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On 22nd
March 2008 the Financial Times carried an item by Glasgow GP Dr
Margaret McCartney (“If it’s in the mind, it’s still the real
thing”) in which she stated that neither ME – to which she referred
as “myalgic encephalitis” instead of the correct term myalgic
encephalomyelitis – nor fibromyalgia (FM), nor repetitive strain
injury (RSI) nor irritable bowel syndrome (IBS) “has a clear
pathological or biochemical abnormality”. She went on to
confirm: “It’s certainly true that many doctors see these kinds
of symptoms as an irritating and time-consuming diversion from
‘real’ pathology”.
Unfortunately for
ME patients in the UK, such comments are nothing new.
The person whose
work has had most impact on their lives is psychiatrist Professor
Simon Wessely, whose twenty-year published record on ME patients
underpins such ill-informed comments, for example:
- “The
description given at the Mayo Clinic remains accurate: ‘The
average doctor will see they are neurotic and he will often be
disgusted with them’ ”
(In: Psychological Disorders in General Medical
Settings, ed: Sartorius et al; Hogrefe & Huber, 1990)
- “Blaming symptoms on a viral infection conveys certain
advantages, irrespective of its validity (and) is beneficial to
self-esteem by protecting the individual from guilt and blame”
(In: Post-Viral Fatigue Syndrome. ed: James Mowbray and Rachel
Jenkins. John Wiley & Sons, 1991)
-
“It
seems that ME sufferers prefer to feel they have a ‘real’
disease – it is better for their self-esteem”
(Pfizer Invicta Pharmaceuticals 1992:4-5)
-
“Patients with inexplicable physical symptoms are generally
viewed as an unavoidable, untreatable and unattractive burden”
(Brit J Hosp Med 1994:51:8:421-427)
-
“Somatisation sufferers consume vast amounts of health resources
for little benefit”
(Clin Exp Allergy 1995:25:503-514)
-
“The
term ME may mislead patients into believing they have a serious
and specific pathological process. Several studies suggest that
poor outcome is associated with social, psychological and
cultural factors”
(Joint Royal Colleges Report on CFS, October 1996
-
“ME
has never been fully accepted as a real condition, says Simon
Wessely”
(The Guardian, 21st April 1998). Note that the World
Health Organisation fully accepted ME as a real condition in
1969 and continues to do so
.
-
“It
is only human for doctors to view the public as foolish,
uncomprehending, hysterical or malingering”
(BMJ 2003:326:595-597)
-
“Science is indeed socially controlled, and so it should be”
(The Guardian, 1st March 2003)
-
“Functional somatic syndromes include chronic fatigue syndrome”
(Rev Bras Psiquiatr 2005:27:3). This is noteworthy, given that
Wessely is on public record as stating: “I don’t classify CFS
as a somatoform disorder” (Wessely Answers Questions. 10th
April 2002: CAME).
From the above
quotations, it seems there may be an explanation why doctors such as
Dr McCartney are so misinformed.
However, not only
does it seem that Dr McCartney has been careless over her
terminology but it also seems she has not kept abreast of the
medical science that has revealed the pathological and biochemical
abnormalities now known to underpin these disorders.
Moreover, she
claims that the recommendation for cognitive behavioural therapy
(CBT) in the NICE Guideline on “CFS/ME” does not imply a
psychological cause because “behavioural treatments can be used
to improve the quality of life of people who have diabetes, asthma,
or cancer”. This is undoubtedly so, but the key differences that
seem to have been overlooked by Dr McCartney are that in those
disorders, appropriate investigations and effective interventions
are not ignored or proscribed and, importantly, behavioural therapy
is an adjunctive and not the primary – indeed the sole – management
recommendation as it is in ME/CFS.
Dr McCartney harks
back to the much-criticised 1999 paper by psychiatrists Simon
Wessely and Michael Sharpe in The Lancet (“Functional somatic
syndromes: one or many?”: Lancet 1999:354:936-939) and she quotes
with seeming approval Professors Wessely and Sharpe: “The
existence of specific somatic syndromes is largely an artefact of
medical specialisation”.
Apart from the
Lancet article to which she refers, Dr McCartney will doubtless be
aware of Wessely’s views on ME/CFS, fibromyalgia (FM), Gulf War
Syndrome (GWS), the Camelford water poisoning catastrophe, the
effects of chronic low-dose organophosphate (OP) poisoning and the
adverse effects of mobile phones, since Wessely has not been
reticent in publicising his views. He is certain that such disorders
do not exist and that people who claim to suffer from them are
deluding themselves because, he says, they are actually suffering
from a mental (somatisation) disorder which, to quote Dr McCartney,
is “the phenomenon of translating mental distress into physical
symptoms”. Wessely is certain that such symptoms are merely
“the modern preoccupation with the state of our environment” and
that they occur in “a few individuals with pre-existing
somatisation disorders (and are) then diverted to fall in line with
the prevailing (“disease”). Future investigations of environmental
incidents should recall that social and cultural factors are as
important as medical ones” (The Legend of Camelford. Anthony S
David and Simon C Wessely. Journal of Psychosomatic Research
1995:39:1:1-9 --- see below).
The denial of the
very existence of such disorders has become Wessely’s trade-mark.
It was captured in the New Statesman almost a
decade ago when in February 1999 Ziauddin Sardar wrote “Ill-defined
notions”: “When is someone sick, really sick? Who decides? By
what criteria? The only thing that is certain is that you are only
ill when someone says you are ill. Consider syndromes. Once this
was a name for a collection of symptoms for which no clear cause had
yet been found. Now it stands for a bunch of symptoms lacking even
the security of certainty that they are actually there. Most
notorious is ‘chronic fatigue syndrome’, known as ‘ME’. Horror
stories abound of people whom the psychiatric experts considered
just to be faking. The same can be said of 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. Recently he published the results of ‘the most
definitive study’ of Gulf War syndrome in the Lancet. It concluded
– surprise, surprise – that there is no such thing as Gulf War
syndrome. Clearly, Wessely is a follower of Groucho Marx: ‘Whatever
it is, I deny it’ ”.
These are
profoundly serious issues in which Professor Wessely seems to have
been shown to be completely wrong, yet no-where has it been possible
to find a retraction of, let alone an apology for, the incalculable
damage that many people believe his misinformed opinions and
policies have caused.
Although
psychiatric disorders are diagnosed on opinion and not on a
definitive diagnostic test, Professor Wessely demands
“evidence-based medicine” supported by a definitive test and
specific biomarkers before he will accept the reality of ME/CFS.
Whilst there is as yet no specific diagnostic test, there is an
abundance of biomarkers which support the diagnosis, but Professor
Wessely continues his determined and sustained denial and dismissal
of this scientific evidence that clearly proves him to be wrong.
As Philip Steer,
Emeritus Professor, Imperial College, London, asks in the current
issue of the British Medical Journal: “Could strict adherence to
evidence-based practice be harmful to patients?” and he notes
that: “‘Conviction politicians’ may be popular, but conviction
doctors are potentially dangerous” (BMJ 2008:336:673).
Of even more
concern is the fact that, despite having been shown to be so wrong
about, for example, the Camelford disaster, Gulf War syndrome, the
dangers of mobile phones, the nature of IBS, the nature of
fibromyalgia and the nature of ME/CFS (for evidence, see below),
Professor Wessely’s influence over Government policy continues
unabated.
The influence of
his team in the NICE Guideline on “CFS/ME” featured in the 2007 R&D
(Research & Development) annual reports by NHS organisations in
England, in which the South London and Maudsley NHS Trust stated in
section 2A (“Examples of impact on health and social care”):
“We begin by summarising key achievements and follow with six
examples that illustrate the impact of our research”.
The section on
“Chronic Fatigue Syndrome” boasts: “In October 2006 NHS Plus
published Occupational Aspects of the Management of Chronic Fatigue
Syndrome: a National Guideline. It was accompanied by two additional
leaflets, one for Health Care professionals and one for employers.
This report was heavily influenced by research carried out at our
Chronic Fatigue (sic) Unit. The NICE CFS/ME guideline
also includes priority recommendations to which our research, led by
Trudie Chalder and colleagues, has contributed: ‘When the adult or
child’s main goal is to return to normal activities, then the
therapies of first choice should be CBT or GET because there is good
evidence of benefit for this condition in mild to moderately
affected adults and some evidence in mild to moderately affected
children’. As a result of our research we have developed
our chronic fatigue syndrome service to include treatment at home.
In addition we now offer telephone treatment routinely after
demonstrating its effectiveness”.
ME/CFS
On 18th
March 2008 The Daily Telegraph carried an item entitled “ME:
‘Invisible disease’ is now easier to read” by Bob Ward, who reported
on the work of Dr Jonathan Kerr of St George’s University of London
(published in the Journal of Clinical Pathology and to be presented
at an ME Research UK [MERUK] biomedical conference at the University
of Cambridge on 6th May 2008 [and also at the Invest in
ME International ME/CFS Conference 2008 in London on 23rd
May 2008]). The article pointed out that Kerr’s team has identified
88 genes that produce different levels of proteins and other
molecules in ME/CFS compared with controls. In 2005 Kerr carried
out a complex analysis and found that patients with ME/CFS can be
divided into seven clinical sub-types according to specific gene
combinations and the severity of symptoms. The most severely
affected patients had 71of the 88 gene abnormalities. In his
follow-up paper to which the Telegraph article referred, Kerr’s
earlier work was confirmed: (J Clin Pathol 2007:
doi:10.1136/jcp.2007.053553): “In this study, for each CFS/ME
subtype, we determined those genes whose expression differed
significantly from that of normal blood donors. Genomic analysis
was then related to clinical data for each CFS/ME subtype.
Genomic analysis revealed some common (neurological, haematological,
cancer) and some distinct (metabolic, endocrine, cardiovascular,
immunological, inflammatory) disease associations among the
subtypes. It is particularly interesting that in these genomically
derived subtypes, there were distinct clinical syndromes, as would
be expected in a disease with a biological basis”.
Other researchers
have noted that patients with ME/CFS can have “a genetic
predisposition to an immunomodulatory response of an inflammatory
nature, probably secondary to one or more environmental insults”
(N Carlo-Stella et al. Clin Exp Rheumatol 2006:24(2):179-182).
One would think
that such evidence would lead to a change in attitude by Wessely
School psychiatrists towards ME/CFS, but as has been noted countless
times by many people, nothing seems to stop Wessely’s influence on
Government policy: a current example is the forthcoming conference
on “CFS” to be held at The Royal Society of Medicine on 28th
April 2008, about which Dr Derek Enlander from New York wrote on 21st
March 2008 to the Editor of the Daily Telegraph: “Your article
on gene research in ME was a breath of fresh air in the stale
atmosphere of UK Government funded research. Over the years it has
been shown to be a physical disease. The cause is obscure (and) this
obscurity has been masterfully used by psychiatrists to claim that
the disease is a manifestation of a psychiatric condition. What
arrogance! The Royal Society of Medicine plays to this theme by
running a conference on ME/CFS. The speakers are dwelling mainly on
psychiatry – rather peculiar for a Society of Medicine. As far as I
know the RSM has not noted these physical aspects. The Government
through NICE continues to waste money on proven bad methods of
treatment which, in a large number of cases, cause relapse. Surely,
by now, the Government should be embarrassed”.
That ME/CFS is not
a somatisation disorder is now beyond doubt because there is
overwhelming evidence confirming it to be a multi-system organic
disorder in which there is disruption of virtually every system in
the body (for evidence, see
http://www.meresearch.org.uk/information/researchdbase/index.html
and
http://www.meactionuk.org.uk -- between them, these sites
contain over 3,000 published papers demonstrating that ME/CFS
is not a psychiatric disorder). The item published on 18th
March 2008 in The Daily Telegraph to which Dr Enlander referred
above was indeed a breath of fresh air. As noted by Dr John
Greensmith in his response: “There has been ample research
evidence for M.E. as a discrete illness since 1956 and it has been
endorsed by the WHO as a neurological illness since 1969, yet the
Government’s advisers, who are dominated by psychiatrists, have
tampered with the M.E. entry in the British version of the WHO
handbook (though it remains untouched in other countries) and have
recommended two treatments on the basis of questionable research
evidence, one of which, cognitive behavioural therapy (CBT) has no
lasting benefit for people with M.E. and the other, graded exercise
therapy (GET) may leave some patients irrecoverably worse. They say
that they do not believe that M.E. is ‘all in the mind’ (but) since
most patients are treated by psychiatrists, using treatments
developed for psychiatric illnesses, most often in psychiatric units
of hospitals, it is hard to think how otherwise they would treat
them if they did believe it was of psychiatric origin. The
situation does not look set to change. Indeed, a Royal Society of
Medicine conference to be held on 28th April 2008, to
which selected delegates have been invited and others told that they
should not attend, is expected to recommend that this unproven
service should be expanded” (drjohngreensmith@mefreeforall.org
).
Nancy Klimas, Professor of Medicine at the
University of Miami and an international expert on ME/CFS, affirmed:
“Our patients are terribly ill, misunderstood, and suffer at the
hands of a poorly informed medical establishment and society” (AACFS
In-coming Presidential Address: Co-Cure 21st March
2005).
In January 2008, Klimas went on record: “As an
immunologist, I once would have said (ME)CFS is clearly an immune
dysfunction state, while an endocrinologist would have called
attention to the adrenal gland irregularities, and a specialist in
the autonomic nervous system would be convinced (ME)CFS is all about
blood pressure abnormalities. Given what we’ve discovered about the
illness, I now tell people (ME)CFS is all of these things. We know
that (ME)CFS has identifiable biologic underpinnings because we now
have research documenting a number of pathophysiological processes
involving the brain, the immune system, the neuroendocrine system
and the autonomic nervous system” (Historical perspective.
Nancy Klimas. In: “Defining Moments – 20 years of making CFS
History”, published by the CFIDS Association of America, January
2008).
It is regrettable that such pronouncements do
not receive anything like the publicity that Professor Wessely’s
pronouncements receive.
The latest evidence demonstrating the key finding
that there is a low-grade inflammatory response in ME/CFS was
published on 21st March 2008 in Clinical Science (VA
Spence et al: Clinical Science 2008:114(8):561-566); this important
paper adds to the existing body of scientific knowledge about ME/CFS
that shows excessive cytokine production, disruption of the HPA axis
and dysfunction of the autonomic nervous system, none of which can
credibly be attributed to a behavioural disorder that is amenable to
psychotherapy.
Professor Wessely and other members of the
“Wessely School” simply ignore all this scientific evidence that
proves them wrong and they remain committed to their own unshakable
beliefs, which many people believe have resulted in unnecessary
suffering of innumerable sick people.
Fibromyalgia
Just as he dismisses ME/CFS as a somatisation
disorder, Professor Wessely likewise asserts that fibromyalgia (FM)
also is a somatisation disorder – indeed, he asserts that it is the
same somatisation disorder (Lancet 1999:354:936-939). He
clearly believes this, but where is his evidence? There is none.
The scientific evidence, especially the more
recent evidence, continues to mount and it does not support
Professor Wessely’s beliefs. He, however, rejects this substantial
body of evidence that he is wrong.
The WHO classifies FM as a discrete disorder in
ICD-10 at M79 under soft tissue disorders, not as a somatisation
disorder.
The Mayo Clinic recently published “Fibromyalgia
myths: The truth about 9 common myths”, which stated
“Fibromyalgia is a specific diagnosis” (http://www.mayoclinic.com/health/fibromyalgia/AR00056
).
Illustrations of research findings in FM include
the following:
In 1997 it was shown that levels of somatomedin C
are lower in FM patients (AL Bennett et al. J Psychiat Res
1997:31:1:91-96).
In 1998 researchers showed that levels of
Substance P are elevated in FM patients (Evengaard B et al. Pain
1998:78:2:153-155).
In 2003 it was shown that endothelin-1 is raised
in FM patients (Pache M et al. Rheumatology 2003:42:493-494).
Research in 2005 indicated that FM is the result
of internal biochemical imbalances that cause the physical symptoms
(Co-Cure MED: 2nd January 2005: Fibromyalgia: new
insights into a Misunderstood Ailment).
Different research in 2005 found elevated
N(epsilon)-carboxymethyllysine levels in muscular tissue and in
serum of patients with FM, with more intensive staining in the
interstitial connective tissue of fibromyalgic muscles (Ruster M et
al. Scand J Rheumatol 2005:34(6):460-463).
Again in 2005, more serious abnormalities were
demonstrated by histologic studies particularly on electron
microscopy, revealing disorganisation of Z bands and abnormalities
in the number and shape of mitochondria: biochemical studies and P31
magnetic resonance spectroscopy showed inconstant abnormalities of
ATP and phosphocreatine levels. The authors noted that
“Mitochondrial abnormalities, reduced capillary circulation and
thickened capillary endothelium may result in decreased availability
of oxygen and impaired oxidative phosphorylation as well as ATP
synthesis” and commented that these abnormalities do not seem to
be the consequences of de-conditioning (Le Goff P. Joint Bone Spine
2005, November 9th).
In 2006, an important review in the Annals of the
New York Academy of Sciences (Sarzi-Puttini P et al, Ann N Y Accad
Sci 2006:1069:109-117) demonstrated orthostatic intolerance in FM,
suggesting underlying abnormalities in cardiovascular neural
regulation: “Research suggests that various components of the
central nervous system are involved, including the HPA axis,
pain-processing pathways, and the autonomic nervous system”
Again in 2006, research showed a greater
prevalence of FM in HTLV-1 (human T cell lymphotrophic virus)
infected individuals, suggesting that FM may be associated with this
viral infection (Cruz BA et al: J Rheumatol: 2006:33(11):2300-2303).
In 2007, researchers at Yale University School of
Medicine showed muscle hypoperfusion induced by regional vasomotor
dysregulation in FM, noting that this vasoconstriction in muscle
would lead to low-level ischaemia and its metabolic sequelae (Katz
DL et al. Med Hypotheses 2007: March 19th).
More research into FM in 2007 demonstrated
bladder symptomatology (Brand K et al. Clin Rheumatol 2007: May 3rd).
Further research in 2007 showed that autoimmune
thyroiditis is present in an elevated percentage of FM patients and
that patients with thyroid autoimmunity showed a higher percentage
of dry eyes, burning or pain with urination, allodynia, blurred
vision and sore throat (Bazzichi L et al. Clin Rheumatol 2007: May 9th).
In 2007, Bazzichi et al also showed evidence of
abnormal levels of cytokines in FM: “The higher levels of
cytokines found in FM patients suggest the presence of an
inflammatory response system (IRS) and highlight a parallel between
the clinical symptoms and biochemical data” (Clin Exp Rheumatol
2007:25(2):225-230).
Another paper in 2007 revealed a conspicuous
pattern of altered brain morphology, suggesting that FM is
associated with structural changes in the central nervous system of
patients (Schmidt-Wilcke T et al. Pain: 2007: June 21st).
In January 2008 researchers provided compelling
evidence of a demyelinating polyneuropathy in FM, with
electrodiagnostic (EDX) evidence of both polyneuropathy and
demyelination. The authors concluded that 33% of FM patients have
clinical and EDX findings of chronic inflammatory demyelinating
polyneuropathy / CIDP. (Caro XJ et al. Rheumatology (Oxford)
2008:47(2):208-211).
In February 2008 researchers from McGill
University, Montreal, Canada, presented evidence that “neurotransmitter
studies show that FM patients have abnormalities in dopaminergic,
opioidergic, and serotonergic systems” and that “studies of
brain anatomy show structural differences between the brains of FM
patients and healthy individuals” (Schweinhardt P et al.
Neuroscientist 2008: February 12th).
Also in 2008, in a blinded study, skin biopsy
samples showed electron microscopic evidence of unusual patterns of
unmyelinated nerve fibres as well as associated Schwann cells, which
the researchers considered may contribute to the lower pain
threshold seen in FM patients (Kim SH et al. Clin Rheumatol
2008:27(3):407-411).
In a study published in March 2008, US
researchers noted that previously, functional magnetic resonance
imaging (fMRI) had shown that the insula displays augmented activity
in FM, which means that neurons in FM patients are more active in
this part of the brain. This linked to their own findings that pain
decreased when levels of the brain molecule glutamate went down,
glutamate being a neurotransmitter that conveys information between
neurons in the nervous system (Clauw D et al. Arthritis and
Rheumatism 2008:58:3).
Such research findings cannot rationally be
dismissed, yet Wessely et al still insist that fibromyalgia is a
somatisation disorder and they have deliberately included FM
patients in the Medical Research Council’s behavioural intervention
trials on patients with “CFS/ME” in which “Wessely School”
psychiatrists are the investigators, a diagnostic inaccuracy that
would seem to make a mockery of the MRC’s claim that it funds only
studies of the highest scientific calibre, especially as in July
2004 a Minister of State (Dr Stephen Ladyman MP) made it known at a
House of Commons All Party Parliamentary Group on FM that doctors
were to be offered financial incentives to persuade patients with
fibromyalgia to enter these MRC trials.
Gulf War Syndrome
From even before 1996, the time when he and
fellow psychiatrist Anthony David were awarded $1million (£666,000)
by the US Department of Defence in a Pentagon-funded study to
investigate Gulf War illness among UK veterans (BMJ1997:314:95),
Wessely continually denied the existence of Gulf War Syndrome.
In their official report on GWS published in the
Lancet in January 1999 (Catherine Unwin et al. Lancet
1999:353:169-178), Wessely et al concluded that there is no such
thing as Gulf War Syndrome and that the pathway of such illness
could be the “perceived” risk of chemical attack, and that it
was this “psychological” effect that might be contributing to
the ill-health of Gulf War veterans.
In October that same year a study carried out by
the well-respected Rand Corporation for the US Defense Department
did not support Wessely’s conclusions. As a result of this two-year
study by Dr Beatrice Golomb, the Penatgon changed its policy and
admitted that there could be a link with GWS and the use of
pyridostigmine bromide (PB, or anti-nerve gas) tablets which the UK,
US and Canadian troops were forced to take during the first (1991)
conflict in the Gulf.
In his testimony to the Gulf War Illnesses Public
Inquiry held at the Palace of Westminster in 2004 and chaired by The
Rt Hon The Lord Lloyd of Berwick, Robert Haley, Professor and
Director of the Division of Epidemiology and Preventative Medicine
at the University of Texas South Western Medical Centre, Dallas, an
acknowledged world authority on the nature and causes of
neurological disease in Gulf War veterans, said of Wessely et al:
“Studies using nonspecific definitions of Gulf War neurological
syndrome are biased toward finding negative results.
Early in the history of
Gulf War illness research, around 1993, a decision was made in the
government to the effect that ‘there is no Gulf War syndrome’, and
this led to pressure on researchers who wanted government funding
not to use a case definition of the illness in their research.
Without at least a provisional case definition, however, it is
virtually impossible to design studies that will elucidate the
nature of the illness, or illnesses, and connect them with causes.
“The most important example of the unproductive
use of a nonspecific case definition concocted was the series of
studies from the Kings College London group. In place of a case
definition describing the disease that veterans were complaining of,
they defined Gulf War illness as having a score of greater than 72.2
on the SF-36 questionnaire, which measures functional impairment
regardless of the cause. This case definition essentially counted
veterans as having Gulf War illness if they had any condition that
caused them to feel bad. Consequently, many veterans with diseases
other than Gulf War neurological syndrome that made them feel bad
were mistakenly counted as cases, and conversely, many with typical
symptoms of Gulf War neurological syndrome but who were not very ill
with it were not counted as cases. This severe degree of
bidirectional misclassification has caused all studies from the
Kings College London group to reach spuriously negative
conclusions”.
Professor Haley
also provided evidence (against Professor Wessely’s studies) that:
“Studies using nonspecific measures of nerve agent exposure are
biased toward finding negative results”.
Wessely told the
Inquiry: “The Gulf war syndrome debate is really just of academic
importance” but Lord Lloyd (a former law lord) said there was
“every reason” to accept the existence of a “Gulf War
Syndrome” (The Independent Public Inquiry on Gulf War Illness.
Report published on 17th November 2004).
In March 2008, The US National Academy of
Sciences published another report by Dr Beatrice Golomb (of the
University of California, San Diego, and Chief Scientist to the US
Congress-appointed Committee on Gulf War Illnesses); this report
found evidence linking the symptoms experienced by the Gulf War
Veterans – including muscle and joint pain, rashes and breathing
problems – to a particular class of chemicals, specifically to the
anti-nerve gas agent given to the troops, to the pesticides used to
control sand-flies, and to the nerve gas sarin. Dr Golomb told
Reuters that: “Convergent evidence now strongly links a class of
chemicals – acetylcholinesterase inhibitors – to illness in Gulf
War veterans”. She said that a lot of attention had been given
to psychological factors, but that “psychological stressors are
inadequate to account for the excess illness seen” (http://www.bbc.co.uk/1/hi/health/7288902.stm
). The Proceedings of the National Academy of Sciences is specific:
“Increasing evidence suggests excessive illness in Persian Gulf
War veterans can be explained partly by exposure to organophosphate
and carbamate acetylcholinesterase inhibitors, including
pyridostigmine bromide (PB), pesticides and nerve agents (and) this
exposure may be causally linked to excess health problems in Gulf
War veterans” (Proc. Natl. Acad. Sci. USA,
10.1073/pnas.0711986105).
This study was
reported in The Economist (War of nerves. 13th March
2008), which also reported Professor Wessely’s comments about these
irrefutable findings: “This may encourage sick veterans that a
cause of their suffering could finally be found, but Simon Wessely,
a professor at the Institute of Psychiatry’s centre for military
health research, is sceptical. He says that the review is ‘an
opinion piece that continues a line of argument Dr Golomb has put
forwards for some time’”.
In a response to
The Economist, Malcolm Hooper (Emeritus Professor of Medicinal
Chemistry and Chief Scientific Adviser to the UK Gulf War Veterans)
wrote: “The casual and dismissive comments by Professor Simon
Wessely about the recent review by Professor Beatrice Golomb that
makes clear the link with chemicals used in the first Gulf War are
unacceptable. (They are) indicative of the resistance to extensive
American research studies that have identified serious damage to the
brains of sick soldiers, major heart and cardiovascular disorders,
as well as immune, respiratory and neuromuscular disorders,
including an excess of motor neurone disease. Despite no official
funding, UK research has found excess osteoporosis and severe
endocrine damage in UK veterans. The neglect of these veterans is
shameful. Golomb’s paper challenges us to seek and speak the truth
and to act accordingly”.
It seems strange
that Professor Wessely should reject the science reported in the
Proceedings of the New York Academy of Sciences (which has an
impressive impact factor rating) in favour of his own speculation.
Moreover, it seems
that he fails to see that he is doing exactly that of which he
accuses Dr Golomb – i.e. his own view is nothing more than “an
opinion piece that continues a line of argument” that he
has “put forward for some time”. The big difference that
Professor Wessely seems to have missed -- either by accident or by
design -- is that Dr Golomb has got actual evidence to support her
findings, whereas he has none.
Toxicity of
organophosphate and organochlorine compounds
Professor Wessely
has a long published record of rejecting the validity of
environmental illness (for example: BMJ 1993:307:747-748; Clin & Exp
Allergy 1995:25:503-514), particularly illness arising from
exposure to chemicals, and he has apparently commented with seeming
satisfaction that in the modern world it is impossible to avoid
daily contact with a multiplicity of chemicals.
In numerous
publications, he has seemed to disparage and denigrate patients with
symptoms of environmental illness, repeating the same message time
and again, both in medical journals and in the media:
“These
total allergy syndromes are akin to culture-bound syndromes
afflicting modern developed societies where sufferers from
unexplained symptoms no longer see themselves as possessed by devils
or spirits but instead by gases, toxins and viruses”
(Clin Exp Allergy 1995:25:503-514).
“In a
previous era, spirits and demons oppressed us. Although they have
been replaced by our contemporary concern about invisible viruses,
chemicals and toxins, the mechanisms of contagious fear remain the
same. To the majority of observers, including most
professionals, these symptoms are indeed all in the mind”
(NEJM
2000:342:2:129-130).
“The
release of poison gas into a crowded Tokyo subway killed 12 people.
Since then there have been several reports of sudden episodes of
panic among crowds of Japanese commuters. These were probably
examples of mass hysteria. Mass hysteria is far from new. A classic
book on the subject has just been reissued. It is an account of the
follies of mass behaviour throughout the ages. In previous times,
mass hysteria would be blamed on demons, spirits and diabolical
possession. Nowadays we are oppressed by equally invisible gases,
viruses and toxins”
(“Have you heard? We are being poisoned”. The Times, 4th
July 1995, page 14).
“Like many hospital specialists, I have seen a steady
stream of patients with many mysterious symptoms. The sufferers
usually blame their ill health on factors such as solvents,
pesticides, pollution, food additives or dental amalgam. Many report
exquisite sensitivity to such everyday substances as perfumes,
deodorants, tap water and hairspray. Such people are sometimes
labelled as suffering from ‘total allergy syndrome’. All
explanations have much in common. First, there is no personal
blame. Second, all appear to be modern worries. Third, all are
linked by another modern theme – the immune system in trouble. I
doubt it is a coincidence that multiple chemical sensitivity, and
total allergy, rose to prominence in parallel with the rise of HIV.
The idea that the immune system might give way because of an
invisible external agent is now embedded in popular consciousness.
But just how new are these modern illnesses? The things that we
blame for making us feel ill change over the years. Medieval man
was oppressed by spirits and demons. Nowadays we blame similar ills
on mysterious viruses and allergies (which are) an ever-changing
parody of scientific advances of the day. ‘Modern’ illness is far
from modern”
(“Sickness of the century. Simon Wessely sees a connection to fears
of the past”. The Guardian 28th May 1996, page 13).
“ ‘People
always believe they are oppressed. They seize on explanations that
are credible and make sense within their world view: 300 years ago,
people believed in possession by demons’. These days, he writes in
an editorial
(in the
New England Journal of Medicine),
those demons have been replaced by our ‘concern about invisible
viruses, chemicals and toxins’. So how do you deal with a mass
psychogenic / sociogenic illness? ‘The challenge is to convey the
scientific reality without being seen as blaming the victims’,
writes Wessely
(The
Guardian 25th January 2000, pp8-9).
“The threat of chemical and biological weapons could
have serious long-term social and psychological consequences,
leading to outbreaks of panic-induced illness, according to a
leading psychiatrist, Simon Wessely. Outbreaks of mass sociogenic
illness are already appearing, (with) worries about reproductive
outcomes, such as impaired fertility or damaged babies”
(“Panic could be biggest illness”. The Guardian, 19th
October 2001).
It is indeed
impossible to avoid daily contact with chemicals, over 30,000 of
which have not been fully evaluated toxicologically, so their
combined effects on humans are unknown. Lindane, an organochlorine
pesticide (OCP), was widely used as an insecticide in the farming
industry because of the need for ever-increasing food production.
The nation (and indeed the world) has been deluged with ever more
complex agrochemicals, some of which have now been banned. DDT was
found in the food chain and was banned in the 1970s, but OCPs can
still be found in environmental and biological matrices due to their
persistence (“Man-Made Chemicals in Food Products”. TNO Report,
2006: Netherlands Organisation for Applied Scientific Research).
These products are not effectively metabolised so they just
accumulate in the body.
There have been
innumerable items in the press about falling sperm counts and rising
cancer levels, as well as the fact that the UK now has the highest
incidence of asthma in Europe.
In June 2003 the
Royal Commission on Environmental Pollution, chaired by Sir Tom
Blundell FRS, FMed Sci, presented its 24th Report
“Chemicals in Products” to Parliament by Command of Her Majesty. It
caused a media frenzy. Some illustrations include the following:
“Thousands
of chemicals are being used every day without proper safety tests,
exposing the public to a ‘gigantic experiment’ experts warned
yesterday. The potential dangers posed by flame retardants,
plastics, glues and even some toothpastes are uncertain, because
only 40 of 30,000 chemicals in large-scale use have been tested
fully, says the Royal Commission on Environmental Pollution. Because
of this, ‘the chemical disasters of the past are likely to be
repeated in the future’”
(“Chemical timebomb”. Daily Express, 27th June 2003).
“The
government is experimenting with people’s lives by failing to test
properly tens of thousands of man-made chemicals used in everyday
life, according to a leading biochemist who chairs the Royal
Commission on environmental pollution”
(“Failure to test chemicals ‘puts lives at risk’ ”. The Guardian, 27th
June 2003).
On 22nd
April 2004 the Daily Mail carried an item by Robin Yapp, Science
Reporter (“Revealed, the toxic chemicals invading our bodies”) in
which he wrote: “A huge cocktail of toxic chemicals can be found
in every adult’s blood, research revealed yesterday. Scientists say
the chemicals – found in everything from TVs to sofas, cosmetics, to
computer screens – are now so widespread in the environment that
no-one is likely to escape contamination”.
Concern was
expressed that most testing of chemicals is done on individual
compounds, but possible syngergistic effects of the compounds in
multiple formulated products are generally not tested at all.
In 2005, the Pesticide Action Network UK
published “The alternative pesticide residues report: What the
Government doesn’t tell us”. This report provides striking examples
of where the current regulatory system does not appear to protect
consumers, particularly in relation to pesticide residues in food,
and notes the uncertainties about the impact of pesticides on human
health, particularly chronic illnesses, endocrine disruptors and the
effect of a ‘cocktail’ of pesticides.
It cannot have been overlooked by Wessely et al
that the work of Dr Jonathan Kerr of St Georges, London, has linked
ME/CFS to OPs (J Clin Path 2005:58:826-832). Kerr et al suggest
that patients with (ME)CFS “have reproducible alterations in gene
regulation”, noting that “sixteen genes were confirmed as
having an expression profile associated with (ME)CFS. These genes
can be grouped according to immune, neuronal, mitochondrial and
other functions. These findings are consistent with
previous work showing that patients with (ME)CFS have evidence of
immune activation, such as increased number of activated T cells and
cytotoxic T cells, and raised circulating cytokine concentrations.
NTE (neuropathy target esterase) is a target for
organophosphates and chemical warfare agents, both of which may
precipitate (ME)CFS. EIF2B4 is a mitochondrial
translation initiation factor and one of the EIFB2 family, within
which mutations have been shown to be associated with central
nervous system hypomyelination and encephalopathy. The
involvement of genes from several disparate pathways suggests a
complex pathogenesis involving T cell activation and abnormalities
of neuronal and mitochondrial function, and suggests possible
molecular bases for the recognised contributions of organophosphate
exposure and virus infection”.
In his subsequent paper referred to above (J Clin
Pathol 2007), Kerr stated: “We have previously documented
upregulation of NTE in (ME)CFS. NTE is the primary site of action
of organophosphate (OP) compounds. Exposure to OP compounds may
trigger CFS/ME and Gulf War Illness”.
Neuropathy target esterase (NTE) is inhibited by
several OP pesticides, chemical warfare agents, lubricants, and
plasticisers, leading to OP-induced delayed neuropathy in humans,
with over 30,000 cases of human paralysis (Gary Quistad et al. PNAS
June 24, 2003:100:13:7983-7987).
Although ostensibly not personally involved in
the report of the joint working party of the Royal Colleges of
Physicians and Psychiatrists (“Organophosphate sheep dip: clinical
aspects of long-term low-dose exposure”; November 1998), Professor
Wessely’s influence shines through and a large number of the 85
references are his or those of his close colleagues who share his
views. His frequent co-author -- psychiatrist Anthony David -- was
a member of the working party.
Commenting on the composition of the Royal
Colleges’ working party, Dr Richard Horton, editor of The Lancet,
said: “All together there are ten members, including six
professors. A committee with such a distinguished provenance would
seem immune from criticism. Far from it. Not one of its members
has direct experience of looking after patients exposed to OPs. The
committee’s conclusions are bound to be based on wholly incomplete
evidence. Pompous and complacent scientists are seen to be
pompous and complacent” (Observer Life 3rd August
1997:41).
It is a matter of
note that the 1996 findings of neurologist Professor Peter Behan
from the University of Glasgow linking ME/CFS to chronic low-dose OP
exposure were excluded from the Report of the Royal Colleges, given
that Behan found ME/CFS to be clinically identical to chronic
low-dose OP exposure and that such OP exposure “in some way
prepared the patients for the later development of (ME)CFS”.
Behan reported that the abnormalities found in both ME/CFS and in OP
poisoning were “compatible with a decreased responsiveness of CNS
type II glucocorticoid receptors, (confirming) the hypothesis of
brain steroid receptor resistance in patients with the delayed
response to OPs and in (ME)CFS” (J Nutrition & Environmental
Medicine 1996:6:341-350).
The Royal Colleges’
Report on OPs predictably recommended that treatment for those who
have been exposed to OPs should be cognitive behavioural therapy and
anti-depressants and it claimed that a “vicious circle” of
self-maintaining symptoms, including “illness beliefs and fears
about the meaning of symptoms” perpetuate ill-health. Again
predictably, the Report urged against what many would regard as
appropriate investigation, claiming that investigations “may bias
the consultation towards a narrow physical orientation”.
The Report barely mentioned the problems of
anaesthesia for those with OP exposure, an omission which might well
have given rise to a charge of scientific misconduct, given that in
1987 the Stationary Office had published a Guidance Note MS17 which
unambiguously warned about the dangers of anaesthesia, especially
the commonly-used muscle relaxant succinyl choline, in people who
have been exposed to OPs. Further, in 1995 The Royal College of
Anaesthetists had warned members about the dangers of OP compounds
and anaesthesia.
Neither document
was mentioned in the Report of the Royal Colleges on OPs.
Despite the large
number of papers from both US and UK researchers that show clear
links between neurotoxicity and organophosphate pesticides – effects
exacerbated by synergistic action with other pesticides – Professor
Wessely continues to insist, without any convincing evidence, that
there is no link.
This is not
science, but opinion wedded to fanciful postulates of somatic
illness which are rejected by other psychiatrists.
There is
well-established evidence of the neurological toxicity that is
well-recognised in the literature, including work from the US
National Institutes of Health, from the MRC Toxicology Unit at the
University of Leicester, UK and from prestigious institutions such
as The Scripps Research Institute, La Jolla, California.
The target enzyme
systems involved in the toxicity of these compounds include not only
acetylcholinesterase and butyrylesterase but also much more
sensitive brain enzymes and neuropathy target esterase which play a
role in nerve function and in the development of motor neurone
disease (MND).
It is well-known
that OPs affect brain esterase enzymes at much lower dosages than
those producing significant inhibition of acetlycholinesterase
commonly regarded as the target enzymes for OPs.
OP compounds have
traditionally been associated with the inhibition of esterase
activity (Paul G Richards et al. Molecular Pharmacology
2000:58:3:577-583).
It is widely known
that cholinesterase inhibitors such as OPs are commonly used as
insecticides and pesticides and the chemically closely-related (and
more toxic) organophosphonates are used (and may be stored) in
biological warfare agents.
Researchers have
demonstrated that the time and exposure levels of these agents have
considerable relevance in determining possible brain injury (Lola
Roldan-Tapia et al. Neurotoxicology and Teratology 2005:27:259-266).
Low dose exposure
to both pesticides and nerve agents gives rise to delayed chronic
neurotoxicty (Abou-Donia et al. Archives of Environmental Health
2003:58:484-497).
Abou-Donia and
Garrettson have identified auto-antibodies to neuronal proteins as a
marker for OP neurotoxicty (Environmental Epidemiology and
Toxicology 2000:2:27-41).
It is a matter of
public record that the incidence and prevalence of Alzheimer’s
disease are increasing rapidly (Pritchard et al. Public Health
2004:118:268-283).
As well as
providing a target for the action of pesticides, the cholinergic
system plays an important role in the progression of Alzheimer’s
disease and there is strong correlation between the severity of the
dementia and the cholinergic deficits (Paul G Richards et al.
Molecular Pharmacology 2000:58:3:577-583).
In a paper looking
at the neurotoxicity of chronic exposure to moderate levels of
pesticides, Kamel et al analysed cross-sectional data from 18,782
individuals over a four year period in relation to 23 neurological
symptoms. Among chemical classes of insecticides, associations were
strongest for organophosphates and organochlorines. Results suggest
that neurological symptoms are associated with cumulative exposure
to moderate levels of organophosphate and organochlorine
insecticides (Freya Kamel et al. Environmental Health Perspectives
2005:113:7:877-882).
Changes in
erythrocyte enzymes in humans have been reported after exposure to
different pesticides, including OPs, one of which appears to be an
important biological indicator of pesticide exposure (Antonio F
Hernandez et al. Toxicology Letters 2005:159:13-21).
From just these few illustrations, it is clearly
untenable for anyone to claim that symptoms of low-dose OP poisoning
are a somatisation disorder.
The Camelford
catastrophe
Wessely is equally dismissive of the Camelford
drinking water contamination, where in July 1988 twenty tonnes of
aluminium sulphate were pumped into the drinking water supplies of
the Cornish town, resulting in the death of seven people, with
25,000 people suffering serious health effects and with 40,000
animals affected (The Ecologist 1999:20:6:228-233). The death toll
has since risen – see The Daily Telegraph, 20th April
2006: “Alzheimer’s fear grips poisoned water town” by Medical Editor
Celia Hall. Bone biopsies carried out over six months later showed
stainable aluminium. Although noting that some peoples’ hair, skin
and nails turned blue, in their paper in the Journal of
Psychosomatic Research (The Legend of Camelford: 1995:39:1:1-9)
Wessely and his co-author Anthony David were not to be moved: they
claimed that it was all mass hysteria (BMJ 1995:311:395) and that
the “somatic” symptoms were the result of heightened perception of
normal and benign symptoms and irresponsible reporting by the press,
though they have not explained by what mechanism hysteria affects
animals.
In 1999 it was
conclusively shown by Paul Altmann et al that there was objective
evidence of considerable organic brain damage compatible with the
known effects of exposure to aluminium and that it was this
exposure, not anxiety or hysteria, which was the cause of the
symptoms exhibited by those who had been exposed to the contaminated
water (BMJ 1999:319:807-811).
More recently,
Exley and Esiri described severe cerebral congophilic angiopathy
coincident with increased brain aluminium in a resident of Camelford
(JNNP 2006: doi:10.1136/jnnp.2005.086553), causing Walter Lukiw,
Associate Professor of Neuroscience at Louisiana State University
Health Sciences Centre, to note that as over-expression of
stress-sensing, pro-inflammatory and pro-apoptotic genes have been
observed in aluminium sulphate-induced neurotoxicty, “careful
attention should be paid to the neurological status and
neuropathological outcome of the thousands of unfortunate victims at
Camelford” (eBMJ, 21st April 2006).
In December 2007,
the West Somerset Coroner Michael Rose ordered the police to re-open
the Camelford pollution case following allegations of a cover-up
(Guardian, 13th December 2007).
Responding to this
announcement, a spokesperson for a UK charity and the mother of a daughter severely affected by
ME wrote to The Guardian on 16th December 2007: “I and
many others await with interest the outcome of any police inquiry. A
1995 paper by two psychiatrists asserted that mass hysteria and / or
anxiety were responsible for the supposed suffering of those in the
Camelford area at the time. (One of these ‘experts’) has also given
his expert opinion on many other ‘non-illnesses’ and ‘unfounded
health worries’. He happens to be the Government expert on
electricity pylons, mobile phone masts, Gulf War Syndrome and
myalgic encephalomyelitis”.
The Coroner’s
conclusions are still awaited, but clearly the existing evidence
does not support Professor Wessely’s beliefs that the Camelford
disaster was merely contagious mass hysteria.
Irritable bowel
syndrome
Another of
Professor Wessely’s targets for somatisation disorder is irritable
bowel syndrome or IBS (The Lancet 1999:354:936-939) but the evidence
does not support such a model.
The following are
illustrative of a wide body of evidence:
At the 68th
Annual Scientific Meeting of the American College of
Gastroenterology held in 2003 at Baltimore, important findings were
presented by lead investigators from the University of Vermont
(Peter Moses, Associated Professor of Medicine and Director of
Clinical Research in the Digestive Diseases, and Gary Mawe,
Professor of Anatomy and Neurobiology): “Serotonin is a critical
signalling molecule necessary for normal gut function. Our finding
that key elements of serotonin signalling are changed in IBS lends
credibility to the notion that IBS is not simply a psychological or
social disorder as was once thought, but instead due to altered gut
biochemistry and interactions between the gut and the brain. Now we
have a perspective on molecular changes in the intestines of
individuals with IBS that we did not have before. We identified a
significant decrease in the serotonin transporter in cells that form
the inner lining of the bowel. Because the transporter is diminished
in IBS, serotonin stays around longer, and this can lead to changes
in motility, secretion, and sensitivity” (Ecotoxicology 2003:12
(1-4):345-363).
In 2006, the BMJ
Learning programme by a Clinical Research Fellow and a Professor of
Medicine and Gastroenterology featured IBS (BMJ 2006:332:280-283).
This programme pointed out that a number of pathophysiological
abnormalities can often be identified: “IBS is now clearly
understood to be a multifactorial condition, rather than its just
being due to psychopathology. These include motility, visceral
sensation, central processing, genetics, inflammation and
neurotransmitters”.
At the American
Academy of Neurology 59th Annual General Meeting held
in Boston in April / May 2007, researchers from Brazil showed
that people with inflammatory bowel disease were at risk for
subsequent neurological disorders and presented convincing evidence
of the link between IBD and peripheral neuropathy: “Based on
these results, we believe IBD itself is directly related to the
neuropathy and that neuropathy in these patients is much more common
than previously thought”.
In ME/CFS specifically, there is evidence that
the disorder is accompanied by an increased transloctaion of
endotoxins of gram-negative enterobacteria through the gut wall,
with signs of activation of the inflammatory response system and
IgG3 subclass deficiency (Maes M et al. Neuro Endocrinol Lett
2007:28:6).
Clearly, the out-dated hypothesis that IBS is a
psychosomatic disorder has been abandoned by those who fulfil their
contractual obligations to keep up-to-date with medical science, yet
Professor Wessely et al seem unaware of this progress in medicine.
Mobile phone
sensitivity
In 2003 Professor
Wessely’s team was awarded a research grant of £405,000 to
investigate the psychological and biological effects of mobile phone
radiation in healthy subjects and subjects with self-reported mobile
phone hypersensitivity. Professor Wessely was Principal
Investigator. The study was expected to last until April 2006.
When this was
announced, one astute ME sufferer observed: “That’s one more
negative result, then!”.
On 2nd
September 2003 the Countess of Mar wrote to Professor George
Szmukler, Dean of Psychiatry at the Institute of Psychiatry about
Professor Wessely’s involvement in this study:
“As Principal
Investigator of the (new) Mobile Phone Research Unit at Kings
College Hospital, doubtless (Professor Wessely) is soon to
‘discover’ mobile phones have no biological consequences for human
health other than the aberrant beliefs of those using them”.
Perhaps
importantly, the study was jointly funded by the Programme
Management Committee of the MTHR (Mobile Telecommunications and
Health Research programme), which itself is jointly funded by the UK
Department of Health and the mobile telecommunications industry.
The study was
published on 15th April 2006 in the BMJ
(2006:332:886-891).
As widely
anticipated, Professor Wessely’s study concluded: “We found no
evidence that self-reported sensitivity to mobile phone signals has
a biological basis”. However, the study also noted: “That
symptom severity did increase during exposure is interesting. These
symptoms were not trivial. Indeed, for some they were so severe
that exposures had to be stopped early or the participants withdrew
from the study”.
Undeterred, the
authors still advised: “In terms of their clinical implications,
these results do not suggest that attempting to reduce exposure to
mobile phone signals will be a useful strategy for patients who
report sensitivity to them. Although such interventions might be
actively sought by patients, in the longer term a danger exists that
they will reinforce a patient’s view of himself or herself as being
sensitive to electromagnetic fields. Instead it may be better to
encourage such patients to test alternative explanations for their
symptoms by using cognitive behavioural therapy. The symptoms
reported by ‘sensitive’ people may be primarily psychological in
origin”.
It is notable that a study from Finland that was
published the same year as Professor Wessely’s study came to
interesting conclusions, namely, that mobile phones affect brain
blood flow: “Mobile phones create a radio-frequency
electromagnetic field around them when in use. We studied the
effects of a commercial mobile phone on regional cerebral blood flow
(rCBF) in healthy humans using positron emission tomography (PET)
imaging (in) a double blind, counterbalanced study. Explorative and
voxel-based statistical analysis revealed that a mobile phone in
operation induces a local decrease in rCBF beneath the antenna in
the inferior temporal cortex and an increase in the prefrontal
cortex, suggesting that the electromagnetic field (EMF) emitted by a
commercial mobile phone affects rCBF in humans. These results are
consistent with the postulation that EMF induces changes in neuronal
activity” (Sargo Aalto et al. Journal of Cerebral Blood Flow &
Metabolism 2006:26:885-890).
Whilst the Finnish study did not seek to identify
hypersensitivity to mobile phones, it did provide actual evidence
that they affect brain blood flow.
Arthur Firstenberg is unequivocal: “The most
basic fact about cell phones and cell towers is that they emit
microwave radiation; so do wireless computers, cordless phones and
their base units. A cell phone that is on but not in use is also
radiating. It is a fact that we are all being bombarded, day in and
day out, whether we use a cell phone or not, by an amount of
radiation that is some ten million times as strong as the average
natural background. A cell phone, like a microwave oven, heats you
from the inside out, not from the outside in. The presence of
albumin in the brain is always a sign that blood vessels have been
damaged and that the brain has lost some of its protection.
Researchers have found, consistently for 18 years, (that) microwave
radiation, at doses equal to a cell phone’s emissions, causes
albumin to be found in brain tissue. In research published in 2003,a
single two-hour exposure to a cell phone just once permanently
damaged the blood brain barrier. Two minutes on a cell phone
disrupts the blood brain barrier; two hours on a cell phone causes
permanent brain damage” (Leif G Salford et al. Environmental
Health Perspectives: 2003:111:7:881-883).
Firstenberg continues: “Diseases that have
increased remarkably in the last couple of decades (which) there is
good reason to connect with the massive increase in radiation in our
environment, include asthma, sleep disorders, multiple sclerosis,
ALS, Alzheimer’s disease, fibromyalgia, chronic fatigue syndrome,
hypothyroidism, diabetes, malignant melanoma, testicular cancer,
and heart attacks and strokes in young people. The literature
showing biological effects of microwave radiation is truly enormous,
running to tens of thousands of documents. I am amazed that
industry spokespersons are getting away with saying that wireless
technology has been proved safe or – just as ridiculous – that there
is no evidence of harm. A 1998 survey by the California Department
of Health Services indicated that at that time 120,000 Californians
– and by implication one million Americans – were unable to work due
to electromagnetic pollution” (California EMF Program: The Risk
Evaluation. 2002).
Firstenberg is clear: “The ranks of these
so-called electrically sensitive are swelling in almost every
country in the world, marginalized, stigmatised and ignored”.
The full paper can be found at -
http://www.eldoradosun.com/Archives/01-06_issue/Firstenberg.htm
.
Wessely et al apparently do not accept such
findings, preferring instead to endorse findings of a three-year
study at the University of Essex for the UK Health Protection Agency
(HPA), which found “Phone mast allergy ‘ in the mind’ ”. Perhaps it
is relevant that, as in the case of Professor Wessely’s study, this
study was funded by the Mobile Telecommunications and Health
Research programme, a body which itself is funded by industry and
Government.
Conclusion
In defiance of the extensive published evidence
that ME/CFS and other disorders mentioned above are not
psychosomatic, Professor Wessely’s unremitting insistence that they
are in reality but one single behavioural disorder seems
indefensible.
In April 2000 an Opinion from a leading Queen’s
Counsel (who is a member of the House of Lords) was obtained about
Professor Wessely’s dogma on ME/CFS. That Opinion is concise:
“On the document
you have sent me there is an overwhelming case for the setting up of
an immediate independent investigation as to whether the nature,
cause and treatment of ME as considered by the Wessely School is
acceptable or consistent with good and safe medical practice. There
is substantial doubt as to whether such could be the case. It is, of
course, open to patients (and) their parents to seek Judicial
Review”.
In her letter of 2nd
September 2003 to Professor Szmukler referred to above, the Countess
of Mar wrote:
“Through his
prolific output Professor Wessely has introduced his personal
beliefs into the UK medical literature and those beliefs are aimed
at changing the perception of ME/CFS held by both medical and lay
people. Through the shortcomings of the peer-review system, his
personal beliefs have become medical doctrine, effectively turning
patients into victims”.
Without doubt, there is substantial evidence in
the public domain that Professor Wessely himself has carried out an
unremitting campaign of denigration of ME sufferers. One of the most
notorious was his involvement with a poll run by the British Medical
Journal in 2002 in which doctors were asked to vote on what they
considered to be “non-diseases”. It is understood that it was
Professor Wessely himself who nominated ME. Along with big ears and
freckles, ME was duly voted a “non-disease” that should be left
medically untreated.
It must be due in large part to such disgraceful
antics and to the fact that Professor Wessely and other members of
the Wessely School are Government advisers on “CFS” that people with
ME/CFS are suffering politically-driven health discrimination which
is contrary to the Disabled Discrimination Act.
There is a broad
body of informed opinion – national and international -- that
Professor Wessely belittles other peoples’ work without addressing
the issues.
For a detailed
exposition of the tactics of dismissal used by the Wessely School,
see “The Mental Health Movement: Persecution of Patients? A
Consideration of the Role of Professor Simon Wessely and Other
Members of the ‘Wessely School’ in the Perception of Myalgic
Encephalomyelitis (ME) in the UK. Briefing Paper for the House of
Commons Health Select Committee” by Malcolm Hooper et al http://www.meactionuk.org.uk/SELECT_CTTEE_FINAL_VERSION.htm
Apart from the
Wessely School’s own studies, there is little published evidence to
support the notion that CBT actually works in ME/CFS, and
their own studies have been the subject of criticism on the grounds
that many of their studies are deemed to be methodologically flawed,
principally because of the authors’ selection bias (i.e. they are
not studying cases of true ME/CFS, but are then claiming that their
results relate to ME/CFS).
For many years Professor Wessely has achieved
considerable coverage of his views in the UK media on topics ranging
from dental amalgam, “blaming mummy for a bad tummy” “the power of
the placebo”, “how long should a sick leave last?”, bogus miracle
cures, and total allergy syndrome to RSI (repetitive strain injury),
so the national press coverage of the apparently exponential
increase in rates of psychosomatic disorder and the alleged efficacy
of CBT is substantial, with Professor Wessely being frequently
quoted in the broadsheet newspapers.
Also, due in no small measure to Professor
Wessely’s apparent control over what gets publicly funded on ME/CFS
(perhaps due his previous positions on three MRC Boards and to the
fact that “Wessely School” members hold influential positions at the
MRC) and what gets published on ME/CFS in the UK (perhaps exercised
through his position as a member of the Scientific Advisory Panel to
the Science Media Centre which was founded in 1999; it is funded by
pharmaceutical companies and operates like a newsroom to promote the
views of industry and to launch fierce attacks against those who
question them), the medical journals frequently publish highly
uncritical assessments of CBT which focus on the few studies which
support its use, whilst ignoring those controlled trials which did
not find CBT to be effective (and which warned about the dangers of
exercising beyond fatigue).
This matter is the
subject of an article entitled “A Subgroup Analysis of Cognitive-Behavioral
Treatment Studies” by Fred Friedberg (JCFS: 1999:5: 3-4:149-159;
co-published simultaneously as “Chronic Fatigue Syndrome: Advances
in Epidemiologic, Clinical and Basic Science Research (ed) Roberto
Patarca-Montero, Haworth Press Inc. 1999).
Friedberg, clinical professor in the Department
of Psychiatry at the State University of New York, made the
following cardinal points:
“Several studies of graded activity-oriented
cognitive behavioural treatment for (ME)CFS, all conducted in
England, have reported dramatic improvements in functioning and
substantial reductions in symptomatology.
“On the other
hand, cognitive behavioural interventions conducted in Australia and
the United States have not found significant improvements in
functioning or(ME)CFS symptoms.
“Furthermore,
descriptive studies of CF (chronic fatigue) patients in England, the
US and Australia suggest that the (ME)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 closely resemble fatiguing neurological illnesses”.
Professor Friedberg
notes the “widely divergent clinical presentations” and he
notes specifically that because all the apparently successful CBT
studies 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 CBT could be made.
Professor
Friedberg’s paper was published almost a decade ago, yet Professor
Wessely’s influence in the UK remains undiminished.
In a paper dated 8th
March 2008 entitled “The Year of No Compromise” Greg Crowhurst, a
health care professional whose wife is one of the most severely
affected ME/CFS sufferers in the UK, said the following
“This is a simple summary of the inferred
messages underpinning the psychiatric paradigm, currently being
heavily promoted in the UK”.
Although written
specifically in relation to ME/CFS, the summary applies equally to
all disorders designated by Wessely et al as being “medically
unexplained” which these psychiatrists assert are Functional Somatic
Syndromes (FSS), including the disorders outlined above. These
“Wessely School” psychiatrists in fact believe that ME/CFS, FM, IBS,
non-ulcer dyspepsia, pre-menstrual syndrome, chronic pelvic pain,
atypical chest pain, “hyperventilation syndrome”, tension headache,
temperomandibular joint pain, globus syndrome and multiple chemical
sensitivity are but one single psychiatric disorder (Lancet
1999:354:936-939).
Crowhurst’s summary
exactly captures the situation in the UK:
“The recommendations:
·
do not investigate ME/CFS patients
·
do not provide special facilities for ME/CFS
patients other than psychiatric clinics
·
do not offer special training to doctors about
the disorder
·
do not offer appropriate medical care for ME/CFS
patients
·
do not offer respite care for ME/CFS patients
·
do not offer State benefits for those with
ME/CFS
·
do not conduct biomedical research into the disorder
The tactics:
·
the wreaking of havoc in the lives of ME/CFS
patients and their families by the arrogant pursuit of a psychiatric
construct of the disorder
·
the attempts to subvert the international
classification of this disorder from neurological to behavioural
·
the propagation of untruths and falsehoods about
the disorder
·
the building of affiliations with corporate
industry
·
the insidious infiltration of all the major
institutions
·
the denigration of those with ME
The practices:
·
the attempt to make "ME" disappear in a sea of
chronic fatigue
·
the refusal to see or acknowledge the
multiplicity of symptoms
·
the ignoring and misinterpretation of the
biomedical evidence
·
the suppression of published findings
·
the vested interests
The impact:
·
the arresting and sectioning of protestors
·
the silencing of ME patients, through being given
a psychiatric label
·
the suppression of dissent
·
the labelling of ME patients as the "undeserving
sick", as malingerers
·
the forcible removal of sick children and adults
from their homes.
“It is poignant how an institutionally supported
prejudice against people with ME has arisen, based on nothing more
substantial than supposition and opinion, carefully disseminated.
“You have to be very careful how you discern the truth; it is an
important issue in the corporate wall of collusion surrounding the
physically sick people who have ME.
“We have to be very clear about what is the truth about ME and what
is either deliberate, naive or ignorant misinterpretation or
misrepresentation. The impact of the above strategy on peoples’
lives is catastrophic”.
Crowhurst’s article can be accessed at
www.metrainingco.org.uk
As noted by Hooper et al, the malign influence of
Wessely School dogma extends throughout Government departments,
throughout the NHS, and even extends to the Judiciary, with one
Claimant being told at a High Court Hearing that “Judges regard
ME as psychological self-indulgence”. One Local Health Board
will only fund treatment for ME/CFS where the focus is CBT/GET. A
spokesman for Grampian NHS Trust is on record in 2003 (disturbingly,
this was a year after the publication of the UK Chief Medical
Officer’s Working Group Report) as stating “ME is not a condition
we recognise or treat” (see “Illustrations of Clinical
Observations and International Research Findings from 1955 to 2005
that demonstrate the organic aetiology of ME/CFS”
http://www.meactionuk.org.uk/Organic_evidence_for_Gibson.htm ).
The damage perpetrated on those with ME/CFS by
Wessely School adherents cannot be quantified. The Wessely School
argument that syndromes like ME/CFS cause “unnecessary
expenditure of medical resources” has been criticised by a
leading US researcher for its pernicious public policy implications
(Lancet, 11th December 1999:354: number 9195).
In the UK, patients with ME/CFS, particularly
children, have suffered gross and barbaric abuse and persistent
denigration as a consequence of the beliefs of Wessely School
psychiatrists who are attempting to control the national agenda for
this complex and severe neuro-immunological disorder and who by
their words and deeds have wreaked havoc in the lives of many ME/CFS
patients and their families by their arrogant pursuit of a
psychiatric construct of the disorder in clear defiance of the
clinical and scientific evidence of the organic nature of ME/CFS.
There have been persistent and frequently covert
attempts by these psychiatrists to subvert the international
classification of ME/CFS, with destructive consequences for those
affected.
It seems that Professor Wessely is accountable to
no-one for his role in determining UK Government policy that the
disorders mentioned above do not exist as discrete entities and that
such patients should be “managed” by psychotherapy.
Instead, Professor Wessely has been lauded and
honoured.
On 27 August 2003, Dr George Szmukler, Dean of
Psychiatry, Institute of Psychiatry, King’s College Hospital,
London, wrote to the Countess of Mar about Professor Simon Wessely:
“Professor Wessely must be judged one of the most
outstanding researchers in the UK, and indeed internationally.
Professor Wessely has been awarded a Research Medal by the Royal
College of Physicians specifically for his work on CFS and he has
served on many prestigious scientific committees, further attesting
to the high regard in which he is held by the scientific community”.
Not everyone – including doctors and
medical scientists from around the world -- shares that view.
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