Q&A November

Q

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Fly Agaric >Dont eat

This mushroom (toadstool) is called the fly agaric, although it is an amanita mushroom. It is rather unmistakeable Don’t eat it. The “Death cap” is deadly poisonous amanita

To stay clear of this and the fly agaric “Don’t eat mushrooms with white gills”. They both grow from a mushroom egg (volva) and the white spots are from the top of the egg. With the rule of “don’t eat mushrooms with white gills” would avoid the mushroom (False parasol) below. Some posionous mushrooms have non-white gills.

False parasols of North America. Eat this and you are may get a runny bottom and it will be barf-o-rama ,as it is also known as the vomiter.

The false parasol apparently doesn’t occur in the South East of England.

Below is an “edible” parasol I found in a field. (a) Size matters…ensure your mushroom is over 12cm as umbrella looking mushrooms below 12cm may be poisonous (Dapperlings). The parasols can be over 20cm. (b) The gills in the cap are white. The false parasol has green spores where you see green tinge on the gills (above). (c) The white double ring on the stem moves up and down on the stem. However, there is a look-alike in the UK called the “Shaggy parasol” which grows over 12cm. This makes some people (1 in 25) ill. Importantly if you cut the shaggy parasol the stem stains pink.

Parasol. Would you eat it? Look at the stem.

However the stem of the shaggy parasol and the false parasol are consistent and a single colour

(d) Importantly below the ring you get a snake-like colouring (Stretch-mark) caused by the rapid growth….This apparently indicates a Parasol. Cap was nice in Breadcrumbs.

parasol mushroom

As always with mushrooms….If in doubt chuck it out…Don’t eat anything you are not sure of.

About the author

MouseDoctor

160 comments

  • What to do when enough is enough. There is no cure. Doctors don’t even have the answer its all a mystery. The patient is a guinea pig. One can even end up worse off from one of these drugs!

    • An argument can be made and it is subject of a trial that I guess has been put on hold due to COVID-19…I guess we know the answer based on real life data but this should put the issue to bed.

    • No. No matter what spin is put on it. The mortality rate is 0.6. Alemtuzumab does exactly the same, completely destroys the immune so when it grows back its forgotten about the attack on myelin. Regardless of plasma cells in spinal fluid. As its more t reg biased as well. HSCT is a sledge hammer to crack a nut. As well as after the treatment you will have the immune of 80 year old.

      • Regarding the T reg point and alemtuzumab, I suggest once you get past the spin, an accompanying large pinch of salt.

        • Yeah. I’ve had this discussion before with MD and we agreed to disagree. As follows. Football match 10000 supporters and 5000 police. After Afternalentuzimab. 10000 supporters and 1000 police Although all cell populations come down. But the rstios come up so hence the anti-inflammatory response. I guess what I’m really asking is it possible to disagree with barts and still be considered smart?

  • I’m curious about something I’ve been told fairly recently, but have never come across in all my varied readings over the past five years about MS and all the crap that goes with MS. I’ve had two people tell me in the past year that even with people who have NEVER had any vision problems as part of their MS (even with PPMS) that there is still damage to the optic nerve evident on MRI, with evoked potentials testing, and on autopsy. Quote: “Numerous studies are being published that … the incidence of asymptomatic optic neuritis is quite high and the appearance of optic nerves can mimic glaucoma after optic neuritis.”

    Prof G – given your extensive and expert MS specialist knowledge, I’d be most interested in reading your thoughts on this.

    • Yes there are lots of papers this is why they are using retinal scanning as a surrogate of brain involvement. If you have optic neuritis you get inflammed optic nerves and as the optic nerves go through small holes in the skull (Optic foramen) and then you get loss of nerves in the retina because this is where the heads of the optic nerves live. However, if have MS in the brain the connections to the eye can also be damaged but the inflammation is in the brain and may not be in the optic nerve so you dont notice the damage. Also you can loose quite a few nerves before you notice it. In diabetes you can loose 80% of your insulin beta cells before you notice you have diabetes

      • 1) what specific benefit and use is a VEP to treatment/ management? 2) What type of training or specialist is qualified to interpret VEP? There are few actual neuroopthalmolgists in the US, which may be why ophthalmologists And neuropathologists are able to label themsevles as neuro othalmolgists. I was told by the only dr who worked as a so called “neuro ophthalmologist” in my area (for a reputable big city clinic) that my VEP was normal and I was “staring” at things too long. After living with self doubt about my visual symptoms For years, I inadvertently later learned that that my VEP test had clear slow latencies, which had been dismissed by dr. I raised issue with my current care team and was told slow latencies just show there was damage and already knew there was damage in my brain. So how does VEP really supplement MRI and clinical measurements?

        • OCT was also supposed to be a faster, less intrusive way to monitor progression but enthusiasm has waned. As for VEP, the authors feel that this biomarker will be of benefit for demyelination studies indicating repair.

        • VEP is a measurement to highlight a problem. The latency is associated with demyelination. They only become useful to confirm the essistence of the problem and is of value when there is a treatment. There are no approved repair agents

          Training in electrophysilogy, however often you put a head covering with electrtrodes on and give stimulus by looking at a picture or a light.

          So effects are obvious, so will take a trained eye.

          A pathologist deals with dead people or tissue an ophthalmologist looks at the eyes

  • Concerning the ill-fated Biotin Phase III trial recently published in Lancet

    https://www.thelancet.com/journals/laneur/article/PIIS1474-4422(20)30347-1/fulltext

    “..About 12% of patients in the MD1003 group and 9% of in the placebo group improved in either EDSS or TW25 at month 12, with confirmation at month 15 (odds ratio [OR] 1.35; 95% CI, 0.81 – 2.26; P = .31)..”

    How does one have nearly 10% of the study population on placebo spontaneously improve? Is this level of placebo effect normal in your experience?

    If it were to be somewhat above average, would you encourage anyone to go it alone with Biotin given the apparent nearly 1:7 possibility of sustained EDSS improvement?

    After all, nowadays there are Swiss pharma treatments for progressive patients out there with a lower reported chance of success..

    • As a low-BMI individual, I was interested to read this about the biotin trial (from https://www.medscape.com/viewarticle/939866):

      No significant therapeutic benefits were observed in any prespecified subgroups. Interestingly, those with lower body mass index [BMI] seemed to benefit from the intervention whereas those with higher BMI appeared to benefit from placebo, leading to a neutral effect in the overall population.

      Not statistically significant, however.

  • If I take tysabri, in case of covid positivity can they treat me with a monoclonal drug such as Regeneron or Remdesivir?

        • Below was my question i think it is generalized…

          does flair T2 hyperintense lesion on an mri report mean inflamation currently present ?
          if not how is inflamation present phrased in an mri report i.e would it be enhancing lesion ?
          whats the diffrence between enhancing lesion and hperintensity ? any info or feedback is apreciated 🙂 also is there any other research apart from the info on ms society you are aware of on alpha lipoic acid ?

          • Not sure how correct this site is but I found it quite useful when reading my own MRI Reports! – https://radiologyassistant.nl/neuroradiology/multiple-sclerosis/diagnosis-and-differential-diagnosis
            This may help with your question
            “Enhancement is another typical finding in MS.
            This enhancement will be present for about one month after the occurrence of a lesion.
            The simultaneous demonstration of enhancing and non-enhancing lesions in MS is the radiological counterpart of the clinical dissemination in time and space.
            The edema will regress and finally only the center will remain as a hyperintense lesion on T2WI.”

          • T2/FLAIR signal depends on the local concentration of water in spaces between cells. As MRI’s have greater sensitivity to subtle changes in brain water content, they are better at visualising WMH’s. These areas are hyperintense on T2-weighted (T2) and fluid-attenuated inversion recovery (FLAIR) MRI sequences, and by consensus are now referred to as “white matter hyperintensities” (WMH), or “subcortical hyperintensities” where deep gray matter is also involved.

            Some potential neuropathological associations are:

            Demyelination and axonal loss
            Reduced glial density and atrophy
            Cortical thinning and cerebral atrophy
            Endothelial and immune activation
            Ischaemic damage
            Hypoxia and hypoperfusion

            Active inflmmation is associated with T1 gadolinium enhancement. However that can be argued with, But indicates active blood brain barrier dysfunction.

            Enhancement is T1 and the hyper intensity to show lesion is T2 relaxation

          • MRI is ProfK territorry

            T2/FLAIR signal depends on the local concentration of water in spaces between cells. As MRI’s have greater sensitivity to subtle changes in brain water content, they are better at visualising WMH’s. These areas are hyperintense on T2-weighted (T2) and fluid-attenuated inversion recovery (FLAIR) MRI sequences, and by consensus are now referred to as “white matter hyperintensities” (WMH), or “subcortical hyperintensities” where deep gray matter is also involved.

            Some potential neuropathological associations are:

            Demyelination and axonal loss
            Reduced glial density and atrophy
            Cortical thinning and cerebral atrophy
            Endothelial and immune activation
            Ischaemic damage
            Hypoxia and hypoperfusion

            Active inflmmation is associated with T1 gadolinium enhancement. However that can be argued with, But indicates active blood brain barrier dysfunction.

            Enhancement is T1 and the hyper intensity to show lesion is T2 relaxation

    • In addition the MDs who often answer the questions do not answer clinical questions as we cant give advice and we are not going to comment on personal question, talk to your neurologists/nurses for that information

  • Hi Prof G,

    What are your thoughts are on Ocrevus causing worsening function over time. I experienced worse balance on the 2nd day post infusion, which lasted for 2 weeks or so.

    From your experience, any idea why a patient might have such a reaction? Would this occur with each and every 6mthly infusion? Am I more at risk for “deterioration” due to the drug in the long run as other have mentioned?

    • I wonder if cytokine release from killed B cells aggravating old lesion areas might be responsible for this? Similar situation reported after alemtuzumab infusion but the dosing interval is much longer.

      • MD2,

        This was also my experience after my first 2 half doses i.e. an explosion of previous symptoms. I posted on the Ocrevus facebook group about it and a large number of people reported similar. I am surprised if the killing of B-cells does kick off a potentially damaging inflammatory process such as ‘cytokine release’ then there is not more evidence / research on the subject. Adams talks about worsening functioning over time. If the culprit is ‘cytokine release’ would this not just be a temporary process. So for instance, it would aggravate lesions and cause temporary symptoms rather than making anything permanently worse? There were a number of questions on the October Q and A session on this topic

          • I would say 1-2 days after on each occasion. Basically once the steroids had worn off. When I asked my neuro, he likened it to how a cold could cause a pseudo relapse

          • I had extreme flu like symptoms for 3-4 days after each infusion. In addition, my overall symptoms progressively got worse the two years I was on the DMT. Became “allergic” after my 4th cycle and experienced severe infusion related reactions (anaphylaxis) and have not felt the same since I stopped. Just sharing my experience (again) with the group. Stay positive!

            ……before someone asks, please study this blog and you will find several previous posts with comments related to my experience and frustrations. Currently in the middle of a bad relapse now, and big surprise, since I can still see and walk, I was told there is NOTHING they can do to help my pain, which continues at 10+++++ level. Steroids and pharmaceuticals are getting old.

        • Infusion reactions are very common with ocrelizumab and notably with alemtuzumab. The cytokine release seems to act on older lesions. On culprit is suggested to be Tumour necrosis but there are others. This is why you get the the steroids anti-histamines etc etc. but cells are being bust open and stuff gets released. This is avoided with cladribine as cell implode rather than explode

          • Is it best to initiate cladribine with a clean slate, meaning an immune system not altered by previous DMT use. Or does the data suggest it is okay to initial while the immune system might still be altered from a previous DMT mode of action.

  • Is oocyte cryopreservation contraindicated for women with MS? Does the process of ovarian stimulation with hormones pose a risk for relapse/disease progression?

  • COVID-19 vaccines are expected for early 2021. Most of thema are RNA and vector-based vaccines. In the Phase I and II trials there were relatively strong systemic side effect (chills, headache, myalgia, fever >38), far more than with “traditional” vaccines. The “Oxford vaccine” had a case of transverse myelitis. Today, thera are no approved RNA vaccines for use in humans. Immunocompromised people are excluded from the Phase III studies. So in your opinion: will these new types of vaccinations be safe for pwMS and especially for those on Ocrelizumab, Cladribine, Fingolimod, DMF etc. ??? I would appreciate a traditional inactivated vaccine, like developed by Sinovac, for pwMS.

    • You are giving a live virus and your immune response kills adenovirus so the immune response with kill the adenovirs and in response make responses to SARS-COV-2 in the process…. Part of this is fever…it is an anti-infection response. These effects may be expected.

      Adenovirus is a particularly immunogenic virus in the early trials of adenovirus gene therapy the first generation was not manipulated to stop viral replication…it got into the liver….the liver was destroyed and patient was dead and that was the end of adenoviral vectors for gene therapy.

      Know we know that 80% of people who have been infected with COVID-19 (the UK figure is 71% I blieve) are asymtomatic and we also know that 75% of people can make T cell immune responses even in the absence of an antibody response, against cold causing cornona virus and the dominant response is againinst the Spike (S1/S2) proteins that are being targetted by the virus. If we have symptomatic people making up 6% of the population then there are over 4% who are immune and more likely to make a more exaggerated immune response to vaccines…leading to side effects.

      Once a vaccine is availlable I am sure trials will be done so that is monitored. Clearly we need to know what happens with ocrelizimab for example

      The recipients of the vaccine will have either already have had SARS-CoV-2 infection or

      • Tony Blair was on World at One today on R4 excitedly declaring that even if a vaccine doesn’t work very well, it should be rolled out asap. Side effects didn’t seem to occur to him. But he’s a ‘has been’, so is anybody listening to him.

  • Suppose I start one of the gabapentinoids for spasticity. Is this pretty much a one way road or is it possible / likely to get off them after a while?

    FWIW, the lorazepam I take for sleep very rarely knocks out pain perfectly for 12-18h but obviously that is not in any way sustainable

  • I know everyone is bored of covid but seeing as we are in lockdown part 2 I figure this is an important one:

    Do people on anti-CD20 need to shield?

    I look at the extremely clinically vulnerable list on gov.uk and I don’t think we count although we do count as clinically vulnerable. Do you agree?

    • My own conclusion: the risk to develop severe covid for people on anti CD20 seems to be about twice the normal rate. Given that severe covid is fairly rare for otherwise healthy patients below 50 or even 60, I still go to the office for now, FWIW.

      To reduce risk, I do wear FFP2 masks on public transport and while shopping, though mostly rely on distancing and hygiene in the office (wearing FFP2 all day is impractical and I doubt surgical masks do too much for the person wearing them).

    • I believe people at Barts are not being asked to shield but the ABH is issuing new guidelines soon.

      Based on or reading of the literature there is limited increased risk. ProfG may post on what we are up to

  • When is it likely for the higher dose of ocrevus trial for relapsing remitting ms to be approved for use in the general ms population ?

    • Potentially it could have no benefit, also long-term results are what we really want to see. Adios study may be more important by the time results is released for someone who’s already on OCR today.

  • I’m keen to know about what the long term resolution of secondary autoimmunity post alemtuzumab is like.

    There seems to be a set risk period for development of these conditions, but what happens once you’ve had them? Do you just carry it forward for the rest of your life or does your immune system eventually normalise? What would be the biological process at work here?

    For context I had a particularly stormy course with 3 new autoimmune problems (graves, refractory ITP and AIHA). I’m 4+ years past my last infusion and all has been quiet now for about 18 months. Long term steroids bring side effects, but it’s hard to balance these against what my actual risk is! There doesn’t seem to be any literature on this so we are flying blind 🙁

  • Could adding alpha lipoic acid ( 1200 mg ) as an add on increase the risk of having PML ( jc virus reactivation ) depending on your treatment ( could it increase your odds of having PML if you are on anti-cd 20 or dimethyl fumarate or any other DMT ) ?

    I don’t know if i am worrying for nothing but since alpha lipoid acid has anti-inflammatory proprieties I thought maybe it could increase your odds of having PML when used as an add on to certain DMT but then again I don’t know if I am worrying for nothing. Thanks in advance.

      • I have been wondering if nature, to preserve immunological memory, developed a way to turn naive b cells to memory b cells in absence of the antigen but in presence of antibody secreted by the plasma cells.
        I mean you have immunity to antigen X. All memory b cells are gone for a random reason. B cells start to repopulate. Plasma cells then turn these new naive b cells to memory b cells capable to recognize their target restoring immunological memory and also APC functions.

        It would be intriguing… yet I don’t see evolutionary reasons to select this characteristic.

    • During Lock-down I have developed an interest in mushrooms and have been watching them arrive in our local woods…the fly agarics appeared in large numbers 1-2 weeks ago along with the trooping funnels, the common puff balls and honey fungus a week before that, false death caps before them, the death caps and shaggy inkcaps and before them and we had the blushers, a few other aminitas, loads of boletes, including porcini (penny buns) and giant puffballs. Found a lovely late parasol last week and this week amythst decievers and wood blewits.

      Maybe next year it will be Gourmet MD 🙂 and if I get it wrong Dead MD :-(.

      • Same type and sequence of mushrooms also here… last weekend I found saffron milk caps or red pine caps and lots of grey knights, a few kilograms both (around 1300 mt asl). Many km away but same sequence, wonderful!!!

      • There’s a lot in between gourmet and dead, e.g. nasty taste, bad trip, liver damage, severe case of the sh*ts. Bit like DMTs.

        • Totally agree made a mistake once. I will never do it again…

          With a false parasol actually. I did not know the existence of a false parasol.

          • I have heard of the false parasol, also known as the “vomiter”, so know about the problems of both ends of the intestine. However I dont have that concern as I am led to believe that the do not occur in Engaland but are a common cause of problems in North America. However, you have to look at the stipe/stem/stalk. The snake skin stretch marks on are characteristic of the parasol. I’ll add a picture

        • Very good…:-)
          Know your shrooms….know your DMT…..to reduce chances of the adverse effects. Yep there are a few good shrooms…same for DMT:-)

          At the start of “shroom” season we decided that we would only look for a few safe bets…and MrsMouse did not even want to go near the safe bets…I have been the Queens poison (food) taster. We a few years ago we found a Chanterelle patch wouldnt touch them until we got a local forager to check each one. I now know the distinguishing features

          • The two ends story is the way I described what happened next. You have to be quick to understand which end deserves the priority seat… by the way intoxication may kick in after 2 days or more. Yep false parasol should be white on the stem.

            For chanterelle there are just a couple of mushroom that can be confused and one of them is very toxic but it grows on wood. It is said to be bioluminescent. One should look to the gills, they are very different from the one of the chanterelle.

            Just had pumpkin soup with dried and ground horn of plenty. I was recently told that dried and ground is not the best way to taste them. I was suggested to dry them and then add to risotto few minutes before it is ready.

          • The bioluminescent on wood sounds like Jack O Lantern on the wood (poisonous). Chantrelles have folds and not true gills and another feature is the inside is white when you cut it.The false chantrelle (poisonous) has real gills is yellow on the inside (I haven’t found it), but I guess you know this. I have never seen a horn of plenty. I got a dryer to try and save the pile of porcini that I found, I got my Zip code wrong. I used work zip code and my real address and by the time I got it a week later the season was ended. Maybe next year

          • Just read the edit of the Q&A post. Messed up with the colour of the false parasol stem good I remembered the snake pattern. The one I hate is likely the one that turns reddish when scratched/cut.

            About tasters, I used to bring friends and tell them to test russulae. Last time a friend asked if a huge russula he found was good so I told him to try to taste it. He didn’t want to check the others he found later. Actually, this always happen with all my friends that come with me: they see a big russula mushroom and they want to know if it is edible, they try and they get disappointed.
            Stopped collecting russulae except two very good species that are also easy to identify, others did not have such a taste it is worth collecting, cleaning and so on. It’s a boring task.

          • The false parasol would have the snake pattern so I would have avoided apparently it is about 1 in 25 who react.
            As for russulae…They are not on my radar maybe in future when I have more knowledge however there are too many of them. Apparently they are not deadly poisonous and if you try a nibble and spit out and it is spicy it is not good to eat, the hotter it is the worse eaters they are. I would only try if I could positively identify and as they are not choice I will avoid for now.

          • Woke up this morning and for some reason fancied a mushroom omelette. I wonder why? I’m looking at you MD and Fabio!

    • Thanks it supports what we know from SARS-Cov where T cell responses are detecteable for over 5 years compared to the memory B cell response, there is data of that they can be found for 11 years.

      They find T cell responses outside of Spike we know this already in fact we know every thing already but confirms the smaller studies

  • Are barts going to relocate their infusions for DMTs to the dental hospital like the last time there were a significant number of hospital admissions?

    Thanks

  • Can anyone recommend anything that eases the itch from injection sites? I can go weeks without a problem and then suddenly it’s like my body thinks, “I don’t think so” and the site is lumpy and itchy for days. I’ve tried arnica gel that I keep in the fridge so it’s cool, but it doesn’t really make a difference.
    Thanks for any tips!

  • Hello. I was under the impression, in fact I’m sure it states on the patient information leaflet, that if you are on Tecfidera you should avoid live vaccines. Therefore my understanding is that we will not be offered the covid vaccine when it becomes available and if for some reason we are offered it we should decline. Do you know if any dead vaccines will become available for Covid that will then be suitable for us. I think there are still substantial numbers of people on Tecfidera so I presume others are wondering about this. Thanks

    • Live vaccines are not recommended for most MS DMT.
      The Oxford Vaccine in a live chimpanzee virus but it cant replicate so it should not matter if you are immunosuppressed it can’t create an infection, unlike an attenuated virus but I would suspect they avoid risk and wont recommend it.
      There are two RNA vaccines in very late stage development they are not live and are an alternative. A comparative paper was published today I will do a post.
      Then there is two dead virus (coronaVax Covaxin) in late development too

      • I listened to a presentation from a guy who works for a clinical research company who is managing the trials for 4 different COVID vaccines. He was specifically asked if immunosuppressed people could be given the Oxford vaccine, he response was that as they don’t replicate there was no clinical reason that they couldn’t have the vaccine, but at this point in time it obviously hadn’t been tested in such populations.

  • My puppy has got Kennel Cough, the vet on the video call tonight said immunocompromised people can catch it – so be careful around my dog.
    I’m on Ocrevus. Should I be worried? I can message MS Nurse tomorrow… but just incase anyone sees this and knows if I can catch a dog disease. I’ll be raging if I catch bloody Kennel cough before Covid to be honest…

    • Humans can catch this for example ” A 43-yr-old female presented with a 2-day history of increasing swelling of the face and right upper extremity (They had immune-related cancer). In addition, she had one week history of fever, progressive shortness of breath, and cough with yellow sputum production.” Obviously if you do develop such symptoms you should ensure you tell your doctor so they dont just think covid. Yellow sputum is not necessarily a covid feature but sometimes people get infected with a bacteria. A course of antibiotics should clear up the dog. The sooner you can do this the less likely it will be infective to you and other dogs Bordetella in humans responds to erythromycin.

      One of the most common culprits is a bacterium called Bordetella bronchiseptica which is why kennel cough is often called Bordetella.
      In humans a different Bordetella pertusssis is called whooping cough. Your B cells control bacteria infections. Most dogs that become infected with Bordetella are infected with a virus at the same time. These viruses, which are known to make dogs more susceptible to contracting Bordetella infection, include canine adenovirus, canine distemper virus, canine herpes virus, parainfluenza virus and canine reovirus. Most of the canine viruses cannot be transmitted to humans. However, the main bacteria Bordetella bronchiseptica can infect humans, though this is very rare and only a risk factor for people with weakened immune systems. There is also very little evidence that humans can contract the bacteria from animals.

      No harm to contact your nurse but the first solution is to treat the dog…No kissiing the puppy no matter how cute

      • Thanks Mouse, I thought you may know about this with your animal experience! I am taking him in tomorrow hopefully, for anti-biotics. Yes, she did say it is likely Bordetella, as you said and that this is what human can get too! Been kissing him all weekend… oops.

        He is vaccinated with Nobivac DHP – “vaccine provides core immunisation to dogs for distemper, hepatitis (canine adenovirus) and canine parvovirus.”

        And he’s 5 months old now so id hope he was protected and has generated his immune response ..unless he’s secretly on anti CD20 too 😀

        Good to know what antibiotics are good for that in human, i’ll contact GP if I get symptoms and spare the nurse my neurosis! I am more worried he gave it to my parents elderly dog 🙁

  • MD – I was expecting more chihuly this month; however, mushrooms present their own unique artistic beauty. Plus, some strains have been shown to provide therapeutic benefits, particularly with military veterans. Across the pond, a few of the States just voted to legalized therapeutic mushrooms.

    My question……..would the data/research suggest a spike in t-cell lymphocyte subsets during b-cell repopulation after discontinuing treatment with anti-CD20? I know you have reported on how anti-CD20 therapies also alter t-cells (not just b-cells), yet I do not recall any information on total subset levels during repopulation. I am having difficulty finding this data. Thank you for the continued insight.

    • As an avid reader, commenter, and supporter of this blog, it is disheartening to see no response to my general research question above. Silly me, I thought this was a research blog.

      Frustrating when one of the best MS centers in the US says “we don’t have enough robust research”. So I ask the research blog, no response.

  • Sodium propionate: I have just started a 2 week trial to see if I can feel an effect. Now I read that it can have a toxic effect on the brain,, increasing levels of GABA. Please enlighten me: is there a real risk?

    • I know nothing about Sodium propionate but is an acid and we never recomend self-experimentation unless part of a clinical trial, where the dose is carefully selected and people are monitored for adverse effects.You expose yourself to all sorts of risks

  • Sorry if this has already been asked, but will people with MS be able to have the Pfizer vaccine (in the news today)? Thanks.

    • Yes if you can get your hands on it, 10million doses offered for this year if they are sensible they will save these for immunosuppressed people

  • MUSHROOMS
    After taking these:
    Chaga, Cordyceps, Shiitake, Reishi, Lions Mane, Maitake
    In capsule form -supposedly for neuroregeneration- I was in an ambulance with the siren going. I had fainted and had fast AF. My heart is ok. I chucked the capsules, and the cannabis oil and have been fine since.
    Be warned!

  • Very sorry to hear what happened to Prof G. Get well soon!

    I’d like to ask what are the potential factors for the random worsening of symptoms (which recovers within next day or next few days). And if there is a way to control these factors.

    I understand stress is one of the factors.

  • Dont blame it all on ms

    Low fitness linked to higher depression and anxiety risk

    People with the lowest combined aerobic and muscular fitness had 98% higher odds of depression, 60% higher odds of anxiety, and 81% higher odds of having either one of the common mental health disorders, compared to those with high levels of overall fitness.

    The researchers

    • Fitness! It’s so marvellous to read the different areas of research, reports on clinical trials, ideas on possible trigger factors, lifestyle management, treatment strategies, medication adjustment. What is happening in the field of neuro physiotherapy?

    • MS is it Smart-2. OK I’ll have a go, but obviously I have inside knowledge and you know rule number 1 what happens in a camel club stays in a camel club..The choice is yours was a horse designed?

    • Sid, from previous posts i assume that you are using Prof G’s neuroprotective cocktail. Can i ask what dose of lipoic acid you are taking and whether this is of the R or S variety. I am struggling to find an answer on this. Thank you

      • I am taking 1200 mg as per clinical trial NCT01188811. It says racemic so 50% R and 50% S. Synthetic source. R has different activity bioavailability. Pure R enantiomeric form would be VERY expensive.

        I am taking it as 2 doses each 600 mg approximately 8 hours apart between meals.

      • Anon,

        I take 650mg of Alpha Lipoic Acid a day (one tablet). The bottle doesn’t indicate whether it is R or S variety. I think the earlier trials used 1200mg a day. I see there is a planned trial trialling 1200mg.

        I also take one 10,000IU Vit D tablet a day.

        I’m 6 months into the Keto diet and have lost 30 pounds (now the same weight as in my early 20s). My blood pressure is in the normal range.

        I walk the dog for 25 mins every morning and cycle c.30 mins every day.

        I would like to try Metformin but don’t have diabetes. I’d be interested in getting on a trial where this is offered. I don’t have high cholesterol so cannot be prescribed statins, but will await the results of the MS Stat trial (some years off). Perhaps in the next 5 years, neuros will offer a cocktail of therapies (eg Alpha Lipoic Acid, statin, Metformin) after an induction therapy.

        Good luck.

  • Question

    If you are a big pharma ceo that believes your vaccine its going to be of great value for the company and shareholders and have anounced fantantic trial result

    What do you do?

    Sell stock
    🙂

  • Dear mouse doctor,

    At the current rate of things, how long do you think it will take for a phase 3 antiretroviral trial targeting EBV to get started not completed just started ?

    Also at the rate of things, how long do you think it will take for a phase 3 EBV vaccine for multiple sclerosis to get started not completed just started ?

    Thanks in advance 🙂

    • 1. ProfG and ProfG down under have been waiting to start for ages for EBV drug..EBV is a DNA virus retrovirals work against RNA viruses as they have to convert to viral DNA to reproduce

      2. Moderna started their phase III in March and it is now Novemember (They were allowed by the regulators to skip the pre-clinical), they could run the risk of failure by doing trials all at the same time because there was USA government behind them..for EBV they havent started trials yet.

      • Thank you for your response. So most likely it will take a few years then before completing phase 1 and 2 before reaching phase 3 for the EBV vaccine unless a global alliance is made to accelerate it just like covid-19.

        I thought antiretrovirals used for HIV had efficacy against EBV partly because of this poster in the 2019 ectrims. The title was : Several ‘anti-retroviral’ nucleoside analogues have in-vitro efficacy against Epstein-Barr virus.

        Also, thank you once again I was not aware as to how the covid-19 vaccine managed to be developed quickly. I understand the mechanic behind these trials a little better now. 🙂

        Thank you once again for your response and I hope you will have a great week 🙂

        https://onlinelibrary.ectrims-congress.eu/ectrims/2019/stockholm/278864/natalia.drosu.several.anti-retroviral.nucleoside.analogues.have.in-vitro.html?f=menu%3D6%2Abrowseby%3D8%2Asortby%3D2%2Amedia%3D2%2Ace_id%3D1603%2Aot_id%3D21650

        • In HAART for example there are cocktails of anti virals some are anti viral some are anti retro viral

          Look up operaion Warp Speed https://en.wikipedia.org/wiki/Operation_Warp_Speed $10 billion could fund 10,000 investigator studies, hundreds of pharma trials. Normally you do things sequentially one after the other in this case they were doing stuff in at the same time, wasteful if you get it wrong but saves time. Pfizer have been manufacturing for months thats how they have 50 million doses before Christmas

          • Interesting thank you for sharing the link I have taken a quick look but i will be sure to read it more in depth. We just need to convince the USA government sufficiently enough to demonstrate that EBV causes multiple sclerosis. They would consider the EBV a pandemic since it causes cancers, multiple sclerosis and potentially other autoimmune diseases.

            More efforts into a vaccine would arise i suppose if we could show exactly how from a molecular perspective EBV causes multiple sclerosis.

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