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CO-CURE Medical & Research Posts Only Digest - 6 Nov 2006 to 13 Nov 2006 (#2006-51)

There are 17 messages totalling 2268 lines in this issue. Topics of the week:
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Date:    Tue, 7 Nov 2006 14:20:02 -0500
From:    "Bernice A. Melsky" <bernicemelsky@VERIZON.NET>
Subject: RES: How Do We Know That the Pain in Fibromyalgia Is "Real"?

How Do We Know That the Pain in Fibromyalgia Is "Real"?

Current Pain and Headache Reports 2006, 10:403-407
Current Science, Inc. ISSN 1531-3433

Richard E. Harris and Daniel J. Clauw
Corresponding author:Daniel J. Clauw

Department of Medicine, Division of Rheumatology, University of Michigan
Medical Center, 24 Frank Lloyd Wright Drive, PO Box 385, Ann Arbor, MI
18106, USA.
Email: dclauw@umich.edu


Fibromyalgia is a common idiopathic pain condition often resulting in
increased morbidity and disability in patients. The lack of peripheral
abnormalities in this disease has led clinicians and researchers alike to
question if this syndrome represents a valid entity.

Recent genetic findings suggest that specific gene mutations may predispose
individuals to develop fibromyalgia. In addition, neurobiological studies
indicate that fibromyalgia patients have abnormalities within central brain
structures that normally encode pain sensations in healthy pain-free controls.

Future studies that focus on central neurobiological and/or genetic
influences in fibromyalgia may bring insight into mechanisms of this
problematic disease and ultimately result in improved treatments.


Copyright © 2006 by Current Science, Inc.

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Date:    Tue, 7 Nov 2006 14:27:44 -0500
From:    Fred Springfield <fredspringfield@VERIZON.NET>
Subject: RES: Long-term efficacy of cognitive-behavioral therapy by  general practitioners for fatigue: A 4-year follow-up study

Long-term efficacy of cognitive-behavioral therapy by general practitioners
for fatigue: A 4-year follow-up study.

J Psychosom Res. 2006 Nov;61(5):601-7.

Leone SS, Huibers MJ, Kant I, van Amelsvoort LG, van Schayck CP,
Bleijenberg G, Knottnerus JA.

Department of Epidemiology, Maastricht University, Maastricht, The Netherlands.

PMID: 17084137


OBJECTIVE: In an earlier study, we found that cognitive-behavioral therapy
(CBT) delivered by general practitioners (GPs) for fatigue among employees
on sick leave was not effective after 12 months. In this study we aim to
assess the long-term efficacy of CBT by GPs for fatigue. It was
hypothesized that the intervention could prevent deterioration as well as
relapse of fatigue complaints and relapse into absenteeism in the long term.

METHODS: Patients who participated in the original randomized controlled
trial were followed up 4 years later. Fatigue and absenteeism were the main
outcomes.

RESULTS: Fatigue and absenteeism were high in the intervention and control
groups at the 4-year follow-up. There was no significant difference between
the intervention group and the control group on fatigue and absenteeism.
The intervention group however tended toward less-favorable outcomes as
compared with the control group.

CONCLUSIONS: Like that of chronic fatigue syndrome, the prognosis of
less-advanced fatigue is rather poor. CBT delivered by GPs is not effective
in the long term.

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Date:    Tue, 7 Nov 2006 15:01:24 -0500
From:    "Bernice A. Melsky" <bernicemelsky@VERIZON.NET>
Subject: RES: Fibromyalgia: a disease of psychic trauma

[Fibromyalgia: a disease of psychic trauma.]
[Article in French]

Presse Med. 2006 Nov;35(11 Pt 2):1683-9.

El-Hage W, Lamy C, Goupille P, Gaillard P, Camus V.

Clinique psychiatrique universitaire, CHRU, Tours (37).

PMID: 17086126


Chronic unexplained pain may be a somatic manifestation of psychological
distress - often untreated distress. The association between psychic trauma,
posttraumatic symptoms, psychic dissociation, and somatoform disorders is
currently well documented.

When examining a patient with chronic pain syndrome, it is important to
consider its psychic dimension early on and to look for a history of
psychic trauma. This can help avoid prolonged chronic effects and the
emergence of psychiatric comorbidity.

There is currently no consensual medication strategy for treatment of
unexplained chronic pain syndrome. Multidisciplinary outpatient management
is necessary in these complex cases, which require simultaneous medical and
psychiatric referrals.

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Date:    Tue, 7 Nov 2006 15:04:40 -0500
From:    "Bernice A. Melsky" <bernicemelsky@VERIZON.NET>
Subject: RES: Higher prevalence of fibromyalgia in patients infected  with human T cell lymphotropic virus type I

Higher prevalence of fibromyalgia in patients infected with human T cell
lymphotropic virus type I.

J Rheumatol. 2006 Nov;33(11):2300-3.

Cruz BA, Catalan-Soares B, Proietti F.

PMID: 17086610


OBJECTIVE:. Inflammatory rheumatic conditions including rheumatoid
arthritis and Sjogren's syndrome have been reported in individuals infected
with human T cell lymphotropic virus type I (HTLV-I). Other chronic
lymphotropic virus infections such as hepatitis C and human
immunodeficiency virus are associated with fibromyalgia (FM). There are no
reports about the association between HTLV-I infection and FM. We evaluated
the association between FM and HTLV-I infection.

METHODS: We conducted a case-control study with prevalent cases. Ex-blood
donation candidates with HTLV-I infection from a blood bank cohort, and
healthy blood donors as a control group, were submitted to rheumatologic
evaluation to compare the prevalence of FM. The following covariables were
also evaluated: other rheumatic diseases, age, sex, personal income, level
of education, and depression.

RESULTS: One hundred individuals with HTLV-I infection and 62 non-infected
blood donors were studied. Thirty-eight (38%) HTLV-I infected individuals
and 3 (4.8%) individuals from the control group presented the diagnosis of
FM (OR 12.05, 95% CI 3.53-41.17). Other rheumatic diseases were also more
prevalent in the infected group (37% vs 12.9%; OR 3.80, 95% CI 1.63-8.86).
In multivariate analysis adjusted by the covariables, the association
between HTLV-I and FM was statistically significant (OR 9.14, 95% CI
2.42-34.52).

CONCLUSION: Our study shows a greater prevalence of FM in HTLV-I infected
individuals, suggesting that FM may be associated with this viral infection.

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Date:    Tue, 7 Nov 2006 22:19:26 -0500
From:    "CF-Alliance <cf_alliance@YAHOO.COM> (via Co-Cure Moderators
        
        
        
        
         <co-cure-mod@listserv.nodak.edu>)" <auntiem6@PTD.NET>
Subject: RES:Childhood Trauma Raises CFS Risk

Childhood Trauma Raises CFS Risk


  Researchers Also Say Stress Is a Factor in Chronic Fatigue Syndrome

 

 

 

 

  http://www.webmd.com/content/article/129/117419

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Date:    Wed, 8 Nov 2006 16:17:06 -0500
From:    Fred Springfield <fredspringfield@VERIZON.NET>
Subject: RES: A follow-up study of chronic fatigue syndrome in children  and adolescents: symptom persistence and school absenteeism

A follow-up study of chronic fatigue syndrome in children and adolescents:
symptom persistence and school absenteeism.

Journal: Clin Child Psychol Psychiatry. 2006 Jan;11(1):126-38.

Authors: Sankey A, Hill CM, Brown J, Quinn L, Fletcher A.

Affiliation: Southampton City Primary Care Trust, UK.
alison.sankey@scpct.nhs.uk

NLM Citation: PMID: 17087490


This is a follow-up study of 28 young people aged between 7 and 17 meeting
the Oxford criteria for the diagnosis of chronic fatigue syndrome treated
in a specialist paediatric/psychiatric service. Retrospective case note
analysis revealed a wide range and duration of symptoms together with high
levels of school absenteeism prior to the diagnosis. The mean follow-up
interval after discharge from the specialist service was 3 years and
although most of the young people regarded themselves as fully recovered by
this time, improvement was variable and about one third were still
experiencing disabling symptoms. The illness had impacted on the education
or career plans of all the young people to some extent with 15 experiencing
difficulty returning to school. This article highlights the need for early
recognition and diagnosis of chronic fatigue syndrome in young people and
the importance of continuing paediatric support to reduce symptom
persistence in the sensitive recovery period. Maintaining school attendance
by close liaison between health and education services both before and
after diagnosis and treatment is also vital if long-term morbidity is to be
reduced.

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Date:    Wed, 8 Nov 2006 19:31:47 -0500
From:    "Bernice A. Melsky" <bernicemelsky@VERIZON.NET>
Subject: RES: Chronic Low Back Pain in Older Adults: What Physicians  Know, What They Think They Know, and What They Should Be Taught

Chronic Low Back Pain in Older Adults: What Physicians Know, What They
Think They Know, and What They Should Be Taught.

J Am Geriatr Soc. 2006 Nov;54(11):1772-1777.

Cayea D, Perera S, Weiner DK.

Department of Medicine, Division of Geriatrics and Gerontology, School of
Medicine, Johns Hopkins University, Baltimore, Maryland.

PMID: 17087707


Chronic low back pain (CLBP) is a common and debilitating problem in older
adults. Little exists in the literature about primary care physicians'
(PCPs') knowledge of and confidence in managing this problem. A
self-administered survey was mailed to PCPs in western Pennsylvania to
measure knowledge of the evaluation and treatment of common contributors to
CLBP in older adults, confidence in diagnosing these contributors through
physical examination, and the association between confidence levels and
knowledge.

The survey combined items with an ordinal scale on which PCPs ranked their
confidence in detecting various contributors to CLBP (e.g., fibromyalgia)
using physical examination and patient vignettes followed by multiple
choice questions designed to assess knowledge. One hundred fifty-three of
634 surveys were returned (24.1%).

Overall, the majority of PCPs did not feel "very confident" in their
ability to diagnose any of the contributors of CLBP listed (most items
<40%). PCPs felt most confident in detecting scoliosis and least confident
detecting myofascial pain of the piriformis muscle. There was a wide range
in the number of respondents answering all questions related to a
particular topic correctly (3.9% for sacroiliac joint syndrome to 70.4% for
hip osteoarthritis). There was no relationship between knowledge scores and
confidence ratings (P>.05 for all comparisons).

The results point to a need for more PCP education about CLBP in older
adults. It also suggests that accurate needs assessment should not rely on
physician confidence ratings alone.

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Date:    Thu, 9 Nov 2006 14:04:19 -0500
From:    "Bernice A. Melsky" <bernicemelsky@VERIZON.NET>
Subject: RES: At the Crossroads Between Tension-type Headache and  Fibromyalgia

At the Crossroads Between Tension-type Headache and Fibromyalgia.

Curr Pain Headache Rep. 2006 Dec;10(6):463-6.

Lenaerts ME, Gill PS.

Department of Neurology, Headache Section, Oklahoma University Health
Sciences Center, 711 Stanton L. Young Boulevard, #215, Oklahoma City, OK
73104, USA. marc-lenaerts@ouhsc.edu.

PMID: 17087873


Fibromyalgia syndrome and tension-type headache have multiple clinical
features in common, and pathogenic mechanisms partly overlap. Significant
differences need to be recognized as well. Studying the correlations of
these often comorbid conditions represents a unique opportunity to gain
insight into their pathophysiology and that of other chronic pain
syndromes, to increase the accuracy of their diagnosis, and to improve the
therapeutic armamentarium.

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Date:    Fri, 10 Nov 2006 15:50:20 -0500
From:    "Marcia Harmon <MLHarmon@cfids.org> via Co-Cure Moderators"
        
        
        
        
         <co-cure-mod@LISTSERV.NODAK.EDU>
Subject: RES: Limited Studies of Early-Life Stress Put in Context

 From Marcia Harmon <MLHarmon@cfids.org>:


Limited Studies of Early-Life Stress Put in Context

Two studies published in the November 6, 2006, issue of the Archives of
General Psychiatry associate trauma in early life with CFS and CFS-like
illness. However, each study has important limitations to consider and the
authors' conclusions should not be overgeneralized.

Both new studies focused on a narrow set of adverse events and excluded
others, such as infection, serious injury and malnutrition, shown to be
important in other conditions, and that warrant further exploration in CFS
as well.

Adverse events in early childhood have been shown to be predisposing
factors in other serious conditions, including cardiovascular disease,
diabetes and depression. A report compiled by the National Scientific
Council on the Developing Child at
http://www.developingchild.net/papers/excessive_stress.pdf summarizes this
literature in layman's terms. No broader discussion of this literature is
included in either paper and thus is being overlooked by the media.

Studies like these that rely solely on unverified self-report of childhood
experiences occurring 35-50 years earlier, particularly of people with
later-life physical and psychological health issues, have many limitations
that are well-documented in the medical literature. Although the mean age
of subjects in the Heim study was 50.5 years and subjects in the Kato study
were 42 years or older, this limitation is only acknowledged in the Kato
paper, as described below.

Christine Heim, PhD, of Emory University is the lead author of a study
titled, "Early Adverse Experience and Risk for CFS: Results from a
Population-Based Study." She is no longer affiliated with the Centers for
Disease Control and Prevention's CFS Research Group. Dr. Heim describes the
small study of 43 CFS patients as "exploratory" and states that results
"should be considered as preliminary." The researchers found that CFS cases
reported significantly higher levels of childhood trauma and
psychopathology compared to healthy controls. Exposure to childhood trauma
was associated with three-to eight-fold increased risk for CFS across the
trauma types assessed. The authors state, "our results also clearly
demonstrate that not all cases of CFS have a history of childhood trauma."

The second study, by Kenji Kato, PhD, et al., of the Karolinska Institutet,
presents similar findings from a study nested within a Swedish Twin
Registry of 19,192 twin pairs born between January 1, 1935, and December
31, 1958. All twins were screened for the symptoms of CFS by telephone, but
investigators did not conduct thorough physical and mental status exams to
confirm CFS diagnosis. Thus, conclusions are based on "CFS-like illness,"
and not CFS as strictly defined. In all, 447 subjects fit the description
of "CFS-like illness." Study results indicate an association between
"emotional instability" and self-reported stress and chronic
fatigue/CFS-like illness. In examining differences between twin pairs, the
researchers reported that, "certain genetic propensities may ameliorate or
exacerbate the effect of stress. At the same time, genetic influences on
emotional instability also contribute to the development of fatiguing
symptoms." The authors state that "a number of cases might have been
misclassified owing to recovery or recall bias by the time of the interview."

As the November 3, 2006, announcements by CDC director Dr. Julie Gerberding
underscore, the important story about CFS is much larger than any single
study or pair of studies. The media coverage over the last week, of which
only a small fraction relates to these studies, reflects the bigger picture
too. That said, all people, including the subset of CFS patients described
by these studies, whose lives have been affected by trauma in their
childhood years certainly deserve compassion and careful study so that the
biological and psychological impact of these early-life events is better
understood.

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Date:    Fri, 10 Nov 2006 16:08:15 -0500
From:    Fred Springfield <fredspringfield@VERIZON.NET>
Subject: RES: Odds ratio based multifactor-dimensionality reduction  method for detecting gene-gene interactions

Odds ratio based multifactor-dimensionality reduction method for detecting
gene-gene interactions.

Journal: Bioinformatics. 2006 Nov 8; [Epub ahead of print]

Authors:  Yujin Chung [1], Seung Yeoun Lee [2], Robert C. Elston [3], and
Taesung Park [1 *]

Affiliations:
[1] Department of Statistics, Seoul National University, San 56-1
Shillim-Dong, Kwanak-Gu, Seoul 151-747, Korea
[2] Department of Applied Mathematics, Sejong University, 98 Gunja-Dong
Kwangjin-Gu, Seoul 143-747, Korea
[3] Department of Epidemiology and Biostatistics, Case Western Reserve
University, 10900 Euclid Avenue Cleveland, Ohio 44106-7281, USA

[*] To whom correspondence should be addressed.
Taesung Park, E-mail: tspark@snu.ac.kr

NLM Citation: PMID: 17092990


MOTIVATION: The identification and characterization of genes that increase
the susceptibility to common complex multifactorial diseases is a
challenging task in genetic association studies. The multifactor
dimensionality reduction (MDR) method has been proposed and implemented by
Ritchie et al. (2001) to identify the combinations of multilocus genotypes
and discrete environmental factors that are associated with a particular
disease. However, the original MDR method classifies the combination of
multilocus genotypes into highrisk and low-risk groups in an ad hoc manner
based on a simple comparison of the ratios of the number of cases and
controls. Hence, the MDR approach is prone to false positive and negative
errors when the ratio of the number of cases and controls in a combination
of genotypes is similar to that in the entire data, or when both the number
of cases and controls is small. Hence, we propose the odds ratio based
multifactor dimensionality reduction (OR MDR) method that uses the odds
ratio as a new quantitative measure of disease risk.

RESULTS: While the original MDR method provides a simple binary measures of
risk, the OR MDR method provides not only the odds ratio as a quantitative
measure of risk but also the ordering of the multilocus combinations from
the highest risk to lowest risk groups. Furthermore, the OR MDR method
provides a confidence interval for the odds ratio for each multilocus
combination, which is extremely informative in judging its importance as a
risk factor. The proposed OR MDR method is illustrated using the dataset
obtained from the CDC Chronic Fatigue Syndrome Research Group
(http://www.cdc.gov/ncidod/diseases/cfs/).

AVAILABILITY: The program written in R is available.

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Date:    Fri, 10 Nov 2006 18:00:24 -0500
From:    "Bernice A. Melsky" <bernicemelsky@VERIZON.NET>
Subject: RES: Cognitive Dysfunction in Fibromyalgia and Chronic Fatigue Syndrome: New Trends and Future Directions

Cognitive Dysfunction in Fibromyalgia and Chronic Fatigue Syndrome: New
Trends and Future Directions.

Curr Rheumatol Rep. 2006 Dec;8(6):425-429.

Glass JM.

University of Michigan, Institute for Social Research and Department of
Psychiatry, 426 Thompson Street, Room 5256, Ann Arbor, MI 48106-1248, USA.

PMID: 17092441


Fibromyalgia (FM) and chronic fatigue syndrome (CFS) patients often have
memory and cognitive complaints. Objective cognitive testing demonstrates
long-term and working memory impairments. In addition, CFS patients have
slow information-processing, and FM patients have impaired control of
attention, perhaps due to chronic pain. Neuroimaging studies demonstrate
cerebral abnormalities and a pattern of increased neural recruitment during
cognitive tasks.

Future work should focus on the specific neurocognitive systems involved in
cognitive dysfunction in each syndrome.

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Date:    Fri, 10 Nov 2006 19:05:32 -0500
From:    Co-Cure Moderators <co-cure-mod@LISTSERV.NODAK.EDU>
Subject: NOT,MED: Kaiser Family Foundation Issues New and Updated Resources on Medicare Drug Plans as November 15 Annual Sign-Up Period Approaches for People with Medicare [US]

Friday, November 10, 2006
Kaiser Family Foundation Issues New and Updated Resources on Medicare Drug
Plans as November 15 Annual Sign-Up Period Approaches for People with Medicare


CONTACTS:
Craig Palosky
(202) 347-5270
cpalosky@kff.org

Sarah Carkhuff Fizell
(202) 347-5270
scarkhuff@kff.org


Starting on November 15, all 43 million people with Medicare will have six
weeks to decide whether to continue with or make changes in how they get
their drug coverage and other benefits for the coming year. In advance of
the 2007 open enrollment period for 2007 for Medicare drug plans, the
Kaiser Family Foundation today issued a series of new and updated resources
related to the Medicare drug benefit. These resources include:

Updated fact sheet (at http://www.kff.org/medicare/7426.cfm ) with
state-by-state Medicare Part D plan characteristics for 2007. This fact
sheet provides state-specific data about Medicare drug plan options for
2007, including the number of stand-alone drug plans and Medicare Advantage
plans, and information on premiums, gap coverage, and availability to
beneficiaries who qualify for full low-income assistance. Premiums for
stand-alone plans will range from $9.50 to $135.70 in 2007. Beneficiaries
in 39 states can choose stand-alone plans that provide coverage for
brand-name drugs in the benefit gap in coverage (the so-called "doughnut
hole"). In the 11 other states that do not have that option, beneficiaries
may choose plans that cover generic drugs in the gap.


Updated Medicare Prescription Drug Benefit fact sheet (at
http://www.kff.org/medicare/7044.cfm ), with a revised estimate of people
affected by the coverage gap. This fact sheet includes the latest
information and data about the benefit, including an overview of Part D
plans in 2007 and an updated estimate that 4 million people with Medicare
will reach the coverage gap in 2006. The estimate, based on analysis by the
Actuarial Research Corporation for the Kaiser Family Foundation, reflects
current enrollment and low-income subsidy participation as well as updated
Medicare per capita drug spending.


Updated Talking About Medicare consumer guide (at
http://www.kff.org/medicare/7067/index.cfm), reflecting changes in benefits
for 2007. This online consumer guide, Talking About Medicare, is designed
to help people with Medicare and their families understand options and make
decisions about Medicare coverage based on their personal situations. The
guide includes general information about the Medicare drug benefit, key
considerations for selecting a Medicare drug plan, and information about
financial assistance for those with limited incomes. The guide also
provides information about eligibility and other covered benefits and
explains supplemental insurance options and the Medicare Advantage program.

The new and updated resources are part of the Foundation's broader research
into the Medicare prescription drug benefit, including periodic surveys of
the views and experiences of seniors. Key resources are available online at
http://www.kff.org/medicare/rxdrugbenefit.cfm .

In addition, Kaisernetwork.org will host a live webcast at 2 p.m. E.T. on
Tuesday, Nov. 14
(see
http://www.kaisernetwork.org/health_cast/hcast_index.cfm?display=detail&hc=1935),
to answer questions about the Medicare drug benefit in advance of the open
enrollment period. The discussion will include Leslie Norwalk, acting
administrator of the Centers for Medicare and Medicaid Services; Judith A.
Stein, executive director, Center for Medicare Advocacy; and Juliette
Cubanski, principal policy analyst, Kaiser Family Foundation. Viewers can
send questions in advance to ask@kaisernetwork.org or call 1-888-524-7378
during the live broadcast.

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Date:    Sat, 11 Nov 2006 15:34:19 -0500
From:    "Bernice A. Melsky" <bernicemelsky@VERIZON.NET>
Subject: RES: Are patients with systemic lupus erythematosus at  increased risk for fibromyalgia?

Are patients with systemic lupus erythematosus at increased risk for
fibromyalgia?

Curr Rheumatol Rep. 2006 Dec;8(6):430-5.

Staud R.

Department of Medicine, McKnight Brain Institute, University of Florida,
Gainesville, Florida 32610, USA. staudr@ufl.edu.

PMID: 17092442


Widespread chronic pain, fatigue, and distress do not represent risk
factors for future systemic lupus erythematosus (SLE) or other autoimmune
syndromes. On the other hand, SLE seems to be a significant risk factor for
fibromyalgia (FM). Up to 47% of SLE patients fulfill FM criteria. SLE
patients with concomitant FM are often highly symptomatic and
dysfunctional. The presence of FM symptoms in SLE patients, however, does
not predict more extensive organ involvement or lupus activity.

The high concordance of SLE with FM suggests common mechanisms related to
pain and distress in both patient groups. Recent research suggests
involvement of N-methyl-d-aspartate (NMDA) and neurokinin receptor systems.
Thus, autoimmune activity against these receptor systems in SLE patients
could result in pain, cognitive defects, and chronic pain states including
FM. Conversely, treatment of SLE-FM patients with inhibitors of NMDA or
neurokinin receptors may prevent or alleviate cognitive abnormalities and
chronic pain, as well as FM.

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Date:    Sun, 12 Nov 2006 12:38:07 -0500
From:    "Bernice A. Melsky" <bernicemelsky@VERIZON.NET>
Subject: RES: Coexistence of fibromyalgia, temporomandibular disorder, and masticatory myofascial pain syndromes

Coexistence of fibromyalgia, temporomandibular disorder, and masticatory
myofascial pain syndromes.

Rheumatol Int. 2006 Nov 10; [Epub ahead of print]

Leblebici B, Pektas ZO, Ortancil O, Hurcan EC, Bagis S, Akman MN.

Department of Physical Medicine and Rehabilitation, Faculty of Medicine,
Baskent University, Ankara, Turkey, bleblebici@baskent-adn.edu.tr.

PMID: 17096090


The purpose of this study was to determine the association of fibromyalgia
(FM) with temporomandibular disorder (TMD) and masticatory myofascial pain
(MMP).

Thirty-one consecutive women diagnosed as having FM according to American
College of Rheumatology criteria and 21 consecutive women diagnosed as
having TMD were included in this prospective study. All patients were
examined by a dentist and a physiatrist to identify the coexistence of FM
and TMD.

In the FM group, TMD was found in 25 (80%) patients, and only 6 (19%)
patients had arthrogenous origin with MMP, whereas 19 (81%) patients had
only MMP without arthrogeonous orgin of those 25 women exhibited TMD. In
the TMD group, the prevalence of FM was 52%, which was significantly higher
in those with TMD of arthrogenous origin with MMP.

Our results indicate that coexistence of FM and TMD with MMP is high. Pain
and tenderness in the masticatory muscles appear to be an important element
in FM, so in some patients it may be the leading complaint.

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Date:    Mon, 13 Nov 2006 20:16:06 -0000
From:    Stephen Ralph <stephen.e.ralph@MEACTIONUK.ORG.UK>
Subject: ACT,RES: Klimas, Wessely and NICE: Redefining CBT? - Margaret Williams - 10th November 2006

Permission to Repost

http://www.meactionuk.org.uk/Klimas_Wessely_and_NICE_-_Redefining_CBT.htm

Klimas, Wessely and NICE: Redefining CBT?

Margaret Williams

10th November 2006

Patent Foramen Ovale (PFO) is the persistence (or the acquired re-opening)
of the normal foetal opening between the right and left atria of the heart.
In his September 2006 seminar (see below), Dr Paul Cheney from North
Carolina - who has seen over 5,000 patients with (Myalgic Encephalomyelitis)
/ Chronic Fatigue Syndrome -- states that PFO is "tightly associated" with
(ME)CFS to the order of at least 80% or more of patients.

Despite the fact that the UK medical defence unions have advised doctors
that exercise regimes (which form part of a cognitive behavioural therapy
regime) must be prescribed with just as much caution as pharmacological
interventions, it seems that the National Institute for Health and Clinical
Excellence (NICE) may have overlooked the implications of this advice: in
its Draft Guideline on "CFS/ME", the only recommended management regime is
cognitive behavioural therapy (CBT), including graded exercise therapy (GET)
and, for the severely affected, "Activity Management".

There is no warning that patients with ME/CFS might have PFO. On the
contrary, the NICE Draft Guideline advises against even looking for such
pathology in those with ME/CFS.

Why is the UK ME/CFS community so collectively opposed to the NICE Draft
Guideline?

The answer is because NICE is recommending CBT and GET as the only
management regime and those whose lives are struck down by ME/CFS know full
well that the UK CBT/GET regime has already been shown to be at best of
little help, and at worst, dangerous.

The UK definition of CBT is contained in the Chief Medical Officer's Working
Group Report of January 2002: "Cognitive behavioural therapy is a tool for
constructively modifying attitude and behaviour".

The UK definition of GET is contained in the NHS Plus National Guideline on
Occupational Aspects of CFS of October 2006: "GET involves structured
activity management that aims for a gradual increase in aerobic activities".

According to Cheney, aerobic exercise may kill the patient with (ME)CFS, so
patients are rightly wary, because for almost 20 years Wessely School
psychiatrists have claimed that ME does not exist except as an aberrant
belief, and that "CFS" is a psychiatric disorder in which patients refuse to
confront their "faulty illness beliefs" (ie. that they have a physical, not
a mental, illness). These psychiatrists believe it is such "faulty" beliefs
that prevent people from recovering, therefore the "faulty" beliefs must be
modified in order to get people who harbour misperceptions about their
bodily sensations off welfare benefits and back into work. Patients who do
not - or physically cannot-comply have had their benefits stopped. There has
been little evidence that CBT is a tool to support patients or to help them
cope with the ravages of serious organic disease.


Confusion about CBT in the UK

Confusion abounds in almost every aspect of ME/CFS, including what is now
meant by "CBT/GET", and in the UK there seem to be signs of expedient change
as to the type of CBT/GET that is to be delivered to those with ME/CFS, as
well as the purpose of it; in other words, it seems the nature of CBT is
being re-defined.

For example, in October 2006 at the Sheffield (UK) Conference, CBT was
described by Professor Anthony Pinching as "a valuable tool for managing
chronic disabling illness in patients who are having difficulties in
adjustment". Given Pinching's published track record, notably his article in
Prescribers' Journal in 2000, this seems to represent a significant shift,
because in that article he stated that CFS is not related to on-going
exertion; that patients should not be "over-investigated" because
investigating them causes them "to seek abnormal test results to validate
their illness"; that approaches can be "behavioural"; that "the benefits of
graded exercise have been shown by randomised controlled trials", and that
"the essence of treatment is activity management", relying heavily upon
Wessely School studies, many of which promote the delivery of CBT/GET in a
coercive and overly-inflexible way (Prescribers' Journal 2000: 40:2:99-106).

But Pinching's is not the only apparent turn-around: given that at the
behest of Wessely School psychiatrists who believe "CFS/ME" to be a
behavioural disorder, the Government rushed to invest £8.5 million in "CBT
for CFS" by setting up new Centres that are to deliver CBT/GET for those
with ME/CFS, it now seems to be wondering - in the light of so much
incontrovertible evidence of serious organic pathology in ME/CFS that cannot
be denied forever - if this may have been the wisest way of addressing the
problem, and as a consequence, some Government bodies seem to perceive a
pressing need to justify by any means possible the expenditure of such large
amounts of money on what may be seen as inappropriate interventions.

And so the NICE Draft Guideline states: "The Guideline Development Group was
clear that CBT was not about unhelpful advice or dictation of illness
beliefs, but about changes in lifestyle and learning to achieve improvements
with the patient's abilities. The GDG did not regard CBT or other
behavioural treatments as curative or directed at the underlying disease
process. Rather, such treatments can help some patients cope with the
condition and consequently experience an improved quality of life" (6.3.7 /
Deriving Recommendation / Discussion of the Evidence).

Noble-sounding words, but this sweet-talking does not stop the UK ME
community from seeing such surreptitious amendment as a case of "Come into
my parlour, said the spider to the fly", especially given that NHS Plus has
not waited for the final NICE Guideline but has gone ahead and published its
64-page Policy Document referred to above (Occupational Aspects of the
Management of Chronic Fatigue Syndrome: a National Guideline". Department of
Health: 6th October 2006: 273539) that is grounded entirely on the
psychosocial model of ME/CFS and which recommends that patients who are
still working should be advised to stay at work even if they feel "tired".
Importantly, it stipulates that no-one with a diagnosis of ME/CFS should be
permitted to retire until they have undergone "rehabilitation" by means of
CBT/GET. It is noted that the key players in this document are Professor
Trudie Chalder, Professor Mike Sharpe and Professor Peter White, all of whom
are well-known for their intransigent belief that "CFS/ME" is a behavioural
disorder. It is also noted that the "Guideline Leader" does not work for the
NHS but for a private medical insurance company.

To accompany this Policy Document, NHS Plus has produced three booklets: one
for employers, one for employees and one for healthcare professionals, all
of which contain misinformation about ME (about which the parent document
states: "The descriptive term CFS is preferable to previously used terms
such as post-viral fatigue syndrome or ME").

The booklet for employers states: " This leaflet summarises the
evidence-based guidance on how to support individuals back into, and to
remain in, work. CFS is an illness characterised by severe, disabling
tiredness. A feeling of being tired all the time is very common. ME and
post-viral fatigue syndrome are terms that people with CFS often use (but)
most healthcare professionals prefer the term CFS. (Appropriate treatments)
for CFS (are) CBT, a structured form of psychotherapy (and) GET, a
structured programme designed to increase aerobic activity. If an individual
complains of fatigue, an employer should refer them to an occupational
health professional. Ill-health retirement should only be considered if
appropriate treatments such as CBT and GET have been explored".

The booklet for employees says much the same: "It is a good idea to try to
stay at work even though you feel tired. CBT and GET are treatments that
research has shown can increase the chance of returning to work. Ill-health
retirement is not a first choice".

The booklet for healthcare professionals is even more damaging: "The
perpetuation of CFS may include deconditioning, inappropriate avoidance of
activity as a coping mechanism, personal conflicts and fears about the
condition itself. Management (is by) a biopsychosocial approach. There are
two interventions supported by good quality evidence (sic): CBT involves
cognitive restructuring to tackle negative beliefs. (Its) effectiveness may
be limited by excessive focus on bodily symptoms and taking medical
retirement or disability benefit during the treatment. (In) GET, patients
'negotiate' an aerobic exercise programme. Patients should be advised
against seeking early medical retirement until all rehabilitation strategies
have been explored". The reference to support this last statement says:
"Evidence from expert opinion".

There is no reference to the research evidence that has demonstrated
serious, multi-system pathology: employers and healthcare professionals (ie.
the decision-makers) are given no information about the proven dysfunction
of virtually all body systems, including cardio-vascular, respiratory,
gastro-intestinal, musculo-skeletal, opthalmic, neurological, and most
importantly, the immune system (with the evidence of autoimmunity). Not to
do so is, by any standards, deceptive.

Curiously, Professors Peter White and Mike Sharpe seem to be somewhat
confused: whilst on the one hand they say that the effectiveness of CBT may
be limited by being in receipt of disability benefit, in the same document
they also say: "being in receipt of sickness benefit at the start of
treatment may be a marker of severity".

Thus in the UK things are far from transparent: the NICE Draft Guideline
says one thing, but the NHS Plus documents have pre-empted the NICE
Guideline (due in April 2007) and say another thing entirely.

Those in the UK ME community who might be tempted to accept the NICE Draft
Guideline's assurances that CBT is not about "dictation of illness beliefs"
need to remember that the psychotherapy it recommends will still be
delivered in psychiatric units at the behest of psychiatrists who will still
harbour their ill-founded prejudices against ME patients.


Confusion about CBT in the US

In November 2006 Nancy Klimas, Professor of Medicine at Miami, and Anthony
Komaroff, Professor of Medicine at Harvard (both of whom are not only
clinicians but also long-time researchers into ME/CFS) attended the launch
by the US Centres for Disease Control (CDC) of its "CFS Toolkit" and its
campaign to advance knowledge of (ME)CFS.

At the launch, Professor Klimas said: "Historically, the lack of credibility
afforded this illness has been a key obstacle to understanding it. Today,
with solid evidence that CFS has identifiable biologic underpinnings, and
with evidence that people with CFS experience a level of disability equal to
that of patients with multiple sclerosis, advanced HIV disease and
undergoing chemotherapy, I hope we can begin to put an end to the stigma
surrounding this illness."

Also at the launch, Professor Komaroff said about the lingering belief that
(ME)CFS is psychological and somehow imagined: "That debate raged for 20
years, and now it's over".

As reported on 3rd November 2006 by United Press International, there are
over 3,000 research papers that have established (ME)CFS as a valid
physiological illness, with evidence of inflammation, reduced blood flow and
impaired cellular function. It was described as a "brutal" disease which
often occurs in conjunction with other diseases such as lupus and Lyme
disease, and its symptoms can be as severe and painful as renal failure,
AIDS or multiple sclerosis.

Importantly, distinctions were drawn to the two different types of (ME)CFS:
one that occurs immediately after an infection and one that develops
gradually over time, and to the fact that the two types seem to differ
genetically.

Many parts of the Toolkit are helpful: the CDC points out (and accepts) that
irritable bowel syndrome, multiple chemical sensitivity, fibromyalgia and
Gulf War Syndrome may be co-morbid conditions; that allergies are seen in
many patients and that many (ME)CFS patients are very sensitive to
medications; that alternative therapies should be considered (and that the
practitioner should remain open-minded about them); the need to be alert to
dizziness in patients and the need to refer them a neurologist and / or a
cardiologist before initiating treatment; that there is considerable
variation in symptom expression and severity; that symptoms are
unpredictable; that the disorder can have a profound impact on daily life,
requiring significant lifestyle changes; that (ME)CFS is an 'invisible
illness' in which patients often do not look sick and that this contributes
to patients being misunderstood and isolated; that a therapy which works for
one patient may be of little benefit for another; that advising patients to
engage in aerobic activity can be detrimental as it can cause a full-scale
relapse that can last for weeks, and that patients with (ME)CFS can lose
their jobs, economic security and home.

However, when it comes to treatment, there seems to be confusion, with
Klimas saying at the launch: "Although there's no single treatment-no hoped
for 'magic bullet'-that fixes the illness at its core, there are treatments
that can improve symptoms, increase function and allow CFS patients to
engage in activities of daily living. Current best practices for clinical
care include a combination of symptom management, activity management and
exercise therapies."

This seems at variance with her previous on-the-record views about CBT, for
example:

· "I don't take the British view that CBT is the one thing you can do to
effectively treat (ME)CFS. But it's a tool that helps some patients" (The
Science and Research of CFS: CFIDS Chronicle Special Issue, 2005-2006)

· "The question arises whether a formal CBT or GET program adds anything to
what is available in the ordinary medical setting. A well informed physician
empowers the patient by respecting their experiences, counsels the patients
in coping strategies, and helps them achieve optimal exercise and activity
levels within their limits in a common sense, non-ideological manner"
(ME/CFS: Clinical Working Case Definition, Diagnostic and Treatment
Protocols. Bruce M Carruthers, Nancy G Klimas et al JCFS 2003:11:1:7-115).

How is it that in 2003, Klimas said that a competent physician would give
his patient common sense counselling in coping strategies, but three years
later she now says the same patient should be handed over for psychotherapy?

Is the answer that CBT has been "redefined" in the US also, so in the
absence of any remotely therapeutic intervention, Klimas might well
recommend CBT to help patients with ME/CFS cope with it (whereas in the UK
Wessely et al have used it to deny the very existence of ME/CFS)? Klimas is
also on record as saying at the CDC: "It's critical for patients and their
healthcare providers to know that there is hope and that we can help".

On the matter of management, some of what the Toolkit says is hardly
controversial, namely that the objective of an effective management
programme is threefold: (1) to help patients develop effective coping
strategies (2) to relieve symptoms and (3) to teach patients to manage
activity levels so as to avoid post-exertional malaise on the one hand and
deconditioning on the other.

However, it also states: "The goal of CBT is to change perceptions and
behaviours that can contribute to symptom expression" and "Working with a
CBT therapist, (ME)CFS patients can examine their beliefs and coping
behaviours and modify these as necessary to manage the illness more
effectively".

As in the UK, there seem to be a confusing divergence about the nature of
CBT for those with (ME)CFS.


Changes in the UK?

Are things changing in the UK? On the basis of the Wessely School
psychiatrists' chameleon stances (depending on whether their audience is in
the US or the UK), they may currently see advantages in creating the
illusion that the aim of CBT has always been to help patients cope with
overwhelming illness: if so, are we witnessing the construction of an escape
route made necessary by the realisation that -- in the light of such
substantial and convincing biomedical evidence -- they've been wrong ?

For illustrations of the pliability of Wessely School opinions about the
efficacy of CBT depending on the country in which they were delivered, see
http://www.meactionuk.org.uk/Concerns_re_NICE_Draft.pdf

So why is the Wessely School model of CBT/GET not only unsuitable but
potentially dangerous for those with ME/CFS? The following notes, taken from
Cheney's DVD (a two disc boxed set: for details, send an email to
videos@dfwcfids.org as notified on Co-Cure on 27th October 2006), may
provide some answers.

It should be compulsory viewing for every member of the NICE Guideline
Development Group on "CFS/ME".


Cheney's Seminar

Others have already reported on Cheney's seminar, so what follows is a
simplistic summary and makes no attempt to explain the disrupted metabolic
and biochemical pathways that were demonstrated in detail by Cheney.

Cheney - who has been involved with (ME)CFS since the Lake Tahoe outbreak in
the early 1980s -- began by acknowledging his debt to the work of Peckerman,
who had found that half of the patients studied had low cardiac output as
measured by impedance cardiography. (Peckerman noted that this could be due
to the heart itself, but that it could also be due to problems in the
peripheral blood vessels). This fascinated Cheney, who in 2003 underwent a
successful heart transplant because of dilated cardiomyopathy, as a result
of which he had observed at first hand the spiralling effects on differing
body systems of low cardiac output.


Important Clinical Findings

There is an objective database in key medical literature that includes
evidence (sic) of diastolic dysfunction and heart failure in (ME)CFS. PFO is
found in at least 80% of patients with (ME)CFS.

Oxygen should not be transported into a cell that cannot use it without
effective defences against its by-products (oxygen being the precursor of
free radical formation).

Symptoms are usually manifestations of defence responses and reflect but do
not cause the underlying problem.

Symptom-based treatment alone is therefore flawed at best and dangerous at
worst: to treat symptoms without understanding the underlying disease
process can cause death: the third leading cause of death is treatment by
physicians, which kills 250,000 people per year (the first being heart
disease and the second being cancer) -- most drugs are not aimed at the
primary cause of disease but at symptoms and are therefore dangerous (see
below for Cheney's view about the dangers of giving Prozac to those with
(ME)CFS).


Principles that are important in (ME)CFS

Adaptation to chronic disease is generally coded as a phenotype shift (ie.
one still has the same genes but they are expressing themselves
differently). There is an emerging literature that shows phenotypic
adjustments are defining illnesses by which genes are changing. Why is this
going on? Is the gene shift causing the disease, or is it defending the
host? It is mostly the latter, and this is very important, so we need to
treat the underlying cause as, once changed, the patient can never return to
his/her original phenotype. If genes have changed (and there is evidence
that they have), a patient can be genotypically shifted as well and
phenotypically shifted, and this is a big issue that stands in the way of a
quick fix solution: if chronic disease can never be fixed, how can people be
helped to feel better? The answer lies in suppressing the defence mechanism,
but this is not very good, because if you fix the defence mechanism, at some
deep level you can worsen symptoms.

A key principle is not to use too much oxygen (because it kills). (ME)CFS
protects against almost certain death by adapting to a low energy state.

Patients withdraw from activity: they have a dynamic dysfunction that is
more than simply an adaptation - there is something about the disease that
is making them this way.


The (ME)CFS Case Definition

Cheney outlined the case definition, saying that the classic triad is: no
energy, brain dysfunction, and pain. If a patient does not have pain, s/he
does not meet the (ME)CFS case definition: (ME)CFS is very much a painful
disorder.

Cognitive dysfunction occurs in 99% of cases (processing speed; short-term
memory loss; sensory and information overload; information searching;
multi-tasking problems; spatial disorganisation). "Fatigue features in so
many other disorders, but what makes (ME)CFS special is the brain component".

Mood disturbances occur: depression is rarely severe and is reactive;
anxiety disorders abound, as does mood lability, but 40% do not have any
mood disorder, so (ME)CFS is not a psychiatric disease.


The evolution of (ME)CFS

There are four phases:

1. the onset, or trigger phase

2. the triad phase

3. the dynamic dysfunction phase (although the fatigue and pain and brain
dysfunction are a little better, patients in this phase can do less than
when they were more sick)

4. DNA phenotype adaptation phase (there is a phenotypic adaptation that
locks this in at gene level).


Key scientific articles

Phase 1: (immune activation: fever, swollen glands, sore throat, malaise:
general indications of immune activation)

· Suhadolnick et al (Temple University, USA)

· Komaroff et al (Harvard, USA)

· Klimas et al (Miami, USA)


Phase 2: (the centre of gravity of this illness: fatigue, brain problems and
pain; xenobiotic toxicity coming from the gut and the environment)

· McGregor et al (Newcastle University, Australia)

· Pimental (UCLA, USA)


Phase 3: (the brain and heart component)

· Demitrack et al (NIH, USA)

· Moorkens et al (Antwerp, Belgium)

· Schwartz et al (Harvard, USA)

· Peckerman et al (NMJ & D, USA)

· Drexler et al (Hanover, Germany)


Phase 4: (phenotypic and genotypic adapatation & oxidative stress)

· Vernon et al (CDC, USA)

· Kerr et al (London, UK)

· Urowitz et al (Berkeley, USA)

· Pall (WSU, USA)

· Kennedy et al (Cheney's overhead stated "USA", but if he means Kennedy and
Spence, it should be Dundee, Scotland)

Oxidative stress links (ME)CFS to fibromyalgia, multiple chemicaL
sensitivity and Gulf War Syndrome.


Do people recover from (ME)CFS?

Functional recovery is seen: one's ability to do things can improve, but it
can go the other way, or there may be no change over time. In functional
improvement, do patients really get better, or do they just adapt? The
longer things go on, the more difficult it is to see functional recovery.
Komaroff's data from Harvard is that after 10 years of illness, there is
only a 30% chance of any functional recovery.


The Physical Examination

In phase 1: (immune activation), one sees

· Lymphyodynia (seen in 80-90%)

· Crimson crescents bilaterally on soft palate (seen in 80%)

· Sub-normal temperature


In phase 2: one sees

· Evidence of subcortical brain injury

· Vestibular dysfunction (seen in 94%)

· Hyper-reflexia, especially of the knees and ankles (seen in 70%)


In phases 3 and 4: the most interesting are the metabolic disturbances:

· There is shortened breath-holding capacity (seen in 60%)

· There is very poor oxygen transport (seen in 90%): pulse oximetry readings
measuring saturation of haemoglobin show a significant inhibition to
desaturate

· There is finger-print destruction (seen in 50%): cross-hatching occurs,
with degradation of the ridges; punch biopsies found perivascular lymphoid
infiltrates ie. an inflammatory cuffing exactly as seen in lupus, which
signifies a non-specific immune activation issue (so the finger-print
changes could be reflecting much more than just loss of finger-prints and
may represent a vasculopathy)

· There is sub-normal temperature (seen in 80%)

· There is low systolic blood pressure (in 50% of patients it is less than
100)

· There is orthostatic B/P or pulse changes (seen in 70%)

· Hypertension is very rare

These findings portend significant physiological issues, chief of which is
that oxygen is being prevented from getting into the cell, and if there's no
oxygen, there's no energy.


Magnetic Resonance Spectroscopy

· 70% of patients show elevated lactate levels in the ventricular system
(the lactate elevation is not normal and indicates a defect in energy in the
brain: (ME)CFS patients have significantly elevated lactate levels and the
fatigue correlated significantly with the level of lactate)

· 10% have evidence of neuronal destruction and elevated choline peaks,
typically in the perivascular areas.


Magnetic Resonance Imaging

· 78% of patients have punctate lesions which are most consistent with small
strokes and there is evidence to support this (ie. they are not caused by a
virus or by inflammation).


Mixed venous blood gas picture

· PvO2 is 25 (it should be 40)

· PvCO2 is 55 (it should be 45)

This is a differential hypoxia with hypercarbia. There are only two diseases
where this is seen: one is pulmonary hypertension; the other is (ME)CFS.

The arterial side is normal.

Where does the oxygen go? It's being transported somewhere, but not to the
mitochondria. (ME)CFS patients have been shown to have increased pooling of
extra-cellular fluid in the belly, pelvis and legs which might contain this
dissolved oxygen, but it is more likely being consumed by the oxidative
pathway to create superoxide in massive amounts. Superoxide is the
progenitor of all free radicals. The consequences are increased
intra-cellular oxdidative stress.

If you intervene and give Prozac, you up-regulate superoxide, which is why
serotinergic drugs kill neurons.

Intervening with drugs in situations not fully understood breeds chaos and
kills patients.

(ME)CFS as cellular metabolic dysfunction

There are problems at cell level in energy production, and because of this
degraded energy problem, patients suffer a defect in the ability to detoxify
toxins, especially in the portal circulation (giving rise to gut toxicity as
seen in phase 2). Gene alterations (seen in phase 4) generate a massive
disturbance in the development of energy at the cell level. If you lose
energy, you lose glutathione, but the more glutathione you give, the more
you just create oxidised glutathione, which generates loss of citrate,
causing a left shift on oxyhaemoglobin desaturation. Citrate also binds to
magnesium, so over time the patient will develop a severe magnesium
depletion syndrome. When that happens, you've had your last good night's
sleep: when you lose magnesium, you can't sleep any more.

How and why would a low energy state lead to an inability to transfer
oxygen? Cheney concludes that it's part of a bigger picture that uses low
oxygen transport to stablise the system.

In (ME)CFS, these serious issues are a big problem, especially in the brain,
the heart and in muscle. (ME)CFS is a compensatory response to down-regulate
energy production and oxygen transport in order to reduce tissue damage.

Attempts to push beyond energy limits will cause injury.

Prolonged energy deficits can cause semi-permanent DNA phenotype adaptations
and complications can occur, especially within energy-sensitive systems such
as the heart, the brain and the muscles.

The most likely cause (not trigger) of (ME)CFS is a disruption in handling
the toxic by-products of oxygen utilisation.

In (ME)CFS, catalase is deficient in the heart, lungs and liver (catalase is
the most protective enzyme in the body against the ravages of superoxide),
and Cheney noted that electromagnetic fields [EMFs] "screw up" superoxide
dismutase (SOD), which is a major anti-oxidant scavenger.


Is there an (ME)CFS-associated cardiomyopathy?

(ME)CFS patients have a high heart rate but a low cardiac output. In (ME)CFS
there is a cardiac dimension that is independent of (but not excluding)
autonomic function or blood volume.

82% of patients have abnormal cardiac impedence.

It's hard to talk about a low cardiac output without talking about the
involvement of the brain and the adrenal glands.

A mismatch between metabolic demand and cardiac output, even very briefly,
will kill.

If the cardiac output goes down, in order not to die, there is a rise in
noradrenergic tone (also involving the adrenal glands) to bring the output
back up. In (ME)CFS, this is a serious problem, because when the adrenals
are exhausted, there will be low cardiac output.

There is no such thing as an (ME)CFS patient who is NOT hypothyroid: this
has nothing to do with thyroid failure, but everything to do with matching
metabolic demand and cardiac output.


Order of sacrifice in cases of declining microcirculation

First is the skin; second is the muscles and joints; third is the liver and
gut (patients can usually only tolerate a few foods); fourth is the brain;
fifth is the heart; sixth is the lung and lastly is the kidney (for a more
detailed discussion of this order of sacrifice, see
http://www.meactionuk.org.uk/The_MRC_Profits_before_Patients.htm ).

Among the major causes of death in (ME)CFS is heart failure: Jason et al
(August 2006) found that 20% die of heart failure.

There are two types of heart failure: systolic (which is a failure to eject)
and diastolic (which is not a failure to eject, but a failure to fill
properly).

There are two types of diastolic heart failure: primary relaxation deficit
giving rise to decreased cellular energy as seen in (ME)CFS and secondary
relaxation deficit as seen in hypertension, diabetes and the elderly over
age 75.

Primary relaxation deficit is a disorder that seems to have gone right under
the radar of most cardiologists (who focus on the secondary relaxation
deficit).

Diastolic heart failure was first described in the 1980s but there was no
significant literature until the 1990s, and no significant way to measure it
until 2001.

In July 2006 The New England Journal of Medicine carried a significant paper
on more than 4,500 patients studied with diastolic heart failure (which is
higher than those with systolic heart failure). This is unexplained, but is
accelerating (is it in fact an explosion of (ME)CFS?).

One is just as likely to die of diastolic heart failure as from systolic
heart failure.

Doppler mitral in-flow velocities show diastolic dysfunction.

Concluding the first disc, Cheney stated there is (quote) "a whopping
percentage of (ME)CFS people with diastolic dysfunction".

In the second DVD, Cheney expounds on PFO in relation to (ME)CFS.

He says that at least half of patients exhibit atrial cavitation, and that
when these patients stood up, in 80% the filling volume collapsed. He tested
this with magnesium and the results were significant: magnesium restored 12%
of energy in one minute. Magnesium affects the intracellular energetics,
proving that patients have a "tremendous" energy problem that is very
sensitive to magnesium. (The reason magnesium is so important is that
without it, ATP cannot be converted to ADP for the production of energy).

(ME)CFS patients "squeeze the hell" out of their left ventricle, resulting
in a "whopping" 70% increase in left ventricular wall motion thickness. The
reason why patients are squeezing so hard is because they do not have enough
energy to fill the chambers of the heart properly so they are trying to
compensate by squeezing a lot harder (ie. the way patients are compensating
for this loss of cardiac output is by squeezing the left ventricle much
harder).

There are significant consequences of this. One consequence is that (ME)CFS
patients become asynchronised (ie the heart can be filling and ejecting at
the same time).

If out of synchrony, the ventricle cannot cope, so cardiac output is
severely degraded.

A second consequence is that patients develop a strain pattern, which is an
indication of ischaemia. Cheney has seen ischaemic changes in the inner
ventricular wall because of the increased squeezing.

PFO is a hole in the heart producing a right to left shunt of unoxygenated
blood full of carbon dioxide as well as products of liver metabolism - the
liver is literally draining into the right heart and that blood is being
shot straight to the brain (this was demonstrated on the DVD by means of
Trans Cranial Doppler bubbles).

The assumed cause of the PFO is the same as in the foetus - to protect the
body from oxygen: in (ME)CFS patients are shifted left to right, not because
they have an immature way (as in the foetus) of handling oxygen, but because
they have a defective way of handling oxygen.

In (ME)CFS patients, there is increased left ventricular strain, with
increased R-L shunting, and cardiac ischaemia develops, and because of too
much squeezing, the PFO (that closed at birth) is opened up, resulting in
significant oxygen toxicity, with ischaemic reperfusion-type changes.

The diastolic dysfunction that causes dilatation of the left atrium can
actually break the seal of the sealed Foramen Ovale (ie. the increased
pressure blows through a previously sealed PFO).

It is increasingly clear that in (ME)CFS, a diminished threshold for oxygen
toxicity exists, and that each patient will have a unique threshold.

These findings have a significant negative effect on Emergency Room (A&E)
and operating theatre uses of oxygen during surgery - a patient with (ME)CFS
could be given too much oxygen and be killed on the operating table.

Hyperbaric oxygen could have a very negative impact on some (ME)CFS
patients.

The ultimate consequence of this is low cardiac output, arising from a
problem of energy production.

The complications of PFO include:

· Cerebral aneurysm

· Multiple mini-strokes

· Cerebral hypoperfusion produces pressure headaches; migraine, cognitive
impairment and a lower seizure threshold

· Venous hypoxia complications are fundamentally linked to intracellular
acidosis which depletes electron buffers

· Depleted acid buffers leads to increased sensitivity to diet, drugs and
the environment.


PFOs cause significant instability.

There is a difference between diastolic dysfunction and diastolic failure:
in diastolic dysfunction there is a filling problem but the body is
compensating for it and achieving enough cardiac output to match metabolic
demand. Diastolic failure begins when the body can no longer compensate and
there is a reduction in cardiac output. Cheney repeated that this is seen in
80% of (ME)CFS patients.

If patients draw down their lifestyle to live within the means of the
reduced cardiac output, then progression into congestive cardiac failure
(CCF) is slowed down, but if things continue to progress, a point will be
reached where there is no adequate cardiac output, and dyspnoea will
develop, with ankle oedema and other signs of congestive cardiac failure.

The message from Cheney is clear: in order to stay relatively stable, it is
essential for the (ME)CFS patient not to create metabolic demand that the
low cardiac output cannot match.


The message for NICE

The message for NICE is that (ME)CFS patients instinctively know that they
simply cannot cope with aerobic exercise (as in graded exercise therapy),
and that their instincts have been proved correct by Cheney's
ground-breaking research.

Many (ME)CFS patients are formerly high achievers who do not need to be
patronised by psychiatrists with their behavioural management regimes about
how not to exceed their own limits: they know their limits and live within
them daily in order to survive.

As has been pointed out to NICE, what such patients need is not
multi-million pounds to be given to psychiatrists to try to prove that
(ME)CFS patients will recover with aerobic exercise: what is needed is
biomedical research to find the cause, without which there can be no hope of
effective treatment or a cure.

In the meantime, as NICE has also been informed, patients urgently need
practical support services, including help with personal care, shopping,
housework, cooking, adaptations in the home (such as a chairlift) ie. basic
support for the very ill.

But NICE has already indicated that it is not listening.

[Return to top]

------------------------------

Date:    Tue, 14 Nov 2006 01:00:51 +0100
From:    Jan van Roijen <j.van.roijen@CHELLO.NL>
Subject: res: CORvalen -positive results ME/CFS & FMS

~~~~~~~~~~~~~~~~~~~~~~~~~~~~


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http://www.bizjournals.com/twincities/stories/2006/11/13/daily2.html


Study:

Bioenergy sugar product useful for chronic fatigue syndrome

Minneapolis/St. Paul Business Journal - 12:13 PM CST

Mondayby Steve LeBeauStaff Writer



A study published Monday in the Journal of Alternative and
Complementary Medicine shows positive results for patients
with chronic fatigue syndrome and fibromyalgia who are treated
with CORvalen, a product produced by Bioenergy Life Science
Inc.

The study, conducted by Jacob Teitelbaum, medical director of
the Fibromyalgia and Fatigue Centers Inc., found that two-thirds
of patients reported a average of 45 percent improvement in
energy and a 30 percent improvement of quality of life in the first
12 days following the treatment.


Patients with fibromyalgia, a syndrome characterized by fatigue
and muscle pain, reported less muscle pain and stiffness.

The study focused on the effects of certain specialized sugars
on cellular metabolism. CORvalen contains D-ribose, a type of
sugar produced by the body that promotes the synthesis of
compounds that improve the production of energy at the cellular
level, said the company in a statement.

Bioenergy Life Science Inc., a subsidiary of privately-owned
Minneapolis-based Bioenergy Inc., currently markets CORvalen
to heart patients who need more energy.

slebeau@bizjournals.com | (612) 288-2108

``````````````````

http://biz.yahoo.com/prnews/061113/cgm023.html?.v=74


Press Release Source: Bioenergy Life Science, Inc.


Unique Sugar Improves Energy, Pain and Quality
of Life in Fibromyalgia and Chronic Fatigue Patients!
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~

Monday November 13, 9:30 am ET

New Study on D-ribose Published in Journal of Alternative and
Complementary Medicine


MINNEAPOLIS, Nov. 13 /PRNewswire/

Following the recent announcement by the Centers for Disease
Control and Prevention that Chronic Fatigue Syndrome (CFS) is
a major public health concern, the Journal of Alternative and
Complementary Medicine (12:9, 2006, 35-40) published a study
unveiling a new and promising treatment for CFS and
fibromyalgia (FMS).


The research conducted by Jacob Teitelbaum, MD, Medical
Director of the Fibromyalgia and Fatigue Centers, Inc., and
author of two books on the topic, found a full two-thirds of his
patients reported improvement of their symptoms in the first 12
days following a course of CORvalen® treatment. The average
improvement in energy was 45%, and quality of life improved an
average of 30%. Patients reported less muscle soreness and
stiffness, better ability to overcome fatigue, as well as simply
feeling better.

CORvalen®, developed by Bioenergy Life Science, contains
D-ribose, a unique sugar made by the body to synthesize many
important compounds, including DNA, RNA, and most
importantly, Adenosine Triphosphate (ATP), the 'energy
currency' of the cells. According to some experts, FMS and CFS
patients suffer from cellular energy depletion. CORvalen®
D-ribose provides metabolic support to accelerate cellular
energy recovery and normal cellular functioning.

According to Teitelbaum, principal researcher in the open label
feasibility study, the findings of the study are significant. "The
results are outstanding for a single entity product," he says.
"More specifically, the research helped us pinpoint the
energy-building benefit of CORvalen® and how it substantially
reduces the debilitating symptoms of these conditions. I think
this study, and follow-up studies now underway, will make
CORvalen® one of the most important new nutrients evaluated
over the next few years."

Bob Baurys, founder and CEO of the Fibromyalgia and Fatigue
Centers, Inc. says that CORvalen® is a standard therapy for
patients with FMS and CFS. "The Fibromyalgia and Fatigue
Centers around the country were founded on the principle that
these patients need specialized, focused treatments for their
complex medical conditions in order to see improvement," he
explains.

Baurys, himself a fibromyalgia patient, knows first-hand what it's
like to struggle with the disease. "Our six step integrated
treatment program is designed to not only help relieve the
patient's symptoms, but also to address the underlying cause of
those symptoms," he says. "One of those six steps is promoting
cellular energy, and we have had success doing that with
CORvalen®, an all-natural dietary supplement."

The Fibromyalgia and Fatigue Centers are playing an important
role in the research into these mysterious and frequently
debilitating conditions -- reviewing the latest science, examining
complex case studies and sharing information through the FFC
physician network. Centers are now open in Amarillo, TX,
Atlanta, Cleveland, Dallas, Denver, Detroit, Ft. Worth, Houston,
Las Vegas, Los Angeles, Norwalk, CT, Pittsburgh, Philadelphia,
Salt Lake City and Seattle.

Bioenergy, Inc. is a privately held, Minneapolis-based life
sciences company whose core technology lies in the
development and commercialization of products based on the
physiological benefits of D-ribose in health and wellness.
Bioenergy's clear mission is to develop products that increase
the quality of its customers' lives by improving their metabolic
health. Bioenergy Life Science, Inc., its subsidiary, markets
ribose-based products to the functional food and clinical nutrition
markets. Bioenergy Life Science products include Bioenergy
RIBOSETM, a functional ingredient in the active lifestyle market;
as well as CORvalen® and CORvalenM®, clinical nutrition
products giving metabolic support to patients with heart and
muscle disease.

Source: Bioenergy Life Science, Inc.

[Return to top]

------------------------------

Date:    Tue, 14 Nov 2006 03:15:32 +0100
From:    Jan van Roijen <j.van.roijen@CHELLO.NL>
Subject: med: D-ribose -warning

~~~~~~~~~~~~~~~~~~~~~~~~~~~~


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Dear Readers,

I started with D-ribose on Friday 3 November.

I felt some better after some days.

Before I got ME, I practised yoga every day for at least one hour.

On Monday 6 November I decided to do one stomach exercise:

While lying flat with my back on the floor, I lifted my legs with my
abdominal muscles for about 30 - 40 (?) sec.

The next day I was very sick and I still am; I can't handle my
bulletin currently.

The moral of this story: please be careful, when you try D-ribose
or CORvalen.


~jan

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------------------------------

End of CO-CURE Medical & Research Posts Only Digest - 6 Nov 2006 to 13 Nov 2006 (#2006-51)

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