CBT/GET to be formally recommended for NHS fatigue patients

Discussion in 'Fibromyalgia Main Forum' started by KelB, Oct 2, 2006.

  1. KelB

    KelB New Member

    A study commissioned by the National Institute for Clinincal Excellence (sets policy for the NHS) is going to formally recommend CBT and GET as the standard treatment for CFS patients in the UK. Research has apparently been published in the Journal of the Royal Society of Medicine.

    Full article here (BBC news-only site, non commercial):


    Very disappointing news.

    CBT has helped me, but it was given as a coping mechanism and not the "cure" that seems to be implied by NICE. In my area, there is a waiting list of 6 months minimum to get counselling and even then, there are very few who specialise in CBT for CFS (and fewer still that are sensible about it).

    Heaven help us.
    [This Message was Edited on 10/03/2006]
  2. Smiffy

    Smiffy Member

    The standard treatment? It makes me want to scream! The M.E. Association & the 25% severely affected Group have been saying for years that these can make us very much worse.
  3. KelB

    KelB New Member

    Bumping for UK bods
  4. tansy

    tansy New Member

    is the only way to describe how awful the situation has become for most of us in the UK. What angers most of us is Action for ME's role in all of this; they are clearly more concerned about selling themselves (as confirmed in their presentation to the Gibson Enquiry than they are about those they claim to represent.

    I am ony briefly back on the internet but I wanted to briefly check out what the response to NICE's guidelines will be. The post below was written by Dr Charles Shepherd.

    ME Action UK (not Action for ME) are one of the most outspoken critics of the current situation, The 25% group are too. Supporting these organisations and their efforts is essential; the Wessely School have achieved what they set out to do and it's not just PWME/CFS who will pay the price.

    TC, Tansy

  5. tansy

    tansy New Member



    This is a brief summary of some of the key points that were discussed at a
    National Institute for Health and Clinical Excellence (NICE) meeting held
    at the Royal Overseas League in London on Thursday 5 October 2006.


    Among those attending were:

    Representatives from three ME/CFS charities:
    Doris Jones (25% Group)
    Angela Murphy (AfME)
    Charles Shepherd (ME Association)

    Representing the Royal Colleges and other health profession organisations:
    Professor Leslie Findley (Royal College of Physicians)
    Professor Peter White (Royal College of Psychiatrists)
    Sue Luscombe (British Dietetic Association)
    Sue Pemberton (College of Occupational Therapists)
    Kevin Smith (Royal Pharmaceutical Society)

    Representatives of the Guideline Development Group:
    Professor Richard Baker (Chairman)
    Dr Esther Crawley (Consultant Paediatrician)

    Representatives from existing ME/CFS clinical services:
    Pat Noons (Peninsula Medical School)
    Gillian Walsh (Manchester Clinical Network)

    Representatives of Goverment Departments:
    Cathy Harrison (DWP)

    In addition, there were representatives from all the various arms of the
    NICE bureaucracy - some of whom gave presentations during the meeting - and
    the National Collaborating Centre.

    There were a considerable number of apologies for non attendance.

    The meeting was chaired by Dr Gillian Leng (Implementation Systems Director
    at NICE).


    Dr Leng opened by explaining that this was a one-off meeting that had been
    called to essentially discuss the way in which the NICE guideline would be
    implemented once it is published in early 2007. The meeting would
    therefore concentrate on matters relating to the standard NICE
    implementation process - including costings, training, and education
    programmes - rather than entering into a wide-ranging discussion on what
    people thought about the September draft of the guideline.


    We were informed that the September draft, which has now been placed in the
    public domain (more information and links are available on the ME
    Association news blog) was the final draft. The Guideline Development
    Group (GDG) would take note of all the comments that are forwarded to it as
    a result of the consultation process that is now taking place with the

    A final version of the guideline will then appear in early 2007.

    The guideline itself will be published on the fourth Wednesday of April
    2007 (a date for the diary).


    Despite the intention to concentrate on guideline implementation, the
    presentation from Professor Richard Baker on what NICE regard as the 10 key
    priorities relating to their conclusions and recommendations gave everyone
    an opportunity to raise specific concerns and objections. A substantial
    part of the meeting was then devoted to discussing the actual guideline.

    As a result, NICE officials were left in no doubt that there were very
    serious and constructive objections from some sections of the patient
    community about many of the key conclusions and recommendations being put
    forward in the September draft.

    The MEA stated that we would not be willing to endorse the draft in its
    current form - as there are far too many aspects that we believe are either
    unacceptable, unbalanced or potentially harmful to some people who
    currently come under the umbrella diagnosis of ME/CFS. I went as far as to
    say that I personally thought that certain key parts of the guideline were

    What the MEA wants is a guideline that is going to contain recommendations
    on diagnosis and management that are acceptable to everyone who comes under
    the very unsatisfactory diagnostic umbrella of ME/CFS (and PVFS). This is
    not going to be easy to achieve but we believe it is possible if NICE were
    to take proper notice of patient opinion.

    Other ME/CFS charities will no doubt make their positions clear in their
    own public statements.

    Below are some of the main concerns and objections that were raised by the MEA:

    1 The way in which the guideline has considerably widened the existing
    (Fukuda et al) research criteria for CFS into a new clinical definition
    which includes almost anyone with four months or more of unexplained
    chronic fatigue plus one other symptom from a list that now includes
    palpitations but not orthostatic intolerance, and refers to dizziness but
    makes no mention of the need to examine patients to assess both balance and
    vestibular function.

    2 The failure to cover the fact that there is a wide spectrum of clinical
    and patient opinion on both the possible benefits and the possible harm
    from the only two treatments that the guideline recommends should be first
    choice treatments for anyone with mild to moderate ME/CFS - ie CBT and
    GET. In particular, the sort of feedback contained in the Chief Medical
    Officer's report in which around 65% found that CBT was of no value and
    around 50% saying that GET had made their condition worse. Reference was
    also made to the most recent study on CBT (ref: Cognitive behaviour therapy
    in chronic fatigue syndrome: a randomised controlled trial of an outpatient
    group programme. Health Technology Assess. 2006 Oct; 10 (37): 1-140)
    which had failed to demonstrate any major overall benefit when CBT was
    compared to either education and support or standard medical care.

    There also appears to be a complete failure to appreciate that prominent
    use of the term 'exercise' in the guideline is not an appropriate
    description for the type of energy/activity management that needs to be
    applied with considerable flexibility according to the stage, severity and
    variability of an individual's illness.

    Exercise is, of course, a totally misleading term for energy management in
    the severely affected group - as well as for a significant proportion of
    those with what the guideline describes as a moderate degree of severity.

    3 The failure to explain how management in the very early stages (ie the
    weeks and first few months following an acute onset), and during
    relapse, often needs to be significantly different to the management of
    this illness once it enters a more stable or chronic phase. In particular,
    we strongly object to the implication that a period of increased rest and
    sleep is often inappropriate during the very early stages following an
    acute infection, or during an acute relapse once the illness become chronic.

    NB: Some of the new NHS clinics have a very inflexible policy about not
    accepting referrals to their waiting lists until symptoms have been present
    for six months or more. The MEA believes this is unacceptable and is not
    consistent with the need for early and accurate diagnosis. This important
    point was also discussed at the meeting.

    4 The completely inadequate and/or unsatisfactory coverage of a number of
    key aspects of management. These include alternative and complementary
    approaches; sickness and disability benefits (in particular the fact that
    people need medical support to help end the current situation whereby they
    all too often have to go to appeal in order to obtain Disability Living
    Allowance); diet ; relapses or 'setbacks' as they are referred to in the
    guideline; and symptomatic relief (pain in particular) - all of which are
    highly relevant to primary care.

    5 The way in which the severely affected are described in the guideline
    (including the lack of reference to the more serious neurological symptoms
    noted in section the Chief Medical Officer's report) and some of
    the suggestions regarding how this group should be managed. In particular,
    the lack of evidence regarding CBT and GET in this group; the almost
    complete lack of in-patient and domiciliary services in many parts of the
    UK; and the need for practical help and support in the home.

    Questions were also asked by the MEA about:

    1 Where the money was going to come from if everyone with mild to moderate
    ME/CFS (180,000 as a rough starting point but this figure would rapidly
    rise once everyone with chronic unexplained fatigue is included as well)
    were to be referred to hospital based clinics for medical assessment and
    then treatment with CBT and/or GET (at a cost of possibly around £1,000 per
    course of treatment). It was also pointed out that most PCTs regard ME/CFS
    as a low priority issue, and in the current NHS funding crisis services are
    now being reduced in many areas.

    2 How current hospital based services for people with ME/CFS, which are
    almost non-existent in some parts of the UK, are also going to be able to
    take over the on-going management of vast numbers of people with mild to
    moderate unexplained chronic fatigue - a population which is far higher
    than current estimates of how many people have research defined CFS.

    Some of us found the answers to these very difficult financial questions
    most unconvincing!

    NB: These points and questions obviously represent the position of the MEA
    on the September draft. The 25% Group went into more detail about issues
    that were relevant to the severely affected group. I was not taking
    detailed notes during the meeting and will therefore leave it to other
    charities who were present (or not present) to make their position clear on
    both the content of the meeting and the content of the guideline.

    SUMMING UP.....

    The meeting was chaired with fairness, good humour and common sense by Dr
    Leng .

    Those of us who had a lot of constructive points to make, even if some were
    slightly 'off topic', were allowed to do so.

    I came away with the impression that the deep concerns and objections
    expressed by patient representatives - as well as consultant neurologist
    Professor Leslie Findley, who made an excellent contribution - had been
    listened to and that some of them would now be the subject of further
    discussion at NICE.

    Unfortunately, I was also left with the impression that the guideline would
    not be the subject of major change at this late stage in the development
    process. So while some subtle changes in content, emphasis and language
    will almost certainly occur as a result of this meeting, I doubt if we are
    going to see a guideline that the MEA can endorse - certainly on the basis
    of the responses that were given on Thursday.

    What may lead to a more significant change in mind is if it becomes clear
    to NICE that this guideline is just not acceptable to a very wide selection
    of patient opinion. So the MEA would urge as many people as possible to
    read the guideline (stick to the 48 page shortened version but check with
    the full version where necessary) and let us know what you think.

    The next step for the MEA is to provide a draft of our detailed response to
    the September draft. This should be available by mid October. We will
    then want to know whether people believe that our criticisms and objections
    are justified!


    Please get involved in the consultation process. This guidance from NICE
    is going to have a major affect how your illness is managed for several
    years to come.

    For more information on the September draft, and links to NICE
    publications, go to the MEA news blog at: http://meassocnews.blogspot.com

    The MEA welcomes comments from its members on the current draft as this
    will obviously help us to formulate our detailed response. There is no
    immediate hurry to pass on this feedback (the consultation process runs
    until 24 November 2006) and members may find it helpful to read the first
    draft of our response, which we intend to publish on the MEA website within
    the next week or so.

    If you belong to one of the other MEA charities who are stakeholders in the
    guideline development process you may wish to pass on your comments to them


    A copy of this summary is being sent to Professor Richard Baker, along with
    an offer to publish a response from NICE on the MEA website - if they wish
    to make one.

    Dr Charles Shepherd
    Medical Adviser, ME Association

    [This Message was Edited on 10/12/2006]
  6. tansy

    tansy New Member

    Some Concerns about the National Institute for Health & Clinical Excellence (NICE) Draft Guideline issued on 29th September 2006 on Diagnosis and Management of Chronic Fatigue Syndrome / Myalgic Encephalomyelitis in Adults and Children

    Margaret Williams
    (Nominated Respondent with The 25% ME Group for the Severely Affected)

    19th October 2006

    This document can be read at

    [This Message was Edited on 11/29/2006]
  7. tansy

    tansy New Member

    Klimas, Wessely and NICE: Redefining CBT?

    Margaret Williams 10th November 2006

    Patent Foramen Ovale (PFO) is the persistence (or the acquired re-opening) of the normal foetal opening between the right and left atria of the heart. In his September 2006 seminar (see below), Dr Paul Cheney from North Carolina – who has seen over 5,000 patients with (Myalgic Encephalomyelitis) / Chronic Fatigue Syndrome -- states that PFO is “tightly associated” with (ME)CFS to the order of at least 80% or more of patients.

    Despite the fact that the UK medical defence unions have advised doctors that exercise regimes (which form part of a cognitive behavioural therapy regime) must be prescribed with just as much caution as pharmacological interventions, it seems that the National Institute for Health and Clinical Excellence (NICE) may have overlooked the implications of this advice: in its Draft Guideline on “CFS/ME”, the only recommended management regime is cognitive behavioural therapy (CBT), including graded exercise therapy (GET) and, for the severely affected, “Activity Management”.

    There is no warning that patients with ME/CFS might have PFO. On the contrary, the NICE Draft Guideline advises against even looking for such pathology in those with ME/CFS.

    Why is the UK ME/CFS community so collectively opposed to the NICE Draft Guideline?

    The answer is because NICE is recommending CBT and GET as the only management regime and those whose lives are struck down by ME/CFS know full well that the UK CBT/GET regime has already been shown to be at best of little help, and at worst, dangerous.

    The UK definition of CBT is contained in the Chief Medical Officer’s Working Group Report of January 2002: “Cognitive behavioural therapy is a tool for constructively modifying attitude and behaviour”.

    The UK definition of GET is contained in the NHS Plus National Guideline on Occupational Aspects of CFS of October 2006: “GET involves structured activity management that aims for a gradual increase in aerobic activities”.

    According to Cheney, aerobic exercise may kill the patient with (ME)CFS, so patients are rightly wary, because for almost 20 years Wessely School psychiatrists have claimed that ME does not exist except as an aberrant belief, and that “CFS” is a psychiatric disorder in which patients refuse to confront their “faulty illness beliefs” (ie. that they have a physical, not a mental, illness). These psychiatrists believe it is such “faulty” beliefs that prevent people from recovering, therefore the “faulty” beliefs must be modified in order to get people who harbour misperceptions about their bodily sensations off welfare benefits and back into work. Patients who do not – or physically cannot—comply have had their benefits stopped. There has been little evidence that CBT is a tool to support patients or to help them cope with the ravages of serious organic disease.

    Confusion about CBT in the UK

    Confusion abounds in almost every aspect of ME/CFS, including what is now meant by “CBT/GET”, and in the UK there seem to be signs of expedient change as to the type of CBT/GET that is to be delivered to those with ME/CFS, as well as the purpose of it; in other words, it seems the nature of CBT is being re-defined.

    For example, in October 2006 at the Sheffield (UK) Conference, CBT was described by Professor Anthony Pinching as “a valuable tool for managing chronic disabling illness in patients who are having difficulties in adjustment”. Given Pinching’s published track record, notably his article in Prescribers’ Journal in 2000, this seems to represent a significant shift, because in that article he stated that CFS is not related to on-going exertion; that patients should not be “over-investigated” because investigating them causes them “to seek abnormal test results to validate their illness”; that approaches can be “behavioural”; that “the benefits of graded exercise have been shown by randomised controlled trials”, and that “the essence of treatment is activity management”, relying heavily upon Wessely School studies, many of which promote the delivery of CBT/GET in a coercive and overly-inflexible way (Prescribers’ Journal 2000: 40:2:99-106).

    But Pinching’s is not the only apparent turn-around: given that at the behest of Wessely School psychiatrists who believe “CFS/ME” to be a behavioural disorder, the Government rushed to invest £8.5 million in “CBT for CFS” by setting up new Centres that are to deliver CBT/GET for those with ME/CFS, it now seems to be wondering – in the light of so much incontrovertible evidence of serious organic pathology in ME/CFS that cannot be denied forever – if this may have been the wisest way of addressing the problem, and as a consequence, some Government bodies seem to perceive a pressing need to justify by any means possible the expenditure of such large amounts of money on what may be seen as inappropriate interventions.

    And so the NICE Draft Guideline states: “The Guideline Development Group was clear that CBT was not about unhelpful advice or dictation of illness beliefs, but about changes in lifestyle and learning to achieve improvements with the patient’s abilities. The GDG did not regard CBT or other behavioural treatments as curative or directed at the underlying disease process. Rather, such treatments can help some patients cope with the condition and consequently experience an improved quality of life” (6.3.7 / Deriving Recommendation / Discussion of the Evidence).

    Noble-sounding words, but this sweet-talking does not stop the UK ME community from seeing such surreptitious amendment as a case of “Come into my parlour, said the spider to the fly”, especially given that NHS Plus has not waited for the final NICE Guideline but has gone ahead and published its 64-page Policy Document referred to above (Occupational Aspects of the Management of Chronic Fatigue Syndrome: a National Guideline”. Department of Health: 6th October 2006: 273539) that is grounded entirely on the psychosocial model of ME/CFS and which recommends that patients who are still working should be advised to stay at work even if they feel “tired”. Importantly, it stipulates that no-one with a diagnosis of ME/CFS should be permitted to retire until they have undergone “rehabilitation” by means of CBT/GET. It is noted that the key players in this document are Professor Trudie Chalder, Professor Mike Sharpe and Professor Peter White, all of whom are well-known for their intransigent belief that “CFS/ME” is a behavioural disorder. It is also noted that the “Guideline Leader” does not work for the NHS but for a private medical insurance company.

    To accompany this Policy Document, NHS Plus has produced three booklets: one for employers, one for employees and one for healthcare professionals, all of which contain misinformation about ME (about which the parent document states: “The descriptive term CFS is preferable to previously used terms such as post-viral fatigue syndrome or ME”).

    The booklet for employers states: “ This leaflet summarises the evidence-based guidance on how to support individuals back into, and to remain in, work. CFS is an illness characterised by severe, disabling tiredness. A feeling of being tired all the time is very common. ME and post-viral fatigue syndrome are terms that people with CFS often use (but) most healthcare professionals prefer the term CFS. (Appropriate treatments) for CFS (are) CBT, a structured form of psychotherapy (and) GET, a structured programme designed to increase aerobic activity. If an individual complains of fatigue, an employer should refer them to an occupational health professional. Ill-health retirement should only be considered if appropriate treatments such as CBT and GET have been explored”.

    The booklet for employees says much the same: “It is a good idea to try to stay at work even though you feel tired. CBT and GET are treatments that research has shown can increase the chance of returning to work. Ill-health retirement is not a first choice”.

    The booklet for healthcare professionals is even more damaging: “The perpetuation of CFS may include deconditioning, inappropriate avoidance of activity as a coping mechanism, personal conflicts and fears about the condition itself. Management (is by) a biopsychosocial approach. There are two interventions supported by good quality evidence (sic): CBT involves cognitive restructuring to tackle negative beliefs. (Its) effectiveness may be limited by excessive focus on bodily symptoms and taking medical retirement or disability benefit during the treatment. (In) GET, patients ‘negotiate’ an aerobic exercise programme. Patients should be advised against seeking early medical retirement until all rehabilitation strategies have been explored”. The reference to support this last statement says: “Evidence from expert opinion”.

    There is no reference to the research evidence that has demonstrated serious, multi-system pathology: employers and healthcare professionals (ie. the decision-makers) are given no information about the proven dysfunction of virtually all body systems, including cardio-vascular, respiratory, gastro-intestinal, musculo-skeletal, opthalmic, neurological, and most importantly, the immune system (with the evidence of autoimmunity). Not to do so is, by any standards, deceptive.

    Curiously, Professors Peter White and Mike Sharpe seem to be somewhat confused: whilst on the one hand they say that the effectiveness of CBT may be limited by being in receipt of disability benefit, in the same document they also say: “being in receipt of sickness benefit at the start of treatment may be a marker of severity”.

    Thus in the UK things are far from transparent: the NICE Draft Guideline says one thing, but the NHS Plus documents have pre-empted the NICE Guideline (due in April 2007) and say another thing entirely.

    Those in the UK ME community who might be tempted to accept the NICE Draft Guideline’s assurances that CBT is not about “dictation of illness beliefs” need to remember that the psychotherapy it recommends will still be delivered in psychiatric units at the behest of psychiatrists who will still harbour their ill-founded prejudices against ME patients.

    Confusion about CBT in the US

    In November 2006 Nancy Klimas, Professor of Medicine at Miami, and Anthony Komaroff, Professor of Medicine at Harvard (both of whom are not only clinicians but also long-time researchers into ME/CFS) attended the launch by the US Centres for Disease Control (CDC) of its “CFS Toolkit” and its campaign to advance knowledge of (ME)CFS.

    At the launch, Professor Klimas said: "Historically, the lack of credibility afforded this illness has been a key obstacle to understanding it. Today, with solid evidence that CFS has identifiable biologic underpinnings, and with evidence that people with CFS experience a level of disability equal to that of patients with multiple sclerosis, advanced HIV disease and undergoing chemotherapy, I hope we can begin to put an end to the stigma surrounding this illness."

    Also at the launch, Professor Komaroff said about the lingering belief that (ME)CFS is psychological and somehow imagined: “That debate raged for 20 years, and now it’s over”.

    As reported on 3rd November 2006 by United Press International, there are over 3,000 research papers that have established (ME)CFS as a valid physiological illness, with evidence of inflammation, reduced blood flow and impaired cellular function. It was described as a “brutal” disease which often occurs in conjunction with other diseases such as lupus and Lyme disease, and its symptoms can be as severe and painful as renal failure, AIDS or multiple sclerosis.

    Importantly, distinctions were drawn to the two different types of (ME)CFS: one that occurs immediately after an infection and one that develops gradually over time, and to the fact that the two types seem to differ genetically.

    Many parts of the Toolkit are helpful: the CDC points out (and accepts) that irritable bowel syndrome, multiple chemical sensitivity, fibromyalgia and Gulf War Syndrome may be co-morbid conditions; that allergies are seen in many patients and that many (ME)CFS patients are very sensitive to medications; that alternative therapies should be considered (and that the practitioner should remain open-minded about them); the need to be alert to dizziness in patients and the need to refer them a neurologist and / or a cardiologist before initiating treatment; that there is considerable variation in symptom expression and severity; that symptoms are unpredictable; that the disorder can have a profound impact on daily life, requiring significant lifestyle changes; that (ME)CFS is an ‘invisible illness’ in which patients often do not look sick and that this contributes to patients being misunderstood and isolated; that a therapy which works for one patient may be of little benefit for another; that advising patients to engage in aerobic activity can be detrimental as it can cause a full-scale relapse that can last for weeks, and that patients with (ME)CFS can lose their jobs, economic security and home.

    However, when it comes to treatment, there seems to be confusion, with Klimas saying at the launch: "Although there's no single treatment—no hoped for ‘magic bullet’—that fixes the illness at its core, there are treatments that can improve symptoms, increase function and allow CFS patients to engage in activities of daily living. Current best practices for clinical care include a combination of symptom management, activity management and exercise therapies."

    This seems at variance with her previous on-the-record views about CBT, for example:

    • “I don’t take the British view that CBT is the one thing you can do to effectively treat (ME)CFS. But it’s a tool that helps some patients” (The Science and Research of CFS: CFIDS Chronicle Special Issue, 2005-2006)

    • "The question arises whether a formal CBT or GET program adds anything to what is available in the ordinary medical setting. A well informed physician empowers the patient by respecting their experiences, counsels the patients in coping strategies, and helps them achieve optimal exercise and activity levels within their limits in a common sense, non-ideological manner” (ME/CFS: Clinical Working Case Definition, Diagnostic and Treatment Protocols. Bruce M Carruthers, Nancy G Klimas et al JCFS 2003:11:1:7-115).

    How is it that in 2003, Klimas said that a competent physician would give his patient common sense counselling in coping strategies, but three years later she now says the same patient should be handed over for psychotherapy?

    Is the answer that CBT has been “redefined” in the US also, so in the absence of any remotely therapeutic intervention, Klimas might well recommend CBT to help patients with ME/CFS cope with it (whereas in the UK Wessely et al have used it to deny the very existence of ME/CFS)? Klimas is also on record as saying at the CDC: “It’s critical for patients and their healthcare providers to know that there is hope and that we can help”.

    On the matter of management, some of what the Toolkit says is hardly controversial, namely that the objective of an effective management programme is threefold: (1) to help patients develop effective coping strategies (2) to relieve symptoms and (3) to teach patients to manage activity levels so as to avoid post-exertional malaise on the one hand and deconditioning on the other.

    However, it also states: “The goal of CBT is to change perceptions and behaviours that can contribute to symptom expression” and “Working with a CBT therapist, (ME)CFS patients can examine their beliefs and coping behaviours and modify these as necessary to manage the illness more effectively”.

    As in the UK, there seem to be a confusing divergence about the nature of CBT for those with (ME)CFS.

    Changes in the UK?

    Are things changing in the UK? On the basis of the Wessely School psychiatrists’ chameleon stances (depending on whether their audience is in the US or the UK), they may currently see advantages in creating the illusion that the aim of CBT has always been to help patients cope with overwhelming illness: if so, are we witnessing the construction of an escape route made necessary by the realisation that -- in the light of such substantial and convincing biomedical evidence -- they’ve been wrong ?

    For illustrations of the pliability of Wessely School opinions about the efficacy of CBT depending on the country in which they were delivered, see http://www.meactionuk.org.uk/Concerns_re_NICE_Draft.pdf

    So why is the Wessely School model of CBT/GET not only unsuitable but potentially dangerous for those with ME/CFS? The following notes, taken from Cheney’s DVD (a two disc boxed set: for details, send an email to videos@dfwcfids.org as notified on Co-Cure on 27th October 2006), may provide some answers.

    It should be compulsory viewing for every member of the NICE Guideline Development Group on “CFS/ME”.

    Cheney’s Seminar

    Others have already reported on Cheney’s seminar, so what follows is a simplistic summary and makes no attempt to explain the disrupted metabolic and biochemical pathways that were demonstrated in detail by Cheney.

    Cheney – who has been involved with (ME)CFS since the Lake Tahoe outbreak in the early 1980s -- began by acknowledging his debt to the work of Peckerman, who had found that half of the patients studied had low cardiac output as measured by impedance cardiography. (Peckerman noted that this could be due to the heart itself, but that it could also be due to problems in the peripheral blood vessels). This fascinated Cheney, who in 2003 underwent a successful heart transplant because of dilated cardiomyopathy, as a result of which he had observed at first hand the spiralling effects on differing body systems of low cardiac output.

    Important Clinical Findings

    There is an objective database in key medical literature that includes evidence (sic) of diastolic dysfunction and heart failure in (ME)CFS. PFO is found in at least 80% of patients with (ME)CFS.

    Oxygen should not be transported into a cell that cannot use it without effective defences against its by-products (oxygen being the precursor of free radical formation).

    Symptoms are usually manifestations of defence responses and reflect but do not cause the underlying problem.

    Symptom-based treatment alone is therefore flawed at best and dangerous at worst: to treat symptoms without understanding the underlying disease process can cause death: the third leading cause of death is treatment by physicians, which kills 250,000 people per year (the first being heart disease and the second being cancer) -- most drugs are not aimed at the primary cause of disease but at symptoms and are therefore dangerous (see below for Cheney’s view about the dangers of giving Prozac to those with (ME)CFS).

    Principles that are important in (ME)CFS

    Adaptation to chronic disease is generally coded as a phenotype shift (ie. one still has the same genes but they are expressing themselves differently). There is an emerging literature that shows phenotypic adjustments are defining illnesses by which genes are changing. Why is this going on? Is the gene shift causing the disease, or is it defending the host? It is mostly the latter, and this is very important, so we need to treat the underlying cause as, once changed, the patient can never return to his/her original phenotype. If genes have changed (and there is evidence that they have), a patient can be genotypically shifted as well and phenotypically shifted, and this is a big issue that stands in the way of a quick fix solution: if chronic disease can never be fixed, how can people be helped to feel better? The answer lies in suppressing the defence mechanism, but this is not very good, because if you fix the defence mechanism, at some deep level you can worsen symptoms.

    A key principle is not to use too much oxygen (because it kills). (ME)CFS protects against almost certain death by adapting to a low energy state.

    Patients withdraw from activity: they have a dynamic dysfunction that is more than simply an adaptation – there is something about the disease that is making them this way.

    The (ME)CFS Case Definition

    Cheney outlined the case definition, saying that the classic triad is: no energy, brain dysfunction, and pain. If a patient does not have pain, s/he does not meet the (ME)CFS case definition: (ME)CFS is very much a painful disorder.

    Cognitive dysfunction occurs in 99% of cases (processing speed; short-term memory loss; sensory and information overload; information searching; multi-tasking problems; spatial disorganisation). “Fatigue features in so many other disorders, but what makes (ME)CFS special is the brain component”.

    Mood disturbances occur: depression is rarely severe and is reactive; anxiety disorders abound, as does mood lability, but 40% do not have any mood disorder, so (ME)CFS is not a psychiatric disease.

    The evolution of (ME)CFS

    There are four phases:

    1. the onset, or trigger phase
    2. the triad phase
    3. the dynamic dysfunction phase (although the fatigue and pain and brain dysfunction are a little better, patients in this phase can do less than when they were more sick)
    4. DNA phenotype adaptation phase (there is a phenotypic adaptation that locks this in at gene level).

    Key scientific articles

    Phase 1: (immune activation: fever, swollen glands, sore throat, malaise: general indications of immune activation)

    • Suhadolnick et al (Temple University, USA)
    • Komaroff et al (Harvard, USA)
    • Klimas et al (Miami, USA)

    Phase 2: (the centre of gravity of this illness: fatigue, brain problems and pain; xenobiotic toxicity coming from the gut and the environment)

    • McGregor et al (Newcastle University, Australia)
    • Pimental (UCLA, USA)

    Phase 3: (the brain and heart component)

    • Demitrack et al (NIH, USA)
    • Moorkens et al (Antwerp, Belgium)
    • Schwartz et al (Harvard, USA)
    • Peckerman et al (NMJ & D, USA)
    • Drexler et al (Hanover, Germany)

    Phase 4: (phenotypic and genotypic adapatation à oxidative stress)

    • Vernon et al (CDC, USA)
    • Kerr et al (London, UK)
    • Urowitz et al (Berkeley, USA)
    • Pall (WSU, USA)
    • Kennedy et al (Cheney’s overhead stated “USA”, but if he means Kennedy and Spence, it should be Dundee, Scotland)

    Oxidative stress links (ME)CFS to fibromyalgia, multiple chemical sensitivity and Gulf War Syndrome.

    Do people recover from (ME)CFS?

    Functional recovery is seen: one’s ability to do things can improve, but it can go the other way, or there may be no change over time. In functional improvement, do patients really get better, or do they just adapt? The longer things go on, the more difficult it is to see functional recovery. Komaroff’s data from Harvard is that after 10 years of illness, there is only a 30% chance of any functional recovery.

    The Physical Examination

    In phase 1: (immune activation), one sees

    • Lymphyodynia (seen in 80-90%)
    • Crimson crescents bilaterally on soft palate (seen in 80%)
    • Sub-normal temperature

    In phase 2: one sees

    • Evidence of subcortical brain injury
    • Vestibular dysfunction (seen in 94%)
    • Hyper-reflexia, especially of the knees and ankles (seen in 70%)

    In phases 3 and 4: the most interesting are the metabolic disturbances:

    • There is shortened breath-holding capacity (seen in 60%)
    • There is very poor oxygen transport (seen in 90%): pulse oximetry readings measuring saturation of haemoglobin show a significant inhibition to desaturate
    • There is finger-print destruction (seen in 50%): cross-hatching occurs, with degradation of the ridges; punch biopsies found perivascular lymphoid infiltrates ie. an inflammatory cuffing exactly as seen in lupus, which signifies a non-specific immune activation issue (so the finger-print changes could be reflecting much more than just loss of finger-prints and may represent a vasculopathy)
    • There is sub-normal temperature (seen in 80%)
    • There is low systolic blood pressure (in 50% of patients it is less than 100)
    • There is orthostatic B/P or pulse changes (seen in 70%)
    • Hypertension is very rare

    These findings portend significant physiological issues, chief of which is that oxygen is being prevented from getting into the cell, and if there’s no oxygen, there’s no energy.

    Magnetic Resonance Spectroscopy

    • 70% of patients show elevated lactate levels in the ventricular system (the lactate elevation is not normal and indicates a defect in energy in the brain: (ME)CFS patients have significantly elevated lactate levels and the fatigue correlated significantly with the level of lactate)
    • 10% have evidence of neuronal destruction and elevated choline peaks, typically in the perivascular areas.

    Magnetic Resonance Imaging

    • 78% of patients have punctate lesions which are most consistent with small strokes and there is evidence to support this (ie. they are not caused by a virus or by inflammation).

    Mixed venous blood gas picture

    • PvO2 is 25 (it should be 40)
    • PvCO2 is 55 (it should be 45)

    This is a differential hypoxia with hypercarbia. There are only two diseases where this is seen: one is pulmonary hypertension; the other is (ME)CFS.

    The arterial side is normal.

    Where does the oxygen go? It’s being transported somewhere, but not to the mitochondria. (ME)CFS patients have been shown to have increased pooling of extra-cellular fluid in the belly, pelvis and legs which might contain this dissolved oxygen, but it is more likely being consumed by the oxidative pathway to create superoxide in massive amounts. Superoxide is the progenitor of all free radicals. The consequences are increased intra-cellular oxdidative stress.

    If you intervene and give Prozac, you up-regulate superoxide, which is why serotinergic drugs kill neurons.

    Intervening with drugs in situations not fully understood breeds chaos and kills patients.

    (ME)CFS as cellular metabolic dysfunction

    There are problems at cell level in energy production, and because of this degraded energy problem, patients suffer a defect in the ability to detoxify toxins, especially in the portal circulation (giving rise to gut toxicity as seen in phase 2). Gene alterations (seen in phase 4) generate a massive disturbance in the development of energy at the cell level. If you lose energy, you lose glutathione, but the more glutathione you give, the more you just create oxidised glutathione, which generates loss of citrate, causing a left shift on oxyhaemoglobin desaturation. Citrate also binds to magnesium, so over time the patient will develop a severe magnesium depletion syndrome. When that happens, you’ve had your last good night’s sleep: when you lose magnesium, you can’t sleep any more.

    How and why would a low energy state lead to an inability to transfer oxygen? Cheney concludes that it’s part of a bigger picture that uses low oxygen transport to stablise the system.

    In (ME)CFS, these serious issues are a big problem, especially in the brain, the heart and in muscle. (ME)CFS is a compensatory response to down-regulate energy production and oxygen transport in order to reduce tissue damage.

    Attempts to push beyond energy limits will cause injury.

    Prolonged energy deficits can cause semi-permanent DNA phenotype adaptations and complications can occur, especially within energy-sensitive systems such as the heart, the brain and the muscles.

    The most likely cause (not trigger) of (ME)CFS is a disruption in handling the toxic by-products of oxygen utilisation.

    In (ME)CFS, catalase is deficient in the heart, lungs and liver (catalase is the most protective enzyme in the body against the ravages of superoxide), and Cheney noted that electromagnetic fields [EMFs] “screw up” superoxide dismutase (SOD), which is a major anti-oxidant scavenger.

    Is there an (ME)CFS-associated cardiomyopathy?

    (ME)CFS patients have a high heart rate but a low cardiac output. In (ME)CFS there is a cardiac dimension that is independent of (but not excluding) autonomic function or blood volume.

    82% of patients have abnormal cardiac impedence.

    It’s hard to talk about a low cardiac output without talking about the involvement of the brain and the adrenal glands.

    A mismatch between metabolic demand and cardiac output, even very briefly, will kill.

    If the cardiac output goes down, in order not to die, there is a rise in noradrenergic tone (also involving the adrenal glands) to bring the output back up. In (ME)CFS, this is a serious problem, because when the adrenals are exhausted, there will be low cardiac output.

    There is no such thing as an (ME)CFS patient who is NOT hypothyroid: this has nothing to do with thyroid failure, but everything to do with matching metabolic demand and cardiac output.

    Order of sacrifice in cases of declining microcirculation

    First is the skin; second is the muscles and joints; third is the liver and gut (patients can usually only tolerate a few foods); fourth is the brain; fifth is the heart; sixth is the lung and lastly is the kidney (for a more detailed discussion of this order of sacrifice, see http://www.meactionuk.org.uk/The_MRC_Profits_before_Patients.htm ).

    Among the major causes of death in (ME)CFS is heart failure: Jason et al (August 2006) found that 20% die of heart failure.

    There are two types of heart failure: systolic (which is a failure to eject) and diastolic (which is not a failure to eject, but a failure to fill properly).

    There are two types of diastolic heart failure: primary relaxation deficit giving rise to decreased cellular energy as seen in (ME)CFS and secondary relaxation deficit as seen in hypertension, diabetes and the elderly over age 75.

    Primary relaxation deficit is a disorder that seems to have gone right under the radar of most cardiologists (who focus on the secondary relaxation deficit).

    Diastolic heart failure was first described in the 1980s but there was no significant literature until the 1990s, and no significant way to measure it until 2001.
    In July 2006 The New England Journal of Medicine carried a significant paper on more than 4,500 patients studied with diastolic heart failure (which is higher than those with systolic heart failure). This is unexplained, but is accelerating (is it in fact an explosion of (ME)CFS?).

    One is just as likely to die of diastolic heart failure as from systolic heart failure.

    Doppler mitral in-flow velocities show diastolic dysfunction.

    Concluding the first disc, Cheney stated there is (quote) “a whopping percentage of (ME)CFS people with diastolic dysfunction”.

    In the second DVD, Cheney expounds on PFO in relation to (ME)CFS.

    He says that at least half of patients exhibit atrial cavitation, and that when these patients stood up, in 80% the filling volume collapsed. He tested this with magnesium and the results were significant: magnesium restored 12% of energy in one minute. Magnesium affects the intracellular energetics, proving that patients have a “tremendous” energy problem that is very sensitive to magnesium. (The reason magnesium is so important is that without it, ATP cannot be converted to ADP for the production of energy).

    (ME)CFS patients “squeeze the hell” out of their left ventricle, resulting in a “whopping” 70% increase in left ventricular wall motion thickness. The reason why patients are squeezing so hard is because they do not have enough energy to fill the chambers of the heart properly so they are trying to compensate by squeezing a lot harder (ie. the way patients are compensating for this loss of cardiac output is by squeezing the left ventricle much harder).

    There are significant consequences of this. One consequence is that (ME)CFS patients become asynchronised (ie the heart can be filling and ejecting at the same time).

    If out of synchrony, the ventricle cannot cope, so cardiac output is severely degraded.

    A second consequence is that patients develop a strain pattern, which is an indication of ischaemia. Cheney has seen ischaemic changes in the inner ventricular wall because of the increased squeezing.

    PFO is a hole in the heart producing a right to left shunt of unoxygenated blood full of carbon dioxide as well as products of liver metabolism – the liver is literally draining into the right heart and that blood is being shot straight to the brain (this was demonstrated on the DVD by means of Trans Cranial Doppler bubbles).

    The assumed cause of the PFO is the same as in the foetus – to protect the body from oxygen: in (ME)CFS patients are shifted left to right, not because they have an immature way (as in the foetus) of handling oxygen, but because they have a defective way of handling oxygen.

    In (ME)CFS patients, there is increased left ventricular strain, with increased R-L shunting, and cardiac ischaemia develops, and because of too much squeezing, the PFO (that closed at birth) is opened up, resulting in significant oxygen toxicity, with ischaemic reperfusion-type changes.

    The diastolic dysfunction that causes dilatation of the left atrium can actually break the seal of the sealed Foramen Ovale (ie. the increased pressure blows through a previously sealed PFO).

    It is increasingly clear that in (ME)CFS, a diminished threshold for oxygen toxicity exists, and that each patient will have a unique threshold.

    These findings have a significant negative effect on Emergency Room (A&E) and operating theatre uses of oxygen during surgery – a patient with (ME)CFS could be given too much oxygen and be killed on the operating table.

    Hyperbaric oxygen could have a very negative impact on some (ME)CFS patients.

    The ultimate consequence of this is low cardiac output, arising from a problem of energy production.
    The complications of PFO include:

    • Cerebral aneurysm
    • Multiple mini-strokes
    • Cerebral hypoperfusion produces pressure headaches; migraine, cognitive impairment and a lower seizure threshold
    • Venous hypoxia complications are fundamentally linked to intracellular acidosis which depletes electron buffers
    • Depleted acid buffers leads to increased sensitivity to diet, drugs and the environment.

    PFOs cause significant instability.

    There is a difference between diastolic dysfunction and diastolic failure: in diastolic dysfunction there is a filling problem but the body is compensating for it and achieving enough cardiac output to match metabolic demand. Diastolic failure begins when the body can no longer compensate and there is a reduction in cardiac output. Cheney repeated that this is seen in 80% of (ME)CFS patients.

    If patients draw down their lifestyle to live within the means of the reduced cardiac output, then progression into congestive cardiac failure (CCF) is slowed down, but if things continue to progress, a point will be reached where there is no adequate cardiac output, and dyspnoea will develop, with ankle oedema and other signs of congestive cardiac failure.

    The message from Cheney is clear: in order to stay relatively stable, it is essential for the (ME)CFS patient not to create metabolic demand that the low cardiac output cannot match.

    The message for NICE

    The message for NICE is that (ME)CFS patients instinctively know that they simply cannot cope with aerobic exercise (as in graded exercise therapy), and that their instincts have been proved correct by Cheney’s ground-breaking research.

    Many (ME)CFS patients are formerly high achievers who do not need to be patronised by psychiatrists with their behavioural management regimes about how not to exceed their own limits: they know their limits and live within them daily in order to survive.

    As has been pointed out to NICE, what such patients need is not multi-million pounds to be given to psychiatrists to try to prove that (ME)CFS patients will recover with aerobic exercise: what is needed is biomedical research to find the cause, without which there can be no hope of effective treatment or a cure.

    In the meantime, as NICE has also been informed, patients urgently need practical support services, including help with personal care, shopping, housework, cooking, adaptations in the home (such as a chairlift) ie. basic support for the very ill.

    But NICE has already indicated that it is not listening.
  8. tansy

    tansy New Member


    Margaret Williams 17th November 2006

    Whilst not written in relation to the current confusion about ME/CFS, an NHS consultant physician recently responded to an article in the BMJ on the issue of “policy versus evidence”: “Over the past few decades the practice of Medicine has moved from a basis of experience and understanding of the disease process and its treatment towards the application of authorised protocols and guidelines. (This) raises concerns about the situation in which an inadequate evidence base has become canonised into established guidelines (and) Government policy. It takes a bold man indeed to challenge this set of Emperor’s clothes” (Nick Hardwick: eBMJ re BMJ 2006:333:912-915).

    Can anyone doubt that it is the transformation of “protocols and guidelines” into “canonised policy” that has resulted in the morass that is ME/CFS?

    For what disorder is NICE preparing its Guideline on “CFS/ME”? Is it ME or is it “CFS”? Are they the same disorder? NICE is relying on two definitions of “CFS” (the 1991 Oxford criteria and the 1994 Centres for Disease Control criteria), neither of which defines authentic ME. A quick look at the evidence makes interesting if disturbing reading.


    It is commonly accepted that in 1988, the disease that had previously been called ME was renamed “CFS” by Holmes et al from the US Centres for Disease Control, but is this true, or has there been one of the most devious subterfuges perpetrated in the history of medicine?

    It has long been believed that the introduction of the name “CFS” in 1988 emerged from a collaboration involving Dr Stephen Straus from the US Centres for Disease Control (CDC) with the medical insurance industry, the intention being to curtail benefit payments for the rapidly increasing incidence and prevalence of an existing (and chronically incapacitating) disorder that was known as ME. It was apparently anticipated that such curtailment could be achieved by focusing on the single symptom of chronic “fatigue” (a ubiquitous symptom for which benefit payments could expediently be denied).

    That people were seriously sick with what international ME experts regarded as ME is not in doubt (see Osler’s Webb: Inside the Labyrinth of the Chronic Fatigue Syndrome Epidemic. Hillary Johnson. Crown Publishers Inc, New York: 1996). Quite certainly the advisory committee that was to produce the 1988 case definition of “CFS” included two of the leading experts in ME, Dr Alexis Shelokov from the US and Dr Gordon Parish from the UK.

    However, both these experts withdrew from the deliberations as they were unable to endorse the new definition of “CFS” because it was so far removed from what, as experts, they knew ME to be, since it excluded the cardinal and well-documented neurological and vascular features of ME and focused instead on “fatigue”. The experts were dismayed that the essential characteristics of ME were no longer to feature in the “new” definition that was claimed to be preferable, ostensibly because it made no assumptions about aetiology.

    It is recorded that Holmes himself wanted to keep the term ME but was over-ruled.
    If in 1988 “CFS” was indeed meant to be a new name for ME, in 2005 it was acknowledged to have been a major error by one of the physicians on the committee, Professor Anthony Komaroff: “None of the participants in creating the 1988 CFS case definition, and the illness name, ever expressed any concern that it might trivialise the illness. We simply were insensitive to that possibility, and we were wrong” (http://www.cfidsreport.com/Articles/NIH/NIH_CFS_4.htm ).
    In that definition (Chronic Fatigue Syndrome: A Working Case Definition. Gary P Holmes et al. Ann Intern Med 1988:108:387-389), no mention was made of ME or of its cardinal features (either in the text or in the references), only of the chronic Epstein-Barr Virus Syndrome: “We propose a new name for the chronic Epstein-Barr virus syndrome – the chronic fatigue syndrome” (EBV being one of the herpes family of viruses seen in mononucleosis, not one of the enteroviruses more commonly seen in ME).

    Holmes et al also stated that their case definition described “a possibly unique clinical entity”, but how could such a description apply to ME, given that ME had been documented in the medical literature since at least the 1930s and had been formally classified as a neurological disorder in the International Classification of Diseases since 1969 and had been recognised as a nosological entity in 1978 by the UK Royal Society of Medicine?

    Further, the listed symptoms of the newly-defined “CFS” included fever; sore throat; painful lymph nodes; generalised muscle weakness; myalgia; sleep disturbance; headaches; depression; decreased memory and prolonged generalised fatigue after exercise, all of which might result from EBV infection. In other words, the symptoms were those seen in a typical (and commonly transient) post-viral state that were usually of little consequence.

    Was the over-riding intention to deflect medical and scientific attention away from the world-wide explosion of the devastating and chronic disorder ME and to create a “new” disorder called “CFS” that was of considerably lesser significance and impact, and therefore of less financial consequence for the CDC and the insurance industry?

    In the 1988 “CFS” definition, no mention was made of the fact that in ME, there is a sub-normal temperature (not fever), nor of the additional signs and symptoms that define ME (for example, difficulty in standing and walking; neuro-muscular incoordination; vertigo and balance problems with observable nystagmus; abnormal reflexes; blurred vision; frequency of micturition and other evidence of autonomic instability; fasciculation; marked tremor; difficulty swallowing; hair loss; respiratory, cardiac and vascular problems; pancreatic problems; liver involvement; bowel problems including explosive diarrhoea; increased allergies and hypersensitivities; marked variability of symptoms; sensory storms, and the cardinal symptom of angor animi – a feeling of imminent death).

    A further notable difference is that patients who develop CFS following EBV may succumb to every opportunistic infection and sore throat doing the rounds, whereas those with ME rarely, if ever, get a sore throat or common cold (as noted in the literature on ME, as well as in patients’ own accounts).

    Of interest is that in November 2006, the CDC “CFS Toolkit” launch noted that there are two distinct types of “CFS”, one with rapid post-viral onset and the other with a gradual onset and – significantly -- that the two types appear to differ genetically.

    The question therefore arises as to what disorder the 1988 “new” case definition was defining if, according to the ME experts, it was not ME?

    The alternative question is whether the key features of ME were deliberately omitted in order to portray “CFS” as a less serious (and therefore less expensive) disorder?

    It seems that in 1988, ME was considered to be a physical disease that was henceforth to be renamed “CFS”, but whether this in fact occurred (or whether a different entity from ME was created) is open to conjecture.


    In 1991, the much-criticised “Oxford” case definition appeared, having been compiled by psychiatrists Michael Sharpe, Peter White and Simon Wessely, amongst others (A report – chronic fatigue syndrome: guidelines for research. MC Sharpe et al. JRSM 1991:84:118-121). This report makes it clear that Holmes et al were indeed referring to ME in their 1988 case definition of “CFS”. However, the 1991 criteria state that the authors were looking at patients “with a principal complaint of disabling fatigue” and that “the aim of the meeting was to seek agreement amongst research workers for future studies of patients with chronic fatigue”. As in the 1988 case definition of “CFS”, the key symptomatology of ME was missing, yet Sharpe et al claimed to be including “ME” in their definition. How could they be looking at ME when the cardinal features were specifically excluded from their definition? (It is this 1991 “Oxford” definition that NICE relies upon in its Draft Guideline for “CFS/ME”).

    It is important to remember that Wessely School psychiatrists’ on-the-record goal is to consider all cases of “chronic fatigue” -- from whatever source -- under one umbrella, because they want to determine the role of “fatigue” in psychiatric disorders.

    In this respect, why are patients with ME so relentlessly targeted for psychotherapy as the management regime of choice, when patients with leukaemia or multiple sclerosis (both of which cause fatigue) are not so targeted and admonished that they must “exercise back to fitness”?

    It is also important to recall that Wessely’s cherished aim has long been to “eradicate” ME as a distinct entity: if a disorder does not officially exist, then no-one can suffer from it and there would be no need for expensive provision for it and benefits need not be paid for it. This also seems to have been his modus operandi in the case of Gulf War Syndrome.


    In July 1992 the WHO published the tenth revision of the International Classification of Diseases (ICD-10), in which an alternative term for ME was listed as “CFS”, which subsequently gave rise to the term “ME/CFS”.

    Also in 1992, the US Physicians’ Handbook published by the National Institutes of Health (NIH) stated: “CFS does not appear to be a new disorder. Epidemics (most often called myalgic encephalomyelitis or ME) have been described in the medical literature for at least 60 years”.


    During one of the meetings at which the 1994 CDC revised definition of “CFS” was formulated, in response to a direct question from a physician who was present, Dr Keiji Fukuda (not an ME expert, but lead author of the CDC 1994 definition) stated that the numerous ME epidemics, including the one at the Royal Free Hospital in London in 1955, were definitely not CFS. As in the CDC 1988 case definition, the CDC 1994 revised case definition makes no mention of ME or of its key signs and symptomatology. Instead it emphasises that the exclusion of persons with psychiatric disorders including depression and anxiety “would substantially hinder efforts to clarify the role that psychiatric disorders have in fatiguing illnesses”, adding for good measure that “chronic fatigue cases preceded by some, but not all, psychiatric syndromes can be classified as the chronic fatigue syndrome”. Of significance is the fact that the 1994 CDC revised criteria for “CFS” state unequivocally: “We dropped all physical signs from our inclusion criteria. Whether to retain any symptom other than chronic fatigue generated the most disagreement among the authors”. Thus it seems beyond doubt that ME was not included within the compass of the 1994 CDC revised case definition of “CFS”, no matter what Sharpe (one of the 1994 authors), Wessely, White et al claimed in 1991 (and subsequently). It is, however, this definition that has been used in research that has revealed the major pathology that underlies (ME)CFS.

    Why therefore does the ME community use the composite term “ME/CFS”? For two reasons: firstly because the WHO ICD states that they are the same disorder and secondly because the international research literature makes little mention of “ME”, thus to refuse to use the term “CFS” would exclude the major research literature spanning the last two decades.

    So – in 1988, ME was not the same disorder as CFS (because the ME experts said so), but in 1991 and 1992 (according to Wessely School psychiatrists, the WHO and the NIH), ME was the same disorder as CFS, yet in 1994, according to Fukuda, ME was not the same disorder as CFS (even though Wessely School psychiatrists continue to claim that it is).

    In other words, CFS was not ME when ME was deemed to be a physical disorder, but as soon as ME came to be considered a psychiatric disorder (by Wessely School psychiatrists), suddenly CFS was ME after all.

    Given this conundrum, for what disorder is NICE producing its Guideline?

    On what rational grounds does NICE refuse to accept the advancement of medical science and take as its starting point the Canadian case definition (Carruthers, Klimas et al 2003) that incorporates the cardinal features of authentic ME with the international biomedical research on “CFS” into a composite entity?

    Confusion over case definition has resulted in confusion over the safety of management regimes

    The NICE Draft Guideline for “CFS/ME” is clear that the only recommended interventions are cognitive behavioural therapy, graded (aerobic) exercise and “activity management”.

    Is it safe for people with authentic ME to engage in graded exercise?

    In a submission to NICE on behalf of the UK 25%ME Group for the Severely Affected, mention was made of the 5th edition (2002, reprinted 2004) of a medical textbook that is likely to be on the desk of every GP in the country (having won the “Highly Commended” BMA Award) and to the fact that it contained statements about ME by psychiatrists Peter White and Anthony Clare that are insupportable. The 6th edition (2005) of the same medical textbook is equally inaccurate. Within the section on CFS (in Functional or Psychosomatic Disorders starting on page 1281), White and Clare talk about “dysfunctional beliefs and behaviours” and refer to the “management of functional disorders” as being “rehabilitative therapy” which includes CBT (to “challenge unhelpful beliefs and coping strategies”) and they recommend three months’ GET “to reduce inactivity and improve fitness”.

    This is in line with the NICE draft recommendations about aerobic exercise and also with the NHS Plus Policy Document of October 2006 concerning the occupational aspects of CFS that reflect the Wessely School psychiatrists’ strongly-held beliefs.

    However, Dr Derek Enlander MD (a former virologist who specialises in ME/CFS, previously Assistant Professor at Columbia University and then Associate Director of Nuclear Medicine at New York University; currently Physician-in-Waiting to the Royal Family and to members of HM Government when they visit New York) is on record about aerobic exercise for patients with ME/CFS: “I do not want my patients in an aerobic class. I feel this causes considerable damage to (ME)CFS patients”.
    (Derek Enlander: Update on the Treatment of Chronic Fatigue Syndrome and Fibromyalgia, 8th November 2006).

    Equally, Dr Paul Cheney, who has been studying the disorder since the Lake Tahoe outbreak in 1984, is adamant that such patients should not engage in aerobic exercise: indeed they are unable do so, because the lack of energy generation results in low cardiac output that is not equal to the metabolic demand created by aerobic exercise. (For further information on Cheney’s evidence, see

    http://www.meactionuk.org.uk/Klimas_Wessely_and_NICE_-_Redefining_CBT.htm ).

    The Canadian Guidelines are unequivocal: graded exercise showed the highest negative rating of all management interventions: “The question arises whether a formal CBT or GET programme adds anything to what is available in the ordinary medical setting. A well-informed physician helps (the patient) achieve optimal exercise and activity levels within their limits in a common-sense, non-ideological manner which is not tied to deadlines or other hidden agenda” (ME/CFS: Clinical Working Case Definition, Diagnosis and Treatment Protocols. Bruce M Carruthers, Kenny L De Meirleir, Nancy G Klimas et al. JCFS 2003:11:1:7-115).

    Moreover, the CDC “CFS Toolkit” released at the beginning of November 2006 is equally clear: “This kind of exercise (aerobic) can precipitate a full-scale relapse that lasts for weeks or months”.

    It is already known that ME/CFS experts agree that aerobic exercise can cause serious relapse and that it can be dangerous to the extent that it could be life-threatening for some such patients.

    CBT/GET is already known not to be effective.

    CBT/GET has already been shown to have no lasting benefit.

    CBT/GET is already known to be very expensive.

    It is already known that, logistically, CBT/GET cannot be delivered without recruiting, training and supervising many more therapists at vast expense.

    It is therefore a misuse of funds that could – and should – be better spent on biomedical research.

    Why, therefore, is NICE continuing to pay no heed to the evidence and to recommend CBT/GET as the only management regime for those with “CFS/ME”?

    Is it because NICE is taking advice from only one source ie. from the Wessely School, whose members are, on their own admission, heavily engaged in social engineering and to which they are so committed? (see “Biopsychosocial Medicine: An integrated approach to understanding illness” edited by Peter White; OUP 2005; chapter 12).

    It is such social engineering that turns an inadequate evidence-base into canonised Government policy.

    Is this social engineering taking place because the truth is not to be tolerated under any circumstances (the truth being contained in a memo sent on 17th November 2006 from the Director of the US CDC, Dr Julie Gerberding, to CDC staff: “When we launched the national CFS awareness campaign this month, we demonstrated credible evidence of a genomic and an environmental basis for this condition”.

    In other words, ME/CFS is environmentally acquired. Why is no research permitted in the UK into the “environmental basis” of the condition, but only denial of its very existence?

    Already there is evidence that patients are suffering as a direct result of the NICE Draft Guideline: Professor Leslie Findley from the Essex Neurosciences Unit at Romford has confirmed that in this last week, two Primary Care Trusts have altered, or turned down, treatment for patients with ME/CFS on the basis of the content of the Draft Guideline and asks that people should be made aware that the Draft Guideline is currently being misused.

    At the All Party Parliamentary Group on ME held at Westminster on 16th November 2006, a representative from NICE was instructed by the APPG Chairman (Dr Des Turner MP) to report back to NICE that NICE would be very unwise to publish its Draft Guideline on “CFS/ME” as it stands, and that Turner was at a loss to know why NICE was doing this and also about what NICE hoped to achieve by it. Sir Michael Rawlins, Chairman of NICE, was to be invited to attend the next APPGME.

    For a brief comparison of the difference in the UK and the US about the validity and reality of ME/CFS, the following quotations are taken from the Press Conference held on 3rd November 2006 at the launch of the CDC “CFS Toolkit”:

    Dr Julie Gerberding, Director of the US CDC:

    “One of the things that CDC hopes to do is to help patients know that they have an illness that requires medical attention, but also to help clinicians be able to understand, diagnose and help people with the illness. But more importantly, to be able to validate and understand the incredible suffering that many patients and their families experience in this context”.

    “I have heard from hundreds and hundreds of people who are telling their stories – their courage, their commitment to try to live the best possible life they can (and) the tremendous impact that this is having on their ability to function”.

    “We are committed to improving the awareness that this is a real illness and that people need real medical care and they deserve the best possible help that we can provide”.

    “The science has progressed (which has) helped us define the magnitude and understand better the clinical manifestations (and this has) led to a sorely needed foundation for the recognition of the underlying biological aspects of the illness. We need to respect and make that science more visible”.

    Dr William Reeves, Chief of Chronic Viral Diseases Branch at CDC:

    “We’ve documented the prevalence of (ME)CFS – the illness affects at least a million Americans”.

    “(ME)CFS is responsible for an impact of about $9.1 billion annually in lost earnings”.

    “We’ve documented, as have others, that the level of impairment in people who suffer from (ME)CFS is comparable to multiple sclerosis, AIDS, end-stage renal failure, chronic obstructive pulmonary disease. The disability is equivalent to that of some well-known, very severe medical conditions”.

    “We found that (ME)CFS follows a pattern of remitting and relapsing symptoms, the symptoms can change over time, and that spontaneous recovery is rare”.

    “We found that the best predictor for (ME)CFS was intensity of the initial infectious disease. The sicker the patient when s/he first got infected, the more likely they were to have persisting chronic symptoms. There were no other factors, psychological or biological, that held up under thorough analysis”.

    Professor Anthony Komaroff of the Harvard Medical School:

    “There are now over 4,000 published studies that show underlying biological abnormalities in patients with this illness. It’s not an illness that people can simply imagine that they have and it’s not a psychological illness. In my view, that debate, which was waged for 20 years, should now be over”.

    “A whole bunch of studies show that the hormone system is different in patients with (ME)CFS than in healthy people, people with depression and other diseases”.

    “Brain imaging studies have shown inflammation, reduced blood flow and impaired cellular function in different locations of the brain”.

    “Many studies have found that the immune system appears to be in a state of chronic activation (and) genes that control the activation of the immune system are abnormally expressed in patients with this illness”.

    “A number of studies have shown that there probably are abnormalities of energy metabolism in patients with this illness”.

    During the Question and Answer session, the question was asked: “You’ve cited quite a bit of research that validates that (ME)CFS is actually a real disease. Why is there still such a level of scepticism in the medical community? Is it simply a lack of awareness among health professionals?”

    Komaroff replied: “There are an awful lot of sceptics I’ve met who really just haven’t read the research literature (and) don’t even know there are 4,000 peer-reviewed published papers out there. I think that’s probably the biggest factor, combined with the fact that those people took a stand early on as to what they believe and have been reluctant to back off in the face of the evidence that they’ve not made themselves aware of”.

    Professor Nancy Klimas, Professor of Medicine, University of Miami:

    “I’ve treated over 2,000 (ME)CFS patients. I’ve seen patients (who) were angry, frustrated, trying to convince their physicians, their families, their friends that this is a real illness. I’ve seen other patients (who) hid their diagnosis because of the stigma attached and suffered in silence. It’s been the lack of credibility in this illness that has been one of the major stumbling blocks to making progress”.

    “Today, there is evidence of the biological underpinnings. And there’s evidence that the patients with this illness experience a level of disability that’s equal to that of patients with late-stage AIDS, patients undergoing chemotherapy, patients with multiple sclerosis. And that has certainly given it a level of credibility that should be easily understood”.

    “I’m less enthusiastic about the advances in the clinical care of patients”.

    “We need disability insurance carriers to believe this is an illness – a disabling illness and do what they should do, and pay our patients when they are disabled”.

    “There are diagnostic criteria that enable clinicians to diagnose (ME)CFS in the primary care setting”.

    “Key to the effective management of illness is the effective partnership with the patient and the physician. It’s also important for patients to take a proactive role and become informed and seek appropriate care to manage the illness and its impact on their lives”.

    “I call on my colleagues in the medical profession to treat (ME)CFS patients with the kind of respect and compassion necessary to make this first step”.

    The full Press Conference transcript is available at

    Whatever the motives or mistakes in the past, it is apparent that whatever it is called, ME/CFS can no longer be regarded as a behavioural disorder as the Wessely School has insisted for the last two decades.

    It might be wondered what will be the reaction of Wessely, White, Sharpe et al to know that it has been publicly recognised that from their irrefutable published record (although not named personally), they must be included amongst those responsible for the debate that was waged for twenty years against severely physically – and not mentally – sick people, a debate that has both caused and prolonged incalculable suffering and which, despite all the contrary evidence, Wessely et al are still endeavouring to promote under the auspices of NICE, Government Policy Documents and textbooks of medicine.


  9. cherylsue

    cherylsue Member

    bumping to read thoroughly later

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