1. Patients launch $1.27 million crowdfunding campaign for ME/CFS gut microbiome study.
    Check out the website, Facebook and Twitter. Join in donate and spread the word!
9th Invest in ME International ME Conference, 2014 - Part 2: Pathogens and the Gut
Mark Berry continues his series of articles on the 9th Invest in ME International ME Conference in London, with the emphasis shifting from autoimmunity to pathogens and the gut ...
Discuss the article on the Forums.

Dr. Enlander tackles a poor paper "Fear of movement and avoidance behaviour..."

Discussion in 'Latest ME/CFS Research' started by snowathlete, May 31, 2013.

  1. WillowJ

    WillowJ Senior Member

    Messages:
    3,151
    Likes:
    2,854
    WA, USA
    John H Wolfe not all papers are equal. "avoidance behaviour" could mean the researcher notes that a patient is acting disabled, but the researcher doesn't believe the patient actually is disabled (see the comments on this thread for an evaluation of another such study).

    this it the age-old fallacy of: we haven't run the right tests or the right tests don't yet exist, so it must be entirely or partially a personal/behavioural problem of the patient. This has happened to MS, RA, and a host of other diseases, and it is far past time to be disavowed entirely.

    Most non-BPS practitioners use CBT to help people learn to cope with their disease and maybe teach pacing skills. Do you have a link of what you are talking about regarding Rowe? Rowe, incidentally, at the FDA conference mentioned the dismal results of the PACE Trial, which was among other things a trial of CBT based on the 'fear-avoidance model of illness'.

    I am not aware of any cases where avoidance behaviour could possibly be preventing anyone from reducing PEM/PER/PENE. The only thing we know for certain reduces this is pacing. Other than that, doctors can make recommendations for various things but in the end the patient is always the one who decides to take or not to take any medical treatment.

    And there is no evidence for a strong recommendation for any particular treatment.

    There is some risk of harm from any treatment or therapy or supplement or anything that we might try, and it risks coercion to try to convince people to try a certain thing when they have expressed a disinclination to that.

    Kina, yes, if you were thinking to spin off some of these posts to a new thread, that sounds fine to me.

    @thread The thing about people who improve with this or that treatment is that we generally don't have large-scale studies which prove it's from the treatment in question.
     
    Valentijn likes this.
  2. John H Wolfe

    John H Wolfe Senior Member

    Messages:
    220
    Likes:
    37
    London
    Indeed not

    Until the pathology is better understood it seems unhelpful not to attempt to find out what the optimal panel of tests might be, and to further develop existing ones, by extension

    Clearly such an assertion that does not follow, however nor does the assertion that elements of our illness cannot have anything to do with personal attitudes and associated patterns of behaviour (e.g. in relation to mode, frequency, level, and longevity of activity vs. rest)

    Yes, here are some links for your perusal, along with a brief, excerpt based, chain of relations that help explain the implication of his working hypothesis re: inactivity:

    vi) Nerve Hypersensitivity: Professor Peter C. Rowe et al. (2013a:I, 2013a:II, 2013b) highlight diminished neurodynamics, proposing that nerve tissue tension and associated neuromuscular strain may give rise to central sensitisation (CS) via peripheral nerve tissue stress signaling: Neural Hyper-Sensitivity Syndrome (NHSS), increasing as per the following:​
    • “Relatively brief period of inactivity following surgery or during an acute illness”
      • “Exhausted ability to compensate for soft tissue and neurodynamic restrictions”
        • “Increased noxious afferent input from the irritable peripheral nerves”
          • “Further central sensitisation”
            • “Heightened sensitivity of peripheral nerves to further loading”
    He seems like 'one of the good guys' to me too - there is no agenda here (so far as I can see) other than helping his patients better tolerate the parts of his protocols involving physical rehabilitation

    This is just the way it should be. Rowe's angle offers important insights, and the prospects of the design and bespoke implementation of supportive tools that aid just about any strategy, including pacing (with or without a graduated element)

    It does when studies like the one in the OP translate into 'must push patients harder (regardless of opposition/reported harms)' attitudes, I concurr

    Indeed, cause for further investigation, but perhaps not cause for outright rejection of the possibility that they could well be more broadly beneficial..
     
  3. John H Wolfe

    John H Wolfe Senior Member

    Messages:
    220
    Likes:
    37
    London
    Ah yes, thanks. I'm familiar with this article and did find it interesting I must say, indeed I popped a bit in my article on it:

    "Meirleir et al. (2013) note the increasingly widely held belief that immune responses to HERVs lead to autoimmunity through molecular mimicry; they find that, compared with controls, certain immune cells are uniquely immunoreactive to antibodies to HERVsin 2/3 of those PWME assayed"

    In conjunction with "inflammation", in this article De Meirleir mentions:

    Alterations in the gut e.g. GI immunity~ may be linked to disorder arising in relation to (vertebral/joint) structural/positional abnormalities and (associated) nerve tensioning (irritation), pinching (irritation/ischemia), hypovolemia/hypotension (ischemia/irritation). I cover/hint at some of these linkages in the discussion in my hypothesis article

    He suggests HERV protein expression in pDCs may lead to (a core) pathological link but that their expression may merely be the result of inflammation associated with the disease (and the genetic/epigenetic elements involved in the emergence of the disease state post 'onset'), or perhaps a combination of both

    In the context of my research and the relative scale of the problem of ME/CFS in the post-modern era my sense is that the later is the most likely; for me there is room for genetic predisposing factors (possibly including autoimmunity, or at least the potential for it) but there is no room for an absence of epigenetic factors, which affect central mechanisms and hence cannot conceivably not impact on autoimmune processes

    If I have missed other mentions of sources of inflammation please do let me know
     
  4. user9876

    user9876 Senior Member

    Messages:
    796
    Likes:
    1,963
    I think it is not a case of running the right tests but that a researcher making an observation that someone is not active and then infering their intent from that. Science should be about recording observations and fiting them to a hypothesis rather than letting the hypothesis influence the recording system. It is also very hard to measure peoples intentional state as asking questions can be very suggestive (depending on the questions, the order of the questions etc.)
     
    WillowJ and Valentijn like this.
  5. Richie

    Richie

    Messages:
    46
    Likes:
    29
    I agree with a lot of what you say. but I think while we are dependent on criteria based diagnosis, those who have fitted the criteria and then become asymptomatic have a good claim to say that they have recovered. Of course they may be in remission, their underlying pathology may have been quite different from that of other sufferers etc, but with criteria based diagnosis appropriate symptoms = illness, symptoms gone = better, which gives rise to all the claims that this or that therapy is the cure for ME/CFS.
    As you suggest we need proper science...
    Hope you had agood rest.
     
  6. Richie

    Richie

    Messages:
    46
    Likes:
    29
    Valentijn
    If sb is highly symptomatic, undergoes a certain therapy and no longer complains of symptoms over the long term I am inclined to believe them, just as I believe symptomatic people are ill. Post or prompter hoc is a fair question, but I think doubting recovery stories in principle is wrong. The pertinent question imo is what was the underlying biology (or even psychology) in the first place.

    The last keystone is pretty hard (impossible???) to achieve if we don't know what is being recovered from. Rational and scientific are of course not synonyms. It has recently been "proven" by science that sage assists memory. It was entirely rational for herbalists to recommend sage in certain circumstances prior to this scientific validation, but it was not waht would be called "science based medicine".

    Again, if we don't know what conditions are being referred to under the term ME or CFS, we can't have a single rationale. What e.g. Gupta talks about may have no relevance whatever to x% of the patient pop'n but be relevant to y%, with these groups confounded by the use of symptomatic diagnosis. They have not been validated by trial but I would return tot he example of sage. Anecdote is not data but neither is it valueless. As you say

    You may be right here. There is evidence from sports science that mental attitude does affect performance, and this must be physiologically mediated but the fact that mind can affect body has no specific implications for ME/CFS or lupus or MS or Sjogren's or whatever. No sports team throws out all the doctors, physios and podiatrists in favour of shrinks. I take your point. Problem again is how many people with a diagnosis have these protein problems.

    Re. scientific validity, I think it is quite common for helpful therapies to attract definitive theories re. their mode of working and the condiitions themselves. The intervention may be helpful but the theory wrong or overblown. E.g. guaifenesin, which, I at least believe, has helped some people for FM. I can believe that without beleiving the theory of phosphate excretion esp as guai has now been found to affect the immune system and the pop'n may be heterogenous and responding to guai for a variety of reasons
     
    MeSci likes this.
  7. Firestormm

    Firestormm Guest

    Messages:
    5,824
    Likes:
    5,982
    Cornwall England
    You too are right I think in what you have said here Richie. Where we are now - with the science and understanding - at a personal level - who cares how someone feels they have recovered and are no longer meeting the diagnostic criteria for ME. I don't. Just appreciate people who relate their tales in such a way that doesn't purport they alone have the answer. Also that 'experts' who are selling something are upfront about the evidence for their claims. And then there's the whole pandora's box in how such folk liaise with the media. A little more care to evidence and to what and how they say things - wouldn't go amiss either :)
     
    WillowJ likes this.
  8. alex3619

    alex3619 Senior Member

    Messages:
    7,726
    Likes:
    12,655
    Logan, Queensland, Australia
    John H Wolfe

    Yesterday it occured to me that the autoimmune issues we see in ME might be from just a deranged methylation cycle or oxidative stress. Both deplete glutathione. Without glutathione antibodies might not fold properly (its needed for sulfide bridges) and so might have altered reactivity. In other words the antibodies might be for something else but because they are misfolded (something seen in ME) then they have altered specificity. This is also consistent with Maes' research. We have such a large range of autoantibodies that regular immunological explanations fail.
     
    John H Wolfe likes this.
  9. MeSci

    MeSci ME/CFS since 1995; activity level 6

    Messages:
    3,882
    Likes:
    4,644
    Cornwall, UK
    I have a problem with the idea of rehabilitation for a physical illness without first treating the illness. When I have come across people on a UK ME forum saying they have been referred for rehabilitation, it has always turned out to be CBT/GET.

    If you have cancer, you may have rehabilitation after the actual cancer has been treated, to get you back to fitness.

    If you have broken or sprained a limb, you will have physiotherapy - a type of rehabilitation - after the specific damage has been addressed (sometimes during the recovery process).

    If you have had heart surgery, you may have physio/rehabilitation afterwards.

    But rehabilitation on its own is not treatment, at least not in my understanding of the word.

    As others have said, as one's body starts to function better, one can feel that it is possible to do more, and one therefore does more. That is exactly what I am experiencing as a result of my low-carb/gluten-free/supplement regime. Fat has fallen off, muscle is building up, and as a consequence I am using those muscles again - a delightful and unfamiliar feeling. If I had just tried exercise to get rid of the fat and get the muscles working, it would just have worsened the ME. I know - I have worsened it before through unavoidable exertion.

    I recall an occasion in hospital when the health professionals tried to get me to walk again prematurely after I had had an operation on my foot. I KNEW that it was premature, and told them so. The skin felt very tight where the stitches were - it felt as though it would come open if I put any weight on the foot. The staff insisted. The wound came open almost immediately, and became infected, leading to worse scarring, more time in hospital and prolonged incapacity.

    When you have lived in a body all your life, you tend to know it better than anyone else!
     
    Dolphin, WillowJ, ahimsa and 8 others like this.
  10. Richie

    Richie

    Messages:
    46
    Likes:
    29


    Agreed
     
  11. John H Wolfe

    John H Wolfe Senior Member

    Messages:
    220
    Likes:
    37
    London
    Interesting, thanks for sharing; if that is indeed the case then idiosyncratic autoimmunity may indeed relate to epigenetic factors (as per Dr. Van De Kirk's breakdown)

    "Alex (2013) notes the role of glutathione in (di)sulfide ‘bridging’ or ‘bonding’. Its absence effects protein structure (misfolding has been identified in ME/CFS), stability and biological function. Hence there is the potential for altered specificity of antibody proteins e.g. epigenetic autoimmunity (as malformation turns antibodies into autoantibodies)"

    I'm not (yet) aware of the extent to which Van De Kirk explored the relation with PENE (in his menu of things that "stress the body out"), but, for me, direct inflammatory responses associated with neural sensitivity (and indirect ones associated with neurogenic sensitisation*) remain on the table as one such source of systemic stress

    This is why I believe PWME have little choice but ascend a precarious tightrope between illness and wellness (avoiding falling off along the way on either the overdoing it or underdoing it sides) and must be careful to set this 'tightrope' at an appropriate degree of tension or we may run into trouble/never reach our destination (as the thing has no 'give' if it's too tight, or sags in the middle if too loose)

    This is the basis upon which I welcome all studies into PENE: triggers, impacts (yes, including psychological so long as they are approached/presented responsibly and relevant to disease processes/management), mitigation, pathophysiology, and hopefully also amelioration/alleviation going forward (as the pathology is better understood)
     
  12. John H Wolfe

    John H Wolfe Senior Member

    Messages:
    220
    Likes:
    37
    London
    Me too or, rather, 'beginning to treat the illness, and ensuring conditions are right for recovery'*

    This has become increasingly the norm over the past few decades as health practitioners have realised that leaving people in bed on hospital wards and putting rehab off until tomorrow is detrimental to the health of these patients. Of course a careful balance must be struck (at the individual level), as your own example demonstrates only too clearly!

    I've seen some of the reasons for this trend mentioned in a number of realms but perhaps of most significance for PWME in the realms of neurogenic sensitisation (most of us already have issues with hypersensitivity), circulatory abnormalities e.g. cardiomyopathy/hypovolemia (most of us have OI), and suboptimal respiration (many of us already have issues with hypoxia/hypocapnia)

    Indeed not

    So that my position is better understood, let's call that phase 1

    I advocate introduction of supportive nerve mobilisation therapy (may be pursued independently, or, ideally, with reference to a suitably qualified/informed physical therapist) at phase 2, where a PWME is at the point where other elements of a suitably well designed/implemented personal protocol have been pursued, and they have had sufficient time to recover relative stability, such that they have energy available to dedicate to non-essential activities

    This is where CBT may be thought of as a useful tool and where any 'fears', however rational, may need to be addressed e.g. by explaining the purportedly insidious role of (inactivity linked) neurogenic sensitisation, in order to legitimise the energy investment and perseverance in the face of likely (albeit hopefully minimised) adverse neurogenic effects

    Phase 3 would be the stage at which nerve glide, and tolerance thereof, is demonstrably improved to the extent that physical rehabilitation (as most would understand it e.g. doing more than simply stretches/PT) is well tolerated (back to baseline energy/functionality by the following day and no PENE) and may be pursued

    Fantastic :)

    First and foremost we try to read the signals our bodies send us, a point I make explicitly in my protocol. However, it is perhaps unwise to assume that we necessarily interpret every signal 100% correctly or indeed that the body itself isn't confused/simply fed up e.g. by the disorder, and possibly inauspicious activity and suboptimal rest on top

    That's awful, sorry to hear that
     
  13. MeSci

    MeSci ME/CFS since 1995; activity level 6

    Messages:
    3,882
    Likes:
    4,644
    Cornwall, UK
    I would never suggest that we interpret every signal 100% correctly. But innumerable experiences with health professionals where my interpretation has been correct and theirs wrong have led to my trusting my own interpretation more than theirs. I have not regretted it. It's just very unfortunate that they have dismissed my interpretations (and of course never admit to their errors later). It has been costly to me in terms of health, time and money, and also to the taxpayer, due to the need for repeated consultations and even a repeat emergency hospital admission on the way home from a prior one the same day, after the emergency doctor dismissed my suggestion of hyponatraemia. Guess what it was...and near-life-threatening too.

    It is not just me. It is widespread.
     
  14. SOC

    SOC Senior Member

    Messages:
    5,369
    Likes:
    6,489
    USA
    Additionally, research should not involve the researcher's belief as part of the design. This is a critical fundamental failure of all BPS research I've seen -- it's based on the researchers' belief that the patients are not truly ill. The researchers are not required (I don't know why) to prove that belief through extensive testing (immune function, exercise testing, appropriate pathogen testing, etc, etc). At best, their research should contain clear and complete statements of that basic, and critical, assumption: This research assumes a priori that the patient participants have no physical illness. Testing was not done to verify this assumption.
     
    Dolphin, WillowJ, snowathlete and 5 others like this.
  15. MeSci

    MeSci ME/CFS since 1995; activity level 6

    Messages:
    3,882
    Likes:
    4,644
    Cornwall, UK
    Perhaps the psychos were not taught the scientific method. The version that was taught to me when I started as an undergrad struck me and some fellow-students as rather odd, being that one formulated a hypothesis and then tried to disprove it.

    Here is another explanation of the scientific method:

    http://teacher.nsrl.rochester.edu/phy_labs/appendixe/appendixe.html

    SOC is correct in that assumptions should be reported in published papers.
     
  16. John H Wolfe

    John H Wolfe Senior Member

    Messages:
    220
    Likes:
    37
    London
    Well that makes sense, and I'm sure we're not alone in being somewhat pessimistic about the 'expertise' we receive from conventional, run of the mill, health professionals

    To be fair, however, ours is a tricky/enigmatic illness so it would be perhaps a little unreasonable for us to expect them necessarily to come at it from the right angle from the get-go, although it would be nice if more was done ('top-down') to ensure we hit the ground running with our GPs

    I suppose this is where these sorts of studies may be viewed as being most potentially harmful - where they serve as to highlight one select aspect, of one select part of the disease picture (of varying significance in the population of PWME at large), and hence detrimentally colour/skew the views of certain health professionals

    I've attended a session with medicine students designed to put them in contact with, and hence better understand, the reality of living with neurological disorders. It's encouraging to see the medical establishment taking such steps to bridge certain gaps which invariably lead to the kind of gulf between prescription and practical reality that you describe; it's also encouraging to see young doctors-in-waiting taking such an interest and being willing to listen and learn from us

    It's one thing to make a serious error, quite another to ignore the considered concerns of a patient, and quite another still to then demonstrate a lack of humility when your decisions cause that same patient harm. Such is the world we live in

    Nice to see some accountability starting to creep in, in the wake of these recent scandals at the top (NHS) mind :)

    I wonder what your treatment protocol for hyponatraemia is like?

    I've never had this investigated but I do have POTS and do supplement with salt now, throughout the day (and have contemplated it at night - to aid nocturnal water retention vs. disruptive diuresis)
     
  17. MeSci

    MeSci ME/CFS since 1995; activity level 6

    Messages:
    3,882
    Likes:
    4,644
    Cornwall, UK
    My experiences have by no means all involved ME. I am really trying to use examples to illustrate a general point about patients often having a better understanding of their own bodies than do health professionals, and my experience has included consultants, one being regarded as a 'top man' in his field.

    or of no significance at all. Having participated in ME forums for some time, my clear picture is of a patient group less likely than any other I can think of to be underactive, and more likely than any other I can think of to be OVERactive.

    To avoid the thread wandering off-topic, I will give you a link to a page where I have detailed this:

    http://forums.phoenixrising.me/index.php?threads/has-anyone-seen-dr-kogelnik.6148/page-5#post-345626
     
    ahimsa, WillowJ, alex3619 and 2 others like this.
  18. John H Wolfe

    John H Wolfe Senior Member

    Messages:
    220
    Likes:
    37
    London
    You may well be right; of course it is important to address this (as well), when a swift/smooth recovery is the objective

    Thanks :)
     
  19. WillowJ

    WillowJ Senior Member

    Messages:
    3,151
    Likes:
    2,854
    WA, USA
    I agree with you that what you said may be a large contributor to the problem. Insufficient testing (and possibly lack of knowledge to even understand the relevant tests; this was certainly alleged in 1996 in UK re: the Royal Colleges report) seems to be another important contributor.
     
  20. Dolphin

    Dolphin Senior Member

    Messages:
    6,872
    Likes:
    6,169

See more popular forum discussions.

Share This Page