Saturday, February 28, 2015

Psychiatrists commenting on immunological abnormalities, typical science media Center crap

By Utting Wolff:

  "The Science Media Centre surpassed itself in its coverage of the Columbia University study[6]. Of seven experts chosen to respond to the study, not one gives a positive analysis, no medical adviser from an ME charity or, non-psychosomatic promoting, ME researcher is quoted.

  The featured experts are: Professors Michael Sharpe and Peter White, and Dr Esther Crawley, all notorious proponents of the psychogenic ME model.

  Professor Stephen Lawrie, head of The Division of Psychiatry at the University of Edinburgh: ‘This is a small study’ he states[6]; a study encompassing 20 participants is small professor Lawrie, one involving over 600 participants is not[1]. One has to ask why is a psychiatrist being consulted?"

Thursday, February 26, 2015

IOM: ME/CFS "is a medical—not a psychiatric or psychological—illness"

@ PubMed:


Beyond Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: Redefining an Illness.


Committee on the Diagnostic Criteria for Myalgic Encephalomyelitis/Chronic Fatigue Syndrome; Board on the Health of Select Populations; Institute of Medicine.



Myalgic encephalomyelitis (ME) and chronic fatigue syndrome (CFS) are serious, debilitating conditions that affect millions of people in the United States and around the world. ME/CFS can cause significant impairment and disability. Despite substantial efforts by researchers to better understand ME/CFS, there is no known cause or effective treatment. Diagnosing the disease remains a challenge, and patients often struggle with their illness for years before an identification is made. Some health care providers have been skeptical about the serious physiological—rather than psychological—nature of the illness. Once diagnosed, patients often complain of receiving hostility from their health care provider as well as being subjected to treatment strategies that exacerbate their symptoms. 

Beyond Myalgic Encephalomyelitis/Chronic Fatigue Syndrome proposes new diagnostic clinical criteria for ME/CFS and a new term for the illness - systemic exertion intolerance disease(SEID). According to this report, the term myalgic encephalomyelitis does not accurately describe this illness, and the term chronic fatigue syndrome can result in trivialization and stigmatization for patients afflicted with this illness. Beyond Myalgic Encephalomyelitis/Chronic Fatigue Syndrome stresses that SEID is a medical—not a psychiatric or psychological—illness. This report lists the major symptoms of SEID and recommends a diagnostic process. One of the report's most important conclusions is that a thorough history, physical examination, and targeted work-up are necessary and often sufficient for diagnosis. 

The new criteria will allow a large percentage of undiagnosed patients to receive an accurate diagnosis and appropriate care. Beyond Myalgic Encephalomyelitis/Chronic Fatigue Syndrome will be a valuable resource to promote the prompt diagnosis of patients with this complex, multisystem, and often devastating disorder; enhance public understanding; and provide a firm foundation for future improvements in diagnosis and treatment.
Copyright © 2015, National Academy of Sciences.


    Free Books & DocumentsFree full text

    Tuesday, February 24, 2015

    The real reason why Prof Edward Shorter is ridiculing and attacking severely ill patients

    So why did professor Edward Shorter write his 2 very aggressive / hostile / vile articles in psychologytoday, attacking patients who are severely ill?

      Even though he is a psychiatrist and a medical historian, he shows a total lack of knowledge about basic facts about this disease and totally ignores all clinical evidence etc that what he says is total rubbish / nonsense.

      The answer to the question can be found in one of his tweets, ie his new book is out on the 7th of march.

      @DrEdwardShorter: "… The pub date for this is Mar 7 but Amazon up now. Theme: what should have been in but wasn't and shouldn't but was."

      So all he cares about is selling books, earning money and getting his name in the paper, that he has to ridicule and attack severe ill patients to do so, is obviously no problem to him or to psychologytoday.

      And that's the sad state of affairs of psychiatry and psychology in 2015.

      See also Prof Edward Shorter and the psychic epidemic of ignoring clinical evidence


    Monday, February 23, 2015

    Prof Edward Shorter and the psychic epidemic of ignoring clinical evidence

    A phenomenon well familiar to historians of medicine is the psychic epidemic of ignoring clinical evidence by psychiatrists and medical historians, a belief that spreads epidemically, until the evidence become so overwhelming that it becomes clear that these people have been telling porkies for decades, and then their nonsense is forgotten.

      In the 20th century, psychiatry fostered such an epidemic with the belief that ego masturbation caused their bank accounts to inflate. Many medical historians and psychiatrists obsessed for years over the thought that their “self-abuse” had pleased their bank managers.

      Another epidemic focused on the toxic  effects of ignoring clinical evidence on the ovaries. Many male medical historians and male psychiatrists would plead for ovariectomies, on the grounds that their irritated ovaries were blocking clinical evidence which their penis had spotted, to go all the way to their brain. And that this was leading to erectile dysfunction and the inability to have an orgasm.

      Once their ovaries were removed, their penis size increased by more than 5 inches. So all these male medical historians and male psychiatrists were pleading their doctors for ovariectomies.

      In the late 1980s the belief spread epidemically that reading clinical evidence caused irreversible brain damage, and a number of leading medical historians and psychiatrists wrote books full of advice about eating small meals upside down, with your eyes closed and your brain in hibernation mode, to make sure that clinical evidence would not reach your brain to prevent brain damage.

      I realize that these words will fall unreceptively upon some ears, and I regret that some medical historians and psychiatrists, especially from Toronto, may feel slighted by the clinical evidence that is readily available, if only they where willing to turn on their computer and were willing to read biomedical research, for example the fMRI studies from Stanford, or the PET scan study from Japan. 

      Yet there are larger stakes here. In the way that lives were once ruined with such toxic diagnoses as hysteria, which in this day and age is called MS, millions of lives today are ruined by medical historians and pinocchio psychiatrists who have made a fortune out of ignoring clinical evidence.

      Many psychiatrists and medical historians choose their profession so that they didn't have to become productive members of the community.  (The IOM report dwelled upon the dangers of severely ill patients being abused by the medical profession.) 

      Such a waste of human potential is tragic, and if there are lessons that we may draw from the history of medicine, it is that doctors who discover the underlying metabolic problem or cause of such diseases, which medical historians and psychiatrists call psychosomatic, even though they do not have any evidence to back up this claim, will go on to win the Nobel prize for medicine, as the Nobel Prize winner in medicine, Dr Barry Marshall stated a few years ago.

    Friday, February 20, 2015

    Social sciences lecturer Angela Kennedy: Psychogenic explanations for physical illnesses are almost always fatally flawed


    Since the advent of "medicine" as a discrete practice, beliefs that bodily illness can somehow be caused by psychological, emotional, and behavioural "disorder" have been claimed by many in the discipline. Such beliefs became less creditable as scientific methods of detecting disease developed, with discoveries such as the physiological and anatomical abnormalities in Parkinson's disease and Multiple Sclerosis, for example, and the organisms causing syphilis and duodenal ulcers.

      Nevertheless, psychogenic explanations for illnesses still appear frequently within medical and academic literature, in "common sense" public discourses, and in medical diagnoses of patients. But how plausible are these explanations? Authors of our Own Misfortune? proposes that psychogenic explanations for physical illnesses are subject to a complex mix of confusing concepts, accompanied by certain moralistic and ideological assumptions about people and their illnesses.

      Most crucially, such explanations are also, almost always, fatally flawed, both scientifically and logically.

      Furthermore, the widespread, uncritical acceptance and use of such explanations has had serious and specific adverse effects on the people upon whom they are used.

      This is a timely, groundbreaking book about a critical theme in medicine. It provides rigorous analysis of the claims made about "mental disorder" and bodily illness, using current "medical controversies" (such as, but not limited to, Myalgic Encephalomyelitis and Chronic Fatigue Syndrome) to demonstrate the problems with and adverse effects of such claims. Authors of our Own Misfortune? is essential reading for academics, health professionals, and those directly or indirectly affected by psychogenic explanations for illness.

      Angela Kennedy is a social sciences lecturer and researcher at a number of universities in London, and author of numerous articles, papers and books in lay, professional and academic media over a 30 year career.

      Her academic research interests include: the social stratification, scapegoating and social exclusion of disadvantaged groups, and the effects of these; constructions of moral panics; and the sociology of science and medicine, including manifestations of the 'science wars'.

    Monday, February 16, 2015

    The denial of this illness by doctors means that patients are suffering slow, horrific deaths

    By Kristy Muir, 13th February 2015 :

      "The 37-year-old Bribie Island woman is in the fight of her life against a debilitating disease and consequential infections.

      In February 2013 Amara was diagnosed with Lyme disease (borrelia), bartonella, babesia and multiple other infections.

      Prior to that she suffered chronic fatigue syndrome, diagnosed when she was 23. Amara's condition means she suffers severe seizures daily, as well as photophobia (sensitivity to light), severe cramps and muscle spasms."


      ""Amara is desperately unwell with late (stage) neurological Lyme disease," Ms Collingwood said.

      "What makes her illness different is that the medical profession do not recognise Lyme disease in Australia, despite the fact that thousands of Australians have tested positive to Lyme (via testing facilities in overseas labs) and the numbers are only continuing to increase.

      "The denial of this illness in Australia by the health fraternity means that there is very little to no treatment available here.

      "People are suffering slow, horrific deaths and it is completely unnecessary.""

    Saturday, February 14, 2015

    The Guardian: ME/CFS, a serious disease dismissed as laziness says The Institute of Medicine

    The Guardian, 13 February 2015:

      "People often dismiss sufferers of chronic fatigue syndrome as lazy because the seriousness of the disease is not understood."


    • "“Having called this serious disease by an inappropriate and frankly insulting name is one of the factors that kept doctors, friends, family members, even employers from affording it the seriousness it deserves,” she said."

    Friday, February 13, 2015

    The causative role of alum adjuvant in vaccines in slow brain translocation and delayed neurotoxicity in ME/CFS

    Front. Neurol., 05 February 2015; FULL article @
    REVIEW ARTICLE Biopersistence and brain translocation of aluminum adjuvants of vaccinesimageRomain Kroum Gherardi* , imageHousam Eidi, imageGuillemette Crépeaux, imageFrançois Jerome Authier  and imageJosette Cadusseau * Faculté de Médecine and Faculté des Sciences et Technologie, INSERM U955 Team 10, Université Paris Est-Créteil, Créteil, France Aluminum oxyhydroxide (alum) is a crystalline compound widely used as an immunological adjuvant of vaccines. Concerns linked to the use of alum particles emerged following recognition of their causative role in the so-called macrophagic myofasciitis (MMF) lesion detected in patients with myalgic encephalomyelitis/chronic fatigue/syndrome. MMF revealed an unexpectedly long-lasting biopersistence of alum within immune cells in presumably susceptible individuals, stressing the previous fundamental misconception of its biodisposition. We previously showed that poorly biodegradable aluminum-coated particles injected into muscle are promptly phagocytosed in muscle and the draining lymph nodes, and can disseminate within phagocytic cells throughout the body and slowly accumulate in brain. This strongly suggests that long-term adjuvant biopersistence within phagocytic cells is a prerequisite for slow brain translocation and delayed neurotoxicity. The understanding of basic mechanisms of particle biopersistence and brain translocation represents a major health challenge, since it could help to define susceptibility factors to develop chronic neurotoxic damage. Biopersistence of alum may be linked to its lysosome-destabilizing effect, which is likely due to direct crystal-induced rupture of phagolysosomal membranes. Macrophages that continuously perceive foreign particles in their cytosol will likely reiterate, with variable interindividual efficiency, a dedicated form of autophagy (xenophagy) until they dispose of alien materials. Successful compartmentalization of particles within double membrane autophagosomes and subsequent fusion with repaired and re-acidified lysosomes will expose alum to lysosomal acidic pH, the sole factor that can solubilize alum particles. Brain translocation of alum particles is linked to a Trojan horse mechanism previously described for infectious particles (HIV, HCV), that obeys to CCL2, signaling the major inflammatory monocyte chemoattractant. Billions of humans have been vaccinated and marked regression or eradication of several severe infectious diseases was observed. Nowadays, the potential applications of vaccines extend far beyond prevention of infectious diseases, and vaccination is considered to be a most promising weapon against a variety of different conditions. Vaccine safety has been regarded as excellent at the level of the population (1 ), but adverse effects have also been reported (2 ). Concerns about the use of aluminum adjuvants have emerged following (i) recognition of their role at the origin of the so-called macrophagic myofasciitis (MMF) lesion in 2001 (3 , 4 ), which revealed fundamental misconception of their adjuvant effect and pointed out their unexpectedly long-lasting biopersistence (4 ); and (ii) demonstration of their apparent capacity to migrate in lymphoid organs and then disseminate throughout the body within monocyte-lineage cells and progressively accumulate in the brain (5 ). The present paper will review these emerging characteristics of alum adjuvant particles that raise concerns about innocuity of this widely used compound.

    Tuesday, February 10, 2015

    NO !!

    IOM: psychiatrists beliefs are wrong, ME/CFS is a "serious, complex, multisystem disease"

    By Miriam E. Tucker, February 10, 2015:

    "The illness that has been called "chronic fatigue syndrome" (CFS) in the United States and "myalgic encephalomyelitis" (ME) elsewhere is a "serious, complex, multisystem disease" that physicians need to view as "real" and diagnose, the Institute of Medicine (IOM) says in a new 235-page report."


    The etiology is unknown, but evidence  of biological disease has been mounting for the last several years.


    According to Dr Rowe, "It was a unanimous committee report.... It was interesting for us who are clinicians in the field to see how obvious the direction of the evidence was for those who are scientists, but not specialists in this area." < br >

    "the condition's hallmark defining symptom, postexertional malaise, the report proposes a new name be adopted, "systemic exertion intolerance disease (SEID),"


    "It's time to stop saying that this is a just figment of people's imagination. This is a real disease, with real physical manifestations that need to be identified and cared for," Committee Chair Ellen Wright Clayton, MD, JD, professor of pediatrics and director of the Center for Biomedical Ethics and Society at Vanderbilt University, Nashville, Tennessee, told"Medscape Medical News".


    In particular, the panel found sufficient evidence linking the illness to immune dysfunction, especially diminished natural killer cell function, and infection, particularly Epstein-Barr virus.


    She added, "The level of response is much more than would be seen with deconditioning," with reference to the belief voiced by some clinicians that physical abnormalities in these patients are merely a result of their lack of activity. Indeed, Dr Rowe noted, "That argument is untenable with people who have been physically active, some of them athletes, [before becoming ill]. The deconditioning argument is flawed in that respect."

    Treating ME/CFS with the cancer drug Cyclophosphamide

    Research project

      Cyclophosphamide by myalgic encephalomyelitis / chronic fatigue syndrome (ME / CFS) 

      Scientific title:  Cyclophosphamide BY myalgic encephalomyelitis / chronic fatigue syndrome (ME / CFS)

      Part A, for up to 30 patients with ME / CFS: An open phase II trial with 6 cyclophosphamide infusions 4 weeks apart

      Part B, for up to 20 patients with severe and very severe ME / CFS: An exploratory study with up to 6 cyclophosphamide infusions 4 weeks apart, in collaboration with local health services

      Project description:  The purpose of this study is to investigate whether cyclophosphamide infusions given every four weeks is associated with clinically significant responses and acceptable side effects in ME / CFS patients, and whether such treatment if necessary. Workable in patients with severe and very severe ME / CFS. The primary endpoint will be based on patients' self-report of symptom development.

      The application relates Part A: An open-label phase II study for up to 30 patients with ME / CFS (not mild) with six infusions cyclophosphamide every fourth week, 12 months follow-up. If at least 40% response rate in Part A, then part B: A descriptive study with up to 20 patients with severe and very severe ME / CFS, with the same treatment, but where monitoring and intervention carried out in collaboration with healthcare close patient home.  (Project Manager project) 

      Ref. No .: 2014/1672 EudraCT Number: 2014-004029-41 Project start: 01.01.2015 Project End: 30/06/2017

      Treatment Status: Approved  Research Status: Ongoing  Project: Øystein Fluge  Research Responsible (s): Haukeland University Hospital Initiator: Contributions Research  Financing: Study researcher initiated. There is no external sponsor of the clinical trial. Research Group for ME / CFS Oncology Haukeland University Hospital has support from the Kavli Foundation, essential for research purposes to better understand the pathogenetic mechanisms of ME / CFS. Kavli Fund has granted a 50% nurse position for 12 months., To help with the study. This is thought transferred to clinical research Post by HUS which will then be responsible for implementation and interventions (study Part A) in collaboration with the study management at Oncology, HUS.

      Drug costs are very low (less than 200 NOK per infusion), ie 1200 NOK per patient for the entire treatment, and will be covered over the research group for ME / CFS Oncology their budget. It is drawn own drug insurance for study. There is no financial compensation for study participants. Research Data: Drug Testing, Human biological material Humans  Selection: Patients / clients 

    Saturday, February 7, 2015

    Breaching the do NO harm principal: GET and CBT for ME/CFS



      SIGN NOW please

      Dear NHS England, in view of the current dire state of NHS funding due to Govt cuts, we the UK ME community are happy to accept a total cut of the funding that goes to GET & CBT treatment for ME patients.

      “The whole idea that you can take a disease like this and exercise your way to health is foolishness. It is insane.” Dr Paul Cheyney

      CBT and GET are at best useless and at worst extremely harmful for Myalgic Encephalomyelitis patients. Patients with myalgic encephalomyelitis, particularly children, have suffered gross and barbaric abuse and persistent denigration as a consequence of the beliefs of certain psychiatrists who are attempting to control the national agenda for this complex and severe neuro-immunological disorder.

      These psychiatrists are shown to be clearly in breach of the first tenet of medicine --- first do no harm--- in that by their words and deeds they have wreaked havoc in the lives of M.E.

      The Hummingbird Foundation for ME

      SIGN NOW please


    Thursday, February 5, 2015

    Very sad news, if only the Pinocchio Psychiatrists had done their job as a doctor

    Another 4 ME patients have died because the Pinocchio Psychiatrists have lied their socks off about a debilitating neuroimmune disease for decades. Shameful and disgraceful doctoring

    RIP Brenda Duncan, Gayle M. Marie, Vanessa Li and Daniel Strenge

    PACE trial authors admit in the BMJ, "exercise increases symptoms" in CFS and is therefore HARMFUL

    By Trudie Chalder Professor,
    Kimberley Goldsmith, Peter White, Michael Sharpe, Andrew Pickles King's College London, Department of Psychological Medicine, King's College London, Weston Education Centre, Cutcombe Road, London, SE5 9RJ,

    in the BMJ, 29 January 2015:

    "We found that fear avoidance beliefs mediated both CBT and GET. This does not mean that these beliefs cause the illness.

    We would like to clarify that we did not say that fear avoidance was the cause of CFS [3,4]. We did not state that the illness was psychological or an exercise phobia. Nor did we say that fear of exercise in CFS was “irrational”. Rather, in an illness where exercise increases symptoms, we believe that being cautious about engaging in activity is understandable [4]."

    MY PS:
    Gradually increasing exercise is something people with ME can NOT do, if they can, they are in remission or the diagnosis is WRONG !!! 

    Many ME patients have made been bedridden, including myself, thanks to a severe relapse caused by Graded Exercise Therapy.

    And therefore Exercise therapy contravenes the do NO HARM principle of medicine / the GMC, and doctors who continue to use or promote it should fail their revalidation !!! 

    And the PACE trial authors now basically ADMIT, without using those words, in this rapid response that exercise therapy is HARMFUL !!!

    Tuesday, February 3, 2015

    PACE trial authors admit in the BMJ, fear of exercise in CFS is not irrational

    By Trudie Chalder Professor,
    Kimberley Goldsmith, Peter White, Michael Sharpe, Andrew Pickles King's College London, Department of Psychological Medicine, King's College London, Weston Education Centre, Cutcombe Road, London, SE5 9RJ,

      in the BMJ, 29 January 2015:

      "We found that fear avoidance beliefs mediated both CBT and GET. This does not mean that these beliefs cause the illness.

      We would like to clarify that we did not say that fear avoidance was the cause of CFS [3,4]. We did not state that the illness was psychological or an exercise phobia. Nor did we say that fear of exercise in CFS was “irrational”. Rather, in an illness where exercise increases symptoms, we believe that being cautious about engaging in activity is understandable [4]."

    Monday, February 2, 2015

    Game fixing in and by the PACE trial

    PACE trial's extensive, major, post-trial revisions, without adequate justification would be game fixing in the world of sport ...

      By Alem Matthees, :

      AllTrials supporters may be interested in the multiple major deviations/additions to the PACE Trial protocol, apparently occurring almost exclusively after the authors were already unblinded to the trial data and familiar with the distribution of various outcomes. This latest paper on mediators by Chalder et al. appears to continue this tradition.[1]

    The protocol was published in BioMed Central on the basis that "the authors/investigators are unlikely to be able to make revisions to their protocol". The editor(s) "strongly advise readers to contact the authors or compare with any published results article(s) to ensure that no deviations from the protocol occurred during the study."[2] BioMed Central "believes that publishing study protocols will help to improve the standard of medical research by: [...] enabling readers to compare what was originally intended with what was actually done, thus preventing both 'data dredging' and post-hoc revisions of study aims."[3] It is therefore concerning that the protocol underwent extensive, major, post-trial revisions, without adequate justification. All changes substantially decreased the stringency of the thresholds, made the tested therapies appear much more effective or less harmful than they otherwise would have, and lead to widespread media hype.

    The primary endpoint was completely abandoned after the trial ended. For fatigue this had been either 50% improvement or a Chalder Fatigue Questionnaire (CFQ) bimodal score of ≤3/11 points. For physical function this had been either 50% improvement or a Short-Form-36 physical function (SF-36/PF) score of ≥75/100 points. The "clinically useful difference" for individual participants (≥2/33 points CFQ Likert score and/or ≥8/100 points SF-36/PF) was introduced post-hoc and was significantly less stringent than the "positive outcome"(s) as previously defined.[4][5]

    The recovery criteria (a secondary analysis) underwent extensive, major, post-hoc changes, which made it much less stringent to the point of being highly doubtful whether anyone genuinely recovered.[6] It became possible to be classified as completely "recovered" without clinically significant improvements to either fatigue or physical function. None of these changes, described below, were included in the statistical analysis plan that was finalized shortly before data unblinding.[7]

    1) The previously required CFQ bimodal score of ≤3/11 points was changed to a CFQ Likert score of ≤18/33. The change of scoring method obscures direct comparison, but a Likert score of 18 can be a bimodal score of between 4 to 9, which the protocol regarded as abnormal or excessive fatigue. About 1% of participants simultaneously met both definitions of 'normal fatigue' (CFQ Likert ≤18/33) and 'severe fatigue' (CFQ bimodal ≥6/11) at baseline.[8] Questions have therefore arisen over the method and normative population sample used to calculate this threshold.[9-12]

    2) The previously required SF-36/PF score of ≥85/100 points was lowered to ≥60; worse than trial eligibility criteria for 'significant disability' (≤65).[6] About 13% of participants simultaneously met both definitions of 'normal physical function' (a criterion for complete recovery) and 'significant disability' at baseline.[8] The post-hoc revised threshold was derived from an inappropriate statistical calculation using a non-representative population sample which included the elderly and disabled.[13] CFS occurs at all ages but in this trial of adults, 97% were aged under 60 years at baseline, and a diagnosis of CFS requires that other chronic disabling conditions which explain the fatigue etc are excluded. The stated justification for this drastic change, erroneously asserted that about half the general working age population score under 85, but it is actually 17.6%. Note that 92.3% of the 'healthy' working age English population score 85 to 100, and 61.4% score 100.[13]

    3) The required CGI score of 1 ("very much better") was relaxed so that 2 ("much better") also counted towards recovery. The next option 3 ("a little better") was regarded as a non-improvement. A moderate improvement in CGI score is non-specific, could be a result of improvement to one complaint while multiple major symptoms remain, and on its own does not guarantee any clinically significant improvements to the primary efficacy measures of fatigue and physical function.[14-15]

    4) No longer meeting Oxford CFS criteria did not guarantee real-world recovery, because participants who otherwise still met Oxford criteria as usually applied and still experienced either severe fatigue or significant disability, could be disqualified by failing ad hoc criteria for either, even if their CFQ and SF-36/PF scores remained abnormal or one remained unimproved.[16] (The optional requirements of not meeting CDC CFS criteria or London ME criteria were superfluous, not entry requirements, stricter than the Oxford CFS criteria, made no difference to the results, and were improperly applied.[6,17])

    The technical details of the "planned" mediation analysis[1] are not adequately covered in the published protocol[4] or the statistical analysis plan.[7] It is unknown what methodological changes occurred during this exploratory analysis or whether it was influenced by 'data dredging' and 'post-hoc revisions'. Earlier results were described in 2011 as: "There was modest mediation of CBT and GET effects (approximately 20% of the total effect)."[18] Now much higher figures are being reported, even for individual mediators, including, "fear avoidance beliefs, the strongest mediator, accounted for up to 60% of the overall effect."[1] Interestingly, Chalder et al.[1] and the accompanying editorial by Knoop & Wiborg[19] conceded that the causal relationships between mediators and outcomes were unclear.

    The 60% figure compared GET with a non-representative version of pacing (APT), but news articles have misrepresented this as strong evidence that patients recover by overcoming their fears and exercising. This is contradicted by "an almost complete absence of improvements in objectively measured outcomes", including the fitness step-test which indicates that participants failed to exercise more, despite GET aiming to substantially increase activity/function e.g. 30 minutes of exercise at 60-75% maximum heartrate at least 5 times per week.[20] The exception (GET walking distances) was not clinically significant and was not due to improved fitness.[19] These results dispute the deconditioning model and instead reflect an activity ceiling determined by post-exertional symptoms and abnormal (pathophysiological) responses to exercise.[21,22]

    This non-blinded trial tested therapies aimed to change participants' beliefs about symptoms and impairments, so the discrepancy between subjective and objective outcomes raises plausible concerns about biases with self-reports.[23,24]









    9. http

    Sunday, February 1, 2015

    ME expert Dr Enlander: editors should REFUSE to publish papers, like the PACE trial, which use the Oxford criteria

    By Derek Enlander, ME Expert:

      We read with interest the Psychiatric statement that fear was a major cause of Exercise not being effective in the treatment of ME CFS. I suppose we may expand this notion of treatment failure due to fear to any research. Ridiculously it could be said that the claim of fear of treatment not only affects ME CFS but other disease entities, thus any treatment research project which fails could be attributed to such fear.

    The Oxford criteria for the diagnosis of ME CFS was almost uniquely used by the group publishing this paper and form a mainstay of their criteria. The Oxford criteria are not accepted by the National Institutes of Health and other oversight bodies.

    It is the reviewers' responsibility and the editors' responsibility to refuse publication of papers which do not use correct criteria, indeed the BMJ should publish a note of errata.

    Competing interests: No competing interests 26 January 2015 Derek Enlander Physician ME CFS Center New York 860 Fifth Avenue New York NY


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