Saturday, January 16, 2010

The Event Horizon | CFS Un-Tied Blog

An open e-mail to Professor M. McClure - retrovirologist at Imperial College

An open e-mail to Professor M. McClure - retrovirologist at Imperial College

(With thanks to Sheila Campbell on MEActionUK)

15th January 2010

With Reference to Wessely, Cleare and Collier's' Response on the PLoS One

I found the following statement in Point 3 of Dr Anthony Cleare's response
(below) to be quite extraordinary:

"We follow the same psychiatric exclusion criteria as mandated by the Fukuda
criteria......In addition, we also exclude patients with chronic
somatisation disorder as defined by DSM-IV, which is not required by the
Fukuda criteria, but most experts and clinicians agree are a different

Why extraordinary?

Because of Professor Wessely and colleagues' long held and widely publicised
view that CFS is a somatisation disorder (or medically unexplained syndrome,

This theory is promoted in complete defiance of the scientific evidence
which clearly shows CFS to be an organic disease. As such, by definition,
CFS cannot be a somatisation disorder.(8)(9)

Somatoform disorder is defined in DSM-IV as follows:

"The most common characteristic of the somatoform disorder is the appearance
of physical symptoms or complaints for which they have no organic basis."(6)

With such a profound turn around in thinking (if this really is the case)it
would be helpful to all concerned if the authors could please clarify the
following points:

1. Could you please state how all the authors defined CFS at the time of
carrying out this research and do you still hold that perspective?

Lombardi et al unequivocally, on the basis of the scientific evidence, view
CFS as an organic disease.

2. Could you please explain why you did not state in the paper that you had
excluded patients with somatoform disorders.

3. If, as you say, you excluded patients in this research who had
somatisation disorders, can you please explain why you cited papers in your
reference list (for example, reference 9 by Wessely et al, "Chronic fatigue
syndrome. A Practical Guide to Assessment and Management", 1997) which
clearly classes CFS as a somatisation disorder.

3. And could you please explain why you did not cite papers, such as in Ref
8 & 9 below, which clearly show the organic basis of this disease?

4. Could you please inform us when the 186 blood samples were taken, since
at least up until March 2009, Professor Wessely viewed CFS as a somatisation
disorder(2) You could ask Professor Wessely if the blood drawn from his
patients *after* he had changed his mind with Dr Cleare about CFS being a
somatoform disorder or if the blood was drawn before they both changed their

5.Could you please explain what has led to such a change of mind, no longer
viewing CFS as a somatisation disorder?

Thank you for your time.



Chronic fatigue syndrome: an overview.
Cho HJ, Wessely S.
Rev. Bras. Psiquiatr. vol.27 no.3 São Paulo Sept. 2005 "Chronic fatigue
syndrome is an exemplar of a medically unexplained syndrome."

"Similarly, functional somatic syndromes refer to groups of symptoms lacking
disease-specific, demonstrable abnormalities of structure, and are usually
defined by specialty or organ system. They include irritable bowel syndrome,
fibromyalgia, chronic fatigue syndrome, multiple chemical sensitivity,
chronic pelvic pain, temporomandibular joint dysfunction and more recently
Gulf War syndrome."

This paper is titled "CFS: An Overview" yet please note that the
references,(consisting of 6 papers) do not include any papers on biomedical


New Scientist, Opinion, "Mind over body?", Professor Simon Wessely, 13 March
2009. Please note that there is no mention of all the biomedical research
showing CFS to be an organic disease, hence readers may understandably have
thought that it does not exist.


Research carried out at the Institute of Psychiatry, Kings College London,
where three of the authors of this paper are based.

Part 4 - The Project and the Post "Background: Anorexia Nervosa (AN) and
Chronic Fatigue Syndrome (CFS) are classical psychosomatic
disorders......Aberrant emotional processing is a strong candidate as a
maintaining factor for these disorders."


From "Corporate Collusion?" by Professor Malcolm Hooper, Eileen Marshall and
Margaret Williams, comments made by Professor Wessely over the years about
CFS and CFS patients clearly showing how he views these patients and the

"Wessely is on record as asserting that ME is merely a "belief" held by
those who think they suffer from it; that ME patients' muscle weakness is
"simulated"; that efforts are made to over-interpret laboratory findings;
that the average doctor will see ME patients are neurotic and will often be
disgusted with them; that blaming a virus for the illness conveys advantages
by protecting the victim from personal blame; that symptoms are simply
normal sensations and are the result of "body-watching"; that ME is a
"myth"; that ME is "learned helplessness"; that once validation is granted
by a doctor, the ME patient may assume the "advantages of the sick role --
sympathy, time off work, benefits etc"; that ME symptoms have no anatomical
or physiological basis; that patients' aberrant beliefs are maintaining
factors and that patients with ME exert a large and avoidable financial
burden on health and social services.

(For individual references, see the December 2003 Briefing Paper for the
House of Commons Health Select Committee: The Mental Health Movement:
Persecution of Patients? which is available online at  )."


Medically Unexplained Symptoms: Exacerbating Factors in the Doctor-patients
Encounter, L A Page, S Wessely, Journal of the Royal Society of Medicine
2003:96:223-227 "This term (MUS) is now used in preference to "somatisation"

However I cannot find MUS in the DSM-IV


Definition of somatisation disorder


"Wessely's Way: Rhetoric or Reason?"
Professor Malcolm Hooper and Margaret Williams 22nd March 2008


List of reference and abstracts for some of the many biomedical research
papers on CFS, plus inquest and autopsy information, see item 47 and 48.

9. Two further important references, 2009.

J Clin Pathol. 2009 Dec 2.
Microbial infections in eight genomic subtypes of Chronic Fatigue Syndrome /
Myalgic Encephalomyelitis (CFS/ME).
Zhang L, Goudh J, Christmas D, Mattey D, Richards S, Main J, Enlander D,
Honeybourne D, Ayres J, Nutt DJ, Kerr J.
St George's University of London, United Kingdom;

J Transl Med. 2009 Nov 12;7:96.
Plasma cytokines in women with chronic fatigue syndrome.
Fletcher MA, Zeng XR, Barnes Z, Levis S, Klimas NG.


Official Cause of Death

Note: While the essay below from NurseWriter's blog doesn't address CFS
specifically, it is a good primer for understanding why it is as important
to study and report death as it is to study diseases prior to death.

As noted by Dr. Jason elsewhere, deaths in CFS patients tend to occur two
decades earlier than is normal for the general population. Deaths from
virally related cancers are very prominent as is suicide (which may be
correlated with both the severity of the disease and/or the amount of
stigmatization patients routinely face).

Dr. Andrew Lloyd and the psychiatrists from the Kings College Institute of
Psychiatry automatically exclude CFS patients who have cancer. It doesn't
mean that if you have cancer that you no longer have CFS, it is simply one
way of winnowing out patients so that the population studied fits the
researcher's hypothesis. The argument being that the cancer is causing the
symptoms not CFS therefore the patient does not have CFS. It also allows the
argument to be made that CFS can be triggered by acute infection, but that
patients rapidly recover and somehow continue to think they are sick. That
this defies logic is not addressed.

This line of thought may also allow researchers with this viewpoint to
ignore other research that shows the continuing reactivation of viruses in
CFS may perpetuate the disease in patients. The insistence that patients
cannot be diagnosed with CFS until they have signs and symptoms for at least
six months also means that viral damage to organs such as the brain and
heart may be irreversible by the time patients are diagnosed.  Nor does this
specific view point take into account which appeared first: the CFS or the
cancer or allow for co-morbidity.

The protocol for acknowledging that diseases may not directly result in
death, but are closely associated with diseases that do cause death in a
specific population is already in place. All doctors have to do is use it
properly. As in the example below, HIV doesn't cause death in AIDS, but
other diseases and infections may be a consequence of AIDS or HIV.  This can
also be applied to CFS. *


*Official Cause of Death *

A question recently hit my inbox about what the official cause of death
would be listed as on a death certificate of a person who died of cancer. As
I don't deal much with that end (pun not intended) of the health care
spectrum, I did a bit of digging and found out that writing the "cause of
death" statement is surprisingly complex and yet also a thing of simple
beauty. Ok, so I'm a bit morbid.

A typical cause of death statement might read:

*Acute Myocardial Infarct *

Now, if you aren't an MD or a nurse, that might look like a load of
gibberish, but really it just says "heart attack". Simple, right? er... not
quite as simple as that. Actual cause of death statements are written in two
parts. The purpose of these statements is to allow tracking bodies to
develop statistics on diseases and processes that kill people, *and the
things that put us at greater risk for these conditions*. So if a coroner or
MD writing a death certificate has more information (ie from medical history
or an autopsy), they are going to fill this section in with as much data as

*Part I*

The purpose of part 1 is to determine the series of medical events that lead
up to the death, in reverse order, starting from the most recent condition
and working backwards to the oldest relevant condition that lead directly to
the death. So that very basic heart attack up there would become something
more like heart attack due to hardening of the arteries that feed the heart,
or in medical jargon:

*Acute myocardial infarct*
due to or as a consequence of *Athrosclerotic coronary artery disease*

As another example, if you had someone die of a pneumonia because they had
AIDS, their cause of death statement would look like:

*Klebsiella Pneumonia*
due to or as a consequence of *Acquired Immune Difficiency Syndrome*
due to or as a consequence of *Human Immunodeficiency Virus infection*

If there isn't a lot of data on what lead up to the death, or if the person
was terminally ill from a known disease but there isn't a way to determine
what complication of that terminal disease exactly killed the patient, you
can sort of guess or just leave it off. As below:

*Acute myocardial Infarct*
Due to or as a consequence of *Probable Atherosclerotic coronary artery

Or simply:

*Adenocarcinoma of the prostate*

*Part II*

Part II is to list risk factors that lead to the sequence of events that
lead to the death. These can include other diagnoses, like high blood
pressure (hypertension) or diabetes (diabetes mellitus type I or type II),
or behaviors, like alcohol abuse, IV drug abuse, etc..

*Do's and Don'ts*

*Don't report signs or symptoms as the cause of death*

So a person cannot be said to have died of a cough, fever, or elevated blood
alcohol level. They can die of pneumonia (that caused the cough), or a
specific infection (that caused the fever), or alcohol toxicity (with the
high blood alcohol level would diagnose, but the blood alcohol level itself
is a test, not a diagnosis).

*Don't report mechanistic causes of death*
Mechanistic causes of death are the physical process that stopped or failed
due to disease or trauma, rather than the disease or trauma itself.

As in cardiac arrest caused by a heart attack, or respiratory arrest caused
by pneumonia.

*Do be specific and exact*

Don't oversimplify or under-report.

For instance, a doctor wouldn't write that high blood pressure killed
anybody. High blood pressure may have lead to stroke that killed someone, or
it could have lead to hardening of the arteries and a heart attack.

It's better to include too much information rather than too little.
* *

*Why is cause of death important?*

Cause of death statements also allow us to track which diseases and problems
are killing us, and thereby allow us to work harder on cures, treatments,
and solutions to those same diseases and problems. Keeping mortality and
morbidity statistics is one of the best ways to start tracking the impact of
disease and death. (This is one of the CDC's jobs.)

Of course, the cost of disease and death can't just be measured in death.
Quality of life, healthcare costs, the costs to survivors, and other factors
must be weighed as well.

Thursday, January 14, 2010

An Indefatigable Debate Over Chronic Fatigue Syndrome

thanks to Kim500 at the PhoenixRising forums for the full text of the article

Science 15 January 2010:
Vol. 327. no. 5963, pp. 254 - 255
DOI: 10.1126/science.327.5963.254

News of the Week

An Indefatigable Debate Over Chronic Fatigue Syndrome
Sam Kean

Here we go again. The search for the cause of chronic fatigue
syndrome, which just months ago seemed to be gaining traction, now
seems likely to descend into the same confusion and acrimony that
characterized it for years, as a supposed viral link to CFS published
just last autumn might be unraveling.

Many patients with CFS—long-term fatigue and other ailments that have
no known biological cause—report that their symptoms began after an
acute viral infection, and scientists have tried many times, but never
successfully, to pin CFS to viruses such as Epstein-Barr. Patients
have faced skepticism for years over whether CFS is a "real" disease;
a viral trigger could vindicate them and explain their nebulous

That's why a paper published online 8 October 2009 in Science
( caused such a
stir. A U.S. team reported finding DNA traces of a virus, XMRV, in the
blood cells of two-thirds of 101 patients with CFS, compared with 4%
of 218 healthy controls. Strangely, XMRV, a rodent retrovirus, had
previously been implicated in an aggressive prostate cancer. No one
knows how XMRV might contribute to either or both diseases, but the
authors argued that the link made some sense: XMRV ravishes natural
killer blood cells, which attack both tumors and cells infected by

Other scientists thought the link dubious, criticizing the team, led
by Vincent Lombardi and Judy Mikovits at the Whittemore Peterson
Institute for Neuro-Immune Disease in Reno, Nevada, for not explaining
enough about the demographics of their patients or the procedures to
prevent contamination (Science, 9 October 2009, p. 215). Several
virologists around the world practically sprinted to their labs to
redo the experiments, and the discovery that a clinic associated with
some people at Whittemore was selling, among other CFS services, a
$650 diagnostic test for XMRV made the issue more pressing. A U.K.
team already exploring the XMRV–prostate cancer link won the race,
submitting a paper to PLoS ONE challenging the claim on 1 December
2009. It was accepted for publication after 3 days of review.

The British team, led by retrovirologist Myra McClure of Imperial
College London, examined DNA from the blood of 186 CFS patients
ranging in age from 19 to 70, with an average age of 40. Most were
markedly unwell. McClure's team used a PCR machine—which copies and
amplifies scraps of DNA—to search for two viral sequences, one from
XMRV and the other from a closely related virus. They discovered
nothing. At a press conference discussing the results, published
online 6 January in PLoS ONE, McClure was blunt and confident: "If
there was one copy of the virus in those samples, we would have
detected it."

This null result prompts the question of what—if anything—was wrong
with the original paper. The PLoS ONE authors seem to suggest that
contamination was at fault, stating that they were careful to work in
labs that had never handled XMRV and use PCR machines that analyze no
mouse tissues. But McClure says her group merely wanted to make that
explicit, not accuse anyone.

The U.S. team followed the same procedures, retorts Lombardi, a
biochemist. He also expressed bewilderment that the McClure group
didn't search its CFS samples for the same DNA sequence as his team
had, raising the possibility that they had different results because
they searched for different things. The McClure team, however, looked
for not only an XMRV sequence but also a sequence in a closely related
virus, MLV. That MLV sequence, highly conserved among viruses of its
class, would presumably have been found if XMRV was present, they

One distinct possibility, says John Coffin, a microbiologist at Tufts
University in Boston who studies retroviruses and wrote a separate
analysis for Science when the original paper was published
(, is that both
papers are right. He called the PLoS ONE paper too "preliminary" to
settle the debate and said XMRV could show more genetic variety, and
thus be harder to detect, than anyone assumed. It's also possible that
distinct strains of XMRV appear in different parts of the world, as do
the retroviruses HIV and HTLV (a leukemia virus). Intriguingly,
although research teams in the United States have linked XMRV to
prostate cancer, multiple teams in Germany and Ireland have failed to
find a connection.

Coffin says one more possibility, raised by many scientists, is that
CFS is actually a suite of diseases that present the same symptoms and
so might have many causes. Lombardi agrees. "It's naïve to think that
everyone with chronic fatigue has the same etiology. There's probably
going to be a subset of people with CFS that have XMRV, and it will
probably end up being classified as XMRV-related CFS."

All of this leaves doctors and patients in a muddle. There's no doubt
they're hungry for information. Out of curiosity, Lombardi did a
Google search on "XMRV" the day before the Science paper hit and found
about 22,500 hits. Three months later, there are 400,000.

But some scientists, including Coffin and McClure, fear that the Viral
Immune Pathology Diagnostics clinic (VIP Dx) took advantage of that
hunger by offering the $650 diagnostic test for XMRV, 300 of which
have been administered so far and which already has a 4 to 6 week
backlog. "Leaving aside the issue of who's right and who's wrong,"
says Coffin, "the original paper did not establish the virus [caused
CFS] and didn't establish it as a viable marker." So it's not clear
what a patient or physician could do with a positive result. Steve
Kaye, a colleague of McClure's at Imperial College London and a
co-author of the PLoS ONE paper, noted with some alarm that the
authors of the Science paper had speculated about treating XMRV with
antiretroviral drugs, which can have harsh side effects.

However, VIP Dx developed its XMRV test only after a different company
began offering one; VIP Dx officials saw their test as a more expert
alternative. What's more, Lombardi—an unpaid consultant for VIP Dx who
helped set up and manage the testing program—argues that the test is
useful. Patients could in theory avoid infecting other people with
XMRV and can have their diagnoses validated, if nothing else. His test
results also bolster the science in the original paper; he says 36% of
tests have detected XMRV, including a few from the United Kingdom.
(Test proceeds roll back into research and development at Whittemore,
which licenses the test to VIP Dx. VIP Dx has also received financial
support from the Whittemore family in the past.)

To resolve the dispute, both sides say they are willing to work with
the other and possibly test each other's samples. In the meantime,
more papers exploring the link are slated to appear in the next few
months, and each side says it knows of work supporting its results.
All that suggests that the field will continue to churn. As McClure
told Science, "we take no pleasure in finding colleagues wrong or
dashing the hopes of patients, but it's imperative the truth gets

What part of “Give us our damn data” do you not understand?

Games medical care providers play so they don't have to give you your records, and the excuses they'll use.

Wednesday, January 13, 2010

Angela Kennedy's Response to PLOSone


The authors' reply to the concerns about patients selection for research for this paper raises more problems in addition to those of the original paper. My comments here should be read in addition to other problems raised by authors on this forum.

Firstly, the authors express some resentment towards those legitimately have questioned this research cohort and the criteria over the years, which is rather surprising. Contrary to the insinuation by the authors, no person on the Plosone responses forum has insinuated that the research cohort they use are somehow 'less deserving' than say, the WPI cohort, purely that they are a different type of patient, using different criteria that select a different population, and that this may cause problems with the findings, and claims made based on those findings, with regard to the British 'CFS' population. This is a reasonable concern to express, and such a deduction can be made based on the evidence the authors provide themselves in their paper, citations, and their response. For example, their paper states:

"Patients in our CFS cohort had undergone medical screening to exclude detectable organic illness".

In the authors' response here, they also write:

"Thus patients in our service have also co operated in studies of PET and fMRI
neuroimaging, autonomic dysfunction, neurochemistry, respiratory function,
vitamin status, anti nuclear antibodies, immune function, neuroendocrine
function and genetics "

While patients being processed for a research cohort may well, indeed are likely, to have co-operated and had such tests done, this does not necessarily mean that patients with positive results are part of the research cohort. Indeed, positive results, which would indicate organic abnormality, would surely be likely to prevent a patient being selected for a cohort, by the very logic described in the author's paper here, by their own response (the additional tests are considered `not clinically necessary'?) and in at least one of their citations (Quarmby et al)? In the Quarmby et al paper, the cohort is described, in which the criteria used (in addition to 'Fukuda/CDC') is 'Oxford'. The Oxford criteria (Sharpe et al 1991) in particular actually do allow for patients who fulfil organic abnormality to be selected out of a research cohort. Indeed,  Anthony David, referring to these, commented at the time:

"British Investigators have put forward an alternative, less strict, operational definition which is essentially chronic (6 months or more) severe disabling fatigue in the absence of neurological signs with myalgia, psychiatric symptoms and previous viral infections as common associated features."

Here special attention needs to be paid to the term `previous viral infections' and `absence of neurological signs', in order to contextualise the cohort selection process applied using the Oxford Criteria.

It is therefore quite reasonable to presume that patients in the cohort described in the Erlwein et al paper are less likely to be suffering from organic abnormalities associated with 'CFS' populations than in other research cohorts. It is also rational to be concerned that the cohort described here may not be representative of many people diagnosed with 'CFS' in Britain. NICE guidelines for example, acknowledge that very little research has been done on `severely affected' patients, who comprise, possibly at least 25% of the population of people given a `CFS' diagnosis (though so little research has been done on `severely affected` in Britain, the true number is not yet clear). While patients potentially destined for a research cohort which weeds out `detectable organic abnormality' may be subjected to a rigorous amount of investigations, those not undergoing this process do not undergo such testing, at least not in the NHS. Indeed, such investigations of clinical patients are severely proscribed in the majority of `guidelines': NICE, and the RCPCH guidelines as just two examples. Ironically, Fukuda guidelines also make the following comment:

    "The use of tests to diagnose the chronic fatigue syndrome should be done only
    in the setting of protocol-based research.

    In clinical practice, no additional tests, including laboratory tests and
    neuro-imaging studies, can be recommended. Examples of specific tests (which
    should not be done) include serologic tests for enteroviruses; tests of
    immunologic function, and imaging studies, including magnetic resonance imaging
    scans and radionuclide scans (such as single photon emission computed tomography
    (SPECT) and positron emission tomography (PET) of the head.

    We consider a mental status examination to be the minimal acceptable level of
    assessment." (1994:)

That clinical populations are not to be afforded the types of investigations given to research populations makes the whole idea of `medically unexplained' or `unexplained by disease', or 'functional' (as synonymous with 'non-organic' or not discernibly organic`) as common characterisations of CFS (including by at least one of the authors themselves in previous publications, for just one example, Page et al, 2003) highly problematic at best.

It is also significant that `CFS' is so often described as a `diagnosis of exclusion' (see, for example, the Centre for Disease Control CFS information website (Footnote: . Certain research case definitions comply with this assumption, such as the Oxford Criteria (Sharpe et al, 1991) and CDC Criteria (Fukuda et al, 1994) Here, `diagnosis of exclusion' also functions as a euphemism of `medically unexplained'. The key problem within this recurring theme in the literature, which most frequently remains un-addressed, is how a clinical patient's condition can all too easily become `medically unexplained' because of the practice of encouraging doctors to severely limit investigations in the first place: except, it would appear, ironically, in research populations in which `organic' illness is being weeded out to provide the type of cohort that might fulfil `not organically ill' definitions.

The issue of `disability' also needs to be clarified. The references cited in the Erlwein paper to support the statement that the patient cohort was of 'high levels of disability' refer only to 'disability' in psycho-social terms or feelings of `fatigue`, and not in terms of physical impairment, a key omission. Mundt et al's paper in particular focuses on specific mental health problems and the social exclusionary effects of living with these. While in no way invalidating or trivialising the disability caused by mental health problems, it must be pointed out that both Mundt et al and Chalder Scales nevertheless fail to elucidate a high level of physical or physiological (say, for example, neurological, mitochondrial and/or cardiovascular) impairment, key problems present in people given a clinical diagnosis of `CFS', usually related to specific organic abnormalities that can be found, if they are tested for in the first place.

With regard to the Canadian criteria (Carruthers et al), in fact they have undergone some `validation'. Jason et al found:

"…Canadian criteria selecting cases with less psychiatric co-morbidity, more physical functional impairment, and more fatigue/weakness, neuropsychiatric, and neurologic symptoms. The overall findings suggest that the Canadian clinical criteria appear to select a more symptomatic group of individuals than the CFS criteria, and these individuals do demonstrate less current and lifetime psychiatric impairment than those selected according to the CFS criteria. In contrast, the CFS group was not significantly different from the Chronic fatigue-psychiatric group in psychiatric impairment. Predictably, the Chronic fatigue-psychiatric group evidenced the highest frequency of current and lifetime psychiatric disorders… Overall, there were 17 significant symptom differences between the Canadian and Chronic fatigue-psychiatric group, but only 7 significant symptom differences between the CFS and Chronic fatigue-psychiatric group. Findings suggest that the Canadian criteria select a group of patients with more symptoms, and the Canadian criteria identify a group with higher levels of physical functional impairment and less psychiatric comorbidity. Findings from the present study indicate that the Canadian criteria does capture many of these cardiopulmonary and neurological abnormalities, which are not currently assessed by the current CFS case definition (Fukuda et al., 1994). However, it is worth noting that when the Fukuda et al. (1994) CFS case definition was conceived, the research had not yet been done investigating these abnormalities. In combination with symptom patterns, it is possible to conclude that the Canadian group does select individuals with greater impairment, particularly given the physical composite score, fatigue/weakness, neurologic and neuropsychiatric symptoms, as these symptoms can interfere with daily living and occupational performance. Results from this present investigation highlight the importance of contrasting different diagnostic criteria in order to gain a greater understanding of the syndrome now known as CFS. The findings do suggest that the Canadian criteria point to the potential utility in designating post-exertional malaise and fatigue, sleep dysfunction, pain, clinical neurocognitive, and clinical autonomic/ neuroimmunoendocrine symptoms as major criteria for future attempts to define this syndrome..." ( )

In addition to using the Carruthers et al criteria (or `Canadian Criteria`), the WPI give this information about their patient cohort in their supporting online material:

"Their diagnosis of CFS is based upon prolonged disabling fatigue and the presence of cognitive deficits and reproducible immunological abnormalities. These included but were not limited to peturbations of the 2-5A synthetase/RNase L antiviral pathway, low natural killer cell cytotoxicity (as measured by standard diagnostic assyas) and elevated cytokines particularly interleukin-6 and interleukin-8. In addition to these immunological abnormalities, the patients characteristically demonstrated impaired exercise performance with extremely low VO2 max measured on stress testing..." ( )

It is therefore highly unlikely, as the authors indeed acknowledge in their reply here, that Erlwein et al were testing the same type of patient as those tested by the WPI, which inevitably makes the Erlwein et al findings- and perhaps some of the wilder claims that they have `cast serious doubt' on the WPI`s findings, unfortunately made in some of the lay media- not scientifically tenable. The failure of Erlwein et al to include such type of patient in their cohort, however. does not mean that such patients do not exist in Britain. Copious patient anecdotal experience, research reports, and charity surveys indicate that they do exist. Whether XMRV  is present or not is another matter, but there are enough identifiable problems around patient selection alone with the Erlwein et al paper to indicate this is not a definitive disproving of the existence of the virus in Britain.

Ongoing neglect of the importance of establishing a possible `CFS' patient population in Britain, clinically and in research settings, using the Canadian Guidelines, is preventing the development of knowledge that might help extremely ill and disabled people here in Britain.

The problems I have briefly outlined here do not fully express the range and depths of problems with regard to: the identity of an accurate `CFS' population; the instabilities of `CFS' criteria per se; the faulty concepts of `medically unexplained' or `functional` and relation to `psychogenic` explanations for somatic illness; the vagaries of criteria that claim to facilitate a `diagnosis of exclusion'; and the psychogenic dismissal of serious organic dysfunction of patients given a 'CFS' diagnosis, problems that have happened for many years. These problems are relevant to the Erlwein et al paper. Furthermore, they are highly relevant to all research that claim a psychological and/or behavioural aetiology to the condition or conditions that get deemed as `CFS'.


Carruthers, B. et al (2003) "Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: Clinical Working Case Definition, Diagnostic and Treatment Protocols" Journal of Chronic Fatigue Syndrome, Vol. 11(1), pp 7 - 115.
Chalder, T. Berelowitz, G. Pawlikowska, T. Watts, L. Wessely, S. Wright, D. Wallace, E. P. 'Development of a fatigue scale' Journal of Psychosomatic Research Vol 37: Issue 2: Feb 1993: 147-153.
David, A.S. `Postviral syndrome and psychiatry` British Medical Bulletin: 1991: 47: 4: 966-988
Fukuda K, Straus SE, Hickie I, Sharpe MC, Dobbins JG, Komaroff A. 'The chronic fatigue syndrome: a comprehensive approach to its definition and study' Ann Intern Med. 1994 Dec 15;121(12):953-9.

Jason LA, Torres-Harding SR, Jurgens A, Helgerson J. "Comparing the Fukuda et al. Criteria and the Canadian Case Definition for chronic Fatigue Syndrome". Journal of Chronic Fatigue Syndrome 12(1):37-52, 2004

Mundt, J.C. Marks, I.MShear, K. Griest, J.H. 'The work and social adjustment scale: a simple measurement of impairment in functioning' British Journal of Psychiatry (2002) 180: 461-443

Page, L.A. Wessely, S. 'Medically unexplained symptoms: exacerbating factors in the doctor–patient encounter' J R Soc Med 2003;96:223-227

Sharpe MC, Archard LC, Banatvala JE, Borysiewicz LK, Clare AW, David A, Edwards RH, Hawton KE, Lambert HP, Lane RJ, et al ' Chronic fatigue syndrome: guidelines for research' J R Soc Med. 1991 Feb;84(2):118-21.

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The mitochondria in each cell supply energy to the body in the form of adenosine triphosphate (ATP), and CoQ10 is needed for them to do their job. So it's not surprising that low CoQ10 is implicated in many diverse illnesses - from heart disease and cancer to Alzheimer's, ME/CFS, and migraine.

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There already has been an effort to sell XMRV as the cause of
another disease: ALS (amyotrophic lateral sclerosis).

See 'Neurology Today' (March 6, 2008, Vol. 8, #5, pp 1-14),
The paper concludes,
   The retrovirus, however, remains elusive. The serum and
   CSF tested negative for XMRV.

Reno Gazette Journal on XMRV

Source: Reno Gazette Journal
Date:   12 jaqnuari 2010
Author: Lenita Powers

Reno researchers dispute British challenge to virus discovery

Reno scientists who found a link between a retrovirus and people
with Chronic Fatigue Syndrome are scoffing at a challenge from
British researchers who claim the discovery was false.

Researchers at the nonprofit Whittemore-Peterson Institute for
Neuro-Immune Disease at the University of Nevada, Reno made
headlines worldwide last October when they reported discovering
a new infectious human retrovirus, XMRV, in the blood of 68 of
101 people with Chronic Fatigue Syndrome.

In a story scheduled to appear Friday in the print edition of
Science magazine, Myra McClure, a professor of retrovirology at
Imperial College London, said her team of researchers examined
DNA from the blood of 186 people with Chronic Fatigue Syndrome
for XMRV and a closely related virus, but found neither.
"If there was one copy of the virus in those samples, we would
have detected it," McClure said.

But McClure and her team did not duplicate the scientific techniques
used by the Whittemore-Peterson Institute in collaboration with
the National Cancer Institute and the Cleveland Clinic, Judy
Mikovits, a lead researcher at the institute, said Tuesday.
"You can't claim to replicate a study if you don't do a single
thing that we did in our study," she said. "They skewed their
experimental design in order to not find XMRV in the blood."

The Whittemore-Peterson Institute issued a statement saying the
British study was published after only three days of review as
opposed to the institute study that underwent six months of
vigorous peer review plus confirmation by three independent
laboratories before it was published in Science magazine.

The statement also cited different techniques used in the British
study that make its conclusions meaningless, including the use of
a molecular plasmid control in water instead of a positive blood
sample. "They paid to have their study published in the Public
Library of Science, and it was then picked up by Science (magazine),"
said Mikovits said, who suspects insurance companies in the United
Kingdom are behind attempts to sully the findings of the Reno study.

She said the Whittemore-Peterson Institute has been flooded with
calls from patients with Chronic Fatigue Syndrome discouraged by the
conclusions made by McClure and her team. "They want to know if we
are going to give up because a few people are attacking us, but no,
we are not going to give up," Mikovits said. "We are still trying
to develop drugs to treat Chronic Fatigue Syndrome. That was our
goal, and nothing has changed."

The Whittemore-Peterson Institute continues to form new collaborations
with researchers who are trying to replicate its study, said Annette
Whittemore, president and founder of the institute. "Our goal has
always been to translate our research into diagnostics and therapeutics
for patients," she said. "We think XMRV is, at the very least, a
biomarker for a subset of patients with Chronic Fatigue Syndrome."

(c) 2010 Reno Gazette Journal

A doctor's observations on PLOS One

The dogma of the last 20 years has been created by the system that has had
control of "CFS/ME".

If Professor Wessely and his colleagues had no fear of finding XMRV in
patients with a diagnosis of Chronic Fatigue Syndrome then they would not be
frightened of using a selection criteria not used previously ie. the
Canadian Consensus Criteria.

If Lombardi et al were able to effectively utilise the Canadian Criteria as
they were then why were those at Imperial not allowed to use patients
selected the same way?

Surely if one wants to replicate a groundbreaking study with the best
possible source material then one would want to do things in accordance with

The only reason I can see for the failure to replicate the Lombardi patient
selection protocol is that those behind the patients selected for the
Imperial study were actually afraid of the outcome had they used the same
methods for selecting patients.

What other explanation can there be?

Sure it would have taken longer but then that would have prevented the rapid
publication but then again I was always told that if you wanted to do a job
well you should do it thoroughly regardless of rushing yourselves to get a
quick yet flawed result or outcome.

I guess for Imperial that did not come into their deliberations.....

Wessely, Cleare and Collier claim that their patients were not mental health
patients yet time and again Wessely, Cleare, White, Sharpe et al discuss
their patients in terms of mental health perpetuation and treat their
patients with CBT and Graded Exercise.

Two examples of exactly how the "Wessely School" demonstrate their beliefs
surrounding mental health and Chronic Fatigue Syndrome are given in my
previous e-mail that includes the PLOS One comments.

Another observation -

Why exactly were the same old patients chosen for this study?

Why were no severely affected patients chosen who have never had the luxury
of attending a clinic run by Professor Wessely or one of his colleagues?

The 25% ME Group have a membership list of prime candidates all severely
affected patients with G93.3 Myalgic Encephalomyelitis who are too ill to
take part in CBT and Graded Exercise.

Why exclude those too ill to be "regulars" at Professor Wessely's clinic and
why use patients already "screened" by Professor Wessely and his colleagues.

As there are potential conflicts of interest with the involvement of ANY
psychiatrists such as Cleare, Wessely, White, Sharpe et al, why accept a
study that has any involvement of any of the usual collaborators?

This may be unfair but on a very basic level, one XMRV positive patient
previously diagnosed with CFS is one less recruit for a CBT and Graded
Exercise session or indeed one less participant for the PACE trial.

So when are we going to get a genuine replication study that isn't tainted
by any interests that could possibly pollute or distort the outcomes?

Lombardi et al did their work diligently and produced their study over a
period of six months.

Lombardi et al tested their study over three centres of excellence to ensure

All of their work was vigorously assessed by those who published the study
in Science.

They did not on the other hand knock out a "quickie" study in an obscure
journal to grab some misleading news media headlines in the space of only a
few weeks.

If any UK study is to be worthy of any scientific credibility then it has to
be a genuine independent objective replication study with no conflicts of

It has to use the precise patient replication process employing Fukuda AND
the Canadian Consensus Criteria that was so apparently easy to employ by
Lombardi et al yet impossible and overly complicated to use here in the UK.

Why the complication - surely those wanting to get it right would want to
make an effort to do it right?

Any studies worth reading are also obliged to use the precise testing and
analysing protocols used by Lombardi et al. such as isolating the white
blood cells to concentrate the sample instead of diluting the samples by
only looking at whole blood.

Anything less would lead any scientist to wonder why a study has
deliberately chosen not to replicate.

Anything less than genuine replication is open to legitimate questions and
deconstruction including the motivations of those deliberately failing to
replicate when there is no real reason why they could not do so.

We live in interesting times and I have a feeling that this is not going to
be the first study from the UK, produced in association with psychiatrists
with vested interests where 0% of patients test using non-replication of
Lombardi et al find their results being plastered all over the media for
superficial but effective political gains at that.

Should we be surprised - absolutely not.


Stephen Ralph DCR(D) Retired.

* * *
Someone has noted that since the US researchers found XMRV in 4% of healthy controls, it should raise suspicion that the UK study claims 0% XMRV in either patients or controls.

Tuesday, January 12, 2010

Whittemore Peterson Institute researcher makes major breakthrough

'Whittemore Peterson Institute researcher makes major breakthrough in
Chronic Fatigue Syndrome'
By Nicole Frost. Photo by Theresa Good Medicine Danna-Douglas
Nevada Silver & Blue
Crippling disease may be linked to XMRV virus

Dr. Judy Mikovits, research director for the Whittemore Peterson
Institute at the University of Nevada, Reno, vowed in childhood to
find a cure for cancer following her grandfather's early death from
lung cancer. Although she has yet to accomplish that lofty goal, in
her quest to solve the riddle of one of the most pernicious and deadly
diseases known to humankind, she has fortuitously made a major
breakthrough in understanding the origins of Chronic Fatigue Syndrome,
a debilitating disease that affects more than one million people in
the United States.

In October, the Whittemore Peterson Institute announced that a
recently identified retrovirus called the "XMRV virus" had been linked
to the neuro-immune disease, Myalgic Encephalomyelitis/Chronic Fatigue
Syndrome (ME/CFS). An infection with XMRV virus was detected in 67 out
of 101 patients tested in the study.

Mikovits—whose patients affectionately call her "Dr. Judy"—along with
Whittemore Peterson Institute colleagues and collaborators from the
National Cancer Institute and the Cleveland Clinic, recently published
their groundbreaking findings in the journal, Science, one of the
world's leading journals of original scientific research, global news
and commentary.

Researchers speculate that XMRV infection of certain immune system
cells causes the chronic inflammation and immune deficiency that these
patients exhibit, thereby resulting in their inability to mount an
effective immune response to opportunistic infections.

"This is an incredibly significant discovery for those with Chronic
Fatigue Syndrome, and it has important implications for the world of
science and medicine," said University President Milton Glick.
"Scientific breakthroughs are often iterative, and a finding of this
magnitude can lead to additional discoveries and new research

In less than three years since she was hired as the research director
at the Whittemore Peterson Institute, Mikovits and her team have
identified a genetic susceptibility marker to Chronic Fatigue
Syndrome, developed a cytokine signature describing Chronic Fatigue
Syndrome as an inflammatory disease, produced a sensitive and accurate
test for coinfections, and described an abnormal number of pathogens
in this population. Taken together these biomarkers reveal the
significant number of biological challenges that ME/CFS patients face.

These unique findings led Mikovits to encourage her team to keep
looking for an underlying pathogen capable of producing the disease.
She enlisted the help of eminent retrovirologist, Dr. Frank Ruscetti
of the National Cancer Institute, Dr. Bob Silverman
of the Cleveland Clinic, Dr. Vincent Lombardi '06 Ph.D. (biochmeistry)
of the Whittemore Peterson Institute, and many other collaborators.
Since that time, Mikovits' team has found that more than two-thirds of
the samples are antibody positive.

This finding could be life-changing for the 17 million sufferers of
ME/CFS worldwide. It not only creates the strongest link to a
biological cause of disease in patients with ME/CFS but has
implications for an untold number of other diseases as well. The
discovery of XMRV as a human infectious pathogen may give rise to a
new field of medicine. Finding XMRV to be infectious and replicating
in blood samples supports the need for new diagnostic tools for its
detection, and the development of effective treatments to end the
destructive cycle of disease, including the cancers that patients
commonly suffer.

In contrast to HIV, which is a complex retrovirus, XMRV is a simple
retrovirus, making it an easier target for the development of a
preventative vaccine. "It's not going to be easy, but it's going to be
easier," to find a vaccine or drugs to target XMRV compared to HIV,
said Mikovits.

Mikovits spent more than 20 years at the National Cancer Institute in
Frederick, Md., earning her doctorate in biochemistry and molecular
biology and investigating mechanisms by which retroviruses dysregulate
the delicate balance of cytokines—secreted
substances that carry signals from cell to cell— in the immune
response. Later in her career there, her work helped in the
development of novel therapeutic agents for AIDS and AIDS associated
malignancies (Kaposi's sarcoma).

She agreed to work in Reno after attending a presentation by Dr.
Daniel Peterson, medical director of the Whittemore Peterson
Institute, in which he discussed an unusually large number of rare
cancers that occur in patients with long-standing Chronic Fatigue

"I met and talked to several patients and I became convinced that I
could help," Mikovits says. "I truly thought this work would not only
lead to the answers to these patients' illnesses, but it might also
lead us to the discovery of another new viral cause of cancer."

In addition, Mikovits was moved by talking to Annette Whittemore '74
(elementary education/special education), founder and president of the
Whittemore Peterson Institute, whose daughter, Andrea, has suffered
for many years from Chronic Fatigue Syndrome.

In the fall of 2006, the Whittemore Peterson Institute hired Mikovits
to lead a unique program of translational research. She began forming
a comprehensive research plan using her extensive background in
immunology and virology. Armed with this intriguing data, she began
contacting her many friends at the National Institutes of Health to
join in these efforts.

Mikovits realized that the field of neuroimmune disease lacked a
comprehensive biological research program that could answer the many
questions of patients and their doctors, but she faced longstanding
prejudice in the medical community against even recognizing Chronic
Fatigue Syndrome as a bona fide disease. "There's a significant lack
of federal funding and an institutional bias against biological
research of ME/CFS and other neuroimmune diseases, which has created
incredible hurdles to basic research for years," she says. "We believe
that situation will change with the knowledge of this important viral

Nonetheless, she engaged the world's best virologists, immunologists,
microbiologists, geneticists and epidemiologists. Using the latest
scientific technologies, which were acquired by the Whittemore
Peterson Institute through private and federal funding, she opened her
lab on the University campus and set the research program in motion.

"I have a strong team of the world's best scientists and the financial
support of the Whittemore Peterson Institute, coupled with the
University's supportive environment," she notes. "All of these factors
allowed us to begin our research without waiting years for a federal
grant to fund. I also work with a great team of young scientists from
this University, including Dr. Vincent Lombardi, Katy Hagen, Max
Miller and Dr. Isabel Silvestre."

Formally trained as a cell biologist, molecular biologist and
virologist, Mikovits has studied the immune response to retroviruses
and herpes viruses. In addition, she has coauthored more than 40
peer-reviewed publications that address fundamental issues of viral
pathogenesis, the production of blood cells and cytokine biology.

Ironically, Mikovits may soon realize her childhood dream of curing
cancer—since finding a cure for Chronic Fatigue Syndrome will also
cure the cancers associated with it—while also helping millions of
people who suffer from chronic neuro-immune diseases. When asked
what's next on her agenda, she says:

"In the world of science a new discovery brings more questions than
answers. We will continue our studies to determine what other diseases
are impacted by this virus and define the human immune defects related
to XMRV infection. I am also interested in codeveloping diagnostic
tools and new effective treatments. Many of these studies are already
underway in our lab. I tease Annette that I am going back to the beach
[Mikovits lived in Ventura, Calif. prior to moving to Reno]. But she
knows that I am committed to helping her find the answers for Andrea
and all the other patients before I leave."

Monday, January 11, 2010

Why Bright Light Worsens Migraine Headache Pain

Dr. Teicheira, Chronic Pain, and New Theories

Dr. Teicheira's theory on fibromyalgia is that it's caused by untreated pain; essentially, the nerves are trained to interpret every signal, even neutral ones, as pain, because the majority of the signals they receive are pain.  Teicheira would like to draw and quarter any doctor who tells a patient "just tough it out" rather than prescribing pain pills; since it took me 7 years between first request and finally getting the RX (while hearing every ridiculous excuse in the book), I'll gladly hold them down while he does the "surgery".
Just heard about a woman with a chronic pain condition whose doctor has the theory that by putting her in a medically-induced coma, he can re-boot the system and re-train the nerves.
Which is when it dawned on me that I'm still working on my July refill of Vicodin.  Apparently we've achieved the same thing without the hospitalization: got the nerves used to not feeling pain so now they only signal pain when I've actually done something stupid (like lift a 50-lb box), which is why I was looking at the date on the pill bottle. 

Was referring to these notes from a lecture I went to a few years ago, and  thought it was worth a re-visit here, too.

- - - - -

DAVID TEICHEIRA, M.D.   Sacramento Pain Clinic

"Pain is not well understood"

The International Association for the Study of Pain defines pain as: "An 
unpleasant sensory and emotional experience associated with actual or
potential  tissue damage, or described in terms of such damage"

ACUTE pain is an alarm system    nociceptive pain

nerve impulses are translated by the limbic system   if you  didn't have a
limbic system, you wouldn't have emotions

PERSISTENT pain is a complex state of mind that is the result of many 

people with chronic pain have trouble sleeping   stimulation of 
thalmic/limbic system

if severe pain is allowed to persist for more than 24 hours, neuroplastic  changes associated with the development of intractable chronic pain syndromes  are evident --  damaged mechano-receptor nerve grows over the nociceptor  nerve after 24-48 hours; the nociceptor atrophies.  -- This may be  permanent  
no one knows.

Referred pain uses the same set of nerves

Prescriptions do not take pain away, they just make it easier to ignore 
your pain

You only feel your pain when you're paying attention to it   when  you are
thinking about your pain, that's your cue to do ANYTHING ELSE

as a result of intense pain, neurons in the spinal cord that help to  prevent pain transmissions actually die.  At the same time,  pain-transmitting neurons grow more connectors to other nerves, become more  sensitive, and react more strongly to a painful stimulus

CFS/FMS deal abnormally with pain as a memory.  On a PET scan, the  brain is all lit up all the time.  The process is abnormal, but the pain is  real.

Chronic back pain patients lose 5-11% of their cortex.

Your brain can't tell the difference between chronic pain and new  injury  
flares are not damage indicators

He recommends work through the pain, but don't fight through the pain

muscle  relaxants
anti-neuropathic agents

Chronic pain is different   it's pathological

Neurontin wasn't a good seizure drug, but decreases rate of nerve firing,  no known long-term effects

morphine and other opiates are incredibly safe.

RX doesn't make the pain go away   there's a plateau where more  doesn't do
more   they're better than nothing

pseudo-addiction means you're undertreating   if patient asks for  more, it
usually means more works better

only two ways to entirely take away pain:
local  anesthetic
Saponin SP (for Substance P)   FDA approved only  for use on elderly
animals who'll die in a few days, because it kills all the  pain nerves   doing
this will cause more damage in the long run

distinct neurological pathways for acute vs. chronic pain

NNT   Number Needed to Treat   number of people who  need to take the drug
to get one to feel better
Neurontin's NNT is 3.4  = only 1/4 will get relief
Morphine's NNT is 8 = only 1 in 8 will get  relief
Ibuprofen's NNT is 5 = only 1/5 will get relief

both chronic pain and long term memory  require the NMDA pathway for
mice with poor memory didn't  develop chronic pain if they were deficient
but with 2x NMDA,  they had a great memory and developed chronic pain easily

intense pain can result in permanent changes in the Central Nervous System 
resulting in phantom pain   this can take years to develop

chronic pain does go away for most people
chicken pox ends up in  your RNA => shingles => nerve damage

reticular activating system   pain and sleep are connected

Devil's claw  extract   the most effective dosage for both osteoarthritis
and low  back pain is 50 mg of harpagophytum procumbens daily for at least
2-3  months
Bromelain   ananas comosus, pineapple   shown to  significantly decrease
Substance P release
Turmeric root   curcuma  longa   1125 to 2500 mg/day
Omega 3 fatty acids   salmon,  halibut, cod, herring, mackerel and tuna,
flax seeds, canola oil and  walnuts   1200 to 2400 mg daily

Research links pain sensitivity to gene   Johns Hopkins  neuroscientist
George R. Uhl, M.D., Ph.D.

The symptoms of  fibromyalgia may be the result of a central nervous system
that "remembers" pain  sensations for an abnormally long time, according to
research presented at the  American College of Rheumatology Annual
Scientific Meeting in  Philadelphia.  Fibromyalgia affects about 2% of the US

Researchers at the University of Florida applied heat stimuli to the hands 
of healthy controls and fibro patients.  Fibro patients experienced 
CUMULATIVE pain, indicating abnormalities in spinal cord pain processing, and 
RESIDUAL pain when the stimuli were applied at intervals.  Researchers  found
that the residual pain experienced by fibromyalgia patients was widespread 
and not limited to a single area of the body.

"Because the effect of the first experimental stimulus does not rapidly 
decay in fibromyalgia patients, the effect of subsequent stimuli adds to the 
first, and so on, resulting in ever increasing pain sensations," said lead 
investigator Roland Staud, M.D.  "Our findings provide evidence for 
abnormal central nervous system mechanism of pain in fibromyalgia patients and 
have significant implications for future therapies, which need to target these 
abnormal central pain mechanisms."