WITHOUT PREJUDICE FOR INFORMATION
CONCEPTS OF ACCOUNTABILITY ?
Following the release of the Montague / Hooper document of 1st May 2001 entitled Concerns about the forthcoming UK Chief Medical Officer’s Report on Myalgic Encephalomyelitis (ME) and Chronic Fatigue Syndrome (CFS), notably the intention to advise clinicians that only limited investigations are necessary, the Medical Director of the UK ME Association (Dr Charles Shepherd) continues to press for a formal investigation by the Vice Chancellor of the University of Sunderland into the “conduct” of Professor Hooper. The present document outlines some of the background which lies behind the writing of the original Montague / Hooper paper.
This present document should be read in conjunction with the amended original Montague / Hooper paper (which was amended on 30 July 2001 in order to clarify issues raised by Dr Shepherd and by HealthWatch) and with the Response to criticisms about their paper by Montague and Hooper also dated 30 July 2001.
Sally Montague
Malcolm Hooper
and associates
25 August 2001
CONCEPTS OF ACCOUNTABILITY ?
FOREWORD
On 1st May 2001 Professor Malcolm Hooper and Sally Montague produced a paper entitled “Concerns about the forthcoming UK Chief Medical Officer’s Report on Myalgic Encephalomyelitis (ME) and Chronic Fatigue Syndrome (CFS), notably the intention to advise clinicians that only limited investigations are necessary”.
As is customary, Professor Hooper’s mail address at the University of Sunderland was provided as the contact for correspondence. ‘Sally Montague’ is a composite pseudonym for a group of medical scientists, researchers, clinicians and others, some of whom are themselves severely affected by ME and who for professional reasons and reasons of ill-health do not at present wish to reveal their identity. The document was not submitted to any journal for publication and no deceit took place.
The release of the original Montague/Hooper document brought forth poignant worldwide gratitude from researchers and patients alike; it also brought forth an immediate barrage of letters which essentially amounted to a threatening campaign against the authors; these letters were written almost entirely by Dr Charles Shepherd, Medical Director of the UK ME Association and member of the CMO’s Key Group charged with preparing the forthcoming report, whose membership of HealthWatch was mentioned by Montague and Hooper in their paper. On his own written admission Dr Shepherd caused the Chairman of HealthWatch (solicitor Malcolm Brahams of Messrs David Wineman, Craven House, 121 Kingsway, London WC2B 6NX) to send official letters to Professor Hooper.
The issues raised by Dr Shepherd and Malcolm Brahams were addressed in a written response to the solicitors on 30 July 2001 by Montague and Hooper. Dr Shepherd, however, refuses to accept the evidence and clarification provided in the authors’ response. Because of this, and because
Dr Shepherd’s campaign shows no sign of abating, Montague and Hooper and their associates have set out in more detail in this present document some of the background to their original paper.
The authors would like to confirm again that they did not put their original document on the internet. No responsibility is accepted by the authors for any amendments or alterations which have not been authorised by them. The authors have no responsibility for or connection with any website. The authors point out that any criticisms levelled against their paper must relate to their authorised document and to no other.
CONTENTS
The need for the Montague/Hooper document………………………..……………..4
Brief Historical Summary………………………………………………………… 4
What is ME?………………………………………………………………………. 8
Physical signs found in ME……………………………………………………….. 10
What is CFS?…………………………………………………………………….. 10
The 1996 Joint Royal Colleges’ Report on CFS………………………………….. 12
The Petition “Fighting for Truth”…………………………………………………. 14
The WHO Guide to Mental Health in Primary Care………………………………..14
The evidence that ME/CFS may be virally or chemically induced……………… .. 16
Evidence that there is a need for careful subgrouping within “CFS”……………… 17
The view of Dr Derek Pheby on the need for subgroups………………………… …19
The views of others involved on the need for subgroups…………………………….20
The apparent change of mind by the WG about the need for subgroups………… …20
Implications for treatment……………………………………………………………23
Other areas of the CMO’s report which cause concern………………………………23
The actions of Dr Shepherd after release of the Hooper paper……………………. ..24
Note on Government Advisory Committees………………………………………….30
Note on Cognitive Behaviour Therapy and Professor Wessely………………………31
HealthWatch…………………………………………………………………………34
The published views of HealthWatch Founder on ME/CFS………………………….37
Other views of HealthWatch………………………………………………………….39
The known views of other HealthWatch members on ME/CFS………………………41
The known views of HealthWatch members and others on vitamin and
nutritional therapies and on ‘alternative’ allergy treatments………………………….42
Dr Shepherd and the journalist Duncan Campbell………………………………….. .47
Dr Shepherd’s support for pharmaceutical trials in ME/CFS………………………. .48
HealthWatch members and a Royal College of Physicians’ Report……………….. ..49
HealthWatch members and the Bristol Cancer Help Centre………………………….51
HealthWatch and the book “Dirty Medicine”………………………………………. .52
Points for consideration…………………………………………………………….. 53
The Plight of ME/CFS sufferers…………………………………………………… 55
Testimony of Dr Paul Cheney to the US FDA Scientific Advisory Committee……. ..57
The known opinion of the Deputy Chief Medical Officer………………………….. ..57
The known opinion of the Chief Medical Officer……………………………………..58
The Patients’ Voice………………………………………………………………… 58
Support for Professor Hooper……………………………………………………… 60
References………………………………………………………………………….. 63
The need for the Montague / Hooper document
Montague and Hoooper and their associates are aware that the matters addressed in their document are of substantial public interest. Specifically they are concerned that in the UK Chief Medical Officer’s forthcoming Report on Chronic Fatigue Syndrome / Myalgic Encephalomyelitis, advice is to be given to UK clinicians that CFS and ME are entirely synonymous and that in cases of CFS/ME, only limited investigations are necessary. Such advice may have long-term consequences for many very sick people and their families who have already suffered for too long from what has been called by the Bristol-based ME charity Westcare the “psychiatric fallacy”.
Since the late 1980s, the use by some UK researchers of heterogeneous patient cohorts has hampered progress in understanding this group of complex disorders. There has been too much reliance placed upon the results of studies which have used different case definitions of chronic fatigue syndrome (CFS) whilst not even looking at those with ME, resulting in the invalid comparison of contradictory research findings, and there has been a lack of standardised laboratory tests (1).
In light of these problems, Montague and Hooper and their associates believe it is time to challenge advice that only limited investigations are necessary in CFS/ME.
Brief historical summary
Crucial to understanding the complexity which underlies the entire problem is the question of case definition and related nomenclature.
Myalgic encephalomyelitis (ME) has been documented in the medical literature since 1934 (2); the Wallis description was in 1957 (3); Sir Donald Acheson’s (a former UK Chief Medical Officer) major review of ME was in 1959 (4); the disorder used to be known as “atypical poliomyelitis” but was given the term benign myalgic encephalomyelitis in 1956 (5); in 1962 the distinguished neurologist Lord Brain included ME in the standard textbook of neurology (6); the Royal Society of Medicine held a symposium on ME on 7 April 1978, at which ME was accepted as a distinct entity; the symposium proceedings were published in The Postgraduate Medical Journal in November 1978 (7) and the Ramsay case description was published in 1981 (8).
ME was formally classified as a disease of the nervous system in the World Health Organisation International Classification of Diseases in ICD 8 (which was approved in 1965 and published in 1969): it is listed both in the tabular list and in the Code Index as Code 323, page 173.
ME continued to be classified as a disease of the nervous system in ICD 9 (approved in 1975 and published in 1979), both in the tabular list and in the Code Index, where it is coded as 323.9, page 182.
ME continues to be listed as a neurological disorder in the current ICD 10 at section G.93.3.
By direct communication with the WHO in Geneva, the authors have been informed that when considering the correct classification of ME, the syndrome should be regarded as neurological and not as psychiatric; moreover, there are no plans to reclassify ME in the psychiatric section in the next ICD revision (Version 10.2) which is due in 2003.
Specifically, the authors were advised that the fatigue states including neurasthenia which are currently classified in the ICD at section F 48 as “Behavioural and Mental Disorders” do not refer to ME. This information clearly counteracts the claim made frequently by psychiatrists of the Wessely School (see below).
“Chronic Fatigue Syndrome” is now included in the Code Index in ICD 10 as one of the many names used by some when referring to ME.
Here a difficulty arises, because “Chronic Fatigue Syndrome” (CFS) means different things to different people. There are currently two different interpretations of “CFS”, one used by international researchers and clinicians which relates to a clearly organic
(ie. physical) disorder which is the same as or very similar to ME, the other used by a group of UK psychiatrists led by Simon Wessely, now Professor of Epidemiological and Liaison Psychiatry at Guy’s, St Thomas’ and King’s School of Medicine, London, which relates to a clearly psychiatric disorder. These psychiatrists have become known colloquially as the “Wessely School” (9).
Wessely heads the CFS Research Unit at King’s College Hospital, as well as the Gulf War Illness Research Unit. He is renowned for his belief that ME does not exist other than as a belief that it exists (see below), and for his published belief that there is no such thing as Gulf War Syndrome (10). He is also renowned for his belief that the symptoms reported by the residents of Camelford (Cornwall) as a result of the drinking water disaster in 1988 (when 20 tonnes of aluminium sulphate were accidentally pumped into the town’s drinking water supplies) were due to heightened perception of normal bodily sensations being attributed to an external cause such as poisoning, and that such behaviour was due to anxiety and preoccupation with the state of the environment over chemical toxins. Writing about this catastrophy in the Journal of Psychosomatic Research (11), Wessely and his frequent co-author Anthony David (a psychiatrist who supports the Wessely School view of ME) claimed that such fears often appear in controversial fields such as environmental medicine and clinical ecology; they stated that individuals with long histories of multiple physical complaints divert their symptoms to fall in line with the prevailing issue (in that case, water pollution).
In an article in the BMJ based on a re-assessment of the Wessely and David paper in the Journal of Psychosomatic Research, Bernard Dixon wrote that “mass hysteria was largely responsible for the furore” (12). In the Camelford incident, seven people died, 25,000 suffered serious health effects and 40,000 animals were affected (13); a study commissioned by lawyers acting on behalf of the Camelford plaintiffs and funded through Legal Aid (as opposed to the Department of Health) showed conclusively that those residents who were exposed to aluminium sulphate-contaminated drinking water suffered considerable damage to cerebral function which was not related to anxiety, and that there is objective evidence of organic brain damage which is compatible with the known effects of exposure to aluminium (14).
In a BBC Radio 4 interview on 14 August 2001 on the “Today” programme (the day when, after thirteen years, a further independent enquiry into the episode was announced), the lead author of that study (Paul Altman from Oxford) made the salient point that when studied in detail, abnormalities were found. Speaking on television on the same subject, Paul Tyler, Member of Parliament for the area, said that having to suffer the ill-health was bad enough, “but the cover-up is the real disaster”.
Professor David sat on the Royal College of Physicians and Royal College of Psychiatrists’ Working Party which produced the report on organophosphate sheep dip (15); the report suggested that the ill-health suffered by farmers and others after chronic exposure to OPs was possibly due to “severe anxiety or depression, which have intuitively been attributed by the sufferers to OP exposure”.
On 5 February 1999 the New Statesman carried an article by Ziauddin Sardar entitled “Ill-defined notions” which featured Wessely and which commented on his dismissal of such illnesses as ME and Gulf War syndrome; “Even though 400 veterans have actually died and some 5,000 are suffering from illnesses related to Gulf War Syndrome, the syndrome does not officially exist … Wessely has been arguing that ME is a largely self-induced ailment that can be cured by the exercise programme on offer at his clinic…. Wessely, who occupies a key position in our socio-medical order, denies the existence of Gulf War Syndrome, just as he denies the existence of ME. Clearly, he is a follower of Groucho Marx: ‘Whatever it is, I deny it’. Not surprisingly, lots of people hate him”.
In 1991, the Wessely School of psychiatrists and supporters re-defined ME and adapted the US 1988 Holmes et al “Chronic Fatigue Syndrome” (CFS) case definition (16)
(see below) to include psychiatric illness of which on-going fatigue is a prominent symptom. The 1991 definition is known as the Oxford criteria (17). When used by these psychiatrists, the term CFS is often referring to other fatigue states in which the primary symptom is tiredness or “fatigue”. The Oxford 1991 case definition specifically states “There are no clinical signs characteristic of the condition”.
In 1994 the US Centres for Disease Control (CDC) produced another revision of the working case definition of CFS; that revised definition specifically states “We dropped all physical signs from our inclusion criteria” (18).
Notably, in correspondence dated 26 February 2001 Dr Charles Shepherd (Medical Director of the UK ME Association) denies this outright, writing “It’s just not true that the 1994 criteria specifically exclude patients who have physical signs”, yet the 1994 CDC criteria document plainly says this (page 957).
As with the formulation of the Oxford criteria for CFS, UK psychiatrists Simon Wessely and Michael Sharpe were involved with the 1994 US revision. Notwithstanding Shepherd’s assertion, the two case definitions of CFS emphasise that there are no physical signs; by comparison, those with ME always have observable physical signs (see below).
This confusing state of affairs was noted in the 1994 UK National Task Force report (1), which states unequivocally that “ME” and “CFS” do not represent the same patient populations (see below).
However, in the US the term “CFS” has come to represent patients with what is probably “ME”, and much of the international research literature refers to “CFS”. This dichotomy has been encapsulated by Fred Friedberg, Clinical Professor in the Department of Psychiatry at the State University of New York (19):
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 and phobic patients, while the US and Australian
research sample have been clearly distinguished from depression patients and
more closely resemble fatiguing neurological illnesses”.
Disturbingly, the prime authors of the UK Chief Medical Officer’s report on CFS/ME are apparently determined to equate ME with “CFS” as one single entity, which they refer to as “CFS/ME” (see below). To do so takes no account of the different interpretations of the undifferentiated term “CFS” and it is likely to perpetuate the existing confusion to the detriment of those with non-Oxford defined CFS. It is already known that the CMO’s Report on CFS/ME will recommend psychiatric management approaches: such approaches may be appropriate when considering the Oxford definition of CFS but may be harmful when considering the international interpretation of “CFS” which more closely equates with ME.
Montague and Hooper believe that by seeking to equate one specific syndrome or subgroup with another syndrome or subgroup which does not have the same features, the CMO’s Working Group may be doing a grave disservice to both patients and medical science: they believe it is scientifically unacceptable that one name should refer to two different case definitions, each of which having different symptom profiles. Montague and Hooper are concerned at the repeated refusal by the CMO’s Key Group to acknowledge the clinical difference between ME and other forms of CFS, a difference which many believe has important implications for management and treatment outcomes, as well as for service provision.
What is ME?
ME is a multi-system disorder sometimes associated with enteroviruses related to the poliomyelitis virus (20); it occurs in both epidemic and sporadic form. There are acknowledged similarities and overlaps between ME / non-Oxford CFS and the post-polio syndrome (PPS), particularly concerning the nature and source of the pathophysiology, including virological evidence that enteroviruses persist in the human central nervous system. The mechanism of the incapacitating exhaustion is identical in the two conditions (ie. in ME and PPS). (21).
In ME, different people have different symptoms but the general pattern and evolution of major symptoms are remarkably coherent. Organ systems may be differentially affected and within organ systems there may be a mosaic of affected and unaffected cells, the sum of which defines the degree of organ dysfunction.
The chronicity and severity of ME, together with the degree of disablement, the disruption of the family unit and the inevitable social isolation make this disorder a nightmare.
The most striking feature is overwhelming and incapacitating post-exertional muscle fatigueability, which is quite distinct from “fatigue”, “tiredness” or “sleepiness”, together with extreme malaise. All muscles are affected, including the heart. Cardiac symptoms often mimic coronary thrombosis and it can seem to patients that they are having a heart attack but the usual cause of chest pain is chronic benign pericarditis. The presence and behaviour of the pericardial rub is independent of the intensity of the pain (22).
Research from Glasgow has provided firm laboratory evidence demonstrating delayed muscle recovery from fatiguing exercise and it shows convincingly that in ME/CFS there is continued loss of post-exertional muscle power (giving an additional loss of power), with recovery delayed for at least 24 hours, whereas sedentary controls recovered full muscle power after 200 minutes (23).
ME commonly starts with diarrhoea, together with a persistent headache and or vertigo (dizziness is a particularly striking and chronic feature), with a stiff neck and back, together with generalised muscle pain. It affects not only the central nervous system but the autonomic and peripheral nervous systems as well. Sympathetic nervous system dysfunction is integral to ME and “core” CFS pathology (24).
There may be significant and permanent damage to skeletal or cardiac muscle as well as to other end-organs including the liver, pancreas, endocrine glands and lymphoid tissues (25), with evidence of dysfunction in the brain stem. Injury to the brain stem results in disturbance of the production of cortisol (required for stress control) via damage to the hypothalamus and to the pituitary and adrenal glands. The later effects include not only muscle but joint pain; many patients can walk only very short distances and require a wheelchair.
There is difficulty with breathing, with sudden attacks of breathlessness, problems with swallowing and voice production, thermodysregulation with sweating and shivering, and low blood pressure. There is difficulty with simple tasks such as climbing stairs and dressing, and with short-term memory (26). Cognitive impairment includes difficulty with memory sequencing, processing speed, word searching, spatial organisation and calculation.
Sleep is characteristically unrefreshing. Uncharacteristic emotional labilty is prevalent. There are usually chronic problems with diarrhoea and frequency of micturition, including nocturia. Vascular headaches are common and recurring (27). Patients have to be cautious about drugs, especially those acting on the central nervous system ie. anaesthetics, as there is an increased occurrence of adverse reaction (28). (see also Appendix 1 to the Response dated 30 July 2001 by Montague and Hooper).
Pain is often extreme and intractable: in his three-day CFS/ME intensive Workshop for practitioners given in Australia in August 1995, world expert Dr Paul Cheney emphasised that the control of pain in very sick patients can easily be the most challenging problem in ME/CFS management
ME is a potentially severe, chronic and disabling disorder from which complete recovery is unlikely. Cycles of severe relapse are common, together with characteristic evolution of further symptoms over time. Death occurs almost entirely from end-organ damage, mainly from cardiac or pancreatic failure. Suicide is not uncommon and is related to the current climate of disbelief and rejection of welfare support (29).
Despite claims from some quarters to the contrary, in ME there is evidence of inflammation of the central nervous system (CNS); that is what helps to differentiate ME from other forms of CFS. There are many references in the medical literature to inflammation of the CNS in ME and in “core” CFS (30,31,32,33,34) but such CNS inflammation is not found in all variants of CFS. It is incorrect to deny the existence of CNS inflammation in at least some forms of CFS (ie. in ME), even though such inflammation is by no means universal in all forms of CFS.
In some cases of ME there is evidence of oligoclonal bands in the cerebrospinal fluid (35,36). It is accepted by the most experienced ME clinicians that some degree of encephalitis has occurred both in patients with ME and in those with post-polio syndrome: the areas chiefly affected include the upper spinal motor and sensory nerve roots and the spinal nerve networks traversing the adjacent brain stem, which is always damaged (37). In nearly every patient there are signs of disease of the central nervous system (38). Recent research continues to support neurological involvement (39,40,41,42,43).
In the UK, patients with neurological signs and symptoms are usually the sickest and as such they are excluded from studies of “CFS”. The results of studies from which such patients are excluded are not representative of the true situation.
Physical signs found in ME
In cases of severe ME there are definite physical signs indicative of physical illness which cannot credibly be ascribed to abnormal illness behaviour. Some of these signs are often present in less severely affected cases but are dismissed or trivialised in order to comply with the definition of CFS.
Not all patients have all signs, but throughout the ME literature, the following are common in the sickest patients. Observable signs include nystagmus; sluggish visual accommodation; abnormality of vestibular function with a positive Romberg test (in his 1995 Australian Workshop, Cheney said that more than 90% of patients have an abnormal Romberg versus 0% of controls); abnormal tandem or augmented tandem stance; abnormal gait; hand tremor; incoordination; cogwheel movement of the leg on testing; muscular twitching or fasciculation; hyper-reflexia without clonus; facial vasculoid rash; vascular demarcation which can cross dermatomes with evidence of Raynaud’s syndrome and / or vasculitis (44) and spontaneous periarticular bleeds in the digits; mouth ulcers (45,46); hair loss (47,48,49); a labile blood pressure; flattened or even inverted T-waves on 24 hour Holter monitoring: a standard 12 lead ECG is usually normal (50); orthostatic tachycardia; shortness of breath: patients show significant reduction in all lung function parameters tested (51); abnormal glucose tolerance curves, liver involvement (an enlarged liver is not always looked for and can be missed) (52,53,54,55) and destruction of fingerprints: atrophy of fingerprints is due to perilymphocytic vasculitis and vacuolisation of fibroblasts (56).
What is CFS?
The term “chronic fatigue syndrome” (CFS) did not come into existence until 1988. In the late 1970s and 1980s there seemed to be a remarkable rise in incidence of a condition virtually indistinguishable from ME, to the extent that the powerful American medical insurance industry became alarmed. The result was a new case definition and from 1988 “ME” was henceforth to be called chronic fatigue syndrome.
As a basis for sound scientific research, the new definition has been a disaster. “CFS” is not a single diagnostic entity: it has become a heterogeneous and non-specific label embracing many different medical and psychiatric conditions in which tiredness and fatigue are prominent. The first (1988 Holmes et al) definition of CFS (16) concentrated on “fatigue” as the primary symptom occurring as a post-viral effect and persisting for at least six months, with a sore throat and tender lymph glands in the neck.
The new “CFS” case definition focused on the symptoms of glandular fever and indeed, the disorder was at that time called the Chronic Epstein-Barr Virus Disease (the virus responsible for glandular fever). The Holmes et al definition was obliged to exclude the cardinal features of ME which had been documented for decades, distinguishable by post-exertional muscle fatiguability, extreme fluctuation and variability of symptoms and chronicity.
In the United States in 1988, the eighteen strong panel of medical scientists and clinicians charged with formulating a new case definition and new name could not agree: two of the most clinically experienced members refused to sign the final document and withdrew from the panel because the proposed definition and new name were too different from the ME with which they were so familiar (57). Those two members were Dr Alexis Shelokov (USA) and Dr Gordon Parish (UK). Dr Parish is the custodian of possibly the world’s largest reference library of the pre-1988 literature on ME, known as the Ramsay Archive, which is now housed in Scotland.
Notwithstanding the position of the Royal Society of Medicine in 1978, the case definition of CFS expediently ignores the overt features of neurological disease seen in ME, a disorder which is often confused with multiple sclerosis (36). There is an increasing literature on the issue of ME/CFS being frequently diagnosed as multiple sclerosis: as recently as 1st August 2001 an internet posting listed the similarity of signs and symptoms (numbering 28) and discussed the similarities of magnetic resonance imaging (MRI) scans in ME/CFS and MS. Dr S.Blair noted that in ME, the ‘unidentified white spots’ tend to be punctate but in MS they tend to be more ovoid. While the MRI scans are similar, those of ME patients show increased signal intensity in the white matter near the white=gray delineation rather than in the white matter of the periventricular area (58).
The case definition of CFS also ignores the evidence that ME / non-Oxford CFS has features of autoimmune disorder (eg lupus 59,60) and features of allergy and multiple chemical sensitivity (MCS) (61,62,63,64,65,66), which is now officially recognised in the International Classification of Diseases (67). Data presented at the American Association for Chronic Fatigue Syndrome (AACFS) Fifth International Research and Clinical Conference in Seattle in January 2001 showed that MCS was present in 42.6% of ME/CFS patients compared with 3.8% of controls (68).
The evidence speaks for itself. Other postviral fatigue states are clinically in contrast to the three cardinal features of ME (69). Other fatigue states which may follow flu, measles, chickenpox, herpes or mononucleosis lack not only the clinical but also the laboratory features of ME (70).
Montague and Hooper again draw attention to the fact that both the Oxford 1991 and the CDC 1994 case definitions of CFS unequivocally state that those with CFS have no physical signs, yet patients with ME always have physical signs. The overriding difficulty is that some clinicians in some medical disciplines apparently fail to see them or have no desire to look for them.
It is a matter of record that those who favour a psychiatric aetiology and who wish to eradicate the classification and even the existence of ME were unhappy about the Report of the UK National Task Force on CFS / PVFS / ME published by Westcare (Bristol) in 1994: indeed, that Report itself acknowledges this, stating “ People who gave us their much-valued help are not necessarily in agreement with the opinions expressed”. Being known to be in disagreement with the Report from the National Task Force (which did not have a psychiatric bias), the proponents of the psychiatric view responded to the Task Force Report by producing their own report (that of the 1996 Joint Royal Colleges (71), in the Preface to which it confirms that the authors of the Joint Royal Colleges’ Report are not in agreement with all the findings of the National Task Force report) and indeed the Joint Royal Colleges’ report on CFS presented the views of the psychiatrists and supporters of the Wessely School to the virtual exclusion of all other credible explanations.
The 1996 Joint Royal Colleges’ Report on Chronic Fatigue Syndrome (CR54)
Ostensibly claimed to have been prepared at the request of the UK Chief Medical Officer as a response to the 1994 UK National Task Force Report on CFS/PVFS/ME and that it was the Presidents of the three Royal Colleges who nominated the expert committee, it is widely believed that Wessely was the instigator and prime mover in the joint Royal Colleges’ report. Out of the fifteen members of the Working Group, eight (53%) are psychiatrists well known for their published views which deny the reality of ME and six were signatories to the 1991 Oxford CFS case definition (which denies any physical signs).
Two members of that Working Group (psychiatrists Anthony David and Simon Wessely) had already made their views very clear, writing in the British Medical Journal (72)
“ The inclusion in the tenth revision of the International Classification of
Diseases (ICD 10) of benign myalgic encephalomyelitis …under Diseases
of the Nervous System seems to represent an important moral victory for
self- help groups in the UK…it is unlikely to lead to advances in our
understanding of the condition….The nineteenth century term neurasthenia
remains in the Mental and Behavioural Disorders chapter under Other
Neurotic Disorders… neurasthenia would readily suffice for ME….Applying
more stringent criteria for CFS in the hope of revealing a more neurological
sub-group succeeds only in strengthening the association with psychiatric
disorders. We believe this latest attempt to classify fatigue syndromes will
prevent people from seeing the world as it actually is”.
In the Joint Royal Colleges’ Report, ME is dismissed. Throughout the report is the relentless assertion that the more severe subgroup (ie those with ME) does not exist as a disease entity, and that antidepressant drugs together with cognitive behavioural therapy is an effective measure which should be used to modulate sufferers’ maladaptive perception of their suffering.
Specifically, the Report recommends that antidepressants should be tried in CFS sufferers even in the absence of depression; it advises of the need to remove children forcibly from their parents and home if this is “in the best interests of the child”, and it stipulates that“ no investigations should be performed to confirm the diagnosis”.
The Report virtually ignored the available literature which describes physical anomalies:
it cited 256 references, of which half were by the same or associated group of authors
(the Wessely School), with 10% of the references being by Wessely himself; nine had not been published or reviewed.
The Report was heavily criticised on both sides of the Atlantic; in one cogently argued critique, Dr Terry Hedrick ( a psychologist and former Assistant Comptroller General for the US Government’s Senior Executive Service) exposed just why it was insidiously biased and potentially harmful (73)
In the Joint Report, the authors mention a paper by Buchwald, Gallo (co-discoverer of the HIV virus), Komaroff et al (reference 128 in the Report) but dismiss it, stating
“White matter abnormalities occur in a number of settings, and their
significance remains to be determined”
However, the paper itself concludes that patients with ME/CFS
“may have been experiencing a chronic, immunologically mediated
inflammatory process of the central nervous system”
and that the MRI scans revealed a punctate, subcortical area of high signal intensity consistent with oedema or demyelination in 78% of cases. This is a clear illustration of the biased and misleading personal interpretation of the available evidence by the authors of the Joint Royal Colleges’ Report.
In that Report, the authors mention a paper by Bombadier and Buchwald (reference 173 in the Joint Report), conveying that it supports their own stance, whereas the paper itself actually states the exact opposite of what is claimed by the authors of the Joint Report:
“The fact that the same prognostic indicators were not valid for the group with
CFS challenges the assumption that previous outcome research on chronic
fatigue is generalizable to patients with chronic fatigue syndrome”.
Another illustration from the Joint Royal Colleges’ report can be found where the authors mention a paper by Sandman (reference 153 in the Joint Report) in apparent support of their own view that the results of neuropsychological testing have been “inconsistent”: the paper referenced in fact concludes that
“the performance of the CFIDS (ME/CFS) patients was sevenfold worse than
either the control group or the depressed group. These results indicated that
the memory deficit in CFIDS was more severe than assumed by CDC criteria.
A pattern emerged of brain behaviour relationships supporting neurological
compromise in CFS”.
As has been commented on in the international medical literature (74), Wessely et al often rely upon a mischaracterisation of the facts: some believe that the frequent use of such practice may even amount to scientific misconduct (75).
As far as the CMO’s forthcoming report on CFS/ME is concerned, as Medical Director of the UK ME Association, ought not Shepherd to be pointing this out and questioning the accuracy of the Wessely School instead of condoning and positively supporting such
mis-representation, which he seems to be doing by virtue of recommending the model of evaluation favoured by the Wessely School (ie. only limited investigations are necessary in CFS/ME)?
The Petition “Fighting for Truth”
Because the published criticisms and the many informed critical responses to the Joint Royal Colleges’ report were ignored and / or were met with dismissive and patronising rebuttal by the Presidents of the three Royal Colleges, the UK ME community organised a petition for it to be withdrawn; the petition was called “Fighting for Truth” (ForT) and was signed by 12,500 people. On 26 November 1997 it was presented in the House of Lords by the Countess of Mar to the Minister of State for Health but was rejected, and the unquestionably biased report was not withdrawn.
It is perhaps worth drawing attention to the fact that Wessely’s determination to classify ME as a mental illness apparently remains undiminished: in the WHO Guide to Mental Health in Primary Care (2000) is to be found the following (Disk 2: 6.2, 6.3):
“What is Chronic Fatigue Syndrome? (It) is an illness in which people
experience extreme fatigue and muscle pain from activity. As a result
they do much less than they used to….It is often known as ME.
What makes people develop chronic fatigue syndrome? The pressures
of life; lifestyle; personality style. What can keep fatigue going?
Too much rest. Avoiding activity. Demoralisation and depression.
Various methods of rehabilitation have been shown to be helpful.
These include cognitive behavioural therapy and.. graded programmes
of exercise….. What is negative thinking? Sufferers often feel…that
any attempt to do more…may lead to an increase in symptoms, which the
sufferer may believe means they are doing themselves permanent
damage”.
The Guide to Mental Health in Primary Care states that it is adapted from the patient management package by Dr Trudi Chalder (a registered Mental Nurse and behaviour therapist), Dr Alicia Deale (a behaviour psychotherapist), both of whom work with Wessely, and Professor Simon Wessely himself, amongst others. It has the benefit of being promoted by the website of the University of Oxford Department of Psychiatry (www.psychiatry.ox.ac.uk), long known as a fervent supporter of the Wessely School, and whose website is mirrored on www.whoguidemhpcuk.org
Referring to the WHO International Classification of Diseases, the Oxford website specifically states
“CHRONIC FATIGUE AND CHRONIC FATIGUE SYNDROME - F48.0
(Known internationally as neurasthenia, may be referred to as ME)
“Presenting complaints: patients may report…feeling tired easily…lack of
energy….Chronic fatigue syndrome is diagnosed when substantial physical
and mental fatigue lasts longer than six months…and where there are no
significant findings on physical examination or laboratory investigation….
A behavioural approach, including cognitive behavioural therapy (and) a graded
programme of exercise can be helpful. Guide developed by the WHO
Collaborating Centre for Research and Training for Mental Health.
Institute of Psychiatry, Kings College, London”.
The Oxford Department of Psychiatry website recommends another website:
“The Institute of Psychiatry’s website includes a full patient management
package…it is a useful resource for the practitioner who is working with
the patient to overcome the condition”.
Clearly, the website of the University of Oxford Department of Psychiatry is informing people that the approved WHO classification of ME is as a mental disorder under ICD 10 section F48; the WHO, however, has confirmed by e-mail dated 22 August 2001 that those responsible for the website are in fact the Institute of Psychiatry, King’s College, London (ie.where Wessely works) and that it is not a WHO publication. Moreover, associates of Montague and Hooper were advised by the editor of the ICD that it was unacceptable for there to be two differing categorisations of ME under the WHO banner (one in a neurological classification and one a mental classification), and that this is something which will be looked into by the WHO. The advice from the WHO is that for legal purposes, the ICD takes precedence over the Guide to Mental Health in Primary Care. This is because the classification in the ICD has been approved by the World Health Assembly, whereas the Guide to Mental Health in Primary Care has not been approved by the World Health Assembly. Moreover, the ICD 10 itself specifically mentions at section F48 (Mental and Behavioural Disorders) that ME / postviral fatigue syndrome is excluded from section F 48.
From the University of Oxford Department of Psychiatry website, it indeed appears that the Wessely School at King’s College Hospital, London have managed to get the name and logo of the World Health Organisation linked to their own beliefs about ME by portraying the WHO logo in a prominent position, but this would seem to be deliberate and calculated deception because the website is carrying incorrect and misleading information which is not condoned by the WHO at all.
As an ME sufferer points out in an internet posting, this is an important issue which ME patients should be able to look to the ME charities to sort out, but most members know that any such intervention is unlikely. An internet posting makes another valid point, namely that the Chief Medical Officer should be alerted to the incorrect inclusion of ME at section F 48 under Mental and Behavioural Disorders: crucially, however, it is members of the CMO’s own Working Group who are responsible for the promotion of this misinformation.
It is remarkable that psychiatrists of the Wessely School apparently see no need to observe the internationally approved classification: the WHO Guide to Mental Health (available from November 2000) will be on all GPs’ desks, and GPs will yet again be subject to more deliberate mis-information about ME, which in turn will undoubtedly cause more inappropriate management and more unnecessary iatrogenic suffering for the unfortunate patients who attend with ME.
The evidence that ME/CFS may by virally and chemically induced
One reason why HealthWatch and at least four of its members have mounted such a campaign against Montague and Hooper could be that in their original paper, the authors referred to research which has demonstrated that an antiviral pathway (the RNase L pathway) is dysfunctional in ME/CFS, and it has been shown that this same pathway is also affected by chemicals (76). The authors also cite researchers in the US who have demonstrated a link between toxic exposure and chronic diseases such as ME/CFS and other autoimmune disorders, they suggest that the huge increase in chemical usage is chronically stimulating the immune system (77).
It is known that the incidence of ME/CFS is rising: this evidence comes from UNUM, one of the largest disability insurers in the United States; in April 1994, UNUM reported that in the five years from 1989-1993, mens’ disability claims for CFS increased by 360%, whilst womens’ claims for CFS increased 557%. No other disease category surpassed these rates of increase. In order of insurance costs, CFS/ME came second in the list of the five most expensive chronic conditions, being three places above AIDS.
Recent studies have demonstrated circulating plasma RNA in Gulf War Syndrome, and at the American Association of Chronic Fatigue Syndromes Fifth International Research and Clinical Conference held in Seattle in January 2001, a study was presented which had been conducted to determine the presence or absence of RNA in ME/CFS patients and to determine if the amplified sequences of RNA were similar to or different from those found in Gulf War Syndrome. All chronic illnesses studied (including Gulf War Syndrome, CFS/ME, AIDS and multiple myeloma) show prominent RNA not observed in normal controls. Prominent RNA bands so far sequenced show homology with human genes which are noted for their tendency for gene rearrangement under severe physiologic stress. The most amplified sequences appear to be disease specific. (78)
Dr N. Afari, Associate Director of the University of Washington’s CFS Research Centre, stated that the disorder appeared to be increasing, and that genetic abnormalities may team up with environmental influences to produce ME/CFS, and that environmental influences which researchers are investigating include the frequent pairing of ME/CFS with food and chemical sensitivities.
Evidence that there is a need for careful subgrouping within “CFS”
There is now an unmistakable recognition that sound research has strengthened the need
for consideration of subgroups (79,80,81,82,83,84,85,86).
A recent Editorial in the Journal of Chronic Fatigue Syndrome (87) makes the point that
“the sorting of patients into subpopulations….is helping in the design and
interpretation of clinical trials for therapeutic interventions aimed at particular
disease manifestations”.
The 1994 CDC criteria for CFS (whilst referring only to CFS) themselves recommend that researchers use stratification techniques to identify subgroups of patients (18).
One clear message which emerged from the National Institutes of Health (NIH) State of the Science Conference on CFS held on 23-24 October 2000 in Arlington, Vancouver was that CFS is heterogeneous and researchers must subgroup patients by features including chronicity, immunology and neuroendocrinology (88). Conference participants included Dr David Bell, Professor Dedra Buchwald and Professor Nancy Klimas, all world-renowned experts on ME/CFS.
Roberto Patarca-Montero, Assistant Professor of Medicine and Director of the Laboratory of Clinical Immunology, University of Miami School of Medicine (who is also Editor of The Journal of Chronic Fatigue Syndrome) emphasises the importance of subsets of patients in his paper “Directions in Immunotherapy” (89).
Experienced researchers and clinicians presented evidence at the Fifth International AACFS Conference held in Seattle, 27-29 January 2001 about the need for subgrouping. Some examples include the following:
--- Professor Leonard Jason from De Paul University, Chicago, concluded (90)
Subtype differences detected may account for some of the inconsistencies in
findings across prior studies that have grouped CFS patients into one category.
Subtyping patients according to more homogeneous groups may result in more
consistent findings which can then be used to more appropriately and sensitively
treat the wide range of illness experience reported by different types of individuals
with CFS
--- Professor De Meirleir from Brussels compared immunological profiles in three different subgroups of CFS patients; he found significant differences between the groups (91).
--- Dr Pascale de Becker from Brussels presented evidence that there is a need to assess the homogeneity of a large CFS population in order to establish those symptoms which can improve differentiation of CFS patients (92).
--- Dr Paul Levine from Washington demonstrated that factor analysis is an important tool for separating subgroups of CFS; he showed that it should be utilised in future attempts to develop case definitions for CFS to identify discrete patient groups, which may have different pathogeneses and responses to treatment (93).
--- Dr Katherine Rowe from Australia presented evidence showing that at least three distinct subgroups can be identified within the CFS syndrome (94).
--- A large international multicentre study of autoimmunity was presented by E.Tan
with, amongst others, participants from The Scripps Research Institute, La Jolla,
California; the University of Washington; Harvard Medical School, Boston; State University of New York and George Washington University, Washington DC. Of interest is that another participant was Simon Wessely from Kings College, London. This large study reflected the heterogeneity from one CFS centre to another; it emphasised the importance of subcategorising CFS studies (95).
In the light of current awareness of the overriding need for consideration of subgroups within CFS, there is concern that if the UK CMO’s Report advises UK clinicians that any difference between ME and “CFS” is simply a matter of semantics and personal philosophy (see below), and if it advises that only limited investigations are necessary,
the report may be immediately dismissed and be held in derision by well-informed clinicians and patients alike.
The views of the CMO’s Key Group member Dr Derek Pheby on the need for subgroups
In February 1999 a member of the CMO’s Key Group (Dr Derek Pheby of The Unit of Applied Epidemiology, Frenchay Campus, Bristol) produced a discussion document for the Working Group to consider. In that document, Pheby is definite about the need for attention to be given to the existence of subgroups and he quotes from the Report of the UK National Task Force on CFS / PVFS / ME (1). The Task Force Report states unequivocally that “Although both the terms “CFS” and “ME” have a range of applications, they do not represent the same populations”.
In his discussion document for the CMO’s Working Group, Pheby explicitly states
(emphasis added ):
“ The National Task Force recommended that five main sets of issues should be
addressed, i.e. Clarify the difference between the various chronic fatigue
syndromes… areas where in the view of the Task Force research needed to be
encouraged included: clear definition of the various chronic fatigue syndromes”
“ CFS is a spectrum of disease” [i.e. not a disease entity in itself (quoting Levine)
who is emphatic that “It is clear that CFS is not a single entity”]
“Variations in prognosis may be attributable once again to the heterogeneity of the
condition, with different subgroups having different prognoses”
“The heterogeneity of CFS has made it very difficult to interpret research results
from different studies which may have been conducted in very dissimilar
populations”
“If progress is to be made, it is necessary to consider…the possible existence of
subgroups within the population of patients with CFS / ME”
“The increasing knowledge of pathological processes occurring in CFS / ME has
led to a belief that it should be possible to define subgroups on the basis of
biomarkers and thus to draw a distinction between CFS and ME”
“It has been argued by many that not only can ME be differentiated from CFS
by biological markers, but that its clinical features also differ”
Under “Priority Areas for Research”, Pheby concludes
“Certain areas for research have been identified as being important in
enabling the Working Group to achieve its objectives. These include…
systematic reviews to consider subgroups”
The views of others involved on the need for subgroups
On 24th August 2000 Helen Wiggins of the NHS Executive (who co-compiled chapters
1 and 2 of the CMO’s draft report version 6) e-mailed a correspondent as follows:
“ I would also like to assure you that the CFS/ME Working Group is aware that
treatment that works for one person does not necessarily work for another. Hence
the fact that the team undertaking the Systematic Review will look at evidence that
subgroups of patients respond differently to treatment”.
On 18th August 2000 the Deputy Chair of the CMO’s Working Group on CFS/ME, Professor Anthony Pinching, wrote to Mrs Anne Crocker of Okehampton:
“…. there is no doubt in my mind that the CMO’s Group is well aware of the
heterogeneity of CFS/ME….obviously “one size” will not fit all….I hope very
much that the final product will adequately address these issues”.
In an e-mail to a correspondent dated 11th December 2000 Professor Pinching wrote:
“ I am all too well aware of the fact that current treatment options are
unsatisfactory and that there is a significant group of patients where our current
very limited armamentarium is either ineffective or worse”.
On 11th January 2001 Pinching e-mailed a correspondent as follows:
“ It may be that we can define subgroups that are useful and I would have no
problem with the concept (I have done this on other disease entities (when)
subgrouping has also been helpful)”.
The apparent change of mind by the authors the CMO’s draft report regarding
the need for subgroups
From what is known of the Working Group’s earlier intentions (examples of which are set out above), many people were hopeful that the matter of subgroups would be addressed, especially given their importance in relation to the implications for treatment outcomes. Seemingly this is not to be: Pheby’s contribution on the need for subgroups has apparently disappeared from the CMO’s report whilst those who wield the most influence appear to have made the decision to amalgamate ME and CFS as one single disorder without subgroups, despite all the evidence to the contrary.
This decision may have been approved by Professor Pinching, because to the consternation of a very considerable number people (not only in the UK but via the internet to a worldwide readership), in 2000 a paper on CFS appeared in Prescribers’ Journal (96). It was authored solely by Pinching whilst holding the position of Deputy Chair of the CMO’s Working Group and it caused an outcry.
It was deemed to be a forerunner of the CMO’s Report on the basis that even when wearing two hats, the same wearer could not credibly hold substantially divergent views. The article was seen as illustrating very clearly the extent of the problem of differentiation between the specific and the generic and just how easy it is for the unwary (or those who are following a pre-determined agenda) to “lump together” ME with other fatigue states.
In the article, Pinching states (emphasis added):
“ CFS …is a clearer appreciation of a pattern of symptoms previously
characterised in many different ways”
“ over investigation can be harmful and counterproductive to the management of
these patients…causing them to seek abnormal test results to validate their
illness”
“ patients may need guidance about claims…. from other practitioners”
“ (patients) …avoid activity, fearing relapse, but then develop symptoms of
deconditioning…or excessive awareness of physiological changes”
“ cognitive behavioural therapy…can substantially optimise rehabilitation”
“ Complementary therapists…sometimes reinforce unhelpful illness beliefs”
“ The essence of treatment is activity management and graded rehabilitation”.
Pinching does not even mention ME or the key manifestations of it and he expressly states that the fatigue found in CFS is “not related to ongoing exertion”. In ME, there is always post-exertional muscle fatigue, without which the diagnosis of ME is unsustainable, yet the intention of the CMO’s report is to unite ME with CFS as a single entity as the following illustrations from the draft version 6 exemplify:
“we do not see that it is either practicable or appropriate to use the term ME to
define a subgroup within CFS, or even distinct from it……there is currently no
clear evidence from the literature formally to differentiate ME from CFS on
grounds of either pathophysiology or response to treatment”
“ The Working Group suggests… that the terms CFS and ME are
used synonymously as the composite CFS/ME for the purposes of this report”.
“For the meantime, it seems appropriate to regard CFS / ME as a single, albeit
diverse, clinical entity……..on present evidence (subdividing categories of CFS)
may be considered a matter of semantics and personal philosophy rather than a
matter of established fact”.
Montague/ Hooper and their associates believe that good science requires attention to detail and not the broad-brush approach, however politically expedient or financially attractive such an approach might be.
To the consternation of those who represent the subset of patients who do have evidence of central nervous system disturbance (including inflammation), the drafts of the CMO’s Report seem to ignore Pheby’s carefully prepared and accurate document and instead to accept Pinching’s personal view -- a view which clearly echoes that of the Wessely School (ie. the psychiatric lobby) as expressed in the 1996 Report of the Joint Royal Colleges (71), as did his article and choice of references in Prescribers’ Journal.
Can this really be called “evidence-based medicine” ?
Montague and Hooper believe that in the final version of the CMO’s Report, clinicians’ view of the impact of the illness will need to reflect both patients’ clinical reality and the established laboratory abnormalities found in the various subgroups, not just the prevailing misconceptions so widely promoted by the Wessely School of psychiatrists. Montague and Hooper and their associates believe those misconceptions to be as follows:
1. a psychological rehabilitation programme is the treatment of choice for those with
ME / CFS
2. any differences between subgroups (or between ME and CFS) are of no clinical
significance
3. brain imaging and / or laboratory abnormalities found in ME / CFS are merely
inconsequential epiphenomena.
The information on the need for subgroups set out above has recently been strengthened: expert medical opinion is now unequivocal that there is a pressing need for the study of sub-groups of CFS, using a variety of investigative criteria. In July 2001 the American Medical Association issued a statement, explaining that 90% of CFS/ME patients show normal test results on basic investigations and that studies designed for specific subgroups are needed. Professor Anthony Komaroff, an undisputed world expert on ME/CFS, said:
“Researchers are already using imaging technology to measure brain hormones and are examining the function of the immune system. There is considerable evidence already that the immune system is in a state of chronic activation in many patients with CFS” (97).
The response of members of the CMO’s Key Group (particularly that of both Dr Shepherd and Professor Pinching) to this developing international scientific opinion is therefore particularly disappointing.
Implications for treatment if the CMO’s final report continues to assert that there is no need for subgrouping.
Montague and Hooper believe that in the pursuit of both medical science and medical practice it is necessary to be as specific as possible. Nowhere is this more true than in relation to the various categories of “CFS”. Not only is a broad brush approach potentially harmful to those with mitochondrial damage (particularly the use of CBT involving aerobic graded exercise regimes) (98), but despite attempts to do so, the claimed success with the approach of just one group of UK psychiatrists and their colleagues has not been replicated in the US or in Australia (19).
As mentioned above, such disparate findings are likely to be the result of different authors studying different subgroups of CFS. Montague and Hooper believe it would reflect badly if the CMO’s Working Group report failed to understand the importance of this concept. To imagine that one treatment modality (ie. the psychological approach of cognitive behaviour therapy with or without a programme of graded exercise) could apply to all cases of ME and “CFS” would indeed be inappropriate or worse, a fact which Professor Pinching appeared to appreciate in his e-mail of 11 December 2000 mentioned above.
Other areas of concern about the CMO’s forthcoming report on CFS/ME
In addition to their concern that investigations be limited in cases of CFS/ME and their concern at the intention of the report to promote CBT as an appropriate management intervention, there are other areas in the CMO’s report about which Montague and Hooper and their associates are concerned, particularly the sections which assert that factors which maintain the syndrome include mood disorder, inactivity and illness beliefs, illness behaviour and illness attributions; and that factors apparently unrelated to prognosis include the patient’s immunological profile. In the opinion of many people, such assertions are not in accordance with the international published literature or with clinical experience or with the known biomarkers and are thus unacceptable.
In the US, physicians are concerned by abnormalities in cell biology in ME/CFS; the emphasis of their research is firmly placed on immunology and Th1 - Th2 shifts; on virology and RNase L abnormalities; on HPA axis dysfunction and neuro-endocrinology; on aberrant RNA amplicons, and on cell membrane dysfunction.
In the UK, attention to such findings seems to be intentionally diverted and instead emphasis is heavily placed on socio-psychological investigation and management.
It is a matter of concern that the CMO’s report is intending to advise UK clinicians that neuroimaging investigations should not be carried out on patients with CFS/ME and that looking for specific immune markers should not be part of the clinical evaluation, yet it is such screening procedures which are delivering evidence confirming serious abnormalities in patients with ME/CFS. If such abnormalities are present, then they impact significantly on management.
Research funded by the ME Association found convincing evidence that changes in different immunological parameters correlate with particular aspects of disease symptomatology and with measures of disease severity, lending further support to the concept ot immunoactivation of T-lymphocytes (99).
How can it be in any patient’s best interests to advise UK clinicians that such significant abnormalities should not even be looked for?
Having set out some of the background which influenced the Montague/Hooper paper,
the authors now consider in more detail matters of relevance and concern.
********
The actions of Dr Charles Shepherd after the release of the Montague / Hooper document
The issues raised by Shepherd and by the Chairman of HealthWatch have been addressed by Montague and Hooper in their response dated 30 July 2001, but certain aspects are incorporated here as they are deemed worthy of closer consideration.
Following release of the Montague / Hooper paper, those associated with it have received much publicly circulated comment contained in letters from Charles Shepherd.
Dr Shepherd has also written many letters to the Vice Chancellor of Professor Hooper’s University as well as many letters to the University’s Head of Corporate Affairs; he has written to Professor Allen Hutchinson (Chairman of the CMO’s Working Group on CFS/ME) and to the Chief Medical Officer (Professor Liam Donaldson). Further, Shepherd requested Malcolm Brahams, solicitor and currently Chairman of HealthWatch, to send letters from Messrs David Wineman of Kingsway, London, to Professor Hooper. In an apparent attempt to prevent Professor Hooper from fulfilling an invitation to address members of the Scottish Cross-Party Parliamentary group on ME, Shepherd has also written to Members of the Scottish Parliament about the document (which he describes as (“scurrilous misinformation”). Shepherd has placed some of his own letters on the internet, including one he wrote on 17 July 2001 to the CMO and one he wrote on
1st August 2001 to the Head of Corporate Affairs at the University of Sunderland.
A list of known letters to date sent by Dr Shepherd and other members of HealthWatch was provided as Appendix 3 to the authors’ response to the letters from the HealthWatch solicitor (acting in his dual capacity as Chairman of HealthWatch) dated 30 July 2001.
Issues raised by Dr Shepherd in correspondence
Shepherd comprehensively rejects the authors’ factual response and continues to insist that the Vice Chancellor of the University of Sunderland should carry out an investigation into Professor Hooper’s “conduct”.
In copious correspondence, Shepherd insists that his complaints about the Montague / Hooper document were justified and that sufficient evidence has been provided by him for the University of Sunderland to instigate a formal investigation into the conduct of Professor Hooper (even though he now appears to accept that there are unauthorised versions in circulation).
Notably, Shepherd makes no attempt to retract any of his own statements which were erroneous, for example:
a) Shepherd asserts that the book Dirty Medicine on which Montague and Hooper relied in their paper had “rightly” been withdrawn from sale: such an assertion is untrue and was clearly refuted in the response dated 30 July 2001 by Montague and Hooper.
b) Shepherd repeatedly refers to the book Dirty Medicine as being “unreliable”. That may be Shepherd’s opinion, but it is not the opinion of others. The book was meticulously referenced and many of the issues it addressed are public knowledge, including such matters as the attack by members of HealthWatch upon Dr Jean Monro which bankrupted her private hospital specialising in allergy treatment; the attack by members of HealthWatch upon Dr Keith Mumby (publicly shown on television) and the involvement of some members of HealthWatch in the attack upon the Bristol Cancer Help Centre which almost caused it to close (see below).
c) On several important matters, Shepherd mis-represents what the original document
actually stated and he continues to do so in a manner which in the authors’ opinion
is irrational and unacceptable.
d) In his letter of 1 August 2001 to the University of Sunderland, Shepherd makes a fundamental error; he states
“Just because HealthWatch received a donation from the Wellcome Foundation
( a registered charity linked to a drug company) back in 1991 does not mean
that the organisation is currently “funded by drug companies”.
The Wellcome Foundation is a drug company, it was never a registered charity, nor is the Wellcome Trust (to which one presumes Shepherd is referring) a registered charity: that is why it is called a “Trust”.
In correspondence, Shepherd states that the Montague / Hooper document contains a number of false or misleading allegations relating to the preparation of the CMO’s report on CFS/ME. What was stated about the preparation of the CMO’s forthcoming Report on CFS/ME was taken from documents prepared by members of the Working Group and the NHS Executive.
In correspondence, Shepherd claims that he is now being accused of acting in ways which are unprofessional and detrimental to those with ME/CFS, and that the Montague / Hooper document is resulting in
“ a growing amount of sometimes quite unpleasant and nasty feedback aimed
in my direction”.
The Montague / Hooper paper does not incite anyone, including ME/CFS sufferers, their families or friends to behave in an aggravating manner towards Dr Shepherd or towards anyone else. The authors of a paper cannot be held in any way responsible for the actions of other people. By encouraging ME/CFS sufferers to contact their Member of Parliament and the media, the authors believe that far from being irresponsible, they acted in a legitimate and sensible manner, given that many people believe that what is happening to the UK ME community is a national scandal which requires public exposure.
In correspondence, Shepherd makes it plain that he regards the Montague / Hooper paper as being “seriously flawed” as far as the “scientific conclusions are concerned”.
Shepherd states in his letter of 17 July 2001 to the CMO that
“much of the scientific argument being put forward by Hooper and ‘Montague’
to justify the use of investigations they advocate (eg immunological, endocrine
and virological screening) is very seriously flawed. They rely on statements
from a highly selective use of references along with omission of references
which fail to support their case….Exactly the same type of flawed logic can
be found when they argue for various other tests to be routinely carried out in the
assessment of these patients”.
The irony of this seems to have escaped Shepherd entirely, because it is precisely that argument which has been levelled at the Wessely School for many years.
Currently, there is no treatment modality which is wholly effective in ME/CFS and the medical profession has nothing much to offer these patients. Until the cause or causes are established, management of the disorder is necessarily somewhat speculative. For Shepherd (in his role as Medical Director of the UK ME Association) to advise UK clinicians not even to look for abnormalities of the immunological or endocrine system (when such abnormalities are well documented as occurring in the disorder) is mystifying.
Far from cherry-picking the available references as Shepherd intimates in his letter to the CMO, Montague and Hooper have instead put forward a broad selection of references which support an organic pathoaetiology for the condition. Such references, even though available, have for too long been either ignored, dismissed or trivialised by those in the UK who prefer a psychiatric model of the illness. Montague and Hooper firmly believe that it is necessary to consider a more balanced approach than one which is limited to the psychiatric literature which has dominated the UK medical journals for so many years.
In support of his opinion that the research relied upon by Montague and Hooper is “seriously flawed”, Shepherd makes the following statement in his letter of 17 July 2001 to the Chief Medical Officer:
“ I acknowledge that I have opposed the inclusion of testing for RNaseL activity
(an antiviral marker) and CFS urinary markers…one of the major problems
with both of these tests is that all the published information so far comes from
researchers who have a financial interest in their promotion – a situation which
involves a clear conflict of interest”.
That seems to be an extremely serious allegation by Shepherd which appears to cast substantial doubt on the integrity of leading ME/CFS researchers, including those of professorial status in America, Belgium and Australia. Despite Shepherd’s claim to the CMO, in the opinion of Montague/Hooper, the integrity and status of these eminent researchers is not open to question.
Concerning the RNase L pathway, in a Workshop given in February 1999 at the International Congress of Bioenergetic Medicine in Orlando, Florida, world expert
Dr Paul Cheney explained that there are three phases of the illness and each phase has to be dealt with differently: in phase one, the RNase L is significantly elevated (for about the first five years), after which time there is a progressive loss of this enzymatic upregulation, and by phase three, it is not seen anymore. It is therefore not a diagnostic marker for the condition, but it does mean that patients need to be fully investigated within the first years of onset.
According to Cheney, in phase two there is a significant down-regulation of RNase L, so patients do not have the underlying protein synthesis disruption that RNase produces. However, patients in phase two cannot do as much as they could in phase one (even though they were in fact more sick in phase one) but they are more limited and are still very sick. Phase two is primarily a toxicity issue, as the RNase activity dysregulates the body’s detoxification system, so patients start getting toxic.
In phase three, patients have no RNase activity but are really locked into their boundaries and are limited by the damage done to deep brain structures, particularly in the hypothalamic region. They are grossly limited by substantial damage to the mitochondrial DNA. It is the loss of mitochondria and (most importantly) the loss of dynamic hormone response which causes the limitations so universally experienced by these patients -- they are severely affected by their low dynamic response to any stressor and it is this hypothalamic injury which is so limiting. According to Cheney, that is the end-point of the disease. He made the chilling observation that there is an end-stage which is resistant to all therapeutic intervention, in that any intervention simply makes the patient even more ill, and that in phase three, because of the injured brain, there will be things which these patients will never be able to do again and they will be locked into significant impairment.
It seems that in the UK those charged with helping patients with ME/CFS have no time for such science: in correspondence dated 26 February 2001 Dr Charles Shepherd wrote
“You are being completely unrealistic if you expect that the docs on the CMO
WG might accept Paul Cheney’s ideas….They won’t.”
Referring to the Montague / Hooper paper, in his letter to the CMO Dr Shepherd wrote:
“Professor Allen Hutchinson (Chairman of the Working Group) has offered to
communicate with the Vice Chancellor (of Professor Hooper’s University) to
discuss the problems which this type of scurrilous misinformation creates
for the Working Group”.
The authors of the Montague / Hooper paper cannot agree that by setting out the known facts, they are guilty of “scurrilous misinformation”. For Shepherd to use such language in place of reasoned argument is a matter of concern.
Robust disagreement between differing factions of opinion is not uncommon in medicine. As has been stated many times by many people, the root of the present disagreement would appear to lie in the great difference of patient populations being studied using varying criteria for CFS, different disciplines and a variety of methodologies.
Uppermost in the mind of those who are being inundated by letters from Dr Shepherd
(Medical Director of the charity The ME Association) are two questions:
(i) On the instigation of Charles Shepherd, HealthWatch has employed the professional services of its own solicitor, so why is Charles Shepherd continuing to send out copious letters in defence of that organisation and trying to drive the situation himself? Even before the solicitor had a chance to consider the response, Shepherd continues to send out letters (assiduously copied to many others) in which he continues to quote passages from the original paper, even though those exact issues have been addressed in the response to the HealthWatch solicitor and are supported by impeccable evidence (including Hansard) which does not rely on distortion or mis-representation, about which Shepherd states
“this pathetic and unconvincing defence of their position will inevitably
diminish their credibility still further”
Given that the reference to HealthWatch in the original Hooper paper made no
deleterious assertions whatsoever ( it merely pointed out that the most influential
members of the CMO’s Working Group are members of or involved with
HealthWatch and it set out the aims of HealthWatch which were taken
directly from the organisation’s own literature), why does Shepherd find it necessary
to react in a way which has drawn far more attention to this issue than did the original
paper?
People are particularly incensed at Shepherd’s blatant attempts to prevent Professor
Hooper from fulfilling an invitation to address the Scottish Parliamentary Cross Party
Group on ME. MSPs, however, are not intimidated by Shepherd and believe they
should hear what Professor Hooper has to say.
(ii) Why does Shepherd not address the central issue, rather than resorting to tactics which seem so obviously diversionary? The central and crucial issue is that Shepherd gave advice to the CMO’s Key Group that only limited investigations are necessary in ME/CFS.
Shepherd’s advice on this point has been perceived not only as a betrayal of the ME
community but as being against the weight of considerable international evidence and
medical opinion which is continuing to accumulate.
In correspondence, Shepherd fails to address the evidence put forward by Montague and Hooper which clearly supports the need for more advanced investigations in this group of complex disorders; instead he states
“Montague and Hooper raise a number of completely irrelevant points about
the scientific content of the paper but make no attempt to respond to my view
that their overall conclusions regarding extensive testing of ME/CFS patients
are seriously flawed, are not supported by the current weight of evidence, and
are not advocated by the overwhelming majority of physicians with expertise
in this illness”.
One can only wonder who in the UK constitutes this “overwhelming majority of physicians with expertise in this illness”.
Given that Shepherd was funded by the UK ME Association to attend the AACFS Fifth International Research and Clinical Conference in Seattle in January 2001, his professional advice that investigations should be limited in cases of ME/CFS is all the more bewildering.
Government Advisory Committees
All those associated with the Montague / Hooper paper are concerned about the manner in which government consultative groups are organised, particularly those on subjects relating to chemicals and health. The lack of facilities for public presentation and cross examination leaves this system wide open to the influence of vested interests be they from the medical profession or the chemical and pharmaceutical industries. Those associated with the Montague / Hooper paper believe that if any members or associates of HealthWatch are appointed to advisory committees, then it should also be the case that an expert in the appropriate field who supports complementary and nutritional medicine should be appointed in order to achieve the necessary balance.