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:
[Return to digest index] --------------------------------------------- This is a special digest of Co-Cure Research & Medical posts only Problems? Write to mailto:firstname.lastname@example.org --------------------------------------------- ---------------------------------------------------------------------- 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: email@example.com 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. [Return to top] ------------------------------ 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. [Return to top] ------------------------------ 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. [Return to top] ------------------------------ 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. [Return to top] ------------------------------ Date: Tue, 7 Nov 2006 22:19:26 -0500 From: "CF-Alliance <cf_alliance@YAHOO.COM> (via Co-Cure Moderators <firstname.lastname@example.org>)" <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 [Return to top] ------------------------------ 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. email@example.com 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. [Return to top] ------------------------------ 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. [Return to top] ------------------------------ 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. firstname.lastname@example.org. 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. [Return to top] ------------------------------ 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. [Return to top] ------------------------------ 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 , Seung Yeoun Lee , Robert C. Elston , and Taesung Park [1 *] Affiliations:  Department of Statistics, Seoul National University, San 56-1 Shillim-Dong, Kwanak-Gu, Seoul 151-747, Korea  Department of Applied Mathematics, Sejong University, 98 Gunja-Dong Kwangjin-Gu, Seoul 143-747, Korea  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: email@example.com 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. [Return to top] ------------------------------ 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. [Return to top] ------------------------------ 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 firstname.lastname@example.org Sarah Carkhuff Fizell (202) 347-5270 email@example.com 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 firstname.lastname@example.org or call 1-888-524-7378 during the live broadcast. [Return to top] ------------------------------ 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. email@example.com. 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. [Return to top] ------------------------------ 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, firstname.lastname@example.org. 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. [Return to top] ------------------------------ 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 email@example.com 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 ~~~~~~~~~~~~~~~~~~~~~~~~~~~~ Send an Email for free membership ~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~ >>>> Help ME Circle <<<< >>>> 13 November 2006 <<<< Editorship : firstname.lastname@example.org Outgoing mail scanned by Norton AV ~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~ 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. email@example.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 ~~~~~~~~~~~~~~~~~~~~~~~~~~~~ Send an Email for free membership ~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~ >>>> Help ME Circle <<<< >>>> 13 November 2006 <<<< Editorship : firstname.lastname@example.org Outgoing mail scanned by Norton AV ~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~ 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 [Return to top] ------------------------------
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