    1. Get you information from reputable journals and neurologists and not from facebook.

      Get your drugs from reputable sources, such as a pharmacist and not from a postman, with drugs produced to standards that are required for human use.

      We have seen one paper published that was a series of ancedotes and heard the take home message of a trial, where we don't really know what the effect is and have been told that 90% of people don't respond. Is it a symptomatic treatment or a remyelination treatment or a bust.

      Delete
    2. Thank you. Wise words, in harmony with my feelings on the subject. It seems to me that biotin has gone viral.

      I thought I felt better for taking 1 mg biotin daily. Then I thought I felt better for stopping it. Placebo / nocebo.

      Delete
  10. What's next in the pipeline in terms of remyelinating therapies? Biotin was kinda good, kinda not sure. Is there anything on the way in 2016 that we know of?

    Second question. Are there ANY trials in the pipeline that address the "repair" aspect of your iceberg; i.e. not just remyelinate, but "regrow nerves"?

    ReplyDelete
    Replies
    1. Edinburgh has been given ~2million to look at activin-A, still waiting to see the light of day of an RXR-g drug from Cambridge in terms of clinical trial.
      Good question on the regeneration hypothesis, remyelination strategy will not work when there are no axons to myelinate. The spinal cord injury guys have been at this for some time, you may have to graft in support structure, add in local nerve growth factors, remove/block the inhibitory milieu (some inflammation helps with this), and recapitulate what happens during development. A cervical spine lesion would be a good place to start...

      Delete
    2. "recapitulate what happens during development"............neuro-progenitor cells

      Delete
    3. Is there no info on activin a yet? From what Ive read it states it has a good chance of working as its a naturally occurring element? do these people not understand time is of the essence?
      Also

      Delete
    4. Clemastine and GSK239512
      http://multiple-sclerosis-research.blogspot.com/2014/09/news-from-actrimsectrims-2014-pharma-in.html

      Biotin trial part II

      nerves... Anti-LINGO-1 should inhibit nerve regrowth repellent signals

      Delete
    5. salt is naturally occurring and you know our thoughts there:-). Trials take time todo and time to get the funding to do the trial in place

      Delete
  11. Big curiosity: why should I expect that there is correlation between depression and MS? Maybe is just correlated with the level of imparment you got because of MS, not with MS. The comparison in terms of depression should be done not with the general population but with people with the same level of disability, otherwise we get a bias result. Again, i red in the blog that brain atrophy might relate with depression. How can you test it for real and not just rely on anecdotal evidence. Moreover, couldn't be the opposite i.e., i get more happy because of brain atrophy? All these statment, I think, need a serious experimental background otherwise are real as the idea that certain kinds of lifestyle might cure MS.

    ReplyDelete
    Replies
    1. Set backs in life cause low mood, give it time you may have depression. It is very difficult match patients for depression in a randomized clinical trial, that is why most of us accept cross-sectional and prospective studies.
      Most neurodegenerative disorders have some form of depression associated with them, take Alzheimer's disease, Parkinson's disease for instance. In frontotemporal dementia, on top of this their is disinhibition. If you lose deep white matter (small vessel diseas) you become apathetic and slow.
      Where RCT trials have been done in depression are in treatment resistant depressive cases, such electroconvulsive therapies, ketamine - it's important that you get it right when the risk associated with the treatments is high.
      I hope this makes some sense!

      Delete
    2. oh the hilarity, set backs in life cause low mood. For sure choking and losing bowel control are going to get the party started.

      Delete
  12. Has lecithin been looked at for remylination?(phosphatidylcholine)

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  13. What's the thoughts on this?
    Why is Dr Burts trial non myeloablative yet here he recommends ablation? Is this his greed to go back to square one!
    http://www.hcplive.com/conference-coverage/cmsc-2015/Stem-Cell-Therapy-Could-Stop-MS-for-Many-Years-But-Funding-is-an-Issue

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    Replies
    1. This is Freedman recommending ablation, not Burt. Freedman has been saying this for a while.

      Delete
  14. http://www.nature.com/nature/journal/vaop/ncurrent/full/nature14432.html
    Discovery of previously unknown lymphatics bridging immune system and the CNS. Who knew that human anatomy still held undiscovered structures?

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    Replies
    1. What's more interesting is the function of sleep demonstrating an internal flushing system in the brain which gets rid of B-amyloid, metabolites etc...
      http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3880190/

      Delete
    2. As stated in the paper: "Yet despite its high metabolic rate and the fragility of neurons to toxic waste products, the brain lacks a conventional lymphatic system." This new discovery should be important for clearance of toxic metabolites in sleep deprived patients with neurodegenerative diseases as well as lymphocyte trafficking. When we tell kids to get to sleep, it's no joke:-).

      Delete
    3. yes the glymphatics...tomorrows post

      Delete
  15. Team G - what are your thoughts on the news from the MS uk org that some folks discovered a direct link between the immune system and the brain not previously known of?

    Is it valuable or hype?

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    Replies
    1. By the way if I win euro millions friday, you mouses have a smooth £10m coming your way to get on your bikes and see if these vessels have anything to do with Ms.
      I've read a little more and the people who made this discovery seem to claim that this discovery could help ms be looked at in a mechanistic manner, do you agree that could be the case? Would it also explain the spinal cord involvement

      Delete
    2. There is a spinal cord lymph gland ..tomorrws post

      Delete
  16. Would this not represent an opportunity for new treatments in Ms?
    Also correct me if I'm being stupid here, but they talk about Alzheimer's not draining correctly etc, would this have any link to ccsvi?

    ReplyDelete
    Replies
    1. No link with CCSVI, but the glymphatics appear to clear the waste

      Delete
  17. Thoughts on this appreciated please ....http://medicalxpress.com/news/2015-06-link-brain-immune.html

    Regards as always.

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    Replies
    1. Hi Andy
      I'd be interested in that too
      It looks as though it may embarrass some scientists
      I would love for it to give potential treatment avenues too!

      Delete
    2. I will have a look, once I can see the paper but not sure why it will embarrass scientists.

      Why because they say that the brain doesn't have good lymphatic drainage when this report suggests that there is lymphactic drainage.

      This is not exactly a new idea

      Transfer of central nervous system autoantigens and presentation in secondary lymphoid organs.de Vos AF, van Meurs M, Brok HP, Boven LA, Hintzen RQ, van der Valk P, Ravid R, Rensing S, Boon L, 't Hart BA, Laman JD. J Immunol. 2002 Nov 15;169(10):5415-23

      Role of cervical lymph nodes in autoimmune encephalomyelitis in the Lewis rat.
      Phillips MJ, Needham M, Weller RO. J Pathol. 1997 Aug;182(4):457-64.

      So Roy from Southampton was talking about lymphatics years ago

      One thing for sure I think it has nothing to do with CCSVI
      But will it change the MS landscape...I doubt it, but i will need to change a view.

      I never really understood why the body needs T cells to leave the CNS, cells are are made every day,if they get in the CNS or tissue and don't find what they want they can die and we'll make some new ones.
      I'll be back

      Delete
  18. Apologies for the multiple posts too but would this not support the EBV glandular fever link too?

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  19. Is this Dacluzimab result a new one?

    http://www.medpagetoday.com/MeetingCoverage/CMSC/51896

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  20. Is this research into the lymphatic system and T cells dysfunction interesting to your guys?
    http://www.nature.com/nature/journal/vaop/ncurrent/full/nature14432.html

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  21. I'd also like to see what the Mouse Pros takes are on the whole "Brain Is Directly Connected to the Immune System" hullabaloo. Specifically, how they envision this changing the MS landscape, if it gets independently confirmed.

    ReplyDelete
  22. Hi mouses docs
    What's your thinking on helminth infection and Ms?
    http://www.scopus.com/record/display.url?eid=2-s2.0-33847679709&origin=inward&txGid=5EE5195959E8FAE77AC1CF06C102F7C0.zQKnzAySRvJOZYcdfIziQ%3a6

    Ive read some info on this and especially in this article there is a strong correlation in shmptoms and infection? The same with another where Ms patients had a drink containing helminth

    ReplyDelete
    Replies
    1. What's happening to the environment....parasite eggs

      I can't access your link as I am not logging into scopus so I have no idea what it is about.
      Maybe post details of the paper.

      I have commented on this approach numerous times but it is proof is in the pudding, is this link going to the proof.

      As to your latter comment symptoms and infections do appear to be linked but getting parasites verses a bacterial or viral infection is different as the immune system does not deal with them in the same way

      Delete
    2. There is conflicting reports the one you commented on in feb seems to dismiss the idea of parasitic worm theory etc but this looks to be a bit different
      There's also varied reports in this but then I guess it depends on the patient choice
      That link is a study where 12 patients had previous helminth infection and 12 no infection, the 12 with had a far more benign course. Two of the twelve that were treated for helminth went on to develop Ms related issues after treatment.

      Delete
    3. with n of 12 the study won't tell us much I suspect. Who wrote the study?

      Delete
  23. Hi MD, I wrote to you at your email listed on this site about crowd funding. If you remember from the discussion earlier this year, I'm the person with experience of using this with non-profits but was relapsing at the time so couldn't make you Open Day to discuss this further with you. As I'm deeply adverse to giving my details on a blog, there in this email, which also lists my ...ahem ...applicable 'credentials' such as a link to a book I wrote about non-profits using the internet for fundraising etc.. So I wonder if it's been consigned to the hinterland of spam by your filters or you no longer need any help.

    ReplyDelete
    Replies
    1. Thanks I have forwarded your email to my bosses and think both have responded

      Delete
    2. one in Canada one in Norway so it takes time look forward to seeing you

      Delete
  24. One more for you
    What's your take on lecithin?
    I know it's rich in Choline and many people claim success from this as it promotes remyelination etc
    But you guys commented on and anti acetylcholine Parkinson drug showing success in Ms? Is this the same choline? Also Wikipedia claims higher levels and choline creative ration in subject with tumefactive Ms? Does this suggest choline is bad for you and hence lecithin is a no go?

    It's a minefield out there!

    ReplyDelete
    Replies
    1. No acetytl choline and choline are not the same thing. Lysophosphatidylcholines (LPC, lysoPC), also called lysolecithins is used to cause demyelination

      Delete
  25. I just wanted to post to all the Barts team a thank you for doing what you do. When I look at the support mechanisms in my life, this blog is near the top of the list. Instead of reaching for Dr Google at frequent intervals, I spend five minutes a day taking in from you what I need to. Then I get on with the really important stuff - i.e. keeping exercised, calm and well. xx

    ReplyDelete
  26. What is the thinking on erythropoietin? I know you guys have commented on it before showing a neuroprotective effect in optic neuritis, but this study shows further help with spinal atrophy and edss scores, is there any further investigations on this.
    http://www.ncbi.nlm.nih.gov/m/pubmed/17728357/

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    Replies
    1. I am not sure maybe I can ask Lance Armstrong:-)
      we tried to get our hands on a version that didn't blood dope but we were unsuccessfil

      Delete
    2. on this basis is lecithin a no go?
      It is suggested by ALOT of people with regards to helping with Ms due to inositol?

      Delete
  27. What are your thoughts on this paper?

    http://www.nature.com/nature/journal/vaop/ncurrent/full/nature14432.html

    Structural and functional features of central nervous system lymphatic vessels

    Antoine Louveau, Igor Smirnov, Timothy J. Keyes, Jacob D. Eccles, Sherin J. Rouhani, J. David Peske, Noel C. Derecki, David Castle, James W. Mandell, Kevin S. Lee, Tajie H. Harris & Jonathan Kipnis
    AffiliationsContributionsCorresponding authors
    Nature (2015) doi:10.1038/nature14432
    Received 30 October 2014 Accepted 20 March 2015 Published online 01 June 2015

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    Replies
    1. wow this one has caught the eye I'll post in the morning

      Delete
  28. Any news on the raltegravir trial?

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  29. Team G,
    I came across this article and tried it out. Useful details are in the supplementray materials. I have constipation sometimes and hemorrhoids.
    So far it is working and i'm giving it a self trial. Applying the pressure stopped any straining.

    http://link.springer.com/article/10.1007%2Fs11606-014-3084-6
    Journal of General Internal Medicine
    April 2015, Volume 30, Issue 4, pp 434-439
    Date: 18 Nov 2014
    Effect of Perineal Self-Acupressure on Constipation: A Randomized Controlled Trial
    Ryan Abbott MD, JD, MTOM, Ian Ayres PhD, JD, Ed Hui MD, Ka-Kit Hui MD

    CONCLUSION
    Among patients with constipation, perineal self-acupressure improves self-reported assessments of quality of life, bowel function, and health and well-being relative to providing standard constipation treatment options alone.

    Helen

    ReplyDelete
    Replies
    1. There's a summary of the study on the university webpage.
      http://newsroom.ucla.edu/releases/suffering-from-constipation

      Delete
  30. I know you have touched on this before in 2012
    But do you see gaba as beneficial for Ms? I know they found it so in mouse studies but we all know that doesn't always correlate
    They also found inflamation lowers gaba, but I know baclofen does the same and that's not really helped
    Any ideas?

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  31. Hello,
    I 've gota question about the methods the scientists and pharmas use to prove efficiacy of so called re myelinisating drugs. As far as I have seen they only used evoked potential to measure the effectiveness to study whether there is an impact or not. Why they don 't use imaging for example Diffusion Tensor imaging to look for improvement? I have Not read a study so far using this kind of imaging to prove this. Is there a reason for this?
    Many thanks for your answer. Greetings from germany.

    ReplyDelete
    Replies
    1. Trials using the optic nerve as a read out have electrophysiology as a core outcome. To put back myelin gives a gold standard signal. There are some trials targeting brain spinal cord and they are using imaging as a read out including MTR. One problem for imaging is the correlates and what are they showing? As imaging is largely about water movement. Couple this with lack of resolution and there is a problem. Can we say with certainy what T 1 and T2 lesions are? Over the years i have heard these lesions to be this or that.

      Delete
    2. Come on mouse what's the thoughts on GABA I'd be interested in that!
      Is the glutathione/gaba/glutamate ratio important? I know glutamate is bad at high levels and when it's high gaba is low, also is glutamate not involved in ocidative stress etc and low GABA levels found in Ms patients?
      Also everything that looks to have shown promise looks to interact with these 3?
      What's the take on GABA supplementing?

      Delete
  32. Study suggests MS patients may have fewer vascular problems.
    http://www.medpagetoday.com/MeetingCoverage/CMSC/51845

    A single-center study shows lower rates of hypertension, hyperlipidemia, and diabetes in some MS patients.

    I have fairly high blood pressure and was diagnosed RRMS two years ago.

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  33. What do think of this Team G?? A diet that includes daily eating of beans, red meat and 100% fruit juice can increase odds of EBV in adolescents.

    http://www.newswise.com/articles/view/632367/
    “Baked beans are also rich in sodium, sugar and fat, and depending on the type, rich in uric acid. Some beans contain lectins that are linked to irritable bowel syndrome, multiple sclerosis, allergies and arthritis. EBV infection has been associated with all of these medical conditions.”

    ReplyDelete
    Replies
    1. There's more on the study on this page
      CHHS researchers shed light on link between diet and Epstein-Barr - See more at:

      http://inside.uncc.edu/news-features/2015-04-02/chhs-researchers-shed-light-link-between-diet-and-epstein-barr#sthash.CnLB2ezA.dpuf

      Delete
  34. We know that GABA receptor stimulation inhibits spasticity and there are theorectical possibilities of other things, the data has not been collected to address this. I have asked the same question too.

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    Replies
    1. Why have you asked this? What's your views on it?
      Is glutathione the bodies natural antioxidant? And GABA interacts with glutamate as in when ones high the others low and vice versa? GABA is low in anxiety stress etc, glutamate is high in those situations and ocd which is implicated by ebv?
      I'm convinced there's a connection there somewhere?
      Look at all the supplements and diets that show promise in Ms, gluten free, caseine free diets. Then inositol, theanine, n acetylcysteine and alpha lipoic acid that all claim some sort of effect on Ms and all act on the glutathione glutamate link
      GABA is the important one I think, then there's this old study http://www.ucsf.edu/news/2009/04/4227/glutamate-identified-predictor-disease-progression-multiple-sclero

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    2. And this
      http://www.ncbi.nlm.nih.gov/m/pubmed/25043416/

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    3. GABA inhibits glutamate and maybe excitotoxicity

      Delete
    4. Do I sense an inquisitive mouse regarding GABA glutamate etc?

      Delete
    5. GABA stimulation is sedative and causes cogfog, there are better ways to tackle the problem....how.? Sorry its top secret when the paper comes out...just have to get idea funded and do the work.

      Delete
  35. What is the thinking behind it? I understand it causes cog fog is this because glutamate is key in transmission between neurons?
    I wonder how else you can approach it, is this thinking a new way to attack progressive Ms?
    I'd be interested to hear what your idea is

    ReplyDelete
    Replies
    1. Yes new way of thinkinģ but not ready for prime time yet..sorry.

      Delete
  36. Is riluzole the alternative?

    ReplyDelete
    Replies
    1. Both riluzole and ibudilast from Ms smart have effects on glutamate. Even fluoxetine decrease the release of microglial glutamate!
      Is glutamate behind the thinkng in all of the Ms smart drugs?
      It certainly looks that way
      Then there's the EBV ocd link and the fact they found higher levels of glutamate in the csf of ocd sufferers than controls. Then you have your study showing ocd subjects have higher edss etc
      Is the control of glutamate the answer to neuropototection?

      Delete
    2. Here's another one for you
      glutamate-oxaloacetate transaminase as a neuroprotective, by blood glutamate scavenging?
      I read some animal and human studies on this one of which staying glutamate and GOT are important factors in the prognosis post stroke, with higher levels of GOT fairing better.
      Again linked to hlutamate but is this a neuroprotective approach that could be considered for Ms?

      Delete
    3. Thanks, but to honest we have more ideas of how to be neuroprotective than we can shake a stick at. The question is demonstrating it. If we don't have the resources to do it then it won't get done. even when we have done it in animals the next challenge is showing it works in MS.

      Unless we get more volunteers for PROXIMUS, this approach is dead meat so you will have the seven year trial route so it may take us a few hundred years to get through the list of candidates.

      There are questions (a) efficacy and (b) Tolerability.....messing around with the glutatamate is often not tolerable to the person or the drugs induce receptor tolerance ant they stop working in one case this was within 24h.

      Delete
    4. Is it worth addressing this with nutrients Ie anti depressant like 5htp theanine etc or is the bodies natural balance the best way to cope?

      Delete
    5. i don't know.
      We wont recommend supplements are these is not evidence one way or another...sorry

      Delete
  37. Is this the reason albuterol has shown some success in treating Ms?

    ReplyDelete
    Replies
    1. What success?

      It was trial years ago with copaxone and it has gone no where since I think.
      As to mechanism...I have no idea...certainly not what the Harvard group were proposing as they wereproposing it to be a DMT affecting relapses not a neuroprotective

      Delete
  38. Could this link with the Charcot project ? http://hms.harvard.edu/news/viral-history-drop-blood

    ReplyDelete
  39. I have had RRMS for 2 years and 4 months now. My MS seems to be progressing fairly rapidly this is not including relapses. I am progressing without recent relapses. I am in pain with stiffness and aching. I have been on Tecfidera for 5 months now.
    I get the feeling Tecfidera may be reducing the number of relapses but it isn't slowing down my progression.
    Is this common in RRMS? Would this be classed as relapsing progressive MS?
    thanks

    ReplyDelete
    Replies
    1. Dear Anon, we do not answer personal case-related queries in this blog as we would be guessing. Please talk to your doctor about your concerns.

      Delete
  40. In response to MD's post this morning I think universities do want to be international. Many students are international. Universities want to be recognised globally by other university academic staff and this would assist with articles being peer reviewed and published.
    If we are going to find a cure for MS I think it will be through collaberative work. To understand the mecanisms of MS is important to investigate how MS is in other countries.
    For example Saudi, I know of an MSer in Saudi they suspect a proportion of Saudi people are vitamin D deficient as the sun is so hot it is very uncomfortable to be out in. Even for a very short time.

    40% of the Worlds population is apparently vitamin D deficent.

    ReplyDelete
  41. I know it's EAE but I thought this is interesting...
    Arch Biochem Biophys. 2015 Feb 1;567:75-82. doi: 10.1016/j.abb.2014.12.017. Epub 2014 Dec 23.
    UV light selectively inhibits spinal cord inflammation and demyelination in experimental autoimmune encephalomyelitis.
    Wang Y1, Marling SJ1, Beaver EF1, Severson KS1, Deluca HF2.

    ReplyDelete
    Replies
    1. Results of study.
      Four out of 10 of the mice exposed to UVB did not develop EAE, whereas all 12 of the mice who weren’t exposed developed the disease.
      UV radiation significantly decreased various markers of inflammation in the CNS by day 30 (p < 0.05) as well as significantly decreased overall disease severity.
      Unlike its outcome within the CNS, UVB did not suppress immune response or decrease inflammation in the PNS.
      If the immune response is intact in the PNS, but selectively inhibited in the CNS after UVB irradiation, it suggests that the migration of T cells or reactivation of Tcells might be diminished by UVB irradiation.
      This study adds to the growing amount of evidence suggesting that sunlight provides benefits above and beyond from stimulation vitamin D production. It’s important to remember that because the study was performed in mice, we can’t be certain that the findings would directly relate to humans.

      I am doing a mid-day mile walk each day to get some sun rays. When I am fatigued I sit in the garden for 15 minutes instead.

      Delete
    2. Being innately cynical, I'm tempted to file under "EAE cure of the week" ( a large repository). Paper not available to read at the moment (site is down for maintenance) but maybe the stress response from sunburn is immunosuppressive?

      Delete
    3. Quite frankly, I'm not -wholly-convinced, although as my sample size is just me, it is impossible to know for sure. But 1) I've walked an average of 6-7 miles a day for over 20 years in winter and summer (that's one benefit of having dogs) and only use sun protection in the summer, and even then I ensure I get 15 -20 minutes exposure sans sunscreen on my body (I'm too vain to do this to my face;)). 2)I've taken D3 for over 15 years, daily at 5000iu (I get my levels monitored every three-months) 3)At least once a year I head to sunnier climbs than the UK for around one month.

      And yet, I still have a brain resembling Swiss cheese but perhaps I'd be in a worse state if I didn't do this .... Who knows!

      Delete
    4. A quick check reveals that the amount of ultraviolet radiation they used in this study would give you a nasty case of sunburn. Once again, poor old mice.

      Delete
    5. Just out of interest anon at 3.26pm what are your vitamin D levels? I'm interested because of your daily exposure to sunlight when walking and a long time taking vit D at 5000 iu.

      Delete
    6. Having spent the first two years of my research life on this probable nonsense, how many and what strains were used. Much of the UVB immunosuprression stuff is wholey unreproducible. To take immune response out of the brain when it is shielded in bone and leaving all of peripheral immune response is a cause for concern. Last but important point is translateablity. Mice are adapted for living in the dark humans are not.... MD2 is probably right. Probably cure of the week.

      Delete
    7. PS The smell of Imac and hair removal will haunt me ☺

      Delete
    8. This reminds me.... Not directly MS related, but a useful related warning for all men worldwide (and a good laugh to read!).
      http://www.amazon.co.uk/product-reviews/B000KKNQBK

      Delete
    9. So funny Matt, thanks for the link.

      Delete
  42. Could anybody tell me why doxycycline has not been further investigated in Ms, there has I believe been two trials both showing efficacy in Ms over four months as an add on therapy?
    Is it not also the antibiotic of choice in Dr Wheldon and the Vanderbeilt protocol?

    ReplyDelete
    Replies
    1. Sarcastic mouse
      Why does logic count when you and other neuros etc have no idea what causes the disease? all you have so far is conjecture and little things that work for some not for others and even when they work you have no real way of knowing as many could have a more benign course

      Are you suggesting the trials that showed success are wrong? Could it not affect ebv?

      Delete
    2. What about the combined antibiotic protocols? An opportunity to wipe out your entire gut flora.

      Delete
    3. I've only taken doxycycline twice in my life; the first time, I had my first ever MS relapse (optic neuritis) 5 days after starting.
      The second time I took it, I had an optic neuritis relapse in the other eye after 4 days.
      Other than that, I've never taken it, and never had another bout of optic neuritis!

      Make of that what you will. Probably just a wild coincidence, I'm sure, but at the back of my mind I'll always wonder...!

      Delete
    4. So I'm guessing you are against this approach

      Delete
    5. I hear that deoxycycline is an anti-malaria, I wonder if Plasmodium is the cause of MS, MS is low in malaria endemic areas...is this sensible, you may ask for proof....I do up to that point anecdote is no antidote for getting of your bum to put some meat on the the idea...armchair science is not going to help any one

      Delete
  43. Do you have any theory with regards to the fluoxetine trial currently ongoing, is there any anecdotal info regarding existing patients using this

    ReplyDelete
    Replies
    1. I struggle with this but it has been suggested to have some anti-glial activity.

      Delete
  44. MD - the picture postcard on the teaching trip - is it an homage to we three kings sung by camels??

    ReplyDelete
    Replies
    1. If they bring me any gifts it can be a homage....duty free ciggies are not an acceptable gift I'm afraid:-)

      Delete
  45. Realistically looking at all the race to cure groups etc, is there ever likely to be a cure when no one knows the cause? Especially when you look at how long it takes to get any trials into humans, that process needs to change

    ReplyDelete
    Replies
    1. So what are MSers doing to change that process....our trial is stalling because insufficeicnt number of people are volunteering

      Delete
    2. If we waited till we knew the definitive cause there wouldn't be any treatments now. As MD says trials can be stalled by lack of interest as senn with the low take up for the PROXIMUS trial, which is disappointing to say the least.

      Delete
    3. I'm interested in this trial but I have to say the LP part scares me hugely. I had one botched excruciating LP on diagnosis, it then had to be done by guided x-ray, any chance of it happening this way in the trial, I mean by guided x-ray?

      Delete
    4. Things have moved on concerning LP. Please see here.
      http://multiple-sclerosis-research.blogspot.com/2014/01/removing-headache-of-lumbar-punctures.html

      Delete
    5. It wasn't a headache but hitting a nerve root. I'm not phobic in general about needles but the excruciating pain this LP caused me is not something I want to repeat. Apart from this, I think I match the criteria (well, next month I will as then 6-months on a DMD) which is why I asked, before I speak to my neurologist, if there is any chance this could be done by guided x-ray.

      Delete
    6. I'll leave this for the neuros to answer.

      Delete
  46. What in your humble mouse opinion without and prejudice currently shows the best promise for treatment in orogressive stages of the disease?

    ReplyDelete
    Replies
    1. sorry but I'm not getting drawn here and so maybe be best to stop asking the questions as you are always going to get a sit on the fence response. It is pointless and I have no desire to set people off getting this or that prescribed on the off chance that I say it may be good for progressive MS. Likewise I am not going to give my ideas away until we have published them

      Delete
    2. Fair comment
      Get bacj on that wheel and get publishing
      I'll leave you alone now too and stop pestering you

      Delete
  47. Team G - can you briefly explain what exactly are T2 lesions?

    I don't understand the difference between T2 and GD-enhanced ones.

    ReplyDelete
    Replies
    1. This post will tell you everything you want to know and in language which is not techno-babble (with pictures as well!). Copy and paste the text for the link into your web-browser or look at the posts for the 10th January 2015
      http://multiple-sclerosis-research.blogspot.com/2015/01/education-whats-mri.html

      Delete
  48. I'm not a doc but I'll have a bash at clearing this up for you...

    Your immune system goes circulating around your body in the blood. Let's pretend your immune cells are rioters, and your blood vessels are streets. These rioters run around the streets looking for rivals (pathogens, viruses, etc.) and if it finds any, it beats them to a pulp. Problem solved. There's a big gate outside your brain called the Blood Brain Barrier. Normally, the rioters can't get through that, so all the property behind it (ie your brain and spine) is safe from being attacked by the rioters, or from becoming collateral damage in one of their scraps!

    In an MS attack, this gate (the BBB) breaks down and these rioters get through into the brain/spine and start wrecking the place. Nobody really knows what makes them do this.

    The police get called to calm them down, but until they get there, this attack rumbles on.

    If you look at your brain on an MRI at this point, you have an *enhancing* lesion - as in the rioters are there causing damage right now. Think of an MRI as a helicopter looking at it from above through one of those heat seeking cameras. You'd see all the rioters (lymphocytes) light up in the brain.

    So. After a while, eventually the police turn up (other immune cells) and calm everything down. Rioters ejected. Big gate (BBB) repaired to keep them out again.

    If you look down from a helicopter now, there's no rioters there, so it wouldn't "enhance". But the buildings there would have damage/debris left over from the riot. That's a T2 lesion. A scar. Damage left over from a previous attack, that's now ended.

    Bit long winded, but hope that helps!

    ReplyDelete
    Replies
    1. Really good :-) the bit with the rioters is outstanding... thank you

      Delete
    2. I did white vans and tarmac bu rioters and carnage good too
      http://www.mssociety.org.uk/ms-resources/research-matters-progression-issue-autumn-2012

      Check out
      http://multiple-sclerosis-research.blogspot.com/2015/01/education-whats-mri.html

      Delete
    3. Thank you all, especially Matt!

      My T2 lesions got smaller - does it mean repair?

      or just water shrinkage?

      Delete
  49. The MS Trust are running an article on the debate for early treatment and are looking for people's views. I've gave mine and cited this blog as being very influential in my own decision to treat early. Keep up the good work.

    ReplyDelete
    Replies
    1. Glad you've found the blog useful in helping to make an informed decision.

      Delete
  50. BBC news aticle about nuts -
    http://www.bbc.co.uk/news/health-33076815

    The premature mortality risk due to cancer, diabetes, respiratory and neurodegenerative diseases was lower among the nut consumers.

    There was an average 23% lower risk of 10-year mortality across all diseases, with a decrease of:

    45% for neurodegenerative disease
    39% for respiratory disease
    30% for diabetes

    Prof Piet van den Brandt, who led the study, published in the International Journal of Epidemiology, said: "It was remarkable that substantially lower mortality was already observed at consumption levels of 15g of nuts or peanuts on average per day."
    There was no benefit for peanut butter, which is high in salt and trans fats.

    ReplyDelete
    Replies
    1. What can I say we've had smoking, and sun and recently cats and now nuts following a study in the Netherlands.....do we say Schtop with the endless list of risk factors or can profG piece these together to come up with the ultimate preventive strategy.

      I'll leave him to comment on this study, as I often see him with a bag of bird food....so he may have a valued opinion on this one. We should all have a bit of fibre in our diets

      So peanut butter is no of benefit, because of high salt....but peanuts are OK...so are these salted peanuts, dry roast or monkey nuts and did they offset those consuming peanuts in the bar...

      Maybe we can have a follow-up study on salted verse salt free peanut butter from the US

      Wonder what will be next.... kippers for breakfast:-)

      Delete
    2. Mouse is there any truth in nuts and seeds have high levels of amino acid arginine. Arginine can encourage herpes viruses. A diet with high levels of arginine can enhance viral infections including shingles, glandular fever, chicken pox and cold sores.
      I guess 15g of nuts a day is quite a small amount.. everything in moderation..

      Delete
    3. Strictly speaking peanuts are not nuts but legumes. Even more strictly speaking neither are Almonds, Walnuts and Brazil nuts but that's probably taking it too far;).

      Delete
    4. Lysine (amino acid) is also in nuts but nuts contain more arginine than lysine. Foods rich in lysine are chicken, fish, vegetables, brewers yeast.
      Lysine helps slow down replication of herpes virus.

      Delete
    5. Lysine is in Copaxone. Chemically, glatiramer acetate is designated L-glutamic acid polymer with L-alanine, L-lysine and L-tyrosine, acetate (salt). Is this correct?

      Delete
  51. Can someone of the docs tell me if aspirin manages to get into the brain to switch off inflammation?

    ReplyDelete
    Replies
    1. Yes it does, which is why it seems to be effective in reducing the incidence of Alzheimer's in those taking low-dose aspirin, presumably by suppressing low-level inflammation mediated by activated microglial cells.

      Delete
    2. thanks MD2 - so what about MS - would it affect MS-related inflammation?

      Delete
    3. It could reduce the low-grade inflammation from activated microglia which could be influencing progression though not the inflammation present in relapses.

      Delete
    4. MD2 - and which one of the known meds could reduce the relapse inflammation other than cortisone?

      Delete
    5. No one told me before that aspirin might slow inflammation leading to progression. Why? I might have used aspirin more instead of paracetamol, and maybe, just maybe it might have made a slight difference? The difference between getting up some mornings and wondering how I'm going to drag my body around today and getting up with the confidence that I will drag it around somehow? This obsession with treatments for RRMS is really starting to get me down. Something that might work for progressive MS (e.g. laquinimod) but doesn't work for RRMS just gets swept to the side. No, it's not interesting if it might only help the relatively small percentage of people with PPMS. And even MS-Smart is only targeting SPMS. How long would a person with PPMS have to wait before a therapy found through MS-Smart is also proven effective for PPMS? It's no ******* wonder people with PPMS get so excited about dismal biotin results and dodgy "neutriceuticals".

      Delete
    6. MD2 I understand ibuprofen relieves pain and inflammation much like asprin does, they do not effect blood clotting in the same way. Could ibuprofen effect low grade inflammation from activated microglia like you mention asprin does? Influencing progression.
      thanks

      Delete
    7. I sympathise with your comment. I have RRMS and agree treatment is very focussed on this. I guess this is because there is more chance of influencing the course of RRMS than PPMS or SPMS. And as you say above, it appears 'it's not interesting if it might only help the relatively small percentage of people with PPMS'. That must make you feel very dismissed and undervalued. I know it would make me feel like this plus angry and a whole gamut of emotions, I'd rather not experience.

      It seems to me from conversations I've had with people with progressive MS, that in the case of SPMS, they were told they could no longer be helped and discharged as patients. I find this shocking and if correct (I've only got this from two individuals) it displays quite a lack of empathy and understanding. I'd love to believe these examples are the exceptions but when I read comments as yours, I begin to wonder if it isn't endemic of our health care system in the UK. I'm really sorry this is the situation you face.

      I too did not know that aspirin *may* help and was very surprised to read this. You can bet I'm going to look into this more.

      Delete
    8. Anon 12:36
      Yes it looks like Ibuprofen could effect activated microglia.
      http://www.sciencedirect.com/science/article/pii/S0304394004013722

      But as memory serves from a recent study there are health implications for the long-term use of ibuprofen due to potential gut issues I guess the same may hold for aspirin.

      Delete
    9. Be very wary of stuffing good 'ole ibuprofen down your gullet with too much frequency. An impact of "frequent and regular use of NSAIDs" (especially ibuprofen) which is not well known is a negative impact on your absorption of folate in your diet. This can lead to a folate deficiency, with a whole heap of related symptoms, including APPALLING FATIGUE. Yes - I am ""shouting" - thanks to the ibuprofen I had to take to stay on Rebif I ended up with a folate deficiency. How much was I taking - two 200mg tablets 3 times a week - and "leafy greens" and other good dietary sources of folate are actually my favourite foods. Ditched the Rebif, took a folate supplement for a few months - feel much better now, thank you very much. Also had improved leg coordination and major improvements in depression levels in just two weeks after stopping Rebif. Rebif was pretty much worse than the MS.

      Delete
    10. The posts on aspirin got me wondering if this means it can help with remylenation. I came across a lot of information around 2013, including the below links. How much credence should be given to this?

      http://www.24-7pressrelease.com/press-release/rush-scientists-identify-a-new-function-of-aspirin-343813.php

      http://www.ncbi.nlm.nih.gov/pubmed/23653362

      Delete
    11. Thanks MD2.
      I have been informed coated asprin is better/ more gentle. Fewer stomach ulcers and less stomach upset but there are concerns the coating may lose some of the heart benefits.

      Delete
  52. Sun exposure and MS studies currently recruiting. Vitamin D and UV arms (using same treatment for psoriasis).
    Interesting podcast with Prof Robyn Lucas from ANU medical school.
    https://www.vitamindcouncil.org/blog/vitamin-d-podcast-07-dr-robyn-lucas/#

    ReplyDelete
  53. Any news on the Charcot front? Have you got the data to analyse yet?

    ReplyDelete
    Replies
    1. Are we anywhere near close?

      Delete
    2. It's like the Terry Jones fairy tale about Far-Away castle. Only, in this story, the only way to get there was actually to give up trying. I'm not sure this will work in research.

      Delete
    3. It's the title character in a Beckett play that never turns up.

      Delete
  54. Released today new guidelines for treatment of MS.
    "The guidelines stress the increasing importance of prompt
    treatment following diagnosis and that people with MS will face complex choices and must play an
    active role in treatment decisions".
    http://www.mstrust.org.uk/downloads/ABN-prescribing-guidelines-2015.pdf

    ReplyDelete
    Replies
    1. http://pn.bmj.com/content/early/2015/06/20/practneurol-2015-001139.full

      After reading the full guidelines I'm a little disappointed. A big step in the right direction for sure but looking at the advice given re step up from category 1 to category 2, I'm glad I escalated my drug of choice when I did. I managed to step up from Interferon to Lemtrada based on 1 new lesion but doubt I'd have been so successful under these guidelines. Timing (and luck) was on my side.

      Delete
    2. Treating of CIS remains ambiguous although the added sentence referring to cerebrospinal fluid may help I hope.

      Delete
    3. Re the sentence. 'Once started on therapy, patients should remain under the supervision of specialist MS neurologists and nurses'.
      Yes but also MSers not on a therapy need to remain under the supervision of MS neurologists. I was under care of a few general neurologists before starting therapy and I am sorry to say their knowledge of MS was not great. I kept discussing MS symptoms that are not common but are still heard of in MS. The general neurologists didn't recognise these symptoms as MS related and were not noted down/recorded in my file.
      It does matter when the patient is new to MS as it can be important to start therapy promptly.

      Delete
  55. Haha that's funny for people with ms

    ReplyDelete
  56. Friday, June 19, 2015
    MedDay reports additional positive data of its pivotal Phase III study with MD1003 in patients with Progressive Multiple Sclerosis.
    http://www.medday-pharma.com/news-and-events/medday-reports-additional-positive-data-of-its-pivotal-phase-iii-study-with-md1003-in-patients-with-progressive-multiple-sclerosis/

    ReplyDelete
    Replies
    1. We have to hope that research efforts into drugs to help progressive MS don't stop with biotin / MD1003. Because a circa 1 in 10 chance of _some_ improvement or a small decreased risk of progression is just not good enough. Heaven help us if that is the best that there is.

      Delete
    2. This drug is unlikely to be neuroprotective in its action as the timings dont make sense so either it is a repair or a symptom control drug. Just as only 30 percent respond to fampridine maybe 10 percent ,respond to biotin. So if so how quichkly does the effect occur. I am guessing quickly as it may be anti symptomatic. This first quedtion that needs addessing

      Delete
    3. MouseDoctor, you are spot on, in my humble opinion. I agree entirely. I won't be bothering too much with biotin until more is known about what it is doing. And thank goodness the scientific community don't down tools every time potential red herrings and white elephants appear. And MedDay's confounded positive spin on the unproven is just plain irritating.

      Delete
    4. yeah but i've been taking it (1.25mg) and my hair is so shiny as never before so at least from cosmetic pov it's great :-))

      Delete
  57. Any thoughts on this?
    Does it suggest treating anxiety would help with pain?

    http://www.neurologyadvisor.com/neuromuscular-disorders/multiple-sclerosis-anxiety-pain-prevalence/article/422317/

    ReplyDelete
  58. http://www.hcplive.com/medical-news/reversing-multiple-sclerosis-damage-with-topical-medications

    Is this the big regenerativr breakthrough?!

    ReplyDelete
    Replies
    1. http://multiple-sclerosis-research.blogspot.com/2015/04/more-remyelinating-drugs.html
      No alas not yet. See above posted 23 april

      Delete
  59. Md1003 is the best by a long shot and team g and Co can't compete! In my sceptical opinion.

    ReplyDelete
    Replies
    1. I think you're wrong but lets agree to disagree.

      Delete
    2. We do not see it as a competition and as we are not pharma we are not even in the race, However we are trying to contribute, if pharma do not want to take the reigns or the system does not want to fund alternatives then ptogress will be slow

      Delete
    3. We hardly know anything about MD1003 so far. Why do only ~10% of people respond? What is the mechanism of action? Is there any lasting effect? So it is hardly off the starting blocks, and has been heavily promoted by MedDay. So please don't stop researching, Mouse Doctors.

      Delete
    4. The reason why this studied biotin is that some people with biotin deficiency had MS and reported good effects, so they did a the study and this is how the ProfGs started with raltegrovir... and then you can construct a mechanism. I suspect MedaDay are trying to do science but I bet their resource is going into developing the trials

      Delete
  60. Retroviruses and Amyotrophic Lateral Sclerosis

    Purpose : A small set of HIV-infected patients have been reported with an Amyotrophic Lateral Sclerosis (ALS)-like syndrome that show reversal with antiretroviral drugs.

    http://www.hervanddisease.com/fichiers_site/a3771gen/contenu_pages/2-Avindra%20Nath%20-Retroviruses%20and%20Amyotrophic%20Lateral%20Sclerosis%20Lyon.pdf

    HERV, and then EBV and then HERV again....HERV everywhere....

    As Gwen Stefani says in her famous song: "What are you waiting for?"

    ReplyDelete
    Replies
    1. i'm aware of this

      Where next what don't they do

      Delete
  61. HERV & DISEASE

    First International Workshop
    on Human Endogenous
    Retroviruses and Diseases

    http://www.hervanddisease.com/m-176-abstract.html

    Here some articles of interest:

    -HERV-W/MSRV/Syncytin-1 activation and multiple sclerosis triggers: the EBV/MSRV dual virus hypothesis

    - From first retroviral detection in Multiple Sclerosis (MSRV) to the human endogenous retrovirus type W family (HERV-W)

    - Remyelination impairment and HERV-W in Multiple Sclerosis

    - HERV RNA in the Brains of Patients with Multiple Sclerosis

    ....and a lot of others very interesting abstracts....have a look...

    Will you be there too, profs.?

    ReplyDelete

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