This document looks in particular at cognitive behavioural therapy (CBT) which, together with graded exercise therapy (GET), is the only management intervention recommended by NICE in its Guideline CG53 on “CFS/ME” of 22nd August 2007. This is in spite of the fact that these interventions have been shown to be at best unhelpful to those suffering from ME/CFS, and is in defiance of the substantial body of scientific and biomedical evidence regarding ME/CFS, evidence which the NICE Guideline Development Group (GDG) ignored.
This document also seeks to provide further supportive background information concerning the nature of ME/CFS, including the fact that it can for some be a fatal condition. This information was also ignored by the GDG.
The key points can be summarised as follows:
(i) Background Information
Myalgic Encephalomyelitis (ME) has been formally classified by the World Health Organisation as a neurological disease since 1969. In 1992 the WHO approved the term “chronic fatigue syndrome” (CFS) as a term by which ME may be known, hence the term “ME/CFS” is used to denote the disorder
The Guideline Development Group (GDG) was directed to subsume the distinct disorder ME/CFS within the label “CFS/ME” that encompasses a wide-ranging group of patients who suffer from a “primary complaint of fatigue for six months or more” and includes those with somatoform psychiatric disorders
ME/CFS and “CFS/ME” are not the same condition
The focus by the GDG on simply “chronic fatigue” is in defiance of all the biochemical abnormalities that have been shown to exist in ME/CFS patients
The GDG does not explain how its recommended psychotherapy management regimes of cognitive behavioural therapy and graded exercise therapy (CBT/GET) can restore the damaged genes, nervous system, cardiovascular, immune, digestive and endocrine system of ME/CFS patients
Members of the GDG were specifically directed not to consider the total evidence-base on ME/CFS in the production of the Guideline. NICE therefore failed in its remit to produce a Guideline to aid diagnosis
The focus on the psychosocial model of ME/CFS brings disrepute on those who perpetuate it, including NICE, who give no credible reason for disregarding so much relevant scientific and biomedical evidence
An explanation for the denial and suppression of such a large body of evidence is the vested interests of those who have gained materially from continuing such suppression and denial
ME/CFS can cause death; “CFS/ME” does not. UK Coroners are now providing incontrovertible statements that ME/CFS can lead to death, something that the ME community has known for many years. However, deaths from ME/CFS due to end-organ failure are usually recorded as such, without the underlying ME/CFS being mentioned on the death certificate
Significant and distressing social isolation is very common in people with ME/CFS, leading to increased and unnecessary suffering; there are many tragic case histories.
(ii) Illustrations of evidence about ME/CFS that NICE ignored
There can be no dispute that there is a substantial body of evidence showing that ME/CFS is not a somatoform disorder and should not therefore be managed as such as recommended by the NICE Guideline
“ME/CFS is associated with physical, psychological and social distress (and) cannot be defined using just one of these dimensions”
“Wessely’s work on depression and CFS is methodologically flawed”
“Excessive physical exertion will exacerbate CFS symptoms and may worsen the course and prognosis”
“Cognitive behavioural intervention studies conducted in Australia and the United States have not found significant improvements in functioning or symptoms”
“Not only do patients with severe (ME)CFS not recover to full health, they remain quite severely ill for many years”
The Oxford criteria for “CFS” (created and used by the Wessely School) specifically include patients with primary psychiatric diagnoses
The symptoms of ME/CFS occur in multiple organ systems and no other disorder can account for them
“Those who think of ME/CFS as ‘fatigue’ and forget the importance of the other symptoms will be at risk of misdiagnosing patients leading to inappropriate treatment recommendations. CBT to convince a patient that s/he does not have a physical disorder is disrespectful and inappropriate”.
(iii) Evidence that CBT is ineffective
The Guideline recommends CBT/GET for all patients in the UK with “CFS/ME”, and states that this includes those with ME/CFS
Not only did NICE ignore the fact that the recommended interventions (CBT/GET) are not effective, it ignored the evidence that subsuming all states of “chronic fatigue” into one functional somatic syndrome is contra-indicated, as well as evidence that most of the randomised controlled trials (RCTs) on CBT on which the GDG relied are seriously flawed
In most of the ten trials of CBT upon which the GDG relied, the methodology does not meet even the most minimally acceptable standards
The trials used give a total of 480 patients out of an alleged UK total of 240,000 patients and is insufficient data upon which to recommend a national strategy
Patients with pre-existing psychiatric co-morbidity were not excluded from the studies relied upon
Nowhere is there any evidence that patients fully recovered
The behavioural model of “CFS/ME” offers relatively little; it is supported only by researchers with a professional interest in psychosocial aspects of illness. This model dominates the NICE management regime
There is no credible evidence to support the GDG’s claim that the best practice evidence-base is the nationwide implementation of CBT/GET for patients with “CFS/ME”.
A basic question never addressed by those who favour the psychosocial model of “CFS/ME” is: if patients are not cured by psychotherapy (which its proponents concede), then what is it that they are not cured from?
Why does the NICE Guideline recommend only psychosocial therapy for “CFS/ME” (which is said to include ME/CFS) that has been clearly shown not to be effective?
Background information and illustrations of evidence that CBT cannot improve ME/CFS
which NICE disregarded
An article in The Times on 21st July 2008 about the National Institute for Health and Clinical Excellence (NICE) made a clear statement: “When (NICE) gives bad advice, people suffer”.
In relation to its recommended management regime for myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), NICE has given bad advice in its Clinical Guideline 53 of 22nd August 2007 (Chronic Fatigue Syndrome / Myaglic Encephalomyelitis (or Encephalopathy): diagnosis and management of CFS/ME in adults and children). Unless that Guideline is revoked and replaced by an accurate and well-informed Guideline, people with ME/CFS will continue to suffer.
Of prime importance in relation to any legal challenge to the NICE Guideline CG53 on “CFS/ME” is the fact that, in defiance of the evidence that myalgic encephalomyelitis / chronic fatigue syndrome (ME/CFS) is a classified nosological entity, the Guideline Development Group (GDG) was directed to subsume this distinct disorder within the contrived and heterogeneous label “CFS/ME”, a label that does not denote people with ME/CFS but which encompasses a wide-ranging group of patients who suffer from “a primary complaint of fatigue for six months or more” and which specifically includes those with somatoform psychiatric disorders.
The deliberate blurring of the distinctions between chronic fatigue, CFS/ME and ME/CFS means that those with ME/CFS will continue to receive a psychiatric diagnosis. This unjustified subsuming of any state of “chronic fatigue” into one single somatoform disorder (CFS/ME) has led, and will continue to lead, to inappropriate management strategies which may be potentially fatal for some people with ME/CFS.
ME has been formally recognised as a neurological disease by the World Health Organisation since 1969. It was described clearly and cogently by Dr Melvin Ramsay of The Royal Free Hospital in London, who was regarded as the Father of ME from his long clinical experience of it (Postviral Fatigue Syndrome. Gower Medical Publishing, 1986; the second edition was entitled Myalgic Encephalomyelitis and Postviral Fatigue States, Gower Medical Publishing, 1988. Ramsay told many people that he always regretted allowing himself to be persuaded not to use the term ME in the title of the first edition and insisted on using it in the second edition).
There is substantial evidence that, even though NICE asserts they are the same condition, ME/CFS is not the same as “CFS/ME” – this is mere opinion held and promoted by psychiatrists of the Wessely School that, in the UK, has been elevated to the status of medical certainty in defiance of and contrary to established scientific evidence. Even if the Wessely School psychiatrists believe in their own myth that there is no such distinct disorder as ME/CFS, their unproven beliefs should not be accorded preference over the medical science that has shown them to be wrong.
By deliberately ignoring the published evidence about the nature of ME/CFS and by supporting the Wessely School hypothesis that it is a behavioural disorder, the NICE Guideline has contributed to the misinformation regarding every aspect of ME/CFS that is propagated by these psychiatrists.
To focus on the single symptom of “chronic fatigue” in its management recommendations that NICE asserts relate to people with ME/CFS, whilst down-playing so many other key symptoms of ME/CFS, and to ignore the evidence of acquired (i.e. not congenital) gene abnormalities in ME/CFS (in particular, clear evidence of prominent RNA not observed in normal controls, with the prominent RNA bands sequenced showing homology with human genes that are noted for the tendency for gene rearrangement under severe physiological stress) is to defy reality. This evidence of gene abnormalities that is found only in ME/CFS was presented at the American Association for Chronic Fatigue Syndrome (AACFS, now the International Association for ME/CFS) International Research Conference held in Seattle in January 2001 and was available to the GDG.
The GDG offers no explanation as to how cognitive behavioural therapy or graded exercise can restore defective genes. Indeed, no explanation or evidence is offered as to how CBT/GET is supposed to correct the damage that has been shown to occur in the central and autonomic nervous system, the cardiovascular system, the immune system, the endocrine system and the gastro-intestinal system of those with ME/CFS.
CBT and GET are based on the belief of their proponents that fear of activity is one of the reasons for continued disability in “CFS/ME” (Pesek J, Jason LA et al: Journal of Human Behaviour in the Social Environment: 2000:3:59-77).
Given the substantial published evidence that psychological factors do not contribute to the extreme illness and disability seen in ME/CFS, it is irrational for NICE to claim that psychological interventions such as CBT and GET contribute to improvements in physical functioning in those who wish to recover.
Nothing detracts from the fact that the Guideline recommends only psychotherapy for people with ME/CFS.
It is disingenuous for NICE to state that CBT is used in diseases such as cancer and heart disease, therefore patients with “CFS/ME” should not reject it on the grounds that it is a psychological intervention: the key difference is that in other medical disorders, CBT is offered as adjunctive therapy, not as the primary (and only) intervention as is the case with ME/CFS, where nothing else is on offer. This is akin to telling cancer sufferers that if they would only change the way they think about their illness, they will improve.
Misleadingly, the implied message of the NICE Guideline is that “CFS/ME” is a psychogenic disorder; unfortunately, UK doctors have a lamentable track record of dismissing and denigrating patients whom they believe to be the creators and perpetrators of their own ill-health, and the present Guideline will perpetuate this abuse.
It was in 1990 that Peter Wakeford wrote in the UK ME Association newsletter: “Psychiatrists want the disease firmly in their domain. They’re gathering even now like locusts to redefine it. I have phone calls from isolated desperate people who say: ‘The psychiatrists are trying to put me away in an institution. They’re taking away my day care. Help me’. It’s appalling that even today, people I know are in psychiatric institutions – and they’ve got ME, which is an organic illness” (Perspectives, Summer 1990; pp 25-27).
A decade later, in 2000 Gwynneth Elias commented in despair at the lack of respect and care afforded to those with ME/CFS. She was a patient at the “CFS” clinic at one of the London Teaching Hospitals and was told by the doctor that she should not be afraid to increase her activity, and that she needed to adopt a positive attitude in order to improve: “The arrogance of their assumptions was truly staggering. I was utterly devastated by the lack of help and courtesy. I was disempowered and tempted to withdraw back into the isolation of the illness, as most before me have done. Less than 5% of those in my local support group see a Consultant; most exist with no support” (Perspectives, January 2000:30).
As Erik Johnson pointed out in the eBMJ in 2004 about inappropriate psychiatric interventions for ME/CFS: “ psychological theorists deliberately disregard or manipulate in an imprudent manner (the evidence) if it jeopardises their conceptual model of the illness or diminishes their influence in its treatment” (eBMJ: 15th July 2004).
Numerous surveys have shown that NHS provision is not addressing the needs of those with ME/CFS (for example, the York & Ryedale ME support group’s survey of 2001, as reported in Perspectives 2001; Autumn:15).
By implying – by recommending only psychotherapy — that ME/CFS is a psychosomatic problem, the NICE Guideline has done nothing to correct or even alleviate the situation. Commenting on a GMTV interview with the Welfare Minister James Purnell on 21st July 2008 about the increased difficulties people with ME/CFS will be likely to experience in obtaining and maintaining State benefits, Sir Peter Spencer, Chief Executive of the charity Action for ME, said: “This creates additional stress which adds to the problems which people already face. It also demonstrates that government departments still fail to understand the clinical realities of ME” ( HYPERLINK “mailto:LocalME@yahoogroups.com” LocalME@yahoogroups.com ).
The GDG was directed to ignore the urgent need to subgroup “CFS/ME”
It has now been confirmed by a member of the GDG that members were specifically directed not to consider the total evidence-base on ME/CFS in the production of the Guideline (J.Infection 2007:55:6:569-571). Such a direction ensured that the GDG failed in its remit to produce a Guideline to aid diagnosis.
There is abundant evidence in the literature of calls to distinguish between individuals with different causes of their fatigue. For example, in 1999 US researchers Professor Leonard Jason et al highlighted such a need:
“One consequence of such patient heterogeneity is that when patients groups are combined, distinctions between individuals with different causes of their fatigue, or different syndromes, are blurred. For years, investigators have noted many biological abnormalities among patients with (ME)CFS, including over-activated immune systems, biochemical dysregulation in the 2-5A synthetase/RNase L pathway, cardiac dysfunction, EEG abnormalities, abnormalities in cerebral white matter, decreases in blood flow throughout the brain, and autonomic nervous system dysfunction. Lack of consistency in laboratory findings might be a function of combining patients into a large heterogeneous group rather than analysing them within sub-groups. To complicate matters further, individuals with (ME)CFS experience different phases of their illness” (JCFS 1999:5:3-33).
By intentionally disregarding the existing evidence-base of published knowledge about ME/CFS and by focusing on only a few methodologically flawed randomised controlled trials (RCTs) in its Guideline on “CFS/ME”, and by relying only on those flawed RCTs for its recommendation of the psychological interventions cognitive behavioural therapy and graded exercise therapy (CBT/GET) as the primary management intervention, NICE has compounded the erroneous view that ME/CFS is a primary psychosomatic disorder.
No-one disputes that, as with virtually all serious and chronically disabling diseases, there may be accompanying psychological problems. However, this is very different from asserting that a disorder is a primary behavioural disorder and must be managed as such, as has been the case with ME/CFS in the UK for the last two decades.
The deliberate ignoring by the GDG of the sheer volume of 70 years’ published evidence that ME/CFS is not a primary behavioural disorder raises important questions, particularly the question as to why such evidence should continue to be ignored by agencies of the State such as NICE, and why the focus of management should be so resolutely centred on changing ME/CFS patients’ rightful belief that they suffer from a devastating organic disorder to the acceptance that their disorder is psychosomatic (a compulsory requirement if people with ME/CFS wish their State benefits to continue, since they are required to undertake “rehabilitation” programmes).
The denial of the nature of ME/CFS by the Wessely School (and thus by NICE)
The denial of medical science in relation to ME/CFS gained momentum in 1987 with the advent of psychiatrists of the Wessely School and has continued unabated, as has their well-documented involvement with the medical insurance industry.
The Wessely School members have been prodigious in proselytising their belief that “CFS” (they did not routinely refer to it as “CFS/ME” until early 2002) is a psychiatric (behavioural) disorder, not only in the mainstream medical journals but in the medical trade magazines such as “PULSE” and “GP”, which have a much larger circulation and readership, being read by virtually every registered doctor in the UK.
For example, in June 1998 psychiatrist Peter White (now an influential lead adviser on “CFS/ME” to the Department for Work & Pensions) advised all UK doctors that exercise helps “CFS” and that: “Most patients with CFS will also have a psychiatric disorder”. White stated that increasing exercise is important, “aiming at a total of half an hour of exercise, five days a week”. He continued: “cognitive behavioural therapy has already been shown to be a useful treatment for patients with the chronic fatigue syndrome and can particularly help to challenge unhelpful illness beliefs and coping strategies” (PULSE: 20th June 1998:86-88).
It was in 1998 that Professor Michael Sharpe, a psychiatrist who, with Wessely and White, is known to be heavily involved with the medical insurance industry and a key player in the Wessely School team of mental health professionals that is dedicated to “eradicating” ME and subsuming it within the heterogeneous “chronic fatigue” label, crystallised their intended approach:
“Cognitive behavioural therapy offers patients (with CFS/ME) a new way to think about their illness. The first application of CBT to chronic fatigue syndrome was by Wessely and colleagues (who proposed) a vicious circle model of the perpetuation of chronic fatigue whereby patients’ beliefs about the illness lead to avoidance of activity and thus to chronic disability. Our group (i.e. the Wessely School) wanted to develop the behavioural approach. CBT helps patients to re-evaluate their beliefs (and) encourages them to change their behaviour. Change in the belief is an important factor in recovery. The trials of CBT have shown that ‘psychological’ treatment is effective in patients with CFS” (Cognitive Behaviour Therapy. Michael Sharpe. In: A Research Portfolio on Chronic Fatigue. Ed: Robin Fox. Published by The Royal Society of Medicine for The Linbury Trust, 1998).
In 2001, a short biography of psychiatrist Peter White stated: “The first claim for Permanent Health Insurance (income protection) because of CFS or ME arose around 1987. CFS/ME is now one of the four commonest reasons for claiming income protection. Poor prognosis with CFS/ME has been found to be precipitated by certain illness beliefs and receiving a disability pension” (Insurance Medicine, 3rd July 2001).
In 2002, Sharpe was equally clear: “Functional symptoms are not going to go away. However, the form they take is likely to change. New functional syndromes are likely to include those associated with pollution (chemical, biological and radiological). As the authority of medicine to define what is a legitimate illness is diminished, increasingly consumer orientated and privatised doctors will collude with the patient’s views that they have a disabling and permanent illness. It will be imperative that health and social policy address this problem. Funding of rehabilitation by commercial bodies has begun in the UK with organisations such as PRISMA and is likely to continue. Both health services and insurers now need to take a more positive approach” (Functional Symptoms and Syndromes: Recent Developments. In: Trends in Health and Disability 2002, Report of UNUM Provident Insurance Company. Michael Sharpe).
The confirmation by Sharpe that CBT — also known as “rehabilitation programmes” in an attempt to sell CBT to patients — is being provided in the NHS by the company PRISMA is of particular interest.
PRISMA stands for “Providing Innovative Service Models and Assessments”. It is based in Germany and is a multi-national healthcare company working with medical insurance companies. It arranges “rehabilitation” programmes and its recommended management is CBT. PRISMA claims to be especially concerned with long-term disability from the perspective of government, service providers and insurance companies. It claims to have developed a “unique treatment programme” for “hopeless” cases (it specifically includes those with CFS), claiming that such patients “avoid physical exercise and social activities, as they fear these may trigger new bouts of complaints”. In the PRISMA Company Information, Professor Simon Wessely is listed as a Corporate Officer. He is a member of the Supervisory Board. In order of seniority, he is higher than the Board of Management. He is listed as a “world expert” in the field of “medically unexplained illnesses including Chronic Fatigue Syndrome” (PRISMA Company Information, 2001).
Concern has been repeatedly raised that Wessely is recommending an NHS management programme for people with ME/CFS that is known to be potentially harmful but which is provided by a company of whose Supervisory Board he is a member.
The relentless focus on the unproven psychosocial model of ME/CFS brings disrepute on those who perpetuate it, including NICE.
NICE provides no credible reason for such blatant disregard of the relevant evidence.
It is completely unacceptable that the unsubstantiated personal beliefs of a few immensely influential psychiatrists with indisputable vested interests (i.e. the Wessely School) should continue to indoctrinate UK medicine regarding ME/CFS.
The matter of possible scientific misconduct by Wessely in his selection and presentation of the available evidence relating to ME/CFS was first raised in public in 1994 (see: The CFIDS Chronicle, Spring 1994:14-18). It is now time that he and his like-minded colleagues be held accountable for their published beliefs about ME/CFS and for the consequences of those beliefs upon many thousands of sick people suffering from a well-established organic disease, including the prevention of informed medical understanding and the loss of the provision of appropriate and compassionate care.
The most likely explanation for decades of denial and suppression of such a large body of scientific and biomedical evidence is the vested interests of all those who have gained materially from such continuing denial and suppression.
There is, however, an alternative explanation: that the phenomenal increase in cases of ME/CFS since the 1980s is linked to unavoidable daily exposure to a multiplicity of chemicals or even to chemical warfare agents. Indeed, a link to chemical warfare agents has been established (see below).
The cost implications for the NHS of providing suitable medical care and respite services for an increasing number of ME/CFS sufferers are enormous, as well as for the medical insurance industry to whom the Wessely School psychiatrists are consultant medical advisers (see, for example, HYPERLINK “http://www.meactionuk.org.uk/Notes_on_the_Insurance_issue_in_ME.htm” www.meactionuk.org.uk/Notes_on_the_Insurance_issue_in_ME.htm). These same psychiatrists are also advisers to NICE via the Systematic Review Team at the Centre for Reviews and Dissemination at York upon whose Systematic Review of the literature the GDG relied so heavily.
Key questions require urgent answers: why were members of the Chief Medical Officer’s Working Group on “CFS/ME” which met from 1998 to 2002 threatened with the Official Secrets Act?
Why are Medical Research Council (MRC) files on ME/CFS locked away in the National Archive at Kew and remain inaccessible until 2023 under the thirty-year rule?
Why has the MRC repeatedly rejected so many well-designed studies of the biomedical aspects of ME/CFS and why does it continue to fund only psychiatric studies of CBT/GET for “CFS/ME”? At a meeting held on 15th July 2008 at the MRC, attended by the Medical Adviser to the ME Association, it was made clear that there is no realistic chance of the MRC providing ring-fenced money for ME/CFS research and that there is no realistic chance of the MRC commissioning biomedical research into the disorder, as was recommended in section 6.5 of the Chief Medical Officer’s report of 2002.
Why is the UK Establishment so determined to disregard the international science and to deny the reality of the nature of ME/CFS, just as in the case of Gulf War Syndrome?
That NICE has chosen to continue the misguided suppression of the ever-mounting evidence of serious organic pathology that has been internationally demonstrated in ME/CFS in its Guideline CG53 unsurprisingly fuels speculation within the ME community.
Evidence has now emerged that this may not be idle speculation after all.
The possibility of chemical contamination was raised during a four day Judicial Review in July 2008 in the High Court in London that was looking into the adverse effects of pesticides (brought by Georgina Downs); when pressed by the Judge about the effects of pesticide exposure, Robert Jay QC, Counsel for the Defendant (DEFRA), conceded that it appears these effects are not adequately covered by the current risk assessment model.
In the High Court, reference was made to the suggestion within the Royal Commission on Environmental Pollution (RCEP) Report that causation of ME/CFS may have links with systemic, long-term exposure to such products (Crop Spraying and the Health of Residents and Bystanders. Sir Tom Blundell. HMSO. September 2005: HYPERLINK “http://www.rcep.org.uk/pesticides/Crop%20Spraying%20web.pdf” http://www.rcep.org.uk/pesticides/Crop%20Spraying%20web.pdf) HYPERLINK “http://www.rcep.org.uk/cropspraying.htm” . That Report states:
“Chronic fatigue syndrome or myalgic encephalomyelitis is a complex disorder. Diverse factors have been proposed as contributing to pathogenesis, including exposure to toxins, pesticides and other chemicals (Komaroff et al: Annual Reviews of Medicine 1998:49:1-13). Currently there are no animal models available to reflect all of the chronic ill health effects that have (been) associated with pesticide spraying, specifically multisystem, multisymptom disorders such as CFS. We are aware of some new animal models that reproduce some aspects of CFS that deserve further study. It is important to ensure that symptoms and syndromes that do not fit within traditional toxicological end-points are not ignored simply through lack of knowledge. This applies to the study of multisymptom illness”.
Mr Jay said it was the Defendant’s position that no solid evidence existed to link exposure from any individual pesticide with (ME)CFS. Although not referring specifically to ME/CFS, the Judge (Collins J), was robust in his observation that if data and evidence are not routinely collected by the relevant authorities, how can the Government be so sure that causation does not exist?
Such a potential link does exist.
In 1999 Professors Vojdani and Lapp from the US looked at the possible differentiation between virally-induced ME/CFS and chemically-induced ME/CFS and demonstrated that ME/CFS can be caused by viruses (as in the early epidemics) but also by chemicals (Immunopharmacol Immunotoxicol 1999:21(2):175-202).
In December 2001, at the Alison Hunter Memorial Foundation International Conference on ME/CFS held in Sydney, Australia, Mohamed Abou-Donia, Professor of Pharmacology, Cancer Biology and Neurobiology, Department of Neurotoxicity, Duke University Medical Centre, Durham NC, demonstrated that stress can intensify the effects of relatively safe chemicals, making them very harmful to the brain and liver; even short-term exposure to chemicals, when combined with stress, is enough to cause wide-spread cellular damage (see, for example, Archives of Environmental Health 2003:58:8:484-497; Journal of Toxicology & Environmental Health 2004: February 27).
Significantly, it has long been known that the stress response is disordered in ME/CFS (see for example: Demitrack M et al; Journal of Clinical Endocrinology and Metabolism 1991:73:6:1224-1234; Crofford LJ and Demitrack MD; Rheum Dis Clin North America 1996:22:2:267-284).
In 2005, an important paper by Kaushik, Holgate, Kerr et al delivered a bombshell: this team studied gene expression in the blood of people with ME/CFS and found remarkable differences between patients and controls. Sixteen genes were identified as having an expression profile associated with ME/CFS. These genes can be grouped according to immune, neuronal, mitochondrial and other functions. A neuronal component was identified that is associated with central nervous system hypomyelination, and the authors specifically noted the association of organophosphates and chemical warfare agents. Further, the authors provided evidence of mitochondrial gene upregulation and observed: “The upregulation identified may represent a common host response to persistent infection with several different viruses” (Gene expression in peripheral blood mononuclear cells from patients with chronic fatigue syndrome. N Kaushik, ST Holgate, JR Kerr et al. J Clin Pathol 2005:58:826-832). Stephen Holgate is MRC Clinical Professor of Immunopharmacology at the University of Southampton; Honorary Consultant Physician, Southampton General Hospital, and a member of The Royal Commission on Environmental Pollution; his research interests include CFS.
Also in 2005, UK researcher Dr Derek Pheby, Co-ordinator of the UK ME Observatory, published Risk Factors for the Development of ME/CFS; this report states: “Of possible risk factors, odds ratios greater than 2 were found for damaging initial treatment, and chemical exposure” (JCFS 2005: [cover date 2004 / publication date 2005]:12:2:47-50).
ME/CFS causes death
People die from ME/CFS, but not from “CFS/ME”.
On 13th December 1988 Brynmor John MP died from ME/CFS. His experience of the illness was all too familiar: ‘Though there is only a slight gradient from our house to the main road, it could have been the North face of the Eiger. I just could not get up it’. He found himself unable to dress; the slightest exertion exhausted him and it took days to regain his strength. He was irritated by the profusion of psychiatric comment and was trying to ensure better understanding of ME/CFS (Perspectives, Summer 1991:28-30). Brynmor John suddenly collapsed and died as he was leaving the House of Commons gym after having been advised to exercise back to fitness.
In 1992, Professor Hugh Fudenberg from South Carolina (a pioneer of clinical immunology and one of the most distinguished minds in the field, being awarded The Medal of the Institut Pasteur at the age of 32; he was also a Nobel prizewinner nominee) stated that there is “a greater death rate than normals in the same age range” (see: The Clinical and Scientific Basis of Myalgic Encephalomyelitis Chronic Fatigue Syndrome: ed. BM Hyde, published by The Nightingale Research Foundation, Ottawa, Canada, 1992: page 644).
Perhaps the most tragic and well-known case is that of Alison Hunter from Australia, who died in 1996 and whose death certificate stated the cause of death as “Severe progressive ME”. She was just 19 years old. The pathologist’s report confirmed that she had severe oedema of the heart, liver and brain. She had also suffered severe ulceration to her throat, seizures, paralysis, other neurological symptoms, and gastrointestinal paresis with failure of the gut and bowel. James Ibister, Head of Haematology at Royal North Shore Hospital, Sydney, said: “To be honest, I felt helpless towards the end. On many occasions I was extremely embarrassed about the way she was treated by the system. A lot of terrible things Alison went through were doctors projecting their own fears and inadequacies. How anyone could not think she had a major medical illness was beyond me”. Alison, he said, suffered “terrible physical distress compounded by insults and inhumanity” ( HYPERLINK “http://www.ahmf.org” www.ahmf.org).
In 1998, an ME/CFS sufferer wrote: “I’ve had ME for nearly five years, 18 months of which were a living hell. The physical suffering (inability to walk unaided, chew, swallow, breathe properly, hold my head up, hands which became spastic) were bad enough, but the brain symptoms were at times unbearable – my brain exploding with stimulus until I thought I’d gone mad (and) the room spun like I was drunk, making me feel physically sick. The bed felt like it was moving. I had explosions of light before my eyes. Worst of all were the ‘seizures’, which felt like I was having a stroke – pins and needles on my head and face, drooping muscles around my mouth, my head would start to tip backwards, absolutely terrifying. I live alone, yet have been refused home care, disability living allowance or any form of medical advice. The public need to be shocked by seeing the severely affected, those being tube fed, shaking, uncontrollable, paralysis, unable to hold up their head, speak, see, control bowel movements. The myth that ME is never fatal must be dismissed. I know of several people who have died of the complications ME can bring” (Perspectives, September 1998:26).
UK Coroners are now providing incontrovertible statements that ME/CFS can lead to death. This is something that the ME/CFS community has known for many years.
It was in 1957 that Dr Andrew Wallis reported the post-mortem histopathology on a female from Cumbria who had died of ME/CFS. The histopathology report (held at the University of Edinburgh) states:
“There are in the entire diencephalon, particularly around the third ventricle, numerous small haemorrhages, which extend into the adjacent parts of the mid-brain. Similar haemorrhages can be seen in the corpora mamillare. The haemorrhages are mostly around the small vessels but some are also to be seen in the free tissue. This is a significant finding”.
It was indeed a significant finding and remains so, given the long history of vasculopathy in ME/CFS that abounds in the medical literature (which NICE entirely ignored): see, for example:
HYPERLINK “http://www.meactionuk.org.uk/Vade_MEcum.htm” http://www.meactionuk.org.uk/Vade_MEcum.htm
HYPERLINK “http://www.meactionuk.org.uk/VASCULAR_PROBLEMS_IN_CFS.htm” http://www.meactionuk.org.uk/VASCULAR_PROBLEMS_IN_CFS.htm
HYPERLINK “http://www.meactionuk.org.uk/The_MRC_Profits_before_Patients.htm” http://www.meactionuk.org.uk/The_MRC_Profits_before_Patients.htm
The UK authorities keep no statistics, so the actual number of deaths from ME/CFS remains unknown.
In 1992, a 30 year old woman in the UK who had suffered from ME/CFS for five years committed suicide; the postmortem study (using polymerase chain reaction) showed enteroviral sequences in samples from her muscle, heart, the hypothalamus and the brain stem. No enteroviral sequences were detected in any of the control tissues. The researchers stated: “The findings further support the possibility that hypothalamic dysfunction exists in the pathogenesis of (ME)CFS (and) they suggest that the chronic fatigue syndrome may be mediated by enterovirus infection and that persistent symptoms may reflect persistence in affected organs” (McGarry et al. Ann Intern Med: 1994:120:11: 972-3).
On 18th June 1995, Consultant Radiologist Dr Eric Booth died from ME/CFS aged 48 years, having had ME/CFS for 16 years. Four years before he died, Booth wrote: “ I have been very seriously ill for the last five years, being totally bedridden (but) am unable to convey this to my medical colleagues. I have come to believe that physicians suffer from compassion fatigue” (BMJ 28 October 1995:311). The autopsy findings were disturbing but were suppressed; Booth’s next of kin was warned by the Official Solicitor that action would be taken against her if she divulged the post-mortem findings, to the extent that she was reduced to a state of chronic fear.
In 1998, there was the well-reported case of Joanna Butler, a young woman aged 24 from Leamington Spa, Warwickshire, who was severely affected by and died from ME/CFS. She was nursed at home by her parents and was bed-bound for the last two years of her life and required tube-feeding. Although she died of ME/CFS, her parents were suspected of having caused her death by administering too high a dose of a medically-prescribed morphine-related compound, and the local paper (Courier) reported that the Warwickshire County Coroner (Michael Coker) ordered a police investigation. This investigation cleared them of blame but they were hounded to such an extent that they were forced to move away from the area (see the press reports in The Observer, 19th March 1998: “Tragic death of young ME victim” and the reports in the local paper, including the Courier, which carried a report on the ‘many who die each year’ of ME).
In January 2003 the wife of Richard Senior died of ME/CFS; the North Wales Coroner entered CFS as the cause of death on the death certificate.
On 4th July 2005 Casey Fero died of ME/CFS at the age of 23 in the US. The autopsy showed viral infection of the heart muscle. The pathologist was shocked at the state of Casey’s heart, which showed fibrosis indicating the presence of a long-standing infection.
In November 2005 Sophia Mirza died of ME/CFS in the UK at the age of 32 and the death certificate of 19th June 2006 gives CFS as the cause of death, with acute renal failure (see below).
The most recent UK death from ME/CFS occurred in May 2008 when a severely affected and courageous woman died in the North of England; her death certificate gives “Myalgic encephalomyelitis” as the cause of death.
Evidence from autopsies of people who have died from ME/CFS is chilling. In Sophia Mirza’s case, there was evidence of severe inflammation throughout 75% of her spinal cord.
Evidence from a 2005 autopsy in the US showed oedema of the lower limbs; the alveolar spaces of the lungs were filled with inflammatory cells and there were small emboli scattered throughout the arteries; there was marked congestion of the liver and spleen; the bowel was ischaemic; there was mild inflammation of the kidneys; there was also evidence of rhabdomyolysis (the breakdown of muscle fibres resulting in the release of muscle fibre contents into the circulation, some of which are toxic to the kidney); the bladder showed a hyperplastic epithelium; the thyroid showed colloid filled follicles, with scattered dystrophic calcifications and calcification of the small arterial walls; the right occipital lobe of the brain showed areas of degeneration and degenerated astrocytes, and the white matter surrounding this defect appeared puckered.
The Medical Director of The National CFIDS (chronic fatigue immune dysfunction, a commonly-used US term for ME/CFS) Foundation, Dr Alan Cocchetto, commented: “Every time you look closely at someone with this disease, you see immense suffering. There appears to be no limit as to the human toll that this disease is capable of exerting on patients” ( HYPERLINK “http://www.ncf-net.org/forum/Autopsy.htm” http://www.ncf-net.org/forum/Autopsy.htm ).
Deaths from ME/CFS complications or end-organ failure such as myocarditis or pancreatitis or liver failure are usually recorded as such, without the underlying ME/CFS being mentioned on the death certificate.
Details of some ME/CFS deaths were presented to the UK Chief Medical Officer (CMO) in person by the Countess of Mar, Dr Elizabeth Dowsett (former President of the ME Association) and Doris Jones (an independent ME/CFS researcher) in March 1998 (The Organic Basis of ME/CFS. EG Dowsett, DM Jones, March 1998, available from DM Jones at cost price: 0208-554-3832).
These details were made available to the subsequent CMO’s Working Group on “CFS/ME” but were ignored. It is a matter of record that five members of the Wessely School who were on the Working Group walked out just before the Report was published, refusing to endorse it because it did not categorically state that “CFS/ME” is a somatoform disorder. Those members were psychiatrists Professor Peter White, Dr Anthony Cleare and Professor Elena Garralda, behavioural nurse therapist Trudie Chalder (now a Professor at the Institute of Psychiatry) and Dr Alison Round, a public health physician who, in a paper co-authored with Dr William Hamilton (a member of the Guideline Development Group and Chief Medical Officer of a major medical insurance company for the past 15 years), concluded that in people who claim permanent health insurance for CFS, abnormal illness behaviour is of greater importance than previously recognised (JRCP 1998:32:1:44-48).
In the sample presented to the CMO, there were seven cases of cardiac failure, including two cases of cryptogenic myocardial fibrosis (as seen at the autopsy of Dr Eric Booth); four cases of cancer (incidence of which is known to be increased in ME/CFS patients: Levine et al, 1994: Clin Inf Dis 18: (Suppl 1):S49-S53; Johnson H, Osler’s Webb 1996: Crown Publishers, New York; Levine et al. JCFS 1999:7:1; Levine et al 1998: Annals of Epidemiology: 8:(4):245-249), and cases of hepatic and renal failure. There are reports of hepatic and splenic involvement in ME/CFS going back to 1977 (for example: BMJ 1977:21 May:1350; Psychiatric Annals 1997:27:365-371; Rev Inf Dis 1991:13: (Suppl 1):S39-S44; J Psychosom Res 2000:48:59-68).
The GDG ignored all this evidence and recommended only behavioural interventions for such people.
Deaths directly implicating ME/CFS are mostly documented as suicide. This is not because patients are psychiatrically ill: it is because they are completely unable to look after themselves and are too sick to survive without the necessary social, medical and financial support which in the UK is consistently denied them due to the misinformation propagated about ME/CFS by the Wessely School.
Significant and distressing social isolation in people with ME/CFS is very common, leading to increased and unnecessary suffering; many case histories are tragic. People with ME/CFS have committed suicide when the intense and unremitting suffering and the battles with State agencies that they had to endure became unbearable.
A few illustrations (some of which were in the presentation to the CMO) are as follows:
A young mother of two children in the west country was brusquely told by a nursing sister to pull herself together; severely sick with ME/CFS, she was driven to take her own life
A young man aged 26 from Ireland went to England in search of treatment for ME/CFS; he returned to Ireland unimproved and took an overdose
A mother of three children from Dublin asked her family what favourite meal they would like for their supper; she prepared it, then took a taxi to the coast and drowned herself because she could no longer endure the ravages of ME/CFS
A young man with ME/CFS from Exeter tied a noose round his neck and attached the noose to a car, ending his life in a particularly gruesome way
A man with ME/CFS from Worcestershire was so upset by the derogatory things written in his medical notes (which said he was a malingerer) that he killed himself
An MP with ME/CFS (Gordon McMaster) killed himself by taking an overdose
A young farmer with ME/CFS aged 31 died after taking an overdose of strychnine; he was found by his sister writhing in arched death throes
A young man of 23 with ME/CFS killed himself by jumping into the River Ness in Scotland
A young man with ME/CFS in Warwickshire hanged himself in the hallway of his home
The wife of a Professor in South Wales committed suicide because of ME/CFS.
In 2001, Carli Berry from Yorkshire committed suicide on her 27th birthday.
Most recently, an inquest in May 2008 heard that a young man of 20 from Colchester, Essex, committed suicide after suffering from ME/CFS for ten years.
These serve only as illustrations; there are many more such tragedies.
From the information and statistics available to the ME Association (partly via a Press Cuttings service), the Medical Adviser is on public record as stating that there is about one ME/CFS suicide per month in the UK.
In 2006, in a study looking at the cause of death in ME/CFS, Jason et al stated:
“(ME)CFS is a severe illness and it can affect virtually every major system of the body. Neurological, immunological, hormonal, gastrointestinal and musculoskeletal problems are all common among people with (ME)CFS. The three leading causes of death in individuals with (ME)CFS were heart failure, suicide and cancer. The fact that approximately 20% of the sample died of heart failure is of importance given the growing evidence of cardiac problems among patients with (ME)CFS. Patients with (ME)CFS might have lower cardiac output, and the resulting low flow circulatory state could make it difficult for patients to meet the demands of everyday activity. Given that (ME)CFS is one of the more common chronic health conditions, affecting potentially 0.42% of the population, it is imperative for international researchers and public health officials to seriously study factors that might influence functioning and mortality of those with this condition”.
Jason found that the age at which people with ME/CFS died was considerably younger than would have been expected in the general population (Causes of Death Amongst Patients with Chronic Fatigue Syndrome. Leonard Jason et al. Healthcare for Women International 2006:27:615-626).
A memorial list of some of the people who have died from ME/CFS is available:
Illustrations of evidence about ME/CFS that NICE chose to ignore
It is known that the selection of the Guideline Development Group members was carefully controlled and that NICE “gave preference to those with day to day clinical experience for managing this condition” (letter dated 23rd December 2004 from Nancy Turnbull, Chief Executive of the National Collaborating Centre for Primary Care to the Medical Adviser to the ME Association, rejecting his offer to be a member of the GDG. The letter says that the NCC-PC is funded “to produce guidelines for the NHS by the National Institute for Clinical Excellence”). This is evidence that only those already engaged in behavioural interventions were favoured as members of the GDG, since there is currently no other management of the disorder in the UK available on the NHS. This would seem to confirm the widely-held view that the GDG was specifically chosen to deliver a pre-determined outcome.
It should be noted that despite the published views of some members of the GDG, there is no evidence of maladaptive beliefs, nor of phobic avoidance of activity, in patients with ME/CFS, but there is evidence that the fatigue is not due to lack of motivation or effort. Longitudinal studies using appropriate measures have shown that patients’ belief in a physical cause of their disease does not affect outcome; moreover, research indicates that a belief in a biological cause is not associated with poor mental health.
The alleged links between ME/CFS and psychiatric disorders reflect the overly-broad Oxford diagnostic criteria compiled by Wessely School psychiatrists and reflect these psychiatrists’ choice of measures for assessing psychiatric morbidity.
There can be no dispute that there is a substantial body of evidence showing that ME/CFS is not a somatoform disorder and should not therefore be managed as a somatoform disorder as recommended by the NICE Guideline.
The illustrations that follow were all available to the GDG but were ignored.
In 1990, Australian researchers Hickie, Lloyd et al studied the pattern of “psychiatric” symptoms in a well-defined sample of patients with ME/CFS and found it to be compatible with that observed in other medical disorders. “Patients were not excessively hypochondriacal. Our results suggest that ME/CFS patients are no more psychologically disturbed before the onset of their illness than members of the general population” (British Journal of Psychiatry 1990:156:534-540).
In 1991, US surgeon Thomas English described his own experience of ME/CFS: “There is nothing in your experience in medical school, residency, or practice with its gruelling hours and sleep deprivation that even approaches the fatigue you feel with this illness. I have talked with scores of fellow patients who went to our profession for help, but who came away humiliated, angry, and afraid. The psychospeculation of their physicians was frightening and infuriating. It told them their doctors had little understanding of the real problem. Many patients had lost careers, homes, families. There is nothing that you hold dear that this illness cannot take away from you. Nothing. This is no illness for cookbook doctors. It is a disease for medical intellectuals with supple and open minds” (JAMA 1991:265:8:964).
In 1991, Yeomans and Conway concluded that: “(ME)CFS is associated with physical, psychological and social distress (and) cannot be defined using just one of these dimensions”. Their study emphasised the ease with which psychiatric rating scales may lead to false positive diagnoses in patients with physical symptoms and concluded: “It is unnecessary and indeed unproductive to force patients into unsuitable diagnostic categories as a condition for treatment” (Journal of Infection 1991:23: (3):263-269).
In 1992, Nicole Phillips from Australia pointed out in the Australian and New Zealand Journal of Psychiatry: “It is important for psychiatrists to be aware of the rapidly expanding body of new literature on this illness. Wessely’s work on depression and CFS is methodologically flawed (because) the group of patients studied were those with ‘a primary complaint of fatigue for six months or more’. They were not diagnosed using the full criteria and therefore included many ‘non-pure’ CFS cases. The nature of the illness should be borne in mind when designing programmes with increasing levels of activity. Excessive physical exertion will exacerbate CFS symptoms and may worsen the course and prognosis. Psychiatrists need to utilise terminology such as ‘the sick role’ and ‘abnormal illness behaviour’ with great caution when discussing chronic illness. Not only will they alienate their medical colleagues but, more importantly, the patients they are trying to help” (Aust & NZ J Psychiatry 1992:26:329-330).
In 1995, Trigwell et al demonstrated that: “Those who see CFS as primarily a psychiatric disorder regard it as a variety of somatisation. Scores on the illness behaviour questionnaire cannot be taken as evidence that chronic fatigue syndrome is a variety of abnormal illness behaviour, because the same profile occurs in multiple sclerosis” (BMJ 1995:311:15-18).
In 1996, US neurologist Ben Natelson et al evaluated patients with ME/CFS for a placebo effect in a randomised, double blind, controlled trial and found no evidence that ME/CFS is an illness due to patients being overly suggestible or that ME/CFS is a psychogenic illness, and that: “No clear effect of any treatment has ever been demonstrated in this devastating illness” (Psychopharmacology 1996:124:226-230).
In 1996, Natelson et al examined the rates of somatisation disorder (SD) in ME/CFS relative to other fatiguing illnesses and found that the diagnosis of SD is extremely problematic in terms of its validity because it involves a series of judgments that can be arbitrary and subjective: “(ME)CFS can be viewed as an organic disease involving many organ systems or as an undifferentiated somatoform disorder. A diagnosis of somatoform disorder may be so arbitrary as to be rendered meaningless in illnesses such as (ME)CFS” (Psychosom Med 1996:58(1):50-57).
In 1997, a Review article by Jason et al found that flaws in the case definition and in the design of early epidemiolgical studies have led to “inaccurate and biased characterisations of (ME)CFS” which incorrectly favour a psychiatric view of the disorder. The authors were clear: “The erroneous inclusion of people with primary psychiatric conditions in (ME)CFS samples will have detrimental consequences for the interpretation of both epidemiologic and treatment efficacy findings. Until more differentiated subgroups are developed, it will be exceedingly difficult to identify characteristics that are common for all people with the diagnosis of (ME)CFS” (American Psychologist 1997:52(9):973-983).
In 1998, a report of an Australian international conference on ME/CFS held in Sydney on 12th –13th February noted the recommendation for “‘fully informing the medical profession….. to increase competence in diagnosis (and to include ME/CFS) in the medical student / training curriculum’.. The guidelines are also intended to ‘redress the harm and distress caused by inappropriate psychiatric referral, placing such misdiagnosis in the context of malpractice in terms of duty of care’ ” (Lancet 1998:351:574).
In 1999, Jason et al noted: “Chronic fatigue syndrome is one of the most debilitating medical conditions when quality of life indicators such as those measuring quality of relationships, financial security, and health status are used. Many physicians believe that most patients with this disease are suffering from a psychiatric illness. These biases have been filtered to the media, which has portrayed chronic fatigue syndrome in simplistic and stereotypic ways. Due to the controversy surrounding a chronic fatigue syndrome diagnosis, people with this illness are sometimes overwhelmed with disbelieving attitudes from their doctors, family and/or friends, and many experience profound losses in their support systems” (AAOHN J. 1999:47(1):17-21).
Also in 1999, Fred Friedberg, Clinical Assistant Professor, Department of Psychiatry and Behavioural Science, State University of New York, pointed out the differences between CBT trials in England and the US: “Several studies of graded activity-orientated cognitive behavioural treatment for CFS, all conducted in England, have reported dramatic improvements in functioning and substantial reductions in symptomatology. On the other hand, cognitive behavioural intervention studies conducted in Australia and the United States have not found significant improvements in functioning or symptoms. Descriptive studies of CFS patients in England, the US and Australia suggest that the CFS population studied in England shows substantial similarities to depression, somatization or phobia patients, while the US and Australian research samples have been clearly distinguished from primary depression patients and more clearly resemble fatiguing neurological illnesses. Because successful trials have all been conducted in England, a replication of these findings in a well-designed US study would be necessary before a general recommendation for graded activity / CBT could be made” (JCFS 1999:5: 3-4:149-159).
Another key paper in 1999 was one by Hill, Tiersky, Natelson et al. This study showed that the prognosis for recovery was extremely poor for the severely affected: the majority showed no symptom improvement and only 4% of the patients recovered: “Not only do patients with severe (ME)CFS not recover to full health, but they remain quite severely ill over many years. These data suggest that in patients who do not have psychiatric diagnoses before (ME)CFS onset, depressed mood is a correlate of illness rather than a risk factor for poor prognosis. The cost of (ME)CFS is great, both to the individual and to our society” (Arch Phys Med Rehabil 1999:80:1090-1094).
In 2000, Friedberg et al evaluated symptom patterns in patients with ME/CFS who had been ill for longer than 10 years; chemical sensitivities were assessed (these being a common feature of ME/CFS, which Wessely School psychiatrists ascribe to somatisation). Chemical sensitivity scores were significantly higher in the long-duration group. The authors found that: “long-range coping behaviour stabilises well before 10 years of illness. (ME)CFS symptom severity scores were significantly correlated with measures of allergy symptom severity. Allergy, confirmed by allergy testing, was the most frequently reported medical condition (88.8%). Evidence for hypersensitivity was found. A hypersensitivity mechanism and viral infection may contribute to illness persistence in (ME)CFS” ( J Psychosom Res 2000:48:59-68).
In January 2002, psychiatrist Alan Gurwitt who has been seeing patients with ME/CFS since 1986 published “Pseudo-science” in which he summed up the problem in the UK: “I have often been embarrassed by and angry at many of my colleagues who fall in line with self-declared ‘experts’ who see somatisation everywhere. Ever since the mid-1980s there have been ‘researchers’ with an uncanny knack at cornering research funds because of their already-formed biases that are in synch with the biases of the funding government organisations (and who) indicate that CBT and graded exercise will do the therapeutic job, thus implying a major psychological causative factor. I have noticed the following deficits in their work, their thinking, their word choices and their methods:
They often fail to distinguish between ‘chronic fatigue’ and CFS
They fail to distinguish between pre-illness psychological functioning and post-onset occurrence of reactive symptoms. This error would disappear if they did thorough psychiatric evaluations. Their failure to do proper in-depth psychiatric evaluations in at least some of their studies is a serious error with drastic implications
Their studies make use of flawed, inappropriate and superficial tests of psychological state which then lead to flawed, inappropriate and superficial conclusions. Their use of large numbers of study subjects gives the impression that they are scientific; in my view it is pseudo-science
They fail to include, or to be aware of, the mounting medical-neurological-immunological evidence demonstrating the medical nature of ME/CFS
They demonstrate instead a morbid preoccupation with psychiatric morbidity” (Co-Cure ACT 11th January 2002).
In response to an article in the BMJ 2002:324:1298 that promoted CBT and GET as the only effective treatments for “CFS/ME”, on 9th June 2002 the following was published in the eBMJ: “More naïve research: As a long-term CFS sufferer and retired psychology lecturer who taught CBT and behaviour modification, I can confirm that I have tried CBT and graded exercise and it does not work. CBT cannot do anything for the underlying physical and neurological problems. Hence CBT is a red herring for most of us long-term sufferers. What we need is serious research into the underlying factors” (James Wolsey).
In 2003, US researchers Tiersky and Natelson et al showed that in patients with ME/CFS, co-morbid psychiatric disorder, including anxiety or depression, is not related to physical disability in those who developed psychiatric disorder after becoming ill, in contrast to other diseases wherein co-morbid psychiatric disease does compromise physical functioning. Tiersky et al found that people with ME/CFS suffer from profound physical impairment, with scores below the standard norm for patients with type II diabetes, arthritis, cancer, congestive heart failure, hypertension and myocardial infarction (J Nerv Ment Dis 2003:191:324-331). It is noted that Natelson was also part of the research team that found left ventricular failure upon exertion in a subset of ME/CFS patients, which again produced hard scientific data using sophisticated tests that showed the profound disability in this disease. This study argues against the claims by Wessely School psychiatrists that the profound disability of ME/CFS is “in the cognition of those affected” (a view that persists in the widely-publicised work of the Wessely School which has in principle been adopted by NICE by virtue of its management recommendations).
In 2004, a US Centres for Disease Control (CDC) Surveillance study found that (ME)CFS subjects did not demonstrate any unique patterns of psychiatric disorders and noted that the CDC places ME/CFS at the top priority of new and re-emerging infectious diseases (EK Axe et al. JCFS 2004:12 (3) ).
In 2005, US researchers Song and Jason investigated whether the psychogenic (behavioural) model of ME/CFS by Vercoulen et al (which characterises patients as having insufficient motivation for physical activity or recovery, lacking self-control, and maintaining a self-defeating preoccupation with symptoms) could be replicated in a community-based sample. The authors noted that for some, ME/CFS was assumed to be a psy
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