CBT cannot improve ME/CFS -Background inf. & illustr. of evidence, which NICE disregarded

[Guest guest]

Dear Readers/Friends,

It was a hell of a job to edit this superb article,

but it was worth the trouble: a MUST for everyone,

who has something to do with the unbearable

disease ME/CFS.

I have two other articles by Margaret ,

which I will spread over several days.

For your convenience I will attach the original

version of this article the next time in doc

format.

~jvr

``````

Ralph

Permission to Repost

Note: I have created a page for all Judicial Review documents

and this can be found on a button at the top of the main page

of my website....

www.meactionuk.org.uk

Alternatively you can find the page directly by clicking on this

link... http://www.meactionuk.org.uk/nicejr.htm

The document below is the first in a series created specifically

for the NICE Judicial Review.

Please note that there is some duplication of documents

already published.

http://www.meactionuk.org.uk/Background_Information_re_CBT.htm

````````

Background information and

illustrations of evidence that

CBT cannot improve ME/CFS

which NICE disregarded

Margaret

25th July 2008

Executive Summary

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 " .

(iv) Conclusion

* 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, 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 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 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

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 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 "

(LocalME ).

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 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 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 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. 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 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. 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,

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, 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:

http://www.rcep.org.uk/pesticides/Crop%20Spraying%20web.pdf).

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 ( 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).

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 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 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

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.

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 " (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 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:

http://www.meactionuk.org.uk/Vade_MEcum.htm

http://www.meactionuk.org.uk/VASCULAR_PROBLEMS_IN_CFS.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 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 , 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

( 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 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 "

(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 Dowsett (former President of the ME Association)

and Doris (an independent ME/CFS researcher) in March

1998 (The Organic Basis of ME/CFS. EG Dowsett, DM ,

March 1998, available from DM at cost price:

0).

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 White, Dr

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

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 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; H, Osler's Webb 1996: Crown

Publishers, New York; Levine et al. JCFS 1999:7:1; Levine et al

1998: ls 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 ls

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,

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 " .

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 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:

(http://www.ncf-net.org/memorial.htm ).

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 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 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, 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 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, 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 naVve 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 " (

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 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 psychologically-determined problem (quoting

Wessely and Sharpe), and that while this model has been

cited frequently, no critical reviews or replication of the

Vercoulen et al study of 1998 (which characterised individuals

with ME/CFS as inclined to improperly associate physical

activity with a worsening of symptoms) have been published.

Song and tested the Vercoulen model six times. The

results showed that the Vercoulen model represented those

with chronic fatigue secondary to psychiatric conditions, but

did not represent those with ME/CFS: " In other words, the

present study does not support a psychogenic explanation for

(ME)CFS " (Journal of Mental Health 2005:14 (3):277-289).

In 2005, Canadian psychiatrist Eleanor Stein (whose practice

specialises in ME/CFS) published Chronic Fatigue Syndrome:

Assessment and Treatment of Patients with ME/CFS: Clinical

Guidelines for Psychiatrists (www.mefmaction.net ). Stein is

clear that the Oxford criteria (created and used by the

Wessely School) fail to exclude patients with primary

psychiatric diagnoses and are not often used by other

researchers. The symptoms of ME/CFS occur in multiple

organ systems and no other disorder can account for the

symptoms.

ME/CFS is not a primary psychiatric disorder; rates of

psychiatric disorder in ME/CFS are similar to rates in other

chronic medical disorders and studies that reported higher

prevalence rates of psychiatric disorder had sampling biases;

rates of personality disorder in ME/CFS are not elevated, and

illness severity, not psychological factors, predict outcome.

Stein is outspoken:

" Despite the preponderance of research to the contrary, a

group of primarily British psychiatrists continue to publish

that ME/CFS is caused and exacerbated by faulty

self-perception and avoidance behaviour. The faulty beliefs

are described as: 'the belief that one has a serious disease;

the expectation that one's condition is likely to worsen;

(patients with ME/CFS adopt) the sick role; and the alarming

portrayal of the condition as catastrophic and disabling'.

It should be noted that neither this paper nor any of the

others with similar views are evidence-based – they are the

personal opinions of the authors.

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.

Grief is a universal issue for people with ME/CFS. The losses

are numerous. Patients with ME/CFS cannot manage ordinary

stressors. The rationale of using CBT in ME/CFS is that

inaccurate beliefs and ineffective coping maintain and

perpetuate morbidity (but) it has never been proven that

these illness beliefs contribute to morbidity in ME/CFS.

It is likely that activity avoidance is necessary for the severely

ill. It is important to note that no CBT study has reported

that patients have improved enough to return to work, nor

have they reported changes in the physical symptoms.

Despite the fact that worsening of symptoms after exercise

is a compulsory criterion for diagnosis of ME/CFS, graded

exercise programmes have often been prescribed for such

patients (but) neither exercise tolerance nor fitness has

been shown to improve with exercise programmes. The

medical literature is clear that ME/CFS is not the same as

any psychiatric disorder " .

In 2005, et al were unequivocal: " Review of further

findings suggests that subtyping individuals with CFS on

functional disability, viral, immune, neuroendocrine, neurology,

autonomic and genetic biomarkers can provide clarification for

researchers and clinicians. Subgrouping is the key to

understanding how CFS begins, how it is maintained, how

medical and psychological variables influence its course, and

in the best case, how it can be prevented, treated and cured "

(Neuropsychology Review 2005:15:1:29-58).

In 2006, Demitrack encapsulated the problem that NICE

declined to address. In his paper Clinical methodology and its

implications for the study of therapeutic interventions for

chronic fatigue syndrome: a commentary, Demitrack was

concise:

" The role of clinical methodology in the study of therapeutics

is not trivial, and may confound our understanding of

recommendations for treatment " .

Demitrack noted the entanglement of physical symptoms

and behavioural symptoms, and the various studies by

certain psychiatrists purporting to show that the likelihood

of psychiatric disorder increased with the number of

physical symptoms.

He noted that " The most extreme view considers these

observations to provide convincing evidence that (ME)CFS is,

in essence, embedded in the larger construct of affective

disorders " .

However, in relation to ME/CFS, he noted that " The

observation of specific protracted fatigue and the absence

of substantial psychiatric comorbidity argues convincingly

that this is an inappropriate and overly simplistic way of

approaching this puzzling condition. A major consideration

in the approach to clinical therapeutics in (ME)CFS is the fact

that it is, by definition, a chronic illness. The magnitude of

disease chronicity is a feature that has an important impact

on overall treatment responsiveness. Given these

observations, it is notable that the specific methodology

used to measure treatment outcome rarely comes under

close scrutiny in studies of therapeutic intervention in this

condition. I believe it is crucial that the quality and

interpretability of past and future therapeutic studies of

(ME)CFS be critically appraised to the extent that they

have considered the impact of these issues in their design

and conclusions " .

Demitrack noted the growing body of central nervous system

(CNS) research, especially neuroendrocrine physiology and

neuroimaging studies, that have reinforced the view that

symptoms may indeed be manifestations of a primary

disruption in CNS function. In relation to interventions,

Demitrack was unambiguous:

" To appropriately design and implement (successful

interventions), it becomes critically important to specify the

patient population most likely to benefit from the proposed

intervention, and exceedingly important to define the

specific symptom, or cluster of symptoms, that may be

presumed to benefit from the intervention.

In the absence of a coherent understanding of disease

pathogenesis, it does not seem plausible that any single

intervention would be helpful in an undifferentiated

majority of patients.

It therefore may not be surprising that current treatment

options for (ME)CFS appear only modestly effective.

Non-response, or partial response is the norm, and more

than half of all patients fail to receive any benefit from

many interventions " .

Commenting on clinical outcomes, Demitrack says:

" Our group has shown that the measurement error of rating

scales can be enormous and can substantially undermine the

presumed statistical power of the study " .

Demitrack concludes: " In the face of accumulating

evidence, there is an increasing realisation that a unitary

disease model for this condition has been a theoretical and

practical impediment to real progress towards effective

therapeutics for (ME)CFS. Many treatment studies have,

unfortunately, neglected to thoroughly consider the

significance of patient selection (and) symptom

measurement " (Pharmacogenomics 2006:7(3):521-528).

In 2006, et al sought to subgroup patients with CFS

based on a battery of basic laboratory tests and identified

infectious, inflammatory and other subgroups. When compared

with controls, all subgroups reported greater physical

disability:

" CFS can impact any number of bodily systems including

neurological, immunological, hormonal, gastrointestinal and

musculoskeletal. Researchers have reported various biological

abnormalities, including hormonal, immune activation,

neuroendocrine changes and neurological abnormalities,

among others. However, studies involving basic blood work

appear to show no typical pattern of abnormality among

individuals with CFS.

" Borish et al (1998) found evidence of low level inflammation,

similar to that of allergies. Natelson et al (1993) found that

those with ongoing inflammatory processes reported greater

cognitive and mental disabilities. Buchwald et al (1997) found

individuals with CFS to have significant abnormalities in

C-reactive protein (an indicator of acute inflammation) and

neopterin (an indicator of immune system activation,

malignant disease, and viral infections). Buchwald et al

(1997) stated that individuals with active low level

inflammatory, infectious processes could be identified and

that this was evidence of an organic process in these patients

with CFS. Cook et al (2001) found that individuals with an

abnormal MRI and ongoing inflammatory processes had

increased physical disability, suggesting an organic basis for

CFS.

" Clearly, individuals diagnosed with CFS are heterogeneous.

" Grouping all individuals who meet diagnostic criteria

together is prohibiting the identification of these distinct

biological markers of the individual subgroups. When

specific subgroups are identified, even basic blood work

may reveal a typical pattern of abnormality on diagnostic

tests (DeLuca et al. 1997; Hickie et al. 1995; et al.

2001).

" The relationship between psychiatric diagnosis and CFS

diagnosis is one that is far from being understood.

Discussing the subtypes found, et al state:

" It is notable that these findings emerged utilising only a

basic battery of laboratory screening tests. Many people

with CFS exhibit only minimal or subtle abnormalities on

these tests, and these abnormalities may not be

acknowledged by the primary care physician.

" The more commonly reported physiological abnormalities

in people with CFS, such as the presence of RNase L

(Suhadolnik et al 1997), adrenal insufficiency with

subsequent low cortisol levels (Addington 2000), the

presence of orthostatic intolerance (Schondorf et al 1999),

and immunological abnormalities (Patarca-Montero et al

2000) can only be assessed using highly specialised tests to

which people with CFS typically have little access.

" This study demonstrates that subgrouping is possible

using laboratory tests that are readily available and can

easily be ordered by primary care physicians.

" The identification of clinically significant subgroups is the

next logical step in further CFS research. Previous

research examining people with CFS as a homogeneous

group may have missed real differences among subgroups

of this illness " (Exploratory Subgrouping in CFS: Infectious,

Inflammatory and Other. In: Advances in Psychology Research

2006:41:115-127. A Columbus (Ed): Nova Science Publishers,

Inc).

In 2007 (although possibly too late to have been considered

by the GDG, had it been minded to do so, but 61 out of 64

references pre-date the Guideline, so were available to the

GDG), an important article by and Richman reviewed two

aspects of ME/CFS: the issues involving the inappropriate

name of the illness favoured by some psychiatrists ( " chronic

fatigue syndrome " , which undoubtedly trivialises the disorder),

and the flawed epidemiological approaches, both of which may

have contributed to the diagnostic scepticism and the stigma

that those with ME/CFS encounter.

The authors suggest that the increases in cases during the

past 15 years are due to a broadening of the case definition to

include those with primary psychiatric conditions (as the

Wessely School and NICE have done). The authors note how

flawed epidemiology can contribute to inappropriate

stereotypes, and stress the need for accurate measurement

and classification in disorders that might be labelled as

'functional somatic syndromes' (as the Wessely School deems

ME/CFS to be). The authors state:

" Accurate measurement and classification of (ME)CFS,

fibromyalgia and irritable bowel syndrome is imperative when

evaluating the diagnostic validity of controversial disease

entities alternatively labelled 'functional somatic syndromes'.

Measurement that fails to capture the unique

characteristics of these illnesses might inaccurately

conclude that only distress and unwellness characterise

these illnesses, thus inappropriately supporting a unitary

hypothetical construct called functional somatic syndromes "

(JCFS 2007:14(4):85-103).

Despite the considerable amount of peer-reviewed

international evidence that it is imperative to subgroup the

heterogeneous condition " CFS " , the GDG stated that there is

no evidence to justify subgrouping (see below) and the

Guideline recommends blanket behavioural management

regimes for everyone (mildly, moderately and severely

affected, and children and adolescents with " CFS/ME " in the

UK.

The evidence that CBT is ineffective

Despite the placatory verbiage in the Guideline, the bottom

line is that it recommends CBT/GET for all patients in the UK

with " CFS/ME " , and this includes those with distinct ME/CFS.

There is abundant evidence that CBT does not work, not only

in ME/CFS but in general, yet this evidence was disregarded by

the GDG (see for example:

http://www.meactionuk.org.uk/Deliberate_deceit.htm and

http://www.meactionuk.org.uk/EVIDENCE_OF_EFFICACY.htm

Although post-dating the NICE Guideline on " CFS/ME " , a

University of East Anglia conference has exploded the

widespread myth that CBT is more effective than other types

of therapy. CBT has been the subject of massive Government

investment, as in the £8.5 million awarded for the setting up

of " CFS " Centres specifically to deliver CBT to " CFS/ME "

patients, and the £2.6 million awarded to the Wessely School

psychiatrists by the MRC to support the claimed efficacy of

CBT in " CFS/ME " , and recently CBT has been the subject of a

£173 million Government grant.

The UEA conference was told: " The Government, the public,

and even many health officials have been sold a version of

the scientific evidence that is not based in fact, but is

instead based on error " . The conference was told that three

combining factors have helped perpetuate the CBT myth: (i)

more academic researchers subscribe to the CBT approach than

to any other; (ii) these researchers get more research grants

and publish more studies on the alleged effectiveness of CBT

and (iii) this greater number of studies is used to imply that

CBT is effective (News Desk, 18th July 2008).

International concern about the efficacy of CBT that definitely

pre-dated the Guideline is to be found on the US CDC website:

" The utility of CBT for CFS is in its formative stages and

much needs to be learned before the limits of its usefulness

are known "

http://www.cdc.gov/cfs/docs/wb3151/appendix-c.pdf

Not only did NICE ignore the evidence that the

recommended interventions (CBT/GET) are not effective,

it also ignored the evidence that subsuming all states of

" chronic fatigue " into one functional somatic syndrome is

contra-indicated, as well as the evidence that most of the

RCTs on CBT on which the GDG relied are seriously flawed.

The GDG's " evidence-base "

The York Review of 2005 (which is the 488 page Appendix I to

the Guideline that was written by Bagnall et al specifically to

support the work of NICE) identified ten trials of CBT that

were deemed suitable for inclusion in the Systematic Review.

There were five RCTs of CBT, one controlled trial of CBT

(Whitehead et al, 2002), and four studies of modified CBT

( 1999, 2002, Friedberg 1994, 2004, which do

not appear to have been fed into the recommendations).

In most of the ten identified trials of CBT, the methodology

does not meet even the most minimally acceptable standards.

Somewhat carelessly, page 198 of the Full Guideline states at

6.3.3.1: " Ten RCTs (sic) met the inclusion criteria for

assessment of CBT or modified CBT in people diagnosed with

CFS according to one of the recognised case definitions. Eight

of the studies reported beneficial effects of CBT. Two studies

with low validity scores showed no significant differences " .

Five out of the ten listed trials of CBT registered no overall

effect (see Full Guideline, Appendix I [York Review 2005] page

94). If the RCT of group-CBT (O'Dowd, 2006) is included, then

six out of eleven trials registered no overall effect. However,

the Full Guideline states on page 198: " Eight of the studies

reported beneficial effects of CBT " . This discrepancy may be

explained as " positive spin " by the GDG, which distinguishes

between some beneficial effect and no overall effect.

Such " positive spin " is also used about the Lloyd et al 1993

study (see below), which was given an overall positive rating

for CBT when in fact the CBT effect was negative, but because

in that study CBT was combined with immunoglobulin therapy

(which had a positive effect), the RCT as a whole was given a

positive outcome and is included in the five successful RCTs of

CBT.

The five specific RCTs of CBT on which the GDG relied were:

1. Deale A, Chalder T, Marks I, Wessely S. Cognitive

behaviour therapy for chronic fatigue syndrome: a randomised

controlled trial. Am J Psychiat 1997:154:408-414 (60

patients)

2. Deale A, Husain K, Chalder T, Wessely S. Long-term

outcome of cognitive behaviour therapy versus relaxation

therapy for chronic fatigue syndrome: a 5-year follow-up study.

Am J Psychiat 2001:158:2038-2042 (this was a 5-year

follow-up of their 1997 study and had 53 patients)

3. Lloyd AR, Hickie I, Brockman A, Hickie C, A, Dwyer

J et al. Immunologic and psychiatric therapy for patients with

chronic fatigue syndrome: a double-blind, placebo-controlled

trial. Am J Med 1993:94:197-203 (90 patients). Note that

there is a discrepancy in the stated number of patients: page

54 in the 488 page Appendix (the York Review of 2005) gives

the number of patients as 49, but this becomes 90 in the JRSM

version of the same study

4. Sharpe M, Hawton K, Simkin S, Surawy C, Hackmann A,

Klimes I et al. Cognitive behaviour therapy for the chronic

fatigue syndrome: a randomised controlled trial. BMJ

1996:312:22-26. (60 patients). Note that there is an error

given on page 54 in Appendix I in relation to this study: the

date is written as 1998 but should be 1996

5. Prins JB, Bleijenberg G, Bazelmans E, Elving DL, de Boo

TM, Severens JL et al. Cognitive behaviour therapy for chronic

fatigue syndrome: a multicentre randomised controlled trial.

Lancet 2001:357:841-847 (270 patients).

The correct number of patients in the Lloyd et al study is 90,

not 49 as stated on page 54 in Appendix I (the York

Systematic Review of October 2005).

Excluding the Deale et al follow-up study of the same

patients, this gives 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.

The 2005 version of the York Review was modified and

published again in the Journal of the Royal Society of Medicine

in October 2006 (before the Guideline was published in August

2007). This version identified seven RCTs of CBT, which

included two RCTs on children (Viner 2004 and Stulemeijer

2005) that were excluded from recommendation.

Those RCTs of CBT using the Oxford criteria (Deale at al 1997;

Deale et al 2001 [i.e. the follow-up of the patients from the

1997 study]; Sharpe et al 1996) cannot be studying people

with ME/CFS, since the pathognomonic feature of ME/CFS is

post-exertional incapacitating fatigability combined with

malaise, and this cardinal feature is excluded from the Oxford

case definition. Despite this, NICE has relied on these studies

to recommend CBT for patients with ME/CFS.

Of the remaining two RCTs, the Lloyd study used the

Australian criteria, which have never been adopted

internationally, and the Prins et al study used their own

modification of the US CDC 1994 Fukuda et al criteria (which

themselves do not exclude patients with somatoform disorder:

Ann Intern Med 1994:121:953-959 and the international

medical literature increasingly expresses doubt about their

usefulness, for example: Salit IE. J Rheumatol

1996:23:540-544; et al. JCFS 1999:5:3-33; et al.

Evaluation and the Health Professions 2003:26:13-22;

Darbishire L et al. BJGP 2003:53:491:441-445; Kennedy G et

al. Ann Epidemiol 2004:14:95-100; et al. JCFS

2004:12:1).

Although technically invalid because by definition it excluded

those with ME/CFS, it is notable that there were many other

methodological flaws in the Deale et al 1997 study. In this

study of 60 patients, half received CBT in the form of " graded

activity and cognitive restructuring " and half received

" relaxation " .

The authors state: " CBT is used to modify behaviours and

beliefs that may maintain disability and symptoms " . Three

subjects withdrew from the CBT group and four withdrew from

the relaxation group.

The authors state that at final follow-up (six months after the

course of CBT and relaxation completed), 19 patients

" achieved good outcomes compared with 5 patients in the

relaxation group " .

Somatisation disorder and severe depression are cited as

exclusion criteria; nine participants, however, are described as

having 'major depression' and there were high levels of

existing psychiatric morbidity in the study cohort.

Outcome measures are said to relate to " subjectively

experienced fatigue and mood disturbance, which are the

areas of interest in chronic fatigue syndrome " .

This statement alone indicates that the study cannot be

considering people with ME/CFS because neither " fatigue " (or

" tiredness " ) nor mood disturbance is a defining feature of

ME/CFS (the defining feature of ME/CFS being post-exertional

muscle fatigability with malaise).

Of concern is the fact that the authors state: " The aim was to

show patients that activity could be increased steadily and

safely without exacerbating symptoms " .

That is a remarkable statement. It demonstrates that the

authors had decided -- in advance of the outcome -- that

activity could be increased without exacerbating symptoms.

This is not merely the authors' hypothesis: that this will be

the outcome is taken for granted. Of note is the fact that the

outcome did not meet the authors' certainty, and the authors

had to concede that:

" cognitive behaviour therapy was not uniformly effective: a

proportion of patients remained fatigued and symptomatic " .

Perhaps for this reason, the presentation of results is mostly

reported as averages, rather than giving actual numbers of

patients. The authors acknowledge that: " The data from all

the outcome measures were skewed and not normally

distributed, with varying distributions at each measurement

point " .

In such circumstances, merely providing " average " figures is

not the most appropriate illustration of findings. In summary,

this RCT has little relevance in general and none whatever to

people with ME/CFS (with grateful acknowledgement to ScotME

for this analysis).

Although once again a technically invalid study in relation to

ME/CFS (because it used the Oxford criteria, of which Sharpe

was the leading author), the Sharpe et al study of 1996 merits

comment.

This again was a small study of just 60 patients, of which only

30 patients received CBT (the other 30 being controls). Sharpe

et al concluded: " CBT was both acceptable and more effective

than medical care alone (but) few patients reported complete

resolution of symptoms and not all improved " .

At the time, the study received much media publicity, with

inflated claims of success. When countered by informed

ME/CFS patients, The Independent published a hostile article

by Rob Stepney (26th March 1996) attacking ungrateful

patients:

" Many sufferers are bitterly opposed to (CBT), arguing that

their condition is physical, not psychological. 'Many patients

have a personality which hinders recovery'. Surprisingly, (the

study) has received a luke-warm response from a source one

might expect to be more enthusiastic. (The ME Association)

says of the Oxford study: 'The full weight of righteous zeal

exhibited by the therapists does not seem to have produced

anything more than a perfunctory change at the margins of the

illness'.

'ME is an escape route for the middle classes' claimed one

psychiatrist " .

What was not made public was the fact that Rob Stepney's

wife was one of the Oxford therapists involved with the trial.

On 30th March 1996 The Independent published a letter from a

trial participant ( Rye):

" I am a sufferer and participated in the trial. The article

implies that a new successful treatment has been found for

ME but that sufferers do not want to accept it. There are facts

about the trial that throw into doubt how successful it is. It

is stated that patients in the control group received standard

medical care. I was in that group but I received nothing.

Patients who 'improved significantly' only increased their score

from 70 to 80 on a scale of general functional ability " .

Despite having to acknowledge the fact that few patients

reported resolution of symptoms, the authors nevertheless

asserted: " The results show that a return to normal

functioning is possible in most cases. We believe that our

results have important implications for the management of

patients with chronic disabling fatigue " .

Once again, Wessely School psychiatrists seemed determined

to confuse chronic disabling fatigue with ME/CFS. The ME

Association's Medical Adviser wrote on 18th January 1996 in

The Times:

" Although 22 patients out of 30 in the Oxford trial of CBT

achieved an improvement of approximately 10% in their

disability rating after a year, the only other two controlled

trials of CBT to be published found no benefit from this

fashionable form of short-term psychotherapy. The ME

Association believes that the results so far obtained do need

to be viewed with a considerable degree of caution " .

Notwithstanding, this study forms the " best practice

evidence-base " for NICE's recommendation of CBT for all

patients with " CFS/ME " in the UK, including those with ME/CFS.

The Prins et al study of 2001 which was included in the " best

practice evidence-base " for the NICE Guideline's CBT

management regime has received perhaps more legitimate

criticism than any of the other three studies.

Prins et al state that out of 476 patients diagnosed with CFS,

only 278 were eligible and willing to take part. Those who

refused to take part, had they done so, may have altered the

outcome substantially. Patients with pre-existing psychiatric

comorbidity (one third of the subjects) were not excluded.

From the outset, the authors excluded those with ME/CFS

because they state that the fatigue they were studying was

" not the result of organic disease or ongoing exertion " .

The authors acknowledge that there was a very high drop-out

rate in the treatment arm, but do not provide reasons for the

drop-outs, nor do they report if there were any adverse effects

from the CBT.

As noted by Bland, Professor of Health Statistics at the

University of York in a personal communication (6th June

2008), loss to follow-up of participants is a serious problem in

this trial and the groups may no longer be comparable because

in this trial, the drop-out is greater in the CBT group than in

the control group.

People who after randomisation refused CBT, or after starting

CBT discontinued it were not followed up, but they should

have been, for the control group contained people who, given

the opportunity, would have refused to start or would have

discontinued treatment, and it might plausibly be thought that

such people would do less well than acceptors. Bland states:

" I think that this invalidates the entire Prins trial. There are

methods which have been developed to impute missing data,

but they do not appear to have been used " .

If drop-outs were due to adverse effects, these should have

been reported, since exclusion of these statistics would allow

over-estimation of the alleged benefits of CBT. Further, people

may drop out of a trial because – although not actively harmed

by it -- they receive no benefit; this again was not included in

the Prins study. Had they done so, it might have distorted

their results in a manner that did not fit their required

outcome, because the trial had " cure of chronic fatigue

syndrome as its explicit goal of therapy " .

Of major importance is the fact that Prins et al used their own

modification of the 1994 CDC Fukuda et al case definition.

Patients were eligible for the study if they met the CDC

criteria with the exception of the requirement for four of eight

additional symptoms (those symptoms being impaired memory

or concentration; sore throat; tender cervical or axillary lymph

nodes; muscle pain; multi-joint pain; new headaches;

unrefreshing sleep, and post-exertional malaise).

If these important symptoms are omitted from the entry

criteria, one is left with idiopathic chronic fatigue, yet Prins et

al refer to their study participants as having " CFS " according to

the CDC 1994 criteria.

This would seem to border on deceit. Nowhere is there any

evidence that the patients fully recovered, and a key outcome

did not support the authors' expectation, because for the CBT

group: " Differences in the time spent working in a job did not

reach the 5% level of significance " .

Despite this evidence, the authors still concluded:

" The results of this trial suggest that CBT can be transferred

from CFS research clinics to therapists with no previous

experience of CBT. To increase accessibility of this treatment

for all CFS patients in future, CBT will have to be implemented

outside university medical settings. This idea accords with

Wessely and colleagues' suggestion of transferring the

diagnosis and treatment of functional somatic syndromes to

general physicians aided by psychiatrists. Ideally, general

practitioners should diagnose CFS and refer patients to

psychotherapists for CBT without detours to medical

specialists, as in other functional somatic syndromes " .

The fact that NICE relied on this particular trial as

the mainstay of its recommendations is disturbing.

Clearly NICE has ignored the cogent published criticisms of the

Prins et al trial, for example:

" Judith Prins and colleagues' report leaves the clear

impression that there is a powerful case for the provision of

CBT as a specific therapy for CFS. However, careful

assessment of published studies suggests that this impression

is not evidence-based. Conclusions about efficacy must be

tentative in view of the paucity of trials; the small number of

patients involved; the difficulties in comparing CBT with

control interventions and, importantly, the potential effect of

publication bias " (Vance A Spence and Neil C Abbot. Lancet

2001:358:9277:239-240).

The Medical Director of the ME Association wrote to The Lancet

pointing out:

" Although the purely psychosomatic explanation favoured by

Prins and colleagues may well apply to one subgroup of

patients with CFS, there are others in whom there is evidence

of neurological, muscular and endocrine abnormalities which

cannot be adequately explained by a psychosomatic model.

Underlying organic pathology may help to explain (why)

objective evidence of substantial and sustained recovery (ie.

return to normal employment) is seldom achieved " .

A notable feature of these four studies is that they had

different entry criteria and different (indeed, very diverse)

outcome measurements, so cannot be compared. Indeed, the

York Review (2005) acknowledged that: " standardisation of

outcomes are a priority for research " . All four studies were

very small, and all have serious methodological flaws.

As noted by Abbot and Spence in 2006, the behavioural model

of " CFS/ME " offers relatively little; it is supported only by

researchers with a professional interest in psychosocial

aspects of illness who have acquired the funding to test their

hypotheses; the evidence-base for the usefulness of this

model consists of a small number of clinical trials which, even

by their own standards, have relatively unspectacular results,

yet this model dominates the canvas (Lancet

2006:307:1574).

This model certainly dominates the NICE management

recommendations.

Based on these four studies (and one follow-up study), it is

illogical for the GDG to recommend CBT as an effective

intervention for all people with " CFS/ME " in the UK, especially

as that term is said to include people with ME/CFS.

That the term " CFS/ME " is deemed by NICE to equate exactly

to ME/CFS has been established by NICE:

" We were not able to find the CDC (US Centres for Disease

Control) statement that the conditions were different? "

(NICE CFS/ME Consultation Draft, 29th September – 24th

November 2006, comments on Chapter 1; NICE CG53 website).

This is a remarkable statement by NICE, because the CDC

website clearly confirms:

" Various terms are incorrectly used interchangeably with CFS.

The name ME was coined in the 1950s to clarify

well-documented outbreaks of disease: ME is accompanied by

neurological and muscular signs and has a case definition

distinct from that of CFS " .

This is the CDC Continuing Education Course WB1032

http://www.cdc.gov/cfs/cme/wb1032/chapter1/overview.html

It is even more remarkable that in its comments on

stakeholders' submissions, despite having had numerous

submissions pointing out the need to subgroup " CFS "

(including from The Royal College of Physicians of London and

The British Psychological Society), the GDG asserted

incorrectly seven times (for example, in their comments on the

submission from The 25% ME Group for the Severely Affected

(page 1 of 575); in their comments on submission from The ME

Association (page 455-456 of 575); in their comments on the

submission from The Young ME Sufferers Trust (page 490 of

575):

" No research evidence was found for defined sub-groups

or different management strategies " .

" While it is generally recognised that (CFS) is

heterogeneous, the evidence does not allow distinctions

between subgroups " .

There is an abundance of evidence, but it is not contained in

the four RCTs of CBT upon which the GDG chose to rely.

Professor Leonard , without doubt one of the world's

leading researchers into the disorder, has clarified this issue:

" The term ME/CFS is now being used in many countries, as

proposed by the Canadian Case Definition (Carruthers et al,

2003).

" It is possible to distinguish between the two conditions,

but if the current case definition of CFS does not identify

patients with specific symptoms (e.g. post-exertional

malaise), then it would be easy to miss some individuals

who really have ME/CFS and to include others who do not

have this illness. If this occurred, it would be impossible to

identify consistent biological markers of this illness, and

then many researchers and clinicians would conclude that

ME/CFS was a psychosomatic illness.

" Clearly, some patients with this illness do have

inflammation and others do not (Exploratory subgrouping in

CFS: Infectious, inflammatory, and other. Corradi, &

-Harding, 2006. In: A Columbus (Ed): Advances in

Psychology Research, Volume 41, pp 115-127; Hauppage, NY:

Nova Science Publishers).

" The current method of grouping all individuals who meet

the CFS diagnostic criteria together is complicating the

identification of biological markers that will help scientists to

unravel the pathophysiology of this illness.

" The name myalgic encephalomyelitis has a 50 year history in

the medical literature and it has been formally classified by

the WHO as a neurological disease in the ICD since 1969 and

remains classified in the current ICD as a neurological disorder

(ICD-10 G93.3). In contrast, Myalgic Encephalopathy is not

defined as a specific condition and has no ICD status. Many

advocates believe that we would lose that 50 years of

historical lineage if we endorsed the term Myalgic

Encephalopathy.

" Many feel that there is considerable benefit of maintaining

the name Myalgic Encephalomyelitis, which is the most

consistently used and most widely recognised name

worldwide, with an established neurological ICD code and a

well-documented history of outbreaks along with extensive

epidemiological investigations.

" Researchers and clinicians need to be aware of the strong

sentiments that patients have for Myalgic Encephalomyelitis,

which is historically correct (Ramsay 1981) and has been used

internationally (Hyde, Goldstein & Levine, 1992) " (Issues

Involved in Name Change Recommendations. Leonard A

et al.

http://listserv.nodak.edu/cgi-bin/wa.exe?A2=ind0705B & L=CO-CURE & D=0 & F=P & I=-3 & P=35\

29 & F

Evidence about CBT for " CFS/ME "

that did not inform the GDG's

management recommendations

Other RCTs that were excluded from the GDG " evidence-base "

have found no difference in outcome after CBT for patients

with " CFS/ME " , for example, Huibers and Beurskens et al's

findings were unequivocal:

" There was no significant difference between the experimental

group and the control group on primary or secondary outcomes

at any point. Cognitive behavioural therapy by general

practitioners for unexplained, persistent fatigue did not prove

to be an effective intervention " (Brit J Psychiat

2004:184:240-246).

It is notable that this trial post-dates the Prins et al study,

whose stated aim was to implement Wessely's intention of

transferring the diagnosis and treatment of CFS to general

practitioners, and that two of the authors were also co-authors

of the Prins 2001 study (Bazelmans and Bleijenberg).

Work by et al that casts significant doubt on the

claimed efficacy of CBT was also ignored. Although his major

review of non-pharmacologic interventions for CFS was

published after the production of the Guideline (in this case, in

December 2007, but members would have been expected to

know about it; moreover, many of the references pre-date the

Guideline so were available to the GDG), it is customary for

authors of systematic reviews to seek, obtain and quote from

articles in press. (For example, in their 2006 up-dated Review

that was published in the JRSM, Chambers and Bagnall et al

ought to have referred to the negative findings of the 2006

O'Dowd study of group-CBT, but they did not do so).

et al are clear: " Despite improvement found in a number

of interventional studies (referring to the Deale et al 1997

study and the Sharpe et al 1996 study upon which NICE

relied), other studies have been less successful. Furthermore,

physician-delivered CBT for CFS participants has not shown

efficacy in two studies. In 2001, Ridsdale et al found that

counselling was as effective as CBT. Given the mixed results

for these cognitive and behavioural interventions, it is unclear

which type of non-pharmacologic intervention is most

effective for participants with CFS " .

et al make the point that even in their own trial of

different forms and combinations of CBT, " the changes in the

present trial were relatively modest and few participants

experienced remission of illness " . The authors also note the

lack of long-term effects when the (very high) drop-put rates

are taken into consideration.

In contrast to the Wessely School, et al support a model

of CBT which " serves as a coping tool that allows the

participant to view his/her reactions to the illness as

understandable adjustments to an unpredictable, disabling

condition " and which " might be considered an important

management tool that can be utilised as part of a

comprehensive plan of medical and psychological treatment

for patients with CFS "

(J Clin Psychol Med Settings 2007:14:4:275-296).

In a personal communication, wrote:

" I continue to believe that although some non-pharmacologic

interventions can be helpful to some people in learning to

better cope with many chronic conditions, from cancer to

AIDS, they should not be used as the only treatment modality,

and as we all know, this all too frequently occurs with

ME/CFS " (25th July 2008).

A meta-analysis of CBT for CFS which does not accord with the

NICE Guideline is that of Malouff et al from Australia; again

this was published in 2007, but only 2 of 55 references

post-date the Guideline (so 53 were available to the GDG).

Malouff et al identified 13 studies that met their inclusion

criteria and the authors were more stringent than the York

reviewers upon whom the GDG relied, as Malouff et al

excluded a study which Bagnall et al (the York reviewers)

decided to include (in which a substantial number of

participants received treatment after the study treatment --

Deale, Husain, Chalder and Wessely, 2001; reference 148 in

the Guideline Appendix I).

This is significant, because in the UK, it was stated on BBC

Radio 4 (You and Yours; 7th November 2007) that Professor

Trudie Chalder claimed that CBT is " curative " for 25% of

patients, basing this assertion on her own study (Deale,

Husain, Chalder and Wessely, 2001); NHS Plus claims that CBT

will return people to gainful employment, based on the same

2001 study, and the NICE Guideline claims there is good

evidence for the efficacy of CBT, again based on the same

study (Deale et al 2001).

However, as pointed out by Hooper & Reid,

(http://www.meactionuk.org.uk/FINAL_on_NICE_for_Gibson.html),

the data in that study was corrupted, so no reliable

conclusions can be drawn from it. Malouff et al agreed, and

declined to include it in their meta-analysis.

There is another interesting comparison: in their up-dated

Review (2005) that was done specifically to support the work

of NICE, Bagnall et al excluded a study by Ridsdale et al

(Chronic fatigue in general practice: Is counselling as good as

cognitive behaviour therapy? A UK randomised trial in primary

care. British Journal of General Practice 2001:51:19-24) which

found that counselling was just as effective as CBT, but

Malouff et al included it as being essential for the comparative

assessment of CBT. Bagnall et al had included this study in

their JAMA 2001 Systematic Review yet, curiously, they

excluded it from their 2005 Systematic Review of the same

literature that was done to support the work of NICE.

This would seem to be yet more evidence supporting the

contention that the NICE Guideline was indeed a case of

" policy-based evidence " and not " evidence-based policy " .

Following rigorous analysis, Malouff et al noted the drop-put

rates (up to 42%) and concluded: " One can conclude that CBT

for chronic fatigue disorders has about the same efficacy as

diverse psychological treatments for a variety of psychological

disorders. There presently appears to be no empirical basis

for including cognitive components in treatment of fatigue

disorders " (Efficacy of cognitive behavioural therapy for

chronic fatigue syndrome: A meta-analysis. Clinical Psychology

Review. 2007. Doi:10.1016/j.cpr.2007.10.004).

Another significant study which does not support the NICE

approach of combining all states of " medically unexplained

fatigue " into a single somatoform disorder is that of et

al which provides clear evidence of how different subgroups of

" CFS " may respond to nonpharmacologic interventions such as

CBT (Baseline Cortisol Levels Predict Treatment Outcomes in

Chronic Fatigue Syndrome Nonpharmacological Clinical Trial.

JCFS 2007:14:4:39-59).

" Early researchers describing nonpharmacologic behavioural

interventions for CFS reported high levels of success (Deale,

Chalder, Marks & Wessely, 1997, Prins et al 2001; Sharpe et al

1996), but more recent studies have had somewhat more

mixed results (Bazelmans et al 2005; Donta et al 2003;

Ridsdale et al 2004; Ridsdale et al 2001). Bazelmans et al

found that those who improved the most had fewer complaints

at baseline.

" Cleare et al (2003) found that response was differentiated by

baseline urinary cortisol levels, i.e. those with normal baseline

levels responded more positively to the intervention than

those with initial abnormally low levels.

" Those individuals with most impaired

hypothalamic-pituitary-adrenal axis (HPA) function might

be the least able to improve with nonpharamcologic

interventions.

" It is possible that some individuals with CFS have a cortisol

deficiency and others do not, but when all are combined

into one large CFS category, these important differences

are ignored.

" Understanding how nonpharmacologic interventions

differentially affect the subgroups of individuals with CFS

might provide insight into the pathophysiology of this

illness " .

In this study, " Among those with abnormal baseline cortisol,

63% had low activity levels at the 12-month follow-up,

whereas among those with normal baseline cortisol, only 35%

had low activity levels at the 12-month follow-up.

" This indicates that those who are most impaired

on HPA functioning might be least able to improve

(with CBT) " .

Noting that immunologic functioning did not improve as a

result of CBT (Peakman et al, 1997), this study also looked at

disturbances of immune function, and found significant

immunological abnormalities in the group with abnormal

cortisol at baseline, suggesting that " a stimulus, present in

these individuals but absent in the normal cortisol group, is

responsible. (This) likely represents an important component

of the immune dysfunction associated with the pathogenetic

process of CFS.

" In summary, subgroups of individuals with either normal

or abnormal cortisol levels exhibited different outcomes in a

nonpharmacologic treatment trial.

" This suggests that cortisol levels may serve as an

important marker for individuals with CFS that might

benefit from CBT.

" This study suggests that subgrouping according to

endocrinologic functioning is a useful strategy for assessing

the effects of treatment " .

It is the case that the NICE Guideline proscribes testing

cortisol levels and regards all cases of " CFS/ME " as a

behavioural disorder.

By strategically limiting its selected " evidence-base " to just

four RCTs of CBT, the GDG has ignored a wealth of good

quality studies and empirical evidence which question the

reliability of those RCTs.

Wessely School psychiatrists often accuse patients with

ME/CFS of " catastrophising " their symptoms, and of holding

" catastrophic illness beliefs " , but the chosen RCTs do not

address symptoms of ME/CFS other than " fatigue " , such as

repeated, prolonged vertigo (which is catastrophic), or

frequent episodes of incapacitating chest pain of similar

intensity to a myocardial infarction (which are catastrophic), or

the inability to look after oneself (which again is

catastrophic). Wessely School psychiatrists exclude such

patients from their studies. Consequently, the NICE Guideline

does not accord such symptoms sufficient prominence.

In summary, there is no credible evidence to support the

GDG's claim that the evidence-base for " best practice " is the

nationwide implementation of CBT/GET for patients with

" CFS/ME " if, as stated, this includes patients with ME/CFS.

Even the authors of the first York Systematic Review (2001)

themselves offered many cautions about their results

(including poor quality evidence; the studies were

methodologically flawed; inconsistencies in case definitions;

exclusion of the severely affected and children etc) but these

caveats were largely missing from the 2005 version that was

compiled by the same authors specifically to support the work

of NICE.

Missing evidence for the

NICE recommendations

It is notable that the RCTs upon which the GDG relied all

promote the Wessely School model of CBT (i.e. the need to

change aberrant illness beliefs about the nature of the

disorder by the re-structuring of cognitions, increase of

physical activity, and the return to work). This required

patients to push themselves beyond their physical capabilities

and was based on the " no pain, no gain " philosophy (eg.

Fulcher and White, BMJ 1997:314:1647-1652, which

stipulated:

" If patients complained of increased fatigue they were

instructed to continue at the same level of exercise and

increase when the fatigue had lessened. All patients were

instructed to continue with regular exercise " ).

A disturbing number of patients have reported in numerous

ME/CFS support group magazines that they were subjected to

rigorous, oppressive and even abusive regimes. In one

shocking case, the mother of a child severely affected by

ME/CFS discovered that the therapist had written a treatment

plan and that this plan stated:

" We expect (her son's name) to protest, as well as the activity

causing him a lot of pain. This may result in screams….it may

feel punitive "

(http://wwwmeactionuk.org.uk/Inquest_Implications.htm).

However, the actual advice in the NICE Guideline has modified

somewhat this disproved model and is more focused on

psychological support and helpful coping strategies that are to

be undertaken with the co-operation of the patient (i.e.

working in partnership with the patient). This is very different

from the original Wessely School model.

Whilst this is to be welcomed, it nevertheless presents

another problem for NICE. There are no RCTs for this modified

version of CBT, so on what best practice evidence-base does

NICE rely for its national policy recommendations?

None is provided.

The Cochrane Collaboration

Review of CBT for " CFS/ME "

It is likely that in its defence of the Guideline, NICE will rely

on the latest revision of the Cochrane Collaboration (CC)

Intervention Review of CBT for CFS ( " Cognitive behaviour

therapy for chronic fatigue syndrome in adults " .

Price et al. Cochrane Database of Systematic Reviews, vol 16

#3, July 2008. Wiley & Sons).

As customary with this body, this Review comes under the

Cochrane Depression, Anxiety and Neurosis Editorial Group,

which means that the WHO-classified CFS is incorrectly

categorised by the CC as a mental disorder, which is in breach

of the WHO taxonomic principles. However, the CC Review

clearly states: " CFS has had many names in recent decades,

including myalgic encephalomyelitis (ME) and post-viral

fatigue syndrome " but, according to the WHO rubric, the

inclusion of ME/CFS as a mental disorder is indefensible.

The CC reviewers claim that " CFS " has been " clearly defined " ,

yet they have failed to consider the evidence that people with

ME/CFS do not suffer from " fatigue " but from post-exertional

fatigability. This pathognomonic feature does not feature at all

in the Wessely School model, which may mean that the

studies in the CC Review have excluded people with ME/CFS.

The process of reviewing the literature for CBT in CFS began in

1997, and in the original CC 2000 Review, no meta-analyses

were performed, since only three studies were eligible for

inclusion at that time, and each of those studies used a

different control intervention. The conclusions of the original

Review stated: " There is no satisfactory evidence for the

effectiveness of CBT in patients with the milder form of CFS

found in primary care or in patients who are so disabled that

they are unable to attend out-patients. Additionally, there is

no satisfactory evidence for the effectiveness of group CBT " .

This latest CC up-date of CBT for CFS includes an additional 12

studies conducted since 1999.

The selection criteria were RCTs involving adults with a

primary diagnosis of CFS assigned to a CBT group compared

with usual medical care (this is not defined) or another

intervention, alone or in combination.

15 studies (1043 participants) were included in the Review, of

which 4 studies (i.e. more than 25%) are unpublished (and

therefore not peer-reviewed).

The four RCTs of CBT that formed the basis of the GDG's

management recommendations are all included in the

up-dated Cochrane Review (Deale et al, Am J Psychiat 1997;

Lloyd et al, Am J Med 1993; Sharpe et al, BMJ 1996 and Prins

et al, Lancet 2001).

The up-dated Cochrane Review found that 40% of people who

received CBT showed clinical improvement, in contrast with

26% who received usual medical care.

The recommendation is that more studies should be carried

out.

However, the CC Review in fact concluded that the results

were inconsistent and the studies did not fit well together,

making it difficult to draw any conclusions.

At follow-up (1 – 7 months after treatment ended), when

people who had dropped out were included, there was no

difference between CBT and usual medical care. Very few

studies reported on the acceptability of CBT and no studies

examined side-effects.

The Cochrane Collaboration is deemed by the Establishment to

be the " gold-standard " of meta-analyses. Cochrane Reviews

are generally assumed to be independent and objective, but

there are known problems with them (Ole Olsen,

Herxheimer et al; BMJ 2001:323:829-832).

Olsen et al noted that whilst the Cochrane Library " remains a

key source of evidence about the effects of healthcare

interventions, its users should interpret reviews cautiously.

Readers should be particularly cautious of reviews with

conclusions that favour experimental interventions when

relatively little evidence is available for the review. Too

often, reviewers' conclusions over-rated the benefits of new

interventions " .

Given this warning, it may be deduced that, despite its own

conclusions that at follow-up there is no difference between

CBT and usual medical care, the CC's latest call for even more

studies of CBT on long-suffering ME/CFS patients shows an

illogical resistance to accept the existing evidence that it is

ineffective unless subgrouping is carefully utilised (which NICE

does not accept).

Conclusion

There is a basic question that is never addressed by those

who favour the psychosocial model of " CFS/ME " : if patients are

not cured by psychotherapy (a fact which the Wessely School

themselves concede: CBT and GET are only " modestly

effective " and " neither approach is remotely curative " – Simon

Wessely, Editorial, JAMA 19th September 2001), then what is

it that they are not cured from?

If, as the Wessely School has advised NICE, " CFS/ME " is a

psychological disorder, then if a psychological therapy has not

cured it, this means either that it is not a psychological

disorder, or else that the psychological therapy does not work.

Why, then, does the NICE Guideline recommend only a

psychological therapy for " CFS/ME " (which is said to include

ME/CFS) that has been clearly shown not to be effective?

Patients would not complain so vociferously and consistently

about a management regime that helped them, whether that

regime be orthodox, alternative, psychological or of any other

type, but with CBT and GET, patients have registered their

complaints and concerns for many years, as has been

demonstrated in the many surveys conducted by the UK ME

charities. The only possible conclusion must be that these

approaches do not work and / or are harmful.

The Guideline Development Group which produced the

Guideline, however, deemed the patients' evidence to be

biased and it was therefore largely disregarded:

" Information gathered through patients surveys is generally

considered as relatively low-level evidence. RCTs are

considered to be at the top of the hierarchy of evidence (and)

when evidence from an RCT is available, it is generally given

priority over other types of evidence, including patient

surveys. The GDG recognised that surveys from self-selected

respondents are subject to bias "

(Full Guideline, 2.6.1, pp 77-78).

This was confirmed by Dr Fred Nye, a member of the GDG:

" All statements which the GDG had rated as 'uncertain' were

submitted to a wider group, of whom the majority were

patients and carers, and was much more confident in its views

than the GDG. This suggests very strongly that its

conclusions were based on opinion rather than on a serious

review of the evidence. Consultation with the wider group was

more like an opinion poll. In my view it did little to increase

the objectivity of our recommendations "

(J Inf. 2007:55:6:569-571).

This would seem to be a gross procedural abnormality,

because not to accord patients' evidence equal weighting with

RCTs is in clear breach of the AGREE Instrument. That NICE is

a member of the AGREE collaboration was confirmed by

Professor Sir Rawlins, Chairman of NICE, on 18th April

2002:

" The ish Intercollegiate Guidelines Network (SIGN) and

NICE are both members of the AGREE (Appraisal of Guidelines,

Research and Evaluation) collaboration. Members of the AGREE

collaboration all develop guidelines according to the same

basic principles and both NICE and SIGN aim to meet the

international standard set by the AGREE guideline appraisal

instrument (available from www.agreecollaboration.org ) "

(Joint NICE / SIGN statement on working together to improve

patient care, 18th April 2002).

In the case of its Guideline on " CFS/ME " , NICE has done little

to improve patient care.