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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 E-Mail mailto:Co-Cure-HMCfirstname.lastname@example.org to unsubscribe --------------------------------------------- ---------------------------------------------------------------------- Date: Wed, 24 Jan 2007 11:13:38 -0500 From: Fred Springfield <fredspringfield VERIZON.NET> Subject: RES: Mitochondrial dysfunction and molecular pathways of disease Mitochondrial dysfunction and molecular pathways of disease. Journal: Exp Mol Pathol. 2007 Jan 17; [Epub ahead of print] Authors: Pieczenik SR, Neustadt J. NLM Citation: PMID: 17239370 Since the first mitochondrial dysfunction was described in the 1960s, the medicine has advanced in its understanding the role mitochondria play in health, disease, and aging. A wide range of seemingly unrelated disorders, such as schizophrenia, bipolar disease, dementia, Alzheimer's disease, epilepsy, migraine headaches, strokes, neuropathic pain, Parkinson's disease, ataxia, transient ischemic attack, cardiomyopathy, coronary artery disease, chronic fatigue syndrome, fibromyalgia, retinitis pigmentosa, diabetes, hepatitis C, and primary biliary cirrhosis, have underlying pathophysiological mechanisms in common, namely reactive oxygen species (ROS) production, the accumulation of mitochondrial DNA (mtDNA) damage, resulting in mitochondrial dysfunction. Antioxidant therapies hold promise for improving mitochondrial performance. Physicians seeking systematic treatments for their patients might consider testing urinary organic acids to determine how best to treat them. If in the next 50 years advances in mitochondrial treatments match the immense increase in knowledge about mitochondrial function that has occurred in the last 50 years, mitochondrial diseases and dysfunction will largely be a medical triumph. [Return to top] ------------------------------ Date: Wed, 24 Jan 2007 11:22:51 -0500 From: Fred Springfield <fredspringfield VERIZON.NET> Subject: RES: Alexithymia in Chronic Fatigue Syndrome: Associations With Momentary, Recall, and Retrospective Measures of Somatic Complaints and Emotions [Note: Alexithymia is defined as "a disorder characterized by cognitive-emotional deficits including: * problems identifying, describing, and working with one's own feelings, often marked by a lack of understanding of the feelings of others; * confusion of physical sensations often associated with emotions with those emotions; * few dreams or fantasies due to restricted imagination; and * concrete, realistic, logical thinking, often to the exclusion of emotional responses to problems." en.wikipedia.org/wiki/Alexithymia ] ORIGINAL ARTICLES Alexithymia in Chronic Fatigue Syndrome: Associations With Momentary, Recall, and Retrospective Measures of Somatic Complaints and Emotions Journal: Psychosomatic Medicine 69:54-60 (2007) Authors: Fred Friedberg, PhD and Joyce Quick, MS Affiliation: From Stony Brook University, Stony Brook, New York. Address correspondence and reprint requests to Fred Friedberg, PhD, Putnam Hall/South Campus, Stony Brook University, Stony Brook, NY 11794-8790. E-mail: email@example.com Objective: The relationship between alexithymia and real-time momentary symptom assessments has not been reported. This cross-sectional study hypothesized that alexithymia would be a predictor of somatic symptoms using three different types of symptom measurement (momentary, recall, and retrospective) in the medically unexplained illness of chronic fatigue syndrome (CFS). In addition, it was hypothesized that negative affect would be a significant mediator of the relationship between alexithymia and somatic symptoms. Finally, the relation of alexithymia to physical illness attribution (a CFS illness predictor) was explored. Methods: Participants were 111 adults with CFS. Alexithymia was assessed with the Toronto Alexithymia Scale. Momentary ratings of current symptoms and affect were recorded in electronic diaries carried for 3 weeks. Weekly recall of these momentary reports was also recorded. Retrospective measures included 6-month ratings of fatigue and pain, the Fatigue Severity Scale, the Brief Pain Inventory-Short Form, a CFS symptom measure, the Beck Depression Inventory-II, the Beck Anxiety Inventory, and an illness attribution rating. Results: Partial correlations, controlling for age and sex, yielded no significant associations between general or specific forms of alexithymia and momentary ratings of fatigue or pain. On the other hand, a significant association, partially mediated by anxiety scores, was found between a specific form of alexithymia and a retrospective pain measure. Finally, physical illness attribution was not significantly associated with alexithymia. Conclusion: Based on assessments of real-time and retrospectively measured symptoms, these data provided only modest support for the alexithymia construct as a predictor of somatic symptoms in people with CFS. Key Words: alexithymia . chronic fatigue syndrome . ecological momentary assessment Abbreviations: CFS = chronic fatigue syndrome; TAS-20 = Toronto Alexithymia Scale-20-item form; DIF = Difficulty Identifying Feelings; DDF = Difficulty Describing Feelings; EOT = Externally Oriented Thinking; FSS = Fatigue Severity Scale; BPI = Brief Pain Inventory; BDI-II = Beck Depression Inventory-Second edition; BDI corr = BDI corrected for somatic symptoms; BAI = Beck Anxiety Inventory; NA = negative affect. © 2007 American Psychosomatic Society [Return to top] ------------------------------ Date: Thu, 25 Jan 2007 14:51:26 -0500 From: Fred Springfield <fredspringfield VERIZON.NET> Subject: RES: CFS Reports from 2006 HHV-6 & 7 Conference CFS Reports from 2006 HHV-6 & 7 Conference Following are abstracts of selected articles dealing with CFS from a 120-page issue of the Journal of Clinical Virology, titled Papers and Abstracts of the 5th International Conference on HHV-6 & 7, 1-3 May 2006, Barcelona, Spain. The publication was made possible with funding from the HHV-6 Foundation. __________________________ Review of Ampligen® clinical trials in Chronic Fatigue Syndrome Journal: Journal of Clinical Virology, Vol. 37, Supplement I, December 2006, p. S113. Author: W. Mitchell Affiliation: Chronic Fatigue Syndrome Clinical Consortium, Department of Pathology, Vanderbilt University School of Medicine, Nashville, TN, USA; Hemispherx Biopharma, Philadelphia, PA, USA. [E-mail: firstname.lastname@example.org ] Summary at http://www.immunesupport.com/library/print.cfm?ID=7638 __________________________ Use of valganciclovir in patients with elevated antibody titers against Human Herpesvirus-6 (HHV-6) and Epstein-Barr Virus (EBV) who were experiencing central nervous system dysfunction including long-standing fatigue Journal: Journal of Clinical Virology, Vol. 37, Supplement I, December 2006, pp. S33-S38. Authors and affiliations: Authors and affiliations: Andreas M. Kogelnik, Kristin Loomis, Mette Hoegh-Petersen, Fernando Rosso, Courtney Hischier, Jose G. Montoya, Andreas M. Kogelnik, Kristin Loomis, Mette Hoegh-Petersen. Stanford University School of Medicine, Stanford, California, USA (Kogelnik, Rosso, Montoya); HHV-6 Foundation, Santa Barbara, California, USA (Loomis, Hischier); Palo Alto Medical Foundation Research Institute, Palo Alto, California, USA (Hoegh-Peterson, Rosso, Montoya). [Contact J.G. Montoya. E-mail: email@example.com ] Abstract available at http://www.immunesupport.com/library/print.cfm?ID=7639 _________________________ Is Human Herpesvirus-6 a trigger for Chronic Fatigue Syndrome? Journal: Journal of Clinical Virology, Vol. 37, Supplement I, December 2006, pp. S39-S46. Author: Anthony L. Komaroff Affiliation: Division of General Medicine, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA. [E-mail: firstname.lastname@example.org ] Abstract at http://www.immunesupport.com/library/print.cfm?ID=7640 __________________________ Activation of human herpesviruses 6 and 7 in patients with Chronic Fatigue Syndrome Journal: Journal of Clinical Virology, Vol. 37, Supplement I, December 2006, pp. S47-S51. Authors and affiliations: S. Chapenko, A. Krumina, S. Kozireva, Z. Nora, A. Sultanova, L. Viksna, M. Murovska. August Kirchenstein Institute of Microbiology and Virology, Riga Stradins University, Riga, Latvia. Abstract at http://www.immunesupport.com/library/print.cfm?ID=7641 _________________________ Active Human Herpesvirus six (HHV-6) infections in patients with Chronic Fatigue Syndrome (CFS) and relapsing-remitting multiple sclerosis (RRMS) Journal: Journal of Clinical Virology, Vol. 37, Supplement I, December 2006, pg. S116. Authors: K.K. Knox and D.R. Carrigan Affiliation: Institute for Viral Pathogenesis, Milwaukee, Wisconsin, USA. [E-mail: email@example.com ] Abstract at http://www.immunesupport.com/library/print.cfm?ID=7642 __________________________ Coagulation disorders in patients with Chronic Fatigue Syndrome (CFS) and HHV-6 viremia Journal: Journal of Clinical Virology, Vol. 37, Supplement I, December 2006, pg. S117. Author: JH Brewer Affiliation: Plaza Infectious Disease and St. Luke's Hospital, Kansas City, Missouri, USA. [E-mail: firstname.lastname@example.org ] Abstract available at http://www.immunesupport.com/library/print.cfm?ID=7643 [Return to top] ------------------------------ Date: Fri, 26 Jan 2007 16:35:41 +0100 From: "Dr. Marc-Alexander Fluks" <fluks COMBIDOM.COM> Subject: RES,NOT,URL: ME-NET has moved Today, ME-NET has moved. The pages on the old web site, http://www.me-net.dds.nl now forward to the corresponding pages on the new site, http://www.me-net.combidom.com Info on the relocation of files can be found at, http://www.me-net.combidom.com/move.htm [Return to top] ------------------------------ Date: Fri, 26 Jan 2007 10:49:24 -0500 From: Jill McLaughlin <jillmclaughlin COMCAST.NET> Subject: NOT,RES: Search for answer to an enduring problem http://www.theherald.co.uk/features/features/display.var.1145256.0.0.php Search for answer to an enduring problem IN 2002, Anna Hemmings was at the peak of her athletic prowess: world kayaking champion. A few months later, she had broken down completely - utterly, incurably exhausted, unable to paddle even for 10 minutes. "I couldn't go on. I no longer had the energy," says Hemmings. "It was strange . . . I looked normal, yet inside my muscles were aching so badly that sometimes I couldn't even hold my hands up to wash my hair in the shower." Hemmings was diagnosed with chronic fatigue syndrome (CFS): crippling exhaustion which makes even moderate exercise unbearable. The illness, which affects around 20,000 Scots per year, is mysterious and often untreatable. It has a number of possible triggers - viral, stress-related, dietary - which may also indicate an underlying genetic predisposition. But despite countless experiments, the cause of chronic fatigue has remained elusive. Now, in search of an explanation and a cure, scientists are turning their approach on its head by studying elite athletes who can withstand fatigue better than others. Dr Paula Robson-Ansley, of the University of Portsmouth, believes endurance athletes may have a specific type of gene that makes them less likely to suffer fatigue. To test her theory, she travelled to the 2006 Merida TransWales Mountain Bike Race where competitors covered more than 500km over rugged terrain in seven days. Each day, Robson-Ansley took blood samples from 80 athletes who took part, before and after the race. Separately, she took blood samples from 85 people around the UK who have been diagnosed with CFS. She is now carrying out a detailed comparison, at the laboratories of Portsmouth's department of sport and nutrition. "The experiment may help explain why some people develop chronic debilitating fatigue for no apparent reason," she says. Robson-Ansley has a personal interest in the research: her own athletic career was cut short by a bout of chronic fatigue, sometimes described as "unexplained underperformance syndrome" (UPS). She was an Olympic-standard rower, training in preparation for the 1996 games, when her body rebelled. A five-kilometre run made her feel like she had just done a marathon. Forced to retire from competition, she set her sights on a new goal: understanding the biological roots of UPS and chronic fatigue syndrome. Robson-Ansley suspects that endurance athletes may carry a different form of a gene, compared with CFS sufferers, a form which protects the athletes from suffering excessive fatigue, during and following endurance exercise. Her test is focusing on Interleukin-6 (IL-6), a messenger molecule in the body that is released when the body is under stress; for example, during infection or illness or when blood sugar levels get low by sending a "distress signal" to the brain. During prolonged exercise, IL-6 levels in athletes increase dramatically. One study found IL-6 levels increasing 100-fold in runners following a marathon. In another, when runners were injected with IL-6 before a 10km trial run, they ran markedly slower. The molecule seems to be sending a warning message to the brain: "Slow down, conserve energy - the body is fatigued and recovery time is needed." So, Robson-Ansley wondered, could it be that endurance athletes have a different version of the IL-6 gene than sufferers of chronic fatigue syndrome? Certainly different versions of IL-6 are known to exist. Previous studies have found that, during infection, people with one variation of the gene - "C-type" - produced less IL-6 during infection than those with the "G-type" version of the gene. Over the course of the mountain-bike event, blood samples were taken every morning at 6am before the cyclists completed that day's stage of the race. IL-6 levels did not change over the seven-day mountain-bike event. But as the mountain bikers became more tired, the study found marked increases in the levels of the IL-6 receptor - the receiver molecule that helps send the IL-6 message to the brain. This "would heighten the athlete's sensitivity to IL-6 when it is produced", says Robson-Ansley. Therefore, "it may be that chronic fatigue sufferers don't necessarily produce more IL-6 but they are more sensitive to its release," she says. If her theory is correct, it may one day be possible to treat some types of CFS with a drug that can block IL-6 receptors in the brain. The good news is, such a drug already exists: an antibody which binds to the IL-6 receptor in the brain, de-activating it. In tests, when this antibody was injected into exhausted athletes, it eliminated the sensation of fatigue - offering hope that it would work as a therapy. Another, more worrying scenario, is that unscrupulous athletes might take IL-6 blockers to train harder, by staving off pain. Robson-Ansley admits this is a possibility, "but it would probably be dangerous", she says. Drug cheats who took it as a performance-enhancer could risk damage to the immune system. The full results of her study into the IL-6 genes are not expected to be released until the middle of this year, but she is confident that she is winning the race to cure chronic fatigue. "I think we now know that there is a lot more going on in the relationship between the IL-6 receptor and fatigue than previously thought," she says. "But one has to be cautious in prescribing the role genes might play in athletic performance as it is still very early days. The history of sport is littered with countless examples of athletes who succeed against all kinds of odds, including physical ones." 12:45am Thursday 25th January 2007 By JAMES MORGAN, Science Reporter [Return to top] ------------------------------ Date: Fri, 26 Jan 2007 14:25:05 -0500 From: "Bernice A. Melsky" <bernicemelsky VERIZON.NET> Subject: RES: Treatment outcomes after multidisciplinary pain rehabilitation with analgesic medication withdrawal for patients with fibromyalgia Treatment outcomes after multidisciplinary pain rehabilitation with analgesic medication withdrawal for patients with fibromyalgia. Pain Med. 2007 Jan-Feb;8(1):8-16. Hooten WM, Townsend CO, Sletten CD, Bruce BK, Rome JD. Departments of Psychiatry and Psychology, Mayo Clinic College of Medicine, Rochester, Minnesota, USA. PMID: 17244099 Objective. This study of patients with a diagnosis of fibromyalgia (FM) was conducted to test the hypothesis that immediate posttreatment measures of psychosocial functioning, health attributes, negative pain-related emotions, and depressive symptoms improve significantly during multidisciplinary pain rehabilitation while concurrently withdrawing analgesic medications. Design. Prospective case series. Setting. Multidisciplinary pain rehabilitation center at a tertiary referral medical center. Patients. In total, 159 consecutive patients with a diagnosis of FM admitted to the pain rehabilitation program from January 2002 to December 2003. Interventions. A 3-week outpatient multidisciplinary pain rehabilitation program based on a cognitive-behavioral model that incorporates analgesic medication withdrawal. Outcome Measures. Multidimensional Pain Inventory (MPI), Short Form-36 Health Status Questionnaire (SF-36), Coping Strategies Questionnaire-Catastrophizing subscale (CSQ-C), and the Center for Epidemiologic Studies-Depression scale (CES-D) were administered at admission and dismissal and the mean differences in scores were compared using paired t-tests. The number of patients using opioid analgesics, nonsteroidal anti-inflammatory drugs (NSAIDs), benzodiazepines, and muscle relaxants at admission and dismissal were compared using chi-squared analyses. Results. The difference in admission and dismissal scores from the MPI, SF-36, CSQ-C, and CES-D demonstrated a favorable response to treatment (P < 0.001). Compared with admission, the number of patients using opioids (P < 0.001), NSAIDs (P < 0.001), benzodiazepines (P < 0.001), and muscle relaxants (P < 0.01) at program dismissal was significantly reduced. Conclusion. The results of this study support the hypothesis that immediate posttreatment measures of physical and emotional functioning are favorable for patients with FM following multidisciplinary pain rehabilitation that incorporates withdrawal of analgesic medications. [Return to top] ------------------------------ Date: Fri, 26 Jan 2007 17:56:41 -0500 From: "Rich Van Konynenburg <Richvank aol.com> [via Co-Cure Moderators] Subject: RES,MED:Treatment of CFS based on Glutathione Depletion--Methylation, Cycle Block Hypothesis January 25, 2007 Suggestions for Treatment of Chronic Fatigue Syndrome (CFS) based on the Glutathione Depletion Methylation Cycle Block Hypothesis for the Pathogenesis of CFS Richard A. Van Konynenburg, Ph.D. I presented the Glutathione Depletion Methylation Cycle Block Hypothesis for the pathogenesis of CFS in a poster paper at the 8th international conference of the International Association for Chronic Fatigue Syndrome in Ft. Lauderdale, Florida, on January 10-14, 2007. This poster paper is available on the internet at the following url: http://phoenix-cfs.org/GSH%20Methylation%20Van%20Konynenburg.htm Since then I have received requests from some clinicians for a description of a treatment approach based on this hypothesis. I am a researcher, not a clinician, and I am well aware that it is one thing to believe that one understands the pathogenesis of a disorder, but quite another to know how to treat patients who suffer from this disorder. Nevertheless, I will respond to these requests to the degree I am able. What I can say in this regard will be based on what I perceive are the most successful treatment approaches currently used in autism, which I believe shares the same basic pathogenetic mechanism with CFS, and also on limited experience in communicating by internet with the small number of CFS patients so far who have elected to try these approaches. Of course, I am counting on clinicians to apply their judgment to what I write here, based on their expertise and clinical experience, since responsibility for treatment falls to them. I suspect that clinicians would like for me to supply a simple, straightforward approach that would be uniformly applicable to all CFS patients and thus readily useable in a typical busy practice in today s medical climate, in which it is practicable to devote only a relatively short time to each individual patient. Believe me, I understand this, and I would very much like to be able to give such a response. Now comes the however. At this point it appears that it will actually be necessary in most cases to devote considerable time to each patient, and to tailor the treatment program to the individual patient. In my opinion, the reasons for this do not appear now to be lack of understanding of the pathogenesis, but to be inherent in the genetic individuality of the patients as well as in the variety of their concomitant medical issues and, for many, in their general state of debility. I now see this need for individual treatment and significant time investment in each patient as the most significant problem in the practicable delivery of treatment to these patients. Hopefully this will become clearer as I explain further, and hopefully also, this problem can be ameliorated to some degree in the future as more experience is gained. If you have read my pathogenesis paper, you know that I now believe that the fundamental biochemical issue in at least a large subset of the CFS patients is that the methylation cycle is blocked. Therefore, I think that the main goal of treatment must be to remove this block and to get the methylation cycle back into normal operation. I believe that it is also true that glutathione depletion is present in these patients and is directly responsible for many of the features of CFS, as I described in my recent poster paper, but I have found in interacting with clinicians as well as with many patients on the CFS internet lists, that it is usually not possible to normalize the glutathione levels on a permanent basis by direct approaches of glutathione augmentation. Instead, it appears that the methylation cycle block must be corrected first, to break the vicious circle that is holding down the glutathione levels. In addition to this, some patients, because of particular genetic polymorphisms, cannot tolerate supplementation with glutathione or other substances intended to help them directly to build glutathione. One clinician estimated to me that this group amounts to about one-third of the patients. Based on what is being done in autism by the Defeat Autism Now! (DAN!) researchers and clinicians and independently by Dr. Amy Yasko, N.D., Ph.D., I am going to suggest two treatment approaches for CFS. The first is a simplified approach which may be applicable to patients who have not been ill for an extended period, and who are not very debilitated. Use of this simplified approach would be based on the hope that the patient does not have certain genetic polymorphisms, which would not be known in this simplified approach. If the patient does in fact have these polymorphisms, the simplified approach will not be successful, and then you will have to move on to the more complex treatment. This simpler treatment approach is based partly on the treatment that was used by Dr. S. Jill James, Ph.D., et al. in the study that found the connection between the methylation cycle block and glutathione depletion in autism (This was Ref. 2 in my pathogenesis paper), but it makes use of supplements that are part of Dr. Amy Yasko s treatment program. The second treatment approach is much more involved and is based on Dr. Yasko s complete autism treatment. I currently believe that the second approach is the type of treatment that will be necessary also for most CFS patients, and certainly those of longer standing or greater debility, as well as those having certain genetic polymorphisms. However, I am including the simpler approach in an effort to match the practical demands of current medical practice, to the degree I understand them. In the simplified treatment approach, potentially applicable to patients who have not been ill for an extended period, who are not very debilitated, and who will initially be assumed not to have certain genetic polymorphisms, one would proceed directly toward the goal of restarting the methylation cycle, together with some general nutritional support. If this treatment is tolerated and is efficacious in a particular case, I think it could actually be relatively straightforward. I think it should be borne in mind, though, that if the simplified approach is not effective for a particular patient, there is the risk that trying it could discourage the patient before she or he reaches the second option. So I think it would be proper and wise to discuss this issue with the patient up front, and to apply considerable clinical judgment as to whether the simplified approach should be tried on a particular patient. The simplified approach would involve giving the following oral supplements daily, all of which are available from Dr. Yasko s supplement website at <http://www.holisticheal.com:>http://www.holisticheal.com: ¼ tablet (200 micrograms) Folapro (Folapro is 5-methyl tetrahydrofolate, an active form of folate, which is sold by Metagenics with a license from Merck, which holds the patent on synthesis). ¼ tablet Intrinsic B12/folate (This includes 200 micrograms of folate as a combination of folic acid, 5-methyl tetrahydrofolate, and 5-formyl tetrahydrofolate, aka folinic acid or leucovorin (another active form of folate), 125 micrograms of vitamin B12 as cyanocobalamin, 22.5 milligrams of calcium, 17.25 milligrams of phosphorus, and 5 milligrams of intrinsic factor) (up to) 2 tablets (It s best to start with ¼ tablet and work up as tolerated) Complete vitamin and ultra-antioxidant from Holistic Health Consultants (This is a multivitamin, multimineral supplement with some additional ingredients. It does not contain iron or copper, and it has a high ratio of magnesium to calcium. It contains antioxidants, some trimethylglycine, some nucleotides, and several supplements to support the sulfur metabolism.) 1 softgel capsule Phosphatidyl Serine Complex (This includes the phospholipids and some fatty acids) 1 sublingual lozenge Perque B12 (2,000 micrograms hydroxocobalamin with some mannitol, sucanat, magnesium and cherry extract) 1 capsule SAMe (200 mg S-adenosylmethionine) 1/3 dropper, 2X/day Methylation Support Nutriswitch Formula (This is an RNA mixture designed to help the methylation cycle. It is not essential, but is reported to be helpful.) Note that I have specified hydroxocobalamin rather than methylcobalamin as the main supplemental form of vitamin B12. I ve done this to accommodate patients who may have downregulating polymorphisms in their COMT (catechol-O-methyltransferase) enzyme, which many CFS patients seem to have. If they do not have these polymorphisms, methylcobalamin would be more effective, but in this simplified treatment, the patient s polymorphisms will not be known. I am also including a small amount of SAMe, which is also a compromise, since the amount needed will again depend on COMT polymorphisms, which will not be known for this simplified treatment. The amount of B12 specified is also a compromise, since those with certain polymorphisms will benefit from a higher dosage than will those without them. After this treatment is begun, you can expect the patient to feel worse initially, and I think it would be proper and wise to make the patient aware of this before the treatment is begun. It is necessary to determine whether this feeling is occurring because the treatment is working and the patient s body is beginning to detox and kill viruses, or whether it is occurring because the patient does in fact have upregulation polymorphisms in their CBS (cystathionine beta synthase) enzyme, in which case you will have to move on to the more complicated complete treatment regimen. Which of these is the case can be determined by taking spot urine samples for a urine toxic metals test and a urine amino acids test from Doctor s Data Laboratories. These can be ordered through Dr. Yasko (at <http://www.testing4health.com>http://www.testing4health.com) if you would like to receive her interpretation of the results, or they can be ordered directly from Doctor s Data Laboratories (<http://www.doctorsdata.com>http://www.doctorsdata.com). If the toxic metals are elevated on the urine toxic metals test, this will indicate that the patient has begun to detox, which is desirable. If taurine and ammonia are elevated on the urine amino acids test, this will suggest that the patient does have CBS upregulation polymorphisms, in which case you will have to stop this treatment and move to the more complicated approach described below. It would be best to do this treatment for a week or two before doing the urine tests, so that meaningful results can be obtained on these tests, unless the patient cannot tolerate it. If the latter is the case, then you will have to go on to the more complicated treatment approach described below. As I have emphasized, the simplified treatment approach may or may not be tolerated by a particular patient, and I will explain why it might not be tolerated later in this discussion. Now I will move on to the more complicated treatment approach that I currently believe will be necessary for most of the patients. I will not supply all the details of this treatment approach in this letter, but will try to give you an overall picture of the sequence of steps involved. I recommend reading Dr. Yasko s book The Puzzle of Autism, and consulting her other materials as well. These are available from <http://www.amazon.com>http://www.amazon.com by searching on Amy Yasko. Before getting into this treatment approach, I first want to discuss some important issues, and then I will discuss the treatment, step by step: 1. It is necessary to minimize the use of pharmaceuticals in treating CFS patients. There are at least two reasons for this. As you know, the use of pharmaceuticals is based on their being eliminated at certain rates by the body s detox system, found primarily in the liver, kidneys and intestines. However, many CFS patients have polymorphisms in their detox enzymes, including CYP450 enzymes and Phase II detox enzymes. (If desired, these can be characterized by the Detoxigenomic panel offered by <http://www.genovations.com>http://www.genovations.com). Because of these polymorphisms, many patients are genetically unable to detox pharmaceuticals at normal rates, and cannot tolerate them. In addition to this, all patients who have the glutathione depletion and methylation cycle block suffer from biochemical inhibition of their detox systems, whether they have these polymorphisms or not. Because of these two factors, CFS patients suffer from the toxic effects of pharmaceuticals. Treatment using nutritional supplements is necessary, and some herbals can be tolerated as well. 2. Because of the broad nature of the current case definition for CFS, the population defined by it is very heterogeneous. It is likely that the pathogenesis model I have presented for CFS will not fit all patients. For this reason, I recommend a relatively inexpensive glutathione measurement initially, such as the red blood cell total glutathione test offered by <http://www.immuno-sci-lab.com>http://www.immuno-sci-lab.com (phone them for details) or by Mayo Laboratories. Perhaps a better test is the serum reduced glutathione test offered as part of the Comprehensive Detox Panel at <http://www.gdx.net/home/assessments/detox/reports/>http://www.gdx.net/home/assessments/detox/reports/. If a below-normal value is found in either of these tests, I think that there is a good chance that this pathogenesis model fits the patient. 3. Different patients have different genetic polymorphisms in the enzymes and other proteins that impact the methylation cycle and the associated biochemical cycles and pathways. Some of these polymorphisms will have important impacts on the choice of specific parts of the treatment program. In using the more complicated treatment approach, it will be necessary to characterize the polymorphisms before it will be possible to make some of the decisions about selection of particular treatment aspects. The most comprehensive panel for this is Dr. Yasko s Comprehensive Basic SNP (single nucleotide polymorphism) Panel I, available from <http://www.testing4health.com>http://www.testing4health.com. Dr. Yasko has selected the polymorphisms on this panel by correlating their presence with severity of autism symptoms and with the results of biochemical testing (mainly spot urine tests for organic acids, amino acids, and essential and toxic metals). This is a somewhat unorthodox method that jumps over the usual intermediate steps involved in studying polymorphisms, and there is not universal agreement about her results in the research community, but I think Dr. Yasko s treatment outcomes are speaking for themselves, as can be seen from the voluntary testimonials of parents of autistic children on the parents discussion group at <http://www.autismanswer.com>http://www.autismanswer.com. As a researcher, of course, I look forward to the day when these polymorphisms will be thoroughly researched and characterized, and have encouraged those involved in such work to forge ahead. The results from this genetic panel require interpretation. One can either study Dr. Yasko s materials to gain her insights on interpreting the results in general, or order her interpretation of the particular results, which is called a Genetic Analysis Report or GAR. The GAR is a computer-generated report with some general material that applies to all the cases, and specific sections that are chosen in response to the particular genetic polymorphisms found in the individual patient. As such, the continuity of the discussion in the GAR is not what would be found in a report written from scratch for each particular patient, and it may have to be read more than once to make all the connections in one s mind, but the material contained is specific to the particular genetic panel results, and Dr. Yasko updates the material used in generating the GARs as more is learned. 4. As I have discussed in my paper, people who have been ill for an extended period of time (many months to many years) will have accumulated significant infections and significant body burdens of toxins, because both their cell-mediated immune response and their detox system will have been dysfunctional during this time. When the methylation cycle is then restarted, both the immune system and the detox system will begin to function better. When they do, pathogens and infected cells will begin to die off at higher rates, and toxins will be mobilized. The resulting detoxification will be unpleasant, and may even be intolerable. If the patient has not been prepared in certain ways, discussed below, she or he may not be willing to continue this and may drop out of the treatment program. 5. One of the most important preparatory activities is to make sure the gastrointestinal system is operating well enough to be able to absorb nutrients, including both food and the oral supplements used in the treatment, and also well enough to be able to dispose of toxins into the stools on a regular basis. If this is not done, it is likely that the treatment will not be successful. Treatments for the G.I. system, as well as for other aspects described below, are discussed in Dr. Amy Yasko s book. Some CFS patients have reported benefit from Xifaxan to treat deleterious bacteria in the gut. This antibiotic is not absorbed from the G.I. tract, so it does not present problems for the detox system. 6. Another very important aspect of the preparation is to deal with the overstimulation or overexcitation of the nervous system that is present in CFS. This probably results from several causes, including depletion of magnesium and in some cases depletion of taurine, low blood flow to the brain because of low cardiac output, glutathione depletion in the brain producing mitochondrial dysfunction, and dietary and other factors causing elevation of excitatory neurotransmitters and depletion of inhibitory neurotransmitters. It is important that this be dealt with because if it is not, the patient will be less able to tolerate the detox inherent in the treatment. 7. Another important step is to ensure that the patient s nutritional status is supported. Many CFS patients are in a rather debilitated state, partly because of deficiencies of essential nutrients. They are also in a state of oxidative stress. Appropriate nutritional supplements can correct these problems at least to some degree and get the overall metabolism of the patient into a better state, so that they can better tolerate the detox part of the treatment. 8. Particular organs or systems may not be functioning well and may need extra nutritional or herbal support. Which ones will vary from one patient to another, so this part of the treatment must be tailored to the individual patient. 9. Chronic bacterial infections should be addressed. According to Dr. Yasko, females in particular appear to be prone to streptococcal infections. She also finds that aluminum appears to be associated with the bacteria, so that when the bacteria die off, aluminum is excreted. While antibiotics can be used, there are downsides to this, both in terms of difficulty in detoxing some of the antibiotics and in terms of killing beneficial intestinal flora and encouraging deleterious ones, such as Clostridia dificile. In addition, some CFS patients have experienced tendon problems from the fluoroquinolone antibiotics. Dr. Yasko prefers natural antimicrobial treatments. 10. When the methylation cycle is restored, the normal detox system is able to deal with more of the toxins. Dr. Yasko also uses low doses of oral EDTA, but not the sulfur-containing chelators (DMSA and DMPS), to help remove aluminum as well as other metals, including mercury. DMSA and DMPS are not used because they can also bind glutathione, so that if a patient who is low in glutathione receives these chelators, their glutathione status can be worsened. Also, DMSA and DMPS are rich in sulfur, and CFS patients with certain polymorphisms cannot tolerate them. She also uses some natural RNA formulas for detoxing, as well as for a number of other purposes during the treatment. These are somewhat costly, and are not required as part of the treatment, but are reported to be helpful. 11. As mentioned in item 3 above, it is important to characterize relevant polymorphisms prior to bringing up the methylation cycle operation. One of the most important aspects of this is to evaluate polymorphisms in the CBS (cystathionine beta synthase) enzyme, which is located at the entrance to the transsulfuration pathway and converts homocysteine to cystathionine. Although this is somewhat controversial within the research community, Dr. Yasko finds that certain polymorphisms cause an increase in the activity of this enzyme. The result is that there is too large a flow down the transsulfuration pathway, and somewhat counterintuitively this results in lowered production of glutathione, as well as elevated production of taurine, ammonia, sulfite and hydrogen sulfide. The last three of these substances are toxins. If a patient has CBS polymorphisms, it is necessary to deal with this aspect before restarting the methylation cycle. If this is not done, efforts to start this cycle will result in increased production of these toxins. This may explain why some patients cannot tolerate direct efforts to build glutathione using sulfur-containing substances, while others derive some benefit from this. Dealing with this CBS upregulation situation can take a month or longer. 12. Only after all these issues have been addressed is the patient ready to start supplementing with larger amounts of the folates and cobalamins to begin major restoration of operation of the methylation cycle. 13. As you can see from the diagram in my pathogenesis paper, there are two possible pathways from homocysteine to methionine. One involves the enzyme methionine synthase, which requires methylcobalamin and is linked to the folate cycle as well, and the other involves the enzyme betaine homocysteine methionine transferase (BHMT), and requires trimethylglycine or one of the phospholipids (phosphatidyl-serine, -choline, or -ethanolamine). Ultimately, it is important to get the methionine synthase pathway back into operation, but in Dr. Yasko s practice it has been found that it is easier to start up the BHMT pathway first. I think the reason is that S-adenosylmethionine (SAMe) interacts with methionine synthase, and by first starting up the BHMT pathway, one ensures that there is enough SAMe to start up the methionine synthase pathway. 14. As these steps are taken, the immune system and the detox system will start to function at higher levels, and die-off and detox will begin. These processes are monitored using periodic spot urine testing, and decisions about when to proceed to the next step in the treatment program are based on this urine testing. 15. Viral infections are dealt with naturally as the immune system recovers, though Valtrex is used in some cases. As the viruses die off, it is observed that heavy metal excretion increases. Heavy metal excretion is tracked using periodic spot urine tests and is plotted as a function of time to determine the progress. 16. When appropriate indications are seen in the urine testing, the BHMT pathway is slowed using dimethylglycine, which is a product of the BHMT reaction, and thus exerts product inhibition on it. This shunts the flow through the parallel methionine synthase pathway. This has the effect of bringing up the folate cycle, which is linked to it, and also bringing up the biopterin cycle, which is linked to the folate cycle. The folate cycle is needed to make new RNA and DNA to proliferate new cells, such as T cells in cell-mediated immunity. The biopterin cycle is necessary for the synthesis of serotonin and dopamine as well as for the operation of the nitric oxide synthases. Some patients benefit from direct supplementation of tetrahydrobiopterin, often in very small amounts. 17. The treatments up to this point should resolve most of the symptoms of CFS. The last step is to support remyelination, which has been dysfunctional during the time when the methylation cycle was blocked, because methylation is necessary to synthesize myelin basic protein. This should improve the operation of the nervous system. That is a rough outline of the treatment process, and again, I refer you to Dr. Yasko s materials for the details. I m sorry that this treatment approach is not simple, quick, easy and inexpensive, but unfortunately, I think this rather complex process is what is required, for the reasons I ve given. I hope this is helpful, and I would very much appreciate it if you decide to try this treatment approach, that you will keep me informed of how it works out for your patients. If I can answer questions that come up, please let me know. Rich Van Konynenburg, Ph.D. [Return to top] ------------------------------ Date: Sat, 27 Jan 2007 10:46:29 -0500 From: "Dr. Bart Stouten via Co-Cure Moderator" <ray CO-CURE.ORG> Subject: NOT, RES: An insight into the situation in Belgium Recently a report evaluating the five CFS reference centres which have been operating in Belgium since 2002 was published. The summary below contains the main points raised in the report. The report (written in Dutch) can be accessed at http://riziv.fgov.be/care/nl/revalidatie/study-sfc-cvs/index.htm Best wishes, Bart Stouten Summary of the evaluation report (2002-2004) of the five CFS reference centres in Belgium * Despite a large amount of national and international research on CFS, a lot remains unknown. There is no general consensus about the aetiology and pathophysiology, required in order to diagnose, how to treat, and how to name the condition. * A working group from the Belgium High Health Council has identified the medical and administrative problems for CFS patients. To cope with the identified problems, RIVIZ was asked to make contracts with reference centres for chronic fatigue syndrome. These centres had to satisfy the following criteria: * multidisciplinary teams and approach * out-patient diagnosis * formulate a therapeutic proposal for the general practitioner * actively participate in scientific research and information * active support for the health professionals Because knowledge and participation in scientific CFS research is mostly limited to universities, the recognition of CFS centres was limited to medical teams associated with a university. Five recognized centres: * four for adults: UZ Leuven, UZ Antwerpen, UZ Gent, and UCL * one for adolescents younger than 18 years: AZ VUB The centres became operational between April 2002 and October 2002. The maximum costs of the five centres together is approximately 1.7 million euros per year. Chronic Fatigue Syndrome criteria of Fukuda et al. (1994) are used. Centres can only accept patients who are referred by their general physician using a standardized intake form that was devised by the `Akkoordraad.' * The first contact between the centre and the patient is a consult with a general physician/internist. The aim is to quickly identify patients who do not meet the criteria for a CFS diagnosis. * Patients suspected to have CFS after this consult enter a phase where they are assessed by a multidisciplinary team consisting of an internist, psychiatrist, and rehabilitation physician. * If the multidisciplinary assessment has made the diagnosis of CFS, then a specific, individually-tailored interdisciplinary therapeutic programme will be advised. The length is at most 12 months, and for adults it should at least include cognitive behaviour therapy (CBT) as well as graded exercise therapy (GET). [Ed note: CBT and GET were given in groups but individual sessions were included where deemed helpful] * For the adolescents, the required length of the complaints for a CFS diagnosis was reduced from six months to six weeks [Ed note: the six week limit also applies to fatigue]. With respect to fatigue, the restriction that the chronic fatigue must have resulted in an absence from school for at least two weeks in a period of six weeks was added. For adolescents, the initial consult is performed by a paediatrician. The adolescent therapeutic programme included GET as well as one of the following: school guidance, system therapy, or CBT. Evaluation measurements are taken at before the programme, immediately after the programme, and 6 and 12 months after the programme. The centres have a certain freedom in their policy. Sometimes, additional criteria are applied, alongside the Fukuda CFS criteria to select patients for a therapeutic programme. The length, intensity, contents and focus of the therapeutic programmes can differ between centres. The centres have the freedom to choose to offer out-patient or in-patient programmes. In practice, there is only one centre (dealing with the adolescents) where patients are hospitalized for ten days during the assessment phase following the intake. Methodological shortcomings as recognized in the report include: 1. Due to lack of objective measures to diagnose CFS and assessing the course of disease, a lot of data on the functioning of patient was collected using interviews and questionnaires. 2. Comparisons between centres was not always easy because each centre had registered the parameters for their own patients, and sometimes this led to compatibility issues between centres. 3. Some centres recorded that certain parameters for a large number of patients were 'unknown,' even though the rehabilitation-contracts indicated that assessment of these parameters was mandatory and included them in the funding for the centre. 4. There are no control groups with patients that e.g. followed no programme, a minimal programme, or an alternative programme. 5. There were large differences in the amount of registered data - mostly related to the number of registered patients- per centre. In particular there were not enough data (<10 patients) to perform a statistical analysis for the centre that treated the adolescents. Furthermore, the overall results are biased by the centre which treated the most participants. Results for the adult centres * Evaluation period: 1 April 2002 30 June 2005. * 1505 patients entered the multidisciplinary assessment phase, 1421 patients completed this phase, 951 specific interdisciplinary rehabilitation programmes were started * Until 31 December 2004, 3042 patients were referred to the CFS centres. Of those, (only) 54% had the mandatory consult with the internist, 37% followed the multidisciplinary assessment phase, 26% entered the specific interdisciplinary rehabilitation phase, and 20% completed the specific interdisciplinary rehabilitation phase. Thus 63% of the referred patients have never been diagnosed or evaluated according to the contracts. * In 94% of the cases the internist judged that the referred patient may have CFS; the CFS diagnosis was subsequently confirmed by the multi-disciplinary team in 96% of those cases. * In 80% of the cases where the diagnosis CFS was confirmed, the specific interdisciplinary rehabilitation programme was recommended. * 89% of the patients continued the rehabilitation programme until the moment that the costs of rehabilitation were no longer covered. For no patients the programme was stopped because the patient was not motivated enough. Only in 2.8% of the cases the programme was ended by the patient. * Complete recovery was never recorded as a reason for ending the rehabilitation. Some centres believed that a complete cure for this chronic condition is not possible. [Ed note: though not mentioned in the main text, annex 3 reveals that other centres did: the centre in Gent estimated that 2-3% were completely cured after rehabilitation; the adolescent centre reported that 2 out of 3 patients in a sample of 14 had completely recovered after rehabilitation.] * For 71% of the patients, the treatment team judged that there was sufficient improvement to transfer the rest of the intervention back to first and second line care. * Most general practitioners (70%) have referred only a single patient. 96% referred three or less patients. Only 1% referred five or more patients to the centres. * The mean age of the patients that were referred to the centres was 40 years and 8 months; 41% were between 40 and 49 years old; 87% was female. * 10% of the patients judged to have CFS worked fulltime, 14% worked part-time, 76% did not have paid work. On average CFS patients worked 17.7% (out of 38 hours) per week. When non-paid (e.g. household) work was taken into account, CFS patients worked 57.2% per week. 26% of the patients had income from professional work, 54% had a disability allowance. * On average, patients had experienced chronic fatigue for 58 months. 38% had chronic fatigue for more than five years. Most mentioned minor symptoms including: muscle aching 95%, memory or concentration problems 94%, non refreshing sleep 92%, post exertional malaise lasting longer than 24 hours 85%. Less frequent complaints were tender lymph nodes 38% and sore throat 54%. * Maximum exercise test indicated that the reference values were on average 73.3% of the nominal values * There was a large difference in the psychopathological conditions between centres. 42% had a somatisation disorder/undifferentiated somatoform disorder (varied from 1-89% between the centres); 13% depressive disorder (0-33%); generalised anxiety disorder 6% (0-26%). The psychiatrists of the centres thought that these differences were related to recording bias and/or interpretation bias. The largest differences between centres were the `undifferentiated somatoform disorder' (varied between 1-89%). The symptom pattern is almost the same as CFS, but the former requires a relation with identifiable social stressors (as a primary aetiological factor). According to the psychiatrists, the large difference between centres reflects the uncertainty in the aetiology of CFS. Results of the treatment programme * Analysis indicated statistically significant improvements in subjective fatigue (measured with CIS20 subscale fatigue), vitality (SF36), memory and concentration problems (CIS20-concentration), self-reported physical activity (CIS20-activity, SF36), and quality of life (SF36 general) for the group as a whole. Despite the improvement, the average scores remained low as compared to a healthy population (e.g. quality of life score after rehabilitation was 39.6 for CFS versus 78.8 for a healthy population). * The effect of rehabilitation on the results of the exercise test were limited and not statistically significant. Furthermore, there seemed to be no relation between the subjectively experienced quality of life and the cardio respiratory capacity. The maximum exercise was very demanding for the patients as it could lead to severe malaise afterwards (abnormal exercise intolerance is characteristic for CFS). Some believed that the maximum exercise test was not in line with the therapeutic goal to avoid maximum exertion. According to some centres, after rehabilitation, some patients stopped the exercise test prematurely because they had learned during rehabilitation to not exert themselves too much. * Before rehabilitation, average amount of paid work was 18.3% (of 38 hours). Immediately after rehabilitation this was reduced to 14.9% (6% worked more, 10% worked less), 6 months later it was 16.7%. Scores at 0 months and at 6 months after rehabilitation as compared to baseline (just before rehabilitation) [Ed note: this table is not complete, but gives an indication of the numbers that are mentioned in the main text of the report; the full tables are in annex 3 of the report] improved deteriorated CIS20-fatigue (0 months)* 61% 21% (6 months)* 60% 25% SF36 vitality (0 months)* 60% 25% (6 months)* 56% 30% CIS20 memory& (0 months)* 52% 32% concentration (6 months)* 56% 29% CIS20 physical (0 months)* 56% 24% activity (6 months)* 56% 28% SF36 phys. (0 months)* 54% 31% functioning (6 months)* 57% 30% SF36 quality of (0 months)* 48% 30% life (6 months) 46% 34% max exercise test -watts (0 months) 38% 38% -O2 (0 months) 58% 39% -basismetabolism (0 months) 55% 44% sub max exercise test -watts (0 months) 43% 30% -O2 (0 months) 56% 37% -basismetabolism (0 months) 56% 39% self-efficacy (0 months)* 57% 32% (6 months) * statistically significant improvement compared to baseline for the group as a whole Comparison to published studies * Comparison of the results of the CFS reference centres with published evidence based studies was difficult as the published studies often used other measurements. Furthermore, scientific studies often used more stringent criteria to select patients. Finally, sometimes the published studies used other selection criteria than the CDC criteria that were applied in the reference centres. * Fulcher et al (BMJ 1997; 314:1647) compared 33 patients with CFS that followed GET with a control group of 33 CFS patients who did flexibility/relaxation exercises. The peak O2 consumption improved by 13% in the group that followed GET (mean improved from 31.8 to 35.8). In the CFS reference centres this is only 2% (from 22.3 to 22.8). The scores on the 'functional functioning' scale (range 0-100) improved from 48.5 to 69 in the Fulcher et al study; in the reference centres the improvement was less (41.8 to 47.6) though still statistically significant. * Prins et al (Lancet 2001; 357:841-47) compared a group of 92 CFS patients who followed CBT/GET with a group who were given guided support and a group that had no intervention (natural course). For the CBT group the mean CIS20-fatigue score before therapy was approximately 52 (range 8-56; higher indicates more fatigue), after therapy approximately 40. For the CFS centres the baseline score was 51.7. Although statistically significant, the score was only improved to 47.0 after rehabilitation. The report remarks that it should be noted that the Prins et al study also included patients that did not satisfy the CDC criteria that they should have at least 4 out of a list of 8 symptoms; patients who used medication or had a conflict with the health insurance were also excluded. * The results of the centres are not good as the results in the published evidence based studies. The report asks if this depends on the way the interventions are organised. The published studies used individual therapy, the reference centres performed group therapy (on average 3 people per group, though in some centres the groups consisted of 10-11 persons), sometimes in combination with a limited number of individual sessions. Conclusion section * Despite the limited effect of the treatment offered by the reference centres, the patients experienced a global improvement of subjective perception of their health (as measured with questionnaires for fatigue, concentration, physical functioning, quality of life, psychological functioning), without an accompanying improvement of their physical capacities (as measured by the exercise test). * In general the final levels of health and functioning were not as good as in the normal population, which had consequences for the possibilities for occupational rehabilitation. Furthermore, there is a large variance in the results. There were also patients that did not improve or even got worse after rehabilitation. The effect of the rehabilitation was decreased at the follow-up phase, which shows the significance of the rehabilitation and raises questions about the length. [Ed note: I omitted the results for adolescents as only 59 patients were referred to the centres until December 2004; of those, 37% were confirmed to have CFS; less than 10 patients had data that could be used to evaluate the rehabilitation, therefore no statistical analysis were performed in the report. The general trend of the results of the <10 patients is that they improved a lot, and after rehabilitation several measurements are within 1 standard deviation of the mean of the normal population; the report warns that these results have to be interpreted with caution due to the small sample size.] [Return to top] ------------------------------ Date: Sat, 27 Jan 2007 14:36:10 -0500 From: "Bernice A. Melsky" <bernicemelsky VERIZON.NET> Subject: RES: Awareness and perceptions of fibromyalgia syndrome: a survey of Malaysian and Singaporean rheumatologists Awareness and perceptions of fibromyalgia syndrome: a survey of Malaysian and Singaporean rheumatologists. Singapore Med J. 2007 Jan;48(1):25-30. Arshad A, Kong KO. Rheumatic Diseases Unit, Putra Specialist Centre, Alor Star 05100, Malaysia. email@example.com. PMID: 17245512 Introduction: Fibromyalgia syndrome (FMS) is a common but controversial condition. There appears to be different levels of belief of its existence and awareness. We set out to explore the variations of perceptions and awareness of this condition among rheumatologists from Malaysia and Singapore. Methods: 48 rheumatologists from Malaysia (28) and Singapore (20) were approached to participate in this survey by answering a specific questionnaire regarding their belief in FMS. 23 respondents from Malaysia and 20 from Singapore completed the questionnaire. Results: 91 percent of Malaysian rheumatologists and 95 percent of the Singaporean believe that FMS is a distinct clinical entity and that this condition is considered an illness rather than a disease. 87 percent and 90 percent of rheumatologists from Malaysia and Singapore, respectively, believe that FMS is a mixture of medical and psychological illness. However, not many of those in the university setting include FMS in their undergraduate teaching. 87 percent and 80 percent of the respondents from Malaysia and Singapore, respectively, also ordered blood tests to exclude other serious pathologies, and 100 percent of the respondents from both countries also prescribed some form of drugs to their FMS patients. Conclusion: This study confirmed that there was a variation of perceptions and knowledge of FMS among rheumatologists from Malaysia and Singapore. The majority of rheumatologists recognise that FMS is a distinct clinical entity, and is diagnosed by excluding other well-defined clinical diseases through a combination of clinical evaluation and screening tests. [Return to top] ------------------------------ Date: Sun, 28 Jan 2007 15:11:30 -0500 From: "Bernice A. Melsky" <bernicemelsky VERIZON.NET> Subject: RES: Biology and therapy of fibromyalgia. Functional magnetic resonance imaging findings in fibromyalgia Biology and therapy of fibromyalgia. Functional magnetic resonance imaging findings in fibromyalgia. Arthritis Res Ther. 2007 Jan 17;8(6):224 [Epub ahead of print] Williams DA, Gracely RH. Chronic Pain and Fatigue Research Center, Department of Internal Medicine, Division of Rheumatology, University of Michigan Health System, University of Michigan, Ann Arbor, MI, USA. firstname.lastname@example.org. PMID: 17254318 ABSTRACT: Techniques in neuroimaging such as functional magnetic resonance imaging (fMRI) have helped to provide insights into the role of supraspinal mechanisms in pain perception. This review focuses on studies that have applied fMRI in an attempt to gain a better understanding of the mechanisms involved in the processing of pain associated with fibromyalgia. This article provides an overview of the nociceptive system as it functions normally, reviews functional brain imaging methods, and integrates the existing literature utilizing fMRI to study central pain mechanisms in fibromyalgia. [Return to top] ------------------------------ Date: Sun, 28 Jan 2007 22:48:19 -0500 From: Jill McLaughlin <jillmclaughlin COMCAST.NET> Subject: NOT,MED: Drained by the brain - The Australian http://www.theaustralian.news.com.au/story/0,20867,21131962-28737,00.html Drained by the brain Yuppie flu is real and may be caused by disruption in the brain. Clara Pirani investigates the disease, which is costing the country $525 million a year The Australian January 29, 2007 LYN Wilson has a blunt message for anyone who doubts that chronic fatigue syndrome is a debilitating physical illness. "Why would anyone want to give up their life and their income, for nothing? People who think we're not sick don't have a clue." The 54-year-old Queensland woman was 37 when she suddenly developed gastroenteritis and began to have trouble staying awake. She was admitted to hospital but doctors were baffled by her symptoms, which included loss of feeling in her legs and difficulty concentrating. During the next 16 months, Wilson was misdiagnosed with multiple sclerosis and lupus, and was told by one doctor that she only needed to start taking aerobics classes to get fit. "I finally went to a diagnostic specialist who diagnosed me with chronic fatigue." By then, Wilson was experiencing crippling headaches and neck pain, had trouble following conversations and had to quit her job as a teacher's aide at a kindergarten. "I was devastated. I absolutely loved my job." Wilson, who wears a neck brace to reduce headaches and walks with a frame, works as a volunteer when she can, helping people with CFS. "Most people I meet, when I tell them what I have, will say, 'Yeah, I get tired like that.' They have no idea. Wearing a neck brace is painful, it's hot, very uncomfortable and it's hardly a fashion statement. "My daughter's wedding is coming up and I'm dreading having to wear it. Why would I do this if I didn't have to?" Wilson, like many of the 140,000 Australians who suffer from the affliction, is fed up with people who question whether CFS, sometimes known as myalgic encephalomyelitis, is a real condition. In the 1980s it became known as the yuppie flu, a vague illness that affected high achievers. Its seemingly unconnected symptoms - including fatigue, joint and muscle pain, disrupted sleep and an inability to concentrate - were questioned by doctors and employers who accused sufferers of being hypochondriacs or malingerers. Even doctors who believed that the symptoms were real dismissed the condition as a psychological disorder. In the past five years, however, research by some of the world's leading medical organisations has shown CFS is a crippling, physical condition that affects people of all ages. The US Centres for Disease Control and Prevention this month launched a campaign to convince the public and medical profession that CFS is a serious illness. CFS costs the Australian community $525million a year, according to research published in The Medical Journal of Australia. Many sufferers are unable to work and between 25,000 and 35,000 are housebound. However, doctors and researchers remain deeply divided on how to diagnose and treat the condition. CFS usually begins with flu-like symptoms but progresses to chronic fatigue. It is not improved by bed rest and exhaustion follows any sort of physical activity. Most people with CFS develop it after a viral infection such as from the Epstein-Barr virus, which causes glandular fever. In 2002 the World Health Organisation classified CFS as a neurological disorder and research conducted in the past five years supports the theory that the illness is caused by a disruption in the brain. Anthony Komaroff, a professor of medicine at Harvard Medical School and a spokesman for the CDC campaign, says brain functioning and cell energy metabolism appear impaired in those with CFS. Last year, James Baraniuk, a researcher at the Georgetown University Medical Centre in Washington, DC, reported that CFS patients have a series of proteins in their spinal cord fluid that are not present in people without the condition. "Our research provides initial evidence that it may be a legitimate neurological disease and that at least part of the pathology involves the central nervous system," Baraniuk says. Andrew Lloyd, professor of infectious diseases at the University of NSW's school of medical sciences, says researchers are starting to reject previously accepted theories that CFS was caused by an infection or some form of abnormal immune response to an infection. "Disorders of blood flow, metabolism or muscles have also been crossed off the list. The current thinking is that it's a disorder of the brain. We just don't know where in the brain or exactly what sort of brain chemical disturbance occurs," Lloyd says. Peter Del Fante, an Adelaide GP who has treated more than 300 patients with CFS, says researchers are increasingly finding physical abnormalities that are only present in people with CFS: "For example, researchers in Japan have found molecular differences in the blood of people with CFS," he says. While Colin Neathercoat, director of the ME/CFS Association of Australia, welcomes the research, he wants doctors to focus on better ways of treating the condition. Neathercoat accuses many Australian doctors of advocating outdated and potentially dangerous treatments. Since 2002, doctors have used treatment guidelines set up by the Royal Australasian College of Physicians, which advocate cognitive behavioural therapy to help patients to cope with the condition, and graded exercise to build up their strength. Lloyd says CBT helps patients deal with their physical and mental limitations. "CBT is a package deal based on helping patients to understand the pragmatic approach to day-to-day management of fatigue. One of the typical things in CFS is that patients find the stuff that they used to do easily, like running for a couple of kilometres, is not possible. They find that if they walk around the block they feel buggered and it takes them hours or even days to recuperate. That phenomenon often drives patients to think it's a bad idea to do anything physical." Lloyd says that encouraging patients to perform short bouts of exercise prevents them from pushing themselves too hard. "They need to learn how to avoid that boom-bust cycle, dividing physical and other activities into smaller, short segments." Neathercoat, however, warns that approach can cause more harm than good. "For some people, they get up and have a shower and that's all they can manage. The more you push these people with work or recreationally, the more severe those symptoms become." Jim Chambers agrees. Eleven years ago his son Jeremy, a 23-year-old student, developed CFS after a bout of glandular fever. His condition deteriorated and he spent three years at home, almost bedridden. "On a good day he was able to make his breakfast and not much else," Chambers says. "His quality of life was zero, he just focused on what he had to do to stay alive." Jeremy remains at home and is unable to work or study. "The prognosis is pretty bleak, Chambers says. "He was a vibrant young man who was a high-distinction student working on his honours. His short-term memory is definitely affected and it's just terribly distressing to have to say goodbye to your dreams as a young person." Chambers says Jeremy suffered relapses whenever he tried to push himself physically or mentally. "The message we have to get out to parents and teachers is to back off and stop telling kids and teenagers to just push on when they are sick. "If a kid is usually a go-getter and suddenly they are not performing and they've got nothing left in the tank, then obviously something is wrong. It's better that they take 12 months off to recover rather than pushing on and becoming critically ill and bedridden." Lloyd admits that graded exercise does not work for all patients. "A lot of GPs looked at the guidelines that were sent out and thought that graded exercise meant that if patients could walk around the block a few times, they should try to walk around the block 10 times the next week. That sort of simplistic formula doesn't work. I have patients who are elite athletes from the Institute of Sport who can still ride for kilometres, but they used to ride for hundreds of kilometres. At the other end of the scale, I have patients who are housebound and their exercise program is a walk to the letterbox and back." Neathercoat and GPs such as Del Fante are also critical of the way the Australian guidelines define CFS. "The Royal Australasian College of Physicians' guidelines set up in 2002 are so vague that basically anyone with a little bit of fatigue would fit into it," Neathercoat says. CFS organisations want Australian doctors to follow the Canadian guidelines. Launched in 2003, they diagnose people with CFS only if they have experienced six symptoms including general fatigue, post-exertion fatigue, sleep dysfunction, pain, cognitive impairment and immune or neuroendocrine problems for more than six months. "We are approaching the Government to adopt the Canadian guidelines, which are also critical of graded exercise as a form of treatment," Neathercoat says. Del Fante says South Australia has developed its own version of the Canadian guidelines, using post-exertion malaise as the identifying symptom of CFS. "If they have to lie down in bed, sometimes for days, to recover from physical exertion, that's CFS. There is nothing else that does that to you but CFS. And if you put those people on an exercise program, unless it is very, very slow and minimal, it's extremely dangerous." ME/CFS Australia is also calling on the medical profession to stop referring to the condition as chronic fatigue syndrome and to adopt the name myalgic encephalomyelitis. "The view of most patient advocacy groups around the world is that not only does the name chronic fatigue syndrome trivialise the condition, but the principal symptom may not be fatigue," Neathercoat says. "There are so many more symptoms to the illness. Changing the name will help people to finally accept that this condition is very real and very serious." Clara Pirani is The Australian's health reporter. ________________________ Sidebar: SICK AND TIRED Chronic fatigue syndrome, also called CFS/ME (chronic fatigue syndrome/myalgic encephalomyelitis) is an illness characterised by extreme exhaustion. It can strike at any age. The cause is unknown and recovery can take years. Some people don't recover at all and some suffer relapses for the rest of their lives. Symptoms Persistent profound weakness, extreme tiredness after any form of exertion, disrupted sleep, pain and neurological and cognitive problems. Other symptoms include: orthostatic hypotension (a sudden drop in blood pressure when you stand up); orthostatic tachycardia (increased heart rate when you stand up); palpitations; shortness of breath with exertion; muscle twitching; nausea; gastrointestinal and urinary problems; sore throat and tender lymph nodes; marked weight change, extreme loss or gain. Cause The cause is unknown but there are avenues under investigation including: an abnormal response from the central nervous system; an unusual response to a virus; blood pressure abnormalities; viruses or bacteria in the intestines. Other issues Lack of community understanding can lead to depression. Some sufferers are too ill to work, study or socialise. As with other disabilities, depression is common, particularly when other people don't take the condition seriously. Source: Victorian Government © The Australian [Return to top] ------------------------------ Date: Mon, 29 Jan 2007 19:23:30 -0000 From: Tom Kindlon <tomkindlon OCEANFREE.NET> Subject: Re: NOT,RES: An insight into the situation in Belgium Following on from Bart Stouten Ph.D's informative post "An insight into the situation in Belgium": http://listserv.nodak.edu/cgi-bin/wa.exe?A2=ind0701D&L=CO-CURE&P=R3379&I=-3 (or http://tinyurl.com/ynug64 ) I thought I would point out that the same documents are also available in french, see : http://www.riziv-inami.fgov.be/care/fr/revalidatie/studies/study-sfc-cvs/index.htm or http://tinyurl.com/2tj42o "Rapport d’évaluation concernant les centres de référence pour le syndrome de fatigue chronique" The french version of the 181-page report in PDF format is at http://www.riziv-inami.fgov.be/care/fr/revalidatie/studies/study-sfc-cvs/pdf/rapport.pdf Or http://tinyurl.com/39rq96 The URL for the version in Dutch has changed to: http://riziv-inami.fgov.be/care/nl/revalidatie/studies/study-sfc-cvs/pdf/rap port.pdf or http://tinyurl.com/3xb4ak Tom Kindlon [Return to top] ------------------------------
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