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Open The Influence of Epigenetic Modifications and Post-Exertional Malaise in People With Myalgic Encephalomyelitis/Chronic Fatigue Syndrome 2021 Polli

Discussion in 'Recruitment into current ME/CFS research studies' started by John Mac, Mar 4, 2021.

  1. John Mac

    John Mac Senior Member (Voting Rights)

    Not yet recruiting

  2. alktipping

    alktipping Senior Member (Voting Rights)

    really aerobic exercise i guess the groups will only have the most mildly effected . otherwise hasn't this already been done by workwell . and more of this sick people need behavioural intervention crap .
    Peter Trewhitt likes this.
  3. Hutan

    Hutan Moderator Staff Member

    Aotearoa New Zealand
    I think the aerobic exercise is just being used as a challenge, to see what happens when people with ME/CFS do physical activity.

    Just looking at BDNF, it seems that the protein might have a role in our symptoms, and that exercise should increase the expression of the gene. So, at first glance, it seems like a reasonable idea to see what exercise does to the expression of the gene in people with ME/CFS.

    (just edited to not have three versions of 'looking' in one sentence)
    Last edited: Mar 5, 2021
    sebaaa, Mij, Andy and 5 others like this.
  4. Effi

    Effi Established Member (Voting Rights)

    [Note: haven't posted in a long time, am cognitively not doing well, hope my writings make sense! will probably be unable to comment further, hope that's ok]

    This is a research group I would label as BPS or at least BPS light. They are part of a chronic pain research consortium: http://www.paininmotion.be/ Just reading the titles of their latest blogs on the homepage should give everyone an idea of where their head is at (Polli is on the members page http://www.paininmotion.be/about-us/members).

    The tricky thing about this group is that their CFS research tends to look biomed (because technically it is!), but their solutions to the problem have so far always been BPS (i.e. your body is giving out "false alarm signals" that can be fixed through pain neuroscience education, basically the same premise as the "false illness beliefs" trope).

    I suppose this research builds upon their own findings of elevated sBDNF in a 2020 study of CFS patients with comorbid FM. The problem I see, is that in Belgium many or most FM patients end up with a CFS diagnosis at some point, following complaints of "fatigue" on top of the FM pain, i.e. it's wildly overdiagnosed. (Not saying ME/CFS+FM doesn't occur, just that it seems like almost every single FM patient here will get a CFS diagnosis at some point, even though many of them clearly don't meet any of the newer/stricter ME/CFS criteria.)

    I wonder if elevated BDNF is linked to chronic pain specifically. According to past comments of this research team, they generally seem to consider both FM and CFS as "fatigue and pain", with FM being more pain related and CFS more fatigue related. They refuse to acknowledge that widespread pain is not one of the most debilitating complaints in 99% of PWME. The studies they do tend to be physically impossible to carry out for patients with moderate ME, let alone severe ME. Therefore, I can't see how their samples would generally not be skewed towards FM, with or without actual ME/CFS. The Pain in Motion website lists their CFS and FM research under one and the same heading, which shows that their FM and CFS research is very much intertwined. An example of this from the same group: Central sensitization: a biopsychosocial explanation for chronic widespread pain in patients with fibromyalgia and chronic fatigue syndrome

    Leonard Jason's group also carried out a BDNF study on ME specifically, in 2014. They checked BDNF in ME patients, MS patients and healthy controls, and found BDNF to be DECREASED in ME patients. The ME sample was small (n=15), but I am infinitely more confident in Jason's very thorough knowledge of correct usage and possible pitfalls of ME(CFS) criteria, so I would expect this to be a small but accurately diagnosed sample.

    I could be mistaken, but it seems like the Polli group first took a sample of CFS patients with comorbid chronic FM pain, in order to show elevated BDNF in CFS (see 2020 study linked above). Now in this current study, they technically skip FM altogether, but as most FM patients have a CFS diagnosis here anyway, that shouldn't necessarily exclude them, as FM isn't listed as an exclusionary illness. That the diagnosis will be made by an "MD experienced in the field of internal medicine and ME/CFS" does not necessarily inspire confidence, as internal medicine MDs have been actively involved in the worst BPS groups for CFS from the very start here. Not saying they will definitely be a BPS minded MD, but seen as this whole group is BPS light at best, there is every chance for this to be a BPS minded MD in internal medicine and we all know the pitfalls of the different criteria, when they are used by someone who doesn't understand the illness, or worse, someone with an agenda. (I know the CCC criteria require PEM, but in the minds of some people, all that means is "more fatigue after exertion".)

    Just wanted to add this info to the conversation. I'm not saying this will definitely be a bad study, but I am not confident that this project will lead us to more useful knowledge, let alone solutions. My hunch is that they are hoping to establish BDNF (or COMT, or HDAC) as a biomarker for biopsychosocial "central sensitisation", which would then give them a biomed rationale for psychosocial/behavioral interventions.
  5. Hutan

    Hutan Moderator Staff Member

    Aotearoa New Zealand
    Thanks for those great insights, Effi, thanks for making the effort.

    I found that Sorenson, Jason 2014 study yesterday with its finding of decreased BDNF, which, as you say, is at odds with the finding of elevated BDNF by this group.

    I found some papers suggesting BDNF is lowered in people with depression:
    So it all seemed quite unclear and, as you say, quite open to possibilities of poorly selected participants, all round. And possibly quite easily confounded by activity levels - because if exercise increases BDNF then it would not be surprising if people with ME/CFS or depression (both probably typically more sedentary than healthy people) had lower levels.

    And then the other two genes the team is looking at did seem to have scope for BPS interpretations. So I too was left feeling uneasy. I meant to post further, but then, you know, ran out of energy.
    Effi, alktipping, Trish and 1 other person like this.

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