Q & A March 2021

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Spring is on its way and if you have a question, you know the drill.

Spring hits MD2’s garden

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MouseDoctor2

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  • can fasciculations be a symptom of ms ? i have had a constant and continuous twitch in the muscle in my left hand below my little finger for two months now, it started out of the blue and nothing stops it. ive had steroids, baclofen, gabapentin all sorts but it just keeps going morning noon and night. i was told by my ms nurse that its not unheard of but my gp says its not common with ms as ms isnt thought to effect the peripheral nerve. i have tried to contact my neuro but no such luck and no one can give me a straight answer if ms can cause this or if i now have something else to worry about.

    i know you guys cant comment on particular cases but just in general could fasciculations be ms ? and can they be constant and drug resistant?

    • Annon with fasciculations, yes, yes, yes, my right hand pinky gets jumpy for a week or two onoccasion. The first time it happened it was a significant flare. Of course we can never really definitively say MS causes my facilitations or other miscellaneous out of the ordinary symptoms, but I take it as a sign to slow down a bit and take care. I got a bit more comfortable with my MS when I began to trust my own experience and not expect a doctor to validate every sensation I get. As another commenter suggested, I do supplement with magnesium, calcium, and zinc tablet when muscle contractions of Hands, feet, or limbs bother me. It’s supposed to relax the muscles. Best wishes.

      • Hey thanks for replying its very kind, my hand has been like it now constantly for over two months so its panicking me a little, never had issues with it before and it just started when i woke up one morning and hasnt stopped.

    • I have fasciculations. Before first ocrevus dose they where almost everywhere arms, legs, shoulders, knees… I was told they are not a symptom of MS but I didn’t have them before last relapse. They almost completely went away shortly after ocrevus first dose.

  • Hi,

    Thanks for a great blog!

    Two questions;
    – Cladribine targets CD19 b-cells while Rituximab, Ocrelizumab etc targets CD20 b-cells. The CD20 drugs appear to be more efficient than Cladribine. Can you explain why this is the case?
    – When will Merck release instructions on re-treatment of Cladribine/ Mavenclad?

    • On what basis is ocrelizumab better than cladribine? As long as they deplete similarly they should be similar. In terms of cladribine dosing I guess you could ask is the dosing optimised higher doses were advoided as low lymphocyte numbers was a sife-effect in 2010…however it is the effect.

      I have no idea when Merck will release data, profG may.

      • I am not saying Ocrevus is better than Mavenclad, I said it was more efficient – on the basis of released data. Yeah, yeah, there is no head-to-head comparison, but if you look at the numbers and study design (which is comparable enough), they favor Ocrevus.

        Back to my question; I will re-phrase it, in hope of an answer – will a 85% depletion of b-cells targeted towards CD19 markers equal the same efficacy as 85% depletion of b-cells targeted towards CD-20 markers?

        I guess they (Merck) have to get their move on. A lot of people are quickly entering their fourth year, and will be looking for alternative meds to keep them protected.

        • CD19 is monitored and not CD20 because ocrelizumab/rituximab would block the staining so it is used with most agents cladribine, orcrelizumab, alemtuzumab,

          Without a trial how do you properly capture the data. But agreed the info is needed

  • My neurologist has suggested I take Siponimod. I’m worried about taking it at this time, as it affects the immune system. What do you think? I have active secondary progressive (had another relapse in September) and my disability is continually worsening in both hands arms and legs. Can’t walk can’t stand up without help.
    If you think I should take it; do I need to wait until after the second dose of the vaccine? I had the first one on 12th Feb

    • We cannot give such personal treatment advice. You will get a more optimised vaccine response if you complete your second cycle. In Europe siponimod is indicated for active secondary progressive MS, in the US there are more options. That you are being offered treatment suggests your neuro thinks it will be of value

  • the ebmt guidlines state that someone with agressive relapsing ms is a good candidate for hsct and may be treated with it instead of having to fail treatments due to quick disability build up where as the nhs guidlines state that you have to fail one of the top tier dmts first unless your ppms with activity which seems to be pretty rare, so does one supersede the other ? if you dont fit nhs criteria but do fit the ebmt would you be offered hsct ? i have also spoken to people in support groups that were treated with hsct after failing less efficacious medication is there a particular reason the would be able to skip the highly effective medication ?

  • I had twitches then fasciculations and it was a symptom of a rather severe magnesium deficit. It’s a PNS symptom rather than a CNS symptom. For me it was secondary to adding vitamin D, not knowing I was already pretty magnesium deficient.

    Obviously I’m not the Bart’s team but this complicated my diagnosis since not directly MS.

  • DMTs and infections – would it be fair to state that as a crude rule of thumb, DMTs increase the risk of infection mostly because of suppression of CD8+ T cells?

  • I’m just about to start year 2 Mavenclad and in the last month definitely back to where I was prior to year 1. It was a great year.

    My question: if Mavenclad reduces by 80% B memory cells per year, growing new naive B cells, could a case be made for two years not depleting enough to manage EBV completely?

    Vs. the continual B cell depletion of Ocrevus.

    How does Kisempta compare to Ocrevus?

    Thank you!

    • ofatumumab is given as a subcutaneous injection monthly ocrelizumab is intravenous 6 monthly recovery rate of ofatumba is aout 40 weeks and 62-70 for ocrelizumab, so maybe B cell subset depletion is different but haven;t seen the data

  • This question is directed to Prof G although any response would be appreciated. Prof G has openly stated that if he had MS his particular poison would be alemtuzumab or HSCT. These are not available to him first line on the NHS. So if diagnosed tomorrow, what is his strategy? accept a CRAB drug and wait for a relapse to access Lemtrada 2nd line? He could fight for Ocrelizumab but that would likely rule him out of clinical trials and would likely get his MS activity under wraps (MRI wise), making it less likely to ‘quaify’ for HSCT or Alemtuzumab in the early phase of his disease. Does he pursue HSCT privately? not in the UK, unless he can demonstrate activity. This leaves the option of seeking treatment abroad. A move that is considered unwise by the Barts team. This is the conundrum facing a number of patients on this blog and i would love to see a post on it / response to this. We hold Prof G in very high esteem and use his advice to challenge our constantly challenge our nueros (which no doubt they all love) but i am struggling to solve this particular puzzle

  • Hi MD & team,

    Is there anything else that pwMS can take to help stop inflammation, other than NSAIDS and Steroids? If you feel the neurological pain and burning sensation from your MS and keep having various infections/viruses (thankfully not the one beginning with ‘C’).

    And a question which may appear a little grim but stay with me…

    If you’re in a lot of pain and stiffness everyday in your say in your 40s/50s how do you look to treat someone, apart from doses of gabapentin/pregabalin or baclofen, long-term? To understand that your future for the next 20/30 (if all goes well) is going to be something that is harder to bear as you’re degenerating everyday with age. How would you advise the best way to manage the pain/stiffness and if the inflammation is there all the time and say in my case, on a DMT – but feeling worsening of symptoms, what would be your plan for a patient to look to the future on the DMT and should you carry on with it? How long would you allow a patient to continue before you start having a deeper conversation about their MS?

    I know you can’t advise but if you could mention some possible past patient scenarios, that would be great.

    Many thanks and all the best to you and the gang 🙂

    • I have found GREAT relief from pain and stiffness by doing the Maltese cross stretch which is done with a strap and props to slowly allow your body to relax. Lying on back, left leg outstretched, strap around ball of right foot and ends of strap held by left hand. Stretch right arm out to the side, slowly cross right foot/leg over the body and allow it to lower to floor- use strap to control the drop, with goal of having the right leg perpendicular to the left leg. Bring right leg back to center over head, place strap in right hand and allow right leg to drop to the right with the left arm outstretched. Repeat 4x doing for a count of 4-5 slow breaths for each time the leg is on the ground. Note, when you cross over your body the left ankle turns so that the outer edge of the foot is touching the ground BUT when the leg drops to its own side, the left foot is centered as if a “Barbie” foot. Then reverse to have the right leg outstretched and the left leg crossing over or off to the side. My pain dropped 50% on day one and now I do this and have minimal pain the rest of the day.

    • I’m a woman in my late 50s with MS and like you experience pain and a sense of inflammation a lot of the time. I’ve been taking 700mg of Gabapentin for some 2/3 years now.
      I find my symptoms are eased with the use of daily stretches, also some mindfulness, a reasonably good diet and IF. Whatever stretches I do depends on how I’m feeling that particular day. I’ve watched loads of YouTube vids and worked with a yoga teacher for a few months and now have a better sense of which stretches I like, that work well for me.

      If you haven’t already you may want to take a look at Aaron Boster for advice on various things including exercise. Also the MS Gym – mainly exercises, but couple of stretching routines also.

      Best wishes with keeping your pain and inflammation to as low a level as possible.

    • 1200 mg of lipoic acid a day should slow down brain atrophy a phase 2 trial showed it slowed it down by 68 %. However depending on the medication you take it could interfere with your medication therefore it is best to talk to your pharmacist and/or your health care provider. A second phase 2 clinical trial of lipoic acid 1200 mg a day will have the results public near the end of 2021.

      A DMT slows or stops new lesions and lipoic acid should in most cases dramatically slow down brain atrophy.

  • Greetings from Norway, and thank you for the oppurtunity to ask questions!

    As far as I’m aware, there is no logical reason why patients should feel worse between infusions of the B-cell depleting agents rituximab and ocrelizumab (CD19+ still usually dead). Yet, I know of quite a lot of patients that experience the so-called ”crap-gap” when closing in on a refill (about 2-4 weeks prior). Has there been any research done on this phenomenon, and if not; do you have your own reflections on why patients might feel worse when closing in on re-fills?

      • Yeah, I guess that could be the explanation. In personal experience, however, my CD19+ was still at 0 last time after 7 months (when I had to postpone rituximab for almost 2 months). So they were still not coming back. Still, I felt worse fatigue-wise for about 5-6 weeks. Got better about a week or two after the refill. No difference in lifestyle either.

        I’ve been wondering whether it could be a psychological effect. I mean, the awareness of the fact that you should get a new infusion might produce an expectation that you should feel worse. Don’t think it could explain my case though, as I’m very logical about the disease. Thanks for answering!

          • Even if there was returned B cells, could they make people “feel” worse that quickly (1~2 month after return)?

  • What are your thoughts on Low Field Magnetic Stimulation as a remyelinating treatment, please? It’s already sometimes used to treat schizophrenia and depression, with pretty acceptable side effects, and I just saw a paper claiming that it promotes remyelination in cuprizone-poisoned mice. Before I saw that, it hadn’t even occurred to me that magnetic fields might influence myelin production, but their results are good enough to be at least interesting, and I would be grateful to hear your thoughts on how likely it is to turn into a useful treatment, please.

    The paper I’m looking at is “Low Field Magnetic Stimulation Promotes Myelin Repair and Cognitive Recovery in Chronic Cuprizone Mouse Model”, Wang et al, CEPP February 2021.

  • If more successful treatments are found for progressive forms of MS, should they be used in relapsing remitting as a combination therapy, to slow down the unseen early progression. Or will they just be strictly for progressive forms of MS

  • Hi, thanks for this q&a. My question is in regards to this article: “Long-Term Clinical Outcomes of Hematopoietic Stem Cell Transplantation in Multiple Sclerosis.”
    The authors show that hsct represents an effective treatment for people with aggressive ms that doesn’t respond to traditional DMTs, as 60% of patients don’t show signs of progression after 10 years.
    It is my understanding that the authors suggest that hcst is a viable therapeutic approach in the types of patients mentioned above (eg. Aggressive ms). I wonder: is it possible that this notion “harms” people with milder forms of the disease, that end up being prescribed DMTs that lower the chance of getting relapses, but don’t work as well on the smouldering component of ms?
    Wouldn’t hsct be even more effective if used in less aggressive ms?
    I hope my question is clear, thanks in advance.

    • The general view seems to be that the risk-return trade off is not as favorable for less aggressive forms (there is some evidence HSCT works better when there is radiologically visible activity tho). I disagree with the risk-return tradeoff but what can we do…

  • Now that the J and J vaccine is approved in the US, is it logical to try to get one of the mRNA vaccines so as to have double the chances of generating a response if on Ocrevus? A recent ACTRIMS study showed only 17% of Ocrevus patients generated antibodies after getting Covid. Is a vaccine likely to be as poor?

  • In general, is the reasonable escalation path from anti-cd20 just alemtuzumab or HSCT or is cladribine also worth looking into?

      • I am giving it a failing grade because while it does something for flulike symptoms (so probably controls inflammation) it does not seem to do much to prevent ever so small deterioration from accruing. Something EDSS frankly will not catch for a long time…

  • One hears a lot about leg weakness in pwMS, but How common is mainly just core weakness in MS? I have trunk weakness. I am mobile, however, my weak core severely limits the amount of time I can comfortably stand, sit, or drive. What interventions have been shown to help strengthen a very weak pwMS’s core? Standard PT with floor exercises and bands didn’t strengthen but aggravated my hip flexors, back, and core.

    • Perhaps the physio advice you’ve been given isn’t specific enough. I didn’t respond particularly well to the exercises given me in the hospital’s physio clinic. It was only when I had a course of one-to-one with a neuro physio that advice was sufficiently tailored. It turned out that it was several areas of weakness that were contributing to the problem with the core, so it had to be tackled via strengthening a number of muscle groups – the hip flexors being the hardest in the body to get at.. The core improved when I combined these very precise physio exercises with her general exercise recommendations. That translated as very regular swimming and Pilates.

      • That’s so great to hear Kay! Thank you for sharing. It will keep me looking for a solution. Finding an expert to help me appears to be the challenge.

  • Re: astra Zeneca and J and J vaccine. Both if these hsve had transverse myelitis as a rare adverse event. I understand the physiology of myelitis post vaccine is not ms, but likely similar to a TM post viral infection. However, if one has had TM, does it not make sense to avoid these vaccines? Is there not a vulnerability in the blood brain barrier that makes you at higher risk for TM?

  • https://www.abstractsonline.com/pp8/#!/9245/presentation/144
    What do you think will/should be the lessons taken from this?
    Raising the current levels of tolerated chronic lymphopenia?
    Standard testing of CD8+ (and CD4+) T lymphophenia in cases of chronic ALC?
    More frequent JCV-testing? Or broader: more vigilance towards all kind of infections?
    Or should we wait for other cases before ‘the need for vigilant lymphocyte monitoring’ is translated into concrete guidelines?

  • Do you know what happens to serum IgG and IgM levels after the first and second (and also 3rd and 4th if known) course of cladribine?

  • Re EB virus, I have PPMS, assuming EB +ve, never had or been aware of having glandular fever but have soreness in neck/throat for some years, sometimes feels like there’s something that gets stuck( like one tissue rubbing over another) often. Could this be related to EB and is it worth treating?
    Anyone experienced similar feeling in neck or anyone seen/heard of similar in patients?
    Had an ultrasound of neck and all ok

  • Where on your blog can I find the most up-to-date information about covid vaccines and dmts and the timing etc?

      • Or rather change their plans. Given that their ms vaccine is less likely to work than EBV they could change their minds eventually ?

        • The theory is that the mRNA MS vaccine should work as a treatment as well as a vaccine (not entirely convinced by that argument, but they seem to believe it), and MS treatments are quite profitable. I’d be surprised if they can make anything like as much out of an EBV vaccine, even if it did prevent MS.

          • EBV in this case is most likely more profitable since their vaccine is likely to fail. Many have tried and failed in the past. ” The antigen is not the same in everyone and that same antigen can change from one year to another within that same individual. ” These were the word of Dr Mark Freedman. If we look at a CMV vaccine it is estimated to have a peek annual sales of a minimum of 2 billion dollars all the way up to 5 billion per year. Therefore an EBV vaccine could also be within that price range so their is a profit to be made in making an EBV vaccine.

          • The unit cost of manufacture will be low and uses the same technology as used for the COVID vaccines

    • Because of the cost. Atara biotherapeutics is a smaller company compared to others so they ( for now ) have a smaller budget. However, they could eventually enroll people with rrms.

    • Because they want to fail?. I have no idea what Atara is doing. There was a presentation at ACTRISM 2021, I have seen this before because this is where there is a spot in the market this is where companies go….in a few year you will never hear of them again. Maybe it will work. The original trials had a logic I am yet to be convinced allogenic cells are the answer

  • Ever considered having a forum on this site? you have a well informed group on PwMS who would benefit from advice / liaison with one another. Admin i suppose would be problematic and the team has enough to do with their day jobs i am sure but if you could find a trustworthy volunteer :-).

    • Thanks I will have a look Martí et al. Mitochondrial arginase-2 is a cell‑autonomous regulator of CD8+ T cell function and antitumor efficacy. JCI Insight. 2019 Nov 21;4(24):e132975……..J Immunol. 2010 Mar 1;184(5):2572-82. doi: 10.4049/jimmunol.0902436. Arginase II restricts host defense by attenuating inducible nitric oxide synthase translation in macrophages

      • I know you can’t give specific advice, but would it be relatively safe to receive rituximab for itp after 2 doses of alemtuzumab for ms 9 & 10 years ago? Am failing other itp treatments.
        And also, could the rituximab potentially give some form of ms protection despite it being a lower dosing regime?

        • If your immune system has recovered then there is a blank slate for other treatments, using ocrelizumab has been performed. If you believe me as opposed to other people rituximab. ofatumumab, cladribine and alemtuzumab all target the cells involved in MS, so rituximab should not be different

          • Many thanks for reply. I believe you & I also appreciate this blog for giving us a place to ask these questions. Thanks again.

  • Epstein-Barr virus (EBV) has long been implicated in multiple sclerosis (MS), though its mechanism of contribution remains unknown. Age-associated B cells (ABCs) are known to expand and persist following viral infection and are increased in MS patients. We hypothesize that EBV infection expands the number of ABCs and skews the population towards a Th1 inflammatory phenotype, leading them to function pathogenically in MS. To explore how the EBV-primed ABC population contributes to MS we have utilized the in vivo models of EBV, gammaherpesvirus 68 (gHV68), and MS, and MOG35–55 experimental autoimmune encephalomyelitis (EAE). We observe that ABCs display distinct phenotypes during gHV68 infection and EAE: ABCs secrete anti-viral IFNg during gHV68 infection and IL10 during EAE. Intriguingly, latent gHV68 infection prior to EAE results in a heterogeneous ABC phenotype, with IL10 and IFNg-secreting subsets. As IFNg is pathogenic during EAE and MS, and IL10 is protective, the gHV68-EAE ABCs display a more pathogenic phenotype compared to EAE alone, corresponding to the enhanced clinical course during gHV68-EAE. Knocking out ABCs results in an amelioration of disease in gHV68-EAE, but not EAE alone, further substantiating that gHV68 infection drives ABCs towards pathogenicity. In MS patients we observe an increased number and altered inflammatory phenotype of circulating ABCs compared to age and sex-matched healthy controls. These findings indicate that gHV68 and EBV prime ABCs to contribute pathogenically during EAE and MS and suggest that ABCs may be a therapeutic target.

    Latent gammaherpesvirus infection licenses age-associated B cells for pathogenicity during EAE and MS

    https://www.jimmunol.org/content/204/1_Supplement/58.10

    • I think we have commented on the work in the past. The work you cite is an abstract from a meeting, once the data is published we may comment on it. It is a route to try and explain MS, however as mouse B cell biology appears different to huumans it may one explanation but may or may not be the right one

  • At the current rate of things how long do you expect it will take until a phase 3 trial of an antiretroviral in MS will take place ? ( Since their is a small antiretroviral in MS happening this year )

  • https://multiplesclerosisnewstoday.com/news-posts/2021/03/04/actrims2021-benign-versus-aggressive-multiple-sclerosis-ms-the-hunt-for-clues/

    “Conversely, other research showed that developing no new brain or spinal cord lesions over three years from MS onset was associated with an overall risk of developing secondary progressive MS of 0.9% versus 53.1% in the event of a new lesion.”

    If no new lesions were achieved with help of DMTs, would the odds ratio be the same? Is the damage the factor here or is it the disease activity the factor here?

      • Thank you MD, I take if no lesions were achieved with help of DMTs, odds of converting SPMS is much closer to 0.9% than 53.1% if damage and lesions are the factors.

  • What is the outlook of a 30 year-old female who just been diagnosed (very average disease activities for a pwMS at onset with spinal cord lesions), started on Ocrelizumab, in 30 years?

    • Young good sign, female good sign, spinal cord lesions less good than optic neuritis, start on high efficacy is good in 30 years better than starting on low efficacy treatment. Where in 30 years no idea…if you went thirty years back from today it is 1990 and not very effecitive treatments, thirty back from that no treatments and much more bleak. Thirty years forward it is bound to be better….who knows maybe no new MS

  • Is there ongoing research on the cost/benefit of DMTs for RRMS-patients in general? (analogous to, e.g., https://journals.sagepub.com/doi/abs/10.1177/1352458518765656)
    I know early treatment is often considered important, but for some patients, the side-effects of DMTs could outweigh the benefits. Arguably, pharma will not be interested in this type of research, but is there academic or non-profit funded research on the determinants of so-called ‘benign’ MS? Or is current research mostly focused on ever stronger DMTs?

  • Is orientation examined by assessing place (city) and time (day, date, month, and year), as part of a VNE fit for purpose?
    I don’t know if it is, as I have good cognition but the days seems to roll into one, especially during lockdown or when busy working. I know of a few HCP’s that get the day of the week and date wrong, due to being so busy.

  • See that Cognito Therapeutics have announced positive phase 2 results for their first digital therapeutic to improve memory, cognition, functional abilities and reduce brain atrophy in Alzheimer’s.
    Be interesting to know if it does well in Phase 3 + whether it can be utilised more widely – including of course in MS.

  • Can you help me understand something re lesions and damage done? I am away that there any many unknowns driving Ms and there i have read about smouldering ms on this blog, but in theory if pwMS has a high lesion load on brain and spine, and relatively low disability/ history of clinical relapses, does this mean that they have been ‘lucky’ ? And if they get on high efficacy drugs, and can prevent further damage accruing through new lesions or aggravation of old lesions, then should their disability remain unchanged? Or is it more likely that these lesions smoulder and further disability will accrue? I suppose what I am wondering is if the extent of the damage felt at the time the lesions accrues likely to be the extent of the damage IF the disease can be got under control?

  • I came across the following BMJ article, from 2017. Its interesting about
    ‘Words that annoy, phrases that grate’.
    https://blogs.bmj.com/bmj/2017/04/07/tessa-richards-words-that-annoy-phrases-that-grate/

    I remember a general neurologist informed me I was suffering from/with MS, after diagnosis. But for me I would say, suffering is too strong a word. The suffering is transient, once I have adjusted to the new me again.

    Another term:
    “Consenting the patient”— the article highlights, ‘Let’s change informed consent to informed request’. It’s an improvement. But also it could be…consent received from the patient? Something a patient gives.

    What do you think? thanks.

  • Cancer risks – is there any DNA tests available for the public that we could do and assess our cancer risks? I know BRCA 1 and 2 for breast cancer. Anything else that is comprehensive and legit?

  • Just reading about chronic fatigue syndrome and how it affects 2.5 million people in US. Strangely, it sounds very similar to MS. Is this another form of MS? More precisely, progressive form? Why does the pathology of both sound identical. Has their been any research to link the new together?

    • I think ‘syndrome’ is what you call something if you don’t know the cause.
      Fatigue can be caused by so many things – including, we seem to be learning now, viruses. I had a viral infection that caused excruciating fatigue for over a year. But it was before covid, and at that time, doctors decided that was not possible;).

    • Probably due to a virus that affects the mitochondri. Hence the fatigue. Don’t hold your breath for a answer.

    • * At the start of the survey if you click on an area other than England it tells you the survey covers England only, shame they couldn’t have mentioned this in the title.

  • Is it possible for an infection to trigger the onset of SPMS, or to ‘accelerate’ MS-symptoms?
    I’m not talking about relapses, but of general worsening (walking, stifness, tingling, fatigue,…). I had an infection 2 years ago that hit me really hard (couldn’t walk, slept constantly, muscle pains, difficult breathing even when resting,…). I’m ‘recovered’, but my general symptoms are so much worse now, and I wonder if the infection ‘speeded things up’.
    Any reference to research would be greatly appreciated!

  • I had an MRI of the spine without contrast fluid, showing a number of new (‘vague’) lesions. According to the neurologist, since there are no colorations on the images, they are probably no active lesions (hence there’s no need to restart medication). I am quite confused by this, since I was under the impression that the way to differentiate between active and non-active lesions on MRI was based on the use of contrast fluid. Or am I being to simplistic here?

  • Suplements work

    Published in the journal Clinical and Translational Medicine, the results of this study show that older humans taking GlyNAC for 24 weeks saw improvements in many characteristic defects of aging, including glutathione deficiency, oxidative stress, mitochondrial dysfunction, inflammation, insulin resistance, endothelial dysfunction, body fat, genomic toxicity, muscle strength, gait speed, exercise capacity and cognitive function. The benefits declined after stopping supplementation for 12 weeks

    GlyNAC improves multiple defects in aging to boost strength and cognition in older humans

    https://medicalxpress.com/news/2021-03-glynac-multiple-defects-aging-boost.html

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