Choline on the Brain? A Guide to Choline in Chronic Fatigue Syndrome
http://phoenixrising.me/research-2/the-brain-in-chronic-fatigue-syndrome-mecfs/choline-on-the-brain-a-guide-to-choline-in-chronic-fatigue-syndrome-by-cort-johnson-aug-2005
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"Exercise Tests Suggest Autoimmunity..." Cort Johnson

Discussion in 'Latest ME/CFS Research' started by Diwi9, Aug 16, 2017.

  1. gregh286

    gregh286 Senior Member

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    But there are medicines that address these....alpha blockers..etc..?
     
  2. Gingergrrl

    Gingergrrl Senior Member

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    Yes, definitely there are many medications for POTS. The two that work best for me are Atenolol & Midodrine (but I was already taking these before learning I had so many autoantibodies).
     
  3. Jesse2233

    Jesse2233 Senior Member

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    Prof @Jonathan Edwards thanks this is encouraging. Do you know of any literature reviews off hand speaking to this increased treatability of autoimmune conditions?
     
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  4. gregh286

    gregh286 Senior Member

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    Good article.https://www.ncbi.nlm.nih.gov/pubmed/28553225
     
  5. Jonathan Edwards

    Jonathan Edwards "Gibberish"

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    There does not seem to be any reason to think that the antibodies to adrenergic or cholinergic receptors actually cause symptoms in ME. Normal people frequently have just as high levels. The slight statistical increase reported in ME is not the sort of difference seen in the autoimmune diseases where antibodies clearly cause symptoms. I do not think anybody should be thinking of treatment based on the presence of these antibodies. In the rituximab study the presence of antibodies did not predict response. The fall in antibodies correlated with response but that does not indicate they are causal.
     
  6. Jonathan Edwards

    Jonathan Edwards "Gibberish"

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    Literature reviews these days are almost always political propaganda pieces. The development of effective treatments for autoimmunity is just a basic fact of medicine over the last twenty years or more that every medical student is aware of so nobody is particularly likely to want to write a review about it I suspect.
     
  7. Kati

    Kati Patient in training

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    How about Cochrane reviews? :D:whistle::nerd:
     
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  8. Gingergrrl

    Gingergrrl Senior Member

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    I am confused why these results are dismissed as unimportant? I understand that they cannot prove or indicate that the autoantibodies are "causal" but if the responders had the autoantibodies AND after treatment, saw the autoantibodies drop, then it seems to me, that this would mean something! Because in order for the autoantibodies to drop (in the responders), it means that they had to be present in the first place.

     
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  9. A.B.

    A.B. Senior Member

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    Blood contains a variety of antibodies already. B cell depletion will lower levels of all antibodies.
     
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  10. Gingergrrl

    Gingergrrl Senior Member

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    But isn't this the mechanism of how Rituximab works (in autoimmunity, not chemo) so the drop in these specific autoantibodies (anti adrenergic and cholinergic) could be significant since these specific autoantibodies were found to drop in the responders (but not in the non-responders) if I am understanding correctly? I think the research article said that the responders had positive ANA titers, these auto-antibodies, and Hashi's autoantibodies (vs. other ones). I'd have to check the article again but it seemed significant to me.
     
  11. Cheesus

    Cheesus Senior Member

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    It sounds to me like it may just be the drug was effective in killing off antibodies in the body generally. So it may tell us that antibodies in some people respond to the intervention, but not which antibodies specifically are clinically significant.
     
  12. Gingergrrl

    Gingergrrl Senior Member

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    @Cheesus... I did not recognize you with your new avatar!!! Okay, back on topic...

    Maybe I am totally confused but I thought the study said that "x" number of people had the autoantibodies and the presence of them did not predict who would be a responder. Then ALL of those people got Rituximab but only the ones in which the autoantibodies decreased were the responders. Meaning there is some connection between the two factors (even it is not "causal" of the person's symptoms or illness). I don't think I am explaining it well but it seems that if ALL people have autoantibodies in their blood AND Rituximab merely decreases autoantibodies, then ALL who get Ritux would be responders, yet this is not the case so there must be another explanation?
     
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  13. bertiedog

    bertiedog Senior Member

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    I had Autonomic testing done at Breakspear about 4 years ago. It showed that after stressing my system with 6 deep breaths over 1 minute I had less than 50per cent of oxygen in my cells than a healthy person & in addition I had raised CO2.

    Dr M stressed this was very bad for me and I should start using an oxygen concentrator for uo to 1 hour 3 times daily. So after hiring one & getting big benefits I bought my own from EBay. Very inexpensive but efficient. I use around 5 litres a minute & only now need 30 minutes max more like 20 minutes on a normal day.

    Looks like I fit the 2nd category of this research because there was nothing wrong with the way my lungs worked . I also experience POTS but this is helped by low dose Propananol usually twice daily.


    Pam
     
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  14. A.B.

    A.B. Senior Member

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    I don't remember any details from that article.

    That antibodies didn't drop in nonresponders could just mean that B cells were not being killed. It tells us that elimination of some antibody makes the difference between response and nonresponse, but not what antibody it is.
     
    Last edited: Sep 25, 2017
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  15. Cheesus

    Cheesus Senior Member

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    @Gingergrrl I feel a bit like I have a new face. I'm not sure I like it.

    I don't know the details of the article. But the way I understood it is the same as A.B.: it just shows that those people for whom Rituximab kills antibodies will have a clinical improvement.

    You could have been monitoring any antibodies in the responders, and you would have seen a drop. The fact that they were monitoring those specific antibodies doesn't make them clinically significant.
     
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  16. ljimbo423

    ljimbo423 Senior Member

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    I wonder if the antibodies that are being lowered in the Rituximab responders are antibodies produced from the antigen(s) Mark Davis spoke about in the Symposium. He said this in regards to the cd8 t cell cloning in cfs-

    Jim
     
  17. Jonathan Edwards

    Jonathan Edwards "Gibberish"

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    It is certainly confusing. You probably have to be an expert on plasma cell dynamics (like me) to have any feel for what it means. If these autoantibodies cause symptoms then you would expect more of them in ME than normal. They seemed to be a bit more common in ME but not much to be honest. You would also expect people with antibodies to be more likely to respond to rituximab but that did not seem to be the case.

    The fact that of those with antibodies those whose antibodies fell more were more likely to respond could fit with the antibodies causing the symptoms but it might simply reflect the fact that these people have rather short lived plasma cells and some other antibodies that were not measured also fell. So there is no clear evidence that the autoantibodies on the tests are relevant ones.

    There is a further problem that this finding was not one that would be most likely predicted. That means that it was a chance finding after doing several analyses of the results. And as soon as you start analysing results lots of ways you are bound to find some correlations by chance.

    I might add that the fall was pretty variable within responders and non-responders. There was a statistical relation but it did not look like a close correlation. When we have looked at antibodies in other diseases correlations tended to be pretty consistent, even if there were some exceptions.

    It is very hard to give a precise explanation why but from looking at the data I did not feel confident that it made a convincing case for these antibodies having a direct role in symptoms. So I think measuring them at present is not going to provide any useful information about whether to be treated or not.
     
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  18. Gingergrrl

    Gingergrrl Senior Member

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    I have read and highlighted the article twice and I still find it confusing!

    I guess I had assumed that B cells were killed (and went down to zero like mine) by the Rituximab in all subjects in the study, but maybe this was an incorrect assumption on my part? I do agree that they could only report on the autoantibodies that they measured and that the responders could in fact have other autoantibodies go down that were not measured.

    I am in this group b/c I have an autoantibody that attacks the calcium channel and anti GAD65 (and probably others that just have not been measured) so it is hard to say which autoantibodies being reduced are causing my improvements. I have also done IVIG prior to, and in addition to, the Rituximab so it is hard to determine causality in my case.

    I'm not sure if I like it either! :D Maybe it is a face that has to grow on you LOL.

    That makes sense but I still find it interesting that these specific autoantibodies dropped in the responders (vs. the non responders).

    I feel relieved that it is confusing to you, b/c then I don't feel so bad that it is confusing to me!

    I think that very few ME patients (and people with autoimmune disease/autoantibodies in general) have been tested for these specific autoantibodies so the sample size would be very small.

    My gut instinct is that I disagree, based on reading that article and on conversations with my doctor, and I feel that these autoantibodies do play a role but I lack the background to be able to back this up with anything significant :(.
     
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  19. A.B.

    A.B. Senior Member

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    These antibodies are known or have been proposed to play a role in POTS, complex regional pain syndrome (CRPS) and CFS, and serious adverse reactions to HPV vaccination.

    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5209415/

    These are G-protein-coupled receptors. Australian researchers presented some data in August during the OMF conference that suggested a very strong genetic predisposition for ME/CFS in individuals with mutations in genes corresponding to G-protein coupled receptors. Maybe these mutations are required for autoimmunity, or maybe ME/CFS can be split into a genetic subtype and one autoimmune subtype.

    Anyway it's getting late and I'm rambling. We will hopefully figure all this out in the next few years.
     
    Last edited: Sep 25, 2017
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  20. Jesse2233

    Jesse2233 Senior Member

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    @Jonathan Edwards is it possible that the presence of these autoantibodies indicate a subgroup of an autoimmune subset (perhaps one more suspectible to POTS) and that the Rituximab responses (with varied autoantibody levels) represent the autoimmune subset (and diffrrent subgroups within)?
     
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