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[Return to digest index] --------------------------------------------- This is a special digest of Co-Cure Research & Medical posts only Problems? Write to mailto:email@example.com --------------------------------------------- ---------------------------------------------------------------------- Date: Wed, 11 Apr 2007 13:56:30 -0400 From: Co-Cure Moderator <ray CO-CURE.ORG> Subject: NOT,MED: Dale Guyer, MD, Discusses the Integrative and Molecular Treatment of Chronic Fatigue Syndrome and Fibromyalgia Dr. Dale Guyer, MD, is a family physician and the Director of The Advanced Medical Center located in Indianapolis, Indiana, where patients are offered a unique blend of traditional and integrative therapies for a number of health-related issues, with a focus on ME-CFS and FM. In the following Q&A Dr. Guyer explains his holistic, evidence-based approach to testing and treatment - which involves use of selected pharmaceutical drugs as an additive to appropriate nutritional support and other measures "to normalize a complex internal bio-chemical milieu." Question: Dr. Guyer, do you see many patients with Chronic Fatigue Syndrome and Fibromyalgia? Dr. Guyer: Yes, I have seen probably several hundred patients who have been given this diagnostic category. Q: How do you go about treating a patient with a weakened immune system? Dr. Guyer: Generally, these individuals require a detailed laboratory analysis to evaluate what components of their immune system are out of balance. For example many individuals have depleted Natural Killer Cell Function and imbalances in the TH1 and the TH2 immune responses. Additionally I like to see a baseline analysis for RNase-L, apoptosis, 2-5A-Synthetase, alpha-interferon, and associated lab work to get a more complete picture. Ultimately, strategies to improve immune system function would include anything that supports overall body health. An essential focus, in my experience, is to identify chronic infections and work to reduce immune burden - either with nutraceutical or anti-infective medication as clinically warranted. I also rely heavily on natural immune modulators such as transfer factor, probiotics,** and immune supporting herbals. Read the complete Q&A at http://www.immunesupport.com/library/showarticle.cfm?id=3725 [Return to top] ------------------------------ Date: Wed, 11 Apr 2007 14:07:12 -0400 From: Fred Springfield <fredspringfield VERIZON.NET> Subject: RES: The chronic fatigue syndrome - an update The chronic fatigue syndrome - an update. Journal: Acta Neurol Scand Suppl. 2007;187:7-14. Author: Wyller VB. Affiliation: Department of Pediatrics, Rikshospitalet-Radiumhospitalet Medical Centre, Oslo, Norway. NLM Citation: PMID: 17419822 Background - In this article, current scientific knowledge on the chronic fatigue syndrome (CFS) is reviewed. The US case definition of CFS (the CDC-definition) is most widespread in research and clinical practice. Estimates of prevalence vary from 0.2% to above 2%. The female-male ratio is approximately 3:1. Clinical Features - Severe fatigue is the dominating complaint; it is worsened from exertions and not substantially relieved by rest. In addition, the patients might have a varying combination of accompanying symptoms. Clinical evaluation should be based upon standardized guidelines, including an assessment of functional impairments. Pathophysiology - The pathophysiology should be interpreted within a biopsychosocial framework. Present knowledge suggests that certain genetic polymorphisms and personality traits might be regarded as predisposing factors, some infections and severe psychosocial stress constitute precipitating factors, whereas disturbances of immunity, skeletal muscle, cognitive abilities, endocrine control and cardiovascular homeostasis are possible perpetuating factors. Treatment - Cognitive behavioural therapy and graded exercise therapy are of proven value in randomized controlled trials. Several pharmaceutical measures have been explored and found to have no beneficial effect. Most patients might expect long-term improvement, but full recovery is rare; however, the prognosis is better among adolescents. [Return to top] ------------------------------ Date: Thu, 12 Apr 2007 12:47:08 -0400 From: Fred Springfield <fredspringfield VERIZON.NET> Subject: RES: Is a full recovery possible after cognitive behavioural therapy for chronic fatigue syndrome? Is a full recovery possible after cognitive behavioural therapy for chronic fatigue syndrome? Journal: Psychother Psychosom. 2007;76(3):171-6. Authors: Knoop H, Bleijenberg G, Gielissen MF, van der Meer JW, White PD. Affiliation: Expert Centre Chronic Fatigue, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands. NLM Citation: PMID: 17426416 Background: Cognitive behavioural therapy (CBT) for chronic fatigue syndrome (CFS) leads to a decrease in symptoms and disabilities. There is controversy about the nature of the change following treatment; some suggest that patients improve by learning to adapt to a chronic condition, others think that recovery is possible. The objective of this study was to find out whether recovery from CFS is possible after CBT. Methods: The outcome of a cohort of 96 patients treated for CFS with CBT was studied. The definition of recovery was based on the absence of the criteria for CFS set up by the Center for Disease Control (CDC), but also took into account the perception of the patients' fatigue and their own health. Data from healthy population norms were used in calculating conservative thresholds for recovery. Results: After treatment, 69% of the patients no longer met the CDC criteria for CFS. The percentage of recovered patients depended on the criteria used for recovery. Using the most comprehensive definition of recovery, 23% of the patients fully recovered. Fewer patients with a co-morbid medical condition recovered. Conclusion: Significant improvement following CBT is probable and a full recovery is possible. Sharing this information with patients can raise the expectations of the treatment, which may enhance outcomes without raising false hopes. Copyright (c) 2007 S. Karger AG, Basel. [Return to top] ------------------------------ Date: Thu, 12 Apr 2007 18:49:03 -0400 From: "Chris Hunter" <chunter ahmf.org> [via Co-Cure Moderators] Subject: Res: Autopsy protocols/tissue bank for ME/CFS Alison Hunter Memorial Foundation "The startling truth is that some of the most conspicuous spokespeople for science horribly misrepresent it: . We have been treated again and again to the stock phrase "there is no evidence that." I have never heard anyone add: "But absence of evidence does not mean evidence of absence" Without that codicil we do not have the whole truth" - Colin Tudge "Physicist heal thyself. Science isn't arrogant , but scientists." (exerpt Australian Financial Review 2/4/2001: reprint from New Statesman) Both 1996 and 1999 CFS Peer Reviews for the Centres for Disease Control CDC recommended the establishment of a CFS patient brain bank for "neuropathological analysis for central nervous system tissues not available by other mechanisms". When referred to this recommendation at the 2004 Madison, Wisconsin IACFS Conference, Dr William Reeves said this would be undertaken "immediately". Dr Susan Vernon expanded on the idea of Tissue Repository Centers in her presentation "The feasability and acceptance of a CFS Research Network". In 2007 while there has been no action to implement the recommendations, research into coping styles, lifetime stressors and fatiguing illnesses appear to have taken priority for the CDC. In 1996 the interest of the University of NSW CFS research team under the direction of Professors Dennis Wakefield, Andrew Lloyd and Ian Hickie was expressed "to receive tissue for research study from patients who die having suffered from chronic fatigue syndrome. In particular our interest would be in studying the brain as it is this organ which we believe to be the critical site in which the unknown disease process is most likely to occur." Yet this team has been amongst those most conspicuous in the field of ME/CFS publications with their promotion of "there is no evidence .." without the codicil. They have encouraged speculative hypotheses with regard to belief systems, and somatisation in those severely affected. Where is the science? Where is accountability? Julie Robotham writes in the Sydney Morning Herald - Health and Science article Thursday 12 April "The development of an autopsy protocol may help unlock some of the mysteries of chronic fatigue syndrome" <http://www.smh.com.au/news/science/victims-give-clues-to-the-answers/20 07/04/11/1175971183260.html> http://www.smh.com.au/news/science/victims-give-clues-to-the-answers/200 7/04/11/1175971183260.html Chris Hunter chunter ahmf.org www.ahmf.org <http://www.ahmf.org/> [Return to top] ------------------------------ Date: Thu, 12 Apr 2007 14:51:51 -0400 From: "Bernice A. Melsky" <bernicemelsky VERIZON.NET> Subject: RES: Treatment of cervical myelopathy in patients with the fibromyalgia syndrome: outcomes and implications Treatment of cervical myelopathy in patients with the fibromyalgia syndrome: outcomes and implications. Eur Spine J. 2007 Apr 11; [Epub ahead of print] Heffez DS, Ross RE, Shade-Zeldow Y, Kostas K, Morrissey M, Elias DA, Shepard A. Chicago Institute of Neurosurgery and Neuroresearch Medical Group, Chicago, USA. PMID: 17426987 Some patients with fibromyalgia also exhibit the neurological signs of cervical myelopathy. We sought to determine if treatment of cervical myelopathy in patients with fibromyalgia improves the symptoms of fibromyalgia and the patients' quality of life. A non-randomized, prospective, case control study comparing the outcome of surgical (n = 40) versus non-surgical (n = 31) treatment of cervical myelopathy in patients with fibromyalgia was conducted. Outcomes were compared using SF-36, screening test for somatization, HADS, MMPI-2 scale 1 (Hypochondriasis), and self reported severity of symptoms 1 year after treatment. There was no significant difference in initial clinical presentation or demographic characteristics between the patients treated by surgical decompression and those treated by non-surgical means. There was a striking and statistically significant improvement in all symptoms attributed to the fibromyalgia syndrome in the surgical patients but not in the non-surgical patients at 1 year following the treatment of cervical myelopathy (P </= 0.018-0.001, Chi-square or Fisher's exact test). At the 1 year follow-up, there was a statistically significant improvement in both physical and mental quality of life as measured by the SF-36 score for the surgical group as compared to the non-surgical group (Repeated Measures ANOVA P < 0.01). There was a statistically significant improvement in the scores from Scale 1 of the MMPI-2 and the screening test for somatization disorder, and the anxiety and depression scores exclusively in the surgical patients (Wilcoxon signed rank, P < 0.001). The surgical treatment of cervical myelopathy due to spinal cord or caudal brainstem compression in patients carrying the diagnosis of fibromyalgia can result in a significant improvement in a wide array of symptoms usually attributed to fibromyalgia with attendant measurable improvements in the quality of life. We recommend detailed neurological and neuroradiological evaluation of patients with fibromyalgia in order to exclude compressive cervical myelopathy, a potentially treatable condition. [Return to top] ------------------------------ Date: Thu, 12 Apr 2007 09:47:22 -0700 From: Steven Du Pre <isaiah40 SONIC.NET> Subject: NOT, MED: Interview with Dr. Peterson, Judy A. Mikovits, Anne Whittmore Re: upcoming Center for Excellence in Nevada Hello, You can view this short interview at the website. The research director & Dr. Peterson have found that there is a percentage of patients who come down with viral-induced cancers with this disease, Myalgic Encephalomyelitis/CFS, due to derangements of the immune system. Since one of the three leading causes of death for Myalgic Encephalomyelitis/CFS is cancer , this is an important finding that has not come to full attention in the American public because of the ignorance of the public agencies involved here in the US . Here's the information on the interview: There is a research center for M.E. /CFS being built on the campus of the University of Nevada, Reno. Here's a link to a interview done with Anne Whittemore, and longtime CFIDS doctor/researcher Dan Peterson. Annette F. Whittemore, Founding Director - Whittemore/Peterson Institute for Neuro-Immune Disease Dr Daniel L. Peterson M.D., Medical Director Judy A. Mikovits, PH.D, Research Director The Center is scheduled for completion 2008-2009. http://www.nevadanewsmakers.com/video/nnmstreamb.asp?showID=396 Steven Du Pre Poetry website: http://www.angelfire.com/poetry/soareagle/index.html "By words the mind is winged." Aristophanes Website for National Alliance for Myalgic Encephalomyelitis: http://www.name-us.org [Return to top] ------------------------------ Date: Fri, 13 Apr 2007 20:35:18 +0900 From:
http://www.cfids-cab.org/rc/Nicolson-1.pdf Some of his articles was posted to the Co-Cure last year I believe but, I can not find them. Hope this helps. Thanx for Ray, one of the Co-Cure moderators, for finding the location of the original article above. Hang in there. Rika Kageyama Tokyo, Japan [CFS+RP since 1979] *CFS: Chronic Fatigue Syndrome *RP: Relapsing Polychondritis [Return to top] ------------------------------ Date: Fri, 13 Apr 2007 13:21:41 -0400 From: "Jill McLaughlin <jillmclaughlin comcast.net> via Co-Cure Moderator" Subject: NOT,MED: Victims give clues to the answers - Sydney Morning Herald - April 12, 2007 http://www.smh.com.au/news/science/victims-give-clues-to-the-answers/2007/04/11/1175971183260.html The Sydney Morning Herald Victims give clues to the answers April 12, 2007 The development of an autopsy protocol may help unlock some of the mysteries of chronic fatigue syndrome, writes Julie Robotham. UNDER the microscope, it could not have been clearer. Sophia Mirza's brain and spinal fluid showed indisputable evidence of inflammation and cell death. The discovery, by the neurologist Abhijit Chaudhuri and a neuropathologist colleague, marked the first time a serious abnormality confined to the central nervous system had been identified at the post-mortem examination of a patient whose principal diagnosis was chronic fatigue syndrome. In turn, that ensured the 32-year-old became the first person in Britain to have the syndrome - also known as myalgic encephalomyelitis - recorded as the cause of her death. In Adelaide last month, Chaudhuri and specialists from all over the world took the first steps towards developing an autopsy protocol that would allow samples to be consistently collected and analysed from the bodies of people who die, like Mirza, after a long battle with the syndrome. These would form the basis of an international tissue bank in an attempt to shed light on what goes wrong in the baffling condition, which often strikes young and previously healthy individuals. It could help "establish the condition as a valid neurological problem", Chaudhuri says, and might lead to treatments. Chaudhuri, a consultant neurologist from the Essex Centre for Neurological Sciences, says the protocol is intended to allow non-specialist pathologists to collect and preserve samples, which could then be examined by a neuropathologist. The move comes amid concern that brain and spinal cord tissues which might shed light on the disorder are being lost because pathologists do not appreciate their significance. In Mirza's case, and in another autopsy on a young British man, "there was no way [their illness] could be explained by a primary psychiatric condition", Chaudhuri says, referring to a widespread assumption that the condition - which typically begins after a viral illness and is estimated to affect up to 140,000 Australians - is related to mental stress. Daniel Peterson, an American physician who specialises in chronic fatigue syndrome, says its name has allowed it to be trivialised. "These are very complex patients to understand," he says. "We've been held back by biases." Peterson, who is establishing a research centre at the University of Nevada, says he is most interested in forms of the condition that arise after recognised infections, which seem to trigger immune disturbances. The specialists' meeting in Adelaide was organised by Christine Hunter, via the Alison Hunter Memorial Foundation, which Hunter formed after the death a decade ago of her teenage daughter, who had chronic fatigue syndrome. As the protocol is formalised, the group will seek endorsement from experts around the world, she says, to accelerate its acceptance by the wider medical community. Elizabeth Salisbury, a senior staff specialist in tissue pathology at Royal North Shore Hospital, says formal guidelines would encourage those conducting autopsies to retain appropriate tissues for later genetic, antibody or biochemical testing. "One of the difficulties with a disease like CFS is [it] is very much an emerging science," says Salisbury, who is not involved in the protocol's development. "We don't necessarily understand all the pathological changes that account for the signs and symptoms." Salisbury says families of patients who die after having chronic fatigue syndrome or other complex, elusive disorders usually support tissue removal. "They really do want the answers," she says. Colin Neathercoat, a director of the advocacy group ME/CFS Australia, says the cost of supporting patients with long-term disability from the syndrome is enormous, and more funding is needed for research into its origins and possible treatments. "We would desperately like to see government engage in this growing problem and recognise its impact on the Australian economy, let alone its impact on sufferers," he says. [Return to top] ------------------------------ Date: Fri, 13 Apr 2007 13:46:42 -0400 From: "Bernice A. Melsky" <bernicemelsky VERIZON.NET> Subject: RES: Accelerated Brain Gray Matter Loss in Fibromyalgia Patients: Premature Aging of the Brain? Accelerated Brain Gray Matter Loss in Fibromyalgia Patients: Premature Aging of the Brain? J Neurosci. 2007 Apr 11;27(15):4004-4007. Kuchinad A, Schweinhardt P, Seminowicz DA, Wood PB, Chizh BA, Bushnell MC. McGill Centre for Research on Pain, Department of Neurology and Neurosurgery, and Department of Anesthesia and Faculty of Dentistry, McGill University, Montreal, Quebec, Canada H3A 2B2, and GlaxoSmithKline, Addenbrooke's Centre for Clinical Investigation, Addenbrooke's Hospital, Cambridge CB2 2GG, United Kingdom. PMID: 17428976 Fibromyalgia is an intractable widespread pain disorder that is most frequently diagnosed in women. It has traditionally been classified as either a musculoskeletal disease or a psychological disorder. Accumulating evidence now suggests that fibromyalgia may be associated with CNS dysfunction. In this study, we investigate anatomical changes in the brain associated with fibromyalgia. Using voxel-based morphometric analysis of magnetic resonance brain images, we examined the brains of 10 female fibromyalgia patients and 10 healthy controls. We found that fibromyalgia patients had significantly less total gray matter volume and showed a 3.3 times greater age-associated decrease in gray matter than healthy controls. The longer the individuals had had fibromyalgia, the greater the gray matter loss, with each year of fibromyalgia being equivalent to 9.5 times the loss in normal aging. In addition, fibromyalgia patients demonstrated significantly less gray matter density than healthy controls in several brain regions, including the cingulate, insular and medial frontal cortices, and parahippocampal gyri. The neuroanatomical changes that we see in fibromyalgia patients contribute additional evidence of CNS involvement in fibromyalgia. In particular, fibromyalgia appears to be associated with an acceleration of age-related changes in the very substance of the brain. Moreover, the regions in which we demonstrate objective changes may be functionally linked to core features of the disorder including affective disturbances and chronic widespread pain. [Return to top] ------------------------------ Date: Sat, 14 Apr 2007 21:18:43 +0200 From: "Dr. Marc-Alexander Fluks" <fluks COMBIDOM.COM> Subject: RES,NOT: Is a Full Recovery Possible after CBT for CFS ? Source: Psychotherapy and Psychosomatics Vol. 76, #3, pp 171-176 Date: April 2007 URL: http://www.karger.com/pps http://content.karger.com/ProdukteDB/produkte.asp?Aktion=ShowAbstract&ArtikelNr=99844&Ausgabe=232878&ProduktNr=223864 Is a Full Recovery Possible after Cognitive Behavioural Therapy for Chronic Fatigue Syndrome? --------------------------------------------------------------------------- Hans Knoop(a), Gijs Bleijenberg(a), Marieke F.M. Gielissen(a) Jos. W.M. van der Meer(b), Peter D. White(c) a Expert Centre Chronic Fatigue and b Department of Internal Medicine, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands; c Department of Psychological Medicine, Barts and the London Queen Mary School of Medicine and Dentistry, London, UK H. Knoop Expert Centre Chronic Fatigue, Radboud University Nijmegen Medical Centre POB 9011 NL-6525 EC Nijmegen (The Netherlands) Tel. +31 243610030, Fax +31 243610041, E-Mail j.knoop nkcv.umcn.nl Abstract Background Cognitive behavioural therapy (CBT) for chronic fatigue syndrome (CFS) leads to a decrease in symptoms and disabilities. There is controversy about the nature of the change following treatment; some suggest that patients improve by learning to adapt to a chronic condition, others think that recovery is possible. The objective of this study was to find out whether recovery from CFS is possible after CBT. Methods The outcome of a cohort of 96 patients treated for CFS with CBT was studied. The definition of recovery was based on the absence of the criteria for CFS set up by the Center for Disease Control (CDC), but also took into account the perception of the patients' fatigue and their own health. Data from healthy population norms were used in calculating conservative thresholds for recovery. Results After treatment, 69% of the patients no longer met the CDC criteria for CFS. The percentage of recovered patients depended on the criteria used for recovery. Using the most comprehensive definition of recovery, 23% of the patients fully recovered. Fewer patients with a co-morbid medical condition recovered. Conclusion Significant improvement following CBT is probable and a full recovery is possible. Sharing this information with patients can raise the expectations of the treatment, which may enhance outcomes without raising false hopes. Key Words Chronic fatigue syndrome, recovery Cognitive behavioural therapy, outcome Introduction Between 50 and 70% of the patients show a significant reduction of symptoms and disabilities after cognitive behavioural therapy (CBT) for chronic fatigue syndrome (CFS) [1, 2]. The nature of this improvement is uncertain. Some suggest that patients improve by adapting better to a chronic condition, while others think that recovery is possible . This debate shows some similarities to the issue of recovery from mood disorders [4, 5]. The attitude of the therapist towards the treatment goals will affect the expectations and perceptions of the patient. If learning to cope with CFS is the jointly agreed maximal goal of treatment, patients will engage with treatment accordingly. If the therapist suggests that recovery is possible, the patient expectations are raised, which in turn may lead to a change in the perception of symptoms as well as disability. This is also the essence of the placebo response. The placebo response of CFS patients to psychological interventions is lower than that related to biomedical interventions and lower than that expected in other medical conditions , suggesting that CFS patients are sceptical of psychological interventions. Since the communication of the aim of a treatment is an intervention that can facilitate change , the controversy about the nature of improvement is clinically important. To find out the tenable goal of therapy-adaptation or recovery - a definition of recovery is needed that can be operationalized and measured. We propose that a definition is used that closely follows the Center for Disease Control (CDC) criteria for CFS . Two key elements of the CDC criteria are that a patient is severely fatigued and disabled. Recovery then implies that the patient's level of fatigue is within the range of healthy controls. We propose operationalizing this criterion as scoring within the range of the mean plus (or minus) 1 standard deviation (SD) of the healthy population. A second aspect of recovery is that a patient will no longer be disabled. This means that patients have no physical disabilities - an often used criterion in CFS - and no disabilities in any other domains of functioning. Again, we propose scoring within the range of the mean plus 1 SD of the healthy population as the criterion for recovery. Although patients who are no longer abnor- mally fatigued or disabled do not meet the CDC criteria for CFS, having a 'normal' level of fatigue and not being disabled is a more satisfactory definition of recovery. For complete recovery the perception of the patient also has to change. The patient has to perceive his fatigue and functioning as both normal and comparable to healthy people. Finally, a comprehensive definition combines changes in fatigue, disability and perception. The objective of this study was to find out whether recovery is possible after CBT. For this, we collected data from a cohort of patients treated with CBT. For comparison we used healthy population norms. By doing this, we assumed that CFS was the only health problem of the patients. However, it is possible that the patient had another medical condition beside CFS, causing disability. Therefore, we measured the confounding effect of co-morbid medical conditions on the outcome. Methods Subjects All consecutive patients with CFS that were treated with CBT at the Radboud University Nijmegen Medical Centre between September 2003 and May 2005 were eligible for the study if they met the following inclusion criteria: 1 CDC criteria for CFS ; 2 severely fatigued and functionally impaired, defined by a cut-off score of 35 or higher on the fatigue severity subscale of the Checklist Individual Strength (CIS-fatigue)  and a weighted score of 700 or higher on the Sickness Impact Profile (SIP) ; 3 completed the pre- and post-treatment assessment. If a medical co-morbidity was present which could not explain the fatigue, it was registered for further analyses. Intervention All patients received CBT for CFS according to a protocol described elsewhere . Assessment The assessment was part of the clinical routine and performed by research assistants not involved in the treatment. Self-Reported Improvement Self-rated improvement was measured after treatment by one question: patients indicated whether they had no symptoms, significantly fewer symptoms, the same complaints or whether the symptoms had become worse . Fatigue The different definitions of recovery are summarized in table 1. The CIS-fatigue indicates the level of experienced fatigue over the past 2-week period and consists of 8 items on a 7-point scale. The score can range between 8 and 56 . A normal group of 53 healthy adults with a mean age of 37.1 (SD 11.5) has a mean score on the CIS-fatigue of 17.3 (SD 10.1). Using this as a reference for the CBT group, there resulted a threshold score of 27, the mean plus 1 SD . Disabilities Physical disabilities were measured with the 'physical functioning' subscale of the Medical Outcomes Survey Short Form-36 (SF-36) [14, 15]. The scores range from 0 (maximum physical limitations) to 100 (ability to do vigorous activity). Healthy adults without a chronic condition  were used as a norm group, with a mean score of 93.1 (SD 11.7). A patient had to score 80 or higher to be considered as recovered. Social functioning was measured with the subscale 'social functioning' of the SF-36, ranging between 0 (no social activities) and 100 (normal participation in social activities). Using the same criterion and reference group as above resulted in a threshold score for recovery of 75 or higher. The SIP measures functional disability in ambulation, home management, mobility, alertness behaviour, sleep/rest, work limitations, social interactions, recreation and pastimes. The eight subscales were added to provide one weighted score of disability (SIP8 total). The mean SIP8 total score of a healthy group of 78 women is 65.5 (SD 137.8) . Recovery was defined as scoring the same or lower than the mean plus 1 SD of this reference group, i.e. scoring 203 or lower. Combining Fatigue and Disabilities This definition of recovery was operationalized by combining cut-off scores on SF-36 physical functioning and the CIS-fatigue. Perception of Health and Fatigue Health perception was assessed with the scale 'general health perception' of the SF-36. This scale measures the evaluation of the health status by a patient, with scores ranging between 0 and 100. The mean in the reference group was 80 (SD 14.5) resulting in a cut-off score of 65. The perception of fatigue was assessed with the Fatigue Quality List (FQL). The FQL consists of 18 adjectives and patients pick which adjectives best fit their experience of fatigue. Factor analysis showed a 4-factor solution; 3 of the 4 factors have negative connotations of fatigue: 'frustrating', 'exhausting' and 'frightening'. About 97% of the untreated CFS patients scored on 1 or more of the 3 factors [Gielissen et al., unpubl. data]. Recovery was defined as no longer scoring on any of the 3 negative factors. Combining Fatigue, Disabilities and Perception This comprehensive definition of recovery was operationalized by combining the cut-off scores on the CIS-fatigue, the SF-36 scales of physical functioning and social disabilities, the general health perception and the FQL. Results Baseline Data Of the 112 CFS patients with a pre-treatment assessment, 3 (3%) did not start with CBT. There were 13 drop-outs (11% of the patients starting with therapy) during treatment, so 96 patients completed the pre- and posttreatment assessment. The mean age of this group was 37.0 years (SD 11.5). Seventy-three patients were women (76%). The mean duration of the illness was 70.8 months (range 12276 months, SD 52.8). Treatment Results Table 2 shows the scores of the patients before and after treatment. Following treatment, 73 (77%) of the 95 patients, who rated their improvement (data were missing for 1 patient), reported that they had no or significantly fewer symptoms. There was a significant decrease in CIS-fatigue and patients also reported significantly fewer disabilities on the SF-36 subscale physical functioning and the SIP8. In total, 66 patients (69%) no longer met the inclusion criteria for fatigue severity and the level of disabilities (SIP8 6 700). Full Recovery as Outcome The percentage of recovered patients was determined for all criteria and ranged between 23 and 59% (table 3). The Effect of Medical Co-Morbidity Twenty-two of the 96 patients (23%) had a medical comorbid condition beside CFS. Fifteen patients had one medical co-morbidity: treated hyperthyroidism, gonadal dysgenesis with normal karyotype, menorrhagia, controlled diabetes mellitus, quiescent ulcerative colitis, ne- phrotic syndrome, controlled asthma, allergy (2), recurrent sinusitis, epilepsy, migraine, periodic leg movement disorder, multiple traumas, intramedullary haemangioma on medication. Seven patients had two co-morbidities: treated hyperthyroidism and epilepsy, controlled diabetes mellitus and Forestier's disease, controlled asthma and chronic low back pain (2), allergy and treated sleep apnoea, single transient ischaemic attack and cervical arthrosis, chronic headache and treated high blood pressure. After CBT, patients with medical co-morbidity had a mean CIS-fatigue score of 35.8 (SD 13.7) compared to a mean CIS-fatigue score of 28.6 (SD 14.0) for the group without (t=2.15, d.f. 94, p=0.034). The group with medical co-morbidity also had more SIP disabilities following CBT, compared to the group without co-morbidity (t=2.22, d.f. 94, p=0.029). The SIP8 total mean scores were 934 (SD 563) and 607 (SD 739), respectively. The SF-36 physical functioning following treatment was lower in the group with co-morbidity [mean of 66 (SD 27.9) and 80 (SD 20.4), respectively; t=2.46, d.f. 94, p=0.016]. Fewer patients with medical co-morbidity recovered (table 4). For social disability, the perception of fatigue, and the combination of all criteria for recovery, the difference in the proportions of recovered patients failed to reach statistical significance. Discussion More than 70% of the CFS patients reported significantly fewer symptoms following treatment with CBT and roughly 70% no longer met the CDC criteria for CFS. This favourable outcome is consistent with the results of earlier controlled studies [1, 2]. Improvement and not meeting research criteria for an illness are different from recovering [18, 19]. To examine if recovery was possible we used different definitions of recovery that encompassed three elements: no longer being severely fatigued, being able to resume all activities, and a perception of health and fatigue that is similar to the perception of healthy persons. Depending on the definition used, up to 59% of the patients recovered. Even if we used the most conservative definition of recovery, 23% fully recovered. We therefore conclude that recovery from CFS following CBT is possible. In the absence of a control treatment group, it is difficult to attribute this effect to treatment with certainty. A comparison with the natural course of CFS provides some useful information. In a review  that used less stringent criteria for recovery, the median recovery rate without treatment was 5% of the patients meeting operational criteria for CFS. As expected, the recovery rates following CBT found in this study were substantially higher. Our study was only concerned with the short-term effects of treatment. The only controlled study investigating the long-term efficacy of CBT for CFS showed lasting benefits 5 years after treatment . Some may argue that it is not possible to recover from CFS and that our recovered patients were misdiagnosed. We found no evidence to support this, with all patients meeting CDC criteria for CFS. Ninety-one of our 96 patients complained of post-exertional malaise, which some suggest is the main characteristic feature of CFS . The criteria for recovery were based on healthy norms. Patients had to score within the range of the mean plus or minus 1 SD. The norm groups were selected for their good health. Assuming a normal distribution, this means that 15% of the healthy subjects (scoring between 1 and 2 SD beyond the mean) had a score that would be considered as deviant from the norm in the present study. One could say that a patient meeting these criteria not only recovered from CFS, but is also more healthy than a sub- stantial part of the healthy general public. Thus, the effect of CBT may be underestimated. In determining the threshold scores for recovery we assumed a normal distribution of scores. However, in the healthy population the SIP and SF-36 scores were not normally distributed. Therefore one could argue that recovery according to the SIP8 has to be defined as scoring the same or lower than the 85th percentile of the healthy reference group. In that case, the recovery rate using the definition of having no disabilities in all domains (i.e. scoring the same or lower than the 85th percentile on the SIP8) would decrease from 26 to 20%. As we do not know the exact distribution of the SF-36 scores, we cannot control for the effects of violation of the assumption of normality. Patients with medical co-morbidities had significantly higher levels of disabilities after treatment. This implies that less stringent criteria for recovery should be used that incorporate the effect of the co-morbidity. Using healthy adults as a reference group will lead to an underestimation of the effect of CBT in those with medical co-morbid conditions. The fact that fatigue, disability and health can return to a 'normal' level following treatment is a promising finding. Keeping in mind that most patients suffered several years of ill health, it is remarkable that such a change in perception can take place. These results suggest that recovery after CBT may be possible when it is applied to other related disorders for which CBT has been found to be helpful, such as fibromyalgia . The first clinical implication of the present study is that a therapist delivering CBT can tell the patient that substantial improvement is likely to occur and that full recovery is possible. By communicating this, the therapist can counterbalance factors that lower the expectations of the patient. Examples of such factors are a negative attitude of certain patient advocacy groups towards behavioural interventions or an oversolicitous attitude of significant others in response to CFS . There is empirical evidence that lower expectations of patients have a negative influence on therapy outcome . The second clinical implication of the present study is that recovery is a construction. The percentage of recovered patients differed depending on the definition of recovery used. It is possible that a patient has another concept of recovery than the therapist. It is important that they jointly (re)formulate a definition which forms the objective of the treatment. Tables Table 1. Operationalization of the different definitions of recovery -------------------------------------------------------------------------------------------- Definition of recovery Measure Criterion used Cut-off -------------------------------------------------------------------------------------------- Level of fatigue comparable CIS-fatigue Mean + 1 SD =<27 to healthy people No physical disability SF-36 physical Mean - 1 SD >=80 No social disability SF-36 social Mean - 1 SD >=75 No disabilities in all domains SIP8 total Mean + 1 SD =<203 Normal fatigue and no physical CIS-fatigue, SF-36 physical Mean + 1 SD, =<27, >=80 disability mean - 1 SD Normal health perception SF-36 general health Mean - 1 SD >=65 No negative perception of fatigue FQL Factor score negative = 0 Combining criteria of Fatigue CIS-fatigue Mean + 1 SD =<27 Physical and social disabilities SF-36 physical and social Mean - 1 SD >=80, >=75 Perception of health SF-36 general health Mean - 1 SD >=65 Perception of fatigue FQL Factor score negative = 0 -------------------------------------------------------------------------------------------- Mean = Mean of healthy norm group. Table 2. Pre- and post-treatment scores of CIS-fatigue, SF-36 physical and SIP8 total (n=96) -------------------------------------------------------------------------------------------- Pre-treatment Post-treatment Treatment 95% CI t d.f. p value mean mean effect value -------------------------------------------------------------------------------------------- Self-rated 77 improvement, % CIS-fatigue 50.0 p/m 5.2 30.3 p/m 14.0 -19.7 -16.8 to -22.6 -13.6 95 <0.001 SF-36 physical 51.8 p/m 19.1 76.3 p/m 23.0 24.5 19.1 to 29.8 9.1 94 <0.001 SIP8 total 1,448 p/m 510 682 p/m 619 -766 -631 to -900 -11.3 95 <0.001 -------------------------------------------------------------------------------------------- t values assessed by pairwise t test. Table 3. Percentage of patients (n = 96) who meet the definitions of recovery following CBT -------------------------------------------------------------------------------------------- Definition of recovery Criterion reached, % -------------------------------------------------------------------------------------------- Level of fatigue comparable to healthy people 48 No physical disability 59 No social disability 55 No disabilities in all domains 26 Normal level of fatigue and no physical disability 44 Normal health perception 54 No negative perception of fatigue 37 Combining criteria of fatigue, disabilities and 23 perception of health and fatigue -------------------------------------------------------------------------------------------- Table 4. Percentage of recovered patients following CBT with (n=22) and without (n=74) medical co-morbidity -------------------------------------------------------------------------------------------- Definition of recovery No co-morbidity Co-morbidity Z value p value % % -------------------------------------------------------------------------------------------- Level of fatigue comparable to 55 23 -2.68 0.007 healthy people No physical disability 65 41 -2.00 0.046 No social disability 59 50 -0.56 0.578 No disabilities in all domains 31 9 -2.05 0.040 Normal level of fatigue and no 50 23 -2.25 0.024 physical disability Normal health perception 58 41 -1.41 0.157 No negative perception of fatigue 41 23 -1.52 0.129 Combining criteria of fatigue, 29 12 -1.17 0.241 disabilities and perception of health and fatigue -------------------------------------------------------------------------------------------- Z values determined by the Mann-Whitney U test. References 1 Whiting P, Bagnall AM, Sowden AJ, Cornell JE, Mulrow CD, Ramirez G: Interventions for the treatment and management of chronic fatigue syndrome: a systematic review. J Am Med Assoc 2001;286:1360-1368. 2 Stulemeijer M, de Jong LWAM, Fiselier TJW, Hoogveld SWB, Bleijenberg G: Cognitive behaviour therapy for adolescents with chronic fatigue syndrome: randomised controlled trial. Br Med J 2005;330:7481-7486. 3 Prins JB, Bleijenberg G, de Boo TM, van der Meer JWM: Cognitive behaviour therapy for chronic fatigue syndrome: correspondence, authors reply. Lancet 2001;358:240-241. 4 Fava GA: The concept of recovery in affective disorders. Psychother Psychosom 1996; 65:2-13. 5 Andrews G: Should depression be managed as a chronic disease? Br Med J 2001;322:419-421. 6 Cho HJ, Hotopf M, Wessely S: The placebo response in the treatment of chronic fatigue syndrome: a systematic review and metaanalysis. Psychosom Med 2005;67:301-313. 7 Di Blasi Z, Harkness E, Ernst E, Georgiou A, Kleijne J: Influence of context effects on health outcomes: a systematic review. Lancet 2001; 357:757-762. 8 Fukuda K, Straus SE, Hickie I, Sharpe MC, Dobbins JG, Komaroff A: The chronic fatigue syndrome: a comprehensive approach to its definition and study. International Chronic Fatigue Syndrome Study Group. Ann Intern Med 1994;121:953-959. 9 Vercoulen JHMM, Swanink CMA, Fennis JFM, Galama, JMD, van der Meer JWM, Bleijenberg G: Dimensional assessment of chronic fatigue syndrome. J Psychosom Res 1994;38:383-392. 10 Van der Werf SP, De Vree B, van der Meer JWM, Bleijenberg G: Natural course and predicting self-reported improvement in patients with a relatively short illness duration. J Psychosom Res 2003;53:749-753. 11 Bleijenberg G, Prins J, Bazelmans E: Cognitive behavioral therapies; in Jason LA, Fennell PA, Taylor RR (eds): Handbook of Chronic Fatigue Syndrome. New York, Wiley & Sons, 2003, pp 493-526. 12 Prins JB, Bleijenberg G, Bazelmans E, Elving L, de Boo TM, Severens JL, van der Wilt GJ, Spinhoven P, van der Meer JWM: Cognitive behaviour therapy for chronic fatigue syndrome: a multicentre randomised controlled trial. Lancet 2001;357:841-847. 13 Vercoulen JHMM, Alberts M, Bleijenberg G: De Checklist Individual Strength (CIS) (The Checklist Individual Strength). Gedragstherapie (Behavioural Therapy) 1999;32: 642-649. 14 Stewart A, Hays R, Ware J: The MOS short form general health survey: reliability and validity in a patient population. Med Care 1988;26:724- 732. 15 Ware JE Jr, Sherbourne CD: The MOS 36-item short-form health survey (SF-36). I. Conceptual framework and item selection. Med Care 1992;30:473-483. 16 Aaronson NK, Muller M, Cohen PD, Essink-Bot ML, Fekkes M, Sanderman R, Sprangers MA, te Velde A, Verrips E: Translation, validation, and norming of the Dutch language version of the SF-36 Health Survey in community and chronic disease population. J Clin Epidemiol 1998;51:1055-1068. 17 Servaes P, Verhagen C, Bleijenberg G: Determinants of chronic fatigue in disease-free breast cancer patients, a cross-sectional study. Ann Oncol 2002;13:589-598. 18 Pasquali R: The biological balance between psychological well-being and distress: a clinician's point of view. Psychother Psychosom 2006;75:69-71. 19 Ryff CD, Dienberg Love G, Urry HL, Muller D, Rosenkranz MA, Friedman EM, Davidson RJ, Singer B: Psychological well-being and ill-being: do they have distinct or mirrored biological correlates? Psychother Psychosom 2006;75:85-95. 20 Cairns R, Hotoph M: A systematic review describing the prognosis of chronic fatigue syndrome. Occup Med C 2005;55:20-31. 21 Deale A, Husain K, Chalder T, Wessely S: Long-term outcome of cognitive behaviour therapy versus relaxation therapy for chronic fatigue syndrome: a 5-year follow-up study. Am J Psychiatry 2001;158:2038-2042 22 White PD, Thomas JM, Amess J, Grover SA, Kangro HO, Clare AW: The existence of a fatigue syndrome after glandular fever. Psychol Med 1995;25:907-916. 23 van Houdenhove B, Egle UT: Fibromyalgia: a stress disorder? Psychother Psychosom 2004;73:267-275. 24 Prins JB, Bos E, Huibers MJ, Servaes P, van der Werf SP, van der Meer JW, Bleijenberg G: Social support and the persistence of complaints in chronic fatigue syndrome. Psychother Psychosom 2004;73:174-182. 25 Bentall RP, Powell P, Nye FJ, Edwards RH: Predictors of response to treatment for chronic fatigue syndrome. Br J Psychiatry 2002;181:248-252. -------- (c) 2007 S. Karger AG, Basel [Return to top] ------------------------------ Date: Sun, 15 Apr 2007 11:13:48 -0700 From: "ME/CFS <firstname.lastname@example.org> [via Co-Cure Moderator] Subject: RES: Astrocyte hypothesis for ME and/or FM ASTROCYTE HYPOTHESIS FOR ME AND/OR FM In Sweden, we have researchers in neurology, Hansson E. and Rönnbäck L, who study astrocytes. Astrocytes are a part of the neural cells in the brain. Their function is to form the blood brain barrier and to regulate exchange between the extracellular space in the brain and the blood capillaries. They do communicate with each other and with other cells. There is a hypothesis that the astrocytes may be involved behind diseases like ME and FM. I have not seen so much about this hypothesis in international research about ME and I think it would be interesting to also have this hypothesis presented in ME conferences. It is sure a part of the ME puzzle that should not be forgotten about. My suggestion is to invite the authors for the astrocyte hypothesis on ME conferences. It shall indeed be mentioned that the researchers Hansson E. and Rönnbäck L do concentrate on ME or FM, but they look at the Astrocyte function in a more general sense. /Kasper REFERENCES:  Rönnbäck L, Olsson T, Hansson E: Astrocyterna - hjärnans doldisar, delaktiga i neurastena symtom. Läkartidningen (97) 24:2956-61, 2000.  Hansson E., Rönnbäck L.: Glial neuronal signaling in the central nervous system. FASEB J. 17, 341-348, 2003. PMID: 12631574 http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=12631574&query_hl=13&itool=pubmed_docsum  Hansson E., Rönnbäck L. 2004: Altered Neuronal-Glial Signaling in Glutamatergic Transmission as a Unifying Mechanism in Chronic Pain and Mental Fatigue. Neurochem Res. Altered neuronal-glial signaling in glutamatergic transmission as a unifying mechanism in chronic pain and mental fatigue. Neurochem Res. 2004 May;29(5):989-96. Review. PMID: 15139297 http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=15139297&query_hl=7&itool=pubmed_docsum  Persson M, Sandberg M, Hansson E, Ronnback L. Microglial glutamate uptake is coupled to glutathione synthesis and glutamate release. Eur J Neurosci. 2006 Aug;24(4):1063-70. Epub 2006 Aug 21. PMID: 16925588 http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=16925588&query_hl=7&itool=pubmed_docsum  Abbott NJ, Ronnback L, Hansson E. Astrocyte-endothelial interactions at the blood-brain barrier. Nat Rev Neurosci. 2006 Jan;7(1):41-53. Review. PMID: 16371949 http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=16371949&query_hl=9&itool=pubmed_docsum  Andersson AK, Ronnback L, Hansson E. Lactate induces tumour necrosis factor-alpha, interleukin-6 and interleukin-1beta release in microglial- and astroglial-enriched primary cultures. J Neurochem. 2005 Jun;93(5):1327-33. PMID: 15934951 http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=15934951&query_hl=9&itool=pubmed_docsum  Läkartidningen nr 14-15 2007 volym 104, »Trött i hjärnan« osynligt handikapp som kan ge stora problem Lars Rönnbäck, professor, överläkare i neurologi, Sahlgrenska Universitetssjukhuset/Sahlgrenska, Göteborg http://www.lakartidningen.se/engine.php?articleId=6451 (with summary in English at the end) http://www.lakartidningen.se/store/articlepdf/6/6451/LKT0714s1137_1142.pdf [Return to top] ------------------------------ Date: Mon, 16 Apr 2007 16:02:19 -0400 From: "Ian McIlroy <ian box52.plus.com> [via Co-Cure Moderators]" Subject: NOT,RES: International Conference on ME/CFS Biomedical Research - ME Research UK - Edinburgh - 25th of May 2007 As a friend of ME Research UK (and of my own bat!), I just wanted to remind people about the International Conference on ME/CFS Biomedical Research, hosted and organised by ME Research UK, and co-sponsored by the Irish ME Trust, which will take place on Friday 25th May 2007 at the Edinburgh Conference Centre, Heriot-Watt University, Edinburgh, UK. The full day's programme consists of invited keynote lectures and shorter research presentations, and will be of interest to a wide range of professionals, people with ME and observers alike. It should be a very interesting conference with a number of international speakers presenting as well as ME Research UK and other UK researchers giving presentations. On Campus accommodation is booked direct with the Heriot Watt Accommodation office which can be contacted by telephoning 0131 451 3669 or emailing email@example.com. The accommodation website is http://www.eccscotland.com/accommodation/allyear.htm. Further information about the conference can be found at http://www.meresearch.org.uk/newhorizons.html and additional details by contacting the ME Research UK Office, at ME Research UK The Gateway North Methven Street Perth PH1 5PP, UK Telephone/Fax: 01738 451234 E-mail: meruk pkavs.org.uk Ian McIlroy Belfast [Return to top] ------------------------------ Date: Tue, 17 Apr 2007 00:45:53 +0200 From: Jan van Roijen <j.van.roijen CHELLO.NL> Subject: not,med: Multiple Chemical Sensitivity Awareness ~~~~~~~~~~~~~~~~~~~~~~~~~~~~ Send an Email for free membership ~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~ >>>> Help ME Circle <<<< >>>> 17 April 2007 <<<< Editorship : j.van.roijen chello.nl Outgoing mail scanned by Norton AV ~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~ http://www.americanchronicle.com/articles/viewArticle.asp?articleID=24334 Governors and Mayor Proclaim May as Multiple Chemical Sensitivity Awareness and Education Month ~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~ Lourdes Salvador April 16, 2007 Governor Bill Ritter of Colorado, Governor Ted Strickland of Ohio, Mayor Josephus Eggelletion of Broward County Florida, Governor Jim Gibbons of Nevada, and Governor Christine Gregoire of Washington are among the first governors and mayors to proclaim the month of May 2007 as Multiple Chemical Sensitivity Awareness and Education Month. Multiple Chemical Sensitivities (MCS) is also known as Environmental Illness (EI), Toxic Injury (TI), Toxicant Induced Loss of Tolerance (TILT), and several other names. Originally identified in a 1989 multidisciplinary survey of 89 clinicians and researchers, and modified in 1999, top consensus criteria (Nethercott et al, 1993) for MCS define the condition as: 1. A chronic condition. 2. Symptoms recur reproducibly. 3. Symptoms recur in response to low levels of chemical exposure. 4. Symptoms occur when exposed to multiple unrelated chemicals. 5. Symptoms improve or resolve when trigger chemicals are removed. 6. Multiple organ systems are affected. Products that MCS patients react to include ANY quantity of exposures to pesticides, secondhand smoke, alcohol, fresh paint, scented products and perfumes, candles, fragrances, food preservatives, flavor enhancers, aerosols, tap water, cosmetics, personal care products, new carpets, petroleum products, formaldehyde, outdoor pollutants, newspaper ink, cleaning compounds, printing and office products, and other synthetically derived chemicals. Some also react to natural products that are highly concentrated such as natural orange cleaners due to high volatile organic compound and pesticide concentration. Symptoms can range from minor annoyances to life-threatening reactions. Prevalence The prevalence of MCS, based on self-reported symptoms by sample populations provides an estimate of 16% of the population who experience reactions to everyday chemicals (Gibson, 2005; Meggs et al, 1996). MCS affects more women than men. All education levels, income levels, and nationalities are affected equally. Etiology (Causation) There is no clear consensus as to what causes the symptoms of MCS. One of the first studies on MCS focused on possible long term potentiation in the hippocampus and neural sensitization as a central mechanism (Pall, 2003). Later studies examined the role of the inflammatory process and found that brain inflammation was correlated with symptoms of MCS (Pall, 2003). In 1999, Meggs proposed that MCS is caused by low molecular weight chemicals that bind to chemoreceptors on sensory nerve C-fibers leading to the release of inflammatory mediators (Meggs, 1999). Many observable and empirical, scientific facts can help identify MCS including SPECT scans and chemical encephalopathy, vitamin deficiencies, mineral deficiencies, excess amino acid deficiency, and disturbed lipid and carbohydrate metabolism (Rea et al, 2006; Ziem, 2001; Callendar et al, 1995; Heuser et al, 1994). McKeown-Eyssen et al (2004) studied 203 MCS sufferers and 162 controls and found that blood tests revealed that genetic differences relating to the body's detoxification processes were present more often in those with MCS than those without. Data showed that five genetic polymorphisms have a statistically significant role in determining MCS prevalence ( McKeown-Eyssen et al 2004). Each of these genes encode proteins that metabolize chemicals previously implicated in MCS, notably the organophosphorus pesticides (PON1 and PON2 genes) and the organic solvents (CYP2D, NAT1 and NAT2 genes) ( McKeown-Eyssen et al 2004). People with a ''high'' expression of two specific genes (CYP2D6 and NAT2) were 18 times more likely to have MCS than those without ( McKeown-Eyssen et al 2004). It was concluded that "a genetic predisposition for MCS may involve altered biotransformation of environmental chemicals" ( McKeown-Eyssen et al 2004). Haley found similar, confirmatory results with the PON1 gene in studies of the Gulf War syndrome veterans. A new study by Schnakenberg et al (2007) confirmed the genetic variation previously found by McKeown-Eyssen and Haley. A total of 521 unrelated individuals participated in the study. Genetic variants of four genes were analyzed: NAT2, GSTM1, GSTT1, and GSTP1. The researchers concluded that individuals who are NAT2 slow acetylators and those with homozygously deleted GSTM1 and GSTT1 genes are significantly more likely to develop chemical sensitivity (Schnackenberg et al, 2007). According to the study, the glutathione S-transferases act to inactivate chemicals, so people without these GSTM1 and GSTT1 genes are less able to metabolize environmental chemicals because "glutathione S-transferases play an important role in the detoxification of chemicals" (Schnackenberg et al, 2007). The deletion of another gene, the GSTP1 gene, leaves individuals more susceptible to developing these diseases, as lack of these genes means a loss of protection from oxidative stress (Schnackenberg, et al, 2007). The NO/ONOO- cycle is implicated by Pall as being a plausible etiology for Multiple Chemical Sensitivities (MCS), Fibromyalgia (FM), Chronic Fatigue Syndrome (CFS), Post-Traumatic Stress Disorder (PTSD), and Gulf War Syndrome. Peroxynitrite (ONOO-) is oxidized from nitric oxide. Excess peroxynitrite depletes energy stores, which is perceived to cause extreme fatigue (Pall, ND). Of more interest to those who suffer from MCS is the fact that peroxynitrite breaks down the blood brain barrier and excess levels allow greater access to the brain (Pall, ND). This greatly increases the effects of chemicals on the brain. Essentially a non-MCS person has a barrier that protects the brain from damage from low-level chemical exposure, however a person who suffers from MCS has little or no barrier making the brain subject to increased damage and reactivity with minute exposures most people do not react to. The key effect of nitric oxide (NO) is that it inhibits cytochrome P-450 activity and slows degradation of hydrophobic organic chemicals (Pall, ND). This means that excess nitric oxide slows down the body's natural detoxification processes leaving MCS patients subject to the effects of chemical exposure longer than non-sufferers. Between a reduced blood-brain barrier and increased time to naturally detoxify the body MCS patients are subject to permanent and long-term brain and nervous system damage which includes toxic encephalopathy. "The only etiologic mechanism proposed for each of these is a vicious cycle mechanism involving elevated levels of nitric oxide and its oxidant product, peroxynitrite. This cycle may be initiated by a variety of diverse short-term stressors, including viral and bacterial infections, physical trauma, severe psychological stress, organic solvent exposure, and exposure to three classes of pesticides, organophosphorus / carbamate pesticides, organochlorine pesticides and pyrethroid pesticides). Each of these short-term stressors are known to be able to trigger responses that lead to increases in nitric oxide levels. Indeed, other initiating short-term stressors, including a protozoan infection, carbon monoxide exposure, thimerosal exposure and ciguatoxin exposure are also known or thought to act to increase nitric oxide levels, as well" (Pall, 2006). Regardless of cause, victims of MCS suffer isolation and require the support of family, friends, and medical providers. The month of May is designated to raise awareness of the condition and foster better understanding of its cause and prevention. With reasonable accommodations, victims can experience increased ability to work, attend school, shop, dine, go to church, and socialize. Accommodations are often simple and involve things such as opening windows, increasing ventilation, and substituting safer products that increase the safety of both the patient and others the general population. References Callender, TJ, et al. (1995). Evaluation of chronic neurological sequelae after acute pesticide exposure using SPECT brain scans. Journal Toxicology & Environmental Health. 41:275-284. Caress, S., & Steinemann, A. (2003). A Review of a Two-Phase Population Study of Multiple Chemical Sensitivity. Environmental Medicine. 111, 1490 - 1497. Davidoff, L. (1989). Multiple Chemical Sensitivities (MCS). The Amicus Journal. Winter. Ferrie, H. (October 2003). Multiple Chemical Sensitivity: Government and Medical Science Finally Recognize Crippling Effects of MCS. Vitality, Retrieved May 17, 2006, from http://www.vitalitymagazine.com/node/112 Gibson, P. (2005). Understanding & Accommodating People with Multiple Chemical Sensitivity in Everyday Living. Independent Living Research Utilization. Haley, RW, Billecke, S, & La Du, BN (1999). Association of low PON1 type Q (type A) arylesterase activity with neurologic symptom complexes in Gulf War veterans. Toxicology and Applied Pharmacology 157(3):227-33. Heuser, G, et al. (1994). Neurospect findings in patients exposed to neurotoxic chemicals. Toxicology & Industrial Health. 10:561-571. McKeown-Eyssen, G, Baines, C, Cole, D, Riley, N, Tyndale, R, Marshall, L, & Jazmaji, V (2004). Case-control study of genotypes in multiple chemical sensitivity: CYP2D6, NAT1, NAT2, PON1, PON2 and MTHFR]. International Journal of Epidemiology 33, 1-8. Meggs WJ, Dunn KA, Bloch RM, Goodman PE, Davidoff AL (1996). Prevalence and nature of allergy and chemical sensitivity in the general population. Archives of Environmental Health. Jul-Aug;51(4):275-82. Meggs, WJ (1999). Mechanisms of allergy and chemical sensitivity. Toxicology and Industrial Health. 15:3-4, 331-338. Nethercott J.R., Davidoff L.L., Curbow B., et al. (1993) Multiple Chemical Sensitivities Syndrome: Toward a Working Case Definition. Arch Environ Health, 48:19-26 Pall, M. (ND). Multiple Chemical Sensitivity: The End of Controversy. Washington State University School of Molecular Biosciences, Retrieved May 18, 2006, from: http://molecular.biosciences.wsu.edu/faculty/pall/pall_mcs.htm Pall, M (2006). The NO/ONOO- Cycle as the Cause of Fibromyalgia and Related Illnesses: Etiology, Explanation and Effective Therapy. Washington State University School of Molecular Biosciences. Pall, M (2003). Elevated nitric oxide/peroxynitrite theory of multiple chemical sensitivity: central role of N-methyl-D-aspartate receptors in the sensitivity mechanism. Environmental Health Perspectives. 111:12, 1461-1464. Pall, M. (2001). Multiple Chemical Sensitivity - The End of Controversy. Washington State University, School of Molecular Biosciences, Retrieved May 17, 2006, from http://molecular.biosciences.wsu.edu/faculty/pall/pall_mcs.htm Schnackenberg,E. et al (2007). A cross-sectional study of self-reported chemical-related sensitivity is association with gene variations of drug-metabolizing enzymes. Environmental Health. Ziem, G (2001). Medical Evaluation and Treatment of Patients with Chemical Injury and Sensitivity. National Institute of Environmental Health Sciences. Disclaimer This is for informational purposes and is not intended to replace the examination, diagnosis and treatment of a licensed physician and no such claims are inferred. The author and publisher will not be responsible for misuse of this information and recommend consulting with a doctor qualified to diagnose MCS if it is suspected. About the Author Lourdes Salvador is a writer and social advocate based in Hawaii. She is the president of MCS America and a featured monthly writer for MCS America News at www.mcs-america.org. She is a passionate advocate for the homeless, working with the local governor to open new shelters and provide services to the homeless based on a presentation of her ideas to the governor. That passion soon turned to advocacy and activism for victims of multiple chemical sensitivity. For more information about Lourdes and her advocacy work, please visit: www.mcs-america.org, www.thetruthaboutmcs.blogspot.com, and www.cafepress.com/mcsamerica. Copyrighted © 2007 Lourdes Salvador [Return to top] ------------------------------ Date: Tue, 17 Apr 2007 01:17:02 +0200 From: Jan van Roijen <j.van.roijen CHELLO.NL> Subject: med: Is this the cure for ME? ~~~~~~~~~~~~~~~~~~~~~~~~~~~~ Send an Email for free membership ~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~ >>>> Help ME Circle <<<< >>>> 17 April 2007 <<<< Editorship : j.van.roijen chello.nl Outgoing mail scanned by Norton AV ~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~ Quote from below: *......Some doctors and health workers believe it is the result of social and psychological factors - and best treated with psychotherapy and exercise. Now it is becoming clear these patients have "a disturbance in their body's natural way of dealing with infection," says Malcolm Hooper, Emeritus Professor of Medicinal Chemistry at the University of Sunderland.....* ~jvr ~~~~~~~~ http://www.dailymail.co.uk/pages/live/articles/health/healthmain.html?in_article_id=386443&in_page_id=1774&ICO=HEALTH&ICL=TOPART Daily Mail Is this the cure for ME? ~~~~~~~~~~~~~~~~~ By JEROME BURNE, Daily Mail Last updated at 11:53am on 16th May 2006 A drug used to treat herpes infections has produced a dramatic improvement in patients severely affected by ME, or fatigue syndrome. Sufferers who for years had been unable to leave their homes now report being able to resume normal life. This is a remarkable result for a treatment for this complex and controversial disorder that is thought to affect as many as 240,000 people in Britain and for which there is no cure. The results, reported at a scientific conference earlier this month by Professor Jose Montoya of Stanford University in California, involved 12 patients who had been given the powerful drug valganciclovir, which targets the human herpes virus (HHV-6). Nine of the patients experienced a great improvement. One of Montoya's cases was onetime champion figure skater Donna Flowers, now aged 50 and working as a physiotherapist, who lives in California's Silicon Valley. "Two years ago, I was spending 14 hours a day in bed and my brain was so fogged I couldn't write a letter," she says. "I wasn't functioning at all. I'd been diagnosed with chronic fatigue, but the doctors didn't have anything to offer. I had to employ a full-time nanny just to look after my three-year-old twins." However, she is now back at work, treating young Olympic hopefuls, the nanny has gone and she's just started ballet lessons. 'Soaring energy levels' "When Donna came to see us, her energy levels were around 10 per cent of what she considered normal,' says Montoya. "Today, she is functioning at 90 per cent." One patient who could barely walk around the block is now cycling three hours a day, while another who could not even get down the stairs to breakfast is now up every day at 7am. The professor reported his findings at a conference on the HHV-6 virus, which was held in Barcelona earlier this month. While it's well known that some patients with CFS have signs of various viral infections, this is the first time that treating one of the viruses has been shown to be so effective. "I was amazed by the results," says Montoya, who runs the infectious diseases clinic at Stanford. "Donna was sent to me because high levels of another virus (Epstein Barr) had been detected in her system. "I found high levels of HHV-6 virus as well, so I treated her with valganciclovir to bring down her viral load. "I'd hoped it might help a bit, but I didn't expect the results to be anything like as dramatic. It was pure serendipity." 'Careful monitoring' Valganciclovir is licensed to treat HHV-6 infections of the eye, which can affect transplant or cancer patients with severely weakened immune systems. HHV-6 is not the same as the herpes virus responsible for cold sores. Most commonly, it causes roseola infantum in children, who get a fever and a rash. "I have treated hundreds of immune compromised patients with the drug, so I am very familiar with it," says Montoya. "It can have serious side-effects including anaemia, so you have to monitor patients very carefully. But so far none of the CFS/ ME patients have reacted badly to it." All the experts agree that a lot more research will have to be done before valganciclovir can be widely used as a treatment. "There is a long history of linking CFS/ME with some sort of viral infection," says Charles Shepherd, a medical advisor to the charity Action For ME. "About 75 per cent of cases begin with an infection which the patient never properly recovers from, so it is quite likely infectious agents lurk in the body. While the role of HHV-6 is certainly plausible, we will have to wait for a larger trial that is properly controlled." Montoya agrees: "These were individual cases and it is always possible the results were due to a effect," he says. However, that is unlikely because we saw a worsening of each patient's condition around week three to four of the treatment, probably when infected cells were dying off. After that came the improvement. "That is not a pattern you get with placebos. But we don't know yet why the drug makes such a difference." The possibility that valganci-clovir could eventually provide an effective treatment for some cases of CFS is just part of a wider picture. Over the past year, genetic research has provided a new understanding of the disease that could eventually lead to new therapies. For years, the conventional view has been that there is no known cause, no way to diagnose it and no effective treatment. Some doctors and health workers believe it is the result of social and psychological factors - and best treated with psychotherapy and exercise. Now it is becoming clear these patients have "a disturbance in their body's natural way of dealing with infection," says Malcolm Hooper, Emeritus Professor of Medicinal Chemistry at the University of Sunderland. "Anti-viral drugs such as valganciclovir may be allowing it to re-set itself." Hooper was one of the speakers at a conference in London for ME Awareness Day on Friday. Another speaker was Dr Jonathan Kerr of St George's Medical School in London, who recently published groundbreaking work on the links between genes and CFS/ME. "We've found that the genes in patients' white blood cells - a key part of the immune system - are switched on and off in an abnormal fashion," he says. The hope is that a relatively old drug, called interferon beta, can help to restore the balance. A controlled trial is planned. What researchers such as Kerr find disheartening is that there seems to be little official support for this biological-based research in Britain. The bulk of the funding has gone to the psychological approach. But many hope a parliamentary inquiry looking at the progress of CFS/ME research will find that research involving genes, viruses and the immune system would benefit patients. [Return to top] ------------------------------
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