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Co-Cure Weekly Digest of research and medical posts only - 22 Jan 2007 to 29 Jan 2007

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Date:    Wed, 24 Jan 2007 11:13:38 -0500
From:    Fred Springfield <fredspringfield VERIZON.NET>
Subject: RES: Mitochondrial dysfunction and molecular pathways of  disease

Mitochondrial dysfunction and molecular pathways of disease.

Journal: Exp Mol Pathol. 2007 Jan 17; [Epub ahead of print]

Authors: Pieczenik SR, Neustadt J.

NLM Citation: PMID: 17239370

Since the first mitochondrial dysfunction was described in the 1960s, the
medicine has advanced in its understanding the role mitochondria play in
health, disease, and aging.

A wide range of seemingly unrelated disorders, such as schizophrenia,
bipolar disease, dementia, Alzheimer's disease, epilepsy, migraine
headaches, strokes, neuropathic pain, Parkinson's disease, ataxia,
transient ischemic attack, cardiomyopathy, coronary artery disease, chronic
fatigue syndrome, fibromyalgia, retinitis pigmentosa, diabetes, hepatitis
C, and primary biliary cirrhosis, have underlying pathophysiological
mechanisms in common, namely reactive oxygen species (ROS) production, the
accumulation of mitochondrial DNA (mtDNA) damage, resulting in
mitochondrial dysfunction.

Antioxidant therapies hold promise for improving mitochondrial performance.
Physicians seeking systematic treatments for their patients might consider
testing urinary organic acids to determine how best to treat them.

If in the next 50 years advances in mitochondrial treatments match the
immense increase in knowledge about mitochondrial function that has
occurred in the last 50 years, mitochondrial diseases and dysfunction will
largely be a medical triumph.

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Date:    Wed, 24 Jan 2007 11:22:51 -0500
From:    Fred Springfield <fredspringfield VERIZON.NET>
Subject: RES: Alexithymia in Chronic Fatigue Syndrome: Associations  With Momentary, Recall, and Retrospective Measures of Somatic Complaints and Emotions

[Note: Alexithymia is defined as "a disorder characterized by
cognitive-emotional deficits including:
* problems identifying, describing, and working with one's own feelings,
often marked by a lack of understanding of the feelings of others;
* confusion of physical sensations often associated with emotions with
those emotions;
* few dreams or fantasies due to restricted imagination; and
* concrete, realistic, logical thinking, often to the exclusion of
emotional responses to problems."
en.wikipedia.org/wiki/Alexithymia ]


Alexithymia in Chronic Fatigue Syndrome: Associations With Momentary,
Recall, and Retrospective Measures of Somatic Complaints and Emotions

Journal: Psychosomatic Medicine 69:54-60 (2007)

Authors: Fred Friedberg, PhD and Joyce Quick, MS
Affiliation: From Stony Brook University, Stony Brook, New York.
Address correspondence and reprint requests to Fred Friedberg, PhD, Putnam
Hall/South Campus, Stony Brook University, Stony Brook, NY 11794-8790.
E-mail: fred.friedberg@stonybrook.edu

Objective: The relationship between alexithymia and real-time momentary
symptom assessments has not been reported. This cross-sectional study
hypothesized that alexithymia would be a predictor of somatic symptoms
using three different types of symptom measurement (momentary, recall, and
retrospective) in the medically unexplained illness of chronic fatigue
syndrome (CFS). In addition, it was hypothesized that negative affect would
be a significant mediator of the relationship between alexithymia and
somatic symptoms. Finally, the relation of alexithymia to physical illness
attribution (a CFS illness predictor) was explored.

Methods: Participants were 111 adults with CFS. Alexithymia was assessed
with the Toronto Alexithymia Scale. Momentary ratings of current symptoms
and affect were recorded in electronic diaries carried for 3 weeks. Weekly
recall of these momentary reports was also recorded. Retrospective measures
included 6-month ratings of fatigue and pain, the Fatigue Severity Scale,
the Brief Pain Inventory-Short Form, a CFS symptom measure, the Beck
Depression Inventory-II, the Beck Anxiety Inventory, and an illness
attribution rating.

Results: Partial correlations, controlling for age and sex, yielded no
significant associations between general or specific forms of alexithymia
and momentary ratings of fatigue or pain. On the other hand, a significant
association, partially mediated by anxiety scores, was found between a
specific form of alexithymia and a retrospective pain measure. Finally,
physical illness attribution was not significantly associated with alexithymia.

Conclusion: Based on assessments of real-time and retrospectively measured
symptoms, these data provided only modest support for the alexithymia
construct as a predictor of somatic symptoms in people with CFS.

Key Words: alexithymia . chronic fatigue syndrome . ecological momentary

Abbreviations: CFS = chronic fatigue syndrome; TAS-20 = Toronto Alexithymia
Scale-20-item form; DIF = Difficulty Identifying Feelings; DDF = Difficulty
Describing Feelings; EOT = Externally Oriented Thinking; FSS = Fatigue
Severity Scale; BPI = Brief Pain Inventory; BDI-II = Beck Depression
Inventory-Second edition; BDI corr = BDI corrected for somatic symptoms;
BAI = Beck Anxiety Inventory; NA = negative affect.

© 2007 American Psychosomatic Society

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Date:    Thu, 25 Jan 2007 14:51:26 -0500
From:    Fred Springfield <fredspringfield VERIZON.NET>
Subject: RES: CFS Reports from 2006 HHV-6 & 7 Conference

CFS Reports from 2006 HHV-6 & 7 Conference

Following are abstracts of selected articles dealing with CFS from a
120-page issue of the Journal of Clinical Virology, titled Papers and
Abstracts of the 5th International Conference on HHV-6 & 7, 1-3 May 2006,
Barcelona, Spain. The publication was made possible with funding from the
HHV-6 Foundation.


Review of Ampligen® clinical trials in Chronic Fatigue Syndrome

Journal: Journal of Clinical Virology, Vol. 37, Supplement I, December
2006, p. S113.

Author: W. Mitchell

Affiliation: Chronic Fatigue Syndrome Clinical Consortium, Department of
Pathology, Vanderbilt University School of Medicine, Nashville, TN, USA;
Hemispherx Biopharma, Philadelphia, PA, USA. [E-mail:
bill.mitchell@vanderbilt.edu ]

Summary at


Use of valganciclovir in patients with elevated antibody titers against
Human Herpesvirus-6 (HHV-6) and Epstein-Barr Virus (EBV) who were
experiencing central nervous system dysfunction including long-standing fatigue

Journal: Journal of Clinical Virology, Vol. 37, Supplement I, December
2006, pp. S33-S38.

Authors and affiliations:  Authors and affiliations: Andreas M. Kogelnik,
Kristin Loomis, Mette Hoegh-Petersen, Fernando Rosso, Courtney Hischier,
Jose G. Montoya, Andreas M. Kogelnik, Kristin Loomis, Mette Hoegh-Petersen.
Stanford University School of Medicine, Stanford, California, USA
(Kogelnik, Rosso, Montoya); HHV-6 Foundation, Santa Barbara, California,
USA (Loomis, Hischier); Palo Alto Medical Foundation Research Institute,
Palo Alto, California, USA (Hoegh-Peterson, Rosso, Montoya). [Contact J.G.
Montoya. E-mail: gilberto@stanford.edu ]

Abstract available at


Is Human Herpesvirus-6 a trigger for Chronic Fatigue Syndrome?

Journal: Journal of Clinical Virology, Vol. 37, Supplement I, December
2006, pp. S39-S46.

Author:  Anthony L. Komaroff

Affiliation: Division of General Medicine, Department of Medicine, Brigham
and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
[E-mail: komaroff@hms.harvard.edu ]

Abstract at


Activation of human herpesviruses 6 and 7 in patients with Chronic Fatigue

Journal: Journal of Clinical Virology, Vol. 37, Supplement I, December
2006, pp. S47-S51.

Authors and affiliations: S. Chapenko, A. Krumina, S. Kozireva, Z. Nora, A.
Sultanova, L. Viksna, M. Murovska. August Kirchenstein Institute of
Microbiology and Virology, Riga Stradins University, Riga, Latvia.

Abstract at


Active Human Herpesvirus six (HHV-6) infections in patients with Chronic
Fatigue Syndrome (CFS) and relapsing-remitting multiple sclerosis (RRMS)

Journal: Journal of Clinical Virology, Vol. 37, Supplement I, December
2006, pg. S116.

Authors:  K.K. Knox and D.R. Carrigan

Affiliation: Institute for Viral Pathogenesis, Milwaukee, Wisconsin, USA.
[E-mail: kknox@ivpresearch.org ]

Abstract at


Coagulation disorders in patients with Chronic Fatigue Syndrome (CFS) and
HHV-6 viremia

Journal: Journal of Clinical Virology, Vol. 37, Supplement I, December
2006, pg. S117.

Author: JH Brewer

Affiliation: Plaza Infectious Disease and St. Luke's Hospital, Kansas City,
Missouri, USA. [E-mail: jbrewer@plazamedicine.com ]

Abstract available at

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Date:    Fri, 26 Jan 2007 16:35:41 +0100
From:    "Dr. Marc-Alexander Fluks" <fluks COMBIDOM.COM>
Subject: RES,NOT,URL: ME-NET has moved

Today, ME-NET has moved.

The pages on the old web site,
now forward to the corresponding pages on the new site,

Info on the relocation of files can be found at,

[Return to top]


Date:    Fri, 26 Jan 2007 10:49:24 -0500
From:    Jill McLaughlin <jillmclaughlin COMCAST.NET>
Subject: NOT,RES: Search for answer to an enduring problem


Search for answer to an enduring problem

IN 2002, Anna Hemmings was at the peak of her athletic prowess: world
kayaking champion. A few months later, she had broken down completely -
utterly, incurably exhausted, unable to paddle even for 10 minutes.

"I couldn't go on. I no longer had the energy," says Hemmings. "It was
strange . . . I looked normal, yet inside my muscles were aching so badly
that sometimes I couldn't even hold my hands up to wash my hair in the shower."

Hemmings was diagnosed with chronic fatigue syndrome (CFS): crippling
exhaustion which makes even moderate exercise unbearable. The illness,
which affects around 20,000 Scots per year, is mysterious and often
untreatable. It has a number of possible triggers - viral, stress-related,
dietary - which may also indicate an underlying genetic predisposition. But
despite countless experiments, the cause of chronic fatigue has remained

Now, in search of an explanation and a cure, scientists are turning their
approach on its head by studying elite athletes who can withstand fatigue
better than others.

Dr Paula Robson-Ansley, of the University of Portsmouth, believes endurance
athletes may have a specific type of gene that makes them less likely to
suffer fatigue.

To test her theory, she travelled to the 2006 Merida TransWales Mountain
Bike Race where competitors covered more than 500km over rugged terrain in
seven days.

Each day, Robson-Ansley took blood samples from 80 athletes who took part,
before and after the race. Separately, she took blood samples from 85
people around the UK who have been diagnosed with CFS.

She is now carrying out a detailed comparison, at the laboratories of
Portsmouth's department of sport and nutrition. "The experiment may help
explain why some people develop chronic debilitating fatigue for no
apparent reason," she says.

Robson-Ansley has a personal interest in the research: her own athletic
career was cut short by a bout of chronic fatigue, sometimes described as
"unexplained underperformance syndrome" (UPS). She was an Olympic-standard
rower, training in preparation for the 1996 games, when her body rebelled.
A five-kilometre run made her feel like she had just done a marathon.
Forced to retire from competition, she set her sights on a new goal:
understanding the biological roots of UPS and chronic fatigue syndrome.

Robson-Ansley suspects that endurance athletes may carry a different form
of a gene, compared with CFS sufferers, a form which protects the athletes
from suffering excessive fatigue, during and following endurance exercise.

Her test is focusing on Interleukin-6 (IL-6), a messenger molecule in the
body that is released when the body is under stress; for example, during
infection or illness or when blood sugar levels get low by sending a
"distress signal" to the brain.

During prolonged exercise, IL-6 levels in athletes increase dramatically.
One study found IL-6 levels increasing 100-fold in runners following a
In another, when runners were injected with IL-6 before a 10km trial run,
they ran markedly slower.

The molecule seems to be sending a warning message to the brain: "Slow
down, conserve energy - the body is fatigued and recovery time is needed."
So, Robson-Ansley wondered, could it be that endurance athletes have a
different version of the IL-6 gene than sufferers of chronic fatigue syndrome?
Certainly different versions of IL-6 are known to exist. Previous studies
have found that, during infection, people with one variation of the gene -
"C-type" - produced less IL-6 during infection than those with the "G-type"
version of the gene.

Over the course of the mountain-bike event, blood samples were taken every
morning at 6am before the cyclists completed that day's stage of the race.
IL-6 levels did not change over the seven-day mountain-bike event. But as
the mountain bikers became more tired, the study found marked increases in
the levels of the IL-6 receptor - the receiver molecule that helps send the
IL-6 message to the brain.

This "would heighten the athlete's sensitivity to IL-6 when it is
produced", says Robson-Ansley. Therefore, "it may be that chronic fatigue
sufferers don't necessarily produce more IL-6 but they are more sensitive
to its release," she says.

If her theory is correct, it may one day be possible to treat some types of
CFS with a drug that can block IL-6 receptors in the brain. The good news
is, such a drug already exists: an antibody which binds to the IL-6
receptor in the brain, de-activating it. In tests, when this antibody was
injected into exhausted athletes, it eliminated the sensation of fatigue -
offering hope that it would work as a therapy.

Another, more worrying scenario, is that unscrupulous athletes might take
IL-6 blockers to train harder, by staving off pain. Robson-Ansley admits
this is a possibility, "but it would probably be dangerous", she says. Drug
cheats who took it as a performance-enhancer could risk damage to the
immune system.
The full results of her study into the IL-6 genes are not expected to be
released until the middle of this year, but she is confident that she is
winning the race to cure chronic fatigue.

"I think we now know that there is a lot more going on in the relationship
between the IL-6 receptor and fatigue than previously thought," she says.
"But one has to be cautious in prescribing the role genes might play in
athletic performance as it is still very early days. The history of sport
is littered with countless examples of athletes who succeed against all
kinds of odds, including physical ones."

12:45am Thursday 25th January 2007

By JAMES MORGAN, Science Reporter

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Date:    Fri, 26 Jan 2007 14:25:05 -0500
From:    "Bernice A. Melsky" <bernicemelsky VERIZON.NET>
Subject: RES: Treatment outcomes after multidisciplinary pain rehabilitation with analgesic medication withdrawal for patients with  fibromyalgia

Treatment outcomes after multidisciplinary pain rehabilitation with
analgesic medication withdrawal for patients with fibromyalgia.

Pain Med. 2007 Jan-Feb;8(1):8-16.

Hooten WM, Townsend CO, Sletten CD, Bruce BK, Rome JD.

Departments of Psychiatry and Psychology, Mayo Clinic College of Medicine,
Rochester, Minnesota, USA.

PMID: 17244099

Objective. This study of patients with a diagnosis of fibromyalgia (FM) was
conducted to test the hypothesis that immediate posttreatment measures of
psychosocial functioning, health attributes, negative pain-related
emotions, and depressive symptoms improve significantly during
multidisciplinary pain rehabilitation while concurrently withdrawing
analgesic medications.

Design. Prospective case series. Setting. Multidisciplinary pain
rehabilitation center at a tertiary referral medical center.

Patients. In total, 159 consecutive patients with a diagnosis of FM
admitted to the pain rehabilitation program from January 2002 to December

Interventions. A 3-week outpatient multidisciplinary pain rehabilitation
program based on a cognitive-behavioral model that incorporates analgesic
medication withdrawal.

Outcome Measures. Multidimensional Pain Inventory (MPI), Short Form-36
Health Status Questionnaire (SF-36), Coping Strategies
Questionnaire-Catastrophizing subscale (CSQ-C), and the Center for
Epidemiologic Studies-Depression scale (CES-D) were administered at
admission and dismissal and the mean differences in scores were compared
using paired t-tests. The number of patients using opioid analgesics,
nonsteroidal anti-inflammatory drugs (NSAIDs), benzodiazepines, and muscle
relaxants at admission and dismissal were compared using chi-squared analyses.

Results. The difference in admission and dismissal scores from the MPI,
SF-36, CSQ-C, and CES-D demonstrated a favorable response to treatment (P <
0.001). Compared with admission, the number of patients using opioids (P <
0.001), NSAIDs (P < 0.001), benzodiazepines (P < 0.001), and muscle
relaxants (P < 0.01) at program dismissal was significantly reduced.

Conclusion. The results of this study support the hypothesis that immediate
posttreatment measures of physical and emotional functioning are favorable
for patients with FM following multidisciplinary pain rehabilitation that
incorporates withdrawal of analgesic medications.

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Date:    Fri, 26 Jan 2007 17:56:41 -0500
From:    "Rich Van Konynenburg <Richvank aol.com> [via Co-Cure Moderators]
Subject: RES,MED:Treatment of CFS based on Glutathione Depletion--Methylation, Cycle Block Hypothesis

January 25, 2007

Suggestions for Treatment of Chronic Fatigue Syndrome (CFS) based on
the Glutathione Depletion Methylation Cycle Block Hypothesis for the
Pathogenesis of CFS

Richard A. Van Konynenburg, Ph.D.

I presented the Glutathione Depletion Methylation Cycle Block
Hypothesis for the pathogenesis of CFS in a poster paper at the 8th
international conference of the International Association for Chronic
Fatigue Syndrome in Ft. Lauderdale, Florida, on January 10-14, 2007.
This poster paper is available on the internet at the following url:


Since then I have received requests from some clinicians for a
description of a treatment approach based on this hypothesis.

I am a researcher, not a clinician, and I am well aware that it is one
thing to believe that one understands the pathogenesis of a disorder,
but quite another to know how to treat patients who suffer from this
disorder. Nevertheless, I will respond to these requests to the degree
I am able. What I can say in this regard will be based on what I
perceive are the most successful treatment approaches currently used in
autism, which I believe shares the same basic pathogenetic mechanism
with CFS, and also on limited experience in communicating by internet
with the small number of CFS patients so far who have elected to try
these approaches. Of course, I am counting on clinicians to apply their
judgment to what I write here, based on their expertise and clinical
experience, since responsibility for treatment falls to them.

I suspect that clinicians would like for me to supply a simple,
straightforward approach that would be uniformly applicable to all CFS
patients and thus readily useable in a typical busy practice in today s
medical climate, in which it is practicable to devote only a relatively
short time to each individual patient. Believe me, I understand this,
and I would very much like to be able to give such a response.

Now comes the however.  At this point it appears that it will actually
be necessary in most cases to devote considerable time to each patient,
and to tailor the treatment program to the individual patient.  In my
opinion, the reasons for this do not appear now to be lack of
understanding of the pathogenesis, but to be inherent in the genetic
individuality of the patients as well as in the variety of their
concomitant medical issues and, for many, in their general state of
debility. I now see this need for individual treatment and significant
time investment in each patient as the most significant problem in the
practicable delivery of treatment to these patients. Hopefully this
will become clearer as I explain further, and hopefully also, this
problem can be ameliorated to some degree in the future as more
experience is gained.

If you have read my pathogenesis paper, you know that I now believe
that the fundamental biochemical issue in at least a large subset of
the CFS patients is that the methylation cycle is blocked. Therefore, I
think that the main goal of treatment must be to remove this block and
to get the methylation cycle back into normal operation. I believe that
it is also true that glutathione depletion is present in these patients
and is directly responsible for many of the features of CFS, as I
described in my recent poster paper, but I have found in interacting
with clinicians as well as with many patients on the CFS internet
lists, that it is usually not possible to normalize the glutathione
levels on a permanent basis by direct approaches of glutathione
augmentation. Instead, it appears that the methylation cycle block must
be corrected first, to break the vicious circle that is holding down
the glutathione levels. In addition to this, some patients, because of
particular genetic polymorphisms, cannot tolerate supplementation with
glutathione or other substances intended to help them directly to build
glutathione. One clinician estimated to me that this group amounts to
about one-third of the patients.

Based on what is being done in autism by the Defeat Autism Now! (DAN!)
researchers and clinicians and independently by Dr. Amy Yasko, N.D.,
Ph.D., I am going to suggest two treatment approaches for CFS. The
first is a simplified approach which may be applicable to patients who
have not been ill for an extended period, and who are not very
debilitated. Use of this simplified approach would be based on the hope
that the patient does not have certain genetic polymorphisms, which
would not be known in this simplified approach. If the patient does in
fact have these polymorphisms, the simplified approach will not be
successful, and then you will have to move on to the more complex
treatment. This simpler treatment approach is based partly on the
treatment that was used by Dr. S. Jill James, Ph.D., et al. in the
study that found the connection between the methylation cycle block and
glutathione depletion in autism (This was Ref. 2 in my pathogenesis
paper), but it makes use of supplements that are part of Dr. Amy
Yasko s treatment program. The second treatment approach is much more
involved and is based on Dr. Yasko s complete autism treatment. I
currently believe that the second approach is the type of treatment
that will be necessary also for most CFS patients, and certainly those
of longer standing or greater debility, as well as those having certain
genetic polymorphisms. However, I am including the simpler approach in
an effort to match the practical demands of current medical practice,
to the degree I understand them.

In the simplified treatment approach, potentially applicable to
patients who have not been ill for an extended period, who are not very
debilitated, and who will initially be assumed not to have certain
genetic polymorphisms, one would proceed directly toward the goal of
restarting the methylation cycle, together with some general
nutritional support. If this treatment is tolerated and is efficacious
in a particular case, I think it could actually be relatively
straightforward. I think it should be borne in mind, though, that if
the simplified approach is not effective for a particular patient,
there is the risk that trying it could discourage the patient before
she or he reaches the second option. So I think it would be proper and
wise to discuss this issue with the patient up front, and to apply
considerable clinical judgment as to whether the simplified approach
should be tried on a particular patient.

The simplified approach would involve giving the following oral
supplements daily, all of which are available from Dr. Yasko s
supplement website at

¼ tablet (200 micrograms) Folapro (Folapro is 5-methyl
tetrahydrofolate, an active form of folate, which is sold by Metagenics
with a license from Merck, which holds the patent on synthesis).

¼ tablet Intrinsic B12/folate (This includes 200 micrograms of folate
as a combination of folic acid, 5-methyl tetrahydrofolate, and 5-formyl
tetrahydrofolate, aka folinic acid or leucovorin (another active form
of folate), 125 micrograms of vitamin B12 as cyanocobalamin, 22.5
milligrams of calcium, 17.25 milligrams of phosphorus, and 5 milligrams
of intrinsic factor)

(up to) 2 tablets (It s best to start with ¼ tablet and work up as
tolerated) Complete vitamin and ultra-antioxidant from Holistic Health
Consultants (This is a multivitamin, multimineral supplement with some
additional ingredients. It does not contain iron or copper, and it has
a high ratio of magnesium to calcium. It contains antioxidants, some
trimethylglycine, some nucleotides, and several supplements to support
the sulfur metabolism.)

1 softgel capsule Phosphatidyl Serine Complex (This includes the
phospholipids and some fatty acids)

1 sublingual lozenge Perque B12 (2,000 micrograms hydroxocobalamin with
some mannitol, sucanat, magnesium and cherry extract)

1 capsule SAMe (200 mg S-adenosylmethionine)

1/3 dropper, 2X/day Methylation Support Nutriswitch Formula (This is an
RNA mixture designed to help the methylation cycle. It is not
essential, but is reported to be helpful.)

Note that I have specified hydroxocobalamin rather than methylcobalamin
as the main supplemental form of vitamin B12. I ve done this to
accommodate patients who may have downregulating polymorphisms in their
COMT (catechol-O-methyltransferase) enzyme, which many CFS patients
seem to have. If they do not have these polymorphisms, methylcobalamin
would be more effective, but in this simplified treatment, the
patient s polymorphisms will not be known. I am also including a small
amount of SAMe, which is also a compromise, since the amount needed
will again depend on COMT polymorphisms, which will not be known for
this simplified treatment. The amount of B12 specified is also a
compromise, since those with certain polymorphisms will benefit from a
higher dosage than will those without them.

After this treatment is begun, you can expect the patient to feel worse
initially, and I think it would be proper and wise to make the patient
aware of this before the treatment is begun. It is necessary to
determine whether this feeling is occurring because the treatment is
working and the patient s body is beginning to detox and kill viruses,
or whether it is occurring because the patient does in fact have
upregulation polymorphisms in their CBS (cystathionine beta synthase)
enzyme, in which case you will have to move on to the more complicated
complete treatment regimen. Which of these is the case can be
determined by taking spot urine samples for a urine toxic metals test
and a urine amino acids test from Doctor s Data Laboratories. These can
be ordered through Dr. Yasko (at
<http://www.testing4health.com>http://www.testing4health.com) if you
would like to receive her interpretation of the results, or they can be
ordered directly from Doctor s Data Laboratories
(<http://www.doctorsdata.com>http://www.doctorsdata.com). If the toxic
metals are elevated on the
urine toxic metals test, this will indicate that the patient has begun
to detox, which is desirable. If taurine and ammonia are elevated on
the urine amino acids test, this will suggest that the patient does
have CBS upregulation polymorphisms, in which case you will have to
stop this treatment and move to the more complicated approach described
below. It would be best to do this treatment for a week or two before
doing the urine tests, so that meaningful results can be obtained on
these tests, unless the patient cannot tolerate it. If the latter is
the case, then you will have to go on to the more complicated treatment
approach described below.

As I have emphasized, the simplified treatment approach may or may not
be tolerated by a particular patient, and I will explain why it might
not be tolerated later in this discussion.

Now I will move on to the more complicated treatment approach that I
currently believe will be necessary for most of the patients. I will
not supply all the details of this treatment approach in this letter,
but will try to give you an overall picture of the sequence of steps
involved. I recommend reading Dr. Yasko s book The Puzzle of Autism,
and consulting her other materials as well.  These are available from
<http://www.amazon.com>http://www.amazon.com by searching on Amy Yasko.

Before getting into this treatment approach, I first want to discuss
some important issues, and then I will discuss the treatment, step by

1. It is necessary to minimize the use of pharmaceuticals in treating
CFS patients. There are at least two reasons for this. As you know, the
use of pharmaceuticals is based on their being eliminated at certain
rates by the body s detox system, found primarily in the liver, kidneys
and intestines. However, many CFS patients have polymorphisms in their
detox enzymes, including CYP450 enzymes and Phase II detox enzymes. (If
desired, these can be characterized by the Detoxigenomic panel offered
by <http://www.genovations.com>http://www.genovations.com). Because of
these polymorphisms, many
patients are genetically unable to detox pharmaceuticals at normal
rates, and cannot tolerate them. In addition to this, all patients who
have the glutathione depletion and methylation cycle block suffer from
biochemical inhibition of their detox systems, whether they have these
polymorphisms or not. Because of these two factors, CFS patients suffer
 from the toxic effects of pharmaceuticals. Treatment using nutritional
supplements is necessary, and some herbals can be tolerated as well.

2. Because of the broad nature of the current case definition for CFS,
the population defined by it is very heterogeneous. It is likely that
the pathogenesis model I have presented for CFS will not fit all
patients. For this reason, I recommend a relatively inexpensive
glutathione measurement initially, such as the red blood cell total
glutathione test offered by
<http://www.immuno-sci-lab.com>http://www.immuno-sci-lab.com (phone them
for details) or by Mayo Laboratories. Perhaps a better test is the
serum reduced glutathione test offered as part of the Comprehensive
Detox Panel at
If a
below-normal value is found in either of these tests, I think that
there is a good chance that this pathogenesis model fits the patient.

3. Different patients have different genetic polymorphisms in the
enzymes and other proteins that impact the methylation cycle and the
associated biochemical cycles and pathways. Some of these polymorphisms
will have important impacts on the choice of specific parts of the
treatment program. In using the more complicated treatment approach, it
will be necessary to characterize the polymorphisms before it will be
possible to make some of the decisions about selection of particular
treatment aspects. The most comprehensive panel for this is Dr. Yasko s
Comprehensive Basic SNP (single nucleotide polymorphism) Panel I,
available from
<http://www.testing4health.com>http://www.testing4health.com. Dr. Yasko has
the polymorphisms on this panel by correlating their presence with
severity of autism symptoms and with the results of biochemical testing
(mainly spot urine tests for organic acids, amino acids, and essential
and toxic metals). This is a somewhat unorthodox method that jumps over
the usual intermediate steps involved in studying polymorphisms, and
there is not universal agreement about her results in the research
community, but I think Dr. Yasko s treatment outcomes are speaking for
themselves, as can be seen from the voluntary testimonials of parents
of autistic children on the parents discussion group at
<http://www.autismanswer.com>http://www.autismanswer.com. As a researcher,
of course, I look forward
to the day when these polymorphisms will be thoroughly researched and
characterized, and have encouraged those involved in such work to forge
ahead. The results from this genetic panel require interpretation. One
can either study Dr. Yasko s materials to gain her insights on
interpreting the results in general, or order her interpretation of the
particular results, which is called a Genetic Analysis Report or GAR.
The GAR is a computer-generated report with some general material that
applies to all the cases, and specific sections that are chosen in
response to the particular genetic polymorphisms found in the
individual patient. As such, the continuity of the discussion in the
GAR is not what would be found in a report written from scratch for
each particular patient, and it may have to be read more than once to
make all the connections in one s mind, but the material contained is
specific to the particular genetic panel results, and Dr. Yasko updates
the material used in generating the GARs as more is learned.

4. As I have discussed in my paper, people who have been ill for an
extended period of time (many months to many years) will have
accumulated significant infections and significant body burdens of
toxins, because both their cell-mediated immune response and their
detox system will have been dysfunctional during this time. When the
methylation cycle is then restarted, both the immune system and the
detox system will begin to function better. When they do, pathogens and
infected cells will begin to die off at higher rates, and toxins will
be mobilized. The resulting detoxification will be unpleasant, and may
even be intolerable. If the patient has not been prepared in certain
ways, discussed below, she or he may not be willing to continue this
and may drop out of the treatment program.

5. One of the most important preparatory activities is to make sure the
gastrointestinal system is operating well enough to be able to absorb
nutrients, including both food and the oral supplements used in the
treatment, and also well enough to be able to dispose of toxins into
the stools on a regular basis. If this is not done, it is likely that
the treatment will not be successful. Treatments for the G.I. system,
as well as for other aspects described below, are discussed in Dr. Amy
Yasko s book.  Some CFS patients have reported benefit from Xifaxan to
treat deleterious bacteria in the gut.  This antibiotic is not absorbed
 from the G.I. tract, so it does not present problems for the detox

6. Another very important aspect of the preparation is to deal with the
overstimulation or overexcitation of the nervous system that is present
in CFS. This probably results from several causes, including depletion
of magnesium and in some cases depletion of taurine, low blood flow to
the brain because of low cardiac output, glutathione depletion in the
brain producing mitochondrial dysfunction, and dietary and other
factors causing elevation of excitatory neurotransmitters and depletion
of inhibitory neurotransmitters. It is important that this be dealt
with because if it is not, the patient will be less able to tolerate
the detox inherent in the treatment.

7. Another important step is to ensure that the patient s nutritional
status is supported. Many CFS patients are in a rather debilitated
state, partly because of deficiencies of essential nutrients. They are
also in a state of oxidative stress. Appropriate nutritional
supplements can correct these problems at least to some degree and get
the overall metabolism of the patient into a better state, so that they
can better tolerate the detox part of the treatment.

8. Particular organs or systems may not be functioning well and may
need extra nutritional or herbal support. Which ones will vary from one
patient to another, so this part of the treatment must be tailored to
the individual patient.

9. Chronic bacterial infections should be addressed. According to Dr.
Yasko, females in particular appear to be prone to streptococcal
infections. She also finds that aluminum appears to be associated with
the bacteria, so that when the bacteria die off, aluminum is excreted.
While antibiotics can be used, there are downsides to this, both in
terms of difficulty in detoxing some of the antibiotics and in terms of
killing beneficial intestinal flora and encouraging deleterious ones,
such as Clostridia dificile. In addition, some CFS  patients have
experienced tendon problems from the fluoroquinolone antibiotics. Dr.
Yasko prefers natural antimicrobial treatments.

10. When the methylation cycle is restored, the normal detox system is
able to deal with more of the toxins. Dr. Yasko also uses low doses of
oral EDTA, but not the sulfur-containing chelators (DMSA and DMPS), to
help remove aluminum as well as other metals, including mercury. DMSA
and DMPS are not used because they can also bind glutathione, so that
if a patient who is low in glutathione receives these chelators, their
glutathione status can be worsened. Also, DMSA and DMPS are rich in
sulfur, and CFS patients with certain polymorphisms cannot tolerate
them. She also uses some natural RNA formulas for detoxing, as well as
for a number of other purposes during the treatment. These are somewhat
costly, and are not required as part of the treatment, but are reported
to be helpful.

11. As mentioned in item 3 above, it is important to characterize
relevant polymorphisms prior to bringing up the methylation cycle
operation. One of the most important aspects of this is to evaluate
polymorphisms in the CBS (cystathionine beta synthase) enzyme, which is
located at the entrance to the transsulfuration pathway and converts
homocysteine to cystathionine. Although this is somewhat controversial
within the research community, Dr. Yasko finds that certain
polymorphisms cause an increase in the activity of this enzyme. The
result is that there is too large a flow down the transsulfuration
pathway, and somewhat counterintuitively this results in lowered
production of glutathione, as well as elevated production of taurine,
ammonia, sulfite and hydrogen sulfide. The last three of these
substances are toxins. If a patient has CBS polymorphisms, it is
necessary to deal with this aspect before restarting the methylation
cycle. If this is not done, efforts to start this cycle will result in
increased production of these toxins. This may explain why some
patients cannot tolerate direct efforts to build glutathione using
sulfur-containing substances, while others derive some benefit from
this. Dealing with this CBS upregulation situation can take a month or

12. Only after all these issues have been addressed is the patient
ready to start supplementing with larger amounts of the folates and
cobalamins to begin major restoration of operation of the methylation

13. As you can see from the diagram in my pathogenesis paper, there are
two possible pathways from homocysteine to methionine. One involves the
enzyme methionine synthase, which requires methylcobalamin and is
linked to the folate cycle as well, and the other involves the enzyme
betaine homocysteine methionine transferase (BHMT), and requires
trimethylglycine or one of the phospholipids (phosphatidyl-serine,
-choline, or -ethanolamine). Ultimately, it is important to get the
methionine synthase pathway back into operation, but in Dr. Yasko s
practice it has been found that it is easier to start up the BHMT
pathway first. I think the reason is that S-adenosylmethionine (SAMe)
interacts with methionine synthase, and by first starting up the BHMT
pathway, one ensures that there is enough SAMe to start up the
methionine synthase pathway.

14. As these steps are taken, the immune system and the detox system
will start to function at higher levels, and die-off and detox will
begin. These processes are monitored using periodic spot urine testing,
and decisions about when to proceed to the next step in the treatment
program are based on this urine testing.

15. Viral infections are dealt with naturally as the immune system
recovers, though Valtrex is used in some cases. As the viruses die off,
it is observed that heavy metal excretion increases. Heavy metal
excretion is tracked using periodic spot urine tests and is plotted as
a function of time to determine the progress.

16. When appropriate indications are seen in the urine testing, the
BHMT pathway is slowed using dimethylglycine, which is a product of the
BHMT reaction, and thus exerts product inhibition on it. This shunts
the flow through the parallel methionine synthase pathway. This has the
effect of bringing up the folate cycle, which is linked to it, and also
bringing up the biopterin cycle, which is linked to the folate cycle.
The folate cycle is needed to make new RNA and DNA to proliferate new
cells, such as T cells in cell-mediated immunity. The biopterin cycle
is necessary for the synthesis of serotonin and dopamine as well as for
the operation of the nitric oxide synthases. Some patients benefit from
direct supplementation of tetrahydrobiopterin, often in very small

17. The treatments up to this point should resolve most of the symptoms
of CFS. The last step is to support remyelination, which has been
dysfunctional during the time when the methylation cycle was blocked,
because methylation is necessary to synthesize myelin basic protein.
This should improve the operation of the nervous system.

That is a rough outline of the treatment process, and again, I refer
you to Dr. Yasko s materials for the details.

I m sorry that this treatment approach is not simple, quick, easy and
inexpensive, but unfortunately, I think this rather complex process is
what is required, for the reasons I ve given. I hope this is helpful,
and I would very much appreciate it if you decide to try this treatment
approach, that you will keep me informed of how it works out for your
patients. If I can answer questions that come up, please let me know.

Rich Van Konynenburg, Ph.D.

[Return to top]


Date:    Sat, 27 Jan 2007 10:46:29 -0500
From:    "Dr. Bart Stouten via Co-Cure Moderator" <ray CO-CURE.ORG>
Subject: NOT, RES:  An insight into the situation in Belgium

Recently a report evaluating the five CFS reference centres which have been
operating in Belgium since 2002 was published. The summary below contains
the main points raised in the report.

The report (written in Dutch) can be accessed at

Best wishes,
Bart Stouten

Summary of the evaluation report (2002-2004) of the five CFS reference
centres in Belgium

* Despite a large amount of national and international research on CFS, a
lot remains unknown. There is no general consensus about the aetiology and
pathophysiology, required in order to diagnose, how to treat, and how to
name the condition.
* A working group from the Belgium High Health Council has identified the
medical and administrative problems for CFS patients.

To cope with the identified problems, RIVIZ was asked to make contracts
with reference centres for chronic fatigue syndrome. These centres had to
satisfy the following criteria:
* multidisciplinary teams and approach
* out-patient diagnosis
* formulate a therapeutic proposal for the general practitioner
* actively participate in scientific research and information
* active support for the health professionals

Because knowledge and participation in scientific CFS research is mostly
limited to universities, the recognition of CFS centres was limited to
medical teams associated with a university.

Five recognized centres:

* four for adults: UZ Leuven, UZ Antwerpen, UZ Gent, and UCL
* one for adolescents younger than 18 years: AZ VUB

The centres became operational between April 2002 and October 2002. The
maximum costs of the five centres together is approximately 1.7 million
euros per year. Chronic Fatigue Syndrome criteria of Fukuda et al. (1994)
are used.

Centres can only accept patients who are referred by their general
physician using a standardized intake form that was devised by the

* The first contact between the centre and the patient is a  consult with a
general physician/internist. The aim is to quickly identify patients who do
not meet the criteria for a CFS diagnosis.

* Patients suspected to have CFS after this consult enter a phase where
they are assessed by a multidisciplinary team consisting of an internist,
psychiatrist, and rehabilitation physician.

* If the multidisciplinary assessment has made the diagnosis of CFS, then a
specific, individually-tailored interdisciplinary therapeutic programme
will be advised. The length is at most 12 months, and for adults it should
at least include cognitive behaviour therapy (CBT) as well as graded
exercise therapy (GET). [Ed note: CBT and GET were given in groups but
individual sessions were included where deemed helpful]

* For the adolescents, the required length of the complaints for a CFS
diagnosis was reduced from six months to six weeks [Ed note: the six week
limit also applies to fatigue]. With respect to fatigue, the restriction
that the chronic fatigue must have resulted in an absence from school for
at least two weeks in a period of six weeks was added. For adolescents, the
initial consult is performed by a paediatrician. The adolescent therapeutic
programme included GET as well as one of the following: school guidance,
system therapy, or CBT.

Evaluation measurements are taken at before the programme, immediately
after the programme, and 6 and 12 months after the programme.

The centres have a certain freedom in their policy. Sometimes, additional
criteria are applied, alongside the Fukuda CFS criteria to select patients
for a therapeutic programme. The length, intensity, contents and focus of
the therapeutic programmes can differ between centres. The centres have the
freedom to choose to offer out-patient or in-patient programmes. In
practice, there is only one centre (dealing with the adolescents) where
patients are hospitalized for ten days during the assessment phase
following the intake.

Methodological shortcomings as recognized in the report include:
1.    Due to lack of objective measures to diagnose CFS and assessing the
course of disease, a lot of data on the functioning of patient was
collected using interviews and questionnaires.
2.    Comparisons between centres was not always easy because each centre
had registered the parameters for their own patients, and sometimes this
led to compatibility issues between centres.
3.    Some centres recorded that certain parameters for a large number of
patients were 'unknown,' even though the rehabilitation-contracts indicated
that assessment of these parameters was mandatory and included them in the
funding for the centre.
4.    There are no control groups with patients that e.g. followed no
programme, a minimal programme, or an alternative programme.
5.    There were large differences in the amount of registered data -
mostly related to the number of registered patients- per centre. In
particular there were not enough data (<10 patients) to perform a
statistical analysis for the centre that treated the adolescents.
Furthermore, the overall results are biased by the centre which treated the
most participants.

Results for the adult centres

* Evaluation period: 1 April 2002  30 June 2005.

* 1505 patients entered the multidisciplinary assessment phase, 1421
patients completed this phase, 951 specific interdisciplinary
rehabilitation programmes were started

* Until 31 December 2004, 3042 patients were referred to the CFS centres.
Of those, (only) 54% had the mandatory consult with the internist, 37%
followed the multidisciplinary assessment phase, 26% entered the specific
interdisciplinary rehabilitation phase, and 20% completed the specific
interdisciplinary rehabilitation phase. Thus 63% of the referred patients
have never been diagnosed or evaluated according to the contracts.

* In 94% of the cases the internist judged that the referred patient may
have CFS; the CFS diagnosis was subsequently confirmed by the
multi-disciplinary team in 96% of those cases.

* In 80% of the cases where the diagnosis CFS was confirmed, the specific
interdisciplinary rehabilitation programme was recommended.

* 89% of the patients continued the rehabilitation programme until the
moment that the costs of rehabilitation were no longer covered. For no
patients the programme was stopped because the patient was not motivated
enough. Only in 2.8% of the cases the programme was ended by the patient.

* Complete recovery was never recorded as a reason for ending the
rehabilitation. Some centres believed that a complete cure for this chronic
condition is not possible. [Ed note: though not mentioned in the main text,
annex 3 reveals that other centres did: the centre in Gent estimated that
2-3% were completely cured after rehabilitation; the adolescent centre
reported that 2 out of 3 patients in a sample of 14 had completely
recovered after rehabilitation.]

* For 71% of the patients, the treatment team judged that there was
sufficient improvement to transfer the rest of the intervention back to
first and second line care.

* Most general practitioners (70%) have referred only a single patient. 96%
referred three or less patients. Only 1% referred five or more patients to
the centres.

* The mean age of the patients that were referred to the centres was 40
years and 8 months; 41% were between 40 and 49 years old; 87% was female.

* 10% of the patients judged to have CFS worked fulltime, 14% worked
part-time, 76% did not have paid work. On average CFS patients worked 17.7%
(out of 38 hours) per week. When non-paid (e.g. household) work was taken
into account, CFS patients worked 57.2% per week. 26% of the patients had
income from professional work, 54% had a disability allowance.

* On average, patients had experienced chronic fatigue for 58 months. 38%
had chronic fatigue for more than five years. Most mentioned minor symptoms
including: muscle aching 95%, memory or concentration problems 94%, non
refreshing sleep 92%, post exertional malaise lasting longer than 24 hours
85%. Less frequent complaints were tender lymph nodes 38% and sore throat 54%.

* Maximum exercise test indicated that the reference values were on average
73.3% of the nominal values

* There was a large difference in the psychopathological conditions between
centres. 42% had a somatisation disorder/undifferentiated somatoform
disorder  (varied from 1-89% between the centres); 13% depressive disorder
(0-33%); generalised anxiety disorder 6% (0-26%). The psychiatrists of the
centres thought that these differences were related to recording bias
and/or interpretation bias. The largest differences between centres were
the `undifferentiated somatoform disorder' (varied between 1-89%). The
symptom pattern is almost the same as CFS, but the former requires a
relation with identifiable social stressors (as a primary aetiological
factor). According to the psychiatrists, the large difference between
centres reflects the uncertainty in the aetiology of CFS.

Results of the treatment programme

* Analysis indicated statistically significant improvements in subjective
fatigue (measured with CIS20 subscale fatigue), vitality (SF36), memory and
concentration problems (CIS20-concentration), self-reported physical
activity (CIS20-activity, SF36), and quality of life (SF36 general) for the
group as a whole. Despite the improvement, the average scores remained low
as compared to a healthy population (e.g. quality of life score after
rehabilitation was 39.6 for CFS versus 78.8 for a healthy population).

* The effect of rehabilitation on the results of the exercise test were
limited and not statistically significant. Furthermore, there seemed to be
no relation between the subjectively experienced quality of life and the
cardio respiratory capacity. The maximum exercise was very demanding for
the patients as it could lead to severe malaise afterwards (abnormal
exercise intolerance is characteristic for CFS). Some believed that the
maximum exercise test was not in line with the therapeutic goal to avoid
maximum exertion. According to some centres, after rehabilitation, some
patients stopped the exercise test prematurely because they had learned
during rehabilitation to not exert themselves too much.

* Before rehabilitation, average amount of paid work was 18.3% (of 38
hours). Immediately after rehabilitation this was reduced to 14.9% (6%
worked more, 10% worked less), 6 months later it was 16.7%.

Scores at 0 months and at 6 months after rehabilitation as compared to
baseline (just before rehabilitation) [Ed note: this table is not complete,
but gives an indication of the numbers that are mentioned in the main text
of the report; the full tables are in annex 3 of the report]

                              improved   deteriorated
CIS20-fatigue     (0 months)*  61%        21%
                   (6 months)*  60%        25%

SF36 vitality     (0 months)*  60%        25%
                   (6 months)*  56%        30%

CIS20 memory&     (0 months)*  52%        32%
concentration     (6 months)*  56%        29%

CIS20 physical    (0 months)*  56%        24%
activity          (6 months)*  56%        28%

SF36 phys.        (0 months)*  54%        31%
functioning       (6 months)*  57%        30%

SF36 quality of   (0 months)*  48%        30%
life              (6 months)   46%        34%

max exercise test
  -watts           (0 months)   38%        38%
  -O2              (0 months)   58%        39%
  -basismetabolism (0 months)   55%        44%

sub max exercise test
  -watts           (0 months)   43%        30%
  -O2              (0 months)   56%        37%
  -basismetabolism (0 months)   56%        39%

self-efficacy     (0 months)*  57%        32%
                   (6 months)

* statistically significant improvement compared to baseline for the group
as a whole

Comparison to published studies

* Comparison of the results of the CFS reference centres with published
evidence based studies was difficult as the published studies often used
other measurements. Furthermore, scientific studies often used more
stringent criteria to select patients. Finally, sometimes the published
studies used other selection criteria than the CDC criteria that were
applied in the reference centres.

* Fulcher et al (BMJ 1997; 314:1647) compared 33 patients with CFS that
followed GET with a control group of 33 CFS patients who did
flexibility/relaxation exercises. The peak O2 consumption improved by 13%
in the group that followed GET (mean improved from 31.8 to 35.8). In the
CFS reference centres this is only 2% (from 22.3 to 22.8). The scores on
the 'functional functioning' scale (range 0-100) improved from 48.5 to 69
in the Fulcher et al study; in the reference centres the improvement was
less (41.8 to 47.6) though still statistically significant.

* Prins et al (Lancet 2001; 357:841-47) compared a group of 92 CFS patients
who followed CBT/GET with a group who were given guided support and a group
that had no intervention (natural course). For the CBT group the mean
CIS20-fatigue score before therapy was approximately 52 (range 8-56; higher
indicates more fatigue), after therapy approximately 40. For the CFS
centres the baseline score was 51.7. Although statistically significant,
the score was only improved to 47.0 after rehabilitation. The report
remarks that it should be noted that the Prins et al study also included
patients that did not satisfy the CDC criteria that they should have at
least 4 out of a list of 8 symptoms; patients who used medication or had a
conflict with the health insurance were also excluded.

* The results of the centres are not good as the results in the published
evidence based studies. The report asks if this depends on the way the
interventions are organised. The published studies used individual therapy,
the reference centres performed group therapy (on average 3 people per
group, though in some centres the groups consisted of 10-11 persons),
sometimes in combination with a limited number of individual sessions.

Conclusion section

* Despite  the limited effect of the treatment offered by the reference
centres,  the patients experienced a global improvement of subjective
perception of their health (as measured with questionnaires for fatigue,
concentration, physical functioning, quality of life, psychological
functioning), without an accompanying improvement of their physical
capacities (as measured by the exercise test).

* In general the final levels of health and functioning were not as good as
in the normal population, which had consequences for the possibilities for
occupational rehabilitation. Furthermore, there is a large variance in the
results. There were also patients that did not improve or even got worse
after rehabilitation. The effect of the rehabilitation was decreased at the
follow-up phase, which shows the significance of the rehabilitation and
raises questions about the length.

[Ed note: I omitted the results for adolescents as only 59 patients were
referred to the centres until December 2004; of those, 37% were confirmed
to have CFS; less than 10 patients had data that could be used to evaluate
the rehabilitation, therefore no statistical analysis were performed in the
report. The general trend of the results of the <10 patients is that they
improved a lot, and after rehabilitation several measurements are within 1
standard deviation of the mean of the normal population; the report warns
that these results have to be interpreted with caution due to the small
sample size.]

[Return to top]


Date:    Sat, 27 Jan 2007 14:36:10 -0500
From:    "Bernice A. Melsky" <bernicemelsky VERIZON.NET>
Subject: RES: Awareness and perceptions of fibromyalgia syndrome: a survey of Malaysian and Singaporean rheumatologists

Awareness and perceptions of fibromyalgia syndrome: a survey of Malaysian
and Singaporean rheumatologists.

Singapore Med J. 2007 Jan;48(1):25-30.

Arshad A, Kong KO.

Rheumatic Diseases Unit, Putra Specialist Centre, Alor Star 05100,
Malaysia. anwararshad@hotmail.com.

PMID: 17245512

Introduction: Fibromyalgia syndrome (FMS) is a common but controversial
condition. There appears to be different levels of belief of its existence
and awareness. We set out to explore the variations of perceptions and
awareness of this condition among rheumatologists from Malaysia and Singapore.

Methods: 48 rheumatologists from Malaysia (28) and Singapore (20) were
approached to participate in this survey by answering a specific
questionnaire regarding their belief in FMS. 23 respondents from Malaysia
and 20 from Singapore completed the questionnaire.

Results: 91 percent of Malaysian rheumatologists and 95 percent of the
Singaporean believe that FMS is a distinct clinical entity and that this
condition is considered an illness rather than a disease. 87 percent and 90
percent of rheumatologists from Malaysia and Singapore, respectively,
believe that FMS is a mixture of medical and psychological illness.
However, not many of those in the university setting include FMS in their
undergraduate teaching. 87 percent and 80 percent of the respondents from
Malaysia and Singapore, respectively, also ordered blood tests to exclude
other serious pathologies, and 100 percent of the respondents from both
countries also prescribed some form of drugs to their FMS patients.

Conclusion: This study confirmed that there was a variation of perceptions
and knowledge of FMS among rheumatologists from Malaysia and Singapore. The
majority of rheumatologists recognise that FMS is a distinct clinical
entity, and is diagnosed by excluding other well-defined clinical diseases
through a combination of clinical evaluation and screening tests.

[Return to top]


Date:    Sun, 28 Jan 2007 15:11:30 -0500
From:    "Bernice A. Melsky" <bernicemelsky VERIZON.NET>
Subject: RES: Biology and therapy of fibromyalgia. Functional magnetic resonance imaging findings in fibromyalgia

Biology and therapy of fibromyalgia. Functional magnetic resonance imaging
findings in fibromyalgia.

Arthritis Res Ther. 2007 Jan 17;8(6):224 [Epub ahead of print]

Williams DA, Gracely RH.

Chronic Pain and Fatigue Research Center, Department of Internal Medicine,
Division of Rheumatology, University of Michigan Health System, University
of Michigan, Ann Arbor, MI, USA. rgracely@med.umich.edu.

PMID: 17254318

Techniques in neuroimaging such as functional magnetic resonance imaging
(fMRI) have helped to provide insights into the role of supraspinal
mechanisms in pain perception. This review focuses on studies that have
applied fMRI in an attempt to gain a better understanding of the mechanisms
involved in the processing of pain associated with fibromyalgia. This
article provides an overview of the nociceptive system as it functions
normally, reviews functional brain imaging methods, and integrates the
existing literature utilizing fMRI to study central pain mechanisms in

[Return to top]


Date:    Sun, 28 Jan 2007 22:48:19 -0500
From:    Jill McLaughlin <jillmclaughlin COMCAST.NET>
Subject: NOT,MED: Drained by the brain - The Australian


Drained by the brain
Yuppie flu is real and may be caused by disruption in the brain. Clara
Pirani investigates the disease, which is costing the country $525 million
a year

The Australian
January 29, 2007
LYN Wilson has a blunt message for anyone who doubts that chronic fatigue
syndrome is a debilitating physical illness. "Why would anyone want to give
up their life and their income, for nothing? People who think we're not
sick don't have a clue."

The 54-year-old Queensland woman was 37 when she suddenly developed
gastroenteritis and began to have trouble staying awake. She was admitted
to hospital but doctors were baffled by her symptoms, which included loss
of feeling in her legs and difficulty concentrating.

During the next 16 months, Wilson was misdiagnosed with multiple sclerosis
and lupus, and was told by one doctor that she only needed to start taking
aerobics classes to get fit. "I finally went to a diagnostic specialist who
diagnosed me with chronic fatigue."

By then, Wilson was experiencing crippling headaches and neck pain, had
trouble following conversations and had to quit her job as a teacher's aide
at a kindergarten. "I was devastated. I absolutely loved my job."

Wilson, who wears a neck brace to reduce headaches and walks with a frame,
works as a volunteer when she can, helping people with CFS. "Most people I
meet, when I tell them what I have, will say, 'Yeah, I get tired like
that.' They have no idea. Wearing a neck brace is painful, it's hot, very
uncomfortable and it's hardly a fashion statement.

"My daughter's wedding is coming up and I'm dreading having to wear it. Why
would I do this if I didn't have to?"

Wilson, like many of the 140,000 Australians who suffer from the
affliction, is fed up with people who question whether CFS, sometimes known
as myalgic encephalomyelitis, is a real condition.

In the 1980s it became known as the yuppie flu, a vague illness that
affected high achievers. Its seemingly unconnected symptoms - including
fatigue, joint and muscle pain, disrupted sleep and an inability to
concentrate - were questioned by doctors and employers who accused
sufferers of being hypochondriacs or malingerers.

Even doctors who believed that the symptoms were real dismissed the
condition as a psychological disorder.

In the past five years, however, research by some of the world's leading
medical organisations has shown CFS is a crippling, physical condition that
affects people of all ages.

The US Centres for Disease Control and Prevention this month launched a
campaign to convince the public and medical profession that CFS is a
serious illness.
CFS costs the Australian community $525million a year, according to
research published in The Medical Journal of Australia. Many sufferers are
unable to work and between 25,000 and 35,000 are housebound.

However, doctors and researchers remain deeply divided on how to diagnose
and treat the condition.

CFS usually begins with flu-like symptoms but progresses to chronic
fatigue. It is not improved by bed rest and exhaustion follows any sort of
physical activity.

Most people with CFS develop it after a viral infection such as from the
Epstein-Barr virus, which causes glandular fever.
In 2002 the World Health Organisation classified CFS as a neurological
disorder and research conducted in the past five years supports the theory
that the illness is caused by a disruption in the brain. Anthony Komaroff,
a professor of medicine at Harvard Medical School and a spokesman for the
CDC campaign, says brain functioning and cell energy metabolism appear
impaired in those with CFS.

Last year, James Baraniuk, a researcher at the Georgetown University
Medical Centre in Washington, DC, reported that CFS patients have a series
of proteins
in their spinal cord fluid that are not present in people without the
condition. "Our research provides initial evidence that it may be a
legitimate neurological disease and that at least part of the pathology
involves the central nervous system," Baraniuk says.

Andrew Lloyd, professor of infectious diseases at the University of NSW's
school of medical sciences, says researchers are starting to reject
previously accepted theories that CFS was caused by an infection or some
form of abnormal immune response to an infection.

"Disorders of blood flow, metabolism or muscles have also been crossed off
the list. The current thinking is that it's a disorder of the brain. We
just don't know where in the brain or exactly what sort of brain chemical
disturbance occurs," Lloyd says.

Peter Del Fante, an Adelaide GP who has treated more than 300 patients with
CFS, says researchers are increasingly finding physical abnormalities that
are only present in people with CFS: "For example, researchers in Japan
have found molecular differences in the blood of people with CFS," he says.
While Colin Neathercoat, director of the ME/CFS Association of Australia,
welcomes the research, he wants doctors to focus on better ways of treating
the condition.

Neathercoat accuses many Australian doctors of advocating outdated and
potentially dangerous treatments.

Since 2002, doctors have used treatment guidelines set up by the Royal
Australasian College of Physicians, which advocate cognitive behavioural
therapy to help patients to cope with the condition, and graded exercise to
build up their strength.

Lloyd says CBT helps patients deal with their physical and mental
limitations. "CBT is a package deal based on helping patients to understand
the pragmatic approach to day-to-day management of fatigue. One of the
typical things in CFS is that patients find the stuff that they used to do
easily, like running for a couple of kilometres, is not possible. They find
that if they walk around the block they feel buggered and it takes them
hours or even days to recuperate. That phenomenon often drives patients to
think it's a bad idea to do anything physical."

Lloyd says that encouraging patients to perform short bouts of exercise
prevents them from pushing themselves too hard. "They need to learn how to
avoid that boom-bust cycle, dividing physical and other activities into
smaller, short segments."

Neathercoat, however, warns that approach can cause more harm than good.
"For some people, they get up and have a shower and that's all they can
manage. The more you push these people with work or recreationally, the
more severe those symptoms become."

Jim Chambers agrees. Eleven years ago his son Jeremy, a 23-year-old
student, developed CFS after a bout of glandular fever.
His condition deteriorated and he spent three years at home, almost
bedridden. "On a good day he was able to make his breakfast and not much
else," Chambers says. "His quality of life was zero, he just focused on
what he had to do to stay alive."

Jeremy remains at home and is unable to work or study. "The prognosis is
pretty bleak, Chambers says. "He was a vibrant young man who was a
high-distinction student working on his honours. His short-term memory is
definitely affected and it's just terribly distressing to have to say
goodbye to your dreams as a young person."

Chambers says Jeremy suffered relapses whenever he tried to push himself
physically or mentally. "The message we have to get out to parents and
teachers is to back off and stop telling kids and teenagers to just push on
when they are sick.

"If a kid is usually a go-getter and suddenly they are not performing and
they've got nothing left in the tank, then obviously something is wrong.
It's better that they take 12 months off to recover rather than pushing on
and becoming critically ill and bedridden."

Lloyd admits that graded exercise does not work for all patients. "A lot of
GPs looked at the guidelines that were sent out and thought that graded
exercise meant that if patients could walk around the block a few times,
they should try to walk around the block 10 times the next week. That sort
of simplistic formula doesn't work. I have patients who are elite athletes
from the Institute of Sport who can still ride for kilometres, but they
used to ride for hundreds of kilometres. At the other end of the scale, I
have patients who are housebound and their exercise program is a walk to
the letterbox and back."
Neathercoat and GPs such as Del Fante are also critical of the way the
Australian guidelines define CFS. "The Royal Australasian College of
Physicians' guidelines set up in 2002 are so vague that basically anyone
with a little bit of fatigue would fit into it," Neathercoat says.

CFS organisations want Australian doctors to follow the Canadian
guidelines. Launched in 2003, they diagnose people with CFS only if they
have experienced six symptoms including general fatigue, post-exertion
fatigue, sleep dysfunction, pain, cognitive impairment and immune or
neuroendocrine problems for more than six months.

"We are approaching the Government to adopt the Canadian guidelines, which
are also critical of graded exercise as a form of treatment," Neathercoat says.
Del Fante says South Australia has developed its own version of the
Canadian guidelines, using post-exertion malaise as the identifying symptom
of CFS.
"If they have to lie down in bed, sometimes for days, to recover from
physical exertion, that's CFS. There is nothing else that does that to you
but CFS. And if you put those people on an exercise program, unless it is
very, very slow and minimal, it's extremely dangerous."

ME/CFS Australia is also calling on the medical profession to stop
referring to the condition as chronic fatigue syndrome and to adopt the
name myalgic encephalomyelitis.

"The view of most patient advocacy groups around the world is that not only
does the name chronic fatigue syndrome trivialise the condition, but the
principal symptom may not be fatigue," Neathercoat says.

"There are so many more symptoms to the illness. Changing the name will
help people to finally accept that this condition is very real and very

Clara Pirani is The Australian's health reporter.



Chronic fatigue syndrome, also called CFS/ME (chronic fatigue
syndrome/myalgic encephalomyelitis) is an illness characterised by extreme
exhaustion. It can strike at any age. The cause is unknown and recovery can
take years. Some people don't recover at all and some suffer relapses for
the rest of their lives.

Persistent profound weakness, extreme tiredness after any form of exertion,
disrupted sleep, pain and neurological and cognitive problems.
Other symptoms include: orthostatic hypotension (a sudden drop in blood
pressure when you stand up); orthostatic tachycardia (increased heart rate
when you stand up); palpitations; shortness of breath with exertion; muscle
twitching; nausea; gastrointestinal and urinary problems; sore throat and
tender lymph nodes; marked weight change, extreme loss or gain.

The cause is unknown but there are avenues under investigation including:
an abnormal response from the central nervous system; an unusual response
to a virus; blood pressure abnormalities; viruses or bacteria in the

Other issues
Lack of community understanding can lead to depression.
Some sufferers are too ill to work, study or socialise. As with other
disabilities, depression is common, particularly when other people don't
take the condition seriously.

Source: Victorian Government

© The Australian

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Date:    Mon, 29 Jan 2007 19:23:30 -0000
From:    Tom Kindlon <tomkindlon OCEANFREE.NET>
Subject: Re: NOT,RES:  An insight into the situation in Belgium

Following on from Bart Stouten Ph.D's informative post "An insight into the
situation in Belgium":
(or http://tinyurl.com/ynug64 )

I thought I would point out that the same documents are also available in
french, see :
 or http://tinyurl.com/2tj42o
"Rapport d’évaluation concernant les centres de référence pour le syndrome
de fatigue chronique"

The french version of the 181-page report in PDF format is at
 Or http://tinyurl.com/39rq96

The URL for the version in Dutch has changed to:
 or http://tinyurl.com/3xb4ak

Tom Kindlon

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End of Co-Cure Weekly Digest of research and medical posts only - 22 Jan 2007 to 29 Jan 2007

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