CO-CURE Medical & Research Posts Only Digest - 18 Sep 2006 to 25 Sep 2006 (#2006-44)
There are 12 messages totalling 2038 lines in this issue.
Topics of the week:
1. RES: Chronic fatigue syndrome [Review]
2. RES: Management of patients presenting with Sjogren's syndrome
3. RES: Interventions for the prevention and management of neck/upper extremity musculoskeletal conditions: a systematic review
4. RES: An investigation of the long-term benefits of antidepressant medication in the recovery of patients with chronic fatigue syndrome
5. ACT,RES: Incessant Belief? - Eileen Marshall Margaret Williams 19th September 2006
6. RES: CFS/ME & FM papers, published since August 2006
7. res: Pediatric Case Definition - ME/CFS
8. res: Chronic fatigue syndrome [Review]-2
9. RES,ACT: The pseudo-science of CBT
10. RES,NOT: U.S. Federal Register: CFS project CDC
11. RES, MED: Vit B3: Helps MS-Protects brain cells-Even in late-stage Multiple Sclerosis
12. NOT,MED: Response to a query about creatine supplements
[Return to digest index]
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This is a special digest of
Co-Cure Research & Medical posts only
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Date: Tue, 19 Sep 2006 09:48:47 -0400
From: Fred Springfield <fredspringfield@xxxxx.xxx>
Subject: RES: Chronic fatigue syndrome [Review]
Review
Chronic fatigue syndrome
Journal: J Clin Virol. 2006 Sep 13; [Epub ahead of print]
Authors: L.D. Devanur and J.R. Kerr [*]
Affiliation: Chronic Fatigue Syndrome (CFS) Group, Department of Cellular &
Molecular Medicine, St. George's University of London, Cranmer Terrace,
London SW17 0RE, United Kingdom
[*] Corresponding author: Corresponding author. Tel.: +44 208 725 5276;
fax: +44 208 725 5260. E-mai<jkerr@sgul.ac.uk>
Received 24 July 2006;
accepted 18 August 2006.
Available online 15 September 2006.
NLM Citation: PMID: 16978917
Chronic fatigue syndrome (CFS) is thought to have a worldwide prevalence of
0.4-1% with approximately 240,000 patients in the UK. Diagnosis is based on
clinical criteria and critically depends on exclusion of other physical and
psychiatric diseases.
Studies of pathogenesis have revealed immune system abnormalities and
chronic immune activation, dysfunction of the
hypothalamic-pituitary-adrenal (HPA) axis, brain abnormalities, evidence of
emotional stress (comprising host aspects) and evidence of exogenous
insults, for example, various microbial infections (Epstein-Barr virus,
enteroviruses, parvovirus B19, Coxiella burnetii and Chlamydia pneumoniae),
vaccinations and exposure to organophosphate chemicals and other toxins
(comprising environmental aspects).
Emotional stress appears to be very important as it reduces the ability of
the immune system to clear infections, it's presence has been shown to
determine whether or not an individual develops symptoms upon virus
infection, and it leads to activation of the HPA axis. But, emotional
stress is distinct from depression, the presence of which precludes a
diagnosis of CFS.
There is no specific treatment for CFS other than the much underutilised
approach of specific treatment of virus infections. Current priorities are
to understand the molecular pathogenesis of disease in terms of human and
virus gene expression, to develop a diagnostic test based on protein
biomarkers, and to develop specific curative treatments.
Keywords: Chronic fatigue syndrome; Virus; Infection; Diagnosis;
Pathogenesis; Gene expression
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Date: Tue, 19 Sep 2006 10:42:54 -0400
From: "Bernice A. Melsky" <bernicemelsky@xxxxx.xxx>
Subject: RES: Management of patients presenting with Sjogren's syndrome
Management of patients presenting with Sjogren's syndrome.
Best Pract Res Clin Rheumatol. 2006 Aug;20(4):791-807.
Venables PJ.
Kennedy Institute Division, Imperial College, London, UK.
PMID: 16979538
Sjogren's syndrome is an autoimmune exocrinopathy that predominantly
affects salivary and lachrymal glands, leading to dry eyes and mouth. The
most common clinical problems faced by the rheumatologist are those of dry
eyes and mouth, parotid swelling, fatigue and extraglandular manifestations.
The first stage in management is to make an accurate diagnosis based on the
American/European consensus criteria. The most frequent differential
diagnoses are dry eyes and mouth symptoms, a variant of chronic fatigue
syndrome and fibromyalgia, and sialosis, which causes a non-inflammatory
enlargement of the parotid glands.
The mainstay of treatment for the sicca symptoms is local therapy, and that
for the milder systemic symptoms is hydroxychloroquine. Steroids and
immunosuppressive drugs are reserved for more severe extraglandular disease.
In spite of intensive research in other systemic treatments including
biologic therapies, there is limited evidence to support their use in
routine clinical practice.
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Date: Tue, 19 Sep 2006 10:48:35 -0400
From: "Bernice A. Melsky" <bernicemelsky@xxxxx.xxx>
Subject: RES: Interventions for the prevention and management of neck/upper extremity musculoskeletal conditions: a systematic review
Interventions for the prevention and management of neck/upper extremity
musculoskeletal conditions: a systematic review.
Occup Environ Med. 2006 Sep 14; [Epub ahead of print]
Boocock MG, McNair PJ, Larmer PJ, Armstrong B, Collier J, Simmonds M,
Garrett N.
Auckland University of Technology, New Zealand.
PMID: 16973739
Whether considered from medical, social or economic perspectives, the cost
of musculoskeletal injuries suffered in the workplace is substantial and
there is a need to identify the most efficacious interventions for their
effective prevention, management and rehabilitation.
Previous reviews have highlighted the limited number of studies that focus
on upper extremity intervention programmes. The aim of the current study
was to evaluate the findings of primary, secondary and/or tertiary
intervention studies for neck/upper extremity conditions undertaken between
1999 and 2004 and compare these results with those of previous reviews.
Relevant studies were retrieved through the use of a systematic approach to
literature searching and evaluated using a standardised tool. Evidence was
then classified according to a 'pattern of evidence' approach. Studies were
categorised into subgroups depending on the type of INTERVENTION: mechanical exposure interventions; production systems/organisational
culture interventions; and modifier interventions. Thirty one intervention
studies met the inclusion criteria.
The findings provided evidence to support the use of some mechanical and
modifier interventions as approaches for preventing and managing neck/upper
extremity musculoskeletal conditions and fibromyalgia. Evidence to support
the benefits of production systems/organisational culture interventions was
found to be lacking. This review identified no one single or
multidimensional strategy for intervention that was considered effective
across occupational settings.
There is limited information to support the establishment of evidence-based
guidelines applicable to a number of industrial sectors.
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Date: Tue, 19 Sep 2006 11:11:07 -0400
From: Fred Springfield <fredspringfield@xxxxx.xxx>
Subject: RES: An investigation of the long-term benefits of antidepressant medication in the recovery of patients with chronic fatigue syndrome
Research Article
An investigation of the long-term benefits of antidepressant medication in
the recovery of patients with chronic fatigue syndrome
Journal: Human Psychopharmacology: Clinical and Experimental, 2006 Sep 18;
[Epub ahead of print] DOI: 10.1002/hup.805
Authors: Marie A. Thomas, Andrew P. Smith
Affiliation: Centre for Occupational and Health Psychology, School of
Psychology, Cardiff University, UK
*Correspondence to Marie A. Thomas, Centre for Occupational & Health
Psychology, 63 Park Place, Cardiff, CF10 3AS, UK. email: Marie A. Thomas
(thomasma@xx.xx.xx)
Funded by: Linbury Trust, Gatsby Foundation
Keywords: Chronic Fatigue Syndrome • antidepressant medication • recovery
Received: 10 April 2006;
Accepted: 9 August 2006
PMID: 16981220
Abstract
Two hundred and seventy-five patients fulfilling the Centre for Disease
Control (CDC) criteria for Chronic Fatigue Syndrome (CFS) completed
measures assessing illness history, global ratings of well being, sleep,
activity and psychopathology at baseline, 6 months, 18 months and 3 year
follow-up.
Forty-nine of these patients had been prescribed antidepressant medication,
namely Tricyclic drugs or Selective Serotonin Re-uptake Inhibitors (SSRI).
Data from the current study suggests that patients in the antidepressant
medication group recover at a faster rate over time when compared to the
untreated patient sample. In addition, the positive effects of
antidepressant therapy are maintained at the 3-year follow-up point.
It appears from these data that the SSRI in particular are responsible for
improvements in the condition. Most importantly, these improvements include
a reduction in the levels of fatigue recorded by patients.
These findings have not been demonstrated in previous studies of the effect
of antidepressant therapy for patients with this illness and this may
reflect the short time periods studied in the earlier research.
Copyright © 2006 John Wiley & Sons, Ltd.
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Date: Tue, 19 Sep 2006 16:51:15 +0100
From: Stephen Ralph <stephen.e.ralph@xxxxx.xxx.xx>
Subject: ACT,RES: Incessant Belief? - Eileen Marshall Margaret Williams 19th September 2006
Incessant Belief?
Eileen Marshall Margaret Williams 19th September 2006
In a recent letter from Heather Finch of the Medical Research Council's
Knowledge and Management Group, the MRC repeated its well-worn mantra about
"high quality" research: "research excellence will continue to be the
primary consideration in funding decisions" (see Co-Cure EDU: 16th September
2006: MRC Doggerel Part I). Of interest is the fact that Ms Finch also
stated: "Awards may be made according to their scientific quality". "May" be
made according to their scientific quality? Why not "are" made according to
scientific quality?
We have previously noted what seems to be a disturbing lack of scientific
rigour on the part of the MRC in relation to ME/CFS issues and have noted
that high scientific standards seem sadly lacking when it comes to funding
research into ME/CFS: see, for example the following:
(1) "Some questions about ME/CFS to which credible answers are urgently
required" (22nd March 2004)
http://www.meactionuk.org.uk/Some_Questions_-_220304.htm
This noted that the Oxford criteria (to be used in the MRC 'CFS' PACE
trials) have been shown to have no predictive validity and that there has
never been international consensus about them: they are used only in
Britain, and it is virtually unheard of for studies to use criteria that
have been superceded. It noted that vested and competing interests had not
been declared and it questioned why such large sums had been granted by the
MRC for more trials of management approaches that have already been shown
not to work for those with ME/CFS. It noted that the financial interests of
the medical insurance industry have been allowed to take precedence over the
needs and care of ME/CFS patients
(2) "Questions for the MRC" (18th June 2005)
http://www.meactionuk.org.uk/Question_for_the_MRC.htm
This noted that on 16th June 2005, Sarah Perkins, Programme Manager of the
MRC's Mental Health Board, stated about the PACE trial: "The main entry
criteria are the Oxford criteria: the exclusion criteria will be used to
exclude neurological conditions. It will not be used to exclude patients
with a diagnosis of ME" and asked seven questions, including (i) why the MRC
is using special pleading in relation to ME when ME is classified as a
neurological disorder by the WHO (ii) on what scientific evidence the MRC is
relying to enable it to disregard this international classification that was
approved by the World Health Assembly (iii) given that Wessely School
psychiatrists seem to be financially encouraged to demand 100% proof of an
organic aetiology before they will 'allow' ME to be accepted as an organic
disorder, why the MRC does not equally require a similar standard of proof
from these psychiatrists that ME is a mental disorder
(3) "Issues re the use of the Oxford criteria for the MRC 'CFS' Trials"
(20th June 2004)
http://www.meactionuk.org.uk/SIGNS_in_ME.htm
This lists many of the signs -- as opposed to symptoms --seen in ME/CFS that
the psychiatrists funded by the MRC consistently ignore
(4) "ME/CFS and Fibromyalgia: additional considerations for the MRC in
relation to the PACE trials"
http://www.meactionuk.org.uk/Additional_considerations_re_MECFS_and_FM.htm
This provides referenced evidence of the distinctions between ME/CFS and
fibromyalgia (the MRC 'CFS' trials having made no distinction between the
two disorders)
(5) "High Standards at the MRC?" (21st April 2005)
http://www.meactionuk.org.uk/High_Standards_at_the_MRC.htm
This addressed and questioned the MRC's claim that it insists on a high
scientific standard being required for funding
(6) "ME Exists: True or False?" (18th August 2006)
http://www.meactionuk.org.uk/ME_Exists_-_True_or_False.htm
This pointed out that the "Wessely School" psychiatric model of ME/CFS is
not evidence-based, nor can it ever be so: it is an hypothesis that cannot
be tested, let alone proven, which contrasts with the biomedical model of
ME/CFS that is supported by respected literature of solid scientific
evidence.
Given its track record, especially the findings in the Report of the House
of Commons Science and Technology Select Committee that under the
Chairmanship of Dr Ian Gibson MP was excoriatingly critical of the MRC (see
The Work of the Medical Research Council: Third Report of Session 2002-2003
/ HC132, March 2003), how can the MRC credibly continue to assert that the
PACE CFS trial meets the stringent and rigorous criteria that it claims to
require?
As ever, the facts speak for themselves: the PACE trial is using criteria
formulated by "Wessely School" psychiatrists that have never been adopted
internationally and which by definition exclude those with authentic ME/CFS
but which include those with psychiatric disorders (the Oxford 1991
criteria); the psychiatrists leading the PACE trial have deliberately
diluted the entry criteria in order to enhance recruitment (see the PACE
Trial Identifier, which states: "We chose these broad criteria in order to
enhance recruitment" and on 19th March 2004 this was expanded by Carolan
Davidge from the MRC: "As for the PACE trial, the Oxford criteria are to be
used (in the FINE trial) since they are perceived to be broader and more
inclusive, and also easier for GPs to screen for"); the same psychiatrists
have intentionally amalgamated those with different disorders, with the
inevitable consequence that the results will be skewed and therefore
meaningless and, crucially, the MRC trials seem to be paying scant heed to
the known dangers of increased oxidative stress for those with severe
ME/CFS.
It has just been announced that the combined MRC / AfME "Summit" has been
re-convened for November 2006 (see Co-Cure NOT: Research Summit - AfME (UK)
14th September 2006); the announcement states: "As far as we know, this will
be the first time that neurologists, immunologists, pain and sleep disorder
specialists, epidemiological psychiatrists, pathophysiologists and others
will work together to explore innovative ways of tackling ME".
What an extraordinary claim: why have the MRC and AfME ignored all the
international Clinical and Research conferences on ME/CFS since 1988, many
of which were reported in AfME's own magazine?
Have the MRC and AfME forgotten the US NIAID (National Institute of Allergy
and Infectious Diseases) Symposium held at the University of Pittsburgh in
September 1988; the Rhode Island Symposium in 1988; the Rome Symposium in
1988; the San Francisco conference in April 1989; the British Post-Graduate
Medical Federation Conference in London in June 1989; the Los Angeles
International Conference in February 1990; the First World Symposium held in
1990 at Cambridge University, UK; the Charlotte Research Conference in
November 1990; the Canadian Workshop at the University of British Columbia,
Vancouver, in May 1991; the Dublin International Symposium in May 1994 (held
under the auspices of The World Federation of Neurology); the First World
Congress (also under the auspices of The World Federation of Neurology) in
Brussels in 1995; the Second World Congress in Brussels in September 1999;
the Bloomington Conference in Minnesota in October 2001, and the
International Clinical and Scientific Meetings presented by the Alison
Hunter Memorial Foundation in Australia, especially the Third International
Meeting in Sydney in December 2001?
Have the MRC and AfME forgotten the biennial International Research and
Clinical Conferences hosted by the American Association of CFS (AACFS, now
the IACFS / International Association of CFS), including the Albany, New
York, conference in October 1992; the Fort Lauderdale, Florida, conference
in October 1994; the San Francisco conference in October 1996; the Boston,
Massachusetts, conference in October 1998; the Seattle conference in January
2001; the Chantilly, Virginia (Washington D.C.) conference in January -
February 2003; the Madison, Wisconsin, conference in October 2004?
Are the MRC and AfME aware of the forthcoming IACFS Professional Research
Conference that is to be held at Fort Lauderdale in January 2007? Will they
be sending representatives?
Have the MRC and AfME forgotten the Scientific Workshops such as the one
co-sponsored by the US National Institutes of Health in June 2003 on
neuro-immune mechanisms in (ME)CFS and the two MERGE workshops (including
the Royal Society of Edinburgh funded Workshop in 2003 and the MERUK
Colloquium in July 2006), which consisted of presentations by key scientists
with a working knowledge of ME/CFS, the aim being to facilitate links
between scientists working towards the common goal of understanding the
biomedical basis of ME/CFS?
The above lists are by no means comprehensive, so it is absurd for the MRC
and AfME to appear to believe that their "Summit" represents the first time
that researchers have collaborated "to explore innovative ways of tackling
ME".
How can it be "high quality" science to ignore the evidence that was
presented at these international meetings over the last 18 years?
Will the immunologist at the MRC / AfME "Summit" be AfME's own Medical
Adviser, Professor Anthony Pinching, who is responsible for the much-derided
CFS Centres that deliver only psychotherapy and who believes that it is
unnecessary to study subgroups of "CFS"?
Why are vascular biologists such as Dr Vance Spence and geneticists such as
Dr Jonathan Kerr missing from the list of specialists to be invited to the
"Summit", when they are the very people who have provided irrefutable
evidence of the organic nature of the disorder?
All this has been pointed out many times before, yet the MRC and the
psychiatrists it so favours continue to ignore the evidence.
In "Letter from America" on 31st December 2001 on the BBC World Service,
Alistair Cooke -- whilst not referring to ME/CFS -- admirably encapsulated
the problems that have for so long beset the ME community, namely that for
years the MRC has supported the Wessely School psychosocial model of ME/CFS:
"By shouting the word often enough they hope to turn it into a reality. It's
a case of what the poet William Empson called 'incessant belief labouring to
create its object' ".
How true. And how spectacularly unscientific.
[Return to top]
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Date: Wed, 20 Sep 2006 07:15:04 +0200
From: "Dr. Marc-Alexander Fluks" <fluks@xxx.xx>
Subject: RES: CFS/ME & FM papers, published since August 2006
Source: NCBI PubMed
Date: September 20, 2006
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 papers 1938-today,
http://www.me-net.dds.nl/library/literature.html#publications
Search papers,
http://www.me-net.dds.nl/library/literature.html#catalogue
Figures computer analysis:
http://www.me-net.dds.nl/library/literature.html#figure
CFS/ME & FM papers, published since August 2006
-----------------------------------------------
___ Thomas MA, Smith AP.
An investigation of the long-term benefits of antidepressant medication
in the recovery of patients with chronic fatigue syndrome.
Hum Psychopharmacol. 2006 Sep 18.
___ Smyth J, Nazarian D.
Development and preliminary results of a self-administered intervention
for individuals with fibromyalgia syndrome: a multiple case control
report.
Explore (NY). 2006 Sep;2(5):426-31.
___ Devanur LD, Kerr JR.
Chronic fatigue syndrome.
J Clin Virol. 2006 Sep 13.
___ Gillis ME, Lumley MA, Mosley-Williams A, Leisen JC, Roehrs T.
The health effects of at-home written emotional disclosure in
fibromyalgia: a randomized trial.
Ann Behav Med. 2006 Oct;32(2):135-46.
___ Lotaif AC, Mitrirattanakul S, Clark GT.
Orofacial muscle pain: new advances in concept and therapy.
J Calif Dent Assoc. 2006 Aug;34(8):625-30.
___ Jamil H, Nassar-McMillan SC, Salman WA, Tahar M, Jamil LH.
Iraqi Gulf War Veteran Refugees in the U.S.:PTSD and Physical Symptoms.
Soc Work Health Care. 2006;43(4):85-98.
___ Arnold LM, Hudson JI, Keck PE, Auchenbach MB, Javaras KN, Hess EV.
Comorbidity of Fibromyalgia and Psychiatric Disorders.
J Clin Psychiatry. 2006 Aug;67(8):1219-1225.
___ Dinler M, Kasikcioglu E, Akin A, Sayli O, Aksoy C, Oncel A, Berker E.
Exercise capacity and oxygen recovery half times of skeletal muscle in
patients with fibromyalgia.
Rheumatol Int. 2006 Sep 9.
___ Bonifazi M, Lisa Suman A, Cambiaggi C, Felici A, Grasso G, Lodi L,
Mencarelli M, Muscettola M, Carli G.
Changes in salivary cortisol and corticosteroid receptor-alpha mRNA
expression following a 3-week multidisciplinary treatment program in
patients with fibromyalgia.
Psychoneuroendocrinology. 2006 Sep 6.
___ Wolfe F, Rasker JJ.
The Symptom Intensity Scale, Fibromyalgia, and the Meaning of
Fibromyalgia-like Symptoms.
J Rheumatol. 2006 Sep 1.
___ Kool MB, Woertman L, Prins MA, Van Middendorp H, Geenen R.
Low relationship satisfaction and high partner involvement predict
sexual problems of women with fibromyalgia.
J Sex Marital Ther. 2006 Oct-Dec;32(5):409-23.
___ El Maghraoui A, Tellal S, Achemlal L, Nouijai A, Ghazi M, Mounach A,
Bezza A, Derouiche el M.
Bone turnover and hormonal perturbations in patients with fibromyalgia.
Clin Exp Rheumatol. 2006 Jul-Aug;24(4):428-31.
___ Alasehirli B, Demiryurek S, Arica E, Gursoy S, Demiryurek AT.
No evidence for an association between the Glu298Asp polymorphism of
the endothelial nitric oxide synthase gene and fibromyalgia syndrome.
Rheumatol Int. 2006 Sep 2.
___ Hickie I, Davenport T, Wakefield D, Vollmer-Conna U, Cameron B, Vernon SD,
Reeves WC, Lloyd A; Dubbo Infection Outcomes Study Group.
Post-infective and chronic fatigue syndromes precipitated by viral and
non-viral pathogens: prospective cohort study.
BMJ. 2006 Sep 16;333(7568):575.
___ Citak-Karakaya I, Akbayrak T, Demirturk F, Ekici G, Bakar Y.
Short and long-term results of connective tissue manipulation and
combined ultrasound therapy in patients with fibromyalgia.
J Manipulative Physiol Ther. 2006 Sep;29(7):524-8.
___ Madden S, Sim J.
Creating meaning in fibromyalgia syndrome.
Soc Sci Med. 2006 Aug 30.
___ Betina Nishishinya M, Rivera J, Alegre C, Alejandra Pereda C.
Non pharmacologic and alternative treatments in fibromyalgia [Spanish].
Med Clin (Barc). 2006 Sep 2;127(8):295-9.
___ Karper WB, Jannes CR, Hampton JL.
Fibromyalgia syndrome: the beneficial effects of exercise.
Rehabil Nurs. 2006 Sep-Oct;31(5):193-8.
___ Blehm R.
Physical therapy and other nonpharmacologic approaches to fibromyalgia
management.
Curr Pain Headache Rep. 2006 Oct;10(5):333-8.
___ Hwang E, Barkhuizen A.
Update on rheumatologic mimics of fibromyalgia.
Curr Pain Headache Rep. 2006 Oct;10(5):327-32.
___ Wood PB.
A reconsideration of the relevance of systemic low-dose ketamine to the
pathophysiology of fibromyalgia.
J Pain. 2006 Sep;7(9):611-4.
___ Thorlacius S, Stefansson SB, Ranavaya MI, Walker R.
Fibromyalgia and anxiety disorder [Icelandic].
Laeknabladid. 2002 Nov;88(11):815-818.
___ McLean SA, Williams DA, Stein PK, Harris RE, Lyden AK, Whalen G, Park KM,
Liberzon I, Sen A, Gracely RH, Baraniuk JN, Clauw DJ.
Cerebrospinal fluid Corticotropin-Releasing factor concentration is
associated with pain but not fatigue symptoms in patients with
fibromyalgia.
Neuropsychopharmacology. 2006 Aug 23.
___ Kerr JR, Christian P, Hodgetts A, Langford PR, Devanur LD, Petty R, Burke
B, Sinclair LI, Richards SC, Montgomery J, McDermott C, Harrison TJ,
Kellam P, Nutt DJ, Holgate ST.
Current research priorities in Chronic Fatigue Syndrome/Myalgic
Encephalomyelitis (CFS/ME): disease mechanisms, a diagnostic test and
specific treatments.
J Clin Pathol. 2006 Aug 25.
___ Hooper M.
Myalgic Encephalomyelitis (ME): a review with emphasis on key findings
in biomedical research.
J Clin Pathol. 2006 Sep 1.
___ Puri BK.
Long-chain polyunsaturated fatty acids and the pathophysiology of
myalgic encephalomyelitis (chronic fatigue syndrome).
J Clin Pathol. 2006 Aug 25.
___ Gibson I.
A new look at Chronic Fatigue Syndrome/Myalgic Encephalomyelitis (CFS/
ME).
J Clin Pathol. 2006 Aug 25.
___ Carruthers B.
Definitions and aetiology of Myalgic Encephalomyelitis (ME): how the
Canadian Consensus Clinical Definition of ME works.
J Clin Pathol. 2006 Aug 25.
___ Hannestad U, Theodorsson E, Evengard B.
Beta-Alanine and gamma-aminobutyric acid in chronic fatigue syndrome.
Clin Chim Acta. 2006 Jul 14.
___ Guedj E, Taieb D, Cammilleri S, Lussato D, de Laforte C, Niboyet J,
Mundler O.
(99m)Tc-ECD brain perfusion SPECT in hyperalgesic fibromyalgia.
Eur J Nucl Med Mol Imaging. 2006 Aug 25.
___ Eriksen W.
Myalgic encephalopathy - an inexact report with doubtful conclusions
[Norwegian].
Tidsskr Nor Laegeforen. 2006 Aug 24;126(16):2144; author reply 2144-5.
___ Bennett R, Nelson D.
Cognitive behavioral therapy for fibromyalgia.
Nat Clin Pract Rheumatol. 2006 Aug;2(8):416-24.
___ Dadabhoy D, Clauw DJ.
Therapy Insight: fibromyalgia - a different type of pain needing a
different type of treatment.
Nat Clin Pract Rheumatol. 2006 Jul;2(7):364-72.
___ Choy E.
Comparing methods for the diagnosis of fibromyalgia.
Nat Clin Pract Rheumatol. 2006 May;2(5):244-5.
___ Williams DA.
Utility of cognitive behavioral therapy as a treatment for insomnia in
patients with fibromyalgia.
Nat Clin Pract Rheumatol. 2006 Apr;2(4):190-1.
___ Simon LS.
Is milnacipran effective in treating pain in patients with fibromyalgia?
Nat Clin Pract Rheumatol. 2006 Mar;2(3):126-7.
___ Staud R, Rodriguez ME.
Mechanisms of disease: pain in fibromyalgia syndrome.
Nat Clin Pract Rheumatol. 2006 Feb;2(2):90-8.
___ Clauw DJ.
Does acupuncture help reduce pain in patients with fibromyalgia?
Nat Clin Pract Rheumatol. 2005 Dec;1(2):76-7.
___ Komaroff AL.
By the way, doctor. I would be most grateful for information concerning
chronic fatigue syndrome, a disorder from which I have suffered for the
past 10 years. Do you see any help on the horizon?
Harv Health Lett. 2006 Aug;31(10):8.
___ Longley K.
Fibromyalgia: aetiology, diagnosis, symptoms and management.
Br J Nurs. 2006 Jul 13-27;15(13):729-33.
___ Osorio CD, Gallinaro AL, Lorenzi-Filho G, Lage LV.
Sleep quality in patients with fibromyalgia using the pittsburgh sleep
quality index.
J Rheumatol. 2006 Sep;33(9):1863-5.
___ Gameiro GH, da Silva Andrade A, Nouer DF, Ferraz de Arruda Veiga MC.
How may stressful experiences contribute to the development of
temporomandibular disorders?
Clin Oral Investig. 2006 Aug 22.
___ Okumus M, Gokoglu F, Kocaoglu S, Ceceli E, Yorgancioglu ZR.
Muscle performance in patients with fibromyalgia.
Singapore Med J. 2006 Sep;47(9):752-6.
___ Havermark AM, Langius-Eklof A.
Long-term follow up of a physical therapy programme for patients with
fibromyalgia syndrome.
Scand J Caring Sci. 2006 Sep;20(3):315-22.
___ Singh SR, Levine MA.
Natural health product use in Canada: analysis of the national
poplulation health survey.
Can J Clin Pharmacol. 2006 Summer;13(2):e240-50.
___ Lucas KE, Armenian HK, Petersen GM, Rowe PC.
Familial aggregation of fainting in a case-control study of neurally
mediated hypotension patients who present with unexplained chronic
fatigue.
Europace. 2006 Aug 18.
___ Bazzichi L, Giannaccini G, Betti L, Italiani P, Fabbrini L, Defeo F,
Giacomelli C, Giuliano T, Rossi A, Uccelli A, Giusti L, Mascia G,
Lucacchini A, Bombardieri S.
Peripheral benzodiazepine receptors on platelets of fibromyalgic
patients.
Clin Biochem. 2006 Sep;39(9):867-72.
--------
(c) 2006 NCBI PubMed
[Return to top]
------------------------------
Date: Wed, 20 Sep 2006 18:38:26 +0200
From: Jan van Roijen <j.van.roijen@xxxxx.xx>
Subject: res: Pediatric Case Definition -ME/CFS
Send an Email for free membership
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Journal of Chronic Fatigue Syndrome
(ISSN: 1057-3321)
Volume: 13 Issue: 2/3
Cover Date: 2006
not yet published
Copyright Date: 2006
CONTENTS
Foreword
Page Range: xvii - xix
DOI: 10.1300/J092v13n02_a
Elke Van Hoof, Kenny De Meirleir, Neil McGregor
ORIGINAL RESEARCH
A Pediatric Case Definition for Myalgic Encephalomyelitis
and Chronic Fatigue Syndrome.
Page Range: 1 - 44
DOI: 10.1300/J092v13n02_01
Leonard A Jason, David S. Bell, Kathy Row, Elke L. S. Van
Hoof, Karen Jordan, Charles Lapp, Alan Gurwitt, Teruhisa Miike,
Susan Torres-Harding, Kenny De Meirleir.
For a diagnosis chronic fatigue syndrome (CFS), most
researchers use criteria that were developed by Fukuda et al.
(1994), with modifications suggested by Reeves et al. (2003).
However, this case definition was established for adults rather
than children. A Canadian Case Definition (ME/CFS; Myalgic
Encephalomyelitis/CFS) has recently been developed, with
more specific inclusion criteria (Carruthers et al., 2003). Again,
the primary aim of this case definition is to diagnose adult CFS.
A significant problem in the literature is the lack of both a
pediatric definition of ME/CFS and a reliable instrument to
assess it. These deficiencies can lead to criterion variance
problems resulting in studies labeling children with a wide variety
of symptoms as having ME/CFS. Subsequently, comparisons
between articles become more difficult, decreasing the
possibility of conducting a meta-analysis. This article presents
recommendations developed by the International Association of
Chronic Fatigue Syndrome Pediatric Case Definition Working
group for a ME/CFS pediatric case definition. It is hoped that
this pediatric case definition will lead to more appropriate
identification of children and adolescents with ME/CFS.
Keywords:
Pediatric CFS, definition, pediatric questionnaire.
Pediatric Chronic Fatigue Syndrome and Muchausen-by-Proxy:
A Case Study
Page Range: 45 - 53
DOI: 10.1300/J092v13n02_02
E. Van Hoof, P. De Becker, K. De Meirleir
Pediatric chronic fatigue syndrome (CFS) posits even more
challenges for professional caregivers in comparison with adult
CFS samples. Most children with CFS display a decrease in
school attendance and a decrease in social activities. As
several conditions such as school phobia, primary psychiatric
disorders or family disturbance present the same
characteristics, the diagnostic process appears more complex.
Family disturbance, moreover, is often specified as child abuse,
neglect or even Muchausen-by-proxy. As skepticism is frequently
associated with a diagnosis of CFS, patients and parents must
fend for themselves fighting allegations of child abuse and
neglect. This case study illustrates what happens when such
allegations are put forward.
Keywords:
Muchausen-by-proxy, pediatric chronic fatigue syndrome, child
protective services.
Psychosocial and Physical Impact of Chronic Fatigue in a
Community-Based Sample of Children and Adolescents.
Page Range: 55 - 74
DOI: 10.1300/J092v13n02_03
Susan R. Torres-Harding, Karen Jordan, Leonard A. Jason
PhD, Renee Arias.
Background:
Few studies have examined the problem of chronic fatigue in
children and adolescents and its potential impact on functioning.
Chronic fatigue may have a negative impact on school
functioning, family activities, psychological well-being, physical
functioning, and severity of medical symptomatology.
Objectives:
This study compared psychosocial, family, and physical
functioning between a randomly selected community based
sample of 36 children and adolescents with chronic fatigue and
a group of 21 children and adolescents without fatigue.
Methods:
Children and parents completed a comprehensive medical
history questionnaire and questionnaires assessing
psychological functioning, family functioning, and school
attendance.
Results:
Results indicated that children with chronic fatigue tended to
have more difficulties in overall physical and psychological
functioning, as measured by the Child Health Questionnaire and
the Child Behavior Checklist. In addition, children in the chronic
fatigue group experienced disruptions in a range of activities
and reported more severe physical symptomatology when
compared to children without fatigue.
Conclusions:
Findings suggest that children and adolescents with chronic
fatigue may have a range of associated difficulties, including
limitations in physical and psychosocial functioning and a
negative impact on the ability to engage in normative activities.
Keywords:
Chronic fatigue, children, adolescents, psychosocial functioning,
physical functioning.
SHORT ARTICLE
Prevalence of Pediatric Chronic Fatigue Syndrome in a
Community-Based Sample.
Page Range: 75 - 77
DOI: 10.1300/J092v13n02_04
Karen M. Jordan, Leonard A. Jason PhD, Cynthia J. Mears, Ben
Z. Katz, Alfred Rademaker, Cheng-Fang Huang, Judith
Richman, William McCready, Penny M. Ayers, Kari K. Taylor
THEORY USED IN CLINICAL PRACTICE
Guidelines for the Diagnosis of Pediatric Chronic Fatigue
Syndrome: Things Parents Need to Know.
Page Range: 79 - 88
DOI: 10.1300/J092v13n02_05
S. D. Bell, E. Van Hoof
In this special issue of the Journal of Chronic Fatigue Syndrome,
chronic fatigue syndrome (CFS) in children and adolescents is
specifically addressed. It is a topic long overdue. It is my sincere
hope that the criteria presented here will begin a process of
rigorous clinical testing and refinement so that pediatricians and
other medical providers will come to have a reliable and
accepted way of making the diagnosis of ME/CFS in a person
under 18 years of age. This short review is meant for parents
and other caregivers as a brief summary of the guidelines that
may be of value. The primary role of these guidelines is to
present a strict and rigorous definition that can be tried and
tested. This summary is to make the process of diagnosis
somewhat easier for parents and caregivers alike until the
testing process is completed. Therefore, for more detailed
symptom description and exclusionary illness description, I
would refer the reader to the primary article. Professional
caregivers and clinicians may offer this article available to inform
parents with a child or/ adolescent suffering from CFS.
Keywords:
Pediatric chronic fatigue syndrome, parents, diagnosis.
Recognizing Pediatric CFS in the Primary Care Practice:
A Practicing Clinician's Approach.
Page Range: 89 - 96
DOI: 10.1300/J092v13n02_06
Charles W. Lapp MD.
Pediatricians and primary care physicians may be
uncomfortable diagnosing Chronic Fatigue Syndrome in children
because a good diagnostic tool has not been available.
Deferring a diagnosis, however, may lead to apprehension,
over-utilization of medical resources in a search for validity, a
delay in treatment, and possibly inappropriate coping
techniques. This case-based article discusses symptoms and
signs seen in adolescent patients with CFS, evaluation of
suspect cases, and both current and future diagnostic case
definitions.
Keywords:
Pediatric chronic fatigue syndrome, primary care, diagnosis.
REVIEW
Chronic Fatigue Syndrome in Children and Adolescents
Page Range: 97 - 115
DOI: 10.1300/J092v13n02_07
James M. Oleske MD, MPH, Kenneth J. Friedman PhD,
Kenneth R. Kaufman MD, MRCPsych, Donna Palumbo LCSW,
Jonathan Sterling MA, Terri Lynn Evans RN.
Objective:
An overview of the unique aspects of Chronic Fatigue Syndrome
in children and adolescents (CACFS) is herein provided for
healthcare professionals who may be called upon to diagnose
and/or treat this illness. Young age of onset, puberty, and
interactions with peers and the educational system provide
greater diagnostic and treatment challenges than found with
adult onset CFS.
Method:
A review of diagnostic procedures and treatment protocols
found in the contemporary literature is coupled with the
professional experiences of the authors in treating CACFS to
delineate the roles and responsibilities of family, healthcare
providers and educators in diagnosing, treating and supporting
the CACFS patient.
Results:
Areas discussed include: pathogenesis, patient evaluation,
clinical evaluation, laboratory evaluation, treatment options,
psychological issues, role of schools, and the roles of primary
and tertiary care providers.
Conclusion:
CACFS can be diagnosed and treated with varying levels of
success if all the professionals involved in the treatment program
have a clear understanding of their roles and responsibilities.
Primary care physicians, pediatricians, other subspecialists,
family members, social workers and educators, may all be
called upon to participate in the treatment program of CACFS.
While it is best to have one, compassionate physician in charge
of care, the CACFS may benefit from the inclusion of
specialized treatment options available from or through a tertiary
care provider. To the extent possible, socialization, education
and psychological support of the CACFS should be provided.
Keywords:
Pediatrics, review, patient evaluation, psychology, primary care,
tertiary care.
[Return to top]
------------------------------
Date: Thu, 21 Sep 2006 23:20:08 +0200
From: Jan van Roijen <j.van.roijen@xxxxx.xx>
Subject: res: Chronic fatigue syndrome [Review]-2
Send an Email for free membership
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19 Sep 2006 Fred Springfield posted the abstract on Co-Cure
of: *Chronic fatigue syndrome [Review]* - Journal: J Clin Virol.
2006 Sep 13; Authors: L.D. Devanur and J.R. Kerr
http://listserv.nodak.edu/cgi-bin/wa.exe?A2=ind0609c&L=co-cure&T=0&P=3117
``````````````````````````````````````````````````````````````````````````````
~jvr: as 'fair use' I add the *treatment * section from this study
`````````````````````````````````````````````````````````````````````````````````
4. Treatment
``````````````````
As we do not understand the pathogenesis of CFS, it is
impossible to make specific therapeutic interventions. The one
exception to this is in the area of infection. For example, if a
particular infection can be identified, then the specific therapy
can be used, and this is often beneficial.
4.1. Specific therapies
The fact that CFS is frequently triggered and perpetuated by
ongoing microbial infection has led to the proposed approach of
exhaustive investigation to find an infectious cause of a patient's
symptoms, which may then indicate a specific anti-microbial
drug regimen that can be used to eradicate that infection with
resultant clinical benefit (Chia and Chia, 2003). There are
sufficient infections whose association with CFS is prominent to
make this approach a useful one in terms of potential benefit to
a large number of CFS patients. For example, Epstein-Barr
virus, enteroviruses, parvovirus B19, C. pneumoniae and C.
burnetii (see above). This approach is standard in the
management of patients with pyrexia of unknown origin (PUO),
often with good results. So, why is it such a barrier for us to apply
these simple and universally accepted practices to a disease in
which infection frequently plays a major role? Along similar lines,
immunestimulant therapy through weekly injections of
staphylococcus toxoid led to marked improvements in the
symptoms of patients with CFS suggesting that immune
activation was key in the clearance of pathogens (Zachrisson et
al., 2002).
Hydrocortisone has been used to correct abnormalities in the
HPA axis (Cleare, 2003); this has been shown to lead to a
significant improvement in symptoms of disease in CFS
patients and a reduction of dehydroepiandrostenedione (DHEA)
to normal levels, but may also be complicated by adrenal
suppression (McKenzie et al., 1998).
4.2. Non-specific therapies
The use of anti-depressants, NSAIDs, anxiolytic drugs,
stimulants, anti-allergy drugs and anti-hypotensive drugs have all
been reported, but are not universally benefi- cial (Afari and
Buchwald, 2003). Recently, the use of methylphenidate, an
amphetamine-derived stimulatory drug, has been shown to
significantly improve fatigue and concentration disturbances in
people suffering from CFS (Blockmans et al., 2006).
Randomised controlled trials have been carried out to determine
the effectiveness of intravenous Ig therapy in the treatment of
CFS with conflicting results. Two such studies have reported no
beneficial effect of IgG therapy on the symptoms of CFS
(Vollmer-Conna et al., 1997; Peterson et al., 1990), however one
study has demonstrated a beneficial effect of Ig therapy (Lloyd et
al., 1990). IVIG therapy is recognized to benefit individual CFS
patients although it is difficult to predict which patients may
benefit.
The failure of conventional therapies to provide adequate relief
from the symptoms of CFS has led sufferers to experiment with
various alternative therapies with markedly differing outcomes
(Tharakan and Manyam, 2006; Gregg, 1997; Sekiya et al.,
2005; Mears, 2005; Sackner et al., 2004; Weatherley-Jones et
al., 2004; Ernst, 2004).
The TNF-a inhibitors may provide benefit in CFS. This group of
drugs has been shown to lead to dramatic improvement in
patients with rheumatoid arthritis, Crohn's disease, psoriasis
and other diseases including asthma. One TNF- inhibitor
(etanercept) has been used with signifi- cant benefit in the
treatment of 6 CFS patients in a pilot study (Lamprecht et al.,
2001). Unfortunately, this trial was not published as a paper, but
only as a meeting abstract. This requires urgent confirmation in
a larger subset of patients.
4.2.1. Psychological therapies
Graded exercise therapy (GET) and cognitive behavioural
therapy (CBT) remain the most common methods of treatment
for CFS available on the NHS. The rationale for GET is that
increasing amount of exercise will 'blow out the cobwebs and
return the patient to a normal or near-normal level of activity. The
rationale behind CBT is that patients are encouraged to gain
insights into the effects that particular activities have on their
physical functioning, and thereby to gain an increased ability to
tailor their activities to their capabilities. Numerous studies have
been conducted to determine the effect of graded exercise
therapy on patients with CFS despite the fact that it is known to
have a detrimental effect on many patients. While some studies
report benefit of CBT, this is admitted by it's proponents to be a
minor benefit and not a cure. In addition, a significant proportion
of patients show no improvement following CBT (Akagi et al.,
2001; Huibers et al., 2004). Neither GET nor CBT are specific
treatments for CFS, as we do not yet understand the
pathogenesis of CFS.
Preventing serotonin uptake has been found to be beneficial in
CFS patients with secondary depression. A pilot study
investigating the possible beneficial effects of the use of the
serotonin receptor antagonists, tropisetron and ondansetron on
fatigue in patients with CFS showed improvement in fatigue but
not any other symptoms (Spath et al., 2000). The use of a
serotonin receptor antagonist, granisetron, has shown promising
results with regard to fatigue levels, albeit in a pilot study with no
placebo (The et al., 2003). The use of the serotonin receptor
antagonist, nefazodone, has shown improvements in symptoms
of pain and insomnia in all three patients and two of the three
patients also showed improvements in NK cell function
(Goodnick and Jorge, 1999).
4.3. Supplements to support normal physiology
The use of vitamin and mineral supplementation is very common
in those suffering from CFS and is in our view advisable if high
quality preparations are used. In addition, use of anti-oxidants in
these preparations is of clear bene- fit due to their role in
reducing inflammation and the toxic effects of superoxide
radicals and excessive oxidation, which is recognised as a
problem in CFS (Kennedy et al., 2005). For example, a 2-month
trial with l-carnitine has shown improvements in fatigue in
patients with CFS (Plioplys and Plioplys, 1997). The use of
l-glutamine is also advisable to aid in repair of the
gastrointestinal tract (GIT) and to reduce the catabolic effects on
muscles of a debilitating illness. It is known that a deficiency in
essential fatty acids may lead to impairment of the immune
response due to a decrease in production of cytokines. In this
regard, oral supplementation with eicosapentaenoic acid has
been found to be beneficial in CFS patients, with two studies
demonstrating the improvement in fatigue (Puri et al., 2004; Puri,
2004), which is consistent with the anti-viral and
immunomodulatory effects of EPA.
[Return to top]
------------------------------
Date: Sat, 23 Sep 2006 22:30:00 +0000
From: Mary Schweitzer <marymsch@xxxxx.xxx>
Subject: RES,ACT: The pseudo-science of CBT
Doug Fraser gave me permission to use citations from two long
(but excellent) posts he sent to the discussion list LocalME.
What we have here is the juxtaposition of two works:
William Epstein, "Psychotherapy as Religion" (University of Nevada, 2006)
and
Vincent Deary and Trudy Chalder, "Case conceptualisation
in chronic fatigue syndrome," Chapter 11 of Chronic
Fatigue Syndrome: Formulation and treatment in clinical
health psychology [I'm sorry; I do not have the full citation
for this]
Trudy Chalder recently testified before the Gibson Inquiry,
the Parliamentary Committee investigating the treatment of
patients with CFS in the UK. "We already know that CBT
works for: Chronic Pain, Chronic Diseases i.e. rheumatoid
arthritis, Cancer (fatigue, distress), Irritable Bowel Syndrome,
Anxiety disorders, Depression, Eating disorders, PTSD,
to name but a few ..."
Epstein's book contains a withering critique of the claims of
omnnipotence for cognitive behaior therapy (CBT) and
psychotherapy.
CBT rates its own chapter.
"CBT appears to be the favored contemporary choice of
psychotherapy, eclipsing psychodynamic and behavioral
treatments as American society intensifies its preference for
personal responsibility over social responsibility, exaggerating
an already exaggerated heroic individualism.
"Yet CBT, like all of psychotherapy, is more akin to the mysticism of
mind cure and faith healing than to clinical science ...
"Despite the enormous amount of research cited to sustain the
different propositions of the cognitive model and thus CBT, the
theory has a contrived, ad hoc quality. It retreats from
disconfirming evidence, proposing the unmeasurable to explain
inconvenient findings.
"Most problematic, the central notion of causal direction, that
cognition rules emotion, behavior, and perhaps even physiology; has
not been adequately proven by any test. Indeed, alternative
assumptions—for example, that the environment or primitive emotion
determines behavior and that cognition is usually expressive post
hoc representation—remain equally plausible. Notably in relation to
cause but also in many other portions of the theory; Beck and others
are evasive....
"It relies on very uncertain discordant research that only allows box-
score summaries of 'many studies' or of 'most research' or of 'most
evidence,' or of seemingly 'reasonabl'e conclusions' or of 'our
review' or of some 'evidence [that] was found."
--------------------------------
Chalder and Deary's essay constitutes a perfect example
of Epstein's "pseudo-science" of CBT and psychotherapy.
The piece reads like a "pundit's" column - It's a matter of
rhetoric and persuasion - not proof.
As Epstein commented, this type of pseudo-science self-
references a lot - that is, everybody in the footnotes is part
of the Royal Colleges school of psychosomatic medicine - and
in fact, there are a lot of references to both Chalder and Deary's
own previous work.
First they present a "THEORY":
CFS can be conceptualised in terms of:
* the factors that predisposed the person to be vulnerable to it
* the factors that precipitated the current period of illness
* the factors that are now maintaining it.
Though they consider it possible - even highly likely - that a virus
is the initiating event, through the entire article they never admit
to the possibility that the 2000+ articles on the physicality of CFS,
the numerous articles on the history of M.E., are in any way accurate.
They do not confront the opposing evidence; they just ignore it.
There is no reference to articles on the biomechanics of ME/CFS,
or the articles on NMH/POTS, or the research on evidence of brain
damage (QEEGs and PET scans), or the research on cardiological abnormalities - and definitely no references to the research on
immunological abnormalities and viruses.
No references to anything except ... other psychotherapists.
The authors do not REFUTE the existing evidence - to repeat,
they simply IGNORE it.
After using persuasion alone to present the three "stages", as
it were, of the disease, they then give us a single patient - not a
real patient, mind you, but a composite.
The composite has the following "typical" personality and disease
characteristics (note the similarities to recent comments by
CDC's Bill Reeves):
Factors that predispose our fictional patient to be vulnerable to CFS:
1. Perfectionist personality
2. Abusive/absent father who sexually abused her two sisters;
3. Needy mother - i.e., both (2) and (3) created damage to "her"
psyche from childhood, probably contributed to (1)
Factors that precipitated the current period of illness:
4. Death of her husband (and they had no children).
5. Virus closely following the loss of her husband.
6. Left her job to "rest".
Factors that are now maintaining it:
7. Given public income support which permits her to continue
to "rest" (and maintain the "sick role")
8. Good support structure - friends help her out.
Results:
Sleeps all the time, experiences anxiety and pain that can
be attributed to tension, and does not even walk
down her hallway.
All of these are "typical", they say, of a CFS patient.
Well.
First, let's blame the parents and the past. It's so easy.
THERE IS ABSOLUTELY NO EVIDENCE THAT PATIENTS WITH
CFS-FUKUDA OR M.E. HAVE MORE LIKELIHOOD OF AN
ABUSIVE CHILDHOOD THAN ANYBODY ELSE.
The basis of the claim that CFS is the result of too much
stress is mainy that CFS patients have abnormally low
cortisol levels (patients with major melancholic depression
have abnormally high levels). "Hypocortisolism may
represent a 'burn-out' of the stress response in the
client; an indication that they were under stress for
a prolonged period and have thus become less able
to deal with it."
But there's no EVIDENCE that is the case!
Nor has the "perfectionist personality" hypothesis been
demonstrated empirically - it is an artifact from the
"yuppie flu" epithet and the first (acknowledged to be
flawed) study by CDC, which indicated that "CFS" was
a disease of upper middle class women trying to have it
all. Demographic studies have now disproved those
theories.
She lost her husband. That is very sad (although we can be
relieved that this was, after all, only a fictional patient.)
Could "she" have been depressed?
She did have a bad virus. She tried to go back to work
too fast and "fell ill" again. Permitting her extended sick
leave without counseling as to how to return to work, and
then permitting her to have indefinite public assistance,
only contributed to her inability to get well.
The support network was the nail in the coffin that has kept her
sick. They "allowed" her to continue to play the "sick role" from
the virus. She would not otherwise have permitted herself to
have these friendships with "the girls."
Now - all of this analysis is predicated on the ASSUMPTION -
never demonstrated (and remember, we are not talking about
a real person) that there is nothing physically wrong with her.
And absolutely nothing proves that these are typical
attributes in patients.
But the stage is set:
In they come with the heroic psychiatric rescue.
First, they have her get out of bed. I found it interesting that
our "typical" patient sleeps all the time - since one of the
distinguishing factors of CFS (at least, CFS-Fukuda) is lack of
refreshing sleep. Difficulty sleeping, not too much sleeping.
Of course, sleeping all the time IS a symptom of depression.
Our imaginary patient is made to get out of bed at a given time,
and try walking up and down the hallway ever few hours.
She is asked to increase the physical activity little by little,
and also to LET GO OF HER SUPPORT NETWORK little by little.
-- and miraculously, she is cured!
While the authors express GREAT sympathy for the problems of the
poor patient (the phrase "crocodile tears" comes to mind), they
essentially are blaming the patient for being sick.
It is the patient who CHOOSES to stay in bed all the time, the
patient who CHOOSES to accept all this help from "well-meaning"
- but clearly misguided - friends.
It is the patient who needs to be "fixed", and the patient has to
do all the fixing by making better CHOICES - just a little at a time.
Kind of a neoclassical economics approach to illness - people
are sick becaue they CHOOSE to be sick.
Which is perfect - because it also fits the strong neo-classical
approach to public policy, a return to the policies of Social
Darwinism of old. Everything is a "choice," including illness.
In this world, there is no such thing as misfortune.
The cruelest part of all this - and the most socially dangerous - is
the continued beat of the drum saying that support groups and
"kind, supportive family physicians" are a major part of the problem.
(Although it provides a very convenient rationale that it's okay
to limit patients' contacts with doctors to 5-10 minutes.)
Deary and Chalder provide a perfect example of the
pseudo-science of CBT. It LOOKS and SOUNDS scientific.
But there is nothing scientific here.
The pity is what this research does to the ability of ME/CFS
patients to get REAL help in the community.
------------------------------------------------
Returning to William Epstein, "Psychotherapy as Religion,"
"The psychotherapeutic emphasis on self-determination
ceremonializes personal responsibiity.
[...]
"[It] translates its clinical inabilities into fables of moral
responsibility: the need for the obese, the beleaguered,
the miscreant, the sad, the violent to take responsibility
for themselves and slim down, cheer up, and stop preying
on others.
[...]
"Unfortunately, the perfidies of psychotherapy play out
ideologically in consistent support of a social policy of
inexpensive, unambitious social-welfare programs that
impose an enormous amount of personal responsibility
on those least able to bear it.
"But just as psychotherapy did not create itself from a
series of tests and proofs of what works, so it is that
people do not form themselves in spite of their heroic
beliefs in self-creation and personal responsibility.
"Psychotherapy is compatible with a society deeply
attached to an ethos of self-invention, a fiction that
dispels the terror of confronting humanity's miserably
evolved self-consciousness, deep ignorance, and vast
inability to control its urges or its environment.
"The benefits of self-deception, perhaps political stability
and cultural coherence, are probably paid for by the
persistence of social problems — actual social progress,
necessitating attention to social problems, being
undercut by an ideology of social progress that denies them..."
-----------------------
Finally, we can end with a reference to Wessely's own work -
patients who present with the MOST "somatic" symptoms
(that is, who insist they have physical problems) are the most
DIFFICULT to deal with in therapy.
(See, for example, Butler JA, Chalder T, and Wessely S,
Causal attributions for somatic sensations in patients with
chronic fatigue syndrome and their partners.
Psychological medicine, 2001 Jan, 31(1):97-105)
That the correlation between "belief in physical symptoms" and
"difficulty following treatment" MIGHT have to do with the
existence of REAL physical smptoms that make psychological
treatment ineffective does not give them a single sleepless night.
Mary Schweitzer
[Return to top]
------------------------------
Date: Mon, 25 Sep 2006 11:07:12 +0200
From: "Dr. Marc-Alexander Fluks" <fluks@xxx.xx>
Subject: RES,NOT: U.S. Federal Register: CFS project CDC
Source: U.S. Federal Register
Volume 71, Number 161, p 48550
Date: August 21, 2006
URL: http://frwebgate3.access.gpo.gov/cgi-bin/waisgate.cgi?WAISdocID=176881187+9+0+0&WAISaction=retrieve
DEPARTMENT OF HEALTH AND HUMAN SERVICES
---------------------------------------
Centers for Disease Control and Prevention
[60Day-06-06BN]
Proposed Data Collections Submitted for Public Comment and Recommendations
--------------------------------------------------------------------------
In compliance with the requirement of Section 3506(c)(2)(A) of the
Paperwork Reduction Act of 1995 for opportunity for public comment on
proposed data collection projects, the Centers for Disease Control and
Prevention (CDC) will publish periodic summaries of proposed projects.
To request more information on the proposed projects or to obtain a
copy of the data collection plans and instruments, call 404-639-5960
and send comments to Seleda Perryman, CDC Assistant Reports Clearance
Officer, 1600 Clifton Road, MS-D74, Atlanta, GA 30333 or send an e-mail
to omb@cdc.gov.
Comments are invited on: (a) Whether the proposed collection of
information is necessary for the proper performance of the functions of
the agency, including whether the information shall have practical
utility; (b) the accuracy of the agency's estimate of the burden of the
proposed collection of information; (c) ways to enhance the quality,
utility, and clarity of the information to be collected; and (d) ways
to minimize the burden of the collection of information on respondents,
including through the use of automated collection techniques or other
forms of information technology. Written comments should be received
within 60 days of this notice.
Proposed Project
Conduct a Chronic Fatigue Syndrome Registry Pilot Test (Bibb
County, Georgia)--New--National Center for Infectious Diseases (NCID)
Centers for Disease Control and Prevention (CDC).
Background and Brief Description
CDC is tasked with establishing a registry of chronic fatigue
syndrome (CFS) and other fatiguing illnesses. The objective of the
registry is to identify persons with unexplained fatiguing illnesses,
including CFS, who access the healthcare system because of their
symptoms. Patients will be between the ages of 12 and 59, inclusive.
Specific aims of the registry are: (1) Identify and enroll patients
with CFS and other unexplained fatiguing illnesses who are receiving
medical and ancillary medical care and describe their epidemiologic and
clinical characteristics; (2) follow CFS patients and patients with
other fatiguing illnesses over time to characterize the natural history
of CFS and other unexplained fatiguing illnesses; (3) assess and
monitor health care providers' knowledge, attitudes, and beliefs
concerning CFS; (4) and to identify well-characterized CFS patients for
clinical studies and intervention trials. These specific aims require
inclusion of subjects in early stages of CFS (i.e., ill less than one
year duration) who can be followed longitudinally to assess changes in
their CFS symptoms. Data on persons with CFS in the general population
has been collected in a separate study and is not an objective of this
Registry.
In order to determine the most effective and cost-efficient design
for achieving the objective and specific aims, CDC will conduct a pilot
test of the Registry of CFS and other fatiguing illnesses in Bibb
County, Georgia. The CFS Registry Pilot Test will assess two Registry
designs for efficacy and efficiency in identifying adult and adolescent
subjects with CFS who are receiving medical and ancillary medical care.
Specifically, the CFS Registry Pilot Test will evaluate surveillance of
patients with CFS identified through physician practices and a
surveillance of CFS patients identified by physicians and other health
care providers.
The proposed study will begin when a provider refers a patient to
the registry. Patients who consent to be contacted for the registry
will be asked to complete a detailed telephone interview that screens
for medical and psychiatric eligibility. Eligible subjects will be
invited to have a clinical evaluation that comprises a physical
examination; collection of blood, urine, and saliva specimens; a mental
health interview; and self-administered questionnaires.
There is no cost to respondents other than their time. Patients who
are clinically evaluated will be reimbursed for their time and effort.
The total annualized burden hours are 2,557.
Estimate of Annualized Burden Hours
----------------------------------------------------------------------------------------
Average
Number of Number of burden per Total burden
Respondent respondents responses per response (hours)
respondent (hours)
----------------------------------------------------------------------------------------
Referring Providers................. 400 2 5/60 67
Patient consent to be contacted..... 677 1 10/60 113
Patient Telephone Interview......... 541 1 30/60 271
Patient Clinical Evaluation......... 234 1 540/60 2,106
---------------------------------------------------
Total Burden.................... 2,557
----------------------------------------------------------------------------------------
Dated: August 15, 2006.
Joan F. Karr,
Acting Reports Clearance Officer, Centers for Disease Control and
Prevention.
[FR Doc. E6-13721 Filed 8-18-06; 8:45 am]
BILLING CODE 4163-18-P
--------
(c) 2006 Federal Register
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------------------------------
Date: Mon, 25 Sep 2006 17:41:11 GMT
From: "mycoreg@juno.com" <mycoreg@xxxx.xxx>
Subject: RES, MED: Vit B3: Helps MS-Protects brain cells-Even in late-stage Mu ltiple Sclerosis
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MYCOPLASMA REGISTRY REPORTS
for gulf war syndrome & chronic fatigue syndrome
=A9 2006 Sean Dudley & Leslee Dudley. All rights reserved.
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=
Vitamin B3 May Help MS
Mouse Study: Vitamin B3 Protects Brain Cells -- Even in Late-Stage Multiple Sclerosis
By Daniel DeNoon
Reviewed By Louise Chang, MD
WebMD Medical News - September 19, 2006
http://www.webmd.com/content/article/127/116752.htm
The newest treatment for multiple sclerosis might be vitamin B3, mouse studies suggest.
Nicotinamide is a form of vitamin B3 closely related to niacin. In a
mouse model of MS, nicotinamide protects brain cells from degeneration.
Given in the early stages of disease, it offered "dramatic
protection." Given in late disease, it protected against further brain
damage and new disease symptoms, report Shinjiro Kaneko, MD, and
colleagues at Children's Hospital, Boston.
Both effects would be welcomed by people with MS. Current MS
treatments work only in the early "relapsing-remitting" phase of the
disease. Nothing currently slows the devastating later "chronic
progressive" stage of MS.
"The earlier therapy was started, the better the effect, but we hope
nicotinamide can help patients who are already in the chronic stage,"
Kaneko said, in a news release. "We hope that our work will initiate a
clinical trial, and that nicotinamide could be used in real patients."
Kaneko and colleagues report their findings in the Sept. 20 issue of
the Journal of Neuroscience.
Nerve Fiber Protection
During multiple sclerosis, nerve fibers -- axons -- are damaged by
self-destructive immune responses. It's possible, Kaneko and
colleagues suggest, that protecting them from further damage could
slow disease -- or even lead to some recovery.
The researchers noticed that in the mouse model of MS, the axons of
mice with hyperactive Wld genes aren't damaged as easily. The Wld
gene, it turns out, makes an enzyme necessary for the production of
another protein called NAD. Kaneko and colleagues found that as mice
progress to MS disease, nerve levels of NAD decline.
Kaneko and colleagues tried treating MS mice with nicotinamide. NAD
can be formed from nicotinamide. They found that this prevented the
decline of NAD -- and protected axons from disease.
"We demonstrate that administering nicotinamide can =85 result in
profound neuroprotection in [the mouse model of MS], providing a novel
therapeutic possibility for MS patients," Kaneko and colleagues
conclude.
Of course, clinical trials will be needed to find out if vitamin B3
really can be a safe and effective treatment for multiple sclerosis.
SOURCES: Kaneko, S. Journal of Neuroscience, Sept. 20, 2006; vol 26,
manuscript received ahead of publication. News release, Children's
Hospital, Boston.
© 2006 WebMD Inc. All rights reserved.
* * * * * * * * * * * * * * * * * * * * * * * * * * *
Protecting Axonal Degeneration by Increasing Nicotinamide Adenine
Dinucleotide Levels in Experimental Autoimmune Encephalomyelitis
Models
Shinjiro Kaneko,1 Jing Wang,1 Marie Kaneko,1 Glenn Yiu,1 Joanna M.
Hurrell,1 Tanuja Chitnis,2 Samia J. Khoury,2 and Zhigang He1
1Division of Neuroscience, Children's Hospital Boston, Harvard Medical
School, and 2Brigham and Women's Hospital, Harvard Medical School,
Boston, Massachusetts 02115
Correspondence should be addressed to Zhigang He, Division of
Neuroscience, Children's Hospital Boston, Enders #379, 320 Longwood
Avenue, Boston, MA 02115. Email: zhigang.he@childrens.xxxxx.xxx
Received May 18, 2006; revised Aug. 3, 2006; accepted Aug. 10, 2006.
J. Neurosci. 2006 26: 9794-9804; doi:10.1523/JNEUROSCI.2116-06.2006
http://www.jneurosci.org/cgi/content/abstract/26/38/9794
Key words: axon degeneration; EAE; NAD; Wallerian degeneration; =
nicotinamide; Wlds
ABSTRACT
Axonal damage is a major morphological alteration in the CNS of
patients with multiple sclerosis (MS) and its animal model,
experimental autoimmune encephalomyelitis (EAE). However, the
underlying mechanism for the axonal damage associated with MS/EAE and
its contribution to the clinical symptoms remain unclear. The
expression of a fusion protein, named "Wallerian degeneration slow"
(Wlds), can protect axons from degeneration, likely through a -
nicotinamide adenine dinucleotide (NAD)-dependent mechanism. In this
study, we find that, when induced with EAE, Wlds mice showed a modest
attenuation of behavioral deficits and axon loss, suggesting that EAE-
associated axon damage may occur by a mechanism similar to Wallerian
degeneration. Furthermore, nicotinamide (NAm), an NAD biosynthesis
precursor, profoundly prevents the degeneration of demyelinated axons
and improves the behavioral deficits in EAE models. Finally, we
demonstrate that delayed NAm treatment is also beneficial to EAE
models, pointing to the therapeutic potential of NAm as a protective
agent for EAE and perhaps MS patients.
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FREE BROCHURE: "How to Get an Accurate Polymerase Chain Reaction
(PRC) Blood Test for Mycoplasmal and Other Infections-with a List of
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------------------------------
Date: Mon, 25 Sep 2006 18:43:19 -0400
From: "Dr Charles Shepherd <charlesbshepherd@xxxxx.xxx> via Co-Cure
Moderators" <co-cure-mod@LISTSERV.NODAK.EDU>
Subject: NOT,MED: Response to a query about creatine supplements
Creatine supplements have been used/misused by athletes for many years in
order to try and increase their physical performance.
And there are certainly some theoretical reasons why creatine might work in
this way.
Firstly, creatine provides a reserve source of energy in muscle cells,
which they can quickly draw on when supplies of adenosine triphosphate
(ATP) are exhausted.
Secondly, creatine speeds up phosphocreatine resynthesis during recovery
periods and so helps to delay the onset of muscle fatigue due to glycogen
depletion.
Thirdly, creatine helps to enhance protein synthesis and so may increase
muscle mass.
Having spoken to experts in sports medicine about creatine it seems that
supplements can prolong peak performance in athletes by about 10% for
activities that involve short bursts of intense exercise. But there don't
appear to be any benefits when it comes to sustained activities. So the
benefits in ME/CFS are going to be very questionable.
The downside to creatine supplementation is that it can cause serious
side-effects on kidney function, and there have been reports in the medical
literature where this has happened to athletes (ref: Renal dysfunction
accompanying oral creatine supplements. Lancet, 1998, 351, 1252 - 1253)
. Whether this is purely dose related or due to individual sensitivity
remains uncertain.
My personal view is that creatine is a very speculative form of treatment
for people with ME/CFS and that it could have serious side-effects. I
don't therefore recommend creatine supplementation to my own patients.
However, it would be interesting to do a small clinical trial on some
people with ME/CFS who have definite evidence of biochemical muscle
dysfunction - but their renal function would obviously have to be carefully
monitored.
There is more information on muscle energy supplements - co-enzyme Q10,
creatine, NADH/Enada etc - in an MEA information sheet and on pages 199 -
200 of 'Living with ME'.
Dr Charles Shepherd
Medical Adviser, ME Association
This information may be reposted
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------------------------------
End of CO-CURE Medical & Research Posts Only Digest (#2006-44)- 18 Sep 2006 to 25 Sep 2006 (#2006-44)
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