More GET Drivel from Australia

By David Tuller, DrPH

Some Australian members of the GET/CBT ideological brigades have published yet more nonsense and drivel about “graded exercise therapy” as a treatment for ME/CFS, or what they are still calling “chronic fatigue syndrome.” The article, simply called “Chronic fatigue syndrome: graded exercise therapy,” is in a peer-reviewed journal from a reputable publisher yet is full of unsupported and questionable claims. It references the PACE trial without discussing the developments that have undermined the trial’s credibility, including published re-analyses that refute the core findings. In fact, it reads as if the authors are unaware that the entire debate has been transformed in recent years–which isn’t surprising, because it is basically a reprise of material created in 2015 by the Royal Australian College of General Practitioners.

The lead author, Professor Paul Glasziou of Bond University, is a general practitioner and director of the university’s Institute for Evidence-Based Medicine. He was also the senior author of a published protocol for a Cochrane “individual patient data” review of exercise therapy for so-called “chronic fatigue syndrome.” That protocol was withdrawn once Cochrane declined to publish the full individual patient data review, which was known to have received scathing reviews from those outside the usual orbit. (This review was not the regular Cochrane exercise review that used aggregated published data from the included studies rather than the raw individual unpublished data from the included studies. A revision of that regular review is expected to be published soon.)

Patient and advocacy groups in Australia have for years criticized the RACGP for its continued advocacy of the GET/CBT paradigm. For unknown reasons, a SAGE journal called InnovAiT: Education and Inspiration for General Practice, has now decided this dated RACGP guidance deserves wider exposure. I assume the article passed some sort of peer review, but perhaps it was reviewed by like-minded colleagues of the authors.

The very first sentence is problematic: “Graded exercise therapy (GET) aims to increase a patient’s ability to undertake physical activity by preventing/reversing the physical deconditioning and exercise intolerance related to prolonged (relative) inactivity.” It is of course true that prolonged inactivity can lead to deconditioning. But there is no legitimate or valid evidence that patients with the illness in question are experiencing their devastating symptoms because of deconditioning. This theory has been promoted for decades by the biopsychosocialists and provides the rationale for GET, but it has not been borne out by research.

There is also no proof that the so-called “exercise intolerance” experienced by patients is reversible through GET. Professor Andrew Lloyd, an infectious disease doc at University of Sydney and the country’s self-styled “leading light” for the illness, is a proponent of the “central sensitization” hypothesis—the unproven notion that a brain glitch is leading to a kind of over-interpretation or exaggeration of routine fatigue signals. That appears to be Professor Lloyd’s current rationale for his insistence that treating the illness requires gradually increased exposure to the stimulus in question—in this case, activity. That approach might work for arachnophobia but there is no reason to assume it is appropriate in this context. Professor Lloyd’s claims to the contrary are based on the same kinds of squishy arguments made by the PACE authors.

The InnovAiT article continues in this vein. In presenting what it claims to be the US Centers for Disease Control’s definition of the illness, it cites the elements of the retired Fukuda definition—including the notion that “fatigue” is the core symptom. It is not a secret that the agency now uses the case definition proposed in 2015 by a report from the Institute of Medicine (now the National Academy of Medicine), which frames “exertion intolerance”—and not fatigue per se—as the characteristic symptom. It is unclear why Professor Glasziou and his colleagues chose not to update such critical information as the case definition used by the lead US public health agency. This sort of obvious misstatement of current reality has no place in the medical literature.

The paper includes other problematic statements, such as this: “Patients are encouraged to see symptoms as temporary and reversible, as a result of the current physical weakness.” This advice is exactly wrong and based on flawed research. That’s why the CDC and Kaiser Permanente, for example, have switched course.

And while the article does mention that surveys of patients have found harms from GET, it rationalizes away these reported harms by asserting that “this finding is believed to be due to inappropriately planned or progressed exercise programmes.” This suggestion—that reported harms in surveys are likely be due to poor implementation of GET rather than GET itself—has become something like accepted wisdom among GET proponents. In fact, this idee fixe is not supported by the evidence, as patient and researcher Tom Kindlon noted in a tweet. Just because the claim “is believed” to be true by the article authors and like-minded pro-GET colleagues does not make it so.

Here’s part of a post about this article from Emerge Australia, an organization based in Melbourne: “Exercise as an answer to ME/CFS is rooted in the outdated idea that patients are somehow ‘deconditioned’ (i.e. have lost muscle tone) through an erroneous or psychiatric belief that they are unwell and that patients can be restored to pre-illness condition simply through exercising. This goes completely against all of the huge progress that has recently been made – including in Australia – identifying biological differences between patients with the condition and healthy controls. Perpetuating the idea that patients have ‘false illness beliefs’ or that ‘the answer is exercise’ increases the stigma surrounding the condition, leads to patients being dismissed by doctors and continues the likelihood that more patients might be harmed by exercise programmes. It also has a direct negative impact on funding decisions that seek to investigate the biomedical basis of ME/CFS.”

The article has also been the subject of a lively discussion on the Science For ME Forum: https://www.s4me.info/threads/“graded-exercise-therapy-chronic-fatigue-syndrome”-by-the-handi-working-group-2019.10469/


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7 responses to “More GET Drivel from Australia”

  1. Gijs Avatar
    Gijs

    I ended up in a wheelchair after GET. I was motivated and still the therapists don’t understand it. Even when they see it with their own eyes theri still blind. These psychiatrists are obsessed by their ideology just like Freud was with hysteria.

  2. Alicia Butcher Ehrhardt Avatar
    Alicia Butcher Ehrhardt

    Prescribing exercise for ME is cheap – national health systems in Australia and the UK love the idea; then, if it doesn’t work, you can blame the victim! A two-fer!

    Follow the money.

  3. Couch Turnip Avatar
    Couch Turnip

    I’m not for one minute suggesting that ME patients are suffering from deconditioning but, if mind and body are truly interconnected/inseparable, shouldn’t it be possible for deconditioned people to think themselves to a muscle-conditioned state? Couch, couch and even more couch, rather than ‘Couch to 5K’?

  4. jimells Avatar
    jimells

    “It is not a secret that the agency [CDC] now uses the case definition proposed in 2015 by a report from the Institute of Medicine”

    Are you sure it’s not a secret? How many US physicians have heard the news, a few percent? When it comes to ME, CDC act like they have no idea how to do public awareness campaigns, in spite of all the TV ads to promote vaccines, which prominently feature the letters “CDC”.

  5. ginger gay bartlett Avatar
    ginger gay bartlett

    prof . Lloyds ‘glitch in the brain/sensitisation ‘ theory holds water for me personally but his treatment method for it is flawed. Having found strong symptom relief from avoiding ‘over stimulation’ of the peripheral nervous system which exercise aggravates when I move my muscles: and instead targeting the root cause of the brain glitch and getting more optimal nerve muscle function through dietary manipulations. I found that a diet rich in Glutamate was triggering the glitches in my brain causing CNS /vegus nerve>muscle dysfunction within the body. Over excitation of the nerve fibres was showing up as spasms and pain & circulation problems . L’glutamate is found naturally in diet with grains, legume, dairy , meat and potatoes is converted into a neurotransmitter essential for nerve conduction. L’glutamate is also added to the food supply through food processing and taste enhancement treatments . But when the glial cells in the body, that are responsible for regulating and uptaking the circulating useable l’glutamate/ glutamine have been impaired from some event such as head trauma, vaccination inflammation/other infective states/ psychological trauma or poisoning from nerve agents , they are unable to cope with the high level of excitatory stimulation the CNS is subjected to and the what the chemical turns neurotoxic on itself . The western diet and environment is saturated with high levels of excito-toxic chemicals , so for those of us whose brains have become injured at some time in our life, too much circulating l’glutamate in the body is simply a recipe for CFS/ME/fibromyalgia symptomology. I believe we sufferers have developed a tolerance threshold of nerve stimulation/excitation activity that is both internally and externally derived (mental , food, muscle, movement and other sensorial exposures) . This certainly explains the difference in peoples degrees of functionality /impairment levels at any given time in their life. Is all subject to their own individually preset ‘ tolerance threshold’ . That when it hits it peak, we then encounter a ‘glitch ‘ in the brain and the cycle repeats its self. By limiting the level of circulating L’gluatame in the body by way of dietary restriction, it allows the glial cells to perform properly which translate into no pain, no muscle fatigue and no more digestive disorders . So until people get the brain glitch sorted out , GET is nothing more than one more nerve irritant.

  6. Steve Hawkins Avatar
    Steve Hawkins

    It seems to me that *a* ‘central sensitisation’ effect may indeed be in play, because so many systems are involved, and many are vagally linked, both visceral and peripheral. But to any sufferer, it is plainly obvious that the biopsychosocial cliques have turned this idea on its head in blaming the reduced ability to exercise that it creates, instead of looking for the cause of the sensitisation.

    I put away some shopping two months ago, and I have not been able to turn, stand, or even just lighten the weight on my spine as in pushing down on a stick to get up, without my back and ribs responding instantly by going into excruciating spasm that often causes me to cry out. Despite this, I still try to get up and do as much as I can before the pain forces me back to bed. This gets less and less each day: not more.

    I’m sure that most patients could tell a similar story: but as the CBT/GET cult will never believe anything that patients tell them, unless it is in the form of their own self serving and simplistic questionnaires, they are conditioned never to see the real evidence that is right before their eyes.

  7. Andrew Avatar
    Andrew

    Here is the evidence base on the effect of GET on fitness, and as you can see, it is quite equivocal.

    Wallman et al. 2004 (peak oxygen consumption during submaximal exercise test, performance at a predefined target heart rate)
    Baseline – post intervention (figures are mean, 95% CI)
    15.6 (13.3–17.7) – 17.1 (14.9–19.2) ml/kg/min
    This seems like an improvement, but the two tailed P=0.32 (n=32).

    Moss Morris et al. 2005. VO2Peak
    Baseline – after 12 week intervention period (figures are mean, SD)
    31.99 (19.94) – 27.21 (5.53) ml/kg/min
    P value = who cares, performance was lower after treatment than before.

    Fulcher, White 1998 VO2Peak
    Baseline – After 12 weeks of treatment (figures are median, IQR)
    31.8 (26.8­-36.8) – 35.8 (30.8­-40.7) ml/kg/min
    Note, there were dropouts so looking at medians can be misleading. Since the figures were not reported as mean/sd or mean/CI, the P value can’t be directly calculated (assumptions need to be made)

    Wearden et al. 1998 VO2peak
    Figures were reported as mean change, not mean/sd at baseline and followup, so it is hard to verify, but the result at 26 weeks was stated as mean change=1.9 (95% CI 0.15-3.69) P=0.03, but authors note: “Most subjects reached subjective exhaustion before they had reached their predicted maximum heart rate and before a plateau in oxygen consumption had been reached; consequently no extrapolation to theoretical maximum oxygen uptake was attempted.” Hence the exercise test was limited by motivation, rather than fitness limits.

    PACE trial, Chalder et al. 2015
    No difference on step test.

    FINE (pragmatic rehabilitation) trial, Wearden and Emsley 2013
    No difference on step test

    ——-
    I can’t see how the above evidence can be in any way conclusive about GET improving physical fitness.