Unrelated Blogger Comments May 2015

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BartsMSBlog

145 comments

  • Docs I forgot to ask you when the publication on anticholinergics and increased risk of dementia, Clemastin and Solifenacin are framed are anti cholinergic more current generation?

  • One feature I would love for you all to have is a drug pipeline tracker or something similar. I always see these one off stories from trials like ocrelizumab, but I don't really know when future phase results will come out. There is obviously uncertainty, but I feel resigned reading a lot of the new drug papers on here because I hear some exciting news and then it just vanishes into the void (for example, biotin).

  • after the excitement caused by MD2 at the research day and then the damp squib which was the AAN, we seem to be in a lull. Is there any interesting research results on the horizon? We appear to be no nearer getting a neuroprotective agent or repair agent on the pharmacy shelves – correct me if I'm wrong.

    • Everything that is reported here is still years away from the pharmacy – that is the sad truth but it's not the docs' fault.

      It is up to us MSers to be realistic while reading the news.

      MD2 was right in being excited because just 1 year ago we were still light-years away from cracking the progressive nut and now we are having the first tangible results.

      Also, biotin is far from over – some study results will be out in December.

    • Well if you think the AAN announcements were a damp squib then I suspect there's no pleasing you.
      And you're wrong, we're getting closer.

    • Anon 9:12
      I agree with you, it's just a start but now there are positive results, the impetus is going to be increased. As I've said before,
      pharma have lots of potential neuroprotectants sitting on their shelves and the phenytoin study should give them all the incentive they need to look at these in MS. Also, should we ever get enough recruited to the PROXIMUS study, then I think given that oxcarbazepine looks to be a much better neuroprotectant than phenytoin in our mouse studies, we should see even better neuroprotection with this, which is why I believe it's so important that we get enough MSers recruited for the study.

    • What about the charcot project results? When are these out and is there any idea of how this is going? Surely even blinded studies if succesful should give an indication if theyre working
      Ie patients reporting improving of symptoms etc or slowing of orogression

    • Is there any idea of when these will be out?
      Am I correct in thinking this was tested on RRMS patients only? Is Dr Michael Pender conducting further tests too
      And on a personal level what is your thinking regarding the trial?

    • I'm sure the llast patient was supposed to conclude in January hence lockdown and data release April/may as you stated previously

    • The data lock has happened and I amsure ProfG downunder willbe pouring through the data

    • What are we thinking timewise
      If the data is locked it can't be long surely and there's no shareholders etc to satisfy
      Do you guys genuinely have no idea how it's gone?

    • no shareholders to satisfy means we dont have to dis lose the results before publication.

    • Would you not release it earlier if you had the results? I know it's nice for you to have a big announcement IF it's good
      But for people with Ms every month is important

  • what's your take on candida and Ms is there a link? Could it be why there are so many diets that look anti candida

  • What's next for progressive msers? Any treyments on the horizon?
    Also would you attempt a treatment of any kind for people with rapidly progressive Ms as discussed by DrK with myself recently

  • A load of fuss being made about Ed Miliband tripping last night, that's what happens every single day when you have MS.

  • Apart from coffee / caffeine, what are the neuroprotectives that one can buy over the counter, at the supermarket, or grow in the garden? Could you possibly give a little list of things you think might be worthwhile? I don't mean "cures" – just things that, with additive effect, might, just might make a little bit of a difference over many years and for which there is some scientific evidence? Turmeric, frankincense, blueberries, grapes…

    (Ducking, in case you are figuratively/mentally/virtually throwing something in my direction for asking about nutriceuticals.)

    • You know me and nutriceuticals….hot air little substance at the doses you typically get over the counter…however happy tobe proved wrong

    • There was an article on here about "Treat PPMS early with neurprotectives" – my question is how many are on them and what are they called. If none are on the market then we have to look elsewhere ie nutrceuticals. Maybe wasting money but it is good to have the feeling that one is doing something. People are stocking up on biotin because their clock is ticking and cant wait for the drug to reach them. My view is if the drug is safe then why not let us have it.

    • Testosterone! Even the Americans are doing a phase 2 114 participant multi site trial of testosterone with ucla
      There has to be something in this, especially given stress worsens Ms and stress produces cortisol which lowers testosterone?
      If testosterone is neuroprotective as will be estriol surely supplementing with this would be an option?

  • A couple of MSers I know have taken Lemtrada and have gone a little further too. After the Lemtrada treatment when their lymphocytes are on the rise again, they've taken a dose or two of rituximab to knock that count back down, particularly the C19/C20 lymphocytes. Does this make the Lemtrada treatment more successful? Is there a downside?

    • Re: "After the Lemtrada treatment when their lymphocytes are on the rise again, they've taken a dose or two of rituximab to knock that count back down, particularly the C19/C20."

      Yes, there is a downside in the sense that we don't know if this strategy works or is sfe. Interestingly, about 4-5 years ago I suggested to Genzyme to test this strategy to see if it would prevent the secondary autoimmunity. If they had started a trial back then we would have an answer by now.

  • Team G, I find the rare basal ganglia disease similar in ways to MS and ADEM with brain lesions but can also include spine. Although basal ganglia disease was thought to be inherited. It is seen in Saudi and more recently Portugal. The attacks come on after injury/trauma, stress and febrile illness such as infection. These are all MS relapse triggers for me i've noticed.

    The patients are reported responsive to a lifetime of biotin with vitamin B1 and the dose given for treatment is biotin 300mg, this may be the inital dose and then lowered or stays the same. If the patients (usually children but can be adults too) come off the biotin and vitamin B1 then they worsen again. Also that the biotin prevents progression and symptoms disappear.

  • Would IV cladribine be an induction treatment? What was the tablet form? Was it a few pills a year forever? If so, how did it effect your immune system

    • iv or subcutaneous cladribine would be an induction therapy. The the tablet movectro was a pro-drug meaning that when you eat it the active cladribine drug is then released to that comming fromthe injections of cladribine. Thiscost apparently about $800,000 to do develop a drug they sold for €20,000 a year verses the generic iv or subcutaneous drug costing €400-2,000 a year.

      It effect is like lemtrada it depletes B cells for much longer than lemtrada and depletes T cells for a long time but less agressively than lemtradaandso doesnot cause the autoimmune side effects of lemtrada

  • What would be the prognoais for a patient presenting with sensory sumptoms that within 5 months has turnes to mild spasticity in all four limbs?
    How would you approach this neuros and mds?

  • A nice blog at another website on MS research, which summarizes a recent phenytoin trial results and the role played by the new mouse model developed by MD:
    http://www.msdiscovery.org/news/essays_opinions/18551-refined-animal-model-led-phenytoin-clinical-trial
    The story was told here already but it's good to see it reported elsewhere (I have absolutely no relation to the sodium channel team! I a just a person with MS who likes reading bout research news)

    • A yes a nice article by Dr Katie Lidster…whilst may idea for the project was indeed from MD and ProfG, it was MD4 (AKA Katie Lidster) that did the hard work to make it happen.

  • I've see you guys state before that ocb negative from an LP suggests a different disease to Ms or at least a different process
    Do you still believe this?
    Also what about ocb positive but mri negative?

    • If you are OCB negative there is a better prognsisI think but I am not sure we have said it is a different disease, I know I haven't
      There will be OCB negative and MRI negative MSers…but MS will eventually show itself it is is MS

    • There's a previous post on here stating that it is almost even possibly a different disease
      Ocb would suggest increased risk of spinal atrophy I guess?

    • MD,

      I'm a different anon. Is it possible that some that are OCB negative do have the Igs present in CSF, just that they are below the sensitivity for the test? (Hence potentially becoming positive later in the disease process?)

      Thanks

  • Please could you clarify should brewers yeast in vitamin tablets be avoided by MSers taking immune suppressing drugs? Brewers yeast is sometimes added to vitamin tablets. Thank you.

  • Why do you continually write that you think Lemtrada is a potential cure? Until these 10 years symptom free Lemtrada treated RRMS'ers go 20 years so we have evidence that is has stopped the progressive phase of the disease I think it is a little short sighted and dangerous to call a drug a cure. We know that MS can go dormant for 15 years+. Unless you know something we don't. I have the same issue with the HSCT treatment, 10 years is fabulous, no progression is great, but it's not a cure. It is remission.

    And before the MD's say they don't call in a cure, you can see it quoted by Prof G a number of times in this Blog.

    • Re: ".. Lemtrada is a potential cure?"

      That is why we use the term potential cure. As you state it will take 20 years to find the answer. Some MSers have now gone past 15 years. It is an experiment in progress. If we don't define what we mean by a cure and look for it we will never find it.

      Please note I don't used the term "cure" only "potential cure"; it is simply too premature to use the former term. The arguments used for alemtuzumab can also be applied to other inductions therapies, i.e. HSCT, cladribine, and possibly anti-CD20 therapies.

    • But if you really think this is a potential cure, why would you prescribe any other current drug? Regardless of if there MS is dormant or under control or active? It doesn't seem to make any sense. You are offering 2nd rate medication.. And don't hide behind NICE guidelines.

    • I am not a Doc but based on listening to the neuros the choice of drug rests with the MSer, NICE, NHS England and their prescription guidlines.

  • Can someone help me understand why raltegravir was chosen as the antiviral therapy for the Charcot project? My understanding is that raltegravir is an integrase inhibitor, meaning that it prevents retroviruses from inserting their DNA into the genome. The Charcot project, however, is built on the premise that it's an endogenous retrovirus which is causing MS. Why would disabling reverse transcription have an effect on a virus which already infects every cell in the body?

    This is outside my field, so perhaps I'm missing something very obvious.

    • Raltegravir has shown to be effective against the Herpes virus family. The drug also blocks an enzyme responsible for virus assembly. Since endogenous HERVs are upregulated in viral expression (EBV, HIV) controlling latent Herpes virus activity may benefit patients.

    • Thanks for your response. There seems to be some controversy in the literature regarding the mechanism for anti-herpes effects of raltegravir. For example, [1] suggests that it's disrupting formation of the procapsid, while [2] suggests that it's disrupting DNA replication. I have a few questions about these studies:
      -Is there any in vivo evidence (outside of case reports) for raltegravir efficacy against herpes?
      -Both proposed mechanisms will disrupt viral replication processes, but are these processes only relevant to the lytic phase of the virus? More generally, is there any evidence that latent EBV activity (which is presumed to be driving MS) requires these processes?

      [1]: http://www.pnas.org/content/107/37/16078.long
      [2]: http://jvi.asm.org/content/88/19/11121.full

    • I believe that I've found the answer to my second question. EBV has a latent phase replication mechanism which is distinct from its lytic phase (and from other Herpes viruses). EBNA1 is the only EBV protein involved in latent phase replication. Raltegravir has not been shown to target this protein, and therefore the documented effects of raltegravir appear relevant only to the lytic phase of the virus.

      Like before, I may be missing something, but I'd be very interested to understand better why raltegravir is expected to be effective for MS.

    • Nobody is interested in responding to this comment? There must be some reason why raltegravir was chosen for the Charcot project. If there's not, then a failure of the Charcot project to meet its clinical endpoint may unfairly cast doubt on the MS-EBV hypothesis.

    • This is the realm of the ProfGs as this project is nothing to do with the MDs and therefore it is inapprorpriate for us to answer as we dont want to say something wrong. But I understand that there was anecdote from ProfG and a few other cases and as to choice of drugs this is one of a number of candidates. I think I understand what they are

  • I would realy like to see Prof G as a patient. Is it possible to get referred from Northern Ireland? I have been in limbo since 2005 with query MS and it is driving me mad. No treatment, discharged from NHS even though I have spasticity and dropped foot.

    Thankyou

  • How common in Ms is it to have symptoms sensory and some motor but a normal neurological exam and normal brain cervical mri?

    • Any thoughts? Also I was told couldn't be spasticity even thiugh legs get stiff when walking as nothing is showing on neuro exam??!

  • Access to early treatments such as DMTs are only available to those people that are not languishing on waiting lists to see a neurologist. I had cancer and wasn't seen by a specialist doctor for nearly 4 months last year. What hope for MS?

  • We know all about lesion load and RRMS
    But does lesion load have any influence in ppms?
    Also does Progression rates In ppms change and plateau or is its constant speed of decline?

    I also assume neuroprotecives would help slow decline speed?

  • Dear Profs,

    What is the evidence for a link between psoriasis and MS? DMF appears to work for both.

    I also note this report:

    Alemtuzumab and chronic plaque psoriasis. British Journal of Dermatology, 169: 184–186. doi: 10.1111/bjd.12226

    This showed an early improvement in rash continuing to 7 months (I assume after first dose).

    Is it likely the the authors of a paper such as this would be able to provide further follow-up? It would seem interesting/potentially useful to know if/when the rash in such a patient returned to see if alemtuzumab acts as an induction therapy for psoriasis, which, if it does, would perhaps support it having a similar effect in MS.

  • MouseDocs et al. – do you know if it is safe to get propofol aneasthetic if one has MS? I will be having a minor surgery and they use propofol – however, I don't know if it's okay with my MS?

    Thanx.

  • I have an urgent question. I am 31 years old and had an MRI scan due to symptoms consistent with optic neuritis, and muscle tremors. The MRI had 2 lesions on it. Am I right in saying that no further investigations are required because even a normal person is are "allowed" one lesion/area of high signal per decade?

    If so, is the criteria for CIS, as a 31 year old, actually 5 lesions (as I'm into my fourth decade so the first four lesions are considered normal?).

    Thanks!

    • There are a number of criteria to consider when assessing lesions on MRI including shape, size, location, change over time, presence of enhancement or not. Hence, whilst it is true one should not jump on "any" MRI detectable lesion as being due to demyelination – there are other causes aplenty – your history, age and symptoms should prompt further investigations, including almost certainly a follow up MRI and probably a spinal tap.

    • Dr K – are you familiar with lesions on MRI (and oligo bands) that are due to a malfunctioning thyroid i.e. Hashimoto's?

      Can MS mimick lesions due to the above malfunctioning?

    • The presentation of Hashimoto encephalopathy is usually quite different from MS, but it is one of the known differential diagnoses. MRI lesions may sometimes resemble those found in MS. Blood tests should help reveal thyroid antibodies. Perhaps surprisingly, oligoclonal bands confined to the CSF do occur in Hashimoto's, though less consistently.

    • Thank you DrK – I've got thyroid antibodies in my blood (quite high) – should I consult an endocrinologists at a clinic about this or who could best help me?

    • This has got me interested. I have been hypthyriod for years. Only got a query MS dx as LP was clear and not enough MR evidence for MS. In my last scan radiologist noted that I should get on ultrasound on my thyriod as it looked enlarged. That was 6 months ago and neurologist didnt think it was necessary. My thyriod tests have been TSH and T4 – are these the thyriod anitibodies. I have been trying to get a DX since 2011.

  • I mentioned on this blog some time ago that bad posture might contribute to some MS symptoms in some way. Causing aching for example. From doing a websearch the alexander technique and MS brings up no results. The alexander technique is movement re-education and covers basic every day movements such as getting up from a chair, sweeping the floor and gardening, bending, carrying, lifting, eating and drinking, driving and working at a desk or computer. It seems to me that I could benefit from this technique for my MS.

    • On reading more on the alexander technique it can help balance and also can help nerves in the spine area. It can help with stress and anxiety.

    • MD2, you don't think that it has something to do with the immune system?

      I get relapses every time I have a common cold. How is that not related.

    • No, I do think it has something to do with the immune system but it's not the whole story and may not be the initial cause of MS but a secondary event. Just focusing on the immune system with the current DMTs has got us so far but we need to do other things such as protecting nerves remyelinating those nerves and ultimately repairing the damage. The study mentioned says MSers have particular cells in their immune system which respond to brain antigens producing particular cytokines (signalling molecules) in contrast to non-MSers. The inference is blocking these may be beneficial, which I think needs to be approached with caution as these molecules are widely used by cells of the immune system that are not MS causing but there to fight infection and interfering with these may have unintended consequences.
      The cytokines produced when you have an infection such as a cold can reactivate microglia in your brain which may be contributing to your relapses.

    • Sexy science indeed, but probably means little to most MSers as the main targets that this study highlights are already known and dealing with the immune system is lower down the unmet need compared to progression and repair. However I do believe antigen-specific therapy is the way forward to treat autoimmunity.

  • Hi Dr K or MDs
    What do you do for someone with Ms like symptoms but normal neuro exam, normal brain and cervical mri x2, clear lumbar puncture, with evidence of disc disease?
    Is it common in early Ms for all to be Normal or does it pretty much point to another cause

    • You send him to a psychiatrist and get him on meds for anxiety.

      Stop searching for illness. If you have it – you will be able to tell.

    • sorry I am not a doc but sounds like you are after a consultation and without the case details it is hard to do and we cant give such advice.

  • MD – is a 3T mri scanner better for a neurologist consultation compared with a 1.5T scanner?

    • As no one gets paid to do this and there are no skins to do what we want, this will be a transition as things change bit by bit, some wont like it some will but hey we are responding to our MSer Advisory group so if you are not happy blame them:-)

  • I would be interested in participating in MS patient focus groups. This could be online or face to face. Are there such groups?
    Where we can discuss for example treatments and what areas of research we feel could be beneficial for MS. I don't mean forums such as the MS Society forum.

    • The MS Society has the Research Network

      http://www.mssociety.org.uk/ms-research/get-involved-in-research/research-network

      If you want to discuss treatments and what areas of research you feel could be beneficial for MS, then this is either a lobby you need to have with the funders or a group where you need to engage the researchers such they are energised to go to the funders for support.

      However, who are the right researchers to engage, because maybe they don't currently have the skill set to full-fill your desire. Maybe ProfG would want a to produce such a focus group

    • Thanks MD. I was thinking about a patient focus group in connection with Barts. It would be good to have discussions with other MSers.

  • Do you find that the two recent articles you have posted in HSCT seem to gather more comments/questions/interest than all the rest?
    Does that show you that people are generally interested in this treatment or at least learning more about it, and that we hope that you will offer it to patients soon?

    • Yes it haz become more interesting with the three recent paperz and raises some fundemental problems with the system.
      Here is a surgical approach without pharma in the way and because of pharma pricing it makez it look like value for money. Will it get approved….shall we take bets.

      If we get a subject which causes opinions it gets more interest but maybe if we had some naysayers it would get even more.

  • I think the lupins complememt the new logo so well its worth posting a comment just to have a look at the picture

  • My Iris -Anvil of Darkness (what a great name for a heavy metal band) is just about to burst into bloom.
    Will take a pic and use for next months unrelated comments 😉

  • What is the standard treatment given for someone with early/mild PPMS who also has very little damage on MRI and clear LP. Disability is only a slight limp – hardly noticeable. I asked my neuro about neuroprtectives and Simvastatin – his reply was did I read about that in a woman magazine! Needless to say I dont have much faith in him

    • I'm not a neuro so can't advise

      but Next time say yeah "I always thought "The Lancet" was a bit girlie!, but I hear it is the rag that most British Doctors read or maybe you just look at the pictures?:-)

  • Doctors 🙁

    I'm so sad that I have MS. I don't want to be labelled as disabled…so lonely and without any hope…

    Lol it's pathetic that I am writing this at 2am in the morning but life is just tough sometimes.

    I hope you lead healthy fulfilling lives.

  • Recent posts have been rather uninspiring – I know you can only post what is being published. I'm guessing Welsh mouse has been muzzled which is a shame. I thought we were on the brink of some big news – neuroprotection, repair, charcot…. We are mid-way through 2015, but no real breakthrough news at all. I live in hope.

    • People have been very busy so ProfG was AWOL last week:-) and as you say we post what is published. You have a sniff of repair and protection for 2015..but that is not enough.

      Therefore, I am now going to disappoint because it seems that the only highlight that counts are the results of phase III trials…I can therefore say that you have had most of them for this year at the AAN.

      Maybe we will get ASCEND, which I predict will be a failure, except that it will stop gadolinium-enhancing progressive MSers.

      Maybe we'll get the GSK remyelination trial data

    • Are the results for biotin regarding remyelination not due next month? Though I fancy they would need to be a lot more interesting than the last rather disappointingly damp squib of an announcement.

    • The biotin trial data was released last month, 90% non-responders I seem to remember.

      I don't know when the paper will come out, the optic neuritis trial is at the end of year

  • Mouse Docs – do you know if selenite in high dosage gets into the brain damping inflammation?

    If it gets in would it make the sodium channels worse or better?

    Need to take selenite for my thyroid so that's why I'm asking-

  • Team G I wondered what your thoughts are on weight training with MS? I've read two views on it one being it may help another being it might cause problems with nerves.
    I feel it might not be the best choice.

    • Resistance training as part of a balanced exercise programme should not be a problem.

  • This is a question for Dr Gnanapavan… in relation to her work on NCAM and progression in MS indicators.

    If you see progression in MS associated with low endogenous NCAM, what do you see causing it?

    I note here (http://www.ncbi.nlm.nih.gov/pubmed/10803571 / http://press.endocrine.org/doi/pdf/10.1210/endo.141.5.7468) that Thyroid hormone T3 also regulates NCAM.

    I wonder what the Thyroid’s role in lowered endogenous NCAM is?

    This caught my eye – recovery from chronic demyelination by thyroid hormone therapy: http://www.ncbi.nlm.nih.gov/pubmed/19109501 (noted here, too: http://www.thyroiduk.org.uk/tuk/research/MS.html)

    MS and Thyroidism: http://www.neurology.org/content/82/10_Supplement/P6.170 and here: http://multiple-sclerosis-research.blogspot.com/2013/04/autoimmune-thyroid-disease-in-ms.html

    So the question is this – is low levels of NCAM a T3 issue? And if so, is there any evidence of thyroid hormone therapy working with PsMS?

    And is there any link between the use of Campath, T3 regulation and hyperthyroidism?

    • The story in the testes ("Thyroid hormone down-regulates neural cell adhesion molecule expression and affects attachment of gonocytes in Sertoli cell-gonocyte cocultures", Endocrinology. 2000 May;141(5):1633-41) is opposite of that of what we normally observe in MS, which is an increase in autoimmune thyroid disease. The difficulty is that NCAM is an adhesion molecule and not only is it involved in axonal growth (and to a some extent myelination), it has other roles around the body and is expressed in the skin, in natural killer cells (a sub-type of immune cells) and can behave differently in other organs compared to the brain. This is demonstrated in your second reference where thyroid therapy in fact induces myelination.

      In fact the story of NCAM and similar adhesion molecules which encourage re-growth is much simpler than this, someone in their wisdom designed the axon so that majority of these molecules congregated around the tip, if you damage this for example by cutting it off or say for instance an errant immune cell attacked it, then you loose the functionality of these molecules and then the rest is history.

      The brain operates under a very finely tune neuro-endocrine system which relies on a concept called negative feedback. If endogenous or externally induced levels of a hormone become elevated the neuro-endocrine sytem (hypothalamus, pituitary also known as the HPA axis) down regulates the endogenous production (or your body's production) of the hormone. So such experiments may work in a Petri-dish but not in a human. High levels required to overcome this system would simply make you unwell.

      As far as I know I don't know of any work of thyoid therapy in PwMS.

      Campath (alemtuzumab) causes hyper and hypothyroidism. It has an effect on the thyroid in an all encompassing fashion and not simply on specific aspect.

    • Thank you for this answer. I wonder what the role of HERV viruses and NCAM is and if this might support Prof G's work and theory. But that is for another post. As ever it seems that MS is a careful inter web of lots of different things going wrong, cascading and then attacking. It does make you wonder whether any money will be made available to look at complimentary pharma therapies (like a mitchondrial stimulant, along with a B cell depletor/T cell regulator, along with an anti-viral agent).

      (there was no Pubmed articles that showed evidence of treatment with thioamide drugs such as propylthiouracil, carbimazole or methimazole, or Lugol's solution. I guess if there was then people with Thyroid problems and MS would have responded well to treatment in both diseases).

      I guess the million dollar question then is how to regulate NCAM levels in PwMS

      Keep up the good work and if you need someone to do lumbar tests on treatment and on NCAM levels then I for one would be interested…

    • One final thing… if I am reading this right…it seems Thyroid T3 levels can be used as a marker towards the efficacy of neuroprotectives… would this, I wonder, sidestep the need to lumbar punctures and speed up the testing and trialling of certain compounds in PwMS?

    • Well it would seem that steroids which are the panacea for everything neurological seems to have a positive effect on NCAM http://www.researchgate.net/publication/11392113_The_role_of_NCAM_in_remyelination
      I think the issue with thyroid dysfunction is the autoimmune disorder behind it. Those who develop thyroid dysfunction in the CAMMS (alemtuzumab) trial demonstrate that it's not a great thing to have.
      There needs to be an objective measure of evaluating neuroprotection in PwMS and progressive MS, like for instance OCT in anti-LINGO and the phenytoin ON trial. CSF neurofilaments are also good way of doing this. If you plan to do a pure clinical study then we're talking about X number of years before you'd know if something has failed. By having biomarkers then you can start large through put screening of compounds.

  • I've a question re MRI & CIS. I was reading the definition of CIS (2010 McDonald criteria) and it says you need one objective clinical lesion. Then in the description says you need a lesion in at least 2 of 4 areas. Confused! One lesion, or two required for dc of CIS?

    • DIS – dissemination in space requires at least one lesion in each of the two areas out of the four listed! So one in each!! The English language is confusing.

  • Dear Profs
    Can anyone tell me how long it takes before DMF is effective? I am about 4 months in and have just had a pretty severe relapse after being in remission for about 6 years.

    • Not sure about DMF in MS as duration for a clinical benefit is difficult to quantify, however with fumaderm in psoriasis there is on average improvement in 3 months (which is easy to see).

    • Good news for M&S shoppers anyway. Unless, like me, you find shop-bought bread generally pretty vile. I'll continue to bake my own and use vitamin D supplements!

    • 400IU I expect. This I mean for the general population to increase vit D intake.

      It seems four slices of bread are recommended (by some) per day. So four slices could provide 30% of the daily requirement of vit D.
      I prefer home made bread too.

    • I will continue to take D3 supplements at 5000 iu, I've done this for over ten years and get my levels monitored every 3 months. I don't eat bread unless gluten free (cealics) and even then I rarely eat more than a few slices a month. But it's good that this will be added to bread for M&S customers, maybe they will also add it to their gluten free range.

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