ME Exists: True or False?

Discussion in 'Fibromyalgia Main Forum' started by tansy, Aug 20, 2006.

  1. tansy

    tansy New Member

    Permission to Repost

    http://www.meactionuk.org.uk/ME_Exists_-_True_or_False.htm

    ME Exists: True or False?

    Eileen Marshall
    Margaret Williams
    18th August 2006

    "If you repeat something often enough, you can perhaps make people believe it. What you cannot do is turn it from being false into being true".

    This well-known adage was quoted by Robert Rowthorn in the Sunday Telegraph
    on 2nd July 2006 in an article exposing as false yet another claim by the UK
    Blair Government.

    This adage being true, it ought to be the case that no matter how often the
    psychiatric and medical insurance lobbies (and the Governments with whom
    they connive) continue to deny the published scientific evidence about
    ME/CFS and to promote their own model of behavioural illness, their doctrine
    remains false.

    And false it certainly is: experienced biomedical researchers regard ME/CFS
    as a multi-system autoimmune overlap disorder, not a mental disorder, and
    give it its place between lupus, diabetes type 1 and MS, referring to it as
    "AFS" which stands for autoimmune fatigue syndrome (see also Chronic Fatigue
    Syndrome: A Biological Approach edited by Patrick Englebienne and Kenny de
    Meirleir; pp 291; CRC Press 2002).

    False though the psychiatric paradigm about the nature of ME/CFS is, it
    nevertheless pervades and indoctrinates all levels of society, especially
    medicine, social services, the judiciary and, in recent years, some of the
    ME/CFS patients' support charities in the UK, with knock-on effects on
    sufferers and their families.

    The recent campaign by Action for ME (AfME)
    to engage Members of Parliament in a candle-lit vigil to save the Government
    "CFS" Centres by securing more funding for those Centres would seem to be a
    case in point, given that the Centres support the psychiatric fallacy about
    the nature of ME/CFS by imposing compulsory and often inappropriate
    behavioural modification strategies such as cognitive behavioural therapy
    and graded exercise regimes, even though the evidence continues to mount
    that these Centres are causing actual harm to unknown numbers of those they
    are supposed to be supporting (see Research into ME [RiME] information on
    Co-Cure, 18th August 2006: "RiME latest - NHS Clinics Condemned - Part 4"
    and see also www.erythos.com/RiME ).

    As solicitor John Batt wrote in The Times Law Section on 11th July 2006:
    "False allegation ruins lives..doctors are always hostage to the knowledge
    that lurks in the future.it is not the legal system that is causing
    miscarriages of justice; it is medical opinions that are not as sound as
    they appear to be. If (a doctor) cannot back (his) opinion with research
    and laboratory results, the judge should openly rule that the opinion may be
    worthless. He should not allow statements like: 'this theory is
    well-established' or 'doctors have known this for years' ".

    Where is the evidence that supports allegations by these "Wessely School"
    psychiatrists (some of whom act as Government advisors and others as
    advisors to the medical insurance industry) that people benefit from
    "adopting the sick-role" conferred by a label of ME/CFS? There is no such
    evidence. There is, however, abundant published evidence of the extensive
    losses, loneliness and extreme suffering endured by those with ME/CFS, as
    well as plentiful evidence of the extra burden forced on them in their fight
    for survival, both medical and financial.

    Why is the existing evidence of biomedical anomalies in ME/CFS continually
    ignored by "Wessely School" psychiatrists, who claim that the only disorders
    that they will "accept" are those supported by "evidence-based" medicine?
    And yet their "de-conditioning" model of ME/CFS is not evidence-based, nor
    can it ever be so: it is a hypothesis that cannot be tested, let alone
    proven, which contrasts with the biomedical model of ME/CFS that is
    supported by respected literature of solid scientific evidence.

    The psychiatrists involved with ME/CFS, however, have assumed control of
    the ME/CFS situation and they continue to reject the substantial biomedical
    evidence of serious organic pathology despite the fact that their own
    assumptions about ME/CFS have never been validated. The reaction of the UK
    authorities to the "Wessely School" view of ME/CFS seems grotesquely to
    reflect the South African government's view of AIDS, ie. it can be cured by
    garlic and lemon juice.

    Is it because of the far-ranging influence of "Wessely School" psychiatrists
    that there was such deceit and misappropriation of funds surrounding ME/CFS
    biomedical research in the US?

    Is it because of the influence of "Wessely School" psychiatrists that
    funding applications to the UK MRC for biomedical research projects in
    ME/CFS are rejected in favour of massive and repeated funding for those
    psychiatrists? It is certainly true that Wessely et al have made ME/CFS
    unfashionable to the elite scientific community, who now see ME/CFS as a
    behavioural illness.

    Is it because of the influence of "Wessely School" psychiatrsists that both
    the UK Government and the US Centres for Disease Control (CDC) continue to
    deny appropriate and necessary investigations for those with ME/CFS? For
    example, as in the UK, the CDC continues to deny the need for SPECT scans
    that researchers have shown to be diagnostic in ME/CFS: "Some (ME)CFS
    researchers have observed apparent differences in the cranial blood flow
    between patients and controls (but) imaging tests should not be performed as
    a diagnostic technique for (ME)CFS" (see the post on 17th August 2006 on
    Co-Cure by Stephen Du Pre: "CDC's Continued State of Denial about ME/CFS").

    It was in 1995 that nuclear imaging expert Dr Durval Costa published his
    brain-stem SPECT imaging paper which clearly demonstrated highly significant
    patterns of hypo-perfusion in ME/CFS patients that were not evident in those
    with major depression or in age and gender matched controls. Despite
    countless requests for referrals to him by desperate patients, these were
    consistently thwarted by NHS consultants working in "CFS" clinics, including
    to our certain knowledge by Professor Tony Pinching (then at St Bartholomew's
    Hospital in London, now medical adviser to AfME) who refused outright to
    allow such referrals.

    Costa eventually gave up in the UK and moved to
    Portugal, where he is now Professor of Nuclear Medicine.

    Why have these important findings been buried for the last eleven years?
    If the psychiatric lobby is 100% convinced that they, and they alone, are
    right that ME/CFS is not a serious multi-system organic disorder, why are
    they so opposed to biomedical research that, according to their own beliefs,
    would be negative, thus proving them to be right after all? Or is it simply
    that the psychiatrists want all the available research money for themselves?

    It is a problem that is unlikely to be solved until there is a workable case
    definition against which patients need to be clinically examined and
    categorised correctly, and the establishing of such a case definition is the
    key to this whole argument.

    Why do "Wessely School" psychiatrists not encourage research into the
    underlying cause of ME/CFS as any true scientist would? Why instead do they
    deny and denigrate instead of investigating and supporting patients? It is
    worth recalling that before the existence of diagnostic tests like MRI in MS
    and EEG in epilepsy and the discovery of dopaminergic pathways in
    Parkinsons, sufferers from these disorders were treated abysmally, so the
    diversion of funds for research that would address the aetiology of ME/CFS
    has historical precedence.

    Is the refusal to fund biomedical research simply a case of wishing to
    curtail care costs and of protecting insurance company profits, or could it
    be that those who are unproductive but expensive to the State economy are
    expediently regarded as "useless eaters"? Many will be familiar with the
    book by Martha Gellhorn entitled "The Face of War" (first published in 1959
    and re-published by Virago Press in 1986) about the Nuremberg Trials and the
    fact that the Nazis actually killed 275,000 of their own people who were
    old, feeble-minded or incurably ill, describing them as "useless eaters".

    If it is not a case of those with ME/CFS being "useless eaters", is the
    unthinkable possible, namely that the remarkable (and documented) increase
    worldwide in incidence and prevalence of ME/CFS is in some way related to a
    bio-warfare agent such as borreliosis? The diagnostic picture would then be
    complicated by the overlap with diseases such as borreliosis, whose myriad
    symptoms are almost indistinguishable from ME/CFS.

    Why, for example, was Elena Cook (the pseudonym adopted of necessity by the
    woman who was instrumental in organising the demonstration on 25th January
    2006 outside Gresham College in London at Professor Simon Wessely's lecture
    on the non-existence of Gulf War Syndrome) subsequently arrested and
    sectioned under the Mental Health Act, having received threats to her life
    and family? (see Co-Cure ACT: 17th July 2006: "Release of anti-Wessely
    lobbyist and lyme disease researcher from psychiatric detention [UK]". Her
    statement about her arrest can be seen at
    http://www.lyme-rage.info/elena/statejun06.html).

    Could this have had anything to do with Wessely's known association with the
    US military or with the exposure of the apparent confirmation by the CDC
    that lyme borreliosis is indeed a biowarfare agent?

    (see "US Government Admits Lyme Disease is a Bioweapon" online at
    http://www.indymedia.org.uk/en/2005/11/328067.html and see also "Borreliosis
    / Lyme & M.E. in the United Kingdom" at
    http://www.mesupport.bigstep.com/generic215.html ).

    As noted by Aaron and Buchwald et al (J Gen Intern Med 2001:16(1):24-31), it
    is the case that chronically fatiguing illnesses are associated with high
    rates of many other clinical conditions that cannot be attributed solely to
    psychiatric illness, and that patients with fatiguing illnesses may present
    a complex clinical picture that poses diagnostic and management challenges.
    However, whilst they would not be included in a case definition, the
    following abnormalities have been regularly documented in patients with
    ME/CFS: whilst the direction of causality of the high burden of co-morbidity
    remains unproven, such co-morbidity gives the lie to the psychiatrists'
    too-facile assertion that the greater the number of somatic symptoms, the
    greater the likelihood of somatoform illness.

    Whilst correlation does not imply causality, it remains beyond reason that
    the existence of so many documented abnormalities in people with ME/CFS
    should simply be disregarded and denied, including the following:


    * abnormalities of the central nervous system include abnormalities of brain
    cognition, brain perfusion, brain metabolism and brain chemistry; there is
    evidence of low blood flow in multiple areas of the brain; neuro-imaging has
    revealed lesions in the brain of approximately 80% of those tested and
    according to the researchers, these lesions are probably caused by
    inflammation: there is a correlation between the areas involved and the
    symptoms experienced; abnormalities on SPECT scans provide objective
    evidence of central nervous system dysfunction; there is evidence of a
    chronic inflammatory process of the CNS, with oedema or demyelination in 78%
    of patients tested; there is evidence of a significant and irreversible
    reduction in grey matter volume (especially in Brodmann's area 9) which is
    related to physical impairment and may indicate major trauma to the brain
    (which could also explain the low recovery rate); there is evidence of
    seizures; a positive Romberg is frequently seen in authentic ME/CFS patients

    * abnormalities of the autonomic and peripheral nervous systems: there is
    evidence of dysautonomia in ME/CFS patients - see "Standing up for ME" by
    Spence and Stewart: Biologist 2004:51(2):65-70; according to Goldstein,
    ME/CFS represents the final common pathway for a multi-factorial disorder
    causing autonomic dysfunction

    * cardiovascular dysfunction: there is evidence of haemodynamic instability
    and aberrations of cardiovascular reactivity (an expression of autonomic
    function); there is evidence of diastolic cardiomyopathy; there is evidence
    of endothelial dysfunction; there is evidence of peripheral vascular
    dysfunction with low oxygenation levels and poor perfusion and
    pulsatilities; there is evidence of abnormal heart rate variability and
    evidence of abnormal orthostasis; there is evidence of abnormally inverted
    T-waves and of a shortened QT interval, with electrophysiological aberrancy;
    there is evidence of abnormal oscillating T-waves and of abnormal cardiac
    wall motion (at rest and on stress); there are indications of dilatation of
    the left ventricle and of segmental wall motion abnormalities; there is
    evidence that the left ventricle ejection fraction - at rest and with
    exercise - is as low as 30%; there is evidence of reduced stroke volume

    * respiratory system dysfunction: there is evidence of significant reduction
    in many lung function parameters including a significant decrease in vital
    capacity; there is evidence of bronchial hyper-responsiveness

    * a disrupted immune system: there is evidence of an unusual and
    inappropriate immune response: there is evidence of very low levels of NK
    cell cytotoxicty; there is evidence of low levels of autoantibodies
    (especially antinuclear and smooth muscle); there is evidence of
    abnormalities of immunoglobulins, especially SIgA and IgG3, (the latter
    having a known linkage with gastrointestinal tract disorders); there is
    evidence of circulating immune complexes; there is evidence of a Th1 to Th2
    cytokine shift; there is evidence of abnormally diminished levels of
    intracellular perforin; there is evidence of abnormal levels of interferons
    and interleukins; there is evidence of increased white blood cell
    apoptosis, and there is evidence of the indisputable existence of allergies
    and hypersensitivities and positive mast cells, among many other anomalies,
    with an adverse reaction to pharmacological substances being virtually
    pathognomonic

    * virological abnormalities: there is evidence of persistent enterovirus RNA
    in ME/CFS patients; there is evidence of abnormalities in the 2-5
    synthetase / RNase L antiviral pathway, with novel evidence of a 37 kDa
    binding protein not reported in healthy subjects or in other diseases; there
    is evidence of reverse transcriptase, an enzyme produced by retrovirus
    activity, with retroviruses being the most powerful producers of interferon;
    there is evidence of the presence of HHV-6, HHV-8, EBV, CMV, Mycoplasma
    species, Chlamydia species and Coxsackie virus in the spinal fluid of some
    ME/CFS patients, the authors commenting that it was surprising to find such
    a high yield of infectious agents on cell free specimens of spinal fluid
    that had not been centrifuged

    * evidence of muscle pathology: this includes laboratory evidence of delayed
    muscle recovery from fatiguing exercise and evidence of damage to muscle
    tissue; there is evidence of impaired aerobic muscle metabolism; there is
    evidence of impaired oxygen delivery to muscle, with recovery rates for
    oxygen saturation being 60% lower than in normal controls; there is
    evidence of prolonged EMG jitter in 80% of ME/CFS patients tested; there is
    evidence of greater utilisation of energy stores; there is evidence that
    total body potassium (TBK) is significantly lower in ME/CFS patients (and
    abnormal potassium handling by muscle in the context of low overall body
    potassium may contribute to muscle fatigue in ME/CFS); there is evidence
    that creatine (a sensitive marker of muscle inflammation) is excreted in
    significant amounts in the urine of ME/CFS patients, as well as choline and
    glycine; there is evidence of type II fibre predominance, of scattered
    muscle fibre necrosis and of mitochondrial abnormalities

    * neuroendocrine abnormalities: there is evidence of HPA axis dysfunction,
    with all the concomitant implications; there is evidence of abnormality of
    adrenal function, with the size of the glands being reduced by 50% in some
    cases; there is evidence of low pancreatic exocrine function; there is
    evidence of an abnormal response to buspirone challenge, with a significant
    increase in prolactin release that is not found in healthy controls or in
    depressives; there is evidence of abnormal arginine - vasopressin release
    during standard water-loading test; there is evidence of a profound loss of
    growth hormone; even when the patient is euthyroid on basic screening, there
    may be thyroid antibodies and evidence of failure to convert T4 (thyroxine)
    to T3 (tri-iodothyronine), which in turn is dependant upon the liver enzymes
    glutathione peroxidase and iodothyronine deiodinase, which are dependant
    upon adequate selenium in the form of selenocysteine (which may be
    inactivated by environmental toxins)

    * defects in gene expression profiling: there is evidence of reproducible
    alterations in gene regulation, with an expression profile grouped
    according to immune, neuronal, mitochondrial and other functions, the
    neuronal component being associated with CNS hypomyelination

    * abnormalities in HLA antigen expression: Teraski from UCLA found evidence
    that 46% of ME/CFS patients tested were HLA-DR4 positive, suggesting an
    antigen presentation

    * disturbances in oxidative stress levels: there is mounting evidence that
    oxidative stress and lipid peroxidation contribute to the disease process in
    ME/CFS: circulating in the bloodstream are free radicals which if not
    neutralised can cause damage to the cells of the body, a process called
    oxidative stress: in ME/CFS there is evidence of increased oxidative stress
    and of a novel finding of increased isoprostanes not seen in any other
    disorder; these raised levels of isoprostanes precisely correlate with
    patients' symptoms (isoprostanes being abnormal prostaglandin metabolites
    that are highly noxious by-products of the abnormal cell membrane
    metabolism); there is evidence that incremental exercise challenge (as in
    graded exercise regimes) induces a prolonged and accentuated oxidative
    stress; there is evidence of low GSH-PX (glutathione peroxidase, an enzyme
    that is part of the antioxidant pathway: if defective, it causes leakage of
    magnesium and potassium from cells)

    * gastro-intestinal dysfunction: there is evidence of objective changes,
    with delays in gastric emptying and abnormalities of gut motility; there is
    evidence of swallowing difficulties and nocturnal diarrhoea; there is
    evidence going back to 1977 of hepatomegaly, with fatty infiltrates: on
    administration of the copper response test, there is evidence of post-viral
    liver impairment -- an increase of at least 200 in the copper level is the
    expected response, but in some severely affected ME/CFS patients the
    response is zero; there is evidence of infiltration of splenic sinuses by
    atypical lymphoid cells, with reduction in white pulp, suggesting a chronic
    inflammatory process

    * reproductive system: there is clinical evidence that some female patients
    have an autoimmune oophoritis; there is evidence of endometriosis; there is
    evidence of polycystic ovary syndrome; in men with ME/CFS, prostatitis is
    not uncommon

    * visual dysfunction: there is evidence of latency in accommodation, of
    reduced range of accommodation and of decreased range of duction (ME
    patients being down to 60% of the full range of eye mobility); there is
    evidence of nystagmus; there is evidence of reduced tracking; there is
    evidence of problems with peripheral vision; there is evidence that the
    ocular system is very much affected by, and in turn affects, this systemic
    condition.


    The above list is by no means comprehensive but merely gives an overview of
    documented abnormalities seen in ME/CFS that can be accessed in the
    literature, as well as in the abstracts and reports of international
    Clinical and Research Conferences. Unfortunately not all are on MedLine. It
    is our intention to provide, with others, a comprehensive list of references
    for an article discussing the above abnormalities in ME/CFS to be submitted
    for publication.

    By contrast, there is no credible evidence --- as distinct from belief and
    assertion --- of abnormal illness behaviour in authentic ME/CFS.

    It is not known if, during the various stages of ME/CFS described by Cheney
    (for which see http://www.meactionuk.org.uk/consideration.htm ) all
    patients with ME/CFS exhibit all the above mentioned abnormalities: this is
    unlikely to be known due to the prevailing dictum by dominant UK
    psychiatrists and their associates that it is neither "necessary nor
    appropriate" to investigate such patients other than by minimal screening
    (and if you don't look, you certainly don't find).

    Instead, the UK policy is to compulsorily brain-wash those with ME/CFS into
    changing their rational belief that they are organically sick into the
    irrational belief that, once they "modify" their thinking, they are fit to
    work and to look after themselves.

    Moreover, not only are no appropriate investigations to be performed on
    patients with ME/CFS, but those few NHS physicians who possess the integrity
    and courage to act in ME/CFS patients' best interests and who go out of
    their way to help them are pilloried by their colleagues and in some
    instances are subjected to "disciplinary" proceedings following complaints
    to the General Medical Council by other doctors with known allegiance to the
    pharmaceutical and medical insurance industries; some have been threatened;
    some have been warned off, and some have had their licence to practice
    medicine restricted, with the possibility of their being struck off the
    medical register being very real. Some have been forced to resign; others
    have had their NHS clinics closed down, with their patients being
    transferred to psychiatrists.

    It seems that the powerful vested interests groups who now control the
    Establishment will tolerate no opposition, with the result that NHS doctors'
    freedom to practice medicine is increasingly proscribed.

    With no hope of funding to establish a diagnostic test and with no will by
    the Royal Colleges or Government to formulate or accept an accurate case
    definition, the situation relating to ME/CFS in the UK cannot improve.

    So many abnormalities have now been shown to occur regularly in cases of
    authentic ME/CFS that it is not only bad science to attempt to dismiss,
    ignore or deny a reality that can be scientifically measured, but to
    continue to do so must, as others have noted, border on the criminal. [This Message was Edited on 08/20/2006]
  2. Tantallon

    Tantallon New Member

    One day, hopefully soon, "The Wessley School of Thought" will be shown for what it is, and as I'm too polite to go into more detail I shall end there.

    Sue
  3. tansy

    tansy New Member

    CBT in ME/CFS -- More Information

    Eileen Marshall
    Margaret Williams
    23rd August 2006

    In our document “ME Exists: True or False?” (see Co-Cure ACT: 20th August 2006) we drew attention to recognised abnormalities in ME/CFS, one of which being the significant loss of grey matter in the brain with irreversible loss of grey cells, especially in Brodmann’s area 9, and mentioned that this may indicate major trauma to the brain.

    If such trauma to the brain exists in ME/CFS, then the chance of cognitive behavioural therapy (CBT) being effective in ME/CFS is probably zero and the MRC PACE trials may be a disaster for the psychiatric lobby.

    The ME/CFS community may be interested in an article by Richard A Friedman MD in the New York Times on 27th August 2002 entitled “Behaviour: Like Drugs, Talk Therapy Can Change Brain Chemistry”.

    To quote Friedman: “New evidence suggests that the talking cure and psychotropic medication have much more in common than had been thought. In fact, both produce surprisingly similar changes in the brain”.

    Friedman refers to three brain imaging studies, one looking at obsessive–compulsive disorder and the other two other at depression, all of which showed that when patients improved, the changes in their brain, as shown on PET scans, looked the same regardless of whether they had received antidepressants or CBT.

    Quoting Friedman again: “Does that mean that antidepressants and psychotherapy are really equivalent? In a word, no”.

    Significantly Friedman (a psychiatrist who directs the Psychopharmacology Clinic at the New York Weill Cornell Medical Centre) then states: “Psychotherapy alone has been largely ineffective for diseases where there is strong evidence of structural, as well as functional, brain abnormalities. It seems that if the brain is severely disordered, then talk therapy cannot alter it”.

    As there are structural brain abnormalities documented in the ME/CFS literature since at least 1992 and as the data discussed by Friedman was known about in 2002 (the same year that the UK CMO’s Working Group Report was published), then it must be asked why this knowledge has been disregarded by the psychiatric lobby, and by the MRC who has granted such generous funding to those psychiatrists to allow them to indulge their belief that CBT is the only effective management (not treatment) regime for ME/CFS.

    As it is known that CBT cannot help those with a severely disordered brain, other acknowledged concerns about CBT assume even more importance, one being the increasing public concern that psychological therapies could be used for brain-washing (see the MRC Neuroethics Report, April 2005: Session 2 (“Altering the brain”). One of the speakers at the Workshop was Professor Michael Sharpe of Edinburgh, who spoke about the implications of psychotherapies.

    The MRC Workshop Report pointed out that a growing understanding of neurotransmission at a molecular level has allowed the design of interventions to alter specific brain functions, one such intervention being CBT: “Psychological therapies such as CBT have now been shown to alter brain function. These developments may alter our view of individuality. What are the risks of changing personality? Is cognitive enhancement acceptable to society?”

    The MRC Workshop concluded that further research is needed to determine whether such therapies are reversible, or if there are persistent adverse effects, noting: “There is already evidence that in certain situations psychotherapy can do harm”.

    Other issues of concern to patients with ME/CFS were discussed at the Workshop: “Psychological treatments also raise a number of issues about consent and coercion. How much information should patients be given about the possible effects of therapy on their brain?”

    In relation to ME/CFS, the MRC Neuroethics Workshop Report noted: “The MRC is funding the PACE trial, the largest trial of CFS/ME treatments (sic) to date. However, the trial has faced serious antagonism from some, but not all, patients groups, mainly because of concerns about the use of a ‘psychological treatment’ for a condition that is seen by many as a medical disorder”.

    Given what is already known about the inherent dangers of CBT for those with ME/CFS (especially the known effects of graded exercise as an inducer of oxidative stress and the effects of compulsory exercise on the cardiovascular problems known from the early part of the twentieth century to be an integral feature of authentic ME/CFS), on what ethical grounds can those already crushed by such a heavy illness burden as that imposed by ME/CFS be subjected --- in some cases by coercion – to a management regime that seems to have no hope of beneficial results?



    This raises once again the disturbing question: in whose best interests is medical science undertaken?
  4. Rosiebud

    Rosiebud New Member

    thanks for posting this. I'm getting it on my profile for future reference.

    love
    Rosie
  5. MsE

    MsE New Member

    Thank you for posting the two articles, Tansy. I appreciate it.