Copied here for those who arent able to find it elsewhere ; MAGICAL MEDICINE: HOW TO MAKE A DISEASE DISAPPEAR Introduction The Medical Research Councils PACE Trial of certain behavioural modification interventions for patients with Chronic Fatigue Syndrome / Myalgic Encephalomyelitis (CFS/ME) is controversial on many levels. PACE is the acronym for Pacing, Activity, and Cognitive behaviour therapy; a randomised Evaluation. The PACE trial is being conducted under the auspices of the Medical Research Council (MRC) and is funded by the MRC, the Scottish Chief Scientists Office, the Department of Health (DoH) and the Department for Work and Pensions (DWP). The PACE Trial is the only clinical trial that the DWP has ever funded. The MRCs PACE Trial seemingly inhabits a unique and unenviable position in the history of medicine: it is believed to be the first and only clinical trial that patients and the charities which support them have tried to stop before a single patient could be recruited. Why would people with a severely disabling disease ?? a disease that manifests the pathology summarised on the preceding two pages ?? seek to stop research into their own condition? To answer this question it is necessary to understand the motives of the trial researchers a group of UK psychiatrists and their adherents who advise that the search for a single identifiable cause is meaningless and whose stated aim is to eradicate Myalgic Encephalomyelitis, a disease that has been classified by the World Health Organisation (WHO) in the International Classification of Diseases (ICD) as a neurological disorder for the last 40 years, currently under Disorders of Brain at ICD?10 G93.3 (to which in ICD?10 the WHO specifically codes chronic fatigue syndrome (CFS), hence the use of the term ME/CFS to signify the neurological disease ME). This is a classification with which these psychiatrists disagree. Instead, they believe ME/CFS (which they call CFS/ME) to be a behavioural disorder that is classified as a fatigue syndrome in ICD?10 at F48.0 under Mental and Behavioural Disorders and that it is perpetuated by the aberrant beliefs of the patients themselves, and they seek to modify such aberrant beliefs using a programme of Cognitive Behavioural Therapy (CBT) designed by themselves, which incorporates aerobic Graded Exercise Therapy (GET). These psychiatrists and their supporters, many of whom work for the medical and permanent health insurance industry, are known as the Wessely School (Hansard: Lords: 9th December 1998:1013), a small but influential group led by Professor Simon Wessely from Kings College Hospital and the Institute of Psychiatry (IoP), London, whose intention is said to be to eradicate ME (Eradicating Myalgic Encephalomyelitis. Pfizer/Invicta: 4?5 /LINC UP, 15th April 1992, Belfast Castle) by dropping ME from CFS/ME when expedient (BMJ 2003:326:595?597) and then to reclassify CFS as a behavioural disorder under syndromes of chronic fatigue under Mental and Behavioural Disorders at ICD?10 F48.0. Indeed, this has already commenced because, using Wesselys own material, in 2000 the first edition of the IoPs Guide to Mental Health in Primary Care included CFS/ME as a mental disorder. (This Guide was wrongly described by Ministers of State as the WHO Guide because as an acknowledged WHO Collaborating Centre on mental health, the IoP is entitled to use the WHO logo). In September 2001, the WHO issued a statement repudiating the unofficial re?classification by the UK Collaborating Centre at the IoP, saying that it was at variance with the WHOs position. An erratum to the Guide had to be issued, but only after 30,000 copies had been sold. The matter was raised in Parliament on 22nd January 2004, when Earl Howe noted that Professor Wessely had: effectively hijacked the WHO logo to give credence to his own view of ME as a mental illness (Hansard: Lords: 23rd January 2004:656:7:1192). 8 Undaunted, these psychiatrists then asserted that the WHO itself had classified the same disorder in two places in ICD?10, once in the Neurological Section (G93.3) and also in the Mental (Behavioural) Section (F48.0). Once again, the psychiatrists claims were repudiated by the WHO, who on 23rd January 2004 confirmed in writing: According to the taxonomic principles governing ICD?10, it is not permitted for the same condition to be classified to more than one rubric. The WHO further confirmed that this means that ME/CFS cannot be known as or included with neurasthenia or any other mental or behavioural disorder, as ME/CFS is a distinct nosological disorder. Wessely, however, does not agree: he believes that ME is a behavioural disorder and that patients ascription of the disease to a virus is somatisation par excellence (see below). It is Professor Wessely who is in charge of the MRC PACE Clinical Trial Unit. There is a significant amount of documented international concern about the Wessely Schools stance and the harm it might do to patients. Another curious factor about the PACE Trial is the role played by one of the patients charities (Action for ME), without whose help the PACE Trial might never have happened see below. It is a Government?funded charity, having received substantial Section 64 funding (Health Services Act 1968) in return for supporting DoH policy priorities (which currently include managing CFS/ME as a behavioural disorder). Good science requires that hypotheses are tested in an objective manner, but there are many disturbing aspects about the MRC PACE Trial. Given that the Investigators have already formed their belief that CFS/ME is a behavioural disorder, it is troubling to observe how they seem to have allowed their beliefs to undermine the objectivity of the trial: participants were to be chosen using criteria designed by the Investigators themselves rather than using criteria accepted by the international medical community the Investigators criteria were financially supported by the Chief Investigator himself the Investigators abandoned their intention to use any objective measurements of outcome and will define the self?reported outcome measures using a scale devised by themselves (which has been described as a parody of modern scientific measurement see below) the Investigators have even redefined the meaning of the word recovery see below. The Investigators have received millions of pounds sterling to carry out this trial, even though they already know the answers and they have publicly acknowledged that for ME/CFS patients their psychotherapy interventions are not remotely curative and that many patients do not benefit from them see below. Part of the Trial therapists training appears to include misleading participants: therapists are told to assure participants they believe their illness is real and to show empathy, whilst also being informed in their training that there is no underlying pathology in CFS/ME, so there is one message for the therapists and another for participants. Therapists and research nurses must achieve positive relationships with participants. Research Nurses (RNs) will be selected and trained to achieve positive relationships with participants. In addition to seeing them for a minimum of 5 times in 52 weeks, we will use techniques commonly employed in cohort studies to maintain participation (Trial Protocol, final version 5.0, 01.02.2006). This involves sending birthday cards to participants in order to create an illusion of warmth and of empathy that is intended to elicit positive 9 associations purely in order to maintain participation, a tactic that may be considered misleading and even a form of coercion. Participants are trained to ignore their symptoms (which a world expert in the disorder described as dangerous in his Witness Statement to the High Court see below). Not only were patients seemingly coerced into the Trial, but they were also to be subjected to thought modification and to engage in incremental aerobic exercise that may at best be of no value and according to some international experts in the disorder at worst might kill them. Fully informed consent may not have been obtained from participants, because the beliefs of the Investigators and the therapists about the disorder were not made explicit to them (ie. that the Investigators consider it to be a behavioural disorder and that the PACE Trial is based on their assumption that participants do not have a physical disease), which takes advantage of participants lack of knowledge. To take advantage of patients is in breach of the General Medical Council Regulations. The PACE Trial started in 2004 and aimed to recruit 600 participants. Originally based in three different Centres (Kings College, London; St Bartholomews Hospital, London and the Western General in Edinburgh), three new Centres subsequently began recruiting participants (the John Radcliffe Hospital in Oxford; the Royal Free Hospital in London and a second Centre at St Bartholomews Hospital, London). The PACE Trial team produces a Newsletter for participants and in Issue 2, March 2007, the Chief Investigator, Professor Peter White, a psychiatrist from St Bartholomews Hospital, wrote: These extra centres will significantly boost recruitment into the study. However, it seems that because of the continued failure to meet the recruitment target, it was deemed necessary to open a seventh Centre at Frenchay Hospital in Bristol, which began recruiting in April 2007. Participants were to be randomly allocated to one of four groups (Pacing, Activity/Exercise, Cognitive Behavioural Therapy, or Standardised Specialist Medical Care) with the objective of achieving four groups of 150 patients from according to the 2002 Chief Medical Officers Working Group Report on CFS/ME ?? 240,000 sufferers in the UK. No severely affected patient and no children were to be included in the trial. Despite such a relatively small number in each arm of the trial, using the trials leitmotif of positive reinforcement, the PACE Participants Newsletter, Issue 3, December 2008 states: The PACE trial retains a significant role as the largest trial ever for comparison of rehabilitative therapies for CFS/ME. The results are due to be published in 2010, originally said to be summer, then autumn, but according to the Chief Investigator now moved forward to the spring. There are some extremely disquieting issues surrounding the MRC PACE Trial, and documents obtained under the Freedom of Information Act allow the full story to be told for the first time. The PACE Trial: source of information The PACE Trial Manuals, as well as Minutes of meetings and related correspondence (amounting to approximately 2,000 pages) were obtained via the Freedom of Information Act (FOIA). Requests were made to various bodies including the MRC, the Department for Work and Pensions and the Scottish Chief Scientists Office and took over twelve months to achieve. There are three PACE Trial Manuals for therapists (relating to Cognitive Behaviour Therapy, Graded Exercise Therapy, and Adaptive Pacing Therapy [APT] respectively) and one for doctors (relating to 10 Standardised Specialist Medical Care or SSMC); apart from the latter, there are also respective versions for participants. It is notable that the West Midlands Multicentre Research Ethics Committees letter of 29th October 2002 confirming approval of Peter Whites application for ethical approval states: MREC noted the importance of the study and wished to commend the researchers on the RCT design (random controlled trial), an unusual commendation which seems to show bias from the outset and may indicate the MRECs ignorance of the issues that lie at the heart of the international disquiet surrounding the MRC PACE Trial. Every effort has been made to view objectively the PACE Trial information that informs these comments. However, the information must be assessed in the light of the significant body of evidence that ME/CFS is not a behavioural disorder; moreover the quotations from the Manuals speak for themselves. Although every Manual states that it is copyright and that no part may be reproduced without permission, the Information Commissioners Office has confirmed that if documents are released under the Freedom of Information Act, they enter the public domain and can be used by members of the public and not only by the person who made the application. It is the case that the MRC was not happy that so much of what it regarded as confidential information about the PACE Trial has been released. A letter dated 14th February 2008 from the Information Commissioners Office to the person who made the FOIA application states: The MRC has expressed its concern over how you came to be in possession (of this information). Given the nature of that information, the MRCs concern may well be justified. The difference between ME/CFS and CFS/ME What the Wessely School refers to CFS/ME is, according to them, a condition of medically unexplained fatigue that is perpetuated by inappropriate illness beliefs, pervasive inactivity, current membership of a self?help group and being in receipt of disability benefits (PACE Trial Identifier, section 3.9) and it should be managed by behavioural interventions (CBT and GET). Simon Wessely believes that it is the same as neurasthenia: Neurasthenia would readily suffice for ME (Lancet 1993:342:1247?1248) and that attribution by patients to a virus is somatisation par excellence (J Psychosom Res 1994:38:2:89?98). The Wessely School believes that there are no physical signs of disease and assert that there is no pathology causing the patients symptoms, simply that patients are hypervigilant to normal bodily sensations (see below). Seemingly because of the Wessely Schools beliefs, children with ME/CFS have been diagnosed as having pervasive refusal syndrome and many have been forcibly removed from their distraught parents (see below), who themselves have been labelled as having Munchausens Syndrome by Proxy, a damaging label that is never deleted from their medical records. Whilst Wessely School psychiatrists continue to believe and teach (and advise Government agencies) that CFS/ME is a behavioural disorder that must be managed by behavioural interventions and incremental aerobic exercise (and which two of the PIs assert can be cured by those interventions), in reality true ME/CFS affects every system in the body and many physiological abnormalities have been documented. At the Press Briefing held on 3rd November 2006 by the US Centres for Disease Control to announce its ME/CFS awareness campaign, two eminent professors who specialise in ME/CFS spoke on public record about the nature of ME/CFS. Anthony Komaroff, Professor of Medicine, Harvard Medical School, said: Its a pleasure to be here today with several people who have dedicated successfully a big part of their lives to trying to understand and get recognition for this terrible illness. 11 Its not an illness that people can simply imagine that they have and its not a psychological illness. In my view, that debate, which was waged for 20 years, should now be over. Brain imaging studieshave shown inflammation, reduced blood flow and impaired cellular function in different locations of the brain(and) they change a persons life. Today we have powerful new research technologies and tools we didnt have even 20 years ago, and they are being put to good use by laboratories all over the world. Nancy Klimas, Professor of Medicine and Immunology at the University of Miami (who at the time was President of the International Association for Chronic Fatigue Syndrome, an organisation of medical professionals and research scientists), said: Ive been waiting for this day for a long time. Over the past 20 years, Ive treated more than 2,000 (ME)CFS patients. Whilst attitudes have improved in recent years, the launch of this national awareness campaign is so important to increasing understanding of this illness. Historically, its been the lack of credibility in this illness that has been one of our major stumbling blocks to making progress. Today there is evidence of the biological underpinnings. And theres evidence that the patients with this illness experience a level of disability thats 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. We need to educate physicians and other health care workers about this illness so that every single doctorknows the diagnostic criteria. There are diagnostic criteria that enable clinicians to diagnose (ME)CFS in the primary care setting. The CFS toolkit should be in the hands of every doctorin the country, because this is the key to moving forward (http://www.cdc.gov/media/transcripts/t061103.htm). Referenced illustrations from the medical literature are provided in Section 2, but an introductory overview of documented abnormalities in ME/CFS include 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 (CNS) 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 Brodmanns 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 12 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 cytotoxicity; 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; recently a direct link between a gammaretrovirus (XMRV, which is the same family as the AIDS virus) and ME/CFS has been demonstrated 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 13 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; there is evidence that abdominal pain is due to unilateral segmental neuropathy; there is significant evidence that people with ME/CFS have increased serum levels of IgA and IgM against the LPS of gram?negative enterobacteria, indicating the presence of an increased gut permeability resulting in the autoimmunity seen in many ME/CFS patients; this indicates that the symptoms of irritable bowel seen in ME/CFS reflect a disorder of gut permeability rather than psychological stress as most psychiatrists believe (gastro?intestinal problems are a serious concern in ME/CFS, and 70% of the bodys immune cells are located in the GI tract) 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. 14 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, all of which is available to the Wessely School. ME/CFS has been defined in the Canadian Guidelines (2003), which have been adopted internationally and are the best aid to the diagnosis of ME/CFS but which the Chief Investigator Peter White insists should not be used in the UK (see below), perhaps because they are unambiguous: 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 empowers the patients 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, which is not tied to deadlines or other hidden agenda. In its 2007 Clinical Guideline 53 on CFS/ME, the National Institute for Health and Clinical Excellence (NICE) specifically recommended that the Canadian case definition of ME/CFS should not be used in the UK. NICE based its decision on a small number of mildly positive clinical trials by the Wessely School, while devaluing evidence from scientific studies and patients own evidence. ME/CFS is the only physical condition for which behavioural modification is the primary (indeed only) management approach in a NICE Guideline. The MRC declines to fund biomedical studies, yet the cost of implementing the Wessely School regime in the UK is 3.75 million annually, in addition to non?recurrent costs of 26.45 million (Breakthrough, MEResearch UK, Spring 2008). There is no cure for ME/CFS According to the Chief Medical Officers Working Group Report on CFS/ME, there is no cure (CMOs Working Group Report: January 2002: 188.8.131.52:48) so it is misleading of the MRC PACE Trial Principal Investigators to imply otherwise and to try to achieve their aim by using techniques of persuasion in an attempt to control the mind of participants by constantly bombarding them with language that seems to misinform them. For the Principal Investigators to state that full recovery is possible with CBT/GET, as Professor Michael Sharpe asserted (There is evidence that psychiatric treatment can be curative. BMB 1991:47:4:989?1005) and as Professor Peter White using the General Practice Research Database to show that social factors affect prognosis in CFS ?? unambiguously asserted (recovery from CFS is possible following CBT.Significant improvement following CBT is probable and a full recovery is possible. Psychother Psychosom 2007:76(3):171?176), implying that patients can recover from ME/CFS if they would only follow the psychiatrists recommended regime of CBT/GET, seems to offer false hope: the recovery statistics simply do not support such a belief. To imply otherwise would seem to be overt misrepresentation of the significant body of peer reviewed published biomedical science. However, in their 2007 paper Knoop, White et al appear oblivious and confidently state: The first clinical implication of the present study is that a therapist delivering CBT can tell the patient that substantial improvement is likely and that full recovery is possible. By communicating this, the therapist can counterbalance factors that lower the expectations of the patient. Examples of such factors are a negative attitude of certain patient advocacy groups towards behavioural interventions or an oversolicitous (sic) attitude of others in response to CFS. There is empirical evidence that lower expectations of patients have a negative influence on therapy outcome. This belief may explain the instructions in the PACE therapists Manuals for the need for repeated positive reinforcement. In the same 2007 paper, Whites definition of recovery is curious: 15 The second clinical implication of the present study is that recovery is a construction. The percentage of recovered patients differed depending on the definition of recovery used. It is possible that a patient has another concept of recovery than the therapist. The Penguin English Dictionary defines recovery as regaining health after sickness. To most rational people, recovery means being restored to previous good health, with the ability to return to school, work, sport, social activities and hobbies with no ill?effects. For them, unlike for Peter White, recovery is not a negotiable term. According to US statistics provided in August 2001 by the Centres for Disease Control CFS Programme Update, only 4% of patients had full remission (not recovery) at 24 months. In 2005, the message was clear: The bitter, unpalatable reality is that ME/CFS patients can be pro?active, they can have a good attitude, they can try various drugs and non?drug interventions, and they can still remain ill, even profoundly disabled (The CFIDS Chronicle Special Issue: The Science & Research of ME/CFS: 2005?2006:59). In 2007, the ME Association Medical Advisor pointed out that: Several research studies looking at prognosis have been published. Results from these studies indicate that ME/CFS often becomes a chronic and very disabling illness, with complete recovery only occurring in a small minority of cases. A recent Systematic Review of 14 studies found a median recovery rate of 7% (ME/CFS/PVFS: An exploration of the key clinical issues prepared for health professionals. Drs Charles Shepherd & Abhijit Chaudhuri, published by The ME Association, 2007). For the Wessely School to offer such people only a management regime that is designed to alter their (correct) perception that they are seriously physically ill, and to imply that restructured thinking and incremental aerobic exercise will result in significant improvement (and even full recovery), is believed by many people to amount to professional misconduct.