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[Return to digest index] --------------------------------------------- This is a special digest of Co-Cure Research & Medical posts only Problems? Write to mailto:firstname.lastname@example.org --------------------------------------------- ---------------------------------------------------------------------- Date: Tue, 12 Jun 2007 16:54:55 -0400 From: "Marcia L. Harmon <MLHarmon cfids.org> via Co-Cure Moderator" Subject: NOT,RES: CFIDS Association Issues Press Release on New CFS Prevalence Study The CFIDS Association has issued a press release about the new CFS prevalence study in Population Health Metrics. The full text of the release can be read at http://www.cfids.org/sparkcfs/pr060807.pdf According to the study authors, it is not certain that the prevalence rate found in Georgia can be extrapolated to the entire United States. But if this rate were to be found to be replicable, the prevalence of adults with CFS in the U.S. would be around 4 million, which is the figure Dr. William Reeves has frequently cited in presentations based on the Georgia study data. The 7.5 million figure in Peter White's commentary appears to include all Americans, not Americans between the ages of 18-59, which is the age demographic strictly applicable to the 2.54% prevalence found in Georgia. The exact prevalence rate will no doubt continue to be revised as researchers learn more about CFS, debate the merits of specific methodology for estimating prevalence, and refine their methodology accordingly in new studies. This has happened over the past decade as methods have evolved and prevalence numbers have been revised especially with regard to large community-based studies. And it will continue in the absence of a lab test or biomarker to more accurately define the number of people who are suffering from CFS. There has long been concern in the patient and scientific communities that earlier prevalence studies may not have reflected the real number of Americans suffering with CFS. The new methodology used in the Georgia study can, and will, be debated over the coming weeks and months in the CFS research community. That debate is healthy and part of a larger scientific process that we all hope leads to progressively more accurate estimates of the number of Americans living with CFS. But in the meantime, we need more research investigating cause and cure and identifying more effective treatments for people who are suffering every day with this life-altering illness. Please look for more information and varying perspectives on the new prevalence study in the next issues of the CFIDS Chronicle and CFIDSLink. Marcia Harmon Director of Communications CFIDS Association of America [Return to top] ------------------------------ Date: Tue, 12 Jun 2007 17:06:40 -0400 From: "Stephanie Barr <sbarr FMAWARE.ORG> via Co-Cure Moderator" Subject: NOT,RES: National Fibromyalgia Association Applauds Results of NIH/NIAMS Study on Gabapentin as Effective Treatment for Fibromyalgia FOR IMMEDIATE RELEASE 12 June 2007 National Fibromyalgia Association Applauds Results of NIH/NIAMS Study on Gabapentin as Effective Treatment for Fibromyalgia ORANGE, Calif----For years, fibromyalgia patients have been anxiously awaiting the day when there will be a drug approved specifically for fibromyalgia, the common, often difficult to treat chronic pain illness many have dismissed as all in the heads of patients. Now, that day is closer than ever. New research supported by the National Institutes of Health's National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) shows that the anticonvulsant medication gabapentin, which is used for certain types of seizures, can be an effective treatment for the pain and other symptoms associated with fibromyalgia. In the NIAMS-sponsored, randomized, double-blind clinical trial of 150 women (90%) and men with the condition, Lesley M. Arnold, M.D., director of the Women's Health Research Program at the University of Cincinnati College of Medicine, and her colleagues found that those taking gabapentin at dosages of 1,200 to 2,400 mg daily for 12 weeks displayed significantly less pain than those taking placebo. Patients taking gabapentin also reported significantly better sleep and less fatigue. For the majority of participants, the drug was well tolerated. The most common side effects included dizziness and sedation, which were mild to moderate in severity in most cases. Lynne Matallana who founded the National Fibromyalgia Association (NFA) in 1997 after spending 2 years in bed and visiting 37 doctors before being correctly diagnosed, applauded the study's findings: "The favorable results of Dr. Lesley Arnold's NIAMS supported clinical study on the use of Gabapentin as an effective treatment for the pain and related symptoms of fibromyalgia, gives the fibromyalgia community renewed hope that science is making inroads into finding effective drugs for the treatment of this chronic disorder," said Matallana. "As this study and other new clinical trials prove the safety and efficacy of certain medications, hope for a future that will include effective treatments is brighter than ever before." NIAMS Director Stephen I. Katz. M.D., Ph.D., remarked that "While gabapentin does not have Food and Drug Administration approval for fibromyalgia, I believe this study offers additional insight to physicians considering the drug for their fibromyalgia patients. Fibromyalgia is a debilitating condition for which current treatments are only modestly effective, so a study such as this is potentially good news for people with this common, painful condition." [The following is reprinted from the NIH/NIAMS announcement released on 6/11]: Fibromyalgia is a chronic disorder characterized by chronic, widespread muscle pain and tenderness, and is frequently accompanied by fatigue, insomnia, depression, and anxiety. It affects three million to six million Americans, mostly women, and can be disabling. The precise cause of fibromyalgia in not known, but research suggests it is related to a problem with the central nervous system's processing of pain. As with some other chronic pain conditions, people with fibromyalgia often develop a heightened response to stimuli, experiencing pain that would not cause problems in other people. Yet, unlike many other pain syndromes, there is no physical evidence of inflammation or central nervous system damage. Although gabapentin has little, if any, effect on acute pain, it has shown a robust effect on pain caused by a heightened response to stimuli related to inflammation or nerve injury in animal models of chronic pain syndromes. Researchers have suspected that it might have the same effect in people with fibromyalgia. The new research, published in the April 2007 edition of Arthritis & Rheumatism, indicates the suspicions were correct. Although the researchers cannot say with certainty how gabapentin helps reduce pain, Dr. Arnold says one possible explanation involves the binding of gabapentin to a specific subunit of voltage-gated calcium channels on neurons. "This binding reduces calcium flow into the nerve cell, which reduces the release of some signaling molecules involved in pain processing," she says. How gabapentin improves sleep and other symptoms is less clear, and there are probably different mechanisms involved in fibromyalgia symptoms. "Gabapentin improved sleep, which is an added benefit to patients with fibromyalgia who often report unrefreshing or disrupted sleep," Dr. Arnold says. What is important is that people with fibromyalgia now have a potential new treatment option for a condition with few effective treatments. "Studies like this give clinicians evidence-based information to guide their treatment of patients," says Dr. Arnold. The mission of the National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), a part of the Department of Health and Human Services' National Institutes of Health, is to support research into the causes, treatment and prevention of arthritis and musculoskeletal and skin diseases; the training of basic and clinical scientists to carry out this research; and the dissemination of information on research progress in these diseases. For more information about NIAMS, call the information clearinghouse at (301) 495-4484 or (877) 22-NIAMS (free call) or visit the NIAMS website at http://www.niams.nih.gov The National Institutes of Health (NIH) The Nation's Medical Research Agency includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. It is the primary federal agency for conducting and supporting basic, clinical and translational medical research, and it investigates the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit www.nih.gov. ABOUT THE NFA: The National Fibromyalgia Association is a non-profit 501(c)(3) organization whose mission is to develop and execute programs dedicated to improving the quality of life for people with fibromyalgia by increasing the awareness of the public, media, government and medical communities. The NFA publishes a quarterly magazine, Fibromyalgia AWARE and hosts an award-winning website at www.FMaware.org. ---#--- [Return to top] ------------------------------ Date: Wed, 13 Jun 2007 15:20:25 -0700 From: "CF-Alliance <cf_alliance yahoo.com>.....................via Co-Cure Moderators Subject: MED: Gabapentin Shown Effective For Fibromyalgia Pain Source: NIH/National Institute of Arthritis and Musculoskeletal and Skin Diseases Date: June 12, 2007 Gabapentin Shown Effective For Fibromyalgia Pain http://www.sciencedaily.com/releases/2007/06/070611122223.htm [Return to top] ------------------------------ Date: Thu, 14 Jun 2007 18:34:38 +0200 From: Jan van Roijen <j.van.roijen CHELLO.NL> Subject: med: Incline Village & Myalgic Encephalomyelitis ~~~~~~~~~~~~~~~~~~~~~~~~~~~~ Send an Email for free membership ~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~ >>>> Help ME Circle <<<< >>>> 14 June 2007 <<<< Editorship : j.van.roijen chello.nl Outgoing mail scanned by Norton AV ~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~ From: DEnlander aol.com Reference: *START recognizing ME!!!!* by LK Woodruff; Help ME Circle, 12 June 2007, who wrote between other things: It is important for all reading this article to remember that the Lake Tahoe outbreak in the '80's appears, in retrospect, to have actually been yet another ME (Myalgic Encephalomyelitis) outbreak. And that USA CDC staff then CHOSE to ignore that illness and it's decades-long corroborating documentation, and instead decided to say they were seeing a new, emerging illness...which they named it 'CFS'. See for the whole article: http://listserv.nodak.edu/cgi-bin/wa.exe?A2=ind0706b&L=co-cure&T=0&P=3428 `````````````` Unfortunately the Incline Village patients were not reported in the context that they suffered from a known disease. A disease that Melvin Ramsay reported previously in 1955. His work at the Royal Free Hospital in London resulted in the term Myalgic Encephalomyelitis. If the correlation would have been made with this work, the outbreak may have received more consideration. However the doctors in this small tucked away ski village, a remote place called Incline Village, were not in contact with a medical library and thought, or wished to think, they had discovered a new disease. Unfortunately, sadly, they have never even now recognized Ramsay and his salutary work. Derek Enlander MD New York [Return to top] ------------------------------ Date: Fri, 15 Jun 2007 05:45:51 +0200 From: Jan van Roijen <j.van.roijen CHELLO.NL> Subject: med,res: Nitric Oxide Cycle & Therapy ~~~~~~~~~~~~~~~~~~~~~~~~~~~~ Send an Email for free membership ~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~ >>>> Help ME Circle <<<< >>>> 15 June 2007 <<<< Editorship : j.van.roijen chello.nl Outgoing mail scanned by Norton AV ~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~ Sources: http://molecular.biosciences.wsu.edu/faculty/pall/pall_main.htm http://www.haworthpress.com/store/find.asp Martin L. Pall, Professor of Biochemistry and Basic Medical Sciences; Washington State University <martin_pall wsu.edu> 509-335-1246 In his new book: *Explaining "Unexplained Illnesses": Disease Paradigm for Chronic Fatigue Syndrome, Multiple Chemical Sensitivity, Fibromyalgia, Post-Traumatic Stress Disorder, Gulf War Syndrome and Others, Haworth Medical Press*, Prof. Martin L. Pall mentions a list of agents predicted to down-regulate NO/ONOO cycle biochemistry ~jvr `````````````` Therapy ~~~~~~ The fifth principle of the NO/ONOO- cycle is that therapy should focus on down-regulating NO/ONOO- cycle biochemistry. In other words, lower the cause of illness. Let me state at the outset that I am a Ph.D., not an M.D. and nothing here should be viewed as medical advice. There are several challenges to therapies aimed at lowering NO/ONOO- cycle biochemistry. * The first of these is that we need to stop doing things that up-regulate this biochemistry and there are various stressors that up-regulate this biochemistry therefore are of obvious concern. * The second is that the complexity of the NO/ONOO- cycle makes it difficult to down-regulate and makes it likely that we will need to use multiple agents in order to be effective in such down-regulation. We don't have a magic bullet to treat these illnesses and may have to rely, therefore, on complex combinations of agents each of which may produce an incremental improvement by lowering aspects of the cycle mechanism. * The third is that peroxynitrite, the most central element in the NO/ONOO- cycle is difficult to effectively scavenge in vivo and therefore approaches based solely on scavenging peroxynitrite may not be expected to be effective. Let's consider the first of these challenges. Such stressors as chemical exposure in MCS, excessive exercise in CFS and psychological stress, especially in PTSD, should be avoided to have any expectation of effective therapy. Each of these stressors are expected to up-regulated NO/ONOO- cycle activity in these individual illnesses. Foods to which individuals have developed food allergies should be avoided, as antibody- antigen reactions cause tissues to increase nitric oxide synthesis. Excitotoxins can stimulate NMDA activity and up-regulate NO/ONOO- cycle biochemistry and should therefore be avoided. Excitoxins include monosodium glutamate, aspartame and possibly certain other flavorings such as hydrolyzed vegetable proteins. In Chapter 15 of my book, I consider 30 different agents or classes of agents that are available today and are predicted to down-regulate NO/ONOO- cycle biochemistry and are predicted, therefore, to be potentially useful therapeutic agents. I will add a 31 st such agent that was suggested to me by Dr. Jacob Teitelbaum. Each of these are listed in the long table that follows. Table 3 Agents Predicted to Down-Regulate NO/ONOO Cycle Biochemistry Agent (or class) Mechanism(s) Evidence Tocopherols/ tocotrienols Chain breaking antioxidants. Gamma-tocopherol may have special role in peroxynitrite scavenging and tocotrienols are reported to have special roles in protecting from excitoxicity Ascorbate Chain breaking antioxidant; may also scavenge peroxynitrite; helps to regenerate other antixoxidants CT Coenzyme Q10 Stimulates mitochondrial function, scavenges peroxynitrite, lowers NMDA activity CT selenium Antioxidant properties, selenium compounds are peroxynitrite scavengers, replete deficiencies carotenoids Scavenge peroxynitrite in membranes flavonoids Complex group of phenolic antioxidants with multiple and variable functions; chain breaking antioxidants, lower NF- kB activity, scavenge peroxynitrite, superoxide and nitric oxide, allow regeneration of other antioxidants CT TMG, choline, SAMe, others Compounds with methyl groups attached to positively charged nitrogens or sulfurs act to relieve reductive stress CT Carnitine/ acetyl carnitine Improved transport of fatty acids into mitochondrion for energy metabolism and regeneration of mitochondrial inner membrane; others? CT phospholipids May allow regeneration of oxidized mitochondrial inner membrane lipids; phosphatidyl choline may act to lower reductive stress CT? Hydroxocobalamin (B 12) Potent nitric oxide scavenger; limited uptake when taken orally; other forms of B 12 may act as precursor but with probable lower efficacy. CT Vitamin B 6; pyridoxal phosphate Lowers excitoxicity by improving balance between glutamate and GABA CO/A Riboflavin and also 5'-phosphate May increase glutathione reductase activity and thus increase reduction of oxidized glutathione Other B vitamins Improve energy metabolism, replete deficiencies Reduced glutathione and precursors Reduced glutathione not effective taken orally; precursors should probably be limited in dosage used. Most important antioxidant synthesized in body, many functions. CO/A a-lipoic acid Helps restore reduced glutathione, antioxidant activity, regenerate other antioxidants, lowers NF- kB activity ; quality of supplements seems to be quite variable Mg 2+ Magnesium acts to lower NMDA activity, improve energy metabolism, replete deficiencies CT Zn 2+, Mn 2+, Cu 2+ Precursors of superoxide dismutases, antioxidant activity, replete deficiencies; doses should be modest riluzole Lowers glutamate release, excitoxicity taurine Lowers excitoxicity, NF- kB activity, iNOS induction, Ca 2+ NMDA antagonists; gabapentin Lower excessive NMDA activity, lower response to chemical exposure in MCS CT Inosine Increases uric acid pools which scavenges, in turn, peroxynitrite breakdown products; may also act to speed recovery of ATP pools; possible down-side may include increased mast cell activity Long chain omega-3 fatty acids Lower iNOS induction, lower NF- kB activity, replete deficiencies CT Agents that lower NF- kB activity Lower NF- kB activity CO/A? Curcumin Similar of flavonoids in actions Algal supplements Rich in antioxidants CT Hyperbaric O 2 treatment May act via hydrogen peroxide to induce synthesis of tetrahydrobiopterin and therefore decrease NOS uncoupling CT Minocycline/ tetracyclines Lowers iNOS induction, NMDA activity creatine Lowers excitotoxicity Lowers vanilloid activity, Panax ginseng? Guaifenesin? Expected to lower vanilloid activity CO/A? carnosine Reported peroxynitrite scavenger, unusual antioxidant TRH Lowers NMDA activity D-ribose Increases recovery of ATP pools after energy metabolism dysfunction; may increase reduction of oxidized glutathione CO/A Evidence is listed as being clinical trial evidence (CT) or clinical observations/anecdotal evidence (CO/A) or none, based solely on studies of CFS, MCS, FM or closely related illnesses. It can be seen from Table 3 that there are many different agents that are promising candidates for therapy. Most of them are nutritional supplements. There is some evidence for efficacy of individual agents based on clinical trials (CT) or from clinical observations and/or anecdotal evidence (CO/A) but in most cases, the individual agents where they seem to be effective, have relatively modest effectiveness. The suggestion is that combinations of these agents may be much more effective than individual agents. This combination therapy has been the approach taken by five different physicians in developing their treatment protocols and such combination therapy approaches appear to be the most promising of all therapeutic approaches for treatment of these illnesses. Five physicians have developed complex treatment protocols for these multisystem illnesses. Three of these have focused on the treatment of chronic fatigue syndrome or closely related fatiguing illness, one on both chronic fatigue syndrome and fibromyalgia and one on chemically sensitive patients. Each of these protocols uses from 14 to 18 different agents or classes of agents that are predicted to down-regulate NO/ONOO- cycle biochemistry! While two of these protocols (Teitelbaum's and Cheney's) contain substantial numbers of agents not obviously related to the NO/ONOO- cycle, each contains many agents predicted to down-regulate the cycle. The treatment protocols are outlined in the lists that follow: Dr. Paul Cheney has developed his treatment protocol based on clinical observations and has honed it over the past two decades of treatment of chronic fatigue syndrome patients. He advises trying to avoid things that exacerbate the NO/ONOO- cycle mechanism, some of the same things that I discussed above. Specifically he suggests attenuating GI tract problems by such strategies as going on a low food allergen diet, minimizing environmental chemical exposure and also minimizing inflammatory diseases, such as around the teeth. The agents that I list are followed, in some cases, by comments on how they may act-those comments are mine, not Cheney's. * High dose hydroxocobalamin (B12) injections- potent nitric oxide scavenger * Whey protein-glutathione precursor * Guaifenesin-vanilloid antagonist? * NMDA blockers * Magnesium-lowers NMDA activity * Taurine-antioxidant and acts to lower excitotoxicity including NMDA activity * GABA agonists-GABA acts as an inhibitory neurotransmitter to lower NMDA activity-these include the drug neurontin (gabapentin) * Histamine blockers-mast cells which release histamine are activated by both nitric oxide and vanilloid stimulation (Chapter 7) and may therefore be part of the cycle mechanism * Betaine hydrochloride (HCl)-Betaine lowers reductive stress, the hydrochloride form should only be used in those with low stomach acid. Betaine (trimethylglycine) is also listed separately in the protocol description Antioxidants listed as follows: * Flavonoids, including "bioflavonoids," olive leaf extract, organic botanicals, hawthorn extract * Vitamin E (forms not listed) * Coenzyme Q10-acts both as antioxidant and to stimulate mitochondrial function * a-lipoic acid * Selenium * Omega-3 and –6 fatty acids * Melatonin-as an antioxidant that may act in the brain * Pyridoxal phosphate-improves glutamate/GABA ratio * Folic acid-lowers uncoupling of nitric oxide synthases Cheney prescribes for his patients a total of 18 distinct agents or classes of agents, each of which can be viewed as down-regulating aspects of the NO/ONOO- cycle. I would argue that this in not just coincidental, that it argues in support of the NO/ONOO- cycle mechanism. Dr. Jacob Teitelbaum has published placebo-controlled trial data supporting the efficacy of one version of his protocol (29,30), something none of these other physicians has done. It seems to be effective on both chronic fatigue syndrome and fibromyalgia patients. I am going to describe a recent version of his complex protocol, focusing on what may be the central parts of the protocol, the parts described as "nutritional treatments" and "mitochondrial energy treatments." The last agent in the list, D-ribose, was added to the protocol recently (personal communication). * Daily energy B-complex-B vitamins including high dose B 6, riboflavin, thiamine, niacin and also folic acid. These fall into four categories that I have listed earlier in the chapter * Betaine hydrochloride (HCl)-lowers reductive stress, hydrochloride form should only be taken by those deficient in stomach acid * Magnesium as magnesium glycinate and magnesium malate-lowers NMDA activity-often uses magnesium injections * a-Lipoic acid-important antioxidant helps regenerate reduced glutathione * Vitamin B 12 IM injections, 3 mg injections (does not state whether this is hydroxocobalamin)-may act as potent nitric oxide scavenger * Eskimo fish oil-excellent source of long chain omega-3 fatty acids. Lowers iNOS induction, anti-inflammatory * Vitamin C * Grape seed extract (flavonoid) * Vitamin E, natural-does not state whether this includes g-tocopherol or tocotrienols * Physician's protein formula, used as glutathione precursor * Zinc-antioxidant properties and copper/zinc superoxide dysmutase precursor * Acetyl-L-carnitine-important for restoring mitochondrial function * Coenzyme Q10-both important antioxidant properties and stimulates mitochondrial function * D-ribose-acts to increase rate of ATP and reduced glutathione regeneration If you consider that the oral B vitamins fall into four categories listed earlier in the chapter, Teitelbaum uses a total of 18 agents or classes of agents that are predicted to down-regulate the NO/ONOO- cycle, in the core part of his treatment protocol. Dr. Garth Nicolson started his scientific career developing the famous Singer/Nicolson, fluid mosaic model of biological membranes, a model that is described in essentially all of the standard biochemistry textbooks. He and his colleagues have published on open label trials of a complex proprietary mixture known as NT factor TM, apparently designed to improve mitochondrial and thus energy metabolism function. The trials have been on a group of older patients with unexplained chronic fatigue, and consequently there is some question whether these patients have CFS. Nevertheless, Nicolson and coworkers (31-33) report statistically significant improvements in fatigue and in several other changes often found in multisystem disease patients, affective/meaning, sensory and cognitive/mood. Many of the NT factor components are predicted to lower much of the NO/ONOO- cycle biochemistry. Unfortunately, there is no detailed description of the concentrations of the components of the NT factor proprietary mixture. The mixture contains the following components that are predicted to lower NO/ONOO- cycle biochemistry: * Polyunsaturated phosphatidyl choline-predicted to lower reductive stress * Other phosphatidyl polyunsaturated lipids-this and the phosphatidyl choline are predicted to help restore the oxidatively damaged mitochondrial inner membrane * Magnesium-lowers NMDA activity, may aid in energy metabolism * Taurine-antioxidant activity and lowers excitoxicity including NMDA activity * Artichoke extract-as flavonoid source? * Spirulina-blue-green alga is a highly concentrated antioxidant source * Natural vitamin E-does not tell us whether this includes g -tocopherol or tocotrienols * Calcium ascorbate-vitamin C * a -Lipoic acid-important antioxidant, key role in regeneration of reduced glutathione, but also has role in energy metabolism * Vitamin B 6-balance glutamate and GABA levels, lowers excitotoxicity * Niacin-role in energy metabolism * Riboflavin-important in reduction of oxidized glutathione back to reduced glutathione; also has important role in mitochondrial function * Thiamin-role in energy metabolism * Vitamin B 12-as nitric oxide scavenger? * Folic acid-lowers nitric oxide synthase uncoupling The way I have categorized these earlier on this site and in Chapter 15 of my book, these agents fall into 15 distinct classes of agents expected to lower NO/ONOO- cycle biochemistry. Dr. Neboysa (Nash) Petrovic is a South African physician who, I believe, also has a clinic in England. His CFS treatment protocol (34) has been described as follows (I am unsure how current this is): * Valine and isoleucine-branched chain amino acids known to be involved in energy metabolism in mitochondria, and may be expected,therefore, to stimulate energy metabolism; modest levels may also lower excitotoxicity * Pyridoxine (B 6)-improves balance between glutamate and * GABA, lowers excitotoxicity * Vitamin B 12 in the form of cyanocobalamin-cyanocobalamin is converted to hydroxocobalamin in the human body but the latter form will be more active as a nitric oxide scavenger, since it does not require such conversion * Riboflavin-helps reduce oxidized glutathione back to reduced glutathione * Carotenoids (alpha-carotene, bixin, zeaxanthin and lutein)-lipid (fat) soluble peroxynitrite scavengers * Flavonoids (flavones, rutin, hesperetin and others) * Ascorbic acid (vitamin C) * Tocotrienols-forms of vitamin E reported to have special roles in lowering effects of excitotoxicity * Thiamine (aneurin)-B vitamin involved in energy metabolism * Magnesium * Zinc * Betaine hydrochloride (HCl)-lowers reductive stress, hydrochloride form should only be used by those deficient in stomach acid * Essential fatty acids including long chain omega-3 fatty acids * Phosphatidyl serine-reported to lower iNOS induction (35,36) According to the way I have listed these agents, his protocol contains 14 agents or classes of agents predicted to down-regulate NO/ONOO- cycle biochemistry. [Return to top] ------------------------------ Date: Sat, 16 Jun 2007 16:53:58 -0400 From: <fredspringfield VERIZON.NET> Subject: RES: History of chronic fatigue syndrome [History of chronic fatigue syndrome] [Article in Japanese] Journal: Nippon Rinsho. 2007 Jun;65(6):975-82 Author: Hashimoto N. Affiliation: Center for Medical Education and Information. NLM Citation: PMID: 17561685 Chronic fatigue syndrome (CFS) is not a new disease. Similar morbidities have been known as different names since past several centuries. For example, neurasthenia, epidemic neuromyasthenia, myalgic encephalomyelitis, Akureyri disease, Royal Free disease, chronic EBV disease, post-viral fatigue syndrome etc. Much of the recent interest in CFS was generated by incidence of infection-like outbreak at Lake Tahoe in Nevada. The Center for Disease Control (USA) realized that correlation was poor between those patients who had virologic evidence of EBV infection and those who had the symptoms of chronic fatigue. This is a review of the history of CFS. (1) Historical perspectives in chronic fatigue cases in past old period, (2) Post-viral infectious fatigue and chronic fatigue (myalgic encephalomyelitis), (3) Recent trend of CFS studies and its clinical similar situation. Finally, I would like to state that we intend to draw up a new diagnostic guideline for CFS in Japan. [Return to top] ------------------------------ Date: Sat, 16 Jun 2007 16:57:03 -0400 From: Fred Springfield <fredspringfield@VERIZON.NET> Subject: RES: Overview of chronic fatigue syndrome focusing around prevalence and diagnostic criteria [Overview of chronic fatigue syndrome focusing around prevalence and diagnostic criteria] [Article in Japanese] Journal: Nippon Rinsho. 2007 Jun;65(6):983-90. Author: Kuratsune H. Affiliation: Faculty of Health Science for Welfare, Kansai University of Welfare Sciences. NLM Citation: PMID: 17561686 Chronic fatigue syndrome (CFS) is an operational concept proposed by Centers for Disease Control and Prevention to clarify the unknown etiology of the syndrome characterized by the sensation of abnormally prolonged fatigue. Lots of investigators reported various abnormalities such as virus infection, immune abnormalities, HPA axis abnormalities, metabolic abnormalities, etc., but there are a few abnormalities common to vast majority cases of CFS. Therefore, lots of people as well as medical doctors are still skeptical about the presence of CFS. However, recent studies reveal that CFS can be understood to be a special condition based on the abnormality of neuroendocrine-immunologic system caused by the psycho-social stress and some genetic components. Under these conditions, a reactivation of various kinds of herpes virus infections and/or chronic infections might occur as a result of immune dysfunction, causing the abnormal production of several cytokines. A distinctive feature of CFS is thought to be the secondary brain dysfunction caused by the abnormal production of several cytokines. In this paper, I show the overview of CFS focusing around prevalence, economic impact and diagnostic criteria in Japan. [Return to top] ------------------------------ Date: Sat, 16 Jun 2007 17:03:42 -0400 From: Fred Springfield <fredspringfield VERIZON.NET> Subject: RES: Viral infections in chronic fatigue syndrome [Viral infections in chronic fatigue syndrome] [Article in Japanese] Journal: Nippon Rinsho. 2007 Jun;65(6):991-6. Authors: Sairenji T, Nagata K. Affiliations: Division of Biosignaling, Department of Biomedical Sciences, School of Life Science, Faculty of Medicine, Tottori University. PMID: 17561687 Chronic fatigue syndrome (CFS) is a heterogeneous illness in which patients can have different, overlapping signs and symptoms. No single underlying cause has been established for all CFS patients. Epidemiological studies reveal that a flu-like sickness precedes the onset in the majority of cases. The major hypothesis of the pathogenesis of CFS is that infectious agents such as viruses, may trigger and lead to chronic activation of the immune system with abnormal regulation of cytokine production. Many studies have been performed to identify the possible microbial triggers and to understand the epidemiological microbial agents. We have summarized the recent progressive literature of virus, rickettsia, and mycoplasma implicated in the pathogenesis of CFS. [Return to top] ------------------------------ Date: Sat, 16 Jun 2007 17:06:10 -0400 From: Fred Springfield <fredspringfield VERIZON.NET> Subject: RES: Genetic background of chronic fatigue syndrome [Genetic background of chronic fatigue syndrome] [Article in Japanese] Journal: Nippon Rinsho. 2007 Jun;65(6):997-1002. Authors: Narita M, Narita N. Affiliation: Graduate School of Medicine, Mie University. NLM Citation: PMID: 17561688 Although previous twin and family studies have suggested the involvement of genetic factor(s) in the pathogenesis of chronic fatigue syndrome (CFS), responsible gene for CFS was not known. We have recently reported the association of serotonin transporter gene polymorphism in CFS. A significant increase of longer (L and XL) alleic variants was found in the CFS patients compared to the controls. Compared to S allele, the L allele is believed to retain higher transcriptional activity, which causes decreased concentration of serotonin in the extracellular space, namely, active serotonin in CFS. These results thus support the serotonin hypothesis in the pathogenesis of CFS. [Return to top] ------------------------------ Date: Sat, 16 Jun 2007 17:23:30 -0400 From: Fred Springfield <fredspringfield VERIZON.NET> Subject: RES: Clinical features of chronic fatigue syndrome--symptoms [Clinical features of chronic fatigue syndrome--symptoms] [Article in Japanese] Journal: Nippon Rinsho. 2007 Jun;65(6):1011-5. Authors: Ban N, Saiki T, Ko G, Kuwahata A. Affiliation: Department of General Medicine, Nagoya University School of Medicine. NLM Citation: PMID: 17561690 Chronic fatigue syndrome (CFS) is a clinically defined condition characterized by long-lasting disabling fatigue, resulting in severe impairment in daily functioning and associated symptoms such as memory and concentration difficulties, muscle aches, sleep disturbances, and headache. Common symptoms encountered in CFS patients were reviewed and top 10 common symptoms were described in detail with special reference to the particular features of each symptom helpful to diagnose CFS. [Return to top] ------------------------------ Date: Sat, 16 Jun 2007 21:21:34 -0400 From: Fred Springfield <fredspringfield VERIZON.NET> Subject: RES: Chronic fatigue syndrome and neurotransmitters [Chronic fatigue syndrome and neurotransmitters] [Article in Japanese] Journal: Nippon Rinsho. 2007 Jun;65(6):1005-10. Authors: Miwa S, Takikawa O. Affiliation: Department of Cellular Pharmacology, Hokkaido University Graduate School of Medicine. NLM Citation: PMID: 17561689 Chronic fatigue syndrome (CFS) is an idiopathic illness characterized by persistent fatigue, which could be caused by a variety of etiologic factors including viral infection, abnormal production of cytokines and abnormal acylcarnitine metabolism. Recent studies suggest that CFS is closely associated with attenuation of central synaptic transmission mediated by neurotransmitters such as serotonin and glutamate. Attenuation of serotonin neurotransmission can be caused by increased expression of serotonin transporter, which results either from viral infection and subsequent production of interferon--alpha or from abnormal promoter for serotonin transporter gene. Other neurotransmitter systems may be also involved in CFS mediated by abnormal acylcarnitine metabolism and autoantibodies for neurotransmitter receptors. In this review, we focus recent data on CFS in terms of neurotransmitters. [Return to top] ------------------------------ Date: Sat, 16 Jun 2007 21:21:50 -0400 From: Fred Springfield <fredspringfield VERIZON.NET> Subject: RES: Sleep disturbance [Sleep disturbance] [Article in Japanese] Journal: Nippon Rinsho. 2007 Jun;65(6):1017-22. Authors: Kumano-go T, Adachi H, Sugita Y. Affiliation: Osaka University Health Care Center. NLM Citation: PMID: 17561691 Attempts to elucidate the complex pathophysiology of chronic fatigue syndrome (CFS) must consider subjective and objective sleep. Several reports of CFS showed the high rate of sleep disturbance such as insomnia, hypersomnia, circadian rhythm sleep disorder, sleep apnea/hypopnea syndrome and so on. To analyze pulse wave continuously in sleep of CFS patients by laser blood flowmeter, we set base line component (0.01-0.08 Hz) and pulse wave component(0.70-1.50 Hz). Results of FFT analysis indicate that the CFS can have at least three subtypes of pulse dynamics in sleep. There probably are different types of illnesses now contained within the CFS construct, in which identifying subtypes of sleep disturbance can be one important key. [Return to top] ------------------------------ Date: Sat, 16 Jun 2007 21:22:18 -0400 From: Fred Springfield <fredspringfield VERIZON.NET> Subject: RES: Identification and application of marker genes for differential diagnosis of chronic fatigue syndrome [Identification and application of marker genes for differential diagnosis of chronic fatigue syndrome] [Article in Japanese] Journal: Nippon Rinsho. 2007 Jun;65(6):1029-33. Author: Kawai T, Rokutan K. Affiliation: Department of Stress Science, Institute of Health Biosciences, The University of Tokushima Graduate School. NLM Citation: PMID: 17561693 Chronic fatigue syndrome (CFS) is a complex disease and has no laboratory biomarkers, which makes diagnosis of CFS difficult. Several research groups challenged to identify genes specific for CFS; however, there are no overlaps between studies. The U.S. Centers for Disease Control and Prevention reported remarkable gene expression profiles of a large scale cohort study recruited 227 people. Reported genes were mostly different from the previously reported genes, again featuring the complexity of CFS. Separately, we identified 9 genes that were significantly and differentially expressed between CFS patients and healthy subjects using an original microarray. The changes in expression of 9 genes were confirmed by quantitative PCR. We also demonstrated the usefulness of 9 genes for differential diagnosis of CFS. [Return to top] ------------------------------ Date: Sat, 16 Jun 2007 21:22:07 -0400 From: Fred Springfield <fredspringfield VERIZON.NET> Subject: RES: Psychological symptoms in chronic fatigue syndrome [Psychological symptoms in chronic fatigue syndrome] [Article in Japanese] Journal: Nippon Rinsho. 2007 Jun;65(6):1023-7. Author: Yoshiuchi K. Affiliation: Department of Psychosomatic Medicine, The University of Tokyo. NLM Citation: PMID: 17561692 Patients with chronic fatigue syndrome (CFS) frequently complain of psychological symptoms including depression, anxiety, and neuropsychological impairment. In addition, patients with CFS have been reported to be more likely to have psychiatric diseases such as major depressive disorder, panic disorder, generalized anxiety disorder, and personality disorder. In the present review article, psychological symptoms and psychiatric comorbidity in CFS patients were introduced. In addition, differentiation between CFS and psychiatric disorders were discussed, because there have been few studies on comorbidity and differentiation between CFS and undifferentiated somatoform disorder although there has been heated debate about the existence of CFS itself. [Return to top] ------------------------------ Date: Sat, 16 Jun 2007 21:22:31 -0400 From: Fred Springfield <fredspringfield VERIZON.NET> Subject: RES: The evaluation of fatigue by using acceleration plethysmography [The evaluation of fatigue by using acceleration plethysmography] [Article in Japanese] Journal: Nippon Rinsho. 2007 Jun;65(6):1034-42. Author: Yamaguti K. Affiliation: Department of Physiology, Graduate School of Medicine, Osaka City University. NLM Citation: PMID: 17561694 We evaluated the fatigue of patients with chronic fatigue syndrome by using acceleration plethysmography. The changes in the acceleration plethysmography were relatively dominant in the sympathetic nervous system from the viewpoint of the autonomic nervous system, and the fluctuation in the time-series data of the acceleration plethysmography was decreased from the viewpoint of chaos or complexity system. We found the relation between the level of fatigue and the changes in acceleration plethysmography. Therefore, the acceleration plethysmography might be useful for the evaluation of fatigue. [Return to top] ------------------------------ Date: Sat, 16 Jun 2007 21:23:08 -0400 From: Fred Springfield <fredspringfield VERIZON.NET> Subject: RES: Spectroscopic diagnosis of chronic fatigue syndrome by multivariate analysis of visible and near-infrared spectra [Spectroscopic diagnosis of chronic fatigue syndrome by multivariate analysis of visible and near-infrared spectra] [Article in Japanese] Journal: Nippon Rinsho. 2007 Jun;65(6):1051-6. Authors: Sakudo A, Kuratsune H, Hakariya Y, Kobayashi T, Ikuta K. Affiliation: Department of Virology, Research Institute for Microbial Diseases, Osaka University. NLM Citation: PMID: 17561696 We have recently evaluated the possibility of visible and near-infrared (Vis-NIR) spectroscopy for diagnosis of chronic fatigue syndrome(CFS). Vis-NIR spectra in the 600-1,100 nm region for sera from CFS patients and healthy donors were subjected to principal component analysis (PCA) and soft independent modeling of class analogy (SIMCA) to develop multivariate models to discriminate between CFS patients and healthy donors. The PCA and SIMCA model predicted successful prediction of the masked samples. Furthermore, taking advantage of Vis-NIR spectroscopy to enable noninvasive analysis, our preliminary results have shown that SIMCA model from Vis-NIR spectra of thumb has achieved 70-80% correct determinations. In this review, we will introduce the potential of the Vis-NIR spectroscopy for CFS diagnosis. [Return to top] ------------------------------ Date: Sat, 16 Jun 2007 21:22:48 -0400 From: Fred Springfield <fredspringfield VERIZON.NET> Subject: RES: Chronic fatigue syndrome and herpesvirus reactivation [Chronic fatigue syndrome and herpesvirus reactivation] [Article in Japanese] Journal: Nippon Rinsho. 2007 Jun;65(6):1043-8. Author: Kondo K. Affiliation: Department of Virology, The Jikei University School of Medicine. NLM Citation: PMID: 17561695 Human herpesvirus 6(HHV-6) and human herpesvirus 7(HHV-7) establish life-long latency, reactivate frequently, and are shed in saliva. To identify the factor(s) of their reactivation, we have studied the association with the reactivation and fatigue. Reactivation was examined for viral DNA by real-time PCR method. As a result, healthy adults shed the reactivated HHV-6 in the saliva during work -induced fatigue, and the copy number of HHV-6 DNA was reduced after holidays. However, no significant HHV-6 DNA increase was observed in chronic fatigue syndrome (CFS) patients. In contrast, increase of HHV-7 reactivation was observed both in the case of work-induced fatigue and CFS. These findings suggest that the amount of HHV-6 and HHV-7 reactivation can be an objective biomarker for fatigue. [Return to top] ------------------------------ Date: Sat, 16 Jun 2007 21:23:41 -0400 From: Fred Springfield <fredspringfield VERIZON.NET> Subject: RES: Antinuclear antibodies [Antinuclear antibodies] [Article in Japanese] Journal: Nippon Rinsho. 2007 Jun;65(6):1067-70. Author: Nishikai M. Affiliation: National Hospital Organization Tokyo Medical Center. NLM Citation: PMID: 17561698 Significance of antinuclear antibodies (ANA) in the patients with chronic fatigue syndrome (CFS) was reviewed. When indirect immunofluorescence with the HEp-2 cells as the substrates was used, prevalence of the positive ANA was reportedly 15-25%. The ANA titers were low and the immunofluorescent staining patterns were heterogeneous. One group in the USA reported that 'nuclear envelope staining pattern' was found in more than 50% of the patients with CFS. This results, however, have not been confirmed by any other research groups. Clinical significance of the positive ANA in the CFS patients resides in differential diagnoses of systemic lupus erythematosus and other diffuse connective tissue diseases. Recently, several ANAs specific to CFS have been described. We reported anti-68/48kD protein antibodies utilizing SDS-PAGE/ immunoblot method. These autoantibodies were found in 13% of 114 CFS patients and 0% in healthy subjects (p < 0.05). Hypersomnia and difficulty in concentration were found more frequently in the CFS patients with this specific autoantibody. [Return to top] ------------------------------ Date: Sat, 16 Jun 2007 21:23:29 -0400 From: Fred Springfield <fredspringfield VERIZON.NET> Subject: RES: Estimation of fatigue state in patient with CFS using actigraph and R-R interval power spectrum analysis [Estimation of fatigue state in patient with CFS using actigraph and R-R interval power spectrum analysis] [Article in Japanese] Journal: Nippon Rinsho. 2007 Jun;65(6):1057-64. Authors: Tajima S, Kuratsune H, Yamaguti K, Takahashi A, Takashima S, Watanabe Y, Nishizawa Y. Affiliation: Fatigue Clinical Center, Osaka City University Graduate School of Medicine. NLM Citation: PMID: 17561697 OBJECTIVES: In this study, we try to estimate the fatigue state using actigraphy and R-R interval power spectrum analysis. RESULTS: Actigraphy analysis showed that mean awake activity was decreased and duration of sleep was prolonged in patients with chronic fatigue syndrome (CFS), significantly (p < 0.001). Both of sleep episodes in wake period and wake episodes in sleep period were significantly increased in CFS patients in comparison with healthy volunteers (p < 0.001) In autonomic nerve analysis, sleep/awake ratio of high frequency component was significantly decreased in patients with CFS (p < 0.05). CONCLUSION: The quality of sleep in patients with CFS was decreased because of increase of wake episodes in sleep period. Also the lack of parasympathetic activation during sleep period might be associated with the deterioration of sleep quality in patients with CFS. [Return to top] ------------------------------ Date: Sat, 16 Jun 2007 21:24:13 -0400 From: Fred Springfield <fredspringfield VERIZON.NET> Subject: RES: Chronic fatigue syndrome: biochemical examination of blood [Chronic fatigue syndrome: biochemical examination of blood] [Article in Japanese] Journal: Nippon Rinsho. 2007 Jun;65(6):1071-6. Authors: Hakariya Y, Kuratsune H. Affiliation: Department of Virology, Center for Infectious Disease Control, Research Institute for Microbial Diseases, Osaka University. NLM Citation: PMID: 17561699 Though patients with chronic fatigue syndrome (CFS) have lots of complaints, abnormal findings cannot be detected by biochemical screening tests. However, some specialized blood tests have revealed neuroendocrine immune axis abnormalities, which is closely associated with each other. Recent studies indicate that CFS can be understood as a special condition based on abnormality of the psycho-neuro-endocrino-immunological system, with the distinguishing feature of CFS seeming to be the secondary brain dysfunction caused by several cytokines and/or autoantibodies. In this paper, we summarize these abnormalities found in CFS and show the neuro-molecular mechanism leading to chronic fatigue. [Return to top] ------------------------------ Date: Sat, 16 Jun 2007 21:24:33 -0400 From: Fred Springfield <fredspringfield VERIZON.NET> Subject: RES: Overview of medical treatment and management of chronic fatigue syndrome [Overview of medical treatment and management of chronic fatigue syndrome] [Article in Japanese] Journal: Nippon Rinsho. 2007 Jun;65(6):1077-81. Authors: Yoshihara K, Kubo C. Affiliation: Department of Psychosomatic Medicine, Graduate School of Medical Sciences, Kyushu University. NLM Citation: PMID: 17561700 A tailor-made management plan that includes various combinations of non-pharmacologic and pharmacologic therapy for patients with chronic fatigue syndrome (CFS) is important. We present an overview of four aspects of our medical treatment and management for CFS: introduction of our medical management system, summary of our management strategy, non-pharmacologic therapy, and pharmacologic therapy; according to foreign guidelines and the latest studies. The main non-pharmacologic therapies for CFS are rehabilitation and lifestyle guidance. Using a graded exercise therapy, we have constructed a broad management strategy for CFS. Herein we introduce our graded exercise therapy. If the symptoms continue despite careful management of the program by the physician, consultation with a psychiatrist or psychosomatic medicine specialist is necessary. [Return to top] ------------------------------ Date: Sun, 17 Jun 2007 13:02:47 -0400 From: Fred Springfield <fredspringfield VERIZON.NET> Subject: RES: Overview of psychiatric therapy for chronic fatigue syndrome [Overview of psychiatric therapy for chronic fatigue syndrome] [Article in Japanese] Journal: Nippon Rinsho. 2007 Jun;65(6):1082-6. Authors: Yamadera W, Itoh H. Affiliation: Department of Psychiatry, Jikei University School of Medicine. NLM Citation: PMID: 17561701 Chronic fatigue syndrome (CFS) is recognized as a special condition based on abnormality of psycho-neuro-endocrine-immunological system, which is caused by several cytokines and autoantibodies. For CFS diagnosis, it is required to exclude psychiatric diseases which could cause chronic fatigue. On the other hand, recent studies proved the effectiveness cognitive behavioral therapy(CBT) for CFS. Distorted cognition relevant to CFS includes the characteristics such as over adaptation, perfectionism, avoidance and so on. In the CBT for CFS, it is important to quit seeking physical causes, to accept the pathological state as it is, to monitor daily activity and recognize the cognitive and behavioral patterns which might prolong fatigue, to maintain a constant activity level and to make planned increases in activity. [Return to top] ------------------------------ Date: Sun, 17 Jun 2007 13:06:03 -0400 From: Fred Springfield <fredspringfield VERIZON.NET> Subject: RES: Attentive consideration for the treatment of chronic fatigue syndrome [Attentive consideration for the treatment of chronic fatigue syndrome] [Article in Japanese] Journal: Nippon Rinsho. 2007 Jun;65(6):1089-92. Author: Murakami M. Affiliation: Department of Psychosomatic Internal Medicine, Nihon University Itabashi Hospital. NLM Citation: PMID: 17561702 The etiology of chronic fatigue syndrome(CFS) is still unknown and under active discussion, but involvement of psychosocial factors appear to be essential for the onset and clinical course of CFS. As CFS patients complain of many stress-related physical and psychological symptom, it is important to understand the CFS from psychosomatic point of view. Not only for the pharmaceutical treatment, attentive consideration is required for treatment of exhaustion of body and mind of CFS patients. Use of anti-depressants or oriental herb medicine is often effective to relieve the anxiety and depressive condition. Furthermore to augment the self-healing potential, psychosomatic approach is important to modify the life style and behavioral characteristics. [Return to top] ------------------------------ Date: Sun, 17 Jun 2007 13:08:41 -0400 From: Fred Springfield <fredspringfield@VERIZON.NET> Subject: RES: A new treatment: thermal therapy [A new treatment: thermal therapy] [Article in Japanese] Journal: Nippon Rinsho. 2007 Jun;65(6):1093-8. Author: Masuda A, Munemoto T, Tei C. Affiliation: Masuda Clinic. NLM Citation: PMID: 17561703 Thermal therapy using far-infrared ray dry sauna was performed for patients with chronic fatigue syndrome (CFS). Symptoms such as fatigue, pain, and low-grade fever were dramatically improved on two patients. And prednisolone administration was discontinued and became socially rehabilitated 6 months after discharge. On other 11 patients with CFS, physical symptoms such as fatigue and pain improved, too. Furthermore, we reported that repeated thermal therapy had relaxation effect and diminishes appetite loss and subjective complaints in mildly depressed patients. These results suggest that repeated thermal therapy may be a promising method for the treatment of CFS. [Return to top] ------------------------------ Date: Sun, 17 Jun 2007 13:11:17 -0400 From: Fred Springfield <fredspringfield VERIZON.NET> Subject: RES: Childhood chronic fatigue syndrome [Childhood chronic fatigue syndrome] [Article in Japanese] Journal: Nippon Rinsho. 2007 Jun;65(6):1099-1104. Author: Miike T. Affiliation: Department of Child Development, Faculty of Medical and Pharmaceutical Sciences, Kumamoto University Graduate School. NLM Citation: PMID: 17561704 Chronic fatigue syndrome in childhood and adolescents(CCFS) is a complex and debilitation with severe morbidity and confusion. It is common condition with up to 3-5% of children and adolescents showing strange fatigue and confusion for more than 30 days. In this condition, four major symptoms are important: sleep disorders, easy fatigability, disturbed learning and memorization and immunological problems. Routine laboratory studies are similar to adult CFS, although abnormalities can be seen on serum pyruvic acid level, OGTT pattern, deep body temperature rhythm, hormonal secretion rhythm, and cerebral blood flow. For a diagnosis of CCFS, a research group supported by Japanese ministry of health, labor and welfare developed CCFS case definition on 2004. Treatment focused to correct disrupted circadian rhythms and supply of energy. [Return to top] ------------------------------ Date: Sun, 17 Jun 2007 13:14:37 -0400 From: Fred Springfield <fredspringfield VERIZON.NET> Subject: RES: The autonomic function and child chronic fatigue syndrome [The autonomic function and child chronic fatigue syndrome] [Article in Japanese] Journal: Nippon Rinsho. 2007 Jun;65(6):1105-12. Author: Tanaka H. Affiliation: Department of Pediatrics, Osaka Medical College. NLM Citation: PMID: 17561705 It is postulated that child chronic fatigue syndrome (CFS) involves the autonomic nervous system, although the precise mechanism has not been clearly indicated. This paper reviews recent reports focusing the role of the autonomic nervous system which plays in CFS. Many of the methods for measuring autonomic function have appeared in the clinical setting in parallel with advancing computer technology, but these are limited when applied in children. In these blood pressure and heart rate changes during orthostatic stress and these variability are favorably used. As a result, one third of children with CFS showed abnormal cardiovascular adjustment during posture change (orthostatic dysregulation: OD) which is characterized by instantaneous orhthostatic hypotension, postural tachycardia or neurally-mediated syncope. Most of the studies using power spectral analysis of heart rate variability showed sympathetic activation, however no consistent finding has been obtained. In conclusion, autonomic function might be partly involved in CFS such as OD, but its priority in causing CFS is unclear. [Return to top] ------------------------------ Date: Sun, 17 Jun 2007 13:17:54 -0400 From: Fred Springfield <fredspringfield VERIZON.NET> Subject: RES: Usefulness of growth chart in children and adolescents with chronic fatigue syndrome [Usefulness of growth chart in children and adolescents with chronic fatigue syndrome] [Article in Japanese] Journal: Nippon Rinsho. 2007 Jun;65(6):1113-9. Authors: Oki J, Okubo J. Affiliation: Department of Pediatrics, Asahikawa Kosei Hospital. NLM Citation: PMID: 17561706 We presented three sheets of growth chart in children with chronic fatigue syndrome. The growth chart in 14-year-old boy (patient 1) showed decreased weight gain because of too much exercise. After that he complained of nausea, abdominal pain, sleep disturbance and debilitating fatigue. The growth chart in 12-year-old girl (patient 2) revealed increased weight gain because of overeating due to the divorce of her parents. She developed syncope, sleep disturbance, and fatigue during overeating. The growth chart in 13-year-old girl (patient 3) showed decreased weight gain after she developed lymph node enlargement. We diagnosed her as autoimmune fatigue syndrome because of persistent positive antinuclear antibody. Although growth chart will not be able to detect childhood chronic fatigue syndrome prospectively, the chart may be useful for detecting some life events in these children. [Return to top] ------------------------------ Date: Sun, 17 Jun 2007 13:20:49 -0400 From: Fred Springfield <fredspringfield VERIZON.NET> Subject: RES: School phobia and childhood chronic fatigue syndrome (CCFS) [School phobia and childhood chronic fatigue syndrome (CCFS)] [Article in Japanese] Journal: Nippon Rinsho. 2007 Jun;65(6):1121-33. Author: Tomoda A. Affiliation: Department of Child Developmental Sociology, Faculty of Medical and Pharmaceutical Sciences, Kumamoto University. NLM Citation: PMID: 17561707 Chronic fatigue occurring in previously healthy children and adolescents is a vexing problem encountered by pediatric practitioners and the impact of fatigue in youngsters should not be underestimated. In its severe form, it is often associated with mood disorders. Findings in children and adolescent cases suggest that severe unexplained fatigue might precede the development of fatigue-related illness, such as childhood chronic fatigue syndrome (CCFS). This is a disabling condition characterized by severe disabling fatigue and a combination of symptoms, the prominent features being self-reported impairments in concentration and short-term memory, sleep disturbances and autonomic symptoms that cannot be explained by medical or psychiatric illness. We have encountered such patients with these complaints; their major symptoms include: general fatigue, fever, headache (not migraine), and memory disturbance. From our clinical experience, we have inferred that patients with CCFS might experience changes in brain function levels, which induce an autonomic imbalance and engender symptoms such as general fatigue, higher-order level cognitive dysfunction, and memory disturbance. [Return to top] ------------------------------ Date: Sun, 17 Jun 2007 13:28:49 -0400 From: Fred Springfield <fredspringfield VERIZON.NET> Subject: RES: Sympathetic predominance of cardiovascular regulation during mild orthostatic stress in adolescents with chronic fatigue Sympathetic predominance of cardiovascular regulation during mild orthostatic stress in adolescents with chronic fatigue. Journal: Clin Physiol Funct Imaging. 2007 Jul;27(4):231-8 Authors: Wyller VB, Saul JP, Amlie JP, Thaulow E. Affiliations: Department of Pediatrics, Rikshospitalet-Radiumhospitalet Medical Centre, Oslo, and Department of Pysiology, Unievrsity of Oslo, Oslo, Norway. NLM Citation: PMID: 17564672 Haemodynamic abnormalities have been documented in the chronic fatigue syndrome (CFS), indicating functional disturbances of the autonomic nervous system responsible for cardiovascular control. This study was designed to explore the pathophysiology in adolescent CFS-patients by analysing RR-interval (RRI) variability and diastolic blood pressure (DBP) variability during mild orthostatic stress, using an algorithm which accounts for non-stationary biosignals. A total of 27 adolescents with CFS and 33 healthy control subjects having equal age- and sex distribution underwent 15 min of 20 degrees head-up tilt (HUT). The spectral power densities of RRI and DBP were computed in the low-frequency (LF) band (0.04-0.15 Hz) and the high-frequency (HF) band (0.15-0.4 Hz) using an adaptive autoregressive algorithm to obtain a time-varying spectrum. RMSSD, a time domain index of RRI variability, was also computed. At rest, all indices of variability were similar in the two groups. During tilt, CFS patients had a larger increase in the LF/HF ratio (P</=0.001) and normalized LF power of RRI (P</=0.01), and a larger decrease in normalized HF power (P</=0.01) of RRI than controls. CFS patients also had trends towards a larger decrease in absolute HF power of RRI and a larger increase in normalized LF power of DBP. These findings suggest that adolescents with CFS have sympathetic predominance of cardiovascular regulation during very mild orthostatic stress. Possible underlying mechanisms are moderate hypovolemia, abnormalities of reflex control or physical de-conditioning. [Return to top] ------------------------------ Date: Sun, 17 Jun 2007 20:21:20 -0400 From: "Bernice A. Melsky" <bernicemelsky VERIZON.NET> Subject: RES: Functional somatic syndrome: how it could be relevant to rheumatologists Functional somatic syndrome: how it could be relevant to rheumatologists. Mod Rheumatol. 2007;17(3):179-84. Epub 2007 Jun 20. Masuko K, Nakamura H. Department of Bioregulation and Proteomics, Institute of Medical Science, St. Marianna University School of Medicine, 2-16-1, Sugao, Miyamae-ku, Kawasaki, 216-8512, Japan, email@example.com. PMID: 17564771 Functional somatic syndrome (FSS) is defined as a group of related syndromes characterized more by symptoms, suffering, and disability than by structural or functional abnormality. The diagnostic criteria and/or symptoms of FSS often overlap, and co-morbidity is commonly found among the diseases of FSS. For example, patients with irritable bowel syndrome often suffer from chronic pain, and a high percentage of co-morbidity can be found with fibromyalgia. Accumulating evidence indicates the presence of visceral and somatic hyperalgesia in FSS as a common feature, and the central sensitization mechanism has been suggested to play an important role in the pathophysiology of FSS. In the present article, the authors introduce the concept of FSS focusing on its possible relevance to rheumatology in terms of pain perception. A possible implication of mast cells and proteinase-activated receptor-2 (PAR-2) in FSS is also reviewed. [Return to top] ------------------------------ Date: Sun, 17 Jun 2007 20:24:56 -0400 From: "Bernice A. Melsky" <bernicemelsky VERIZON.NET> Subject: RES: Menopause related sleep disorders Menopause related sleep disorders. J Clin Sleep Med. 2005 Jul 15;1(3):291-300. Eichling PS, Sahni J. University of Arizona College of Medicine, Sleep Disorders Center, Tucson, AZ, USA. firstname.lastname@example.org PMID: 17566192 Sleep difficulty is one of the hallmarks of menopause. Following recent studies showing no cardiac benefit and increased breast cancer, the question of indications for hormonal therapy has become even more pertinent. Three sets of sleep disorders are associated with menopause: insomnia/depression, sleep disordered breathing and fibromyalgia. The primary predictor of disturbed sleep architecture is the presence of vasomotor symptoms. This subset of women has lower sleep efficiency and more sleep complaints. The same group is at higher risk of insomnia and depression. The "domino theory" of sleep disruption leading to insomnia followed by depression has the most scientific support. Estrogen itself may also have an antidepressant as well as a direct sleep effect. Treatment of insomnia in responsive individuals may be a major remaining indication for hormone therapy. Sleep disordered breathing (SDB) increases markedly at menopause for reasons that include both weight gain and unclear hormonal mechanisms. Due to the general under-recognition of SDB, health care providers should not assume sleep complaints are due to vasomotor related insomnia/depression without considering SDB. Fibromyalgia has gender, age and probably hormonal associations. Sleep complaints are almost universal in FM. There are associated polysomnogram (PSG) findings. FM patients have increased central nervous system levels of the nociceptive neuropeptide substance P (SP) and lower serotonin levels resulting in a lower pain threshold to normal stimuli. High SP and low serotonin have significant potential to affect sleep and mood. Treatment of sleep itself seems to improve, if not resolve FM. Menopausal sleep disruption can exacerbate other pre-existing sleep disorders including RLS and circadian disorders. [Return to top] ------------------------------ Date: Mon, 18 Jun 2007 04:26:22 +0200 From: Jan van Roijen <j.van.roijen CHELLO.NL> Subject: act,med: ME/CFS -Incomprehensible (prevalence) ~~~~~~~~~~~~~~~~~~~~~~~~~~~~ Send an Email for free membership ~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~ >>>> Help ME Circle <<<< >>>> 18 June 2007 <<<< Editorship : j.van.roijen chello.nl Outgoing mail scanned by Norton AV ~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~ Pat Fero is the President of the Wisconsin CFS Association. She was an ME/CFS patient before her son Casey was born, who was also diagnosed with ME/CFS at the age of 9. On July 4, 2005 her son died in his sleep at the age of 23. The University of Wisconsin forensic pathologist found that Casey died of myocarditis. His heart was infected with disease. There was inflammation, and the tissue was full of viral infection. Casey also had old fibrosis, indicating that the viral infection was not of a new onset. Casey Fero died of Chronic Fatigue Syndrome; the pathologist was shocked about this finding. Although it is well known from the UK ME literature, that patients die from this disease. It must be an agony for this sick mother, who's heart is crying for the bereavement of her dearly loved son, to experience how the CDC is trying to hide the real nature of this unbearable disease. They changed ME into the trivial and insulting name *Chronic FATIGUE Syndrome* and are (with the help of the psychiatric Wesseley School) redefining this disease every so much years; and with every change they expand the criteria ad infinitum.... The last manipulations from William C Reeves et all. are unacceptable. Why are they trying to frustrate research into this disease? What have they to cover up? What is the closely guarded secret behind this mysterious, horrible, contagious and deadly disease? Jan van Roijen `````````````` INCOMPREHENSIBLE ~~~~~~~~~~~~~~~~~ By Pat Fero A Madison, Wisconsin woman e mailed me this morning to say that she read an exchange about the new CDC prevalence figures. It scared her because it put her in a HUGE population of invisibles, making the larger population of "well" people even more uncaring. That bothers me. We do not need vulnerable people stressed, so I told her what I thought and decided to send my thoughts to readers. I am not a scientist or statistician. With so many people posting opinions about the CDC new prevalence estimates, I am unable to keep up with those who have that kind of education and experience. The fact is, I do not process numbers all that well. However, as I work on a plan, a collaborative effort to set up a national CFS information co-op with a mission to get information to those 85% not diagnosed, our work just multiplied to incomprehensible levels. So, with a previous estimate of 800,000 people in the US with CFS ages 18 - 69, I can believe that, let us say 80% are not diagnosed = 640,000. More than likely, a good share of these people are misdiagnosed with primary depression and/or generalized anxiety disorder. CFS mythology, lack of clarity of the diagnosis, and WHEN a patient presents in the course of the illness, might logically cause an MD to MISS a CFS diagnosis which could lead to inappropriate treatment options and an increase in patient symptoms. I know this because I have seen it for 20 years. I can not accept the logic that 7 million people in the US might, MIGHT have CFS = 1,400,000 people ages 18 - 69 diagnosed and the other 5,600,000 people undiagnosed. That equals the entire population, kids and elderly, of the state of Wisconsin or the state of Missouri. Considering that we are working on a project to reach those people who might possibly have CFS, be sick, uninformed and possibly alone and broke, we must think this through. If we believe the CDC figures, then we would have to be insane to expect to reach so many people with so few volunteers and so few Founders funding a toll free number to handle all the callers. The CDC study says that possibly 2.54% of the Georgia population might have CFS. Dr. Reeves and colleagues do not extrapolate this percentile to the entire United States. After all, scientists tell us not to jump to conclusions based on preliminary studies. Yet, in scientific publications that followed the NIH and CDC studies several years ago, that is exactly what was done which is how we ended up with the 800,000 figure in the first place. Well here we are and I accept, extrapolation be damned, that close to one million people in the United States may have CFS. If I accept the NEW data and extrapolate, then I would also have to believe that: 1. We have and epidemic. OOPS...never supposed to use the word epidemic. 2. Uninformed, uncaring MD's ignoring the masses have enabled this epidemic. 3. The WI CFS Assn as well as other organizations are so sheltered that millions of people have never found us in all these years. 4. There is collusion with the media and government to keep this quiet so as not to alarm the masses. 5. Despite the 7 million sick and disabled people, there is no scientific interest. 6. Adding a few million people to the disability rolls is possible. 7. We need to work harder to campaign for funding, build community and increase awareness for a potential 7 million CFS patients.. WOW. Nope. I do not accept the new data. It must reflect the population of people with some generalized fatigue state which might tell us how stressed humans are in 2007. This may be real and terribly unfortunate, but it has nothing to do with CFS as I know it. It has nothing to do with Myalgic encephalomyelitis as I know it. I hope that patients online prepare to talk about this in a calm, reasonable way as inquiries might bring them someone close by who is frightened, unaware of funding and politics and just needs to hear that these new studies do not state the facts. As for me, someone will have to hit me over the head with proof, proof, proof that the methods used in the CDC studies are valid. Until that happens, I will ignore anything that comes from further investigations of CFS by the CDC. It feels like I need to get off thin ice and head to safe ground. [Return to top] ------------------------------ Date: Mon, 18 Jun 2007 16:00:36 +0200 From: Jan van Roijen <j.van.roijen@CHELLO.NL> Subject: med: Myocarditis & viruses associated with CFS ~~~~~~~~~~~~~~~~~~~~~~~~~~~~ Send an Email for free membership ~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~ >>>> Help ME Circle <<<< >>>> 18 June 2007 <<<< Editorship : email@example.com Outgoing mail scanned by Norton AV ~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~ Reference: *myocarditis* in the introduction to *ME/CFS -Incomprehensible (prevalence)* by Pat Fero; see Co-Cure: http://listserv.nodak.edu/cgi-bin/wa.exe?A2=ind0706c&L=co-cure&T=0&P=6554 ~jvr ```````` From: Kristin Loomis <firstname.lastname@example.org> Myocarditis and viruses associated with CFS ~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~ Several viruses associated with CFS also cause myocarditis. Stanford infectious disease specialist Jose Montoya believes that a co-infection of two herpesviruses, HHV-6 & EBV is the root cause for a significant subset of patients diagnosed with chronic fatigue syndrome, based on his success with treating a number of theses patients who had elevated antibodies to HHV-6 & EBV. (Kogelnik 2006) He has also successfully treated a number of patients who had been diagnosed with CFS but in fact had parvovirus B-19. Researchers at the Robert Bosch Medical Center in Stuttgart, Germany recently demonstrated that both HHV-6 and parvovirus B-19 are far more common in myocarditis than was previously believed. The common wisdom among cardiologists has always been that the viruses invlolved were adenovirus or coxsackie viruses. Not only did the German group find 35% or 31 out of 87 biopsies positive for HHV-6 at pathogenic levels, they determined that patients with HHV-6 involvement progressed more frequently toward chronic heart failure. Furthermore, unlike patients with parvovirus B-19 (the most common virus found), patients with HHV-6 had no chest pain and often did not seek treatment until the late stages of disease (Mahroldt, 2006) Kuhl et al found in 2005 found HHV-6 in 23% of 172 myocarditis patient biopsies, and also found that when the virus cleared (which happened spontaneously in 44% of the cases) there was patient improvement in left ventricular ejection fraction, while in patients where the virus did not clear, there was progressive impairment. (Kuhl, 2005) Infectious disease specialist Martin Lerner has found 24-hour Holter monitor abnormalities in Chronic Fatigue Syndrome patients with elevated antibody titers to EBV, CMV or HHV-6. Furthermore, he has demonstrated improvement in both fatigue levels and cardiac function in several small trials of antiviral therapy with ganciclovir and valacyclovir. (Lerner 1993, Lerner 2001, Lerner 2002) Another group of CFS researchers found reduced cardiac output as measured by impedance cardiography in patients with chronic fatigue syndrome. (Peckerman 2003) Although the Stanford group believes that the most important site of persistent viral infection is in the CNS tissue, they are studying the possibility that one or more of these viruses could also be causing subclinical myocarditis in a subset of CFS patients. Montoya is currently conducting a placebo controlled trial of the antiviral drug Valcyte for patients with elevated antibodies to HHV-6 and EBV. He treats parvovirus B-19 patients with high dose IVIG. Kristin Loomis Executive Director HHV-6 Foundation Santa Barbara, CA 805-969-1174 805-695-8465 Fax http://www.hhv-6foundation.org/ [Return to top] ------------------------------ Date: Mon, 18 Jun 2007 13:57:27 -0400 From: "Bernice A. Melsky" <bernicemelsky VERIZON.NET> Subject: RES: Hypothesis: Bipolar Illness with Complaints of Chronic Musculoskeletal Pain Is a Form of Pseudofibromyalgia Hypothesis: Bipolar Illness with Complaints of Chronic Musculoskeletal Pain Is a Form of Pseudofibromyalgia. Semin Arthritis Rheum. 2007 Jun 13; [Epub ahead of print] Wallace DJ, Gotto J. Clinical Professor of Medicine, Cedars-Sinai Medical Center, David Geffen School of Medicine at UCLA, Los Angeles, California. PMID: 17570468 OBJECTIVE: To present a hypothesis accounting for the differential response of bipolar patients diagnosed with fibromyalgia (FM) to standard therapies, taking into account the markedly statistically significant increase of its prevalence in the syndrome. METHODS: All articles relating to the heading bipolar illness AND fibromyalgia as well as bipolar illness AND pain were searched using PubMed and Medline since 1966. The prevalence of bipolar illness in our last 100 FM consultations was reviewed. RESULTS: Ten percent of our 100 most recent FM consultations included patients with an established diagnosis of bipolar illness. They had little if no response to traditional FM interventions and appeared to have vague and uncertain tender point examinations. CONCLUSIONS: Bipolar illness may be associated with a form of chronic musculoskeletal pain complaints that is not FM. Studies into the role that neurotransmitters play in bipolar patients with complaints of musculoskeletal discomfort deserve further exploration. [Return to top] ------------------------------ Date: Mon, 18 Jun 2007 14:01:23 -0400 From: "Bernice A. Melsky" <bernicemelsky VERIZON.NET> Subject: RES: Hypothesis: The Chaos and Complexity Theory May Help our Understanding of Fibromyalgia and Similar Maladies Hypothesis: The Chaos and Complexity Theory May Help our Understanding of Fibromyalgia and Similar Maladies. Semin Arthritis Rheum. 2007 Jun 13; [Epub ahead of print] Martinez-Lavin M, Infante O, Lerma C. National Institute of Cardiology, Mexico City, Mexico. PMID: 17570473 BACKGROUND: Modern clinicians are often frustrated by their inability to understand fibromyalgia and similar maladies since these illnesses cannot be explained by the prevailing linear-reductionist medical paradigm. OBJECTIVE: This article proposes that new concepts derived from the Complexity Theory may help understand the pathogenesis of fibromyalgia, chronic fatigue syndrome, and Gulf War syndrome. METHODS: This hypothesis is based on the recent recognition of chaos fractals and complex systems in human physiology. RESULTS: These nonlinear dynamics concepts offer a different perspective to the notion of homeostasis and disease. They propose that the essence of disease is dysfunction and not structural damage. Studies using novel nonlinear instruments have shown that fibromyalgia and similar maladies may be caused by the degraded performance of our main complex adaptive system. This dysfunction explains the multifaceted manifestations of these entities. CONCLUSIONS: To understand and alleviate the suffering associated with these complex illnesses, a paradigm shift from reductionism to holism based on the Complexity Theory is suggested. This shift perceives health as resilient adaptation and some chronic illnesses as rigid dysfunction. [Return to top] ------------------------------ Date: Mon, 18 Jun 2007 17:12:40 -0400 From: Fred Springfield <fredspringfield VERIZON.NET> Subject: RES: Reflections on Relevance: The Fields of Psychosomatics and Psychotherapy in 2006 Reflections on Relevance: The Fields of Psychosomatics and Psychotherapy in 2006. Journal: Psychother Psychosom. 2007;76(4):203-212. Author: Balon R. Affiliation: Department of Psychiatry and Behavioral Neurosciences Wayne State University School of Medicine, Detroit, Mich., USA. NLM Citation: PMID: 17570958 This article reviews several areas of new and interesting development in the fields of psychosomatics and psychotherapy published in the literature during 2006. These areas are: (1) cardiovascular illness and its interplay with depression; (2) risks and predisposing factors in the areas of mental illness and physical illness; (3) new developments in chronic fatigue syndrome, and (4) new or newly explored/modified (psycho)therapies, especially cognitive-behavioral therapy. In addition, an important area of conflict of interest in psychiatry in particular and in biomedical science in general is discussed, as this issue has reached prominence in the biomedical literature. Copyright (c) 2007 S. Karger AG, Basel. [Return to top] ------------------------------
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