Saturday, February 20, 2010

5 More Responses to BMJ

(38 in total are up at the time of writing)

http://www.bmj.com/cgi/eletters/340/feb11_1/c738#231497  

Psychiatric measures will not relieve me of a neurological illness
Andrea Pring   (20 February 2010)

Education the Key to
Richard Simpson   (20 February 2010)

Re: Defeatism and Chronic Fatigue
jill cooper   (20 February 2010)

Re: triumphalism not defeatism
Nasim Marie Jafry   (20 February 2010)

Defeatism leads to CBT/GET
Guido den Broeder   (20 February 2010)


=========================

Psychiatric measures will not relieve me of a neurological illness
20 February 2010
    
Andrea Pring,
Writer/Researcher
I cannot work. PL21 0EG



M.E. is an incapacitating, soul-destroying illness that strips away a
sufferer's entire life. Before I became ill, I was a newly qualified
teacher, with a new husband and home. I was beautiful, vibrant and
ambitious. After a succession of viruses I was struck down with ME/CFS and
finally had to retire at the age of 39. I relied on my doctor to do what was
best for me. However, I had no idea at the time that once labelled with the
illness I would no longer be offered further testing or treatment other than
talk therapy and other psychiatric measures.

Psychiatric measures will not relieve me of a neurological illness.

I stagger and slur, bump into things and fall down stairs. I forget where I
live. I struggle to finish sentences. I shake and tremble when I push myself
beyond my limit, which changes by the minute. I suffer with myoclonus,
ataxia, severe low blood pressure and malaise but rarely tiredness.
I lie
unbathed for days until there is break in the symptoms and I can tend to
myself. My hair sits matted and crusted on my head; often left unwashed for
weeks at a time.

I would like to ask the physicians who are reading this a simple question.
How many of you are aware that M.E. is classified as a NEUROLOGICAL illness by the World Health Organisation, and has been since 1969? It was only when
the psychiatric element adopted the illness back in the 1980's that it was
muddied with the artificial construct, CFS.
Now sufferers are thrown in to
the ME/CFS grab-bag along with a conglomerate of other conditions, ranging
from depression, tiredness and burn out to undiagnosed hypothyroidism and
MS. Since further testing is discouraged, physiological proof will rarely be
found. If I were to be given a simple tilt table test then you would see
that my heart and circulation are damaged. But this is one of the very tests
that are discouraged. Why?
POTS is very common in M.E. yet you will rarely
see this mentioned in any of the text books an NHS doctor will read.

I live my life in solitude, not because I choose to but because I have been
forced to by this abhorrent illness, that can be likened to an opprobrious
partner. One who decides when I can wash and dress myself, when I can read a
book, when I can eat, when I can move and if I can use my legs to walk to
the toilet.

All I ask for is appropriate testing and treatment and a chance to continue
where I got off. Nothing more, nothing less.

Competing interests: An ME/CFS sufferer.

=====================

Education the Key to
20 February 2010
    
Richard Simpson,
Charity Trustee
NR59JB



It is easy to see how the "strange conflation" to which Professor Broome
refers would, of course, create a sense of unease in psychiatrists such as
himself and his more prominent peers. Chronic fatigue may not be a terminal
illness but myalgic encephalomyelitis can be.

The media generally do not portray the condition as a "progressive,
paralysing, and commonly fatal illness".[1] Normally the media follow the
propaganda which elements in King's College have continuously promoted since
the late eighties.

If people with ME had only "bed sores, chest infection and malnourishment"
to contend with then the rest of the patient population would not have to
endure the consequences of the stranglehold which psychiatrists have on this
illness – which is at the expense of patients and despite more and more
evidence showing ME to be a serious and progressive biological condition.

Any pessimism exhibited by those with this illness finds its source not in the condition itself but in the ignorance and mendacity of those who
engineer scarce funding from the MRC in order to support the pretence that ME is a somatoform condition, or who publish research based on flawed diagnostic criteria. In fact those suffering the tremendous disability of severe ME are surprisingly optimistic despite the travails of having to deal with prejudice from the some parts of the medical profession and the media.

To use NICE as an example for promoting the use of CBT and GET is risible
and perverse, yet entirely predictable as biomedical research was
ignored.[2] The fact that 90% percent of ME support groups opposed NICE, the
fact that ME patients took NICE to a judicial review in protest at their
guidelines for ME, the fact that the only support that NICE could muster
from those supposedly supporting the ME community were from organisations
that accept government money and who themselves organise "psychosocial
conferences" on ME – all of this illustrates the lack of confidence which
people with ME and their families have for NICE.

And yet NICE is supposedly there to guarantee excellence in clinical
practice.

But we have long since gone past the point where a small section of
psychiatrists influencing NICE can really persuade anyone that CBT and GET
are serious answers to a neurological illness – we just have to wait for the
psychiatrists to catch up or, more likely, be left by the wayside as real
science establishes beyond doubt the pathology of this illness.

Patients and their families are increasingly aware of this policy- based
evidence making which NICE and those who dominate the MRC promote based on
the policies of the last generation which funds only research projects on ME
which promote the psychosocial view of its aetiology [3].

The problem with the treatment of ME in the UK is essentially, as Professor
Broome's posting demonstrates, down to poor education about the condition
and this stems from the education of medical students and continues, for
many doctors, through their years of practice. It is also heavily influenced
by biased research.

If one is fed a constant diet of biased research then one can expect little
more than ignorance to exist.

But there is hope as biomedical research is progressing as shown by the
latest research by the Whittemore-Peterson Institute/National Cancer
Institute/Cleaveland Clinic with the discovery of a link between the XMRV
retrovirus and ME [4]. Hardly just bed sores and chest pains!

There really is a great deal of catching up to do for some sections of the
medical profession with regard to ME.[5]

Perhaps the editor of the BMJ could be persuaded to attend a biomedical
research conference on ME and write an informative, unbiased article about
it for the readers of this journal.

Ultimately, education really is a progressive discovery of one's own
ignorance.

[1] 1. Santhouse AM, Hotopf M, David AS. Chronic Fatigue Syndrome. BMJ
2010;340:c738

[2] National Institute for Health and Clinical Excellence. NICE clinical
guideline 53: Chronic fatigue syndrome/myalgic encephalomyelitis (or
encephalopathy). 2007. www.nice.org.uk/CG53 .

[3] Magical Medicine: How to Make a Disease Disappear by Professor Malcolm
Hooper (http://www.investinme.org/Article400%20Magical%20Medicine.htm )

[4] Vincent C. Lombardi, Francis W. Ruscetti, Jaydip Das Gupta, Max A.
Pfost, Kathryn S. Hagen, Daniel L. Peterson, Sandra K. Ruscetti, Rachel K.
Bagni, Cari Petrow-Sadowski, Bert Gold, Michael Dean, Robert H. Silverman,
and Judy A. Mikovits. Science [DOI: 10.1126/science.1179052]

[5]
http://www.investinme.org/Documents/Journals/Journal%20of%20IiME%20Vol%203%20Issue%201%20Screen.pdf  

Competing interests: None declared

====================

Re: Defeatism and Chronic Fatigue
20 February 2010
    
jill cooper,
teacher
cv214hl



With respect, in response to Alistair C Young's comments:

1. I am glad if many clinicians feel a sense of defeat with regard to their
interpretation of Chronic Fatigue Syndrome.

2. I do not feel that there has been 'bullying' nor 'badgering' by people
who want biomedical research into this range of diseases. (Lay nor medical).


3. If there is a 'powerful lobby' then that is out of necessity.

4. If that poweful lobby 'will not accept any role for psychological factors
in the cause of this disorder' it is because we are not talking about a
single disorder.

Certainly there will be some people with the diagnosis who have
psychological illnesses.
              
5. We are not likely to discover physical causes if we refuse to look for any.

6. Many 'unfortunate victims' have had the opportunity to experience the
'benefits of the treatments outlined by Santhouse and his colleagues' but
many of these victims are still unwell. (If you recall, some of them are
dead).

7. As we are not talking about a single disease, we are unlikely to find a
standard medical treatment.

Once again, I stress that my comment is 'with respect'.

Competing interests: None declared


======================

Re: triumphalism not defeatism
20 February 2010
    
Nasim Marie Jafry,
author of 'The State of Me', ME for 27 years
EH10 4HS



Exactly, there is no defeatism: we want to get better, we are desperate to
get better. Thankfully, there are researchers digging down to the truth -
the biomedical truth - slowly, but surely.

But that truth is still not being acknowledged by a core of
medics/psychiatrists.

The above article could be re-titled: Psychiatrists' insistence on CBT/GET
is undermining the progress of biomedical research.

It is no wonder some in the ME community are labelled as militants. We are
angry and exhausted and baffled at not being listened to.
When will it end?
What does it take?

Competing interests: None declared


==============

Defeatism leads to CBT/GET
20 February 2010
    
Guido den Broeder,
Chairman of the ME/CVS Vereniging
Igor Stravinskisingel 50, 3069 MA, Rotterdam, the Netherlands


Santhouse, Hotopf and David (SHD) claim that defeatism towards myalgic
encephalomyelitis (ME) is undermining evidence that the illness can be
treated. It cannot be stressed strongly enough that they are right - except
that it's the authors' defeatism that I would like comment on.

It is a sign of defeat to diagnose a postviral disorder of the brain,
involving disfunction of various bodily systems (Carruthers, 2003), as
'chronic fatigue'. It is a sign of defeat to claim that it should be
classified as neurasthenia or somatization, to offer behavioural therapies
as the only remedy, and to keep insisting on this even after they have been
proven not to work. Exactly this attitude displayed here by SHD is
responsible for blocking research and guidance into proper diagnostics and
treatment for ME.

ME can be treated - only not by CBT/GET. Research by NIVEL (De Veer, 2008)
shows that CBT, GET as well as antidepressants offer, of all commonly
applied treatments, by far the worst results.
Even NICE, that produced a
guideline on CFS that many professionals refuse to support (NICE, 2007),
does not recommend CBT or GET for the severely ill as the authors, in their
defeat, appear to do.

Diets, supplements, bedrest, pacing and painkillers, on the other hand, are
among the treatments that are known to, sometimes significantly, improve the
ME patient's quality of life (De Veer, 2008). But that is just the
beginning: they do not cure.

There is no reason why ME should not be curable. We know most of what's
wrong - in fact, we knew that already before the psychiatrists muddied the
scene (see e.g. Hyde, 1992) - so all it takes is good research, which of
course needs funding. The millions that are currently wasted on CBT/GET
would do nicely.

So many people need not have died, or lead a crippled life.

Guido den Broeder

Chairman of the ME/CVS Vereniging (The Netherlands)

www.me-cvsvereniging.nl  

----

Carruthers BM, Jain AK, DeMeirleir KL, Peterson DL, Klimas NG, Lerner AM,
Bested AC, Flor-Henry P, Joshi P, Powles ACP, Sherkey JA, Van de Sande MI
(2003), "Myalgic Encephalomyelitis / Chronic Fatigue Syndrome : Clinical
Working case Definition, Diagnostic and Treatment Protocols", Journal of
Chronic Fatigue Syndrome, Vol. 11

De Veer AJE, Francke AL (2008), "Zorg voor ME/CVS-patiënten. Ervaringen van
de achterban van patiëntenorganisaties met de Gezondheidszorg", NIVEL,
Utrecht, December ("Care for ME/CFS patients. Experiences of the supporters
of patient organizations with health care.")

Hyde BM (ed.) (1992), "The Clinical and Scientific Basis of Myalgic
Encephalomyelitis / Chronic Fatigue Syndrome", Nightingale Research
Foundation, Ottawa, Canada with editorial and conceptual advice from Levine
P and Goldstein J., 724+23p, ISBN 0-9695662-0-4

National Institute for Health and Clinical Excellence (2007), "Chronic
fatigue syndrome / Myalgic encephalomyelitis (or encephalopathy); diagnosis
and management", London, August

Competing interests: None declared

Functional Impairment in CFS, Fibro

This is really worth looking at because it used the Canadian Consensus Criteria, which I would have thought would give a reduced estimate of prevelence - but they came up with a prevalence rate of 1.3% for CFS - and over 7% for CFS for prevalence among women of prime working age.

Furthermore, they showed that the three conditions together impacted one in twenty Canadians.

That's pretty impressive, I think.

http://www.cfp.ca/cgi/content/full/56/2/e57

Mary
 
  





Provision of social support to individuals with chronic fatigue syndrome



Provision of social support to individuals with chronic fatigue syndrome

Journal: Journal of Clinical Psychology

Authors: Leonard A. Jason [1 *], Nicole Roesner [1], Nicole Porter
[1], Brittany Parenti [1], Jennifer Mortensen [2], Lindsay Till [3]

Affiliations:
[1] DePaul University
[2] Michigan State University
[3]Northwestern University


*Correspondence to Leonard A. Jason, Director, Center for Community
Research, 990 W. Fullerton Ave., Suite 3100, Chicago, IL 60614
email: Leonard A. Jason Ljason@depaul.edu.

The authors appreciate the financial assistance provided by the
National Institute of Allergy and Infectious Diseases (grant numbers
AI36295 and AI49720).
We also thank the following people for their help on the project:
Carole Howard, Patrick Holiday, Gail Schoebacher, Mary Thompson,
Sandy Reyes, Samra Cheema, Gina Delucca, Blair Coleman, Kimberly
Korkowski, and Laura Thomas.


Abstract
The present study evaluated a buddy program designed to provide
support for individuals with chronic fatigue syndrome (CFS).

The intervention involved weekly visits by a student
paraprofessional, who helped out with tasks that needed to be done in
an effort to reduce some of the taxing demands and responsibilities
that participants regularly encountered.

This model of rehabilitation focused on avoiding overexertion in
persons with CFS, aiming to avoid setbacks and relapses while
increasing their tolerance for activity.
Participants with CFS were
randomly assigned to either a 4-month buddy intervention or a control
condition.

Post-test results showed that individuals who received a student
buddy intervention had significantly greater reductions in fatigue
severity and increases in vitality than individuals in the control
condition.
There were no significant changes between groups for
physical functioning and stress.

Buddy interventions that help patients with CFS reduce overexertion
and possibly remain within their energy envelopes can be thought of
as representing a different paradigm than nonpharmacologic
interventions that focus only on increasing levels of activity
through graded exercise.


© 2009 Wiley Periodicals, Inc. J Clin Psychol 66: 249-258, 2010.  


* * *
 
I will note that at the point that I decided my health was more important than a spotless house, my health started to improve.  I hired someone to do the essential cleaning, didn't worry about a little clutter, and spent  a lot of my time horizontal.  Voila, my health stopped declining and turned around.



Friday, February 19, 2010

More letters to the editor

7 more Rapid Responses in reply to the BMJ editorial, "Chronic Fatigue Syndrome"


[Note that some people's responses did not go up when they first submitted
them so they contacted the letters' editor to enquire for the reason, edited
their letter slightly and got it through. Tom]

http://www.bmj.com/cgi/eletters/340/feb11_1/c738#231497

A dangerous path to take
Linda A Crowhurst   (18 February 2010)

I adore CBT
A.F. Andrew   (18 February 2010)

"It's wrong and misguided to "Imagine""
Barbara J Robinson, Frances Groen   (18 February 2010)

High time to broaden the field
Jackie A Stableforth   (19 February 2010)

CBT The Mythology
Gerwyn j Morris, Stephanie Fulton   (19 February 2010)

Re: I adore CBT
Dr John H Greensmith   (19 February 2010)

Shedding a little more light on 'Defeatism'
Doris M Jones   (19 February 2010)

----------------------------------------------------------------------------
----
A dangerous path to take 18 February 2010

Linda A Crowhurst,
Very Severe ME Sufferer
N/A



Some of the points made in the Editorial are indeed correct, for example
"the alternative to treatment is no treatment and this can have a disastrous
effect on the patient, who may feel the medical profession has given up on
them as a hopeless case."
There is indeed currently no effective treatment,
no cure and little hope for people who are genuinely suffering from very
severe ME, like I have done for the past 16 years.

What is missing from this article is any acknowledgement that it is the
psychiatric lobby's influence in ME that has led to the confusion over what
ME is and the lack of physical treatment and the lack of proper biomedical
investigations. The psychiatric approach is to deny the physical reality of
an ME patient's illness and to promote the unproven view that a person is
ill because of maladaptive thinking and de- conditioning.

This is a very dangerous path to take , one which has led to a negation of
the severity of illness and of the real physical suffering, that people
endure. It has led to the most severely affected housebound and bed-bound
people being left for decades , like myself, without appropriate physical
investigation and biomedical ME support . It has also led to the shocking
reality that the only front-line treatment currently being promoted,
entirely wrongly, by the NHS, is psychosocial, completely ignoring the
underlying physical dysfunction.

The severely affected are not even involved in research so how can their
needs be known ? How can this article promote CBT and GET for very severely
affected patients , when the psychiatric view is a complete denial of their
very real , totally disabling physical experience ? This article will lead
to further confusion in the medical profession , will potentially endanger
people's lives and lead to untold suffering if followed.

Most people with very severe ME would find it too difficult to even be in a
room with other people, due to acute hypersensitivity and a multiplicity of
severe physical symptoms, let alone engage in therapy of any description,
physical or mental. Yet this issue is not even raised in the article.

Reading this paper you might be convinced that ME is a psychiatric disorder
. In reality ME is a neurological disease with physical multi- system
dysfunction; a fact that is frighteningly downplayed and denied by the
psychiatric lobby.

What is omitted from this article is a warning of the very real dangers of
imposing CBT and GET on very frail, vulnerable, ill people for whom exercise
is contra-indicated and who suffer such devastating levels of cognitive
dysfunction, as a result of their disease, that CBT becomes equally as
dangerous as physical exercise. Mental exertion can have an equally
disastrous impact upon the body , leading to an increase in already severe
symptoms and a deterioration that can be permanent and may lead to death.

Patients with severe ME do not want CBT and GET. What they want is
biomedical research, significant biomedical testing and new tests and
treatments available on the NHS. What they need is the psychiatric
interpretation and powerful influence out of ME altogether. It is long
overdue.

Competing interests: None declared

====================================

I adore CBT 18 February 2010

A.F. Andrew,
Family physician
Perth, Australia



In the wake of Lynn Gilderdale's death, one would have expected an
editorial in the BMJ to acknowledge the devastating effects of severe ME,
and try to lead the way forward to find proper treatment and hopefully a
cure.

One would have expected that such an editorial would mention the fact that
ME has been classified by the WHO as a neurological illness since 1969. A
fact that most doctors, including myself before I fell ill, are not aware
of.

Most doctors are led to believe, by a small group of psychiatrists, that
this illness, either doesn't exist, or is based on false illness believes,
and is all in the mind. That the psychiatrist changed the name 20 years ago
from ME in CFS, and then changed the criteria, is just a small detail.

The basis of CBT for ME/CFS is fantastic. First, you blame the patient for his illness, and then when CBT doesn't cure him, you blame him for not being motivated. When I'm fit and well again, I will use this same principle when I see a patient with for example, a severe infection. If the antibiotic I have prescribed, doesn't solve the problem, then I will blame the patient. That the culture has shown that I prescribed the wrong treatment, is something I will ignore.

According to the three psychiatrists, CBT and GET are super treatments for
ME. Lynn at one stage, couldn't swallow anymore, to brighten up her life
even more. Her doctor then had the choice to treat swallowing problems, with
the so fancied behavioural therapy, i.e. CBT, or with exercise therapy, also
called GET, the other psychiatric favourite. Luckily, Lynn's treating doctor
inserted a tube, so she could be tube fed. Although I agree with the
psychiatrists that CBT is best.

You might still think that ME doesn't exist, or, that it is all in the mind,
and continue to be incredibly hostile to your ME patients. However, you
might be next and become an ME patient as well, just like myself and many
others. And I can assure you, you will be in for a big shock, and at the
same time, you will also find that this illness has got nothing to with what
you have been reading in your magazines, written by CBT psychiatrists. So
hip hip hooray for CBT, because who needs proper treatment for a severe and
very disabling illness anyway?

Competing interests: I am a doctor with ME who simply adores CBT

================================

"It's wrong and misguided to "Imagine""
18 February 2010

Barbara J Robinson,
carer/teacher
Suffolk County Council,
Frances Groen



Dr. Broome, you stated; "I imagine risk to life would be consequent upon
profound immobility and factors such as bed sores, chest infection and
malnourishment, all of which are avoidable."

I'm afraid you imagined wrongly. Where is your clinical evidence for this
statement?

You then state, "There are successful treatments available and several
specialist units in the country for those with severe forms of the illness."
Please tell me how many specialist ME/CFS inpatient beds exist in the UK and
where you managed to ascertain this information?

There are approximately 60, 000 severely affected patients, in my experience
(since 1997), most of who receive little or no support from statutory
services. Most severely affected, housebound patients, are nursed and cared
for by their families.

In my experience, those that approach services such as Social Care, or other
"specialist services" (such as yours) which are sometimes requested by
desperate patients with secondary needs, are, more often than not, refused
even an assessment. Reasons given, Not meeting "the criteria"for assessment
is the norm, or following assessment, being being turned down for support
due to ME patients "not meeting the criteria."- even though these patients
have "critical and substantial" needs, including secondary well being
needs." I know from personal experience.

Many areas have scant, domiciliary ME/CFS services for the housebound. Many
clinics will not serve the severely affected at all, excluding them from
their remit, only coping with "the walking wounded", such as one prominent,
"specialist" unit in London.

What I say may defy believe, but that is the reality of the situation in
2010. I suspect the services currently offered, primarily NICE recommended
CBT, GET etc, have been carefully tailored to the meagre, limited budgets
available from the Department of Health, Strategic Health Authorities and
further "pruned" by local "World Class Commissioning"- a contradiction in
terms if ever there was one.

Typically, this pans out to approximately £700 for a referral, diagnosis,
and basic, time limited advice for management before being passed back to
GPs who mostly admit that they don't have a clue and are not trained or
competent to cope.

No wonder patients fall to the risk of despair and worse; through the total
abandonment of the state currently, and the manifest failure of duty of care
generally. As for access to specialist inpatient care, this rarely gets past
the PCT's Special and Exceptional Funding Committees.

Competing interests: None declared

==============================

High time to broaden the field
19 February 2010

Jackie A Stableforth,
UK diagnosed ME/CFS patient, Former RGN (Staff) Coronary Care, Middlesex
Hospital, W1
n/a



The authors, Santhouse et al state that Lynn Gilderdale's symptoms were so
severe that "clinicians should consider alternative diagnoses that would
better explain the symptoms". It is difficult to know how they would have
done this, as any but the most basic tests and treatments are absolutely
proscribed under current NICE guidelines for CFS/ME, especially after one
has been unfortunate enough to receive such a diagnosis.

In my view, the current system is a recipe for patient - doctor mistrust. If
standard tests come back negative then, as the authors correctly indicate,
when the patient is so ill (many patients initially are too ill even to get
to a surgery on their own, not just 'severe' cases), further testing is
common sense.

However, what currently happens is the patient is advised to undergo 'GET'
(when post exertional malaise was a presenting symptom), or leaves with a
prescription for antidepressants and enrolment on a CBT course fundamentally
designed to manage unhelpful 'illness beliefs'. But without fundamental
robust and appropriate medical treatments for their condition, how can there
be trust? Of course patients despair by this stage.
They have already been
prostrate with illness and exhaustion for months, every aspect of their life
is in tatters (health,finance employment, family relationships, self
sufficiency), the doctor has ignored or overridden basic presenting symptoms as being of any consequence (however well intentioned) and now they have
been effectively discredited. And underneath it all, no one really has any
idea what is essentially wrong and the patient is left effectively back
where they started only now in isolation, wondering where it all went wrong.


The lack of a basic diagnostic test and biomedical treatment is what is most
likely to be hampering physicians (and insurers), not defeatism as such.
This can only be gained by serious investigation into underlying aetiology -
not by application of general 'management tools'. Patients across the entire
spectrum of CFS/ME have many disabling physical abnormalities other than
simple 'fatigue' (which in itself fails to describe the experience). If we
continue to focus simply on 'fatigue' and to limit physicians to basic
tests, then as some biomedical researchers have pointed out, ME/CFS can only
effectively become a 'dustbin diagnosis'.

By way of example, an equally damaging illness Haemochromatosis also can
present with extreme fatigue, headaches, pain and other symptoms common to
CFS and has been mistaken for 'CFS', (according to one GP who diagnosed a
friend of mine). 'Fatigue' can be seriously misconstrued when only the usual
tests are applied - the Serum Ferritin testing he required is also not
standard - and patients are misdiagnosed. However, at least there is a test
for haemochromatosis and once identified, referral to a hospital consultant
and full biomedical treatment in specialist centre. Imagine if his GP had
stopped looking? One shudders to imagine the further damage to his organs
had only CBT and GET been recommended. If only CFS patients could be so
lucky.

Having worked previously as an NHS Staff Nurse (Coronary Care) and coming
from a medical family I truly believed that UK medicine in the NHS was
cutting edge. However once diagnosed with CFS/PVF/ME, I was shocked to find
that a highly trained group of professionals whose intelligence I had always
respected had no answers, but most damagingly, weren't prepared to look much
further for them (and was in one case breathtakingly dismissive). The
'pioneering spirit of the scientists of old' appears to have become bogged
down in 'legal guidelines' and even individual well intentioned doctors are
contrained by budgets, accepted treatments for accepted ICD codes, insurance
purposes and so forth. CFS patients find that in spite of their insistence
that something more serious and physical is afoot, in practical reality
there is so little help to get to the bottom of it. And once this happens,
the patient effectively becomes sidelined from the whole medical process.

What may not readily have been accepted by authors such as Santhouse and
colleagues, is that this is in some respects a new condition/s and set of
circumstances that transcends our previous knowledge base. It does not fit
into the old box, the old belief systems and we don't yet have all, if in
fact any, of the answers. ME/CFS now requires new and adventurous lines of
enquiry - but we are hardly likely to find them if we are clinging onto the
old unproven theories and not looking. For doctors and scientists this could
be an exciting moment of opportunity and outstanding discovery, and an
opportunity to listen to patients, to work with them and their experience of
the illness in the investigative process - not theorise wildly in spite of
them.

When I read articles singing the praises of CBT and GET as if they could
make any real difference in these conditions, I realise that it is not the
patients that are beset with 'mistaken illness beliefs'. However the authors
are right in one regard. There really is "A perception that this is an area
of medicine where contrary views are not to be voiced, and where scientific
enquiry is to be limited, [that] is damaging to science and harmful to
patients."

As a patient therefore, I would now like to finally add my voice. Patients
have been very patient with the tired CBT/GET mantra and have long been
swept along with the current state of affairs to the detriment of their own
health and in the case of Lynn Gilderdale and many like her, their lives. Is
it not time to admit it is not working as hoped? Is it not time to come up
with something more robust, or to leave the field?

If as a doctor you are 'reluctant to get involved', as the authors suggest
some are, we are equally reluctant to have you. ME/CFS patients do not need
fainthearted doctors.
Patients with this destructive illness have had to
withstand decades of social isolation, marginalisation and medical
mismanagement (however inadvertent or well intended), in addition to the
burden of being seriously ill. Any doctor who is unable to stand their
ground side by side with them in the midst of chaos and uncertainty is
unlikely to be suited to the rigourous demands and contradictions of this
budding field of medicine.

It is time to broaden the field, with fresh minds and fresh ideas and to
branch out into something new.

Competing interests: None declared

===================

CBT The Mythology
19 February 2010

Gerwyn j Morris,
Psychologist
SA16 OAZ,
Stephanie Fulton



I refer to the article "Air of defeatism exists within the medical
profession that chronic fatigue syndrome can be treated" This article
trivialises the severity of the illness and contains a number of factual
inaccuracies.

NICE is selectively quoted.Nice actually point out that CFS/ME is a very
serious real illness of yet unknown origin and can be more disabling as
multiple sclerosis or late stage aids---There is no known cure or effective
treatment.

This should have been quoted.

NICE specifically make the point that CBT is not a treatment for the
symptoms but an aid to help patients come to terms with their illness. Is
this what is meant by" working"?

CBT has never shown any objective benefit

Some studies, using self reporting, have shown a subjective benefit on
fatigue i.e as assessed by the patient, but no effect at all on activity
levels when measured scientifically.


The confidence intervals in these studies are so wide as to make
extrapolation into a general ME/CFS population impossible.The studies are
clearly underpowered.

Many sufferers take their lives because living with the symptoms is
unbearable These symptoms cannot be treated

There is no robust scientific evidence to support GET although there was a
recent heart attack!

Would any pharmaceutical product obtain a product licence based on patient
self evaluation----or with the confidence interval values associated with
CBT studies.The answer is a resounding No!

Why therefore are sufferers of ME/CFS classified by the WHO as a
neurological disorder only offered CBT

Why were NICE instructed to ignore all the biomedical evidence when
draughting their guidelines

Yours Sincerely,

G J Morris BSc(Psych) LLB(Lond) Dip Law

Competing interests: None declared

====================================

Re: I adore CBT
19 February 2010

Dr John H Greensmith,
Founder, ME Free For All.org
BS16 5SW



I fear that some advocates and practitioners of the CBT/GET monopoly
treatment recommended for M.E. (Myalgic Encephalomyeltitis) sufferers, by
the NICE (National Institute for Health and clinical Excellence) Guidelines
of 2007, may have missed a certain subtle irony in A.F. Andrew, the Dr From
Oz's, "I adore CBT" declaration of interest (Letters, BMJ.com, 18 February
2010, http://www.bmj.com/cgi/eletters/340/feb11_1/c738#231561) and taken it
as an endorsement to continue and expand the sevice, for which they need
little encouragement.

May I, therefore, draw attention to the latest review study (Twisk and Maes,
September 2009) of the treatments Cognitive Behaviour Therapy (CBT) and
Graded Exercise treatment (GET) for people suffering with M.E., which
confirms the findings of every previous study - including those of the same
people advocating and practising these treatments - that CBT/GET is not only
ineffective but potentially harmful for many patients with M.E.?

So, I say hip, hip replacement for CBT and GET as treatments for M.E.
sufferers.

Yours sincerely
Dr John H Greensmith
ME Free For All.org

Competing interests: None declared

=======================

Shedding a little more light on 'Defeatism'
19 February 2010

Doris M Jones,
Researcher and carer of person with ME
Ilford, IG2 6DZ



The above Editorial (1) contains statements which require further comment;
they may also support assertions made in earlier responses on the complex
condition usually referred to as 'CFS/ME' these days.

Recent media coverage of the tragic death of Lynn Gilderdale and her
mother's acquittal for attempted murder of her daughter was widely welcomed
by the ME community and those who support sufferers. The reason is simple:
For the first time the potential full magnitude of suffering by those
severely affected was aired in public.

Controversies and uncertainties over a diagnosis of Chronic Fatigue Syndrome
(CFS) exist largely because this artificial construct was created and is
much favoured by certain psychiatrists - fatigue being the declared cardinal
symptom. This stands in sharp contrast to Myalgic Encephalomyelitis (ME),
which has been classified as a neurolgical disease by the World Health
Organisation for over 40 years (currently under G93.3 in ICD-10, as
regrettably is CFS). The manifold neurological, immune and endocrinological
manifestations and complications of ME are well documented (2,3), linked
particularly to enteroviral infections, as have cases of death due to
cardiac failure, rare tumours, severe neurological complications or basic
end-organ failure, apart from suicides. Some recent studies confirming such
findings have been mentioned in earlier responses.

These facts and others relevant to ME were brought to the attention of the
then Chief Medical Officer, Sir Kenneth Calman, at a meeting arranged by the
Countess of Mar in March 1998 and supported by a document entitled 'The
Organic Basis of ME/CFS' (4) that included a special section on Severity,
Chronicity and Deaths. A copy of the Hyde et al encyclopaedic volume (2) was
also left with Sir Kenneth and DoH staff on that occasion. The establishment
of the CMO's Working Group on CFS/ME was announced in July that year. This
same information and much more was made available to all Key Group members
of the CMO's Working Group on CFS/ME during its deliberations. Furthermore,
results of 4 surveys on over 3000 patients in total were supplied to that
group, which included psychiatrists who ardently advocated the benefits of
Cognitive Behavioural Therapy (CBT) and Graded Exercise Therapy (GET).
Survey results showed clearly however that these two approaches were the
least effective (CBT) and potentially most harmful (GET) to patients. These
same survey results were also repeatedly presented to members of the
Guideline Development Group who compiled the NICE Guideline on CFS/ME during
its deliberations, but who took scare notice of them. To treat depression
where it exists with common antidepressant drugs has been shown to result in
potentially severe adverse reactions, without bringing about any real
improvement in the underlying physiological problems these patients have.

Had decision makers given more credence to patient surveys and reports and
considered some of the documented readily available evidence of the
organic/physical basis of the disease, the current reported defeatism within
the medical profession and the desperate plight of patients might not have
arisen.

With regard to the specific case of Lynn Gilderdale, it should be born in
mind that here a vaccination as well as infections were linked to the onset
of her illness which resulted in progressive serious health problems. Her
condition was so severe that she was hospitalised 50 times during her 17
years' suffering, as the Panorama programme revealed. - The proximity of
immunisations with onset of ME or an exacerbation of the condition have been
documented (5,6). An earlier longitudinal study from the general medical
literature recorded the fact that most hospital patients with post-vaccinal
neuropathies had a concomitant illness (7).

To discount factors like infections, immunisations, antibiotics, oral
contraceptives for women and drugs in general, and/or exposure to toxic
substances (e.g. OP pesticides, toxic metals etc) in the aetiology of this
disease is tantamount to ignoring key factors in a complex equation, in my
opinion (see also response from Dr Ellen Grant). Of course life-style
factors like nutrition and stress also play a role. As Dr Melvin Ramsay said
in his booklet 'Myalgic Encephalomyelitis and Postviral Fatigue States - The
saga of the Royal Free disease' (8), reflecting on his experiences as the
Consultant Physician at that Hospital during the 1955 outbreak: "I had long
harboured a suspicion that the triggering factor of ME is to be found in the
immunological state of the patient and research is showing that this might
be the case" (p26). Dr Shepherd said in his contribution to a recent Times
article (9), what is needed amongst others is research into the role of the
immune response to infections. It stands to reason that an impaired or
dysregulated immune system cannot deal effectively with infections, and we
are all exposed to countless toxic substances in the environment and in
everyday life.

So can ME patients get better and what helps? In 2001 I carried out a
long-term follow-up study on patients who had earlier completed detailed
questionnaires (10). This was a contribution to the CMO's Working Group on
CFS/ME. 22/174 patients (12.6%) reported that they had either regained
normal health or had almost fully recovered. Most had adopted a combination
of approaches, consisting of pacing their activities, adjusting their diets
and taking various supplements; some had also availed themselves of
Homoeopathy or Acupuncture. Two had regained their health mainly by
allopathic therapies: one by taking Thyroxin for a non- functional thyroid
gland, the other by having long-term antibiotic treatment. In my view
therefore another research area that should be explored with urgency is what
has actually helped patients regain normal or near normal health, other than
CBT and GET, which have had more than their share of funding often
accompanied by misleading publicity.

References:

1. Editorial on: Santhouse A et al. Chronic Fatigue Syndrome - Defeatism is
undermining evidence that CFS can be treated. BMJ 2010;340:738 (11.2.2010)

2. Hyde BM et al (Editors). The Clinical and Scientific Basis of ME/CFS. The
Nightingale Research Foundation, Ottawa, Canada, 1992.

3. Richardson J. Enteroviral and Toxin Mediated Myalgic
Encephalomyelitis/Chronic Fatigue Syndrome and Other Organ Pathologies. The
Haward Medical Press, NY, 2001.

4. Dowsett EG et al. The Organic Basis of ME/CFS. Presentation to Sir
Kenneth Calman, CMO, DoH staff and the Countess of Mar, Richmond House,
London, March 1998.

5. Hyde BM et al (Editors). The Clinical and Scientific Basis of ME/CFS. The
Nightingale Research Foundation, Ottawa, Canada, 1992. Chapters 4 (p29); 12
(p115), 43 (p392), 73 generally.

6. Leeming J. Risks and Benefits. Nursing Standard, 17.5.1995,
Vol.9;34:22-23.

7. Pollock TM et al. Seven Year Survey of disorders attributed to
vaccination in North West Thames Region. Lancet 1983;i:753-57.

8. Ramsay AM. Myalgic Encephalomyelitis and Postviral Fatigue States - The
saga of Royal Free disease. Gower Medical Publishing, London, 1988 (p26).

9. 'Doctors, school, friends thought I was faking it'. Times 2 (Health),
25.1.2010, p6+7.

10. Jones DM. Follow-up Survey of ME/CFS/MCS patients. Contribution to the
CMO's Working Group on CFS/ME. April 2001.

Competing interests: None declared






Thursday, February 18, 2010

The Truth About Penguins (and CFS research)

The Truth About Penguins
By Peter Kemp

I wanted to study the nature of penguins.

The 'Canadian' definition of penguins is that they are:
• Flightless
• They can swim
• Largest species up to 1.2 metres tall
• They eat mostly fish
• They lay 1 or 2 eggs
• They generally live in colonies

The 'CDC' definition of these birds is that they are:
• Flightless
• They sometimes eat fish
• They lay eggs
• They can swim

The 'Oxford' definition is that these birds are:
• Flightless
• They lay eggs

The 'Oxford' criteria was chosen for the research as the others were too difficult to apply. 100 subjects who met the research criteria were studied in Sub-Saharan Africa.

The research found that penguins:
• Live in deserts
• Cannot swim
• Are up to 2.4 metres tall
• Weigh 200 pounds
• Capable of speeds up to 40 mph on land
• Are mostly vegetarian

Conclusion:

The research has discovered the truth about penguins. Those funny black and white birds waddling on the ice and swimming in the sea are making fools of everyone. They are not real penguins and should be excluded from all further research into penguins.
  





Auction for Research Funding

I have the pleasure of informing you that the time has come to begin

The Worldwide Association for ME/CFS Awareness and Research - WAMCARE's
auction of celebrity signed photos and memorabilia.

All items will be auctioned on EBAY a few at a time, and posted with good
quality packaging from the UK to wherever you live, postage rates will
depend on where you are located, and the nature of the item.

*All profits will go straight to top quality research into ME/CFS including
the WPI and MERUK.*

At the moment, our website is full and yet we still have many more quality
items to auction. Therefore stay tuned for updates which will be added over
the next few weeks, including a cast *poster of popular Australian soap
Home and Away signed by most of the cast*, kindly arranged for us by
actress Esther Anderson who has been very supportive to the cause.

Items we have at the moment can be found on the auction page of our
website, here: http://www.wamcare.org/auction.html

you can also find out more about ME/CFS here and why research is essential.

You can follow our blog for auction updates http://wamcare.blogspot.com/

Items include:

·         DVDs for part 1 and part 2 of Merlin Season One signed by the 4
main cast members. Plus cast photos of the 4 main cast members.

·         A top worn by Vicky Entwhistle in Coronation Street.

·         A CD album signed by Katie Melua and 2 by Canadian country singer
Aaron Pritchett (the latter yet to be added to the website.)

·         Photos signed by bands and singers, tv presenters, actors,
celebrity chefs and sports stars amongst others. Including: Jude Law, Helen
Mirren, Matt Lucas and David Walliams from Little Britain, Sir Ian
McKellan, Susan Sarandon, Keira Knightley, Stephen Fry, Daniel Craig, Sara
Ramirez,
Dame Judi Dench, David Tennant and many more on our website, and others yet
to be included.

·         Cast signed and non-signed cast fan cards from cast members of
the soaps EastEnders and Neighbours.

·         Poster signed by Home and Away cast, yet to be added to our
website.

Most items are hand signed, although there are a few autopens and
pre-prints, which are indicated as such. Quality of photos varies from HQ
pictures, to computer prints of various qualities. Quality of all items
will be indicated on EBAY as well as on our website, included any damage
which has occurred during transport from the celebrity to us. Photos are
provided on our website, and higher quality photos will be used on EBAY.
Letters from the agents have been included on the website if they were
present.

We at WAMCARE wish to express our gratitude to all the celebrities and
their agencies that have contributed to this charity fundraising auction.
We have received personal, encouraging letters of support from many
wonderful people, which will soon be available for viewing in the
supporters section of our website. We are moved and grateful that these
busy celebs and their agents took the time to write to us and send us such
terrific items.  We would like to thank them on behalf of the millions of
people affected by ME/CFS worldwide for helping make possible WAMCARE's
continuing mission to improve the lives of everyone affected by this
devastating illness.

Thank you for all your support! Please spread the word about our auction,
so that we can raise as much money as possible for ME/CFS research!

Laura Dunks - President and fundraising

Michelle Martin - Vice President, merchandise, website and newsletter
editor.




Wednesday, February 17, 2010

Shootout over XMRV Research

 
 

'Shootout' over Contradictory XMRV Research Continues

Re: The controversy over the UK-based research study claiming to find no XMRV in patient samples… which may yet escalate, with a second contradictory UK study, by Kerr, et al., published Feb 15. (Representative comments.)

Simon Wessely and company often use a different set of criteria to select the patients for their "CFS" studies (such as the Oxford Criteria). These selection criteria are set up so as to include lots of people that are just depressed, and do not have CFS at all. As a consequence, it is not surprising many studies, based on the Oxford Criteria or similar, find that patients do not have XMRV, or can be cured by antidepressants: they studied the wrong people. In other words, when Simon Wessely says "CFS", he actually is talking about "depression". … The original XMRV research at the Whittemore Peterson Institute used the Canadian Consensus definition of CFS/ME. The advantage of these inclusion criteria is that they actually do select CFS patients. - H

• …The UK team's results speak for themselves. No DNA found during PCR testing, yet people are doubting their testing methods! If it was there, they would have found it. People with CFS/ME are delusional in their belief that it's a viral problem. Only those whose illness is clearly brought on by viral infection can consider this to be the cause. It's a bit like the Emperor's New Clothes this whole XMRV thing. Why are people with ME/CFS so defensive about accepting that the illness is neurological? People seem so frightened by the thought that they may have a biochemical imbalance in their CNS or their brain. It's a disease of the CNS or the brain, accept it, and stop pushing the viral envelope so we can get some real research done…. - R

Why are people SO vehemently opposed to evidence that CFS is more than psychological? Who ARE these people and why do they feel so strongly? Why do they even care if they're not sick? Just wondering why people like us who have an illness are being subjected to out-right attempts at oppression. Why favor the UK findings, a poorly-designed study that as I understand it was shipped off for publication quickly without review, to a study that was confirmed by such influential organizations as the National Cancer Institute and the Cleveland Clinic? What exactly is going on here? - G

Lest you think I am just another defensive patient, I have done plenty of PCRs and know how it works. .. Based on my own knowledge I am not at all convinced by the UK study. - S

If you look at the sensory, adrenergic and immune mRNA responses to intense exercise as in the study by Alan Light, this strongly suggests something interfering at the genetic level. In a large multidimensional study organised by the CDC and published in the Journal Of Pharmacogenetics "suggest strongly that many causes of CFS have links to a handful of brain and immune system - related genes that either harbor small mutations or are working abnormally for some reason" This is classic retroviral interference rather than a group of people wired to handle stress abnormally. I am quite certain that a virus/s is the root cause of many cases of what is diagnosed as CFS and the WPI study is a THOROUGH and welcome start in this field. Hopefully to be replicated, positively or negatively but with the appropriate methodology. This illness is far too serious for the world to be treated lightly or politically as many of us believe the British study was. - I

I have no doubts that this is a virus, producing these symptoms. My great uncle, who looked a lot like me, had this condition starting in his mid thirties and was misunderstood from that point on, until I was diagnosed. Imagine, no one thinking you're really sick, until you are a very old man… just being called lazy. His grandaughter, got it, as well… This very real physical disease without a cure has psychological barriers to every aspect of life…  No matter what the cause of our illness, I hope we can all carve out a life for ourselves while we are waiting. I am very grateful for Dr Mikovits work. I think they are on the right track. It gives me hope; but life goes on. - C

The second article seems more worrisome and distressing to me because of Dr. Kerr's involvement. WPI needs to find out what's happening and partake in testing the blood in tandem with these studies to ascertain if it's methodological/procedural - before we lose steam and hope. - E

 

  





Disability Application Issues: How to Be Your Own Expert Medical Witness

 

Dr. Podell gives some good suggestions, but I've done most of them and still cannot get disability because the judge refuses to accept as true any testimony that I'm really sick.  He will not even acknowledge the abnormal blood test results, because they, too, contradict his opinion that I'm simply faking.
 
As far as the fact that it can take a day or two for the results of exertion to become apparent, before one of my SSDI hearings my lawyer suggested that instead of resting up to ensure I could make it through the hearing, I should spend the day or two before the hearing doing things -- show the judge what I'm like after "working" for a couple of days.  She literally wanted me running on fumes at the time of the hearing, and drove me there herself (if you feel you'll be too exhausted to get yourself home safely after the hearing, ask your lawyer to do that!)





 

Monday, February 15, 2010

XMRV Discussion on Faculty of 1000

In a recent blog posting discussing the pros and cons of the two
currently published studies on XMRV and CFS, which itself is one of
the better reviews I've read, the author refers to a post in a
discussion on Faculty of 1000, which appears to be a kind of forum for
professionals to comment on research papers. There are several
comments made, including one dissenting opinion and an author's
response by Dr. Mikovits. There's not really any back and forth
discussion that I've seen; it's mainly straight commenting. The
comments made thus far are copied and pasted below.

Blog post- http://laikaspoetnik.wordpress.com/2010/02/15/finally-a-viral-cause-of-chronic-fatigue-syndrome-or-not-how-results-can-vary-and-depend-on-multiple-factors/

Link to Faculty of 1000 Biology comments on 'Detection of an
infectious retrovirus, XMRV, in blood cells of patients with chronic
fatigue syndrome'- http://f1000biology.com/article/id/1166366
Link to Faculty of 1000 Medicine comments on 'Detection of an
infectious retrovirus, XMRV, in blood cells of patients with chronic
fatigue syndrome'- http://f1000medicine.com/article/id/1165576

Faculty of 1000 Biology comments on 'Detection of an infectious
retrovirus, XMRV, in blood cells of patients with chronic fatigue
syndrome'-

Ulf Pettersson
Uppsala University, Sweden
Genomics & Genetics

Chronic Fatigue Syndrome (CFS) is an enigmatic disease with an unknown
pathogenicity. In this paper, the authors have tested the hypothesis
that a human gamma retrovirus (XMRV) is a causative agent. The authors
analysed blood from 101 CFS patients and 218 controls. A dramatic
difference was found as 67% of the patients were positive for XMRV
whereas only 3.7% of the healthy controls were positive for the same
virus.

Moreover, the virus was infectious when tested in tissue culture. The
authors conclude with caution that XMRV could be a contributing factor
in the pathogenesis of CFS.
The reported results are undoubtedly
convincing. They should, however, be interpreted with caution as CFS
patients might have a malfunctioning immune system and the virus might
then be an innocent passenger. An interesting implication of the
finding is that XMRV has been suspected to be involved in prostate
cancer and it will be interesting to determine what connection there
could be between CFS and prostate cancer.

Competing interests: None declared
Evaluated 13 Nov 2009
-------------------------

Alan Landay
Rush University Medical Center, United States of America
Pharmacology & Drug Discovery

Lombardi and colleagues have isolated DNA from xenotropic murine
leukemia virus-related virus (XMRV) from the cells of patients with
chronic fatigue syndrome (CFS) and have found antibodies to this
retrovirus in their plasma.

CFS is a disease that has been studied for many years by the medical
community which is diagnosed most often by exclusion. It clearly
affects the immune system, with a response characterized by chronic
immune activation and a reduction in natural killer cell function. A
number of viruses (herpes and enterovirus) have been implicated as an
etiologic agent in CFS but none have been conclusively associated with
the disease. The authors of the current study demonstrate that a large
proportion of CFS patients are infected with XMRV (67%) and in vitro
both T and B cells can be infected with XMRV. The results of this
paper raise a number of interesting questions on the role of XMRV in
the pathogenesis of CFS and the diagnosis and treatment of CFS.

Competing interests: None declared
Evaluated 16 Nov 2009
------------------------

Brigitte Huber
Tufts University School of Medicine, United States of America
Immunology

This paper shows that a high frequency of chronic fatigue syndrome
(CFS) patients are infected with a xenotropic murine leukemia-like
virus (XMRV), compared to only a few normal controls. This is
particularly exciting because CFS is ill-defined and has been
approached with hesitation by scientists.

For the first time, we now have evidence that an infectious agent is
associated with this chronic disease. It remains to be shown whether
XMRV is directly responsible for the symptoms, or induces expression
of other cellular genes that lead to an inflammatory response.
Regardless, these new findings open the door for therapeutic
intervention of this dreaded disease.
This same virus has also been
associated with highly malignant prostate cancer {1}, but, again, the
significance of those results is not yet understood.

Competing interests: None declared
Evaluated 20 Oct 2009

Follow-up: IN RESPONSE TO DISSENTING OPINION: I agree with all the
points raised by Patrick Moore. Unless the published results can be
reproduced in an independent lab, we have to use caution with the
interpretation of the presented data.

Evaluated 18 Nov 2009
------------------------------

Adriano Boasso and
Gene Shearer
National Cancer Institute, National Institutes of Health, United
States of America
Immunology

During the past several years, a debate has raged concerning whether
Chronic Fatigue Syndrome (CFS) is a virally induced condition, or even
a medically relevant phenomenon. This publication is exceptional
because it uniquely identifies, in CFS patients, a human
gammaretrovirus that is a xenotropic murine leukemia virus-related
virus (XMRV), which was recently discovered in a subset of prostate
cancer patients.

In this report, the DNA from XMRV was detected in the blood of 68/101
(67%) CFS patients, but only in 8/218 (3.7%) healthy controls. The env
and gag viral sequences of all positive patients were >99% similar to
those from tumor tissue of XMRV-positive prostate cancer patients. The
possibility that the XMRV genomes were murine leukemia virus (MLV)
contaminants was excluded by the finding that the CFS XMRV sequences
clustered with those from prostate cancer patient XMRV rather than
those from MLV. XMRV proteins were produced by activated T and B
lymphocytes from CFS patients, confirming that both of these cell
subsets were productively infected. Transmission of cell-associated
XMRV was observed in co-culture with activated T cells from CFS and
prostate cancer patients or T cell lines. Cell-free XMRV transmission
(from patients' activated T cell cultures) was demonstrated in primary
T cells from healthy controls. Finally, the plasma of 9/18 patients
compared to the plasma of 0/9 controls contained XMRV antibodies that
exhibited blocking activity, demonstrating that patients can elicit a
virus-specific immune response. The authors carefully emphasize that
their findings indicate an association between XMRV and CFS, and not
necessarily a cause-and-effect relationship.
Furthermore, this
discovery and the virologic and immunologic parameters analyzed here,
as well as the connection with prostate cancer, provide many
intriguing areas for future research. These include the molecular
retrovirology of XMRV and its susceptibility to antiretrovirals, the
mode(s) of XMRV transmission, the genetic susceptibility of
individuals to the virus, how infection by this virus can be
diagnosed, how XMRV is associated with cancer, the immunological
processes involved in XMRV infection, and the development of potential
vaccines.

Competing interests: None declared
Evaluated 21 Oct 2009

Follow-up: Nevertheless, it is important to consider that criticisms
have been made which raise skepticism on the results presented in the
study (see dissenting evaluation). The detection of XMRV in CFS
patients should be confirmed by other groups that have expertise in
XMRV-related virology and CFS, as well as in other cohorts, before
full conclusions can be made on the scientific and medical
implications of these findings.

Evaluated 18 Nov 2009
----------------------

Katie Kelm and
George Breese
University of North Carolina at Chapel Hill, United States of America
Pharmacology & Drug Discovery

When one considers how little is known about chronic fatigue syndrome
(CFS), Lombardi and colleagues have made a major breakthrough in
understanding CFS with the discovery of a highly significant
association between CSF and the xenotropic murine leukemia
virus-related virus (XMRV).

CFS is a disease affecting roughly 17 million people worldwide and
involves multiple symptoms involving the nervous, endocrine and immune
systems {1}.
The cause of CFS is unknown, although there has been
evidence that viruses are environmental triggers. The authors found
that 67% of CSF patients are carriers of XMRV compared to 4% in a
healthy control population. The experimenters isolated the XMRV from
the patients and found that cell-associated and cell-free transmission
of the virus is possible. These results suggest that antivirals might
be effective treatment options for individuals suffering from CFS {2}.
Despite these advances, the cause of CFS is still unknown, as XMRV
could be acquired after CFS because CFS patients have weakened immune
systems.

References: {1} Pae et al. Expert Opin Pharmacother 2009, 10:1561-70
[PMID:19514866]. {2} Harmon K, "Retrovirus Linked to Chronic Fatigue
Syndrome, Could Aid in Diagnosis." Sci Am 2009, Oct 8 please click
here for article.

Competing interests: None declared
Evaluated 7 Dec 2009
-----------------------

David Wang
Washington University in St. Louis, United States of America
Microbiology

A recently identified retrovirus, xenotropic murine leukemia
virus-related virus (XMRV), has been detected more frequently in
patients with chronic fatigue syndrome than in healthy controls,
raising the possibility that there may be a disease association
. These
results underscore the fact that many diseases have poorly understood
etiologies and emphasize the need to identify and characterize
unrecognized pathogens.

XMRV was discovered initially in patients with prostate cancer {1}. In
this study, XMRV was detected in >60% of peripheral blood mononuclear
cells (PBMCs) of patients with chronic fatigue syndrome using a
polymerase chain reaction (PCR) assay. By contrast, <4% of controls
were PCR positive. A subset of the patient samples was analyzed for
the presence of XMRV antigen (by Western blot and
fluorescence-activated cell sorting [FACS]) and for infectious XMRV
virus (by co-culture experiments). These results support the notion
that XMRV is present in numerous patients with chronic fatigue
syndrome. Based on the PCR results of this study, there is a strong
association between XMRV and chronic fatigue syndrome.
It is clear
that larger scale case-control studies need to be performed (and there
will likely be many such studies appearing in the months to come) to
confirm these initial observations. Importantly, this study
illustrates that in this era of rapid identification of new microbes
in the human body, one must be mindful that a given microbe may have
pleiotropic effects (e.g. XMRV may be linked to both prostate cancer
and chronic fatigue or even additional disease states).

References: {1} Urisman et al. PLoS Pathog 2006, 2:25 [PMID:16609730].

Competing interests: None declared
Evaluated 18 Dec 2009
----------------------

Ken Wilson
Duke University, United States of America
Microbiology

Chronic fatigue syndrome (CFS) is prevalent, highly debilitating and
frustrating for both patient and physician. A cause for the syndrome
may have been found at long last. Although etiology cannot at this
point be considered proven, Lombardi et al. present strong
circumstantial evidence that a retrovirus is involved.

CFS is a chronically debilitating syndrome with a prevalence of about
1%. Several aspects of the disease have suggested an infectious
etiology and various infectious agents have been implicated in the
past but causality has never been convincing. Lombardi et al. have
found that XMRV, a retrovirus closely related to murine leukemia
virus, can be detected in 2/3 of patients with CFS versus 3.7% of the
general population. Viral proteins were expressed in patients but not
controls and the patients had an immune response to viral proteins.
Both activated T-cells and activated B-cells were infected, and
infected cells taken from patients were able to transmit infection to
uninfected tissue culture cells. Although further work is clearly
required to prove or disprove a causal link, this paper probably
represents the strongest case so far for a specific etiologic agent in
this disorder.

Competing interests: None declared
Evaluated 7 Jan 2010
-----------------

Charles Chiu
University of California, United States of America
Microbiology

This paper reports the detection of xenotropic murine leukemia
virus-related virus (XMRV) in blood from 67% of chronic fatigue
syndrome (CFS) patients but only 4% of controls in the United States,
a truly exceptional finding if confirmed
(some results have been
controversial). CFS is a devastating systemic, multi-symptom disease
that afflicts more than 17 million people worldwide without a defined
etiology to date.

Our group used a broad-spectrum viral microarray to detect XMRV in
patients with a specific kind of hereditary prostate cancer {1}.
Subsequently published data showed that XMRV was also detectable in
cases of sporadic prostate cancer {2}. This study is the first to look
for XMRV in peripheral blood mononuclear cells (PBMCs) of patients
with CFS using both nucleic acid (PCR) and antigen (Western blot,
FACS) methods. XMRV was detected in 67% of PBMCs from patients with
CFS but only in 4% of controls. This is a remarkable finding that now
associates XMRV with two widely different conditions: prostate cancer
and CFS, and whose data must be scrutinized carefully and confirmed
independently. In their Dissenting Opinion of this article, Moore and
Shuda raise valid concerns regarding the potential for PCR
contamination in this study. Some concerns include 1) the criteria for
defining CFS/ME in the patients and in controls were not explicitly
defined, 2) nested PCR was used and neither in a blinded nor
randomized fashion, 3) the remarkable lack of diversity in the six
fully sequenced XMRV genomes (<6 nucleotide average difference across
genome) -- with Fig. S1 even showing that for one fully sequenced
isolate two of the single nucleotide differences were "N's" -- clearly
the result of a sequencing error, 4) failure to use Southern blotting
to confirm PCR results, and 5) primary nested PCR screening done in
one lab as opposed to independent screening from start to finish in
two different laboratories. Concerns have also been brought up with
respect to the antigen testing. A subsequent publication in the UK has
refuted the results of this paper linking XMRV to cases of CFS {3},
but this can potentially be explained as representing geographical
differences in the condition, as XMRV was not seen in prostate cancer
in samples from European patients either {4}.

References: {1} Urisman et al. PLoS Pathog 2006, 2:e25
[PMID:16609730]. {2} Schlaberg et al. Proc Natl Acad Sci USA 2009,
106:16351-6 [PMID:19805305]. {3} Erlwin et al. PloS One, 5:e8519
[PMID:20066031]. {4} Hohn et al. Retrovirology 2009, 6:92
[PMID:19835577].

Competing interests: None declared
Evaluated 19 Jan 2010
-----------------------

Link to Dissenting Opinions & Author Responses on 'Detection of an
infectious retrovirus, XMRV, in blood cells of patients with chronic
fatigue syndrome'- http://f1000biology.com/article/id/1166366/dissent

Dissenting Opinions & Author Responses on 'Detection of an infectious
retrovirus, XMRV, in blood cells of patients with chronic fatigue
syndrome'-

Masahiro Shuda and
Patrick S Moore
University of Pittsburgh Cancer Institute, United States of America
Microbiology

The discovery of the cause of chronic fatigue syndrome would be an
extraordinary finding. Rather than providing extraordinary proof, this
manuscript has flaws that leave the reader unsure of knowing precisely
what was measured.

To detect the xenotropic murine leukemia-like virus (XMRV), the
authors used nested-PCR on non-randomized and non-blinded samples, a
recipe for uncontrolled PCR contamination. This technique re-amplifies
previously cycled products and is inherently prone to intermittent
false positivity that has occurred in our lab and many others (e.g.
{1} and {2} on which I am the author). This is a concern in light of
post-publication claims that XMRV detection rates among chronic
fatigue syndrome (CFS) patients have climbed from 67% to 95%, and XMRV
tests are now being sold and advertised on the internet at
http://www.redlabsusa.com . Southern blotting, which would allay this
suspicion, was not done. Other results in the study also lack support.
Flow cytometry and immunostaining with murine leukemia virus (MLV)
antibodies were used to directly detect viral proteins in patient
cells (see Figure 2A of the paper). The CFS peripheral blood cells
have robust monotonic staining rather than the bimodal peaks that are
expected from a mixture of infected and uninfected populations of
peripheral blood cells. It is not certain whether this level of
viremia for an exogenous retrovirus is medically possible. It may,
perhaps, be possible but it seems improbable and is a pattern more
consistent with a cross-reactive endogenous retroviral antigen. To
confirm this finding, CFS peripheral blood cells (without negative
controls in Figure 2B) were immunoblotted using cross-reactive spleen
focus-forming virus (SFFV) and MLV antibodies. XMRV gp70 and p30
proteins are found at higher levels in 2 out of 5 CFS peripheral blood
samples (1150 and 1221) than in the positive control -- HCD-57 cells
directly infected with SFFV -- a very remarkable result. Repetition
with negative control samples (see Figure 2C of the paper) has the
higher molecular weight bands cut from the photograph, thus we cannot
interpret potential positivity for p30 gag precursor proteins among
the control samples (see CFS samples 1199 and 1220 in Figure 2B).
Finally, the positive control HCD-57 cell lane in Figure 2C lane 8 has
a completely different banding pattern from the very same control in
Figure 2B lane 7 for the p30 gag protein. The elementary issue of
whether the authors are measuring XMRV has to be clarified. The
fundamental basis for the CFS case and control samples is also not
defined at an appropriate level. The samples (supplementary online
material) were "selected for this study from patients fulfilling the
1994 CDC Fukuda Criteria for Chronic Fatigue Syndrome (S1) and the
2003 Canadian Consensus Criteria for Chronic Fatigue Syndrome/myalgic
encephalomyelitis (CFS/ME) and presenting with severe disability".
These are two separate definitions, the latter published in the
"Journal of Chronic Fatigue Syndrome" (which is no longer in print).
It is unclear how the samples were selected from these two criteria.
No references or cut-offs are given for tests used to clinically
define the CFS patients as cases so we are unable to interpret the
essential basis for the study. In addition, no description is given to
indicate that controls were tested in the same manner as CFS patients;
in fact, there is no description for negative control samples at all.
For a disease whose diagnosis is controversial, a clear statement of
where and how the cases and controls were selected is a critical first
step.

Competing interests: None declared
Evaluated 18 Nov 2009

Author Response:

Judy Mikovits, Whittemore Peterson Institute, Reno, United States

This dissent first discusses "the cause of CFS". We did not imply that
XMRV caused CFS. We specifically state that our observation "raises
several important questions". Is XMRV infection a causal factor in the
pathogenesis of CFS or a passenger virus in the immunosuppressed CFS
patient?
The work presents a testable hypothesis that XMRV has a role
in CFS pathogenesis. The key task for the scientific community is to
define the scope of human disease associated with XMRV infection. We
were highly concerned and vigilant about taking precautions to avoid
PCR contamination. This was minimized using laboratory controls such
as dedicated first- and second-round PCR areas in different buildings
and consistent treatment of instruments and work areas with DNA ZAP
and UV rays. Although the original screen was performed using nested
PCR, PCR positivity on a subset of samples was confirmed using
single-round PCR in a different facility (Fig1A). Although not in the
manuscript, PCR status was verified on identical samples not processed
at WPI in a XMRV-free lab at NCI.
Moreover, in normal samples analyzed
in parallel, amplified sequences were found in only 3.7%, making it
unlikely that 67% positivity reflects "uncontrolled PCR
contamination". We should not have discussed unpublished data,
particularly considering the lay media. To discuss more details about
our more recent studies would repeat that error, but we were able to
culture XMRV virus from plasma and detect antibodies in some samples
which were PCR-negative (e.g. see #1118 in Fig1, 2A, 2D). These
examples compelled us to further study PCR-negative patient samples.
Flow cytometry data in the study were not meant to determine in vivo
levels of XMRV protein expression or the level of clinical viremia.
The goal was to determine if the XMRV DNA sequences detected
represented the presence of infectious viral particles. The studies of
XMRV protein expression in peripheral blood mononuclear cells (PBMC)
were performed after PBMC were activated in culture with
phytohemagglutinin and interleukin-2 for 7-14 days to allow the virus
to spread through the culture. It should have been made clearer.
Although at earlier times these samples did have bimodal peaks, data
shown were when most cells were virus positive. Not included in the
paper was the ability of azidothymidine to block XRMV spread in vitro.
The methodology for the immunoblots was also questioned. We used
monoclonal antibodies which recognized the envelope of all xenotropic
and polytropic but not ectopic murine leukemia viruses and reacted
with XMRV env proteins of expected sizes. Concerning the relatively
weak signal of the positive control, HCD-57/SFFV, test sample lanes
contained 150-200ug of protein, only 30ug was loaded in the HCD/SFFV
lane to prevent the positive control signal from overwhelming adjacent
lanes. This study was the initial finding of infectious XMRV virions
in human blood and a second association of XMRV and human disease. Our
observation of actively replicating virus, as well as antibodies
directed against XMRV (which were not criticized) in the patient
population examined, strengthened the paper and the hypothesis that
this recently discovered virus is a human pathogen. Clinically, CFS is
a heterogeneous syndrome with diagnosis made on the basis of the
exclusion of other diseases. Thus, the basis for diagnosis varies
greatly and we expect there to be XMRV-positive and -negative CFS
patients. Additional large-scale clinical studies using control groups
are essential to determine whether XMRV is the cause of CFS. Also,
rigorous independent validation is crucial. To facilitate this, the
NCI, Cleveland Clinic and WPI are making virus reagents available
through the NIH AIDS repository to any academic investigator by
contacting the investigators involved.

Response added 7 Jan 2010

**********************************************

Link to Faculty of 1000 Medicine comments on 'Detection of an
infectious retrovirus, XMRV, in blood cells of patients with chronic
fatigue syndrome'- http://f1000medicine.com/article/id/1165576

Faculty of 1000 Medicine comments on 'Detection of an infectious
retrovirus, XMRV, in blood cells of patients with chronic fatigue
syndrome'

Angélique van 't Wout and
Hanneke Schuitemaker
Academic Medical Centre, Amsterdam, Netherlands
Infectious Diseases

Xenotropic murine leukemia virus-related virus (XMRV), a novel
gammaretrovirus previously found in prostate tumor tissue, was found
significantly more often in the blood cells of chronic fatigue
syndrome (CFS) patients.

CFS is a disorder of unknown etiology that affects multiple organ
systems in the body, including chronic activation of the innate immune
system and a deficiency in natural killer (NK) cell activity. A number
of viruses, including ubiquitous herpesviruses and enteroviruses have
been implicated as possible environmental triggers of CFS. Previously,
XMRV was found in the tumor tissue of a subset of prostate cancer
patients. Since prostate cancer and CFS have both been linked to
alterations in the antiviral enzyme ribonuclease (RNase) L, the aim of
the authors was to test the association of XMRV with CFS
. The authors
indeed found XMRV sequences and protein expression in peripheral blood
mononuclear cell (PBMC) DNA from CFS patients. Moreover, they showed
the presence of infectious XMRV in PBMCs and plasma from CFS patients
as well as plasma XMRV antibody reactivity. The low frequency and/or
absence of each of these XMRV signals in control patients suggest an
association between XMRV and CFS. However, Koch's postulates remain to
be fulfilled and many questions remain -- e.g. is XMRV cause or
consequence? What is the pathogenic mechanism? Both epidemiological
and laboratory studies will need to confirm and expand on the observed
association between XMRV and CFS.

Competing interests: No potential interests relevant to this article
were reported.
Evaluated 28 Oct 2009

***********************

Link to Faculty of 1000 Biology comments on 'Host range and cellular
tropism of the human exogenous gammaretrovirus XMRV', Stieler K et al.
2010- http://f1000biology.com/article/id/1784956

Faculty of 1000 Biology comments on 'Host range and cellular tropism
of the human exogenous gammaretrovirus XMRV', Stieler K et al. 2010

David Alpers
Washington University School of Medicine, United States of America
Physiology

A viral cause for chronic fatigue syndrome (CFS), often co-morbid with
irritable bowel syndrome (IBS), has been suggested before. A pair of
recent reports has suggested that xenotropic murine leukemia
retrovirus (XMRV) is/is not associated with CFS, and the fascinating
study reviewed here examines the factors that permit and regulate
viral expression in mammalian cells.

XMRV was first associated with prostatic cancer samples in North
America, but the virus was rarely found in samples from Northern
Europe {1,2}. Lombardi et al. reported XMRV in nearly 70% of
peripheral blood cells from patients with CFS in North America {3},
but Erlwein et al. could not confirm this in a UK sample {4}. Stieler
et al. show that the murine lymphotropic virus (MLV) receptor, XPR1,
mediates XMRV uptake but that receptor number could not solely account
for variations in titer in cells. Moreover, some cells could be
infected but not produce complete secreted virus. Whether factors
affecting replication, integration, assembly or release can account
for the reported differences in prevalence in prostatic tumor tissue
in North America and Northern Europe is not yet clear. CFS is a
disabling syndrome, and, if it were shown to be due to an infectious
agent, could revolutionize the approach to many functional co-morbid
syndromes, including IBS. But the original reports that human T cell
lymphotropic virus (HTLV)-type II was associated with over 80% of CFS
cases were not confirmed, nor could other retroviruses be found
associated {4}. XMRV is an exogenous gammaretrovirus, and it is not
clear if the disagreement already reported for CFS is related to
difficulties in demonstrating retroviral presence or to some other
issues. Further studies are needed and based on these early reports
will follow rapidly in numbers large enough to provide the needed
data.

References: {1} Fischer et al. J Clin Virol 2008, 43:277-83
[PMID:18823818]. {2} Hohn et al. Retrovirology 2009, 6:92
[PMID:19835577]. {3} Lombardi et al. Science 2009, 326:585-9
[PMID:19815723]. {4} Erlwein et al. PLoS One 2010, 5:e8519
[PMID:20066031].

Competing interests: None declared
Evaluated 3 Feb 2010

Dangerous Exercise

Dangerous exercise: lessons learned from dysregulated inflammatory responses
to physical activity

Dan Michael Cooper, Shlomit Radom-Aizik, Christina Schwindt, and Frank
Zaldivar, Jr.

J Appl Physiol 103: 700-709, 2007.
First published May 10, 2007;
doi:10.1152/japplphysiol.00225.2007

Pediatric Exercise Research Center, Department of Pediatrics, University of
California, Irvine, California

Exercise elicits an immunological "danger" type of stress and inflammatory
response that, on occasion, becomes dysregulated and detrimental to health.
Examples include anaphylaxis, exercise-induced asthma, overuse syndromes,
and exacerbation of intercurrent illnesses. In dangerous exercise, the
normal balance between pro- and anti-inflammatory responses is upset. A
possible pathophysiological mechanism is characterized by the concept of
exercise modulation of previously activated leukocytes. In this model,
circulating leukocytes are rendered more responsive than normal to the
immune stimulus of exercise. For example, in the case of exercise
anaphylaxis, food-sensitized immune cells may be relatively innocuous until
they are redistributed during exercise from gut-associated circulatory
depots, like the spleen, into the central circulation. In the case of
asthma, the prior activation of leukocytes may be the result of genetic or
environmental factors. In the case of overuse syndromes, the normally
short-lived neutrophil may, because of acidosis and hypoxia, inhibit
apoptosis and play a role in prolongation of inflammation rather than
healing. Dangerous exercise demonstrates that the stress/inflammatory
response caused by physical activity is robust and sufficiently powerful,
perhaps, to alter subsequent responses. These longer term effects may occur
through as yet unexplored mechanisms of immune "tolerance" and/or by a
training-associated reduction in the innate immune response to brief
exercise. A better understanding of sometimes failed homeostatic
physiological systems can lead to new insights with significant implication
for clinical translation.

inflammation; innate immunity; leukocyte; asthma

----------------------------------------------------------------------------
----

Free full text at: http://jap.physiology.org/cgi/content/full/103/2/700  
And
http://jap.physiology.org/cgi/reprint/103/2/700  

-------
[Tom: Somebody summarised this to me with the following "take-home" points:
- exercise is a major stimulus of the immune system
- very little research done on exercise in chronic inflammatory states (p.
705) (which CFS likely has some components of)]
 




 

13 Rapid Responses including "Why do doctors refuse to believe patients?"

Subject: 13 Rapid Responses in reply to the BMJ editorial, "Chronic Fatigue
Syndrome" (replies posted 11-13th February, 2010)


http://www.bmj.com/cgi/eletters/340/feb11_1/c738

Rapid Responses to:

EDITORIALS:
Alastair M Santhouse, Matthew Hotopf, and Anthony S David
Chronic fatigue syndrome
BMJ 2010; 340: c738 [Full text]




Rapid Responses published:



Why do doctors refuse to believe patients?
Ellen Goudsmit   (11 February 2010)

Press ahead with funding bio-medical research into M.E./CFS
Sir Peter Spencer   (11 February 2010)

Welcomed common sense and clarity
Matthew R Broome   (11 February 2010)

Biomedical Research not Wastepaper basket diagnoses
jill cooper   (12 February 2010)

Do CBT and GET really work for Chronic Fatigue Syndrome?
Tom Kindlon   (12 February 2010)

Re: Why do doctors refuse to believe patients?
Ellen Goudsmit   (12 February 2010)

Defeatism and Chronic Fatigue
Alastair C Young   (12 February 2010)

More light needed
Neil H Riley   (12 February 2010)

Severely affected - severely neglected
Dr Charles B Shepherd   (13 February 2010)

CBT/GET is ineffective and potentially harmful. ME/CFS patients seem to die
considerably younger.
Frank N.M. Twisk   (13 February 2010)

There's none so blind as those who will not see
Louise E Ellis   (13 February 2010)

Using the correct tool for the right job
Kelly Latta   (13 February 2010)

No room for complacency
Derek FH Pheby   (13 February 2010)

--------------------------------------------------------------------------------

Why do doctors refuse to believe patients?

11 February 2010

Ellen Goudsmit,
Visiting Research Fellow, UEL
London TW11 9QX


As a patient with a progressive form of myalgic encephalomyelitis (ME), a
psychologist who trained in Clinical as well as Health Psychology and a
specialist in ME and chronic fatigue syndrome (CFS), I consider that I may
have a useful contribution to make in the debate about the needs of people
with fatigue syndromes and the treatments mentioned by Santhouse et al. I am
in the unhappy position of being familiar with both sides of the couch, as
it were. For the record, I differentiate between ME and CFS because the
assumption of equivalence has not been tested and I don't recognise myself
in many descriptions of CFS.

As Sandhouse et al suggested, people with ME and CFS need better access to
specialist clinics. As things stand, too many patients are left to cope on
their own and even the most sympathetic GP is limited in what he or she can
offer, courtesy of NICE.

What patients, groups and professionals like myself have been arguing for
years is that CBT and the other approaches noted by Sandhouse et al are
neither appropriate nor particularly helpful for everyone with fatigue
syndromes. However, the article illustrates that we're simply not believed.

As a psychologist, I recognise that CBT and GET can alleviate fatigue and
that many patients feel better, if only for a few months. However, I submit
that too many commentators have overlooked the methodological flaws in the
various trials and that they have overstated the results. For example, a
recent review supports an earlier meta-analysis that effect sizes tend to be
modest (1). Moreover, there are doubts about the value of the different
elements within the interventions, e.g. CBT may help simply because it
provides support and an opportunity to vent our frustration (2). Similarly,
research using objective measures have shown that improvements following CBT
can not be attributed to increases in activity (
3). So why continue to
include it and risk a relapse?

There are also other arguments that we need more flexible and individualized
programmes. For instance, there is no evidence as yet that CBT and/or GET
help those of us with neurological symptoms like muscle weakness, vertigo
and visual disturbances. As for the tendency for some of us to develop
multiple sensitivities to chemicals and foods, it's disabling and extremely
depressing but often psychologised, trivialised and ignored.

There is now enough evidence for therapeutic options which are as effective
as CBT and GET, but more acceptable (4,5). However, NICE misclassified them
under the wrong headings so didn't realise that there were alternatives and
those of us who alerted them to the problem were dismissed.

In terms of my own experience, I know that things can get worse. Some of my
friends are more disabled than me; they too have tried all the therapies
offered by their consultants, but these have not halted the progession of
their disease and some are now barely able to eat a normal diet. We're all
living on hope and it's hard.

Articles like those by Sandhouse et al reinforce the impression that editors
and researchers are keen to lump everyone with fatigue together because it's
neat and tidy. We're human, we dislike complexity and we prefer simple
solutions. CBT and GET seem to solve a lot of problems but they rely on the
asssumption that any differences within the CFS population are of no
clinical significance. They depend on the concept of CFS as an entity with
no ongoing pathology such as infection. They are perpetuated by discussions
which dismiss evidence to the contrary. And above all, they need decision
makers to question the knowledge and credibility of the patient. Even those
who are Fellows of the BPS (British Psychological Society).

What I don't see is an impartial, evidence-based approach. I see a textbook
example of group-think, where dissident voices are unwelcome
and relegated
to the letters page. I see an 'obsession' with CBT and GET. I understand it,
but the scientific process requires more objectivity and we will all be
better off if we accept that there's more to CFS than fatigue.

1. Godfrey E, Chalder T, Ridsdale L, Seed P, Ogden J. Investigating the
'active ingredients' of cognitive behaviour therapy and counselling for
patients with chronic fatigue in primary care: Developing a new process
measure to assess treatment fidelity and predict outcome. Br J Clin Psychol
2007;46:253-72.

2. Price JR, Mitchell E, Tidy E, Hunot V. Cognitive behaviour therapy for
chronic fatigue syndrome in adults. Cochrane Database of Systematic Reviews
2008; Issue 2. Art No.: CD001027. DOI: 10.1002/14651858.CD001027.pub2.

3. Wiborg JF, Knoop H, Stulemeijer, M, Prins JB, Bleijenberg, G. How does
cognitive behaviour therapy reduce fatigue in patients with chronic fatigue
syndrome? The role of physical activity. Psychol Med, 2010 Jan 5:1-7. [Epub
ahead of print]

4. Jason LA, Torres-Harding S, Friedberg F, Corradi K, Njoku MG, et al.
Non-pharmacologic interventions for CFS: A randomized trial. J Clin Psych
Med Settings 2007;14:275-96.

5. Goudsmit EM, Ho-Yen, DO, Dancey, CP. Learning to cope with chronic
illness. Efficacy of a multi-component treatment for people with chronic
fatigue syndrome. Patient Educ Counseling, 2009; 77:231-6.

Competing interests: None declared

==============

Press ahead with funding bio-medical research into M.E./CFS

11 February 2010

Sir Peter Spencer,
Chief Executive
Action for M.E., 3rd Florr Canningford House, Victoria Street, Bristol, BS1
6BY



The authors are correct when they say that doctors are often uncertain
about what they are dealing with when it comes to M.E., This is why we need
the highest priority to be given to scientific research
into M.E./CFS to
discover the fundamental biology of this devastating chronic condition. Is
it any wonder that those who suffer so badly and yet see so little research
feel such despair?

People deserve better, they deserve answers and ultimately either a cure or
failing that far better treatments than are currently available. The authors
say that severe presentations of M.E./CFS are unusual but there are up to
60,000 severely affected people in the UK. Many of these have fallen off the
radar and given up on the NHS because they feel it has little to offer.

We urge the Medical Research Council and the National Institute for Health
Research to press ahead with funding bio-medical research into M.E./CFS now
and urge all doctors to show more professional objectivity and sensitivity
to their M.E. patients in the meantime

Sir Peter Spencer
Chief Executive
Action for M.E.
www.afme.org.uk

Competing interests: None declared

============

Welcomed common sense and clarity

11 February 2010

Matthew R Broome,
Associate Clinical Professor of Psychiatry
University of Warwick



I was delighted to see the excellent editorial by Santhouse et al. As a
clinician, I felt a great deal of unease with the media coverage of the
Gilderdale case and the strange conflation of chronic fatugue syndrome with
a terminal illness and hence the link with the assisted dying/euthanasia
debate.

As Santhouse and colleagues point out, chronic fatigue syndrome is typically
not a terminal illness, with no excess mortality, and in addition to
suicide, I imagine risk to life would be consequent upon profound immobility
and factors such as bed sores, chest infection and malnourishment, all of
which are avoidable. There are successful treatments available and several
specialist units in the country for those with severe forms of the illness.
However, such treatment typically involves the involvement of a
psychiatrist, clinical psychologist and importantly, a physiotherapist and
occupational therapist. But therapeutic gains can certainly be made and the
pessimism towards the condition displayed by the media should be avoided by
health professionals, particularly as the risk is that such pessimism, as
this case demonstrates, may be transmitted to families.

Competing interests: None declared

===============

Biomedical Research not Wastepaper basket diagnoses

12 February 2010

jill cooper,
Non-militant ME campaigner who does not have ME
Teacher cv214hl



Patients and their families are 'fatigued' with the medical profession's
sloppy attitude towards diseases which the medical profession call
'syndromes'. Instead of admitting that these conditions are, as yet, not
understood, the medical profession have invented hypotheses about mind/body
manifestations which can only be treated by correction of thinking on the
part of the patient.

Cognitive Behavioural Therapy is promoted to 'help patients manage their
symptoms' and to cure 'abnormal illness beliefs'. Graded Exercise Therapy is
aimed at reversing 'de- conditioning'.

The best help a medic can give a patient is to respect that patient's
intellect and admit that not everything is understood about the human body.

Instead, we seem to have a group of very powerful psychiatrists who adopted
the Royal Free Disease in the late 60s, ignored all the evidence of physical
symptoms, and have presented it ever since as a form of hysteria.

As a result, we have patients who are severely physically ill who are
choosing suicide rather than to further endure the cruelty doled out to them
by the medical profession and the rest of society.

I do not include all medical professionals in the above accusation but I do
include many of them.

I urge all medical professionals to look at the already existing evidence
which shows immune, endocrine and neurological abnormalities.

I urge you to support the MRC initiative, led by Professor Stephen Holgate,
to do biomedical research to establish the underlying causes of this range
of 'syndromes' so that these patients can receive suitable care.

Competing interests: None declared

===================

Do CBT and GET really work for Chronic Fatigue Syndrome?

12 February 2010

Tom Kindlon,
Information Officer (voluntary position)
Irish ME/CFS Association



Santhouse and colleagues claim that treatments such as cognitive
behavioural therapy (CBT) and graded exercise therapy (GET) "have been shown
to work" in Chronic Fatigue Syndrome (CFS)/Myalgic Encephalomyelitis
(ME)(1). However, what the literature actually shows is that such therapies
have an effect, which is not necessarily the same thing as "working": a
meta-analysis calculated the average Cohen's d effect size across various
CBT and GET studies to be 0.48, which would generally be described as a
small effect size(2).

A recent review of three Dutch CBT studies found that while patients'
fatigue did improve, their activity levels did not and remained low, calling
into question claims that CBT is an effective rehabilitative strategy(3).

Systematic reviews tend to ignore "real world" data
. An audit of 5 Belgian
rehabilitation clinics, where the treatments offered were CBT and GET, found
that while improvements were recorded in various subjective outcome
measures, there was negligible change in the results from the exercise test
and the average number of hours in paid employment decreased at the end and
at follow-up(4). This was unlikely to be due to under- treatment, as an
average of 41 sessions were undertaken.

Given all this data, and the high rates of adverse reactions from GET that
have reported in surveys(5), patients and their clinicians are entitled to
hope that in the future a greater range of interventions will be available.

Tom Kindlon

References:

1. Santhouse AM, Hotopf M, David AS. Chronic Fatigue Syndrome. BMJ
2010;340:c738

2. Malouff JM, Thorsteinsson EB, Rooke SE, Bhullar N, Schutte NS. Efficacy
of cognitive behavioral therapy for chronic fatigue syndrome: a
meta-analysis. Clin Psychol Rev. 2008 Jun;28(5):736-45.

3. Wiborg JF, Knoop H, Stulemeijer, M, Prins JB, Bleijenberg, G. How does
cognitive behaviour therapy reduce fatigue in patients with chronic fatigue
syndrome? The role of physical activity. Psychol Med, 2010 Jan 5:1 -7. [Epub
ahead of print]

4. Rapport d'évaluation (2002–2004) portant sur l'exécution des conventions
de rééducation entre le Comité de l'assurance soins de santé (INAMI) et les
Centres de référence pour le Syndrome de fatigue chronique (SFC) (2006)
http://www.inami.fgov.be/care/fr/revalidatie/general-
information/studies/study-sfc-cvs/pdf/rapport.pdf (Date last accessed: 11
February 2010).

5. Kindlon T, Goudsmit EM. Graded exercise for Chronic Fatigue Syndrome: Too
soon to dismiss reports of adverse reactions. J Rehabil Med. 2010
Feb;42(2):184-6.

Competing interests: None declared

==========================

Re: Why do doctors refuse to believe patients? 12 February 2010

Ellen Goudsmit,
Registered Psychologist (Health)
London TW11 9QX



Re my post 11th February 2010.

I'd like to apologise to Dr. Santhouse for misspelling his name after the
first citation, which was correct. I also wish to note that reference 1 in
the text relates to reference 2 in the list.

Ellen Goudsmit PhD C.Psychol. FBPsS

Competing interests: None declared

===================

Defeatism and Chronic Fatigue 12 February 2010

Alastair C Young,
Neurologist
Bolton BL1 4QR


Santhouse and colleagues comment on the defeatism of clinicians with regard
to the chronic fatigue syndrome.Much of the blame for this reaction is the
bullying and badgering from a pwerful lobby,predominantly lay but partly
medical, which will not accept any role for psychological factors in the
cause of this disorder.

If there is a physical cause then there is certainly no standard medical
treatment available at present.To encourage the unfortunate victims to
pursue the purely physical approach is to deny them the benefits of the
treatments outlined by Santhouse and his colleagues.

Competing interests: None declared

================

More light needed 12 February 2010

Neil H Riley,
Chairman of The ME Association
7, Apollo Office Court, Gawcott, Buckingham MK184DF
Send response to journal:
Re: More light needed



As both a patient with ME/CFS and the Chairman of a National Charity whose
purpose is to inform, fund research and support those with the illness I
have found little defeatism amongst the medical professionals I have met.
There are those who are perplexed; those who accept the chronicity; those
who believe they know a treatment that will help.

What is missing in this debate is the need to examine more closely the huge
range of patients lumped together under the CFS/ME diagnosis. I have
attended many support groups for this illness and the variety of
presentations of symptoms is wide. Some clearly need active psychiatric
help; others counselling; some are in recovery. But there is a core of
chronically unwell members who are not depressed, whose illness began with a
severe viral infection and who have not recovered. Despite the NICE
Guideline recommended treatments of CBT and GET, those patients remain ill
and we simply do not know why.

Until money is spent and researchers encouraged to look more closely at that
group then this illness will continue to generate much heat but painfully
little light. I and many thousands of others like me have an illness that
limits our lives hugely but we do not have an air of defeatism. We have the
intelligence, the drive and the belief that medical science will eventually
find out why we are so ill.

Neil Riley

Chairman of the ME Association Buckingham. MK18 4DF

Competing interests: None declared

=======================

Severely affected - severely neglected 13 February 2010

Dr Charles B Shepherd,
Hon Medical Adviser
The ME Association, 7 Apollo Office Court, Radclive Road, Gawcott, Bucks
MK18 4DF


Santhouse et al (1) are correct to say that therapeutic defeatism is not
the answer to ME/CFS and that suicidal intentions must always be taken
seriously. However, they make a number of conclusions and observations that
are over-simplistic, premature or inaccurate.

First, the media have, quite rightly, used the tragic case of Lynn
Gilderdale to highlight the fact that severe ME/CFS exists and that there is
a desperate need for biomedical research into the underlying cause. But the
media coverage did not imply that ME/CFS is a 'commonly fatal' condition,
and it was premature of the authors to then go on and conclude - without the
benefit of robust epidemiological data - that mortality is not increased.

Second, a considerable amount of accumuating patient evidence (2) indicates
that a significant proportion of people with ME/CFS find that the two
behavioural treatments being recommended - cognitive behaviour therapy (CBT)
and graded exercise therapy (GET) - are either ineffective (ie CBT) or
harmful (ie GET). And the only research so far to investigate potential risk
factors which are involved in the development of severe ME/CFS (3) has
concluded that there is no evidence to implicate personality or neurotic
traits. It is therefore disingenuous to claim that the use of these two
behaviour-based therapies, in a group of patients who cannot normally travel
to hospital to access them, is going to produce a 'dramatic recovery'.

Third, having dealt with the families of a number of people with ME/CFS who
have committed suicide in recent years, the reasons for doing so are often
related to a combination of factors which predominently involve lack of
medical care and social support, failure to control key symptoms, and
inadequate financial help.. While depression may be a factor in some cases
it is not always present.

People with severe ME/CFS require multidisciplinary services in both a
domiciliary and accesible hospital based setting that matches their complex
individual needs. Having strongly criticised the current lack of care that
is available, we question whether the NHS trusts the authors work for are in
fact putting words into action and supplying domiciliary and in patient
facilities for their severely affected ME/CFS patients.

References

1 Santhouse AM, Hotopf M, David AJ. Chronic fatigue syndrome. BMJ 2010; 340:
738 (13 February)

2 Report of the CFS/ME Working Group. Department of Health; January 2002.
http://www.dh.gov.uk/dr_consum_dh/groups/dh_digitalassets/@dh/@en/documents/digitalasset/dh_4059506.pdf

3 Pheby D and Saffron L. Risk factors for severe ME/CFS. Biology and
Medicine 2009; 1: 50 -74.http://biolmedonline.com/Articles/vol1_4_50- 74.pdf

Competing interests: Medical Adviser to an ME/CFS patient support and
research funding charity. Member of MRC Expert Group on ME/CFS research.

CBT/GET is ineffective and potentially harmful. ME/CFS patients seem to die
considerably younger. 13 February 2010

====================================

Frank N.M. Twisk,
Patient and literature researcher
Limmen, the Netherlands



As has been established by the Bagnall et al. (1) and the Price et al. (2),
the solution proposed by Santhouse (3) cognitive behavioural therapy
(CBT)/graded exercise therapy (GET) reduced "fatigue severity" in 40% of
chronic fatigued people, in contrast with 26% in usual care.

Taking into consideration the placebo effect, the fact that a reduction in
"fatigue" is not reflected by objective improvement (4, 5), the fact that
the evidence base for CBT and GET is almost non-existent, etc. one must
conclude that CBT and GET is not effective.

Moreover, as established by large patient surveys, e.g. (6, 7), and by
clinical practice (5), CBT/GET has a negative effect on the symptomology of
many ME/CFS patients (pain, muscle weakness, neurocognitive impairment etc.)

This can be explained by the fact that exertion, and thus GET, intensifies
the pre-existing pathophysiology: inflammation, immune dysfunction,
immunosuppression, (persistent) infections, oxidative and nitrosative stress
and their sequels, e.g. mitochondrial damage/dysfunction and a disturbed
circulation (8, 9).

All in all, CBT/GET is a non-evidenced based therapy and even potentially
harmful for many ME/CFS patients (10).

Santhouse also asserts incorrectly that 'the greatest risk to life is likely
to be suicide' and 'this is often linked to depression that can be
effectively treated'.

A study into the causes of death by a Jason (11) established that ±20% of
the patients had died from cancer, ±20% had died as the consequence of heart
failure, and ±20% as a result of suicide.

The mean age of those who died from cancer and suicide was 47.8 and 39.3
years, respectively, which is ±24 years younger than those who died from
cancer and suicide in the general population.

The pathological abnormalities established in ME/CFS repeatedly plausibly
explain an increased risk for cancer (12)and heart failure (13).

Certainly it is warranted to treat depression in ME/CFS.

However, succesfully treating depression, e.g. by antidepressants, has no
effect on characteristic physical and cognitive ME/CVS symptoms (14, 15,
16).

In conclusion, the comments made by Santhouse do not seem to be very
appropriate.

Ironically, the CBT/GET mantra by Santhouse and colleagues and denial of
serious biological aberrations is exactly the reason why many patients feel
that 'the medical profession has given up to them'.

It is about time the medical profession takes this devastating illness
seriously by exploring the biological abnormalities in depth and developing
effective therapies aimed at these aberrations.

So the death of Lynn Gilderdale and many others will not be in vain.

  1. Bagnall A, Hempel S, Chambers D, Orton V, Forbes C. The Treatment and
Management of Chronic Fatigue Syndrome/Myalgic Encephalomyelitis in Adults
and Children. Centre for Reviews and Dissemination (CRD), University of
York. 2007; CRD Report 35:161.

2. Price JR, Mitchell E, Tidy E, Hunot V. Cognitive behaviour therapy for
chronic fatigue syndrome in adults. Cochrane Database Syst Rev. 2008 Jul
16;(3):CD001027.

3. Santhouse AM, Hotopf M, David AS. Chronic fatigue syndrome. BMJ. 11
February 2010. doi:10.1136/bmj.c738.

4. Wiborg JF, Knoop H, Stulemeijer M, Prins JB, Bleijenberg G. How does
cognitive behaviour therapy reduce fatigue in patients with chronic fatigue
syndrome? The role of physical activity. Psychol Med. 2010 Jan 5:1 -7.

5. Council of approval with regards to rehabilitation contracts with CFS
reference [Akkoordraad in het kader van de revalidatieovereenkomsten inzake
ten laste neming door Referentiecentra van patiënten lijdend aan het
Chronisch vermoeidheidssyndroom] [Dutch]. Evaluation Report (2002- 2004)
with respect to Rehabilitation Contracts between the RIZIV and the CFS
Reference Centers [Evaluation Report 2002-2004 with respect to
rehabilitation contracts between the RIZIV and the CFS Reference Centers]
[Dutch). 2006, July.

6. Action for M.E./AfME. Scotland M.E./CFS Scoping Exercise Report. 2007.

7. Bjørkum T, Wang CE, Waterloo K. [Patients' experience with treatment of
chronic fatigue syndrome] [Article in Norwegian]. Tidsskr Nor Laegeforen.
2009 Jun 11;129(12):1214-6.

8. Kerr JR, Petty R, Burke B, Gough J, Fear D, Sinclair LI, Mattey DL,
Richards SC, Montgomery J, Baldwin DA, et al. Gene expression subtypes in
patients with chronic fatigue syndrome/myalgic encephalomyelitis. J Infect
Dis. 2008 Apr 15;197(8):1171-1184.


9. Gow JW, Hagan S, Herzyk P, Cannon C, Behan PO, Chaudhuri A. A gene
signature for post-infectious chronic fatigue syndrome. BMC Medical Genomics
2009, 2:38. doi:10.1186/1755-8794-2-38.

10. Twisk FNM, Maes M. A review on cognitive behavorial therapy (CBT) and
graded exercise therapy (GET) in myalgic encephalomyelitis (ME)/chronic
fatigue syndrome (CFS): CBT/GET is not only ineffective and not
evidence-based, but also potentially harmful for many patients with ME/CFS.
Neuro Endocrinol Lett. 2009 Aug 26;30(3):284-299.

11. Jason LA, Corradi K, Gress S, Williams S, Torres-Harding S (2006).
Causes of death among patients with chronic fatigue syndrome. Health care
for women international. 2006; 27 (7): 615–26.
doi:10.1080/07399330600803766.

12. Meeus M, Mistiaen W, Lambrecht L, Nijs J. Immunological similarities
between cancer and chronic fatigue syndrome: the common link to fatigue?
Anticancer Res. 2009 Nov;29(11):4717-26.

13. Maes M, Twisk FNM. Why myalgic encephalomyelitis/chronic fatigue
syndrome (ME/CFS) may kill you: disorders in the inflammatory and oxidative
and nitrosative stress (IO&NS) pathways may explain cardiovascular disorders
in ME/CFS. Neuro Endocrinol Lett. 2009;30(6):677- 93.

14. Vercoulen JH, Swanink CM, Zitman FG, Vreden SG, Hoofs MP, Fennis JF,
Galama JM, van der Meer JW, Bleijenberg G. Randomised, double-blind,
placebo-controlled study of fluoxetine in chronic fatigue syndrome. Lancet.
1996 Mar 30;347(9005):858-61.

15. White PD, Cleary KJ. An open study of the efficacy and adverse effects
of moclobemide in patients with the chronic fatigue syndrome. Int Clin
Psychopharmacol. 1997 Jan;12(1):47-52.

16. Wearden AJ, Morriss RK, Mullis R, Strickland PL, Pearson DJ, Appleby L,
Campbell IT, Morris JA. Randomised, double-blind, placebo- controlled
treatment trial of fluoxetine and graded exercise for chronic fatigue
syndrome. Br J Psychiatry. 1998 Jun;172:485-90.

Competing interests: None declared

==================

There's none so blind as those who will not see 13 February 2010

Louise E Ellis,
Chair of the Manchester M.E. Society
M24 1JX


When is the medical profession in the UK going to wake up to the fact that CBT and GET are not effective treatments for M.E? They may be effective for some patients whose fatigue is of a psychiatric origin. However, as patient surveys repeatedly show, CBT and GET are either of no use or result in worsening symptoms for the majority of M.E. patients.

M.S. was proven not to be 'hysterical paralysis'. How long do we have to wait before the medical profession admits that M.E. is not a treatable
psychosocial illness?

What M.E. patients would like to see is biological research into the
condition. Repetition of the erroneous claim that CBT and GET are the answer
to the condition is only making the situation worse for us.

Competing interests: None declared

==========================

Using the correct tool for the right job 13 February 2010

Kelly Latta,
medical writer
27601



It is unfortunate that neither the editorial staff or Drs. Santhouse,
Hotopf, and David have anything new to add in terms of relevant information.

Like talk therapy, CBT has also been shown to help some patients in some
cases with other organic diseases as well as those who may not even have a
disease. It is not the secret they seem to think it is. But neither is it
the only tool in the shed.

Unfortunately CFS has come to be an umbrella term used to describe anything
from people who are merely tired and weary all the way to severely sick
patients with an organic brain disease (CFS WHO ICD-10 G93.3 Vol.3 pg 528).

It is illogical to assume that any one treatment is going to meet the needs
of such a heterogenous group.

Nor do the authors mention that research with anti-virals and immune system
modulators show that in appropriate subgroups these may be the most
effective treatments.
Nor do they mention pacing.

As to causes of death in CFS, there is not much research, but the research
that exists shows that patients are most likely to die of cancer, heart
failure and suicide decades sooner than their contemporaries in the general
population. (Patients with AIDS don't die of AIDS either, but they do die.)

As for suicide, it is always unfortunate when stigmatization by the medical community has such a negative iatrogenic effect.

Kogelnik AM, Loomis K, Hoegh-Petersen M, Rosso F, Hischier C, Montoya JG.
Use of valganciclovir in patients with elevated antibody titers against
Human Herpesvirus-6 (HHV-6) and Epstein-Barr Virus (EBV) who were
experiencing central nervous system dysfunction including long-standing
fatigue. J Clin Virol. 2006 Dec;37 Suppl 1:S33-8.

Propsner NM.Fatigue that doesn't go away. N J Med. 1999 Jun;96(6):29- 31.

Suhadolnik RJ, Reichenbach NL, Hitzges P, Adelson ME, Peterson DL, Cheney P,
Salvato P, Thompson C, Loveless M, Müller WE, et al.Changes in the 2-5A
synthetase/RNase L antiviral pathway in a controlled clinical trial with
poly(I)-poly(C12U) in chronic fatigue syndrome. In Vivo. 1994
Jul-Aug;8(4):599-604.

Fluge Ø, Mella O. Clinical impact of B-cell depletion with the anti- CD20
antibody rituximab in chronic fatigue syndrome: a preliminary case series.
BMC Neurol. 2009 Jul 1;9:28.

Staines DR, Brenu EW, Marshall-Gradisnik S. Postulated vasoactive
neuropeptide immunopathology affecting the blood-brain/blood-spinal barrier
in certain neuropsychiatric fatigue-related conditions: A role for
phosphodiesterase inhibitors in treatment? Neuropsychiatr Dis Treat.
2009;5:81-9. Epub 2009 Apr 8.

Jason LA, Corradi K, Gess S, Williams S, Torres-Harding S. Causes of Death
Among Patients With Chronic Fatigue Syndrome. Health Care for Women
International, 27:615–626, 2006

Levine, P. H., Atherton, M., Fears, T., & Hoover, R. (1994). An approach to
studies of cancer subsequent to clusters of chronic fatigue syndrome: Use of
data from the Nevada State Cancer Registry. Clinical Infectious Diseases,
18(Suppl. 1),S49–S53.

Peckerman, A., LaManca, J. J., Dahl, K. A., Chemitiganti, R., Qureishi, B.,
& Natelson, B. H. (2003). Abnormal impedance cardiography predicts symptom
severity in chronic fatigue syndrome. The American Journal of the Medical
Sciences, 326(2),55–60.

Green, J., Romei, J., & Natelson, B. J. (1999). Stigma and chronic fatigue
syndrome. Journal of Chronic Fatigue Syndrome, 5, 63–75.

Competing interests: None declared

==================================

No room for complacency 13 February 2010

Derek FH Pheby,
Visiting Professor of Epidemiology, and Project Coordinator, National ME/CFS
Observatory
Faculty of Society and Health, Bucks. New University, 106, Oxford Road,
Uxbridge, UB8 1NA



Santhouse et al (1) quoted with approval Mr. Justice Simon's judgment in
the judicial review of the NICE guidelines on CFS/ME, that there is "... a
perception that this is an area of medicine where contrary views are not to
be voiced, and where scientific enquiry is to be limited, [that] is damaging
to science and harmful to patients" (2). They will therefore not object if I
venture an opinion contrary to theirs.

They cite a recent systematic review (3) as evidence of the effectiveness of
behavioural interventions such as cognitive behaviour therapy and graded
exercise in CFS/ME, yet that same review states: "The protocols for many
clinical studies require patients to attend a clinic for treatment and/or
assessment. These conditions may exclude people severely affected with
CFS/ME from taking part and hence bias the sample towards those with less
severe symptoms." Indeed, the only evidence cited by Santhouse et al that
such interventions may benefit the severely affected is an uncontrolled
pilot study of only nineteen patients, published more than a decade ago (4).

There is no evidence at all that such interventions would have benefited
Lynn Gilderdale, or others in a similar position, or averted the tragic
outcome of this case. A recent large-scale survey by the ME Association
found that over 50% of respondents reported that behavioural treatments such
as cognitive behaviour therapy and graded exercise therapy were either
ineffective or made their condition worse
(5). This is consistent with my
own recently published study (6), which indicated that inappropriate
treatment in the early stages of the illness was an important factor in the
development of severe disease, and a survey by Action for ME in which a
clear majority of severely affected respondents reported delays in diagnosis
and lack of care and support from healthcare professionals
(7).

It is not so much that "...an air of defeatism exists within the medical
profession about this condition, particularly for those who are severely
affected." It is rather that a realistic assessment is that we do not yet
have sufficient understanding of this very unpleasant illness to treat it
effectively, and to suggest that we do is unjustifiably complacent. A much
more positive note was struck by a letter in the "Daily Telegraph",
published in the aftermath of the acquittal of Kay Gilderdale, which was
signed by twenty authorities in the field, including clinicians,
researchers, politicians, and leaders of voluntary organisations (8). This
stated clearly that, if any positive lesson was to be learned from the death
of Lynn Gilderdale and the subsequent trial of her mother, it was that there
is an urgent need for better services for people with ME, and more research,
in order to disentangle once and for all the underlying pathology of this
disease and to develop effective treatments.

References

1. Santhouse AM, Hotopf M, David AS. Chronic fatigue syndrome (editorial).
BMJ 2010; 340: 738.

2. R (Fraser and Short) v NICE Case numbers CO/10408/2007 and CO/10435/2007
(2009).

3. Chambers D, Bagnall AM, Hempel S, Forbes C. Interventions for the
treatment, management and rehabilitation of patients with chronic fatigue
syndrome/myalgic encephalomyelitis: an updated systematic review. J R Soc
Med 2006;99:506-20.

4. Essame CS, Phelan S, Aggett P, White PD. Pilot study of a
multidisciplinary inpatient rehabilitation of severely incapacitated
patients with the chronic fatigue syndrome. J Chronic Fatigue Syndr
1998;4:51-60.

5. Shepherd C. Mind or Body? (Letter). New Scientist 2009; no. 2702 (2nd.
April).

6. Pheby D, Saffron L. Risk factors for severe ME/CFS. Biology and Medicine
(2009); 1(4):50-74.

7. "Severely Neglected", London, Action for ME, 2001.

8. The Countess of Mar et al. Breaking the ME enigma (letter). Daily
Telegraph, 6 February 2010.

Competing interests: None declared