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Never Ask Us if We're Hungry -- The Answer's Always No
There are three of us here and for many years, none of us ever got hungry. When our brains would turn to mush, when our faces would go numb, and we would start the invisible vibration which is the signature dance of ME/CFS, we knew we needed to eat.
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Lipkin finds biomarkers not bugs

Discussion in 'Phoenix Rising Articles' started by Firestormm, Sep 12, 2013.

  1. snowathlete

    snowathlete

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    Is it not possible to use these techniques to look at other parts of the blood? peripheral blood mononuclear cells (PBMC) including lymphocytes, and erythrocytes which dont contain a nucleous?
  2. alex3619

    alex3619 Senior Member

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    I predict that serology will show less EBV than the general population. I suspect, based on numerous anecdotal accounts, that we lose seroconversion. So we can lose seroconversion to EBV. That means we lost the memory of how to fight EBV ... those antibodies are no longer made in quantity.

    In any case nearly all adults should show some serological evidence of prior EBV infection. In part that is why so many doctors have dismissed claims of EBV in CFS and ME before. Its a case of "So what? Everyone has EBV!". For patients with frequent EBV reactivation I think there should be a longtitudinal study ... give blood every month or so for a year. This might show a pattern of reactivation.

    One thing I think does happen is that when patients get the symptoms again, they presume its viral reactivation. I am not convinced it always is, just as I am not convinced most claims of Herxheimer reactions are really Herxheimer reactions. The symptoms are due to immunological changes, and they can have other causes. There is no substitute for confirming viral reactivation in a patient with a viral titre assay.

    We still have no good way to thoroughly assess latent infections however.
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  3. alex3619

    alex3619 Senior Member

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    Yes, its possible. I do not know to what extent these techniques have been developed and tested though.

    Whole blood assays are certainly done for some pathogens.
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  4. August59

    August59 Daughters High School Graduation

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    Montoya does not do his own testing for HHV-6 because he does not have "something" that will let him find it with any consistency. All of his is sent out to a lab in Minnesota (I think), but he has stated that extremely hard to find because most of its time is spent in brain tissue. Montoya has also (and Lerner too) that very high levels of EBV antibodies, especially if the Early Antigen, Viral Capsid Antigen and Nuclear Antigen in the IgG form are all present well beyond normal lab values is indicative of re-activation. After the initial exposure to EBV, when you typically see IgM antibodies will never be produced again and that only IgG antibodies are produced during re-activation.

    It is odd that they found a lot of retroviruses and they do terrible under a thaw and re-freeze environment.

    Have the deep sequencing protocols been used yet. I missed part of the call, but I don't think it was the fecal study, but Dr. Lipkin seemed very positive on another test that they haven't done yet. I thought it had something to do with the gut, but from what I have been reading that is not part of the study? He could get samples from Dr. Chia and Dr. KDM as they both have taken some "gut" samples, but I imagine they were scrapings as I'm not sure if taking a "gut" biopsy is high on anybody's list.

    Here is a link about the study that associated Leptin with fatigue severity in CFS.
    http://www.ncbi.nlm.nih.gov/pubmed/23570606
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  5. Firestormm

    Firestormm Senior Member

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    If you missed aspects of the phone broadcast, you can read our full transcript from Lipkin: here (which is an attachment to our article at the head of this thread) :)
  6. Simon

    Simon

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    Thanks. That suggests that EBV is unlikely to be found in this study until they have done the serology work - and no results were given from this in Lipkin's talk.
    The retroviral sequences were reported as part of Montoya's samples. We don't know if these had been through freeze/thaw samples or not but they will be much more recent than Dan Peterson's spinal fluid samples. Also, Ian Lipkin knows a thing or two about finding retroviruses and I'm assuming that he would be well aware of the problem.

    I'm actully not sure what the difference is between deep sequencing and high-thoughput - the latter was used in the Montoya samples:
    However, near the end of the call, when he is discussing the new CFI cohort (recruited via Nacny Klimas et al) he says:
    Which to me sounds very much like what they did with Montoya's samples, so I'm a little bit confused. I did think that high-throughput and deep-sequencing involved essentially the same approach.
  7. August59

    August59 Daughters High School Graduation

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    Hopefully all this will make more sense when the final study is done and published. I'm sure we only got bits and pieces the other day.
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  8. alex3619

    alex3619 Senior Member

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    Yes, there is no substitute for the published paper.
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  9. August59

    August59 Daughters High School Graduation

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    I know Dr. Lipkin mentioned that they were going to make house calls on some of the most severe cases of ME/CFS. He didn't happen to mention how many and if they were going to be looking for specific pathogens or cytokine malfunctions or were they going in with open eyes and look for every possible thing they can find?
    Simon likes this.
  10. cigana

    cigana Senior Member

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    If they were chosen properly they should have had negative Borrelia blood tests already as an exclusion diagnosis. Perhaps those that get labelled "true CFS" are those that don't have borrelia or antibodies in their blood. LLMD's often say the sickest are the ones who often test negative. It would be interesting to do an antibiotic challenge.
  11. Forbin

    Forbin Forbin

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    Just some thoughts on the apparent distinction between the cytokine levels of patients who have been ill less than three years and those who have been ill longer:

    If some shift if going on in this time frame, might it be related to the long standing observation that those who “recover” from ME/CFS are most likely to do so within the first five years?

    I’m thinking that it might be helpful to investigate the cytokine profiles of those who have “recovered” within the first five years as well. As I recall, this is not an insignificant percentage of patients. Other than Dr. David Bell’s long term evaluation of the actual health of “recovered” patients however*, I don’t think that this group has been studied much. The feeling may be, “Why study 'healthy' people?”

    My guess (and it’s only a guess) would be that the recovered patients would not have perfectly normal cytokine profiles either, but their profiles might also not be the same as the profiles of either the pre- or post-shift groups.

    I’m just saying that studying the profiles of the seemingly ignored “recovered” group might add another data point and give some further insight into what is going on.

    Ideally, with the new knowledge of this shift, I’d think that you would now want to follow a group of “under three year” patients so you could compare their pre- and post-shift profiles, get data from closer to when that shift happens, and also get the profiles of any of those that “recover.”


    [*They were not as well as they thought they were.]
  12. lansbergen

    lansbergen Senior Member

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    I agree
  13. aimossy

    aimossy Senior Member

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    I may have missed a post.
    but would anyone take a wild guess at how long it will be before lipkin publishes?
    miss impatient I know!
    lol
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  14. Firestormm

    Firestormm Senior Member

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    Before the end of the year? Only a guess, I mean, hell, we are still waiting for the Norwegians to publish what they announced back in May, and which has been embargoed ever since then 'pending publication'. Drives you round the bend, doesn't it? :mad: :D
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  15. aimossy

    aimossy Senior Member

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    haha ABSOLUTELY. thanks for the guess!
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  16. Firestormm

    Firestormm Senior Member

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    Morning :)

    Mark was contacted by someone who noted others wanting to donate to Lipkin's work specifically and who were wondering how to do it. This was the email Mark received explaining how it can be done:

    The link has also been added to the article.
    Last edited: Oct 28, 2013
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  17. Firestormm

    Firestormm Senior Member

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  18. Bob

    Bob

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    This is not directly ME related, but there was another story re gut bacteria in the news yesterday.

    A strain of Lactobacillus brevis (KB290) has been found to give an immune boost to mice against a flu virus.
    "The researchers noticed that the bacteria enhanced the production of not just flu-related antibodies but also the immune system molecules IFN-α."
    Interesting that it boosts IFN-α (Interferon alpha.)
    I haven't read the research paper yet, so I don't know how effective it's supposed to be, or what sort of immune boost it gives.
    They haven't tested it in humans yet.

    Scientists Prove That Special Japanese Pickle Prevents Flu Infection
    http://www.scienceworldreport.com/a...anese-pickle-prevents-flu-infection-study.htm

    Preventing flu: Scientists find bacteria in Japanese pickled turnips which could boost immune system
    http://www.independent.co.uk/life-s...-which-could-boost-immune-system-8924768.html

    Japanese Turnip Pickle has Flu-Preventing Bacteria
    http://www.natureworldnews.com/arti...panese-turnip-pickle-bacteria-prevent-flu.htm
    Last edited: Nov 6, 2013
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  19. Bob

    Bob

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  20. Simon

    Simon

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    RE @Firestormm: Science Article: Nov 4, 2013 Gut Bacteria May Cause Rheumatoid Arthritis

    The mysterious microbial world within us is beginning to reveal its secrets

    New research linking gut bacteria to Rheumatoid Arthritis throws more light on the complex relationship between illness and the gut, which may yet prove key to solving ME/CFS. As this thread's blog said:
    Our gut bacteria, aka the 'microbiome', 'microbiota' or 'microflora' are becoming ever more important in our understanding of comlex long-term conditons:
    The new study reported in the prestigous new open access journal eLife shows a strong link between just one bacteria and Rheumatoid Arthritis (RA): 75% of new cases of RA had Prevotella Copri bateria compared with just 21% of healthy controls. New cases are important as they are unmedicated, and drugs themselves could affect the bacterial composition of the gut.

    And while the sample size was small (44 newly-diagnosed RA vs 28 healthy controls), the 21% rate of P. Copri seen in healthy controls is similar to that seen in larger population studies of bacteria, making it less likely that this is a statistical freak. Nonetheless, replication of these findings is critical.

    Assuming the finding is robust, the question is what is its significance? there are 3 possibilities:
    1. Prevotella Copri plays a causal role in RA, perhaps as a trigger
    2. RA leads to changes in the gut, with the effect that Prevotella Copri increases
    3. There is a third, unknown factor that leads to both RA and higher rates of Prevotella Copri, a relationship known as co-association.
    So P.Copri could be a cause of RA, or just a marker.

    Clearly it can't be the cause of RA because only 75% of RA cases had P. Copri, and 21% of healthy controls had the bacterium too. However, RA is known to be a complex illness with many predisposing features so it could still play a causal role for some people, and that would be hugely significant.

    Presumably this is exactly the sort of thing that Ian Lipkin is looking for in his ME/CFS microbiome study.

    More information
    The Human Microbiome Project was set up in 2008 to kick off systematic study of the human microbiome (note that actually the microbiome covers fungi and protozoa too, not just bacteria).
    Last edited: Nov 7, 2013

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