Wessely’s Way -Rhetoric or Reason?

[Guest guest]

Wessely's Way: Rhetoric or Reason?

~~~~~~~~~~~~~~~~~~~~~~

Malcolm Hooper

Margaret

malcolm.hooper@...

22nd March 2008

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: Mowbray and

. 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

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

catastrophy, 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. S 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

Kerr of St '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). 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 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 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@... ).

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. 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 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 ls 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 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 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 ( 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,

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. ne, 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 Kerr of St s,

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 ( 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 --

was a member of the working party.

Commenting on the composition of the Royal

Colleges' working party, Dr 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 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 ( G

s 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 ( G

s 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

( F 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 catastrophy

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

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 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

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, Sue Waddle,

spokesperson for the charity ME Research UK, a

magistrate 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 (

Moses, Associated Professor of Medicine and Director

of Clinical Research in the Digestive Diseases, and

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 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) o 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, in return for his decades of denigration of

patients (for actual quotations from his work see

" Quotable Quotes about ME/CFS " available from the

charity Invest in ME at 01603 – 701980) and for his

denial and dismissal of the published evidence that

he is wrong, and for all the seemingly consequential

suffering and despair arising from his personal

beliefs, Professor Wessely has been lauded and

honoured.

On 27 August 2003, Dr 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