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Co-Cure Weekly Digest of research and medical posts only - 14 May 2007 to 21 May 2007

Topics of the week:
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Date:    Tue, 15 May 2007 12:22:09 -0400
From:    "Bernice A. Melsky" <bernicemelsky VERIZON.NET>
Subject: RES: Imaging Pain of Fibromyalgia

Imaging Pain of Fibromyalgia

Current Pain and Headache Reports 2007, 11:190-200

Dane B. Cook, Aaron J. Stegner, and Michael J. McLoughlin
Corresponding author: Dane B. Cook, William S. Middleton Memorial Veterans
Hospital, Madison, WI 53706; Department of Kinesiology, University of
Wisconsin, Madison, WI 53706, USA. Email: dcook education.wisc.edu

Brain imaging studies have provided objective evidence of abnormal central
regulation of pain in fibromyalgia (FM).

Resting brain blood flow studies have reported mixed findings for several
brain regions, whereas decreased thalamic blood flow has been noted by
several investigators. Studies examining the function of the nociceptive
system in FM have reported augmented brain responses to both painful and
non-painful stimuli that may be influenced by psychologic dispositions such
as depressed mood and catastrophizing.

Treatment approaches are beginning to demonstrate the potential for brain
imaging to improve our understanding of pain-alleviating mechanisms. Data
from other chronic conditions suggest that idiopathic pain may be
maintained by similar central abnormalities as in FM, whereas chronic pain
conditions with a known nociceptive source may not be.

Future neuroimaging research in FM is clearly warranted and should continue
to improve our understanding of factors involved in pain maintenance and
symptom exacerbation.

Copyright © 2007 by Current Science, Inc.

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Date:    Tue, 15 May 2007 12:31:37 -0400
From:    "Bernice A. Melsky" <bernicemelsky VERIZON.NET>
Subject: RES: Substance Use Disorders in a Primary Care Sample  Receiving Daily Opioid Therapy

Substance Use Disorders in a Primary Care Sample Receiving Daily Opioid

J Pain. 2007 May 10; [Epub ahead of print]

Fleming MF, Balousek SL, Klessig CL, Mundt MP, Brown DD.

Department of Family Medicine, University of Wisconsin, Madison, Wisconsin.

PMID: 17499555

The primary goal of this paper was to present a comprehensive picture of
substance use disorders in a sample of patients receiving opioid therapy
from their primary care physician. A second goal was to determine the
relation of positive urine screens and aberrant drug behaviors to opioid
use disorders.

The study recruited 801 adults receiving daily opioid therapy from the
primary care practices of 235 family physicians and internists in 6 health
care systems in Wisconsin. The 6 most common pain diagnoses were
degenerative arthritis, low back pain, migraine headaches, neuropathy, and
fibromyalgia. The point prevalence of current (DSM-IV criteria in the past
30 days) substance abuse and/or dependence was 9.7% (n = 78) and 3.8% (30)
for an opioid use disorder.

A logistic regression model found that current substance use disorders were
associated with age between 18 and 30 (OR = 6.17: 1.99 to 19.12), severity
of lifetime psychiatric disorders (OR = 6.17; 1.99 to 19.12), a positive
toxicology test for cocaine (OR = 5.92; 2.60 to 13.50) or marijuana (OR =
3.52; 1.85 to 6.73), and 4 aberrant drug behaviors (OR = 11.48; 6.13 to
21.48). The final model for opioid use disorders was limited to aberrant
behaviors (OR = 48.27; 13.63 to 171.04) as the other variables dropped out
of the model.

PERSPECTIVE: This study found that the frequency of opioid use disorders
was 4 times higher in patients receiving opioid therapy compared with
general population samples (3.8% vs 0.9%). The study also provides
quantitative data linking aberrant drug behaviors to opioid use disorders.

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Date:    Tue, 15 May 2007 13:33:11 -0400
From:    Fred Springfield <fredspringfield VERIZON.NET>
Subject: RES: Reliability of a Chronic Fatigue Syndrome Questionnaire

Reliability of a Chronic Fatigue Syndrome Questionnaire

Journal: Journal of Chronic Fatgue Syndrome, Volume: 13 Issue: 4,  Page
Range: 41 - 66 (2006)  Pub Date: 4/5/2007

Authors and affiliations:
Caroline Hawk Hines PhD, Spinal Cord Injury Service, Hines VA Hospital,
Hines, IL, 60141-5128
Leonard A. Jason PhD, Center for Community Research, Chicago, IL, 60614,
<ljason depaul.edu>
Susan R. Torres-Harding PhD, Center for Community Research, Chicago, IL

Background: A diagnostic instrument, the CFS Questionnaire, was developed
for clinicians and researchers to administer to their patients as a
screening instrument for CFS. The CFS Questionnaire is comprehensive,
covering the inclusionary and exclusionary self-report criteria of the
current U.S. case definition (Fukuda et al. 1994). The instrument also
assesses past and current activity levels, and symptoms of post-exertional
malaise to ensure these items are adequately assessed.

Objectives: The goal of the present study was to evaluate the diagnostic
reliability of an experimental measure for assessing chronic fatigue
syndrome (CFS).

Methods: This instrument was administered to 15 persons with CFS, 15
persons with major depressive disorder (MDD), and 15 controls. Using the
Fukuda et al. (1994) diagnostic criteria, raters independently reviewed
participants' CFS Questionnaire responses and rated whether each study
participant met criteria for chronic fatigue syndrome.

Results: This instrument demonstrated good inter-rater reliability.
Further, this instrument demonstrated adequate classification accuracy,
with a 9.3 positive likelihood ratio and a .08 negative likelihood ratio.
Overall, the CFS Questionnaire demonstrated good test-retest reliability,
with intra-class correlation coefficients and kappa coefficients at .70 or
higher for most items. Lower test-retest reliability coefficients were
found for some items assessing temporal symptoms or items requiring an
estimate of time.

Conclusion: The present study suggests that the CFS Questionnaire is a
reliable diagnostic tool. Use of the CFS Questionnaire should promote
higher levels of diagnostic reliability because it allows for accurate
classification of individuals with CFS.

Keywords: Chronic fatigue syndrome, depression, symptomatology, diagnostic

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Date:    Wed, 16 May 2007 11:50:07 +0100
From:    Ellen Goudsmit <ellengoudsmit HOTMAIL.COM>
Subject: RES: Update on pacing

My academic paper on pacing has again been rejected by a Health Psychology
journal on the grounds that it deals with clinical aspects of CFS. It
appears that health psychologists in the UK  are being discouraged from
clinical work and encouraged towards more theoretical pursuits.  As clinical
psychologists tend to deal with psychiatric matters, or emotional aspects of
medical disorders, pacing is of little interest to them. (My concept is
based on the evidence such as the abnormal response to minimal exertion,
e.g. in immune function, metabolism etc, not

If anyone would like an academic review of pacing for their book on CFS/ME,
please contact me. I've run out of Health Psychology journals and this
wouldn't interest clinical psychology journals, BMJ, Lancet etc.

A copy of an earlier version is available on Co-Cure.


Ellen M. Goudsmit  CPsychol CSci AFBPsS
Chartered Health Psychologist

For information on ME and CFS, see:

*** This e-mail and any attachments are confidential and solely for the
information of the addressee.  Any copying or disclosure  to a third party
is unauthorised and the sender is not  responsible for any matter  resulting
from changes to the text made by a third party.

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Date:    Wed, 16 May 2007 12:49:45 -0400
From:    Co-Cure Moderator <ray CO-CURE.ORG>
Subject: NOT,MED: Vicious Cycles that Block FM and CFS Healing - A 2007 Update

Richard Podell, MD, is clinical professor at New Jersey's Robert Wood
Johnson Medical School, with special interests in Fibromyalgia, CFS,
stress-related disorders, and clinical nutrition. He discusses tools to
reverse problems with sleep, hyperventilation, deconditioning, low
magnesium, hormonal imbalances, blood sugar instability, tension, and loss
of hope.

Read this article at

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Date:    Wed, 16 May 2007 13:02:29 -0400
From:    Fred Springfield <fredspringfield VERIZON.NET>
Subject: RES: Feeling bad in more ways than one: comorbidity patterns of medically unexplained and psychiatric conditions

Feeling bad in more ways than one: comorbidity patterns of medically
unexplained and psychiatric conditions.

Journal: J Gen Intern Med. 2007 Jun;22(6):818-21.

Authors: Schur EA, Afari N, Furberg H, Olarte M, Goldberg J, Sullivan PF,
Buchwald D.

Affiliation: Department of Medicine, University of Washington School of
Medicine, Seattle, WA, USA.

NLM Citation: PMID: 17503107

BACKGROUND: Considerable overlap in symptoms and disease comorbidity has
been noted among medically unexplained and psychiatric conditions seen in
the primary care setting, such as chronic fatigue syndrome, low back pain,
irritable bowel syndrome, chronic tension headache, fibromyalgia,
temporomandibular joint disorder, major depression, panic attacks, and
posttraumatic stress disorder.

OBJECTIVE: To examine interrelationships among these 9 conditions.

DESIGN: Using data from a cross-sectional survey, we described associations
and used latent class analysis to investigate complex interrelationships.

PARTICIPANTS: 3,982 twins from the University of Washington Twin Registry.

MEASUREMENTS: Twins self-reported a doctor's diagnosis of the conditions.

RESULTS: Comorbidity among these 9 conditions far exceeded chance
expectations; 31 of 36 associations were significant. Latent class analysis
yielded a 4-class solution. Class I (2% prevalence) had high frequencies of
each of the 9 conditions. Class II (8% prevalence) had high proportions of
multiple psychiatric diagnoses. Class III (17% prevalence) participants
reported high proportions of depression, low back pain, and headache.
Participants in class IV (73% prevalence) were generally healthy. Class I
participants had the poorest markers of health status.

CONCLUSIONS: These results support theories suggesting that medically
unexplained conditions share a common etiology. Understanding patterns of
comorbidity can help clinicians care for challenging patients.

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Date:    Wed, 16 May 2007 14:29:57 -0400
From:    "Bernice A. Melsky" <bernicemelsky VERIZON.NET>
Subject: RES: Sleep and the affective response to stress and pain

Sleep and the affective response to stress and pain.

Health Psychol. 2007 May;26(3):288-95.

Hamilton NA, Catley D, Karlson C.

Department of Psychology, University of Kansas, Lawrence, KS, US.
<nancyh ku.edu>.

PMID: 17500615

Objective: The current study examined sleep disturbance (i.e., sleep
duration, sleep quality) as a correlate of stress reactivity and pain

Design and Outcome Measures: An ecological momentary assessment design was
used to evaluate the psychosocial functioning of men and women with
fibromyalgia or rheumatoid arthritis (N = 49). Participants recorded
numeric ratings of pain, the occurrence of a stressful event, as well as
positive and negative affect 7 times throughout the day for 2 consecutive
days. In addition, participants reported on their sleep duration and sleep
quality each morning.

Results: Sleep disruption was not found to be an independent predictor of
affect. However, sleep was found to buffer the relationship between stress
and negative affect and the relationship between pain and both positive and
negative affect.

Conclusion: These results are consistent with a model in which good-quality
sleep acts as a biobehavioral resource that minimizes allostatic load.

((c) 2007 APA, all rights reserved).

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Date:    Wed, 16 May 2007 14:33:33 -0400
From:    "Bernice A. Melsky" <bernicemelsky VERIZON.NET>
Subject: RES: Novel pharmacotherapy for fibromyalgia

Novel pharmacotherapy for fibromyalgia.

Expert Opin Investig Drugs. 2007 Jun;16(6):829-41.

Wood PB, Holman AJ, Jones KD.

Louisiana State University Health Sciences Center--Shreveport, Department
of Family Medicine, Shreveport, LA 71130, USA. <pwood lsuhsc.edu>

PMID: 17501695

Fibromyalgia is a common disorder that is characterized by chronic
widespread pain, tenderness to light palpation, fatigue and sleep
disturbances. The present lack of a well-accepted model of the disorder has
hampered progress towards adequate treatment.

A review of potential models to explain the pathophysiology underlying its
primary symptom (i.e., chronic widespread pain) lends insight on the
therapeutic potential of novel therapies. Following this, a mechanistic
evaluation of those medications that are under consideration for the
treatment of the disorder is offered.

Adequate treatment will be likely to involve the identification of biologic
subgroups within the greater fibromyalgia construct.

Key insights from basic research are the basis for increased optimism for
effective relief among patients and clinicians.

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Date:    Wed, 16 May 2007 14:44:13 -0400
From:    Fred Springfield <fredspringfield VERIZON.NET>
Subject: RES: Lyme Disease Presenting as Chronic Fatigue Syndrome

Lyme Disease Presenting as Chronic Fatigue Syndrome

Journal: Journal of Chronic Fatigue Syndrome, Volume: 13 Issue: 4, Page
Range: 67-75 (2006) Pub Date: 4/5/2007

Author: Samuel Shor MD, FACP, Associate Clinical Professor, George
Washington University Health Care Sciences, Reston, VA, 20190,
<sshor intmednova.com>

Objective: Chronic Fatigue Syndrome (CFS) by definition represents a
diagnosis of exclusion. Late stage or "Chronic Lyme" infection with or
without "co-infections" is a difficult diagnosis to establish. The symptom
complex of both conditions can be very similar. This case study represents
an attempt to support serious consideration for a subpopulation of patients
otherwise diagnosed with "CFS," as actually representing chronic Lyme disease.

Method: A case study is presented of a 33-year-old man, who for two years,
was being managed as having CFS. However, after ~2 years of utilizing
multiple modalities of management with limited success, the diagnosis of
Lyme was reconsidered. Historical exposure risks to Lyme in this individual
were high. He had prolonged exposure in the highly tick-infested mountains
of North Carolina for 18 months, several years prior to becoming ill. More
aggressive investigation confirmed the diagnosis of Lyme. Appropriate
changes in management were associated with an improved level of functioning
that was far in excess of what maximal management of CFS was able to
achieve. The features of CFS and chronic Lyme can be very similar and
include the following: Profound fatigue often associated with cognitive
impairment. Other common symptoms related to both of these conditions
include sleep disturbances, fibromyalgia, and dysautonomias. In pursuing
clarification of this diagnosis, the author was exposed to a contrast in
medical opinion regarding diagnostic tools and criteria that were perceived
as creating potential barriers to the management of patients presenting
with these symptoms.

Conclusion: Acceptance and awareness of the possibility that Lyme disease
can present as CFS has important therapeutic and prognostic implications.

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Date:    Thu, 17 May 2007 16:39:41 +0100
From:    Ellen Goudsmit <ellengoudsmit HOTMAIL.COM>
Subject: RES: More reasons why journals rejected pacing paper.

Re the paper on pacing, I received more comments from the editors alluding
to their preference for a systematic review, the lack of critique and
failure to discuss al the relevant data, the  emphasis on 'how-to', the
absence of strong supportive data etc.

Those who read the paper on Co-Cure a few weeks ago  may have noted that it
was more than a 'how-to' guide, with its details of  background, definition,
survey and trial results, critique of certain versions, limitations of
recommended version, discussion of alternatives with critique, details of
evidence showing why pacing is more appropriate for some patients, and
basically all relevant data we could include within the 30 page maximum.
Remember this is the first scientific paper on this subject, so people can't
really compare it with anything, and no one really has the definition etc to
allow them to do trials on the same technique required for a systematic
review. This concept needed an introductory review and this is what we
offered.  As for the lack of 'strong supportive data', we included details
of four controlled trials, of which 2 were RCTs, and three of which were
included in the CRD's 'best of' review (see NICE draft and Chambers et al).
We mentioend a negative trial and explained why it failed.

The comments effectively deny psychologists the information they need to
subject pacing to the normal scientific process which can lead to
amendments, further trials etc. They also deny patients the evidence-based
advice to help manage limited energy. It keeps pacing as an ill-defined
'idea', and permits the CBT school to dismiss this technique as lacking
empirical support. Without patient groups  promoting pacing as an
evidence-based strategy, doctors and psychologists will remain relatively
uninterested in this alternative to GET, and editors won't be keen to accept
papers on the subject. They like a 'hot' topic and this isn't it.  Hence the
odd comments. I can't do much more, I've run out of journals.

A recent paper by Edwards et al documented the present tendency to discover
pacing by trial and error and the desire for  more formal guidance. There is
guidance, but journals don't wish to publish it. And some versions on the
net are not scientifically robust, and have not been tested,  meaning that
doctors don't accept it.

The paper needs the status of a peer-reviewed publication to be taken
seriously. I'm sorry I wasn't able to help.


Ellen M. Goudsmit  CPsychol CSci AFBPsS

For information on ME and CFS, see:

*** This e-mail and any attachments are confidential and solely for the
information of the addressee.  Any copying or disclosure  to a third party
is unauthorised and the sender is not  responsible for any matter  resulting
from changes to the text made by a third party.

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Date:    Fri, 18 May 2007 04:36:23 -0500
From:    Jim Roache <jfroache SYMPATICO.CA>
Subject: Res: Novel pharmacotherapy for fibromyalgia. Wood PB, Holman AJ, Jones KD.

Novel pharmacotherapy for fibromyalgia.
Expert Opin Investig Drugs. 2007 Jun;16(6):829-41.
Wood PB, Holman AJ, Jones KD.
Louisiana State University Health Sciences Center--Shreveport, Department of
Family Medicine, Shreveport, LA 71130, USA.
PMID: 17501695

I recently wrote the WHO and then read about an article in The Lancet. I
wrote the editor of Lancet as follows:

Comments on: Use of evidence in WHO recommendations
The Lancet - DOI:10.1016/S0140-6736(07)60675-8

Below, I incorporate portions of a letter to:

WHO Regional Office for Europe
8,Scherfigsvej DK-2100
Copenhagen 0, Denmark

I approached WHO because they were responsible for approval of the first
research protocol for a growing epidemic of disabling syndromes affecting
many in the helping professions....FMS,CFS,SLE, Post-Polio Syndrome, etc.

Recently, one of our national associations developed - under the watchful
eye of Health Canada - Consensus Documents for the "clinical" assessment and
management of FMS/CFS (FM-ME), using an International Panel of pre-approved
and certified specialists and researchers. The FM document (over 100 pages)
is available in PDF format on site at :

It has been known for some time by clinicians, patients and support groups
that pure research criteria may not always (or ever) be applicable in a
clinical environment - something brought out in the Lancet article cited

While not looking for grant money, I thought WHO might be able to assist in
locating someone to do gene sequencing, gene scanning or a related project
to identify the under and over active genes in FM, now that this has been
done in ME - but using a modified approach.

A protein transmitter has already been isolated. Runx1 has been shown to
code a "transcription factor," a master regulator of multiple genes. Runx1
is one of a group of such proteins transmitting external sensory stimuli,
e.g. pain, to the CNS.

The central point I want to make is that we have to limit the sample sizes
and standard protocols for two reasons - our inability to 1. Dx FM
accurately enough in relation to overlapping syndromes and symptoms, and 2.
properly Dx and segregate the five subsets or subgroups known to be part of
the FM syndrome - something we simply cannot (to date) do!

I am not proposing simply a test - although that may prove to be an
appropriate place to begin - certainly test exist and are effective in
identifying genetic susceptibility in a number of conditions.

What we need, ultimately, is a genetic research project. The recent findings
by genecetists in regard to FM dictate a modified protocol within the
traditional model. While I realize that the scientific method requires
double blinded testing of bona fide subjects, random sampling of controls,
results that are replicable, etc., I am increasingly concerned about
redundancy in FM research.

I have always felt "in my gut" that it was a CNS Syndrome - sleep, exercise,
uselessness of traditional medications (including the neuropathic and
narcotics) acting on the wrong receptors, muscle biopsies, spinal fluid
tests, blood tests (showing distorted red blood cells), even fMRIs that show
problems with blood circulation to the pain centres of the brain, the
blood-brain barrier problem, the HPA axis, the thyroid (T3/4), etc., have
all come in for consideration. Each in turn has been heralded as a cure, and
each time their sponsors have beaten a hasty retreat....because they are
symptomatic, not curative!

In fact, they confirm the existence (the Dx) of the syndrome/s....they are

That slow onset FM is genetic is self-evident - what isn't? What we need to
do is find the genes beginning with slow onset - because it to my mind is
purely genetic in origin - while other subgroups may involve a
susceptibility that must be triggered environmentally.

Recently, a drug PTC124 was touted by The Times (UK), based on a piece in
"Nature", as capable of "targeting nuisance mutations" that cause symptoms
varying as a function of any "disrupted" gene. Only  two diseases - CF and
DMD - have been identified "promising a revolution in the treatment of
thousands of conditions" --- now that is hyperbole!

PTC Therapeutics published their findings. I was provided copies. As per
usual, they were far short of what was reported - I did understand the low
percentage issue (only 15% of those with the mutation, afflicted with CF or
DMD and treated had positive outcomes), but there were certain words that
pushed buttons for me - perhaps rightly; perhaps wrongly - with reference to
their implications for slow onset FM:

a. Spinal muscular atrophy, muscle integrity (FM muscles under a microscope
look like a mouse has been gnawing at them - all tiny holes and raggedy
threads dangling - and growth hormone does not correct such normal wear and
tear. So, instead of glassy smooth muscle fibres, we get microscopic tearing
and a corduroy effect - friction rather than a smooth passage by one fibre
against it's neighbour - thus friction, tension. lactic acid build up (low
oxygen) and pain;

b. Two lysomal storage disorders caused by genetic defects in one of the
sex chromosomes - note the mutations between my cousin and me in the
commercial FTDNA geno testing (yDNA) - i.e. in the sex hormones - male/male;
I realize that we would have to look in the autosomal DNA, the conduit for
inherited traits (the other 22 pairs of chromosomes) and not just the sex
gene....but there are reasons in our extended family to do just that - to

c.. Dystrophin protein plays an important structural role as part of a
large complex in muscle fibre membranes. When it is absent, non-functional
or compromised, it leads to degeneration of muscle tissue....that we have!

d.. When the ability to regenerate the muscle is exhausted, muscle wasting
occurs, but boys on PTC124 are more active and have greater endurance. (that
we have - we could only wish PTC124 would improve our activity rate and

e.. Multi-organ compromise - there is organ compromise in FM - irritable
bowel, irritable bladder, heart and BP anomalies, the list goes on. People
with FMS (PWFMS) have spoken for years about fascia, specialized connective
tissue which surrounds muscles, bones, and joints, providing support,
protection and giving structure to the body in three layers: superficial
deep and subserous. It has been accepted by many as causative in organ
malfunction in FM.

Lastly and less importantly Trzanidine (Zanaflex) and Baclofen normally used
for MS muscle spasm are useful to a degree in FM.

REF: Perspectives: A View of Family Medicine - Fibromyalgia - Practical
Treatments for the Family Physician - Richard N. Podell, MD (Written for
Perspectives, a journal of the New Jersey Academy of Family Physicians, and
used with permission.)

Richard N. Podell, MD is a Clinical Professor in the Department of Family
Medicine at UMDNJ-Robert Wood Johnson Medical School, in New Brunswick, NJ)

I think overall, this was one of the best clinical papers on FM written in
recent years. In fact, I use zanaflex - with some success - and part of my
own protocol - to achieve what is known as "baseline" pain levels.

I fully realize that gene sequencing would be required to determine in the
first instance what has gone on between my "high pain threshold" third
cousin and my "no pain threshold" self - with some muscle mass loss and
considerable/increasing weakness in the legs and firearms.

The question (if we target the drug PTC124 - and I see no particular
rational for doing so) is: "Do we have/share a "nonsense mutation?" Mutation
is clearly there in the sex hormone section of our DNA and it should not be.
We have documented that his g grandfather and my gg grandfather are
identical - the same man - so why mutations in both a slow and fast moving
marker ---result  35-37? I surely would like to know!

Our problem is which genes to sequence and which lab - not specializing in
the conventional conditions - would want to check our samples for FM -
rather than for those conditions known to be associated with other known

Almost everyone with a neuromuscular disorder has had, or will have, a
creatine kinase test. Normal function of CK isn't as relevant as what
happens to CK when muscle is damaged. During muscle degeneration, muscle
cells break open and their contents find their way into the bloodstream.
Because most of the CK in the body normally exists in muscle, a rise in CK
levels in the bloodstream indicates muscle damage - my creatine levels were
high - BUT assumed to be due to NSAID use - now discontinued. I am also
totally allergic to all known narcotics from codeine to methadone - I did a
trial that left the supervising specialist gobstruck. Others in my family
are also allergic - we are not talking about the normal side effects - we
are talking the effects normally felt by an addict in withdrawal - it is
something to behold. In one trial using oxy when it first came to Canada, I
had to withdraw, much to the frustration of the neurologist in charge who
tried everything - to enable to help me stay in. Yet now it is a problem
drug causing widespread abuse and addiction - yet I was completely unable to
tolerate it???

But dystrophin and muscle (fascia) involvement - whether our mutations prove
to be of the nuisance variety or other - in so few generations - certainly
aroused my curiosity. Even if there were no nuisance mutation involvement,
but a match in other dysfunctional (under/over active genes in the
sequence), we would have a very big clue as to what to look for when
expanding the sample population in future testing - not in the standard
random cohort model, but within an extended multi-generational family ---
with readily available test subjects accurately diagnosed and controls who
do not need to be random because they are so averse to the notion that there
could be anything awry in our gene pool that they dismiss the very notion
out of hand.

I am 60 and my third cousin - a priest - is 87 - so there is some
urgency --- we do NOT wish to "jump the queue" on CF or DMD patients, and
the cited articles overstated the case for that drug in any event.  I doubt
we have the CFTR gene - although I think one person in our extended family
has it.

mRNA + stop codon = protein damage and disease....could be? Long shot, I
realize, but there is a strong indication in our family genetic profile that
ought to be worth checking - yDNA mutation of this sort could easily extend
in the autosonal sections of our genome. Given the pattern we are seeing
emerge - why not look for mutations in autosomal as well as yDNA in at least
the two of us? Why are those approached to date apparently reluctant?

I have been trying to make a case for a one-family, mutli-generational
cohort - me, male third cousin, sister and niece, several other third
cousins and perhaps one uncle with FM - - this is 5-6 generations - PWFMS -
including controls - including some with very high pain thresholds.

The PTC reports provided were helpful and certainly clarify the impression
incorrectly left by the recent headlines. However, I would still be
willing - as would my doctor I'm sure - to at least test for the nonsense
mutation and other minimum findings like the stop codon to ascertain whether
it would be worthwhile to consider FM a potential target treatable by this
new drug.

The same would be true were we to forget about this one drug for now - there
are others upcoming. IF one existed or could be quickly developed, it would
be one of the best selling medications worldwide in years, I can assure you.

Gene sequencing would be required to determine in the first instance what
had gone on between my high pain threshold cousin and my no pain threshold
self - with some muscle mass loss and considerable and increasing weakness
in the legs and firearms.

FM is a pain amplification syndrome. That has to involve neurotransmitters
and to me that spells CNS and heredity - nationally in some cases
(Scandinavian being most pronounced) and familial - undeniably, hundreds of
families with long-term histories (often under conflicting nomenclature)
being the norm.

Since my Haplogroup is R1b1c, I approached the Scandinavians first - and the
WHO Office there. While my sampling has been genogenetic, a third cousin
with two mutations at variance with me obviously jumped off the paper. One
was a slow mutator - and yes, I know FM would be autosomal, the conduit for
inherited traits (the other 22 pairs of chromosomes) and not the sex gene
used in yDNA genogenealogy.

But given his high pain threshold and my non-existent one, given that FM is
widespread to other third cousins, the previous generation and down to my
niece through my sister, why isn't someone interested in checking this out -
there are plenty of familial controls who think we are hypochondriacal?

Where is the "publish or perish brigade" when you need them? At least a good
paper for a journal or a thesis could result for even a graduate student or
a small lab, given our genetic profile, based on an analysis of those 22
pairs of chromosomes....and it could be done quickly and inexpensively.

Other families FM, but many are not all in the slow onset group, and are not
as large with confirmed and control random subjects of both sexes as readily
available as we are, (including people the profession).

Sadly, I was restricted to 500 words in the letter to Lancet...and could
share no further with Lancet readers. Suffice it to say, that we have
learned an amazing amount about this condition in the past 18 months - FM
(slow onset) is clearly genetic and, since it effects the CNS, belongs in
neurology, not rheumatology, nor with medicine's lost child, psychiatry.

Grasping at straws to save their fading profession, they continue to insert
themselves into the research, clinical and legal aspects of a problem
outside their expertise....and much time and energy is spent in deflecting
their efforts to label us "head cases" --- certainly something to be
welcomed by disability insurance plans - public and private, but simply
annoying "junk science" to those of us who have lived with and worked with
this condition and those who suffer a second onslaught by psychiatry.

Suicide is becoming commonplace as people are driven to despair by sceptical
doctors (in the face of an accumulating body of medical evidence); insurers
who now automatically litigate claims and then hound patients to assist with
re-training and re-employment. This is particularly ironic because I know
nobody in the many subjects I have come into contact with over the years who
was not a classic Type A - or a Type B feigning Type A behaviour because
society rewards (reinforces) such behaviour.

One US doctor in Ireland even wrote a book defining the "Fibro-Personality".
His thesis was - reverse the behaviour, eliminate the symptoms. I offered
the publisher, who asked me to review it, to allow me to work with him and
re-write it or to do a second edition - with all my royalties going to an
Irish trust to educate physicians and the public about the condition. They
declined. I understand that his wife was quite annoyed at the suggestion.

In Lancet, I asked (if they use the letter), "Is there a geneticist in the
house - if so, please make contact for the rest of this hypothesis and to
assess the viability of a future research project?" Someone will do very
well financially and do a great service to society if they put the pieces of
this puzzle together....and we are very close right now." Yet again, I "feel
it in my gut"!

Jim Roache
Ottawa, ON
Tel: 1 613 749-7766
E-Mail: jfroache@sympatico.ca


What I could not share with Lancet readers was the longer piece I had
submitted to the WHO in Denmark and North America.

WHO Regional Office for Europe 8,
Scherfigsvej DK-2100
Copenhagen 0, Denmark
Telephone: + 45 39 171 717
Facsimile: + 45 39 171 818
E-mail: postmaster@euro.who.int

I am approaching you because I thought you might be able to assist me in
locating someone to do gene sequencing, gene scanning or a related project
to identify the under and over active genes in FM, now that this has been
done in ME.

A protein transmitter has already been isolated as you will see below. I
feel that we have to narrow the cohort sizes in FM research for two
reasons - our inability to properly Dx the five subsets of FM and our
inability to Dx
it accurately due to overlapping symptoms in a number of similar, but not
identical, conditions.

It is not a test I am proposing - it is a genetic research project - as
outlined below.

I live in Ottawa, ON, but my extended family is spread extensively over both
the US and Canada - literally from FL to CA, back to the seaboard and many
states in between; in Canada - literally from sea to shining sea.

I have fibromyalgia syndrome (FMS, FM) and have had it in "slow onset" form
[to my mind the trunk of the tree from which the other subsets flow] all of
my life on and off. Then, as it does, it settled in permanently from about
age 40. I retired on DI at age 50 and am now 60.

During that time, I have been something of an activist - had my own website
for some years, but when two national organizations formed in Canada and
began to provide the results of the latest studies from good journals - plus
a primer, as I had done - I felt I could step down - no need for redundancy.
My greatly reduced pages are still there but as a clearing house for
inquiries that direct people using older links (URLs) on other sites
worldwide to the proper channels.

When I started my site, we were in the outer darkness and information that
existed was faulty and spread all over the internet. I remain involved with
both organizations here and others elsewhere to the extent my health
permits. I have also worked with various US organizations, as well as one in
AU. I have reviewed books and articles on occasion and compared notes online
and in person with doctors dealing with particularly challenging cases -
mostly male - who contrary to the social myth - try to deny not embrace
their pending disability - and resist conventional therapies and medical
protocols. My web site summaries were often used as source material for and
by support groups in much of the Western World.

I still do peer counselling and, when Usenet news was active, we had a very
robust group from around the world with whom to work and compare notes. It
was particularly useful in defining the subsets (by symptomology), in
developing trial and error protocols and in testing large cohorts using the
latest "wonder drug" en masse and comparing results.

We have had a little help in raising awareness locally from our CTV
affiliate - and there has been on again-off again media and public interest
from time to time - just point and click on (or cut and paste) the links
below. If they work you will see PSAs featuring local personalities:



I see that there has now been a film made in the US to promote


From the beginning, I have known FM was a CNS based syndrome - and all talk
about sleep, exercise, traditional medications (trial and error protocols) -
all acting on the wrong receptors, muscle biopsy, spinal fluid analysis,
blood tests (finding misshapen red blood cells), fMRIs that showed problems
with blood circulation to the pain centres in the brain, the blood-brain
barrier, the HPA axis and the thyroid (T3/4), etc., was close but off
target. Each time one of these modalities was heralded as a cure, their
sponsors beat a hasty retreat -  they were off the track....but not as far
as they feared.

My difficulty with these approaches was not that they were incorrect, but
that all they would do was treat a symptom or patient sub-group when, in
fact, they confirmed the existence of the syndrome - pinpointing symptoms
from among over 50 in at least five subgroups in a condition that overlapped
others and was terribly difficult to tease out of a random sample of
misdiagnosed people with FM-ME, SLE, RA, Post polio, Lyme and even Gulf War

In addition, even if anyone could, they still were left with subsets within
FM itself - only about 15% truly disabled - and others ranging to not
greatly impacted. Thus, any notion of an accurately identified/diagnosed
population of people with the condition and a random control group - basic
scientific method - was simply impossible.

I also knew FM was a pain amplification syndrome. That had to involve
neurotransmitters and to me it all spelled genetics - heredity - nationally
in some cases (Scandinavian being most pronounced) and familial - undeniably
hundreds of families with a long-term histories of the condition (often
under conflicting nomenclature) being the norm.

I have been in more trials, tests, informal experiments and protocols that a
lab rat....even tried some of the more conventional but non-medical
therapies - chiropractors, massage, acupuncture (several types), warm water
aerobics and a number of "gadgets" , e.g. TENS machines, etc.

My sister and I are scheduled for a standard Genetic Test using the Health
Sciences Department in Newfoundland (wait-listed) - likely 6 months or so -
and I have submitted a complete family history and some recent research
studies to help focus their thinking.

There is no doubt that we are "candidates" for testing. These tests are
exciting and proving to be a valuable aid in the battle against disease, due
to innovative research such as the Human Genome Project. However, a test is
not research. A test looking for unknown genetic markers is like trying to
find a "black hole" in outer space - before the concept was universally
accepted. They may turn up similar mutations between us, but what will that
prove - if different, it may well be unclear what if anything of
significance has been found.

Genetic tests are available for more than 25 adult-onset disorders and for
more than 100 genetic disorders affecting newborns and children.

Most offered to adults today are for diseases caused by a mutation in a
single gene inherited from one parent --- autosomal dominant disorders. The
pattern of inheritance is easy and important to recognize; if several close
relatives on one side of a family (maternal or paternal) have been diagnosed
with the same disorder, you are a likely candidate testing.

We are - but in our case, what can they look for - FM markers (under and
over active genes, have not yet been clearly identified.

I was asked to gather as much information as possible about the incidence of
FM in our family. How many close relatives were affected - minimum three
generations: grandparents, parents, aunts, uncles, siblings and cousins. At
what age was each person diagnosed & what was the outcome? This information,
with supporting medical records, will be used to construct a family pedigree
that provides a history of the disease in a family.

While I am pleased to have been selected, they are hunting in the dark
without a flashlight. I am certain my uncle and father had it ....self-
medicated by alcohol and horse liniment, plus other folk remedies until
recently....by earlier generations.

It is in the family as far out as third cousin - documented and
confirmed....in our surname Roache. I have been studying genealogy seriously
for some years. Being from Newfoundland - as much a lab as Iceland - we have
a small founding and total number of families - 30,000 in our case, so we
make an ideal target for researchers. Sadly one group from Texas recently
did a poor job with one project, and there is now great reluctance there to
take part in further research because a bad taste was left in the wake of
that last group.

However, I have been doing genogenealogy (surname testing) using the
commercial company FTDNA which uses the lab at the University of Arizona. It
is very strict and meticulous in comparison of some of the others. Recently
I thought, as group administrator, I should get 37 yDNA markers done, plus a
deep clade test.

Not surprisingly, I tested R1b1c (no number) - because R1bs are so numerous,
they simply haven't identified all the branches yet. R1b1c - for the most
part - is a place to store R1b samples for future, more-detailed

Even though R1b stretches from Iberia (Spain) to Scandinavia, it seems that
we are what is generally closest to the North Germanic-Scandinavian group -
not the European Modal or the more recent Irish Model (Oxford Ancestry) of
Iberia (Spain primarily). I suspect we are Dane, Saxon, Friesian,
etc....given where our profile falls on the R1b continuum....mine is quite
different from others tested and is closer to a Palatine than anyone else.

Even though we have a relatively small sample group in our surname test
group, we have access to other data bases. We have three Haplogroups in our
surname - I (Norse), Eb3 (Middle East and England) and R1b (western
European - Germano-Celtic-Dane).

Recently, I thought I should get a control sample. The only person in my
family to cooperate was an 87 year old priest in PA. His name is James as
well. We have the same first forbear in Newfoundland - port of embarkation -
New Ross, Co Wexford c 1823, born 1817. John Roach and his wife Jane
Cullen - likely of a similar genetic background - judging by historical
references and grouping of families of those names at the time - they were
in the early 1800 pre-famine Diaspora.

All it says in their obit and on their marker is that they we both from Co.
Wexford, Ireland. John Roach was Father James Roche's great grandfather and
my great-great grandfather....making us third cousins - from two different
generations. In testing, I expected a 37-37 marker match or at worst a 37-36
in the case of a rapid mutator.

We tested 37-35??? DYS# 391 did not match - it is NOT a fast mutator! We had
the Scandinavian (West Norway and Dane) 11 & 13 at markers 385 a & b; and in
464, which is fast moving/mutating, we also had a mismatch - meaning on
average only a 31% probability that we both shared a common ancestor in the
last 4 generations. The company says that is not a problem and they consider
it 36-37. But 464 is fragmented into a,b,c,d - plus - e,f.g - the latter not
checked. He has

15 15 15 16 in a,b,c, and d

and I have

15 15 16 17 (two off)

Now in certain branches of our large extended family, I might accept an
"extra marital event", but not in our two. First - we are the backbones of
the Canadian and US cohorts, and second we know the complete history -
documented and otherwise - of each branch. I have spent years triangulating
the records and meeting these people, and I look so much like his late
father, we might be brothers - and very similar to Father James himself at
the same (earlier) age.

We have the same personality and physical characteristics and, to use the
old fashioned term, are people of character; a "good" family.

I am not in denial - because had it been in other branches, my
confidence quotient might not nearly be as high. One deviation in a rapid
mutator - OK; but two? And then a deviation in a non-rapid mutator in R1b1c
in so short a time span certainly aroused my curiosity.

Why? He feels almost no pain! He had a triple bypass operation a few years
ago and amazed his doctors when he refused the usual medication. He does not
have the condition of total numbness in which he might injure himself -
simply a very high pain threshold - as do others in the family who might
serve as controls in any experiment to compare against those with pain
amplification or a low thresholds (plus the usual array of symptoms
documented as fitting the FM Profile). We have plenty of both!

Again, FTDNA says that the possibility that my gg grandfather John and Fr
James' g grandfather John being the same man is normally less than 40%, but
they find that acceptable - given the documentation at hand. The probability
table under these circumstances is:

3 generations is 19.79%
4 generations is 31.42%
5 generations is 43.15%

They argue: "When you look at probabilities, you need to keep things in
perspective. This calculator is based on the average mutation rate for each
marker. Rules in general deal with the statistically relevant range. Some
rules address exceptions, others do not.

"Here is the way to read the calculator for this exception:  there is around
a 31% probability that you both shared a common ancestor in the last 4
generations, and 69% that your common ancestor lived beyond 4 generations.
However, your paper trail confirms that the 31% scenario prevailed in this

When I asked about a possible link to establishing a genetic marker for FM,
they replied: "This is something that would be seen in the autosomal DNA,
which is the conduit for inherited traits (the other 22 pairs of
chromosomes) and not in the sex gene.

What I was really asking is should I not be tested against Fr James for FM
identifiers - autosomal or otherwise - yDNA mutations suggest possible
mutations in autosomal DNA that would seem worth at least a quick look.

They have the samples and we could either provide new ones, have them tested
there or get or someone else to do them. This might produce a good paper for
peer review and, given recent discoveries around protein in the cells of FM
patients, this might narrow the focus for at least "slow onset" - the most
genetically determined of the five known subgroups, in my opinion.

The goal - ultimately - a genetically targeted drug to dampen the genes or
mute the symptoms (pain, fatigue and brain fog) which would make billions,
plus relieve incredible suffering, considering how widespread this problem
has become. Up to 10% of most modern western populations suffer FM or
related chronic pain syndromes with a host of related and overlapping

Researchers have already isolated markers for CFS (Chronic Fatigue
Syndrome). I have never seen the conditions as identical - believing CFS to
have a viral component, while FM is totally CNS and neurotransmitter
channelled while being based in the genes.

Three Big Pharma companies have FMS drugs coming through the system -
numbered only (no names) in the US - but I fear they are neuropathy
related....as such, they will not be effective in FMS (I have tried some
already - off label); and another is based on "nonsense mutations" only.
There has been some interesting research on both - a sample summary or two
will provide you an idea of where these studies are taking us:

Abstract: Utility of the blood for gene expression profiling and biomarker
discovery in chronic fatigue syndrome


Dis Markers 2002;18(4):193-199
Vernon SD, Unger ER, Dimulescu IM, Rajeevan M, Reeves WC.
Division of Viral and Rickettsial Diseases, National Center for Infectious
Diseases, Centers for Disease Control and Prevention, Atlanta, GA 30333,
Chronic fatigue syndrome (CFS) is a debilitating illness lacking consistent
anatomic lesions and eluding conventional laboratory diagnosis.
Demonstration of the utility of the blood for gene expression profiling and
biomarker discovery would have implications into the pathophysiology of CFS.

The objective of this study was to determine if gene expression profiles of
peripheral blood mononuclear cells (PMBCs) could distinguish between
subjects with CFS and healthy controls. Total RNA from PBMCs of five CFS
cases and seventeen controls was labelled and hybridized to 1764 genes on
filter arrays.

Gene intensity values were analyzed by various classification algorithms and
nonparametric statistical methods. The classification algorithms grouped the
majority of the CFS cases together, and distinguished them from the healthy

Eight genes were differentially expressed in both an age-matched
case-control analysis and when comparing all CFS cases to all controls.
Several of the differentially expressed genes are associated with
immunologic functions (e.g., CMRF35 antigen, IL-8, HD protein) and implicate
immune dysfunction in the pathophysiology of CFS.

These results successfully demonstrate the utility of the blood for gene
expression profiling to distinguish subjects with CFS from healthy controls
and for identifying genes that could serve as CFS biomarkers.

PMID: 12590173 [PubMed - as supplied by publisher]

This is fine for CFS - and for many of us with FM who also suffer
debilitating fatigue (CFS?) - I'm uncertain. Both conditions are again
receiving attention - I believe in part because of geneticists and recent
announcements (like the study above).

Runx1 gene research has shown it to code for a protein "transcription
factor," a master regulator of multiple genes. Runx1 is part of a group of
proteins that are key in transmitting external sensory stimuli - like pain
and movement - to the spinal cord and brain (CNS). This moves us from genes
to proteins re CFS/ME - and may well be the conductor in FMS/FM as well.

I think we (our and similar families) would be a great collection of
specimens (5-6 generations - that's the only way third cousins could have
it, as well as my niece). And there are family "controls"....perfect
because, like many, they think we are hypochondriacs.

Studies to date have used larger or small but more diverse cohorts - but we
know there is great difficulty in achieving accurate diagnoses (and
therefore  uniform populations to test), considering the number of
over-lapping symptoms with 8-10 different conditions from chromic fatigue to
post-polio syndrome which manifest similarly. This rigidity in approach
seems to me unnecessary.

It may be possible to do this research more successfully and inexpensively
with one family than with a broader, less uniform or small, diverse and
misdiagnosed sample of the FM population and controls. I realize this is a
deviation from the standard research model, but I think a justified
exception. Studies done on extremely small sample groups are just as
exceptional and only purists object.

Someone must surely want to undertake a project like this - a trial not a
test - a research experiment not a diagnostic process - considering the
potential rewards in terms of peer-reviewed publication, prestige and a
medication that will work at the source and not leave people dealing with
protocols which are largely ineffective.

Consider the offset in DI alone, plus currently lost productivity. Most
people with this condition were "go-getters" - once active, successful,
educated professionals - struck down in their prime. We look normal - we
want to be normal - to be back in the world. Talk of our being slackers or
neurotics is not only misguided, it is insulting!

I think we have a way here to identify the mutated genes, quickly and
effectively. Then, given all the work that has been done on the CNS, and the
medications we have already - the solution may be closer at hand than is the
norm - considering what we know about proteins like the one above.

We are really ready to tackle this at the cellular level if we get the
under/over active genes; then look at the Runx1 and/or similar proteins and
their direct link to the spinal cord and brain (CNS). With luck, we might
take a great leap forward very quickly - using a homogenous familial
sample - including suffers and non-sufferers.

While the three summaries below are suggestive, in North America, the
consensus is that depression comes after onset - that no great psychological
cause and effect exists between affect and FM manifesting; in fact, most
hold it to be the reverse - yet we spend time and energy fending off the
"hired guns" and client-seeking psychiatrists - that would be better spent
collaborating on getting a management modality for the primary symptoms this
returning us to full or nearly full function.

Mechanisms of Disease: genetics of fibromyalgia.
Ablin JN,
Cohen H,
Buskila D.
Department of Rheumatology, Tel-Aviv Sourasky Medical Center, Tel-Aviv
University, 6 Weizman Street, Tel Aviv 64239, Israel. <ajacob post.tau.ac.il>

Fibromyalgia is characterized by widespread pain and tenderness, and has a
significant familial component. The etiology of fibromyalgia remains
unclear, but genetic factors seem to have a significant role, and are
influenced by environmental factors [in some subsets - JFR].

Research over the past two decades has demonstrated that genetic
polymorphisms in the serotoninergic, dopaminergic and catecholaminergic
systems of pain transmission and processing are involved in the etiology of
fibromyalgia, but additional candidates continue to emerge.

Fibromyalgia is thought [by some - others totally and correctly disagree] to
belong to the group of affective spectrum disorders, which include related
psychiatric and medical disorders.

As the concept of affective spectrum disorders continues to evolve, progress
in the understanding of the genetic basis of related functional disorders,
such as irritable bowel syndrome and post-traumatic-stress disorder, is
aiding our understanding of the genetic basis of fibromyalgia.

PMID: 17133252 [PubMed - indexed for MEDLINE]

The genetics of fibromyalgia syndrome.
Buskila D,
Sarzi-Puttini P,
Ablin JN.
1Ben Gurion University, Department of Medicine H, Soroka Medical Center and
Faculty of Health Sciences, Beer Sheva, Israel. <dbuskila bgumail.bgu.ac.il> ,
2L Sacco University Hospital, Senior Rheumatologist, Rheumatology Unit,Via
GB Grassi 74, 20157 Milano, Italy. <sarzi tiscali.it> , 3Tel-Aviv University,
Departments of Rheumatology, Tel-Aviv Sourasky Medical Center and Sackler
Faculty of Medicine, Tel-Aviv, Israel. <ajacob post.tau.ac.il>.

Fibromyalgia syndrome (FMS) is a common chronic widespread pain syndrome
mainly affecting women [woman are more commonly diagnosed, but this may be a
function of the male tendency to soldier on - JFR].

Although the etiology of FMS is not completely understood, varieties of
neuroendocrine disturbances, as well as abnormalities of autonomic function,
have been implicated in its pathogenesis. The exposure of a genetically
predisposed individual to a host of environmental stressors is presumed to
lead to the development of FMS.

Fibromyalgia overlaps with several related syndromes, collectively
compromising the spectrum of the functional somatic disorder. FMS is
characterized by a strong familial aggregation.

Recent evidence suggests a role for polymorphisms of genes in the
serotoninergic, dopaminergic and catecholaminergic systems. These are not
specific for FMS and are similarly associated with additional comorbid
conditions. The mode of inheritance in FMS is unknown, but it is most
probably polygenic.

Recognition of these gene polymorphisms may help to better subgroup FMS
patients and guide a more rational pharmacological approach.

Future genetic studies conducted in larger cohorts of FMS patients and
matched control groups may further illuminate the role of genetics in FMS.
[I contend the reverse may be true - JFR]

PMID: 17187510 [PubMed - as supplied by publisher]

Biology and therapy of fibromyalgia. Genetic aspects of fibromyalgia
Buskila D,
Sarzi-Puttini P.
Department of Medicine H, Soroka Medical Center and Faculty of Health
Sciences, Ben Gurion University, Beer Sheva, Israel.
<dbuskila bgumail.bgu.ac.il>

Genetic and environmental factors may play a role in the etiopathology of
fibromyalgia syndrome (FMS) and related syndromes. There is a high
aggregation of FMS in families of FMS patients. The mode of inheritance is
unknown, but it is most probably polygenic.

There is evidence that polymorphisms of genes in the serotoninergic,
dopaminergic and catecholaminergic systems play a role in the etiology of
FMS. These polymorphisms are not specific for FMS and are associated with
other functional somatic disorders and depression.

Future genetic studies in the field of FMS and related conditions should be
conducted in larger cohorts of patients and ethnically matched control
groups. [Again, I suggest the reverse - respectfully. Since Dx is so
difficult, it is impossible to ensure a universe of people with FM - let
alone which have the different subsets, not to mention those misdiagnosed
when they in fact have other conditions which manifest in  overlapping
symptoms - JFR].

PMID: 16887010 [PubMed - indexed for MEDLINE]

If you hear a boiling sound, it is my blood. To suggest that there is an
affective aspect at the source of this condition, one must ask why everyone
matching that criterion does not have FM. If etiology is unknown and there
are environmental triggers, what is the explanation for slow onset FM? I
will need to be shown someone with somatic or depressive symptoms with
matching markers before I can accept the suggestion that there is such

Speculation - even in a scientific publication - is fine if stated and
interpreted as such. Unfortunately, this notion has been pounced upon by
"special interests" who do not have our welfare as a primary concern. I
am so tied - after all these years of being ill and after seeing so much
junk science and so much unnecessary and wasteful duplication of
unsuccessful past research that I could scream - instead, I would prefer to
work with a geneticist who can think outside the box and build on the good
science we do have in hand.

I think that this might be another opportunity for patient - professional
collaboration to make a real contribution - as with our recent Canadian
Consensus Documents for Clinical Practice by an International Panel of

By connecting the dots from DNA to the protein (above) or another of that
type to cell replication manifesting in the ways always thought to be causes
(now symptoms subject to confirmation), thus possibly finding a way to break
the pain cycle - likely on the outward or downward cascade, it just might be
possible to  muffle the amplification of pain, resolve the fatigue and
reduce brain fog.

I don't think in terms of a cure, but of more effective means to manage
symptoms in the short to medium term.

I thought there was a general consensus emerging that FM was a CNS centred,
genetically-based syndrome - the result being clear manifestations in the
HPA Axis, the thyroid (T3/T4, etc), spinal fluid, neurotransmitter
imbalances, growth hormone levels or malabsorption, etc, as well as fMRIs
indicating impeded blood flow to the pain centres of the brain. Every pain
medication to date is either blocked at the blood-brain barrier or acts on
the wrong pain receptors.

Pain amplification is caused by imbalanced neurotransmitters due to flawed
genetic instruction - gene to protein to cell. Genetic engineering seems out
of reach for now; and we ought to concentrate research on dampening the
under or over active genes, by working on the outgoing side of the pain
signal cascade.

I understood that the objective was to break the closed loop  - the pain
loop - or cycle - much as one would interfere with the outgoing signal from
a thermostat to a furnace to lower the heat - stopping the furnace from
running too hot.

I think "symptom management" - as with the common cold. We cannot yet ensure
a consistently "universe" of people guaranteed to have FM by accurate Dx,
let alone separate them by FM subset, against which to compare controls
(blinded or otherwise), so we simply have to "think outside the box"!

We have to face that fact and say - this may be grounds to consider a
deviation from accepted scientific research protocols....not all that
different from using a small sample set of participants.

That being the case, I suggest we find a large extended family (like ours)
where there is a clear Dx of "slow onset"  FM and compare the DNA of those
members with and without the condition.

Replication would involve using the same research protocol with a similar
family or families....not a sample of poorly or incorrectly Dx'd subjects
against controls.

All this other "stuff" that I see published over and over and over -
psychology (CBT), bio-feedback, meditation, etc., and exercise (with post
exertional malaise for most), new drugs or drug combos (to allow
re-patenting) has been discussed and researched to death in my time (at
least 25 years) as a "patient and activist. It now seems counterintuitive.

But, after approaching a number of labs and organizations, nobody seems
interested - even though my own family is an ideal candidate. We have it
Dx'd to the third cousin and 5-6 generations. The controls think we are
hypochondriacs....meaning they would not believe they had the genetic
profile, even if they did!

It seems to me logical that, given the yDNA results (mutations) between my
third cousin and me, someone (especially in locations with Scandinavian or
in Haplogroup R1b populations) should want to test the autosomal markers
between us (and/or amongst other family members) and see if additional
mutations or under/over active genes present in our samples.

We should have tested 37-37 and we tested 35-37 --- unexplained marker
variances --- what else is divergent in our DNA? We know where to look, but
nobody seems to see the potential. Statistically unexpected mutations in one
region suggest at least the possibility of unexpected mutations in the 22
chromosomes among which one would normally look for inherited predisposition
to medical complications.

I would have thought the "publish or perish brigade" or some "post-doc"
researcher might jump at the chance, but no. Then I see all these papers of
questionable merit published - nothing new - but incredible redundancy with
work done earlier or in other countries or published in other
journals....showing my age and time with the dragon, I suppose.

Someone could go back 10 years and see how many research projects are simply
"sawing sawdust" to be blunt....trying the "same old same old" with minor
tweaking, if any, and producing the same (totally predictable) lack of
practical results, often ending with the observation that further research
may be required.

We know we have the proteins in sight. We even have suspected markers in the
DNA, and we certainly know that the cells in the CNS are (at least in part)
duplicating either as per faulty score genetic instruction  or faulty
instruction in the protein and so the cells can potentially go on their
merry way unexamined despite all the ways in which we can now prove they are
there and what they do as a result of their faulty duplication in the CNS.

The stakeholders each have their staunchly defended notions - but no
conclusive proof. Well, I think we have had enough of looking at the
symptoms - we know the body is often reasonably sound - no real physical
damage as in other diseases - so it is either the proteins - which we now
suspect we know - or those markers, genes, mutations. The challenge is to
isolate the faulty instructions (under and over active markers/genes) and
then try to find a way to blunt their effect....something much more readily
done under the protocol I suggest than under the standard scientific
method - which has gotten us exactly nowhere.

We can't do that by looking at unavoidably diverse samples. We need
consistency - the best being familial - and we need to compare them  marker
by marker, gene by gene in one slow onset family (because there will be
inadequate consistency in a larger more diverse group) - and then do it
again with an identical family a time or two....to get the CNS cells under
control so as to break that circuit or cascade.

Right now, all we do is give the client placebos, or tell them everything
is really fine, the body simply needs therapy or more exercise or some other
foolish thing.

Is there a geneticist in the house???

Any advice or assistance you might provide would be deeply
appreciated....and I suspect at least a good paper or thesis would result
given our unique situation. It would be a real shame to miss this
opportunity. Other families have it, but many are not in the slow onset
group, and many are not as large with confirmed Dx and healthy controls in
both sexes as were are.

Thank you for your time and attention. please feel free to contact me at any
time for further information or clarification.

Jim Roache, MBA

Ottawa, ON
E-Mail <jfroache sympatico.ca>

[Return to top]


Date:    Fri, 18 May 2007 13:46:50 -0400
From:    "David Axford <axford worldonline.co.uk> via Co-Cure Moderator"
Subject: NOT,RES: Latest ME Research

The latest ME & CFS References are now available at:

Click on the:
"Latest Research" button which is in the left-hand column.
You'll then see the "ME/CFS References " clearly marked 1st June 2007 in
the right hand frame. This has a "NEW" graphic alongside. Click on the
button (microscope on top of the globe).

You may also find the article using the SEARCH tool which is on the home page.

It is possible that your browser won't log on first time due to the large
number of people who are accessing the web-site. Please be patient and try
again at different times when it's less busy.

[Return to top]


Date:    Fri, 18 May 2007 14:04:06 -0400
From:    Co-Cure Moderator <ray CO-CURE.ORG>
Subject: NOT,RES: abstracts from the Annual European Congress of Rheumatology

The abstracts from the Annual European Congress of Rheumatology
to be held in Barcelona, Spain 13-16 June 2007 (many of which deal
with fibromyalgia) can be found at


[Return to top]


Date:    Fri, 18 May 2007 18:59:36 -0400
From:    Fred Springfield <fredspringfield VERIZON.NET>
Subject: RES: Depression, Chronic Fatigue Syndrome, and Fibromyalgia:  An Update

Depression, Chronic Fatigue Syndrome, and Fibromyalgia: An Update

Journal: Journal of Chronic Fatgue Syndrome, Volume: 13 Issue: 4,  Page
Range: 77-106 (2006)  Pub Date: 4/5/2007

Authors: Kenneth R. Kaufman MD, MRCPsych, Paul J. Goodnick MD

Affiliation: UMDNJ-Robert Wood Johnson Medical School, New Brunswick, NJ

Centers for Disease Control criteria for chronic fatigue syndrome (CFS)
specifically recognize that patients can have both CFS and depression. The
clinician's challenge is to judge for each individual patient whether the
complaint of fatigue is primarily depression, physical illness, such as
CFS, or a combination of both.

This review differentiates CFS and fibromyalgia, discussed as "chronic
fatigue syndrome and related immune deficiency syndromes" (CFIDS), from
depression in terms of physical signs, symptoms, biological parameters,
brain imaging, immunology, and treatment. The review focuses on practical
applications of research findings with a further focus on future ability to
show clear biologic separation and specific treatment.

When depressive symptoms exist with those of CFS, accurate differentiation
can usually be accomplished by focusing on diagnostic criteria. Presence of
multiple physical signs and symptoms of CFIDS may be of great value. In
terms of laboratory testing, a single helpful test may be measuring the
plasma cortisol, which is usually high in depression and low in CFS. Future
research should focus on the combination of plasma cortisol with an index
of serotonin function, which is high in CFIDS and low in depression.
Additional research should focus on neuroimaging and immune differentiation.

Combination of multiple tests should result in a significant and clinically
useful separation between CFIDS and major depressive disorder (MDD). In
treating patients with significant depression or MDD with CFIDS, one should
think of the noradrenergic approach using bupropion or low-dose tricyclic
antidepressants in combination with a selective serotonin reuptake
inhibitor, especially sertraline, to aid improvement of global, pain, and
immunologic parameters.

Alternatively, serotonin norepinephrine reuptake inhibitors (venlafaxine
and duloxetine) should be considered. Future treatment research should
focus on larger placebo-controlled, double-blind trials of these and other
antidepressants as well as the evaluation of psychostimulants,
electroconvulsive therapy (ECT) and repetitive transcranial magnetic
stimulation (rTMS).

Keywords: Chronic fatigue syndrome, fibromyalgia, depression, treatment,
neurobiology, endocrine, cortisol, 5HIAA, fludrocortisone, P300, immune
modulation, neuroimaging, antidepressant, serotonin, psychostimulant,
atypical antipsychotic, ECT, rTMS

[Return to top]


Date:    Fri, 18 May 2007 19:12:09 -0400
From:    Fred Springfield <fredspringfield VERIZON.NET>
Subject: RES: Service Utilization, Barriers to Service Access, and  Coping in Adults with Chronic Fatigue Syndrome

Service Utilization, Barriers to Service Access, and Coping in Adults with
Chronic Fatigue Syndrome

Journal: Journal of Chronic Fatigue Syndrome, Volume: 14 Issue: 1, Page
Range: 5 - 21 (2007)

Authors and affiliations:
Sachi Thanawala, BOT, OTR/L, Department of Occupational Therapy, University
of Illinois at Chicago, Chicago, IL, 60612
Renée R. Taylor, PhD, Associate Professor, Department of Occupational
Therapy, University of Illinois at Chicago, Chicago, IL, 60612,
<rtaylor uic.edu>

Objective: In a sample of 47 adults with CFS, we aimed to describe patterns
of service utilization, identify barriers to service access, and explore
the relationship between service utilization and coping styles.

Method: A questionnaire assessing service utilization frequency and
barriers to service access was administered to a sample of 47 individuals
with CFS. The Illness Management Questionnaire was used to assess
relationships between coping styles and service utilization.

Results: A Cochran's Q test of homogeneity revealed that medical and CFS
self-help services were most frequently used and rehabilitation services
were least frequently used. In terms of service accessibility, 80.9% of
participants reported at least one barrier. Lack of financial (including
insurance) resources and lack of knowledge about service availability were
the two most frequently reported. In terms of coping styles, symptom
focusing was positively associated with use of CFS self-help services and
with use of in-home services and social service agencies. Information
seeking was negatively associated with use of in-home and social service
agencies and with use of mental health services.

Conclusion: These findings can be used by health-care professionals and
advocacy-based organizations to develop programs focused on mass education
campaigns for health-care providers, increase knowledge of service
availability among individuals with CFS, and to understand relationships
between certain types of coping styles and service preferences.

Keywords: Chronic fatigue syndrome, service utilization, access, coping

[Return to top]


Date:    Fri, 18 May 2007 19:44:09 -0400
From:    "Bernice A. Melsky" <bernicemelsky VERIZON.NET>
Subject: RES: Vitamin D and rehabilitation: improving functional  outcomes

Vitamin D and rehabilitation: improving functional outcomes.

Nutr Clin Pract. 2007 Jun;22(3):297-304.

Shinchuk L, Holick MF.

Boston University Medical Center, 715 Albany Street, M-1013, Boston, MA
02118. <mfholick bu.edu>

PMID: 17507730

Vitamin D inadequacy is pandemic among rehabilitation patients in both
inpatient and outpatient settings.

Male and female patients of all ages and ethnic backgrounds are affected.
Vitamin D deficiency causes osteopenia, precipitates and exacerbates
osteoporosis, causes the painful bone disease osteomalacia, and worsens
proximal muscle strength and postural sway.

Vitamin D inadequacy can be prevented by sensible sun exposure and adequate
dietary intake with supplementation.

Vitamin D status is determined by measurement of serum 25-hydroxyvitamin D.
The recommended healthful serum level is between 30 and 60 ng/mL.
25-Hydroxyvitamin D levels of >30 ng/mL are sufficient to suppress
parathyroid hormone production and to maximize the efficiency of dietary
calcium absorption from the small intestine. This can be accomplished by
ingesting 1000 IU of vitamin D(3) per day, or by taking 50,000 IU of
vitamin D(2) every 2 weeks.

Vitamin D toxicity is observed when 25-hydroxyvitamin D levels exceed 150
ng/mL. Identification and treatment of vitamin D deficiency reduces the
risk of vertebral and nonvertebral fractures by improving bone health and
musculoskeletal function. Vitamin D deficiency and osteomalacia should be
considered in the differential diagnosis of patients with musculoskeletal
pain, fibromyalgia, chronic fatigue syndrome, or myositis.

There is a need for better education of health professionals and the
general public regarding the optimization of vitamin D status in the care
of rehabilitation patients.

[Return to top]


Date:    Sat, 19 May 2007 13:18:52 -0400
From:    "Bernice A. Melsky" <bernicemelsky VERIZON.NET>
Subject: RES: Clinical features of the stomatognathic involvement in fibromyalgia syndrome: a comparison with temporomandibular disorders  patients

Clinical features of the stomatognathic involvement in fibromyalgia
syndrome: a comparison with temporomandibular disorders patients.

Cranio. 2007 Apr;25(2):127-33.

Salvetti G, Manfredini D, Bazzichi L, Bosco M.

Section of Prosthetic Dentistry, Department of Neuroscience, University of
Pisa, Italy. <salve106@inwind.it>

PMID: 17508633

Several studies have reported an involvement of the stomatognathic system
in the course of fibromyalgia (FM) similar to that which characterizes
temporomandibular disorders (TMD). The aim of this study was to investigate
and compare the clinical features of stomatognathic dysfunction in patients
with FM and TMD.

Ninety-three FM patients underwent an assessment according to the RDC/TMD
guidelines. Prevalence of the different RDC/TMD diagnoses and some clinical
parameters of FM patients were compared with those of 181 patients affected
by TMD. Seventy-four (79.6%)

FM patients presented at least one RDC/TMD diagnosis and showed lower mean
maximum voluntary and passive mouth opening values than TMD patients.
Moreover, 34 FM patients presented with trigger and/or tender points.

Results of the present study confirm the high rate of involvement of the
stomatognathic system in the course of FM and support the need for a
careful multidisciplinary approach to patients with TMD, including the

[Return to top]


Date:    Sat, 19 May 2007 13:40:43 -0400
From:    Fred Springfield <fredspringfield VERIZON.NET>
Subject: RES: The Feasibility of Reviewing Chronic Fatigue Syndrome  Clients at a Distance: A Teleconference Pilot Study

The Feasibility of Reviewing Chronic Fatigue Syndrome Clients at a
Distance: A Teleconference Pilot Study

Journal: J of Chronic Fatigue Syndrome, Vol. 14 (1) (2007), pp. 23-32

Authors: Gwyneth C. Weatherburn PhD, MSc, TDCR, ACP, SRR; Amelia Goldsmith
Lister BOT, MSc; Leslie J. Findley CLJ, TD, MB, ChB, MD, FRCP, FACP

Gwyneth C. Weatherbum is affiliated with Research Centre for Health
Studies, Buckinghamshire Chilterns University College, Chalfont St Giles,
HP8 4AD, UK.
Amelia Goldsmith Lister is affiliated with Chronic Fatigue Unit, Oldchurch
Hospita;. Romford, Essex RM7 OBE, UK.
Leslie J. Findley is affiliated with CFS Diagnostic & Management Service,
Essex for Neurological Sciences, Oldchurch Hospital, Romford, Essex RM7

Address correspondence to: Gwyneth C. Weatherburn, Research Centre for
Health Studies, Buckinghamshire Chilterns University College, Chalfont St
Giles, HP8 4AD, (E-mail: <gwyn.weatherburn@bcuc.ac.uk>).

Objective: There continues to be a shortage of clinical staff specialising
in the treatment of CFS (ME). In order to access specialist care, many
clients have to undertake long or difficult journeys that may exacerbate
their symptoms. This exploratory study aimed to reduce these travel
problems by the introduction of a Teleconference Review Clinic (TRC).

Method: A TRC was booked for six CFS clients who would normally have
face-to-face review by specialists 44 miles away. Questionnaires were used
to elicit the views of both clients being reviewed and clinicians
undertaking the review at a distance. Differences in distances travelled by
clients for conventional face to face and telemedicine review were
calculated and comments about the teleconference made by clients and
therapists were noted.

Results: There was general satisfaction with the quality of the pictures
and sound during the reviews. Clinicians were able to obtain all the
information required to undertake all clinical assessments. For two clients
the clinical management was changed after the consultation and for one
client an issue was identified that required referral to another clinician.
For clients who lived nearer to the teleconference hospital, the journey
saved ranged between 1 mile and 85.8 miles, the mean being 64.2 miles.

Conclusion: This pilot study does suggest that telemedicine in this area of
medicine is logistically viable and effective, and indicates that a larger
study is needed.

Keywords: Chronic fatigue syndrome, teleconference, review

[Return to top]


Date:    Sun, 20 May 2007 00:47:02 +0200
From:    Jan van Roijen <j.van.roijen CHELLO.NL>
Subject: res: FM & CFS -Identification of differential genetic profiles


Send an Email for free membership
       >>>> Help ME Circle  <<<<
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Abstract from the Annual European Congress of Rheumatology
to be held in Barcelona, Spain 13-16 June 2007


F. J. Garcia-Fructuoso1, J. Lao-Villadoniga2, E. Olano-Martin3,
C. Santos4, V. Poca-Dias1, J. Fernandez-Sola5, A. Martinez6,
L. Simon3, D. Tejedor3

1Rheumatology Department, CIMA Clinic,
2Molecular Genetics, Dr.Echevarne Laboratory, Barcelona,
3Molecular Genetics, Progenika Biopharma, Derio-Bilbao,
4Biology-CIRN, University of the Azores, Azores, Portugal,
5Internal Medicine, Hospital Clinic, Barcelona,
6Molecular Genetics, Asociacion Genica, Derio-Bilbao, Spain

Fibromyalgia (FM) and Chronic Fatigue Syndrome (CFS) are
two illnesses that presently have a diagnosis exclusively clinical.
Significant differences in the prevalence of FM and CFS (2-4 %
to FM and 0,2-0,5 % to CFS) have been reported in almost all
the works, many publications, as well as the clinical experience,
put forward an important overlapping (40 - 60 %) between both
syndromes, what indicates a dichotomy in the data.

The definition criteria of case for FM and CFS, instead of
defining the diseases by their characteristics, make special
emphasis in the severity of the symptoms to perform a
diagnosis. Thus, in FM it will be the widespread pain and the
generalized tenderness in the methodical touch of predefined
points what will lead us to the diagnosis19; in the CFS we will
need, as a major criterion, a physical and cognitive abnormal
fatigue with an high impact of the premorbid activities of the
patient. Therefore, the stratification of the symptoms makes part
of the diagnosis of both diseases and it is necessary for a
correct therapeutic and prognostic orientation.

The need for subtypes as been established. In this study the
variation in Single Nucleotide Polymorphisms (SNPs) of
different ethiopathogenic pathways, was used to take insights in
the genetic profile of FM and CFS. Furthermore, we related the
severity of both diseases, measured with validated self-report
measures, with the variation in SNPs.

The association study was conducted to test the hypotheses that
FM and CFS are different clinical and genetic entities and that
the phenotypic variation observed in both disease, is in part the
result of a different genetic profile.

The ACR'90 and the Fukuda-CDC'94 diagnosis criteria were
used respectively for the diagnosis of FM and CFS. A group of
403 women (186 FM / 217 CFS) and an independent validation
group of 282 women (126 FM / 156 CFS) were selected. The
FIQ and CDC-Symptom Inventory questionnaires were used to
define severity subgroups.

A total of 107 SNPs belonging to neurotransmitters (dopamine
and serotonin), Propiomelanocortin (POMC), Thioredoxin
reductase, Glucocorticoid receptors, Interleukins (IL), Nitric
Oxide Synthetase (NOS), Tumor Necrosis Factor (TNF),
Corticotropin receptors, Catechol-O-Methyltransferase (COMT)
and Tryptophan hydroxylase (TPH) genes were genotyped for
each patient.

We identified 15 SNPs to be able to discriminate between FM
and CFS patients with a 11.5 Likelihood Ratio (LR+, 95%
specificity). The analysis of further SNPs allowed differential
genetic profiling between the most aggressive FM phenotype
and the mild forms (12.4 LR+) and between a severe CFS
phenotype and milder one (12.4 LR+).

The models described in this paper are suitable for the
differential diagnosis between FM and CFS, as well as to
differentiate subtypes between severe and milder phenotypes of
both diseases, in a female Spanish population.These subtypes
could represent different illnesses or clinical situations that, in
the future, can be differentiate.

[Return to top]


Date:    Sun, 20 May 2007 10:41:16 +0200
From:    "Dr. Marc-Alexander Fluks" <fluks COMBIDOM.COM>
Subject: RES: CFS/ME & FM papers, published since April 2007

Source: NCBI PubMed
Date:   May 20, 2007
URL:                                                             http://www.ncbi.nlm.nih.gov/entrez/query.fcgi
        Topic=((chronic fatigue) OR (myalgic encephalomyelitis)) OR fibromyalgia
Ref:    In the update, you will only find journals that are indexed by
        Medline (PubMed).
        All scientific papers 1938-today,
        Search scientific papers,
        Figures computer analysis scientific papers,
        All popular papers 1900-today,

CFS/ME & FM papers, published since April 2007

___ The G, Bleijenberg G, van der Meer J.
       The Effect of Acclydine in Chronic Fatigue Syndrome: A Randomized
       Controlled Trial.
       PLoS Clin Trials. 2007 May 18;2(5):e19.
___ Salvetti G, Manfredini D, Bazzichi L, Bosco M.
       Clinical features of the stomatognathic involvement in fibromyalgia
       syndrome: a comparison with temporomandibular disorders patients.
       Cranio. 2007 Apr;25(2):127-33.
___ Cook DB, Stegner AJ, McLoughlin MJ.
       Imaging pain of fibromyalgia.
       Curr Pain Headache Rep. 2007 Jun;11(3):190-200.
___ Schur EA, Afari N, Furberg H, Olarte M, Goldberg J, Sullivan PF,
       Buchwald D.
       Feeling bad in more ways than one: comorbidity patterns of medically
       unexplained and psychiatric conditions.
       J Gen Intern Med. 2007 Jun;22(6):818-21.
___ Abeles AM, Pillinger MH, Solitar BM, Abeles M.
       Narrative review: the pathophysiology of fibromyalgia.
       Ann Intern Med. 2007 May 15;146(10):726-34.
___ Wood PB, Holman AJ, Jones KD.
       Novel pharmacotherapy for fibromyalgia.
       Expert Opin Investig Drugs. 2007 Jun;16(6):829-41.
___ Bazzichi L, Rossi A, Giuliano T, De Feo F, Giacomelli C, Consensi A,
       Ciapparelli A, Consoli G, Dell'osso L, Bombardieri S.
       Association between thyroid autoimmunity and fibromyalgic disease
       Clin Rheumatol. 2007 May 9.
___ Balasubramaniam R, de Leeuw R, Zhu H, Nickerson RB, Okeson JP, Carlson CR.
       Prevalence of temporomandibular disorders in fibromyalgia and failed
       back syndrome patients: A blinded prospective comparison study.
       Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2007 May 4.
___ Harth M, Nielson WR.
       The fibromyalgia tender points: use them or lose them? A brief review
       of the controversy.
       J Rheumatol. 2007 May;34(5):914-22.
___ Gracely RH.
       A Pain Psychologist's View of Tenderness in Fibromyalgia.
       J Rheumatol. 2007 May;34(5):912-3.
___ Toda K.
       The prevalence of fibromyalgia in Japanese workers.
       Scand J Rheumatol. 2007 Mar-Apr;36(2):140-4.
___ Brand K, Littlejohn G, Kristjanson L, Wisniewski S, Hassard T.
       The Fibromyalgia Bladder Index.
       Clin Rheumatol. 2007 May 3.
___ Aloush V, Ablin JN, Reitblat T, Caspi D, Elkayam O.
       Fibromyalgia in women with ankylosing spondylitis.
       Rheumatol Int. 2007 May 3.
___ Centers for Disease Control and Prevention (CDC).
       Projected state-specific increases in self-reported doctor-diagnosed
       arthritis and arthritis-attributable activity limitations - United
       States, 2005-2030.
       MMWR Morb Mortal Wkly Rep. 2007 May 4;56(17):423-5.
___ Atarowska M, Samborski W.
       Difficulties with diagnosis of fibromyalgia: case report [Polish].
       Ann Acad Med Stetin. 2006;52 Suppl 2:105-10.
___ Furst G.
       Fibromyalgia - a challenge for interdisciplinary management [German].
       Wien Med Wochenschr. 2007 Jan;157(1-2):27-33.
___ Kalkman JS, Schillings ML, Zwarts MJ, van Engelen BG, Bleijenberg G.
       The development of a model of fatigue in neuromuscular disorders:
       A longitudinal study.
       J Psychosom Res. 2007 May;62(5):571-9.
___ Maquet D, Demoulin C, Croisier JL, Crielaard JM.
       Benefits of physical training in fibromyalgia and related syndromes.
       Ann Readapt Med Phys. 2007 Apr 13.
___ Patkar AA, Masand PS, Krulewicz S, Mannelli P, Peindl K, Beebe KL,
       Jiang W.
       A randomized, controlled, trial of controlled release paroxetine in
       Am J Med. 2007 May;120(5):448-54.
___ Gerdle B, Ostlund N, Gronlund C, Roeleveld K, Karlsson JS.
       Firing rate and conduction velocity of single motor units in the
       trapezius muscle in fibromyalgia patients and healthy controls.
       J Electromyogr Kinesiol. 2007 Apr 23.
___ Staud R, Koo E, Robinson ME, Price DD.
       Spatial summation of mechanically evoked muscle pain and painful
       aftersensations in normal subjects and fibromyalgia patients.
       Pain. 2007 Apr 23.
___ Jones JF, Maloney EM, Boneva R, Jones AB, Reeves WC.
       Complementary and Alternative Medical Therapy Utilization by People
       with Chronic Fatiguing Illnesses in the United States.
       BMC Complement Altern Med. 2007 Apr 25;7(1):12.
___ Iverson GL, Page JL, Koehler BE, Shojania K, Badii M.
       Test of Memory Malingering (TOMM) Scores are not Affected by Chronic
       Pain or Depression in Patients with Fibromyalgia.
       Clin Neuropsychol. 2007 May;21(3):532-46.
___ Tanriverdi F, Karaca Z, Unluhizarci K, Kelestimur F.
       The hypothalamo-pituitary-adrenal axis in chronic fatigue syndrome and
       fibromyalgia syndrome.
       Stress. 2007 Mar;10(1):13-25.
___ Knoop H, Stulemeijer M, Prins JB, van der Meer JW, Bleijenberg G.
       Is cognitive behaviour therapy for chronic fatigue syndrome also
       effective for pain symptoms?
       Behav Res Ther. 2007 Mar 14.
___ Moshiree B, Price DD, Robinson ME, Gaible R, Nicholas Verne G.
       Thermal and Visceral Hypersensitivity in Irritable Bowel Syndrome
       Patients With and Without Fibromyalgia.
       Clin J Pain. 2007 May;23(4):323-330.
___ Fantoni F, Salvetti G, Manfredini D, Bosco M.
       Current concepts on the functional somatic syndromes and
       temporomandibular disorders.
       Stomatologija. 2007;9(1):3-9.
___ Pall ML.
       Nitric oxide synthase partial uncoupling as a key switching mechanism
       for the NO/ONOO- cycle.
       Med Hypotheses. 2007 Apr 18.
___ Calandre EP, Morillas-Arques P, Rodriguez-Lopez CM, Rico-Villademoros F,
       Hidalgo J.
       Pregabalin augmentation of quetiapine therapy in the treatment of
       fibromyalgia: an open-label, prospective trial.
       Pharmacopsychiatry. 2007 Mar;40(2):68-71.

(c) 2007 NCBI PubMed

[Return to top]


Date:    Sun, 20 May 2007 13:16:31 -0400
From:    Fred Springfield <fredspringfield VERIZON.NET>
Subject: RES: Changes in Functional Status in Chronic Fatigue Syndrome  Over a Decade: Do Age and Gender Matter?

Changes in Functional Status in Chronic Fatigue Syndrome Over a Decade: Do
Age and Gender Matter?

Journal: J of Chronic Fatigue Syndrome, Vol. 14 (1) (2007), pp. 33-42

Authors: Rosalind M. Matthews MA, Anthony L. Komaroff MD

Affiliation: Both are affiliated with Brigham and Women's Hospital and
Harvard Medical School, Boston, MA, USA

Objective: Patients with chronic fatigue syndrome (CFS) have substantial
deficits in functional capacity, but the course of these deficits over time
has not often been studied. This study measured functional capacity on
three occasions over a decade, in patients with CFS.

Methods: The study was a longitudinal cohort study, and employed the
Medical Outcomes Study Short Form-36 (SF-36) instrument to assess physical
and mental/emotional functional status.

Results: Physical function, as reflected in several different scales,
improved modestly but significantly over time, particularly for patients
aged 18-60 years and for women. Mental/emotional function was not
substantially impaired at the outset of the study, and did not change over

Conclusion: This study found that physical function tended to improve for
many patients over time, despite the fact that they were aging. Physical
function did not deteriorate with time.

Keywords: CFS, functional status, SF-36, subgroups, over time

[Return to top]


Date:    Mon, 21 May 2007 20:37:43 -0400
From:    Fred Springfield <fredspringfield VERIZON.NET>
Subject: RES: Physiological Responses to Arm and Leg Exercise in Women Patients with Chronic Fatigue Syndrome

Physiological Responses to Arm and Leg Exercise in Women Patients with
Chronic Fatigue Syndrome

Journal: J of Chronic Fatigue Syndrome, Vol 14(1) (2007) pp. 43-53

Authors: Casimiro Javierre MD, PhD; José Alegre MD, PhD; José Luis Ventura
MD, PhD; Ana García-Quintana MD, PhD; Ramon Segura MD, PhD; Andrea Suarez
MD; Alberto Morales MD; Agusti Comella MD, PhD; Kenny De Meirleir MD, PhD

Patients affected by chronic fatigue syndrome (CFS) characteristically show
easy and unexplained fatigue after minimal exertion that does not resolve
with rest and is associated with specific symptoms lasting for more than
six months. Cardiopulmonary exercise testing is a valid procedure for
determining functional capacity in patients with CFS.

We compare cardioventilatory adaptation to exercise between a group of
eighty-five consecutive women patients affected by CFS and a group of
fifteen healthy women extremely sedentary individuals, with the use of
maximum incremental exercise testing on a cycle ergometer and arm
ergometer, assessing possible differences.

The majority of values achieved at peak exhaustive exercise were
significantly lower in CFS patients than controls, including the percentage
of maximum oxygen uptake in arm physical test (37.4±10.0% in CFS vs. 58.9±
15.8% in controls) and leg physical test (53.4±15.0% in CFS patients vs.
76.2 ± 18.0% in controls).

In conclusion, the CFS group shows a lower work capacity in arm or leg
exercise that would not be justified exclusively by their personal
characteristics or deconditioning.

Keywords: Chronic fatigue syndrome, maximal oxygen uptake, lactate

[Return to top]


End of Co-Cure Weekly Digest of research and medical posts only - 14 May 2007 to 21 May 2007

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