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Co-Cure Weekly Digest of research and medical posts only - 9 Apr 2007 to 16 Apr 2007

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Date:    Wed, 11 Apr 2007 13:56:30 -0400
From:    Co-Cure Moderator <ray CO-CURE.ORG>
Subject: NOT,MED: Dale Guyer, MD, Discusses the Integrative and Molecular Treatment of Chronic Fatigue Syndrome and Fibromyalgia

Dr. Dale Guyer, MD, is a family physician and the Director of The Advanced
Medical Center located in Indianapolis, Indiana, where patients are offered
a unique blend of traditional and integrative therapies for a number of
health-related issues, with a focus on ME-CFS and FM.

In the following Q&A Dr. Guyer explains his holistic, evidence-based
approach to testing and treatment - which involves use of selected
pharmaceutical drugs as an additive to appropriate nutritional support and
other measures "to normalize a complex internal bio-chemical milieu."

Question: Dr. Guyer, do you see many patients with Chronic Fatigue Syndrome
and Fibromyalgia?

Dr. Guyer: Yes, I have seen probably several hundred patients who have been
given this diagnostic category.

Q: How do you go about treating a patient with a weakened immune system?

Dr. Guyer: Generally, these individuals require a detailed laboratory
analysis to evaluate what components of their immune system are out of
balance. For example many individuals have depleted Natural Killer Cell
Function and imbalances in the TH1 and the TH2 immune responses.
Additionally I like to see a baseline analysis for RNase-L, apoptosis,
2-5A-Synthetase, alpha-interferon, and associated lab work to get a more
complete picture.
Ultimately, strategies to improve immune system function would include
anything that supports overall body health. An essential focus, in my
experience, is to identify chronic infections and work to reduce immune
burden - either with nutraceutical or anti-infective medication as
clinically warranted.

I also rely heavily on natural immune modulators such as transfer factor,
probiotics,** and immune supporting herbals.

Read the complete Q&A at

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Date:    Wed, 11 Apr 2007 14:07:12 -0400
From:    Fred Springfield <fredspringfield VERIZON.NET>
Subject: RES: The chronic fatigue syndrome - an update

The chronic fatigue syndrome - an update.

Journal: Acta Neurol Scand Suppl. 2007;187:7-14.

Author: Wyller VB.

Affiliation: Department of Pediatrics, Rikshospitalet-Radiumhospitalet
Medical Centre, Oslo, Norway.

NLM Citation: PMID: 17419822

Background - In this article, current scientific knowledge on the chronic
fatigue syndrome (CFS) is reviewed. The US case definition of CFS (the
CDC-definition) is most widespread in research and clinical practice.
Estimates of prevalence vary from 0.2% to above 2%. The female-male ratio
is approximately 3:1.

Clinical Features - Severe fatigue is the dominating complaint; it is
worsened from exertions and not substantially relieved by rest. In
addition, the patients might have a varying combination of accompanying
symptoms. Clinical evaluation should be based upon standardized guidelines,
including an assessment of functional impairments.

Pathophysiology - The pathophysiology should be interpreted within a
biopsychosocial framework. Present knowledge suggests that certain genetic
polymorphisms and personality traits might be regarded as predisposing
factors, some infections and severe psychosocial stress constitute
precipitating factors, whereas disturbances of immunity, skeletal muscle,
cognitive abilities, endocrine control and cardiovascular homeostasis are
possible perpetuating factors.

Treatment - Cognitive behavioural therapy and graded exercise therapy are
of proven value in randomized controlled trials. Several pharmaceutical
measures have been explored and found to have no beneficial effect. Most
patients might expect long-term improvement, but full recovery is rare;
however, the prognosis is better among adolescents.

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Date:    Thu, 12 Apr 2007 12:47:08 -0400
From:    Fred Springfield <fredspringfield VERIZON.NET>
Subject: RES: Is a full recovery possible after cognitive behavioural therapy for chronic fatigue syndrome?

Is a full recovery possible after cognitive behavioural therapy for chronic
fatigue syndrome?

Journal: Psychother Psychosom. 2007;76(3):171-6.

Authors: Knoop H, Bleijenberg G, Gielissen MF, van der Meer JW, White PD.

Affiliation: Expert Centre Chronic Fatigue, Radboud University Nijmegen
Medical Centre, Nijmegen, The Netherlands.

NLM Citation: PMID: 17426416

Background: Cognitive behavioural therapy (CBT) for chronic fatigue
syndrome (CFS) leads to a decrease in symptoms and disabilities. There is
controversy about the nature of the change following treatment; some
suggest that patients improve by learning to adapt to a chronic condition,
others think that recovery is possible. The objective of this study was to
find out whether recovery from CFS is possible after CBT.

Methods: The outcome of a cohort of 96 patients treated for CFS with CBT
was studied. The definition of recovery was based on the absence of the
criteria for CFS set up by the Center for Disease Control (CDC), but also
took into account the perception of the patients' fatigue and their own
health. Data from healthy population norms were used in calculating
conservative thresholds for recovery.

Results: After treatment, 69% of the patients no longer met the CDC
criteria for CFS. The percentage of recovered patients depended on the
criteria used for recovery. Using the most comprehensive definition of
recovery, 23% of the patients fully recovered. Fewer patients with a
co-morbid medical condition recovered.

Conclusion: Significant improvement following CBT is probable and a full
recovery is possible. Sharing this information with patients can raise the
expectations of the treatment, which may enhance outcomes without raising
false hopes.

Copyright (c) 2007 S. Karger AG, Basel.

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Date:    Thu, 12 Apr 2007 18:49:03 -0400
From:    "Chris Hunter" <chunter ahmf.org> [via Co-Cure Moderators]
Subject: Res: Autopsy protocols/tissue bank for ME/CFS

Alison Hunter Memorial Foundation

"The startling truth is that some of the most conspicuous spokespeople for science
horribly misrepresent it: .  We have been treated again and again to the stock phrase
"there is no evidence that."  I have never heard anyone add: "But
absence of evidence does not mean evidence of absence" Without that codicil we do not have
the whole truth"

- Colin Tudge  "Physicist heal thyself. Science isn't arrogant , but
(exerpt Australian Financial Review 2/4/2001: reprint from New

Both 1996 and 1999 CFS Peer Reviews for the Centres for Disease Control
CDC recommended the establishment of a CFS patient brain bank for "neuropathological
analysis for central nervous system tissues not available by other mechanisms". When
referred to this recommendation at the 2004 Madison, Wisconsin IACFS Conference, Dr William
Reeves said this would be undertaken "immediately". Dr Susan Vernon expanded on
the idea of Tissue Repository Centers in her presentation
"The feasability and acceptance of a CFS Research Network".
In 2007 while there has been no action to implement the recommendations,
research into coping styles, lifetime stressors and fatiguing illnesses appear to have
taken priority for the CDC.

In 1996 the interest of the University of NSW CFS research team
under the direction of Professors Dennis Wakefield, Andrew Lloyd and Ian Hickie
was expressed "to receive tissue for research study from patients who die having suffered
from chronic fatigue syndrome. In particular our interest would be in studying the brain
as it is this organ which we believe to be the critical site in which the unknown disease
process is most likely to occur."

Yet this team has been amongst those most conspicuous in the field of ME/CFS publications
with their promotion of "there is no evidence  .." without the codicil.
They have encouraged speculative hypotheses with regard to belief systems, and somatisation
in those severely affected. Where is the science? Where is accountability?

Julie Robotham writes in the Sydney Morning Herald  - Health and Science
article Thursday 12 April
"The development of an autopsy protocol may help unlock some of the
mysteries of chronic fatigue syndrome"


Chris Hunter
chunter ahmf.org
www.ahmf.org <http://www.ahmf.org/>

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Date:    Thu, 12 Apr 2007 14:51:51 -0400
From:    "Bernice A. Melsky" <bernicemelsky VERIZON.NET>
Subject: RES: Treatment of cervical myelopathy in patients with the fibromyalgia syndrome: outcomes and implications

Treatment of cervical myelopathy in patients with the fibromyalgia
syndrome: outcomes and implications.

Eur Spine J. 2007 Apr 11; [Epub ahead of print]

Heffez DS, Ross RE, Shade-Zeldow Y, Kostas K, Morrissey M, Elias DA, Shepard A.

Chicago Institute of Neurosurgery and Neuroresearch Medical Group, Chicago,

PMID: 17426987

Some patients with fibromyalgia also exhibit the neurological signs of
cervical myelopathy. We sought to determine if treatment of cervical
myelopathy in patients with fibromyalgia improves the symptoms of
fibromyalgia and the patients' quality of life.

A non-randomized, prospective, case control study comparing the outcome of
surgical (n = 40) versus non-surgical (n = 31) treatment of cervical
myelopathy in patients with fibromyalgia was conducted. Outcomes were
compared using SF-36, screening test for somatization, HADS, MMPI-2 scale 1
(Hypochondriasis), and self reported severity of symptoms 1 year after

There was no significant difference in initial clinical presentation or
demographic characteristics between the patients treated by surgical
decompression and those treated by non-surgical means. There was a striking
and statistically significant improvement in all symptoms attributed to the
fibromyalgia syndrome in the surgical patients but not in the non-surgical
patients at 1 year following the treatment of cervical myelopathy (P </=
0.018-0.001, Chi-square or Fisher's exact test). At the 1 year follow-up,
there was a statistically significant improvement in both physical and
mental quality of life as measured by the SF-36 score for the surgical
group as compared to the non-surgical group (Repeated Measures ANOVA P <
0.01). There was a statistically significant improvement in the scores from
Scale 1 of the MMPI-2 and the screening test for somatization disorder, and
the anxiety and depression scores exclusively in the surgical patients
(Wilcoxon signed rank, P < 0.001).

The surgical treatment of cervical myelopathy due to spinal cord or caudal
brainstem compression in patients carrying the diagnosis of fibromyalgia
can result in a significant improvement in a wide array of symptoms usually
attributed to fibromyalgia with attendant measurable improvements in the
quality of life. We recommend detailed neurological and neuroradiological
evaluation of patients with fibromyalgia in order to exclude compressive
cervical myelopathy, a potentially treatable condition.

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Date:    Thu, 12 Apr 2007 09:47:22 -0700
From:    Steven Du Pre <isaiah40 SONIC.NET>
Subject: NOT, MED: Interview with Dr. Peterson, Judy A. Mikovits, Anne Whittmore Re: upcoming Center for Excellence in Nevada

    You can view this short interview at the website.  The research
director & Dr. Peterson have found that there is a percentage
of patients who come down with viral-induced cancers with this
disease, Myalgic Encephalomyelitis/CFS, due to derangements of
the immune system.   Since one of the three leading causes of
death for Myalgic Encephalomyelitis/CFS is cancer , this is an
important finding that has not come to full attention in the
American public because of the ignorance of the public
agencies involved here in the US .
     Here's the information on the interview:

There is a research center for M.E. /CFS being built on the
campus of the University of Nevada, Reno. Here's a link to a
interview done with Anne Whittemore, and longtime CFIDS
doctor/researcher Dan Peterson.
Annette F. Whittemore, Founding Director -
Whittemore/Peterson Institute for Neuro-Immune Disease
 Dr Daniel L. Peterson M.D., Medical Director
Judy A. Mikovits, PH.D, Research Director
The Center is scheduled for completion 2008-2009.


Steven Du Pre
Poetry website: http://www.angelfire.com/poetry/soareagle/index.html
"By words the mind is winged."  Aristophanes
Website for National Alliance for Myalgic Encephalomyelitis:

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Date:    Fri, 13 Apr 2007 20:35:18 +0900
From:      http://www.cfids-cab.org/rc/Nicolson-1.pdf

Some of his articles was posted to the Co-Cure
last year I believe but, I can not find them.

Hope this helps.

Thanx for Ray, one of the Co-Cure moderators,
for finding the location of the original
article above.

Hang in there.
Rika Kageyama

Tokyo, Japan
[CFS+RP since 1979]

*CFS: Chronic Fatigue Syndrome
*RP: Relapsing Polychondritis

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Date:    Fri, 13 Apr 2007 13:21:41 -0400
From:    "Jill McLaughlin <jillmclaughlin comcast.net> via Co-Cure Moderator"
Subject: NOT,MED: Victims give clues to the answers - Sydney Morning Herald - April 12, 2007


The Sydney Morning Herald

Victims give clues to the answers

April 12, 2007

The development of an autopsy protocol may help unlock some of the
mysteries of chronic fatigue syndrome, writes Julie Robotham.

UNDER the microscope, it could not have been clearer. Sophia Mirza's brain
and spinal fluid showed indisputable evidence of inflammation and cell death.

The discovery, by the neurologist Abhijit Chaudhuri and a neuropathologist
colleague, marked the first time a serious abnormality confined to the
central nervous system had been identified at the post-mortem examination
of a patient whose principal diagnosis was chronic fatigue syndrome.

In turn, that ensured the 32-year-old became the first person in Britain to
have the syndrome - also known as myalgic encephalomyelitis - recorded as
the cause of her death.

In Adelaide last month, Chaudhuri and specialists from all over the world
took the first steps towards developing an autopsy protocol that would
allow samples to be consistently collected and analysed from the bodies of
people who die, like Mirza, after a long battle with the syndrome. These
would form the basis of an international tissue bank in an attempt to shed
light on what goes wrong in the baffling condition, which often strikes
young and previously healthy individuals. It could help "establish the
condition as a valid neurological problem", Chaudhuri says, and might lead
to treatments.

Chaudhuri, a consultant neurologist from the Essex Centre for Neurological
Sciences, says the protocol is intended to allow non-specialist
pathologists to collect and preserve samples, which could then be examined
by a neuropathologist. The move comes amid concern that brain and spinal
cord tissues which might shed light on the disorder are being lost because
pathologists do not appreciate their significance.
In Mirza's case, and in another autopsy on a young British man, "there was
no way [their illness] could be explained by a primary psychiatric
condition", Chaudhuri says, referring to a widespread assumption that the
condition - which typically begins after a viral illness and is estimated
to affect up to 140,000 Australians - is related to mental stress.

Daniel Peterson, an American physician who specialises in chronic fatigue
syndrome, says its name has allowed it to be trivialised. "These are very
complex patients to understand," he says. "We've been held back by biases."
Peterson, who is establishing a research centre at the University of
Nevada, says he is most interested in forms of the condition that arise
after recognised infections, which seem to trigger immune disturbances.
The specialists' meeting in Adelaide was organised by Christine Hunter, via
the Alison Hunter Memorial Foundation, which Hunter formed after the death
a decade ago of her teenage daughter, who had chronic fatigue syndrome. As
the protocol is formalised, the group will seek endorsement from experts
around the world, she says, to accelerate its acceptance by the wider
medical community.

Elizabeth Salisbury, a senior staff specialist in tissue pathology at Royal
North Shore Hospital, says formal guidelines would encourage those
conducting autopsies to retain appropriate tissues for later genetic,
antibody or biochemical testing.

"One of the difficulties with a disease like CFS is [it] is very much an
emerging science," says Salisbury, who is not involved in the protocol's
development. "We don't necessarily understand all the pathological changes
that account for the signs and symptoms."

Salisbury says families of patients who die after having chronic fatigue
syndrome or other complex, elusive disorders usually support tissue
removal. "They really do want the answers," she says.

Colin Neathercoat, a director of the advocacy group ME/CFS Australia, says
the cost of supporting patients with long-term disability from the syndrome
is enormous, and more funding is needed for research into its origins and
possible treatments.

"We would desperately like to see government engage in this growing problem
and recognise its impact on the Australian economy, let alone its impact on
sufferers," he says.

[Return to top]


Date:    Fri, 13 Apr 2007 13:46:42 -0400
From:    "Bernice A. Melsky" <bernicemelsky VERIZON.NET>
Subject: RES: Accelerated Brain Gray Matter Loss in Fibromyalgia  Patients: Premature Aging of the Brain?

Accelerated Brain Gray Matter Loss in Fibromyalgia Patients: Premature
Aging of the Brain?

J Neurosci. 2007 Apr 11;27(15):4004-4007.

Kuchinad A, Schweinhardt P, Seminowicz DA, Wood PB, Chizh BA, Bushnell MC.

McGill Centre for Research on Pain, Department of Neurology and
Neurosurgery, and Department of Anesthesia and Faculty of Dentistry, McGill
University, Montreal, Quebec, Canada H3A 2B2, and GlaxoSmithKline,
Addenbrooke's Centre for Clinical Investigation, Addenbrooke's Hospital,
Cambridge CB2 2GG, United Kingdom.

PMID: 17428976

Fibromyalgia is an intractable widespread pain disorder that is most
frequently diagnosed in women. It has traditionally been classified as
either a musculoskeletal disease or a psychological disorder. Accumulating
evidence now suggests that fibromyalgia may be associated with CNS

In this study, we investigate anatomical changes in the brain associated
with fibromyalgia. Using voxel-based morphometric analysis of magnetic
resonance brain images, we examined the brains of 10 female fibromyalgia
patients and 10 healthy controls.

We found that fibromyalgia patients had significantly less total gray
matter volume and showed a 3.3 times greater age-associated decrease in
gray matter than healthy controls. The longer the individuals had had
fibromyalgia, the greater the gray matter loss, with each year of
fibromyalgia being equivalent to 9.5 times the loss in normal aging. In
addition, fibromyalgia patients demonstrated significantly less gray matter
density than healthy controls in several brain regions, including the
cingulate, insular and medial frontal cortices, and parahippocampal gyri.

The neuroanatomical changes that we see in fibromyalgia patients contribute
additional evidence of CNS involvement in fibromyalgia. In particular,
fibromyalgia appears to be associated with an acceleration of age-related
changes in the very substance of the brain. Moreover, the regions in which
we demonstrate objective changes may be functionally linked to core
features of the disorder including affective disturbances and chronic
widespread pain.

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Date:    Sat, 14 Apr 2007 21:18:43 +0200
From:    "Dr. Marc-Alexander Fluks" <fluks COMBIDOM.COM>
Subject: RES,NOT: Is a Full Recovery Possible after CBT for CFS ?

Source: Psychotherapy and Psychosomatics
        Vol. 76, #3, pp 171-176
Date:   April 2007
URL:    http://www.karger.com/pps


Is a Full Recovery Possible after Cognitive Behavioural Therapy for Chronic
Fatigue Syndrome?
Hans Knoop(a), Gijs Bleijenberg(a), Marieke F.M. Gielissen(a) Jos. W.M. van
der Meer(b), Peter D. White(c)
a Expert Centre Chronic Fatigue and
b Department of Internal Medicine, Radboud University Nijmegen Medical Centre,
  Nijmegen, The Netherlands;
c Department of Psychological Medicine, Barts and the London
  Queen Mary School of Medicine and Dentistry, London, UK
H. Knoop Expert Centre Chronic Fatigue, Radboud University Nijmegen Medical
Centre POB 9011 NL-6525 EC Nijmegen (The Netherlands) Tel. +31 243610030, Fax
+31 243610041, E-Mail j.knoop nkcv.umcn.nl


Cognitive behavioural therapy (CBT) for chronic fatigue syndrome (CFS) leads
to a decrease in symptoms and disabilities. There is controversy about the
nature of the change following treatment; some suggest that patients improve
by learning to adapt to a chronic condition, others think that recovery is
possible. The objective of this study was to find out whether recovery from
CFS is possible after CBT.

The outcome of a cohort of 96 patients treated for CFS with CBT was studied.
The definition of recovery was based on the absence of the criteria for CFS
set up by the Center for Disease Control (CDC), but also took into account
the perception of the patients' fatigue and their own health. Data from
healthy population norms were used in calculating conservative thresholds for

After treatment, 69% of the patients no longer met the CDC criteria for
CFS. The percentage of recovered patients depended on the criteria used for
recovery. Using the most comprehensive definition of recovery, 23% of the
patients fully recovered. Fewer patients with a co-morbid medical condition

Significant improvement following CBT is probable and a full recovery is
possible. Sharing this information with patients can raise the expectations
of the treatment, which may enhance outcomes without raising false hopes.

Key Words

Chronic fatigue syndrome, recovery Cognitive behavioural therapy, outcome


Between 50 and 70% of the patients show a significant reduction of symptoms
and disabilities after cognitive behavioural therapy (CBT) for chronic
fatigue syndrome (CFS) [1, 2]. The nature of this improvement is uncertain.
Some suggest that patients improve by adapting better to a chronic condition,
while others think that recovery is possible [3]. This debate shows some
similarities to the issue of recovery from mood disorders [4, 5].

The attitude of the therapist towards the treatment goals will affect the
expectations and perceptions of the patient. If learning to cope with CFS is
the jointly agreed maximal goal of treatment, patients will engage with
treatment accordingly. If the therapist suggests that recovery is possible,
the patient expectations are raised, which in turn may lead to a change in
the perception of symptoms as well as disability. This is also the essence of
the placebo response. The placebo response of CFS patients to psychological
interventions is lower than that related to biomedical interventions and
lower than that expected in other medical conditions [6], suggesting that
CFS patients are sceptical of psychological interventions. Since the
communication of the aim of a treatment is an intervention that can
facilitate change [7], the controversy about the nature of improvement is
clinically important.

To find out the tenable goal of therapy-adaptation or recovery - a
definition of recovery is needed that can be operationalized and measured. We
propose that a definition is used that closely follows the Center for Disease
Control (CDC) criteria for CFS [8]. Two key elements of the CDC criteria are
that a patient is severely fatigued and disabled. Recovery then implies that
the patient's level of fatigue is within the range of healthy controls. We
propose operationalizing this criterion as scoring within the range of the
mean plus (or minus) 1 standard deviation (SD) of the healthy population.

A second aspect of recovery is that a patient will no longer be disabled.
This means that patients have no physical disabilities - an often used
criterion in CFS - and no disabilities in any other domains of functioning.
Again, we propose scoring within the range of the mean plus 1 SD of the
healthy population as the criterion for recovery. Although patients who are
no longer abnor- mally fatigued or disabled do not meet the CDC criteria for
CFS, having a 'normal' level of fatigue and not being disabled is a more
satisfactory definition of recovery.

For complete recovery the perception of the patient also has to change. The
patient has to perceive his fatigue and functioning as both normal and
comparable to healthy people. Finally, a comprehensive definition combines
changes in fatigue, disability and perception.

The objective of this study was to find out whether recovery is possible
after CBT. For this, we collected data from a cohort of patients treated with
CBT. For comparison we used healthy population norms. By doing this, we
assumed that CFS was the only health problem of the patients. However, it is
possible that the patient had another medical condition beside CFS, causing
disability. Therefore, we measured the confounding effect of co-morbid
medical conditions on the outcome.


All consecutive patients with CFS that were treated with CBT at the Radboud
University Nijmegen Medical Centre between September 2003 and May 2005 were
eligible for the study if they met the following inclusion criteria:
1 CDC criteria for CFS [8];
2 severely fatigued and functionally impaired, defined by a cut-off score of
  35 or higher on the fatigue severity subscale of the Checklist Individual
  Strength (CIS-fatigue) [9] and a weighted score of 700 or higher on the
  Sickness Impact Profile (SIP) [10];
3 completed the pre- and post-treatment assessment. If a medical co-morbidity
  was present which could not explain the fatigue, it was registered for
  further analyses.

All patients received CBT for CFS according to a protocol described elsewhere

The assessment was part of the clinical routine and performed by research
assistants not involved in the treatment.

Self-Reported Improvement
Self-rated improvement was measured after treatment by one question: patients
indicated whether they had no symptoms, significantly fewer symptoms, the
same complaints or whether the symptoms had become worse [12].

The different definitions of recovery are summarized in table 1. The
CIS-fatigue indicates the level of experienced fatigue over the past 2-week
period and consists of 8 items on a 7-point scale. The score can range
between 8 and 56 [9]. A normal group of 53 healthy adults with a mean age of
37.1 (SD 11.5) has a mean score on the CIS-fatigue of 17.3 (SD 10.1). Using
this as a reference for the CBT group, there resulted a threshold score of
27, the mean plus 1 SD [13].

Physical disabilities were measured with the 'physical functioning' subscale
of the Medical Outcomes Survey Short Form-36 (SF-36) [14, 15]. The scores
range from 0 (maximum physical limitations) to 100 (ability to do vigorous
activity). Healthy adults without a chronic condition [16] were used as a
norm group, with a mean score of 93.1 (SD 11.7). A patient had to score 80 or
higher to be considered as recovered.
Social functioning was measured with the subscale 'social functioning' of the
SF-36, ranging between 0 (no social activities) and 100 (normal
participation in social activities). Using the same criterion and reference
group as above resulted in a threshold score for recovery of 75 or higher.
The SIP measures functional disability in ambulation, home management,
mobility, alertness behaviour, sleep/rest, work limitations, social
interactions, recreation and pastimes. The eight subscales were added to
provide one weighted score of disability (SIP8 total). The mean SIP8 total
score of a healthy group of 78 women is 65.5 (SD 137.8) [17]. Recovery was
defined as scoring the same or lower than the mean plus 1 SD of this
reference group, i.e. scoring 203 or lower.

Combining Fatigue and Disabilities
This definition of recovery was operationalized by combining cut-off scores
on SF-36 physical functioning and the CIS-fatigue.

Perception of Health and Fatigue
Health perception was assessed with the scale 'general health perception' of
the SF-36. This scale measures the evaluation of the health status by a
patient, with scores ranging between 0 and 100. The mean in the reference
group was 80 (SD 14.5) resulting in a cut-off score of 65.
The perception of fatigue was assessed with the Fatigue Quality List (FQL).
The FQL consists of 18 adjectives and patients pick which adjectives best fit
their experience of fatigue. Factor analysis showed a 4-factor solution; 3 of
the 4 factors have negative connotations of fatigue: 'frustrating',
'exhausting' and 'frightening'. About 97% of the untreated CFS patients
scored on 1 or more of the 3 factors [Gielissen et al., unpubl. data].
Recovery was defined as no longer scoring on any of the 3 negative factors.

Combining Fatigue, Disabilities and Perception
This comprehensive definition of recovery was operationalized by combining
the cut-off scores on the CIS-fatigue, the SF-36 scales of physical
functioning and social disabilities, the general health perception and the


Baseline Data
Of the 112 CFS patients with a pre-treatment assessment, 3 (3%) did not start
with CBT. There were 13 drop-outs (11% of the patients starting with therapy)
during treatment, so 96 patients completed the pre- and posttreatment
assessment. The mean age of this group was 37.0 years (SD 11.5). Seventy-three
patients were women (76%). The mean duration of the illness was 70.8 months
(range 12­276 months, SD 52.8).

Treatment Results
Table 2 shows the scores of the patients before and after treatment.
Following treatment, 73 (77%) of the 95 patients, who rated their improvement
(data were missing for 1 patient), reported that they had no or significantly
fewer symptoms. There was a significant decrease in CIS-fatigue and patients
also reported significantly fewer disabilities on the SF-36 subscale physical
functioning and the SIP8. In total, 66 patients (69%) no longer met the
inclusion criteria for fatigue severity and the level of disabilities (SIP8 6

Full Recovery as Outcome
The percentage of recovered patients was determined for all criteria and
ranged between 23 and 59% (table 3).

The Effect of Medical Co-Morbidity
Twenty-two of the 96 patients (23%) had a medical comorbid condition beside
CFS. Fifteen patients had one medical co-morbidity: treated hyperthyroidism,
gonadal dysgenesis with normal karyotype, menorrhagia, controlled diabetes
mellitus, quiescent ulcerative colitis, ne- phrotic syndrome, controlled
asthma, allergy (2), recurrent sinusitis, epilepsy, migraine, periodic leg
movement disorder, multiple traumas, intramedullary haemangioma on
medication. Seven patients had two co-morbidities: treated hyperthyroidism
and epilepsy, controlled diabetes mellitus and Forestier's disease,
controlled asthma and chronic low back pain (2), allergy and treated sleep
apnoea, single transient ischaemic attack and cervical arthrosis, chronic
headache and treated high blood pressure. After CBT, patients with medical
co-morbidity had a mean CIS-fatigue score of 35.8 (SD 13.7) compared to a
mean CIS-fatigue score of 28.6 (SD 14.0) for the group without (t=2.15,
d.f. 94, p=0.034). The group with medical co-morbidity also had more SIP
disabilities following CBT, compared to the group without co-morbidity
(t=2.22, d.f. 94, p=0.029). The SIP8 total mean scores were 934 (SD 563) and
607 (SD 739), respectively. The SF-36 physical functioning following
treatment was lower in the group with co-morbidity [mean of 66 (SD 27.9) and
80 (SD 20.4), respectively; t=2.46, d.f. 94, p=0.016]. Fewer patients
with medical co-morbidity recovered (table 4). For social disability, the
perception of fatigue, and the combination of all criteria for recovery, the
difference in the proportions of recovered patients failed to reach
statistical significance.


More than 70% of the CFS patients reported significantly fewer symptoms
following treatment with CBT and roughly 70% no longer met the CDC criteria
for CFS. This favourable outcome is consistent with the results of earlier
controlled studies [1, 2].

Improvement and not meeting research criteria for an illness are different
from recovering [18, 19]. To examine if recovery was possible we used
different definitions of recovery that encompassed three elements: no longer
being severely fatigued, being able to resume all activities, and a
perception of health and fatigue that is similar to the perception of healthy
persons. Depending on the definition used, up to 59% of the patients
recovered. Even if we used the most conservative definition of recovery, 23%
fully recovered. We therefore conclude that recovery from CFS following CBT
is possible.

In the absence of a control treatment group, it is difficult to attribute
this effect to treatment with certainty. A comparison with the natural course
of CFS provides some useful information. In a review [20] that used less
stringent criteria for recovery, the median recovery rate without treatment
was 5% of the patients meeting operational criteria for CFS. As expected, the
recovery rates following CBT found in this study were substantially higher.
Our study was only concerned with the short-term effects of treatment. The
only controlled study investigating the long-term efficacy of CBT for CFS
showed lasting benefits 5 years after treatment [21].

Some may argue that it is not possible to recover from CFS and that our
recovered patients were misdiagnosed. We found no evidence to support this,
with all patients meeting CDC criteria for CFS. Ninety-one of our 96 patients
complained of post-exertional malaise, which some suggest is the main
characteristic feature of CFS [22].

The criteria for recovery were based on healthy norms. Patients had to score
within the range of the mean plus or minus 1 SD. The norm groups were
selected for their good health. Assuming a normal distribution, this means
that 15% of the healthy subjects (scoring between 1 and 2 SD beyond the mean)
had a score that would be considered as deviant from the norm in the present
study. One could say that a patient meeting these criteria not only recovered
from CFS, but is also more healthy than a sub- stantial part of the healthy
general public. Thus, the effect of CBT may be underestimated.

In determining the threshold scores for recovery we assumed a normal
distribution of scores. However, in the healthy population the SIP and SF-36
scores were not normally distributed. Therefore one could argue that recovery
according to the SIP8 has to be defined as scoring the same or lower than the
85th percentile of the healthy reference group. In that case, the recovery
rate using the definition of having no disabilities in all domains (i.e.
scoring the same or lower than the 85th percentile on the SIP8) would
decrease from 26 to 20%. As we do not know the exact distribution of the
SF-36 scores, we cannot control for the effects of violation of the
assumption of normality.

Patients with medical co-morbidities had significantly higher levels of
disabilities after treatment. This implies that less stringent criteria for
recovery should be used that incorporate the effect of the co-morbidity.
Using healthy adults as a reference group will lead to an underestimation of
the effect of CBT in those with medical co-morbid conditions.

The fact that fatigue, disability and health can return to a 'normal' level
following treatment is a promising finding. Keeping in mind that most
patients suffered several years of ill health, it is remarkable that such a
change in perception can take place. These results suggest that recovery
after CBT may be possible when it is applied to other related disorders for
which CBT has been found to be helpful, such as fibromyalgia [23].

The first clinical implication of the present study is that a therapist
delivering CBT can tell the patient that substantial improvement is likely to
occur and that full recovery is possible. By communicating this, the
therapist can counterbalance factors that lower the expectations of the
patient. Examples of such factors are a negative attitude of certain patient
advocacy groups towards behavioural interventions or an oversolicitous
attitude of significant others in response to CFS [24]. There is empirical
evidence that lower expectations of patients have a negative influence on
therapy outcome [25]. The second clinical implication of the present study
is that recovery is a construction. The percentage of recovered patients
differed depending on the definition of recovery used. It is possible that a
patient has another concept of recovery than the therapist. It is important
that they jointly (re)formulate a definition which forms the objective of the


Table 1. Operationalization of the different definitions of recovery
Definition of recovery            Measure                     Criterion used    Cut-off
Level of fatigue comparable       CIS-fatigue                 Mean + 1 SD       =<27
   to healthy people
No physical disability            SF-36 physical              Mean - 1 SD       >=80
No social disability              SF-36 social                Mean - 1 SD       >=75
No disabilities in all domains    SIP8 total                  Mean + 1 SD       =<203
Normal fatigue and no physical    CIS-fatigue, SF-36 physical Mean + 1 SD,      =<27, >=80
   disability                                                 mean - 1 SD
Normal health perception          SF-36 general health        Mean - 1 SD       >=65
No negative perception of fatigue FQL                         Factor score
                                                              negative = 0
Combining criteria of
 Fatigue                          CIS-fatigue                 Mean + 1 SD        =<27
 Physical and social disabilities SF-36 physical and social   Mean - 1 SD        >=80, >=75
 Perception of health             SF-36 general health        Mean - 1 SD        >=65
 Perception of fatigue            FQL                         Factor score
                                                              negative = 0
Mean = Mean of healthy norm group.

Table 2. Pre- and post-treatment scores of CIS-fatigue, SF-36 physical and SIP8 total (n=96)
                 Pre-treatment  Post-treatment  Treatment  95% CI         t    d.f.  p value
                 mean           mean            effect                    value
Self-rated                      77
  improvement, %
CIS-fatigue      50.0 p/m 5.2   30.3 p/m 14.0   -19.7      -16.8 to -22.6 -13.6  95  <0.001
SF-36 physical   51.8 p/m 19.1  76.3 p/m 23.0    24.5       19.1 to 29.8    9.1  94  <0.001
SIP8 total       1,448 p/m 510  682 p/m 619     -766       -631 to -900   -11.3  95  <0.001
t values assessed by pairwise t test.

Table 3. Percentage of patients (n = 96) who meet the definitions of recovery following CBT
Definition of recovery                                           Criterion reached, %
Level of fatigue comparable to healthy people                              48
No physical disability                                                     59
No social disability                                                       55
No disabilities in all domains                                             26
Normal level of fatigue and no physical disability                         44
Normal health perception                                                   54
No negative perception of fatigue                                          37
Combining criteria of fatigue, disabilities and                            23
  perception of health and fatigue

Table 4. Percentage of recovered patients following CBT with (n=22) and without (n=74)
         medical co-morbidity
Definition of recovery            No co-morbidity  Co-morbidity        Z value      p value
                                  %                %
Level of fatigue comparable to    55               23                  -2.68        0.007
   healthy people
No physical disability            65               41                  -2.00        0.046
No social disability              59               50                  -0.56        0.578
No disabilities in all domains    31                9                  -2.05        0.040
Normal level of fatigue and no    50               23                  -2.25        0.024
  physical disability
Normal health perception          58               41                  -1.41        0.157
No negative perception of fatigue 41               23                  -1.52        0.129
Combining criteria of fatigue,    29               12                  -1.17        0.241
  disabilities and  perception of
  health and fatigue
Z values determined by the Mann-Whitney U test.


 1 Whiting P, Bagnall AM, Sowden AJ, Cornell JE, Mulrow CD, Ramirez G:
   Interventions for the treatment and management of chronic fatigue
   syndrome: a systematic review. J Am Med Assoc 2001;286:1360-1368.
 2 Stulemeijer M, de Jong LWAM, Fiselier TJW, Hoogveld SWB, Bleijenberg G:
   Cognitive behaviour therapy for adolescents with chronic fatigue syndrome:
   randomised controlled trial. Br Med J 2005;330:7481-7486.
 3 Prins JB, Bleijenberg G, de Boo TM, van der Meer JWM: Cognitive behaviour
   therapy for chronic fatigue syndrome: correspondence, authors reply.
   Lancet 2001;358:240-241.
 4 Fava GA: The concept of recovery in affective disorders. Psychother
   Psychosom 1996; 65:2-13.
 5 Andrews G: Should depression be managed as a chronic disease? Br Med J
 6 Cho HJ, Hotopf M, Wessely S: The placebo response in the treatment of
   chronic fatigue syndrome: a systematic review and metaanalysis. Psychosom
   Med 2005;67:301-313.
 7 Di Blasi Z, Harkness E, Ernst E, Georgiou A, Kleijne J: Influence of
   context effects on health outcomes: a systematic review. Lancet 2001;
 8 Fukuda K, Straus SE, Hickie I, Sharpe MC, Dobbins JG, Komaroff A: The
   chronic fatigue syndrome: a comprehensive approach to its definition and
   study. International Chronic Fatigue Syndrome Study Group. Ann Intern Med
 9 Vercoulen JHMM, Swanink CMA, Fennis JFM, Galama, JMD, van der Meer JWM,
   Bleijenberg G: Dimensional assessment of chronic fatigue syndrome. J
   Psychosom Res 1994;38:383-392.
10 Van der Werf SP, De Vree B, van der Meer JWM, Bleijenberg G: Natural
   course and predicting self-reported improvement in patients with a
   relatively short illness duration. J Psychosom Res 2003;53:749-753.
11 Bleijenberg G, Prins J, Bazelmans E: Cognitive behavioral therapies; in
   Jason LA, Fennell PA, Taylor RR (eds): Handbook of Chronic Fatigue
   Syndrome. New York, Wiley & Sons, 2003, pp 493-526.
12 Prins JB, Bleijenberg G, Bazelmans E, Elving L, de Boo TM, Severens JL,
   van der Wilt GJ, Spinhoven P, van der Meer JWM: Cognitive behaviour
   therapy for chronic fatigue syndrome: a multicentre randomised controlled
   trial. Lancet 2001;357:841-847.
13 Vercoulen JHMM, Alberts M, Bleijenberg G: De Checklist Individual Strength
   (CIS) (The Checklist Individual Strength). Gedragstherapie (Behavioural
   Therapy) 1999;32: 642-649.
14 Stewart A, Hays R, Ware J: The MOS short form general health survey:
   reliability and validity in a patient population. Med Care 1988;26:724-
15 Ware JE Jr, Sherbourne CD: The MOS 36-item short-form health survey
   (SF-36). I. Conceptual framework and item selection. Med Care
16 Aaronson NK, Muller M, Cohen PD, Essink-Bot ML, Fekkes M, Sanderman R,
   Sprangers MA, te Velde A, Verrips E: Translation, validation, and norming
   of the Dutch language version of the SF-36 Health Survey in community and
   chronic disease population. J Clin Epidemiol 1998;51:1055-1068.
17 Servaes P, Verhagen C, Bleijenberg G: Determinants of chronic fatigue in
   disease-free breast cancer patients, a cross-sectional study. Ann Oncol
18 Pasquali R: The biological balance between psychological well-being and
   distress: a clinician's point of view. Psychother Psychosom 2006;75:69-71.
19 Ryff CD, Dienberg Love G, Urry HL, Muller D, Rosenkranz MA, Friedman EM,
   Davidson RJ, Singer B: Psychological well-being and ill-being: do they
   have distinct or mirrored biological correlates? Psychother Psychosom
20 Cairns R, Hotoph M: A systematic review describing the prognosis of
   chronic fatigue syndrome. Occup Med C 2005;55:20-31.
21 Deale A, Husain K, Chalder T, Wessely S: Long-term outcome of cognitive
   behaviour therapy versus relaxation therapy for chronic fatigue syndrome:
   a 5-year follow-up study. Am J Psychiatry 2001;158:2038-2042
22 White PD, Thomas JM, Amess J, Grover SA, Kangro HO, Clare AW: The
   existence of a fatigue syndrome after glandular fever. Psychol Med
23 van Houdenhove B, Egle UT: Fibromyalgia: a stress disorder? Psychother
   Psychosom 2004;73:267-275.
24 Prins JB, Bos E, Huibers MJ, Servaes P, van der Werf SP, van der Meer JW,
   Bleijenberg G: Social support and the persistence of complaints in
   chronic fatigue syndrome. Psychother Psychosom 2004;73:174-182.
25 Bentall RP, Powell P, Nye FJ, Edwards RH: Predictors of response to
   treatment for chronic fatigue syndrome. Br J Psychiatry 2002;181:248-252.

(c) 2007 S. Karger AG, Basel

[Return to top]


Date:    Sun, 15 Apr 2007 11:13:48 -0700
From:    "ME/CFS <me_cfs@glocalnet.net> [via Co-Cure Moderator]
Subject: RES: Astrocyte hypothesis for ME and/or FM


In Sweden, we have researchers in neurology, Hansson E. and Rönnbäck L, who
study astrocytes. Astrocytes are a part of the neural cells in the brain.
Their function is to form the blood brain barrier and to regulate exchange
between the extracellular space in the brain and the blood capillaries. They
do communicate with each other and with other cells.

There is a hypothesis that the astrocytes may be involved behind diseases
like ME and FM. I have not seen so much about this hypothesis in
international research about ME and I think it would be interesting to also
have this hypothesis presented in ME conferences. It is sure a part of the
ME puzzle that should not be forgotten about.

My suggestion is to invite the authors for the astrocyte hypothesis on ME
conferences. It shall indeed be mentioned that the researchers Hansson E.
and Rönnbäck L do concentrate on ME or FM, but they look at the Astrocyte
function in a more general sense.



[1] Rönnbäck L, Olsson T, Hansson E: Astrocyterna - hjärnans doldisar,
delaktiga i neurastena symtom. Läkartidningen (97) 24:2956-61, 2000.

[2] Hansson E., Rönnbäck L.: Glial neuronal signaling in the central nervous
system. FASEB J. 17, 341-348, 2003.
PMID: 12631574

[3] Hansson E., Rönnbäck L. 2004: Altered Neuronal-Glial Signaling in
Glutamatergic Transmission as a Unifying Mechanism in Chronic Pain and
Mental Fatigue. Neurochem Res.
Altered neuronal-glial signaling in glutamatergic transmission as a unifying
mechanism in chronic pain and mental fatigue.
Neurochem Res. 2004 May;29(5):989-96. Review.
PMID: 15139297

[4] Persson M, Sandberg M, Hansson E, Ronnback L.
Microglial glutamate uptake is coupled to glutathione synthesis and
glutamate release.
Eur J Neurosci. 2006 Aug;24(4):1063-70. Epub 2006 Aug 21.
PMID: 16925588

[5] Abbott NJ, Ronnback L, Hansson E.
Astrocyte-endothelial interactions at the blood-brain barrier.
Nat Rev Neurosci. 2006 Jan;7(1):41-53. Review.
PMID: 16371949

[6] Andersson AK, Ronnback L, Hansson E.
Lactate induces tumour necrosis factor-alpha, interleukin-6 and
interleukin-1beta release in microglial- and astroglial-enriched primary
J Neurochem. 2005 Jun;93(5):1327-33.
PMID: 15934951

[7]  Läkartidningen nr 14-15 2007 volym 104,
»Trött i hjärnan« osynligt handikapp som kan ge stora problem Lars Rönnbäck,
professor, överläkare i neurologi, Sahlgrenska
Universitetssjukhuset/Sahlgrenska, Göteborg
http://www.lakartidningen.se/engine.php?articleId=6451 (with summary in
English at the end)

[Return to top]


Date:    Mon, 16 Apr 2007 16:02:19 -0400
From:    "Ian McIlroy <ian box52.plus.com> [via Co-Cure Moderators]"
Subject: NOT,RES: International Conference on ME/CFS Biomedical Research - ME Research UK -  Edinburgh - 25th of May 2007

As a friend of ME Research UK (and of my own bat!), I just wanted to remind
people about the International Conference on ME/CFS Biomedical Research,
hosted and organised by ME Research UK, and co-sponsored by the Irish ME
Trust, which will take place on Friday 25th May 2007 at the Edinburgh
Conference Centre, Heriot-Watt University, Edinburgh, UK.

The full day's programme consists of invited keynote lectures and shorter
research presentations, and will be of interest to a wide range of
professionals, people with ME and observers alike.

It should be a very interesting conference with a number of international
speakers presenting as well as ME Research UK and other UK researchers
giving presentations.

On Campus accommodation is booked direct with the Heriot Watt Accommodation
office which can be contacted by telephoning 0131 451 3669 or emailing
reservation@eccscotland.com. The accommodation website is

Further information about the conference can be found at


and additional details by contacting the ME Research UK Office, at

ME Research UK
The Gateway
North Methven Street
Perth PH1 5PP, UK
Telephone/Fax: 01738 451234
E-mail: meruk pkavs.org.uk

Ian McIlroy

[Return to top]


Date:    Tue, 17 Apr 2007 00:45:53 +0200
From:    Jan van Roijen <j.van.roijen CHELLO.NL>
Subject: not,med: Multiple Chemical Sensitivity Awareness


Send an Email for free membership
       >>>> Help ME Circle  <<<<
 >>>>       17 April 2007       <<<<
Editorship : j.van.roijen chello.nl
Outgoing mail scanned by Norton AV


Governors and Mayor Proclaim May as
Multiple Chemical Sensitivity Awareness and Education Month

Lourdes Salvador

April 16, 2007

Governor Bill Ritter of Colorado, Governor Ted Strickland
of Ohio, Mayor Josephus Eggelletion of Broward County
Florida, Governor Jim Gibbons of Nevada, and Governor
Christine Gregoire of Washington are among the first
governors and mayors to proclaim the month of May 2007
as Multiple Chemical Sensitivity Awareness and Education

Multiple Chemical Sensitivities (MCS) is also known as
Environmental Illness (EI), Toxic Injury (TI), Toxicant Induced Loss
of Tolerance (TILT), and several other names. Originally
identified in a 1989 multidisciplinary survey of 89 clinicians and
researchers, and modified in 1999, top consensus criteria
(Nethercott et al, 1993) for MCS define the condition as:

1. A chronic condition.

2. Symptoms recur reproducibly.

3. Symptoms recur in response to low levels of chemical

4. Symptoms occur when exposed to multiple unrelated

5. Symptoms improve or resolve when trigger chemicals are

6. Multiple organ systems are affected.

Products that MCS patients react to include ANY quantity of
exposures to pesticides, secondhand smoke, alcohol, fresh
paint, scented products and perfumes, candles, fragrances, food
preservatives, flavor enhancers, aerosols, tap water, cosmetics,
personal care products, new carpets, petroleum products,
formaldehyde, outdoor pollutants, newspaper ink, cleaning
compounds, printing and office products, and other synthetically
derived chemicals. Some also react to natural products that are
highly concentrated such as natural orange cleaners due to high
volatile organic compound and pesticide concentration.
Symptoms can range from minor annoyances to life-threatening


The prevalence of MCS, based on self-reported symptoms by
sample populations provides an estimate of 16% of the
population who experience reactions to everyday chemicals
(Gibson, 2005; Meggs et al, 1996). MCS affects more women
than men. All education levels, income levels, and nationalities
are affected equally.

Etiology (Causation)

There is no clear consensus as to what causes the symptoms of
MCS.  One of the first studies on MCS focused on possible long
term potentiation in the hippocampus and neural sensitization as
a central mechanism (Pall, 2003).

Later studies examined the role of the inflammatory process and
found that brain inflammation was correlated with symptoms of
MCS (Pall, 2003). In 1999, Meggs proposed that MCS is
caused by low molecular weight chemicals that bind to
chemoreceptors on sensory nerve C-fibers leading to the
release of inflammatory mediators (Meggs, 1999). Many
observable and empirical, scientific facts can help identify MCS
including SPECT scans and chemical encephalopathy, vitamin
deficiencies, mineral deficiencies, excess amino acid
deficiency, and disturbed lipid and carbohydrate metabolism
(Rea et al, 2006; Ziem, 2001; Callendar et al, 1995; Heuser et
al, 1994).

McKeown-Eyssen et al (2004) studied 203 MCS sufferers and
162 controls and found that blood tests revealed that genetic
differences relating to the body's detoxification processes were
present more often in those with MCS than those without. Data
showed that five genetic polymorphisms have a statistically
significant role in determining MCS prevalence (
McKeown-Eyssen et al 2004).

Each of these genes encode proteins that metabolize chemicals
previously implicated in MCS, notably the organophosphorus
pesticides (PON1 and PON2 genes) and the organic solvents
(CYP2D, NAT1 and NAT2 genes) ( McKeown-Eyssen et al
2004). People with a ''high'' expression of two specific genes
(CYP2D6 and NAT2) were 18 times more likely to have MCS
than those without ( McKeown-Eyssen et al 2004). It was
concluded that "a genetic predisposition for MCS may involve
altered biotransformation of environmental chemicals" (
McKeown-Eyssen et al 2004). Haley found similar, confirmatory
results with the PON1 gene in studies of the Gulf War syndrome

A new study by Schnakenberg et al (2007) confirmed the
genetic variation previously found by McKeown-Eyssen and
Haley. A total of 521 unrelated individuals participated in the
study. Genetic variants of four genes were analyzed: NAT2,
GSTM1, GSTT1, and GSTP1.

The researchers concluded that individuals who are NAT2 slow
acetylators and those with homozygously deleted GSTM1 and
GSTT1 genes are significantly more likely to develop chemical
sensitivity (Schnackenberg et al, 2007). According to the study,
the glutathione S-transferases act to inactivate chemicals, so
people without these GSTM1 and GSTT1 genes are less able to
metabolize environmental chemicals because "glutathione
S-transferases play an important role in the detoxification of
chemicals" (Schnackenberg et al, 2007). The deletion of another
gene, the GSTP1 gene, leaves individuals more susceptible to
developing these diseases, as lack of these genes means a
loss of protection from oxidative stress (Schnackenberg, et al,

The NO/ONOO- cycle is implicated by Pall as being a plausible
etiology for Multiple Chemical Sensitivities (MCS), Fibromyalgia
(FM), Chronic Fatigue Syndrome (CFS), Post-Traumatic Stress
Disorder (PTSD), and Gulf War Syndrome.

Peroxynitrite (ONOO-) is oxidized from nitric oxide. Excess
peroxynitrite depletes energy stores, which is perceived to
cause extreme fatigue (Pall, ND). Of more interest to those who
suffer from MCS is the fact that peroxynitrite breaks down the
blood brain barrier and excess levels allow greater access to the
brain (Pall, ND). This greatly increases the effects of chemicals
on the brain. Essentially a non-MCS person has a barrier that
protects the brain from damage from low-level chemical
exposure, however a person who suffers from MCS has little or
no barrier making the brain subject to increased damage and
reactivity with minute exposures most people do not react to.

The key effect of nitric oxide (NO) is that it inhibits cytochrome
P-450 activity and slows degradation of hydrophobic organic
chemicals (Pall, ND). This means that excess nitric oxide slows
down the body's natural detoxification processes leaving MCS
patients subject to the effects of chemical exposure longer than
non-sufferers. Between a reduced blood-brain barrier and
increased time to naturally detoxify the body MCS patients are
subject to permanent and long-term brain and nervous system
damage which includes toxic encephalopathy.

"The only etiologic mechanism proposed for each of these is a
vicious cycle mechanism involving elevated levels of nitric oxide
and its oxidant product, peroxynitrite. This cycle may be initiated
by a variety of diverse short-term stressors, including viral and
bacterial infections, physical trauma, severe psychological
stress, organic solvent exposure, and exposure to three classes
of pesticides, organophosphorus / carbamate pesticides,
organochlorine pesticides and pyrethroid pesticides).

Each of these short-term stressors are known to be able to
trigger responses that lead to increases in nitric oxide levels.
Indeed, other initiating short-term stressors, including a
protozoan infection, carbon monoxide exposure, thimerosal
exposure and ciguatoxin exposure are also known or thought to
act to increase nitric oxide levels, as well" (Pall, 2006).

Regardless of cause, victims of MCS suffer isolation and require
the support of family, friends, and medical providers. The month
of May is designated to raise awareness of the condition and
foster better understanding of its cause and prevention. With
reasonable accommodations, victims can experience increased
ability to work, attend school, shop, dine, go to church, and
socialize. Accommodations are often simple and involve things
such as opening windows, increasing ventilation, and
substituting safer products that increase the safety of both the
patient and others the general population.


Callender, TJ, et al. (1995).  Evaluation of chronic neurological
sequelae after acute pesticide exposure using SPECT brain
scans.  Journal Toxicology & Environmental Health. 41:275-284.

Caress, S., & Steinemann, A. (2003). A Review of a Two-Phase
Population Study of Multiple Chemical Sensitivity. Environmental
Medicine. 111, 1490 - 1497.

Davidoff, L. (1989). Multiple Chemical Sensitivities (MCS). The
Amicus Journal. Winter.

Ferrie, H. (October 2003). Multiple Chemical Sensitivity:
Government and Medical Science Finally Recognize Crippling
Effects of MCS. Vitality, Retrieved May 17, 2006, from

Gibson, P. (2005). Understanding & Accommodating People
with Multiple Chemical Sensitivity in Everyday Living.
Independent Living Research Utilization.

Haley, RW, Billecke, S, & La Du, BN (1999). Association of low
PON1 type Q (type A) arylesterase activity with neurologic
symptom complexes in Gulf War veterans. Toxicology and
Applied Pharmacology 157(3):227-33.

Heuser, G, et al. (1994).  Neurospect findings in patients
exposed to neurotoxic chemicals.  Toxicology & Industrial
Health. 10:561-571.

McKeown-Eyssen, G, Baines, C, Cole, D, Riley, N, Tyndale, R,
Marshall, L, & Jazmaji, V (2004).  Case-control study of
genotypes in multiple chemical sensitivity: CYP2D6, NAT1,
NAT2, PON1, PON2 and MTHFR].  International Journal of
Epidemiology 33, 1-8.

Meggs WJ, Dunn KA, Bloch RM, Goodman PE, Davidoff AL
(1996). Prevalence and nature of allergy and chemical sensitivity
in the general population. Archives of Environmental Health.

Meggs, WJ (1999).  Mechanisms of allergy and chemical
sensitivity.  Toxicology and Industrial Health.  15:3-4, 331-338.

Nethercott J.R., Davidoff L.L., Curbow B., et al. (1993) Multiple
Chemical Sensitivities Syndrome: Toward a Working Case
Definition. Arch Environ Health, 48:19-26

Pall, M. (ND). Multiple Chemical Sensitivity: The End of
Controversy. Washington State University School of Molecular
Biosciences, Retrieved May 18, 2006, from:

Pall, M (2006). The NO/ONOO- Cycle as the Cause of
Fibromyalgia and Related Illnesses: Etiology, Explanation and
Effective Therapy. Washington State University School of
Molecular Biosciences.

Pall, M (2003).  Elevated nitric oxide/peroxynitrite theory of
multiple chemical sensitivity:  central role of
N-methyl-D-aspartate receptors in the sensitivity mechanism.
Environmental Health Perspectives.  111:12, 1461-1464.

Pall, M. (2001). Multiple Chemical Sensitivity - The End of
Controversy. Washington State University, School of Molecular
Biosciences, Retrieved May 17, 2006, from

Schnackenberg,E. et al (2007). A cross-sectional study of
self-reported chemical-related sensitivity is association with
gene variations of drug-metabolizing enzymes. Environmental

Ziem, G (2001). Medical Evaluation and Treatment of Patients
with Chemical Injury and Sensitivity. National Institute of
Environmental Health Sciences.


This is for informational purposes and is not intended to replace
the examination, diagnosis and treatment of a licensed
physician and no such claims are inferred. The author and
publisher will not be responsible for misuse of this information
and recommend consulting with a doctor qualified to diagnose
MCS if it is suspected.

About the Author

Lourdes Salvador is a writer and social advocate based in
Hawaii. She is the president of MCS America and a featured
monthly writer for MCS America News at www.mcs-america.org.
She is a passionate advocate for the homeless, working with the
local governor to open new shelters and provide services to the
homeless based on a presentation of her ideas to the governor.
That passion soon turned to advocacy and activism for victims of
multiple chemical sensitivity. For more information about
Lourdes and her advocacy work, please visit:
www.mcs-america.org, www.thetruthaboutmcs.blogspot.com,
and www.cafepress.com/mcsamerica.

Copyrighted © 2007 Lourdes Salvador

[Return to top]


Date:    Tue, 17 Apr 2007 01:17:02 +0200
From:    Jan van Roijen <j.van.roijen CHELLO.NL>
Subject: med: Is this the cure for ME?


Send an Email for free membership
       >>>> Help ME Circle  <<<<
 >>>>       17 April 2007       <<<<
Editorship : j.van.roijen chello.nl
Outgoing mail scanned by Norton AV

Quote from below:

*......Some doctors and health workers believe it is
the result of social and psychological factors - and
best treated with psychotherapy and exercise.

Now it is becoming clear these patients have "a
disturbance in their body's natural way of dealing
with infection," says Malcolm Hooper, Emeritus
Professor of Medicinal Chemistry at the University
of Sunderland.....*




Daily Mail

Is this the cure for ME?


Last updated at 11:53am on 16th May 2006

A drug used to treat herpes infections has produced a dramatic
improvement in patients severely affected by ME, or fatigue

Sufferers who for years had been unable to leave their homes
now report being able to resume normal life.

This is a remarkable result for a treatment for this complex and
controversial disorder that is thought to affect as many as
240,000 people in Britain and for which there is no cure.

The results, reported at a scientific conference earlier this month
by Professor Jose Montoya of Stanford University in California,
involved 12 patients who had been given the powerful drug
valganciclovir, which targets the human herpes virus (HHV-6).
Nine of the patients experienced a great improvement.

One of Montoya's cases was onetime champion figure skater
Donna Flowers, now aged 50 and working as a physiotherapist,
who lives in California's Silicon Valley.

"Two years ago, I was spending 14 hours a day in bed and my
brain was so fogged I couldn't write a letter," she says.

"I wasn't functioning at all. I'd been diagnosed with chronic
fatigue, but the doctors didn't have anything to offer. I had to
employ a full-time nanny just to look after my three-year-old

However, she is now back at work, treating young Olympic
hopefuls, the nanny has gone and she's just started ballet

'Soaring energy levels'

"When Donna came to see us, her energy levels were around 10
per cent of what she considered normal,' says Montoya. "Today,
she is functioning at 90 per cent."

One patient who could barely walk around the block is now
cycling three hours a day, while another who could not even get
down the stairs to breakfast is now up every day at 7am.

The professor reported his findings at a conference on the
HHV-6 virus, which was held in Barcelona earlier this month.
While it's well known that some patients with CFS have signs of
various viral infections, this is the first time that treating one of
the viruses has been shown to be so effective.

"I was amazed by the results," says Montoya, who runs the
infectious diseases clinic at Stanford. "Donna was sent to me
because high levels of another virus (Epstein Barr) had been
detected in her system.

"I found high levels of HHV-6 virus as well, so I treated her with
valganciclovir to bring down her viral load.

"I'd hoped it might help a bit, but I didn't expect the results to be
anything like as dramatic. It was pure serendipity."

'Careful monitoring'

Valganciclovir is licensed to treat HHV-6 infections of the eye,
which can affect transplant or cancer patients with severely
weakened immune systems.

HHV-6 is not the same as the herpes virus responsible for cold
sores. Most commonly, it causes roseola infantum in children,
who get a fever and a rash.

"I have treated hundreds of immune compromised patients with
the drug, so I am very familiar with it," says Montoya. "It can have
serious side-effects including anaemia, so you have to monitor
patients very carefully. But so far none of the CFS/ ME patients
have reacted badly to it."

All the experts agree that a lot more research will have to be
done before valganciclovir can be widely used as a treatment.

"There is a long history of linking CFS/ME with some sort of viral
infection," says Charles Shepherd, a medical advisor to the
charity Action For ME.

"About 75 per cent of cases begin with an infection which the
patient never properly recovers from, so it is quite likely
infectious agents lurk in the body. While the role of HHV-6 is
certainly plausible, we will have to wait for a larger trial that is
properly controlled."

Montoya agrees: "These were individual cases and it is always
possible the results were due to a effect," he says.

However, that is unlikely because we saw a worsening of each
patient's condition around week three to four of the treatment,
probably when infected cells were dying off. After that came the

"That is not a pattern you get with placebos. But we don't know
yet why the drug makes such a difference."

The possibility that valganci-clovir could eventually provide an
effective treatment for some cases of CFS is just part of a wider
picture. Over the past year, genetic research has provided a
new understanding of the disease that could eventually lead to
new therapies.

For years, the conventional view has been that there is no known
cause, no way to diagnose it and no effective treatment.

Some doctors and health workers believe it is the result of social
and psychological factors - and best treated with
psychotherapy and exercise.

Now it is becoming clear these patients have "a disturbance in
their body's natural way of dealing with infection," says Malcolm
Hooper, Emeritus Professor of Medicinal Chemistry at the
University of Sunderland.

"Anti-viral drugs such as valganciclovir may be allowing it to
re-set itself."

Hooper was one of the speakers at a conference in London for
ME Awareness Day on Friday. Another speaker was Dr
Jonathan Kerr of St George's Medical School in London, who
recently published groundbreaking work on the links between
genes and CFS/ME.

"We've found that the genes in patients' white blood cells - a
key part of the immune system - are switched on and off in an
abnormal fashion," he says.

The hope is that a relatively old drug, called interferon beta, can
help to restore the balance. A controlled trial is planned.

What researchers such as Kerr find disheartening is that there
seems to be little official support for this biological-based
research in Britain. The bulk of the funding has gone to the
psychological approach.

But many hope a parliamentary inquiry looking at the progress of
CFS/ME research will find that research involving genes, viruses
and the immune system would benefit patients.

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End of Co-Cure Weekly Digest of research and medical posts only - 9 Apr 2007 to 16 Apr 2007

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