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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, 13 Mar 2007 21:50:45 -0400 From: "Jan van Roijen <j.van.roijen chello.nl> via Co-Cure Moderator" Subject: not,med: Reply -Question to Dr. Peter Manu ~~~~~~~~~~~~~~~~~~~~~~~~~~~~ Send an Email for free membership ~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~ >>>> Help ME Circle <<<< >>>> 13 March 2007 <<<< Editorship : j.van.roijen chello.nl Outgoing mail scanned by Norton AV ~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~ Reference: *Question to Dr. Peter Manu* - Help ME Circle, 11 March 2007- http://www.me-net.combidom.com/index.htm Reactions are welcome: j.van.roijen chello.nl ~jvr `````````` From: Dr. Peter Manu Attached please find my c.v. I do not favor a psychiatric explanation for chronic fatigue syndrome and I explained my position in my book published in 2004 and reviewed by Dr. Komaroff in NEJM. I recognize the fact that patients diagnosed with CFS suffer and have physical and psychological symptoms, but there is no proof that CFS, as currently defined, is a physical or psychiatric disease. In general, I try to avoid misinterpretations of my position by reminding patients and their families that there is a lot of suffering in this world, but not all suffering is due to a physical or mental disease. The fact that such suffering is accompanied by biological abnormalities does not always constitute proof that a disease process is present. A good example is grieving after the loss of a loved one, a state often associated with a dysfunction in the NK cells activity. This does not mean that grief is an immunological disorder or disease. You may also want to know that I'd be much happier to be able to say that CFS is a mood disorder. After all, we can achieve complete, long-lasting remissions in at least 80% of all those suffering from a depressive disorder, while the remission rate for CFS is unfortunately only in the range of 10-25%. Best wishes, Peter ```````````` Curriculum Vitae ~~~~~~~~~~~~~ Peter Manu, MD Office Address ```````````````````` Zucker Hillside Hospital Glen Oaks, NY 11004 (718) 470-8290 License `````````` 1979 New York Certification ```````````````` 1980 American Board of Internal Medicine Academic Appointments ```````````````````````````````` 2000-present - Professor of Clinical Medicine, Psychiatry and Behavioral Sciences - Albert Einstein College of Medicine 1994-1999 - Associate Professor of Medicine and Psychiatry Albert Einstein College of Medicine 1991-1993 - Associate Professor of Medicine and Psychiatry University of Connecticut School of Medicine 1990-1991 - Associate Professor of Medicine University of Connecticut School of Medicine 1983-1989 - Assistant Professor of Medicine University of Connecticut School of Medicine 1980-1983 - Assistant Professor of Medicine State University of New York at Syracuse Clinical and Administrative Positions ```````````````````````````````````````````````` 1993-Present - Director of Medical Services, Hillside Hospital Long Island Jewish Medical Center 1991-1993 - Medical Director, Alcohol and Drug Abuse Treatment Center University of Connecticut Health Center 1989-1991 - Physician in Charge, General Medicine Clinic Newington Veterans Administration Medical Center Coordinator, Primary Care Residency Program University of Connecticut Health Center 1986-1988 - Associate Chief of Staff for Ambulatory Care Newington Veterans Administration Medical Center 1983-1986 - Staff Physician Newington Veterans Administration Medical Center Coordinator, Undergraduate Medical Education Newington Veterans Administration Medical Center 1981-1983 - Director, Primary Care Residency Program Upstate Medical Center, College of Medicine, State University of New York at Syracuse 1980-1981 - Staff Physician Syracuse Veterans Administration Medical Center Clinical Training `````````````````````` 1977-1980 Medical Resident, Booth - Memorial Medical Center, New York - University School of Medicine 1972-1975 Medical Resident, University Hospitals, Bucharest 1970-1972 Rotating Intern, University Hospitals, Bucharest Medical School ```````````````````` 1964-1970 Institute of Medicine and Pharmacy, Bucharest Honors `````````` Best Teacher Award 1982-1983 - Department of Medicine State University of New York at Syracuse Societies Membership ````````````````````````````` American College of Physicians (Fellow) American Federation for Clinical Research Reviewer For Scientific Publications `````````````````````````````````````````````` Acta Psychiatrica Scandinavica American Journal of Medicine Annals of Internal Medicine Biological Psychiatry International Journal of Psychiatry in Medicine Journal of the American Medical Association Journal of Chronic Fatigue Syndrome Journal of Health Psychology Journal of General Internal Medicine Journal of Psychosomatic Research Medical Care New England Journal of Medicine Psychological Medicine Psychosomatics Psychotherapy and Psychosomatics Grant Support `````````````````` Source - National Institute on Alcohol Abuse and Alcoholism Study - Controlled Trials of Buspirone and Fluoxetine in the Prevention of Relapse in Alcoholics Role - Medical Consultant Funding Period - 1991-1992 Source - National Institute on Drug Abuse Study - Carbamazepine Treatment of Cocaine Dependence Role - Medical Consultant Funding Period - 1991-1993 Source - National Institute of Alcohol Abuse and Alcoholism Study - Matching Alcoholism Treatment to Client Heterogeneity Role - Co-investigator Funding Period - 1991-1993 Bibliography ````````````````` Books ```````` 1. Manu P, Suarez RE, Barnett BJ (Editors). Handbook of Medicine in Psychiatry. American Psychiatric Publishing, Inc. 2006. 2. Manu P. The Psychopathology of Functional Somatic Syndromes, Haworth Medical Press, 2004. 3. Manu P. The Pharmacotherapy of Common Functional Syndromes, Haworth Medical Press, 2000. 4. Manu P (Editor). Functional Somatic Syndromes: Etiology, Diagnosis and Treatment, Cambridge University Press, 1998. B. Research Article ``````````````````````````` 5. Correll CU, Harris JL, Pantaleon Moya RA, Frederickson AM, Kane JM, Manu P. Low-density lipoprotein cholesterol in patients treated with atypical antipsychotics: Missed targets and lost opportunities. Schizophrenia Research, 2007 [Epub ahead of print]. 6. Correll CU, Frederickson AM, Kane JM, Manu P. Does antipsychotic polypharmacy increase the risk of metabolic syndrome? Schizophrenia Research 89; 91-100, 2007. 7. Correll CU, Frederickson AM, Kane JM, Manu P. Metabolic syndrome and risk of coronary heart disease in 367 patients treated with second-generation antipsychotic drugs. Journal of Clinical Psychiatry 60:575-583, 2006. 8. Straker D, Correll CU, Kramer-Ginsberg E, Abdulhamid N, Koshy F, Rubens E, Saint-Vil R, Kane JM, Manu P. Cost-effective screening for the metabolic syndrome in patients treated with second generation antipsychotic medications. American Journal of Psychiatry 162:1217-1221, 2005. 9. Manu P. Long-term disability for chronic fatigue syndrome. Journal of Chronic Fatigue Syndrome 3:19-30, 1997. 10. Manu P, Affleck G, Tennen H, Morse PA, Escobar JI. Hypochodriasis influences quality of life outcomes in patients with chronic fatigue. Psychotherapy and Psychosomatics 65:76-81, 1996. 11. Manu P, Lane TJ, Matthews DA, Castriotta R, Watson R, Abeles M. Alpha-delta sleep in patients with a chief complaint of chronic fatigue. Southern Medical Journal 87:465-470, 1994. 12. Manu P, Burleson JA, Kranzler HR. Predictors of irregular discharge from inpatient substance abuse treatment. American Journal on Addictions 3:122-128, 1994. 13. Manu P, Matthews DA, Lane TJ. Food intolerance in patients with chronic fatigue. International Journal of Eating Disorders 13:203-209, 1993. 14. Manu P. The psychiatric morbidity of patients with chronic fatigue. Medecine et Hygiene 51:1927-1929, 1993. 15. Manu P, Lane T, Matthews D. Chronic fatigue and chronic fatigue syndrome: Clinical epidemiology and aetiological classification. In Chronic Fatigue Syndrome, Ciba Symposium No. 173, John Wiley, London, 23-42, 1992. 16. Manu P, Matthews DA, Lane TJ. Panic disorder among patients with chronic fatigue. Southern Medical Journal 84:451-456, 1991. 17. Matthews DA, Lane TJ, Manu P. Antibodies to Epstein-Barr virus in patients with chronic fatigue. Southern Medical Journal 84:832-840, 1991. 18. Kranzler H, Manu P, Hesselbrock V, Lane T, Matthews D. Substance use disorders in patients with chronic fatigue. Hospital and Community Psychiatry 42:924-928, 1991. 19. Lane TJ, Manu P, Matthews DA. Depression and somatization in the chronic fatigue syndrome. American Journal of Medicine 91:335-344, 1991. 20. Manu P, Lane TJ, Matthews DA. How much practice makes perfect? A quantitative measure of the experience needed to achieve procedural competence. Medical Teacher 12:367-369, 1990. 21. Lane TJ, Matthews DA, Manu P. Low yield of physical examinations and laboratory investigations in patients with chronic fatigue. American Journal of Medical Sciences 299:313-318, 1990. 22. Manu P, Lane TJ, White PP. Risk-rate neglect in decisions involving invasive diagnostic procedures. Methods of Information in Medicine 28:20-23, 1989. 23. Manu P, Lane TJ, Matthews DA, Escobar JI. Screening for somatization disorder in patients with chronic fatigue. General Hospital Psychiatry 11:294-297, 1989. 24. Manu P, Matthews DA, Lane TJ, Tennen H, Hesselbrock V, Mendola R, Affleck G. Depression among patients with a chief complaint of chronic fatigue. Journal of Affective Disorders 12:165-172, 1989. 25. Manu P, Lane TJ, Matthews DA. Somatization disorder in patients with a chief complaint of chronic fatigue. Psychosomatics 30:388-395, 1989. 26. Renfro L, Feder HM, Lane TJ, Manu P, Matthews DA. Yeast connection among 100 patients with chronic fatigue. American Journal of Medicine 86:165-168, 1989. 27. Escobar JI, Manu P, Matthews D, Lane T, Swartz M, Canino G. Medically unexplained physical symptoms, somatization disorder and abridged somatization: Studies with the Diagnostic Interview Schedule. Psychiatric Developments 3:235-245, 1989. 28. Snow SG, Calder EA, Taylor LS, Lane TJ, Manu P, Federici C. Screening for cancer and coronary risk factors through a nurse practitioner-staffed preventive health clinic. Preventive Medicine 18:817-823, 1989. 29. Dziadul J, Teague B, Oshinskie L, Manu P. A comparison of lens disorders using undilated and dilated biomicroscopy. New England Journal of Optometry 40:15-18, 1988. 30. Manu P, Tremml PG, Rippey RM, Voytovich AE. Interpretation by students of clinical laboratory results. Medical Teacher 10:219-225, 1988. 31. Manu P, Louis TA, Gottlieb L, Engel P, Rippey RM. Unfavorable outcomes of drug therapy: Subjective probability versus confidence intervals. Journal of Clinical Pharmacy and Therapeutics 13:213-217, 1988. 32. Manu P, Matthews DA, Lane TJ. The mental health of patients with a chief complaint of chronic fatigue: A prospective evaluation and follow up. Archives of Internal Medicine 148:2213-2217, 1988. 33. Manu P, Lane TJ, Matthews DA. The frequency of chronic fatigue syndrome in patients complaining of persistent fatigue. Annals of Internal Medicine 109:554-556, 1988. 34. Dziadul J, Teague B, Oshinskie L, Manu P. A comparison of lens disorders using undilated and dilated biomicroscopy. New England Journal of Optometry 40:15-18, 1988. 35. Manu P, Tremml PG, Rippey RM, Voytovich AE. Interpretation by students of clinical laboratory results. Medical Teacher 10:219-225, 1988. 36. Manu P, Louis TA, Gottlieb L, Engel P, Rippey RM. Unfavorable outcomes of drug therapy: Subjective probability versus confidence intervals. Journal of Clinical Pharmacy and Therapeutics 13:213-217, 1988. 37. Manu P, Matthews DA, Classen DC, Goodspeed RB. Medical subspecialty training and interest in cost-containment education. Journal of General Internal Medicine 2:229-231, 1987. 38. Matty P, Manu P. Outpatient use of beta-blocking agents: Prescribing preferences of physicians in training. Journal of Clinical Pharmacy and Therapeutics 12:409-414, 1987. 39. Manu P, Goodspeed RB, Matthews DA. A quantitative measure of consumer preference in health care delivery. Medical Care 24:86-88, 1986. 40. Manu P, Landaw SA, Williams WJ, Schwartz SE. Analysis of publication output of internal medicine faculty members. Journal of Medical Education 60:860-864, 1985. 41. Manu P, Runge LA. Testing stable angina: Expert opinion versus decision analysis. Medical Care 23:1381-1390, 1985. 42. Manu P, Runge LA, Lee JY, Oppenheim AD. Judged frequency of complications after invasive diagnostic procedures: Systematic biases of a physician population. Medical Care 22:366-370, 1984. 43. Manu P, Runge LA. Biochemical screening for pheochromocytoma: Superiority of urinary metanephrines measurements. American Journal of Epidemiology 120:788-790, 1984. 44. Manu P, Schwartz SE. Patterns of diagnostic testing in the academic setting: The influence of medical attendings subspecialty training. Social Science and Medicine 17:1339-1342, 1983. 45. Manu P, Varade W. Penicillin therapy for asymptomatic neurosyphilis: inpatient, intravenous or outpatient, intramuscular? Lancet 2 (8304): 924-925, 1982 46. Spinowitz BS, Simpson M, Manu P, Charytan C. Dialysis eosinophilia. Transactions of American Society for Artifical Organs 27:161-165, 1981. 47 Karassi A, Manu P, Chirculescu N. Prognostic value of the P wave terminal force in lead V1 at the onset of acute myocardial infarction. Cor e Vasa 19:291-298, 1977. 48. Manu P, Macarie C, Karassi A, Dimitriu CG. Hypercatecholaminuria at the onset of acute myocardial infarction: An unfavorable prognostic sign. Medicina Interna 28:27-32, 1976. 49. Dimitriu CG, Manu P, Karassi A, Draganovici M, Gavrila F. The effect of propranolol and glucose-insulin-potassium solution on the course and prognosis of the acute myocardial infarction. Medicina Interna 28:199-204, 1976. 50. Macarie C, Sitcai N, Manu P. Catecholamine addiction, an iatrogenic complication of the cardiogenic shock in the course of acute myocardial infarction. Revista Sanitara Militara 2:165-169, 1976. 51. Manu P, Mogos G, Sitcai N. Clinical and functional aspects in a case of Pickwick syndrome. Viata Medicala 22:7, 1975. 52. Manu P, Karassi A, Chirculescu N, Rotaru M. Clinical and prognostic implications in 41 cases of left anterior hemiblock at the onset of acute myocardial infarction. Medicina Interna 27:259-264, 1975. 53. Constantineanu M, Manu P. Nonparoxysmal junctional tachycardia. Medicina Interna 26:11-21, 1974. 54. Manu P, Karassi A, Cazan V, Sitcai N, Dimitriu CG. Value of the glucose, insulin, potassium and magnesium treatment in acute myocardian infarction. Medicina Interna 26:565-576, 1974. 55. Karassi A, Nicolau V, Manu P, Ticmeanu F, Draganovici M, Dimitriu CG. The contribution of the heart rhythm and electrocardiogram surveillance to an improved prognosis of major arrhythmias complicating the course of myocardial infarction. Archives Union Medicale Balkanique 11:315-322, 1973. 56. Karassi A, Manu P, Ticmeanu F, Dimitriu CG. Intensive therapy unit for coronary patients. II. Analytical considerations with reference to 155 patients with acute myocardial infarction. Medicina Interna 25:809-826, 1973. 57. Dimitriu CG, Karassi A, Lack S, Zeana C, Dimitriu M, Manu P, Cazan V, Ghinea A. Ruptures of the ventricular wall in myocardial infarction. Medicina Interna 24:1103-1116, 1972. 58. Burnea D, Manu P. Scanning, X-Ray, and clinical aspects of pulmonary tuberculosis associated with carcinoma of the lung. Probleme de Tuberculoza 11:213-231, 1972. 59. Dimitriu CG, Karassi A, Tumaian A, Gavrila F, Manu P, Sava S, Russe G, Ticmeanu F. Electronic surveillance during the intensive care of the coronary patient. Archives Union Medicale Balkanique 10:609-616, 1972. 60. Karassi A, Manu P, Erena R. Urinary catecholamines excretion in acute myocardial infarction. Medicina Interna 23:1209-1224, 1971. C. Review Articles and Book Chapters `````````````````````````````````````````````````` 61. Manu P, Suarez RE, Barnett BJ. Medicine in psychiatry; What do we need to know? In Manu P, Suarez RE, Barnett BJ (Editors) Handbook of Medicine in Psychiatry, American Psychiatric Publishing, Inc, Washington, DC, xxv-xxvii, 2006. 62. Bennett M, Manu P. Pain in extremities. In Manu P, Suarez RE, Barnett BJ (Editors) Handbook of Medicine in Psychiatry, American Psychiatric Publishing, Inc, Washington, DC, 127-135, 2006. 63. Frederickson A, Manu P. Risk assessment prior to electroconvulsive therapy. In Manu P, Suarez RE, Barnett BJ (Editors) Handbook of Medicine in Psychiatry, American Psychiatric Publishing, Inc, Washington, DC, 517-524, 2006. 64. Manu P. Chronic fatigue syndrome: the fundamentals still apply. American Journal of Medicine 108:172-173, 2000. 65. Manu P. Functional somatic syndromes: definition and etiological theories. In Manu P (Editor) Functional Somatic Syndromes, Cambridge University Press, Cambridge, 1-7, 1998. 66. Manu P. Functional somatic syndromes: Exploring common denominators. In Manu P (Editor) Functional Somatic Syndromes, Cambridge University Press, Cambridge, 271-292, 1998. 67. Manu P. Disability evaluation for chronic fatigue syndrome. Journal of Chronic Fatigue Syndrome 3:9-15, 1997. 68. Manu P, Lane TJ, Matthews DA. Idiopathic chronic fatigue: Depressive symptoms and functional somatic complaints. In Demitrack MA and Abbey S (Editors) Chronic Fatigue Syndrome, Guilford Publications, New York, 36-47, 1996. 69. Worner TM, Manu P. The pharmacology of gastrointestinal complications of alcoholism. In Kranzler HR (Editor) The Pharmacology of Alcohol Abuse, Springer-Verlag, Heidelberg, 395-413, 1995. 70. Manu P. Evaluation of patients with chronic fatigue. Primary Care Update 1:126-129, 1994. 71. Manu P, Lane TJ, Matthews DA. Chronic fatigue syndromes in clinical practice. Psychotherapy and Psychosomatics 58:60-68, 1992. 72. Manu P, Lane T, Matthews D. The pathophysiology of chronic fatigue syndrome: Confirmations, contradictions, and conjectures. International Journal of Psychiatry in Medicine 22:395-406, 1992. 73. Manu P. Chronic fatigue: Practical guidelines for the primary caresetting. Consultant 32 (9):71-77, 1992. 74. Escobar JI, Swartz M, Rubio-Stipec M, Manu P. Medically unexplained symptoms: Distribution, risk factors, and comorbidity. In Kirmayer LJ, Robbins JM (Eds). Current Concepts in Somatization: Research and Clinical Perspectives. American Psychiatric Press, Washington, 63-78, 1991. 75. Buchwald D, Gantz NM, Katon WJ, Manu P. (Gregory T, Ed). Chronic fatigue syndrome. Patient Care 25 (May 30):45-58, 1991. 76. Stewart D, Manu P, Wessely S, Straus S, Salit I, Abbey S. Chronic fatigue syndrome (postinfectious neuromyasthenia). Annals of the Royal College of Physicians and Surgeons of Canada 24:509-511, 1991. 77. Matthews DA, Manu P, Lane TJ. Evaluation and management of patients with chronic fatigue. American Journal of the Medical Sciences 302:269-277, 1991. 78. Dimitriu CG, Manu P. Beta adrenergic blocking agents in the treatment of the ischemic heart disease. Medicina Interna 28:97-103, 1976. 79. Karassi A, Manu P. Summary of the prophylaxis and therapy of major complications of acute myocardial infarction. Viata Medicala 21:2-3, 1974. 80. Dimitriu CG, Zeana C, Karassi A, Manu P. Immunological trends in cardiology. Medicina Interna 26:515-522, 1974. 81. Karassi A, Manu P, Dimitriu CG. Free fatty acids dynamic in acute myocardial infarction. Medicina Interna 26:653-658, 1974. 82. Karassi A, Manu P, Nicolau V, Cazan V. The myocardial consequence of hypovolemia. Archives Union Medicale Balkanique 12:721-724, 1974. 83. Constantineanu M, Manu P. The electrogram of the bundle of His in the diagnosis of atrioventricular conduction disturbances. Medicina Interna 25:797-808, 1973. 84. Dimitriu CG, Karassi A, Manu P, Sava S. Intensive therapy unit for coronary patients. I. General considerations. Medicina Interna 25:783-795, 1973. 85. Manu P. Bioclinical advances in the study of alkaline phosphatases. Viata Medicala 20:229-234, 1973. 86. Dimitriu CG, Karassi A, Filipescu Z, Tumaian A, Manu P. The intensive therapy coronary unit. Viata Medicala 20:393-399, 1973. 87. Manu P. Bretylium tosylate: A major antiarrhythmic drug in acute myocardial infarction. Viata Medicala 20:715-717, 1973. 88. Dimitriu CG, Karassi A, Manu P. Theoretical and practical aspects of the treatment of cardiogenic shock in acute myocardial infarction. Medicina Interna 24:391-399, 1972. 89. Karassi A, Manu P. A tentative to integrate hyperglycemia into the post-aggressive response to acute myocardial infarction and its complications. Archives Union Medicale Balkanique 10:237-242, 1972. 90. Karassi A, Manu P, Dimitriu CG. The sudden coronary death. Medicina Interna 24:1087-1102, 1972. 91. Dimitriu CG, Karassi A, Manu P, Gavrila F. Stress and catecholamines in cardiovascular pathology. Medicina Interna 23:1155-1167, 1971. [Return to top] ------------------------------ Date: Wed, 14 Mar 2007 05:57:03 +0100 From: Jan van Roijen <j.van.roijen CHELLO.NL> Subject: res: Is HHV-6 a trigger for ME/CFS? ~~~~~~~~~~~~~~~~~~~~~~~~~~~~ Send an Email for free membership ~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~ >>>> Help ME Circle <<<< >>>> 14 March 2007 <<<< Editorship : j.van.roijen chello.nl Outgoing mail scanned by Norton AV ~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~ Journal of Clinical Virology Volume 37, Supplement 1 , December 2006, Pages S39-S46 HHV-6: an underestimated virus - Proceedings of the 5th International Conference on HHV-6&7 and Abstracts from the 5th International Conference on HHV-6&7 doi:10.1016/S1386-6532(06)70010-5 Is human herpesvirus-6 a trigger for chronic fatigue syndrome? ~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~ Anthony L. Komaroff, a, a Division of General Medicine, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, 10 Shattuck Street, Suite 602, Boston, MA 02115, USA Abstract Chronic fatigue syndrome (CFS) is an illness currently defined entirely by a combination of non-specific symptoms. Despite this subjective definition, CFS is associated with objective underlying biological abnormalities, particularly involving the nervous system and immune system. Most studies have found that active infection with human herpesvirus-6 (HHV-6) - a neurotropic, gliotropic and immunotropic virus - is present more often in patients with CFS than in healthy control and disease comparison subjects, yet it is not found in all patients at the time of testing. Moreover, HHV-6 has been associated with many of the neurological and immunological findings in patients with CFS. Finally, CFS, multiple sclerosis and seizure disorders share some clinical and laboratory features and, like CFS, the latter two disorders also are being associated increasingly with active HHV-6 infection. Therefore, it is plausible that active infection with HHV-6 may trigger and perpetuate CFS in a subset of patients. Keywords: Human herpesvirus-6; Chronic fatigue syndrome; Human; Review Correspondence address: Tel.: +1 617 432 4714; fax: +1 617 432 4719 [Return to top] ------------------------------ Date: Wed, 14 Mar 2007 11:31:49 -0400 From: Fred Springfield <fredspringfield VERIZON.NET> Subject: RES: Orthostatic Intolerance in Chronic Fatigue Syndrome Orthostatic Intolerance in Chronic Fatigue Syndrome Journal: The American Journal of Medicine, Volume 120, Issue 3, Page e13 (March 2007) Authors: Peter C. Rowe, MDa, Katherine E. Lucas, PhDb Affiliations: [a] Department of Pediatrics, Johns Hopkins University School of Medicine, Baltimore, MD USA [b] Department of Pediatrics, Johns Hopkins University School of Medicine, Department of Epidemiology, Johns Hopkins University Bloomberg School of Public Health, Baltimore, MD USA NLM Citation: PMID: 17349421 To the Editor: The main outcome measure in Jones and colleagues' study of the prevalence of orthostatic intolerance in subjects with chronic fatigue syndrome (CFS)1 was a 45-minute head-up tilt test, performed after exclusion of subjects with other medical conditions and subjects being treated with medications used to treat orthostatic intolerance. These exclusions were methodologically necessary to ensure that the observed rate of orthostatic intolerance was associated with CFS and not with the co-morbid medical conditions, and that medication use did not partially treat (and therefore obscure detection of) the underlying circulatory abnormalities. The exclusions came at a steep methodologic cost to the representativeness of the sample. After the exclusion of 41 subjects, and refusal to participate by 23 more, the tilt portion of the study evaluated 10 subjects, just 14% of the original group of 74. The sample was entirely too small to allow firm conclusions to be drawn about the prevalence of orthostatic intolerance overall in those with CFS, or about the relative prevalence of postural tachycardia or neurally mediated hypotension in this group. While not the main focus of the article, Table 7 summarizing the literature on orthostatic intolerance in those with CFS is incomplete. In addition to the small study by DeLorenzo and colleagues of 5 patients with postural tachycardia (reference 10 in the Table), the authors may not have known of a larger study by the same group. That study enrolled 78 subjects with CFS, 22 of whom (28%) developed hypotension during tilt, versus 0 of 38 controls.2 We would also like to clarify the data abstracted in Table 7 from our randomized trial of fludrocortisone (reference 13). Among 171 with CFS who underwent tilt testing, the rate of neurally mediated hypotension was 62%; a further 4% met criteria for postural tachycardia syndrome alone. The combined prevalence of orthostatic intolerance was 66%, not 62% as reported in Table 7. Those who did not develop hypotension were excluded from the treatment portion of the randomized trial, but none of the 171 eligible subjects was excluded from the data on the prevalence of orthostatic abnormalities. We therefore are not sure what the authors meant by the notation "77% excluded." Table 7 also includes some minor typographical errors: reference 20 appears twice (it should be reference 21 the first time, then reference 8 the second time), and reference 34 in Table 7 should be reference 37. Any debate about the precise prevalence of postural tachycardia syndrome or neurally mediated hypotension in CFS has the potential to neglect a critical point. In our studies of orthostatic intolerance, now totaling over 220 subjects with CFS, quiet upright posture has been a strong and consistent physiologic stressor in over 95%. Even when not accompanied by hemodynamic changes, orthostatic stress typically has been associated with a provocation or exacerbation of characteristic CFS symptoms. Others have shown that these symptoms and hemodynamic abnormalities with orthostatic stress can be reversed upon application of external lower-body compression (reference 37). Whether orthostatic disorders are primary or secondary, this evidence suggests that they play an important contributing role in the phenomenology of the illness for a substantial proportion of affected individuals. In contrast to Jones and colleagues, we would agree with Freeman that a better understanding of the mechanisms of the disordered response to orthostatic stress would go a long way toward improving our understanding of the pathophysiology and treatment of CFS symptoms.3 References 1. Jones JF, Nicholson A, Nisenbaum R, et al.. Orthostatic instability in a population-based study of chronic fatigue syndrome. Am J Med. 2005;118:1415e19-1415e28. Abstract: http://listserv.nodak.edu/cgi-bin/wa.exe?A2=ind0512D&L=CO-CURE&P=R1014 2. De Lorenzo F, Hargreaves J, Kakkar VV. Pathogenesis and management of delayed orthostatic hypotension in patients with chronic fatigue syndrome. Clin Auton Res. 1997;7:185-190. 3. Freeman R. The chronic fatigue syndrome is a disease of the autonomic nervous system (Sometimes). Clin Auton Res. 2002;12:231-233. © 2007 Elsevier Inc. All rights reserved. [Return to top] ------------------------------ Date: Wed, 14 Mar 2007 11:45:32 -0400 From: Fred Springfield <fredspringfield VERIZON.NET> Subject: RES: Can submaximal exercise variables predict peak exercise performance in women with chronic fatigue syndrome? Can submaximal exercise variables predict peak exercise performance in women with chronic fatigue syndrome? Journal: Arch Med Res. 2007 Apr;38(3):350-3. Epub 2007 Jan 30. doi:10.1016/j.arcmed.2006.10.009 Authors: Nijs J, [a,b], Demol S, [a], Wallman K. [c] Affiliations: [a] Department of Human Physiology, Faculty of Physical Education & Physiotherapy, Vrije Universiteit, Brussels, Belgium [b] Division of Musculoskeletal Physiotherapy, Department of Health Care Sciences, University College Antwerp, Antwerp, Belgium [c] Human Movement & Exercise Science, University of Western Australia, Perth, Australia Address reprint requests to: Jo Nijs, Vrije Universiteit Brussel, MFYS/Sport, KRO-gebouw -1, Laarbeeklaan 101, B-1090 Brussels, Belgium Received 1 September 2006; accepted 26 October 2006 published online 31 January 2007. NLM Citation: PMID: 17350488 This study aimed at examining whether physiological exercise variables at the submaximal level, defined as 75% of the age-predicted target heart rate, are able to predict peak exercise performance in women with chronic fatigue syndrome (CFS) (n = 222). Subjects performed a bicycle ergometric test against a graded increase in workload until exhaustion with continuous monitoring of electrocardiographic and ventilatory variables. Oxygen uptake at the submaximal level (VO(2SUBMAX)) correlated strongly with peak oxygen uptake (VO(2PEAK)) (r = 0.70). For the prediction of VO(2PEAK), linear regression analysis determined the line of best fit as: Using this equation, the mean error in the prediction was 14.6 ± 11.2% (range 0.1-63.7%). It is concluded that the prediction of VO(2PEAK) based on VO(2SUBMAX) might be useful for analyzing group differences or treatment effects but not for individual (clinical) purposes. Key Words: Submaximal, Exercise test, Prediction, Chronic fatigue syndrome, Fibromyalgia © 2007 IMSS. Published by Elsevier Inc. All rights reserved. [Return to top] ------------------------------ Date: Wed, 14 Mar 2007 12:01:01 -0400 From: "Bernice A. Melsky" <bernicemelsky VERIZON.NET> Subject: RES: Personality styles in patients with fibromyalgia, major depression and healthy controls Personality styles in patients with fibromyalgia, major depression and healthy controls. Ann Gen Psychiatry. 2007 Mar 9;6(1):9 [Epub ahead of print] Nordahl HM, Stiles TC. PMID: 17349053 ABSTRACT: BACKGROUND: The fibromyalgia syndrome (FMS) is suggested to be a manifestation of depression or affective spectrum disorder. We measured the cognitive style of patients with FMS to assess personality styles in 44 patients with fibromyalgia syndrome (FMS) by comparing them with 43 patients with major depressive disorder (MDD) and 41 healthy controls (HC). METHODS: Personality styles were measured by the Sociotropy and Autonomy Scale (SAS) and the Dysfunctional Attitude Scale (DAS). The Structured Clinical interview for DSM Axis I was applied to Axis I disorders, while the Beck Depression Inventory was used to measure depression severity. RESULTS: Patients with FMS in general have a sociotropic personality style similar to patients with MDD, and different from HC, but FMS patients without a lifetime history of MDD had a cognitive personality style different from patients with MDD and similar to HC. CONCLUSIONS: These findings suggest that a depressotypic personality style is related to depressive disorder, but not to FMS. Trial registration: NCT00184106. [Return to top] ------------------------------ Date: Wed, 14 Mar 2007 15:31:26 -0400 From: "Bernice A. Melsky" <bernicemelsky VERIZON.NET> Subject: RES: Management of musculoskeletal pain Management of musculoskeletal pain. Best Pract Res Clin Rheumatol. 2007 Feb;21(1):153-66. Bergman S. Spenshult Hospital, SE 313 92 Oskarstrom, Sweden. PMID: 17350550 Chronic musculoskeletal pain is a major public health problem affecting about one third of the adult population. Pain is often present without any specific findings in the musculoskeletal system and a strictly biomedical approach could be inadequate. A biopsychosocial model could give a better understanding of symptoms and new targets for management. Identification of risk factors for chronicity is important for prevention and early intervention. The cornerstones in management of chronic non-specific, and often widespread, musculoskeletal pain are non-pharmacological. Physical exercise and cognitive behavioral therapy, ideally in combination, are first line treatments in e.g. chronic low back pain and fibromyalgia. Analgesics are useful when there is a specific nociceptive component, but are often of limited usefulness in non-specific or chronic widespread pain (including fibromyalgia). Antidepressants and anticonvulsants could be of value in some patients but there is a need for more knowledge in order to give general recommendations. [Return to top] ------------------------------ Date: Wed, 14 Mar 2007 15:34:11 -0400 From: "Bernice A. Melsky" <bernicemelsky VERIZON.NET> Subject: RES: Fibromyalgia and Overlapping Disorders: The Unifying Concept of Central Sensitivity Syndromes Fibromyalgia and Overlapping Disorders: The Unifying Concept of Central Sensitivity Syndromes. Semin Arthritis Rheum. 2007 Mar 10; [Epub ahead of print] Yunus MB. Professor of Medicine, Section of Rheumatology, The University of Illinois College of Medicine at Peoria, Peoria, Illinois. PMID: 17350675 OBJECTIVES: To discuss fibromyalgia syndrome (FMS) and overlapping conditions, eg, irritable bowel syndrome, headaches, and chronic fatigue syndrome, within the concept of central sensitivity syndromes (CSS). METHODS: A critical overview of the literature and incorporation of the author's own views. RESULTS: The concept of CSS seems viable. It is based on mutual associations among the CSS conditions as well as the evidence for central sensitization (CS) among several CSS members. However, such evidence is weak or not available in other members at this time, requiring further studies. The biology of CSS is based on neuroendocrine aberrations, including CS, that interact with psychosocial factors to cause a number of symptoms. CONCLUSIONS: CSS is an important new concept that embraces the biopsychosocial model of disease. Further critical studies are warranted to fully test this concept. However, it seems to have important significance for new directions for research and patient care involving physician and patient education. Each patient, irrespective of diagnosis, should be treated as an individual considering both the biological and psychosocial contributions to his or her symptoms and suffering. [Return to top] ------------------------------ Date: Thu, 15 Mar 2007 00:34:57 +0100 From: Jan van Roijen <j.van.roijen CHELLO.NL> Subject: res: Can submaximal exercise variables predict peak exercise performance in women with ME/CFS? ~~~~~~~~~~~~~~~~~~~~~~~~~~~~ Send an Email for free membership ~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~ >>>> Help ME Circle <<<< >>>> 15 March 2007 <<<< Editorship : j.van.roijen chello.nl Outgoing mail scanned by Norton AV ~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~ 14 Mar 2007 Fred Springfield posted the abstract of *Can submaximal exercise variables predict peak exercise performance in women with chronic fatigue syndrome?* Nijs J, Demol S, Wallman K. at Co-cure: http://listserv.nodak.edu/cgi-bin/wa.exe?A2=ind0703b&L=co-cure&T=0&P=7349 -------------------------------------------------------------- ~jvr: as fair use I add the discussion section of this article -------------------------------------------------------------- Discussion There is a need for standardized submaximal ergometer tests not only for patients with CFS but for people with various disorders that require close monitoring during exercise (4). Therefore, the present study aimed at examining whether a standardized submaximal ergometer test was able to predict peak exercise performance (including peak aerobic work capacity) in people with CFS. We utilized an exercise protocol (starting at 10 W with an increase of 10 W/min) that has previously been used for the assessment of peak exercise performance in people with CFS (3,11,12,15,16) and defined the submaximal level in accordance with the Aerobic Power Index Test (8,9). The results of the study suggest that exercise variables at the submaximal level are strongly associated with their corresponding variables at the peak (maximal) level. Despite this observation, the associations appeared too weak to predict peak exercise variables with an error margin <10%. Both VO2PEAK and body weight-adjusted VO2PEAK can be predicted from their corresponding submaximal variable with an error margin of 14.6%. For analyzing group differences or treatment effects (research purposes), an error margin of 14.6% might be acceptable and can be taken into account in an a priori power calculation. However, for individual (clinical) purposes, the error range (0.1 - > 60%) should be taken into account. It is therefore concluded that, for clinical purposes, the submaximal exercise testing protocol used here is unable to make an accurate prediction of peak exercise performance in women with CFS. The results should be interpreted in light of the study limitations. Only 71% of the subjects studied here attained the submaximal exercise level, defined as 75% of the agepredicted target heart rate. Thus, the results (and the regression equations) are applicable solely to women attending a specialized chronic fatigue clinic and able to achieve 75% of the age-predicted target heart rate during graded exercise tests. This limits the external validity of the results. Further studies are warranted, for instance, by using the exercise protocol of the Aerobic Power Index Test (an increase of 25 W every minute) or by applying other exercise testing protocols previously used for studying peak exercise performance in people with CFS. Fulcher and White used a treadmill walking test at a constant speed of 5 kph and a gradient increase of 2.5% every 2 min (17). Sargent et al. applied cycle ergometry starting at 0 W with incrementing the power output by 25 W every 2 min (10). Bazelmans and colleagues applied an individually tailored bicycle ergometer test: the workload was increased every minute in steps of 10% of estimated maximal workload (5). In summary, the results of the study suggest that exercise variables at the submaximal level are strongly associated with their corresponding variables at the peak level in women with CFS. VO2PEAK and body weight-adjusted VO2PEAK can be predicted from their corresponding submaximal variable with a mean error margin of 14.6%, which might be acceptable for analyzing group differences or treatment effects. For individual (clinical) purposes, the submaximal exercise testing protocol was found inappropriate for predicting peak exercise performance in women with CFS. [Return to top] ------------------------------ Date: Thu, 15 Mar 2007 13:59:01 -0400 From: Fred Springfield <fredspringfield VERIZON.NET> Subject: RES: Personality and chronic fatigue syndrome: Methodological and conceptual issues Personality and chronic fatigue syndrome: Methodological and conceptual issues. Journal: Clin Psychol Rev. 2007 Jan 27; [Epub ahead of print] Authors: van Geelen SM [a], Sinnema G [a], Hermans HJ [b], Kuis W. [c] Affiliations: [a] Department of Psychology, Wilhelmina Children's Hospital, University Medical Center Utrecht, The Netherlands [b] Faculty of Clinical Psychology and Personality, Radboud University Nijmegen, The Netherlands [c] Department of Immunology, Wilhelmina Children's Hospital, University Medical Center Utrecht, The Netherlands Received 9 December 2005; revised 29 November 2006; accepted 19 January 2007. Available online 27 January 2007. NLM Citation: PMID: 17350740 Among clinical psychologists, consulting physicians, scientific researchers and society in general an image has emerged of patients with chronic fatigue syndrome (CFS) as perfectionist, conscientious, hardworking, somewhat neurotic and introverted individuals with high personal standards, a great desire to be socially accepted and with a history of continuously pushing themselves past their limits. The aim of this article is to (a) give a concise review of the main recent studies on personality and CFS, (b) address the major methodological problems in the study of personality in CFS and (c) discuss some of the conceptual assumptions that seem to limit the research on personality and CFS. The results of the reviewed studies range from no evidence of major differences between the personalities of patients with CFS and controls, to evidence of severe psychopathology and personality disorder in patients with CFS. Although personality seems to play a role in CFS, it is difficult to draw general conclusions on the relation between personality and CFS. It is argued that this is partially due to the diversity and heterogeneity in study methods, patient populations, control groups and CFS case definitions. Personality should be regarded as an important factor to be studied in CFS. However, additional studies are needed, not focusing exclusively on personality disorder, or personality considered on a general trait level. In recent developments in personality research, the continually evolving life narrative that makes sense of, and gives direction to, an individual's life is also regarded as an important aspect of personality. New insights into personality and CFS might be gained by systematically studying the self-narratives of patients with the syndrome. Copyright © 2007 Elsevier Ltd All rights reserved. [Return to top] ------------------------------ Date: Thu, 15 Mar 2007 17:31:47 +0100 From: Jan van Roijen <j.van.roijen CHELLO.NL> Subject: not,med: International ME/CFS Conference 2007 ~~~~~~~~~~~~~~~~~~~~~~~~~~~~ Send an Email for free membership ~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~ >>>> Help ME Circle <<<< >>>> 15 March 2007 <<<< Editorship : j.van.roijen chello.nl Outgoing mail scanned by Norton AV ~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~ International ME/CFS Conference 2007 ~~~~~~~~~~~~~~~~~~~~~~~~~~~~~ Westminster, London 1st May - ME Awareness & Support Day 2nd May - Professionals Conference Day The International ME/CFS Conference 2007 An Update on Clinical Diagnosis, Treatments, Support and Research of Myalgic Encephalomyelitis (ME / CFS) Conference Update: A reminder of the International ME/CFS conference in London in May. News Opening Speech: IiME have pleasure in announcing the opening speech of the International ME/CFS Conference will be given by Mr Norman Lamb, Liberal Democrat Shadow Health Secretary. As work is underway on the new Whittemore Peterson Nevada CFS centre for Neuro-Immune disorders it is an opportune time to remind all that Mrs. Annette Whittemore will be at the London conference discussing this important new centre. (See the full list of presenters below) CPD Accreditation from the Royal colleges has now been given to the IiME International ME/CFS conference. Twelve credits will be given for attendance on both days. Six credits are given to each day and delegates may choose to attend the Professionals Day (2nd May) or the Pre-Conference Day (1st May) - or both days. Discounted rate - Sponsor a Medic: IiME are offering a discounted rate for healthcare staff who are recommended to attend by a local ME Support Group. IiME welcome all professionals who are working with, or have an interest in, ME/CFS. We are very pleased that we have received many enquiries for this scheme. Background: Invest in ME is again holding the International ME/CFS Conference in London in May, 2007. Our ME/CFS conference of 2006 attracted presenters and delegates from eight countries and our DVD of the conference was distributed to over 20 countries including countries in Europe, USA, Canada, Australia and New Zealand. Myalgic Encephalomyelitis (ME) is a serious neurological illness (classified by the World Health Organisation under ICD-10-93.3) that causes severe problems for an estimated 250,000 people in the UK, of whom 25,000 are estimated to be children and young people. It is five times more prevalent than HIV/AIDS in the UK and the leading cause of long term absence of children from school. 2007 will be a critical year for healthcare staff and ME patients. The key-note speaker for Professionals' Day is Dr. Ian Gibson, MP for Norwich North who recently chaired the Parliamentary Inquiry into ME which reported that ME needed to be treated with the same urgency as cancer or heart disease. We expect to have an up-to-date progress report on the status regarding future research strategy from Dr. Gibson and the Medical Research Council. This year the NICE Guidelines on ME are also to be published. The conference will be a unique opportuniy to be informed of the latest research and information from some of the leading experts on ME/CFS in the areas of diagnosis, treatment, epidemiology, paediatrics and research. Conference Information: * The conference takes place over two days * Either one or both days may be attended. * Both days carry maximum CPD accreditation. ME Awareness & Support Day (1st May) is for individuals, ME Patient Groups and Healthcare staff to discuss important issues regarding treatment, guidelines and research of ME/CFS. Professionals Day (2nd May) is for healthcare staff, clinicians, GPs, Paediatricians, researchers, occupational therapists and academics who wish to hear the formal lectures on research, treatments, epidemiology and paediatrics related to ME/CFS. NOTE: Both days are open to all interested in ME/CFS. Discounted rates apply for attendance on both days. Our speakers include some of the foremost experts, researchers and clinicians working with ME/CFS including - * Professor Malcolm Hooper - Emeritus Professor of Medicinal Chemistry, University of Sunderland * Dr. Byron Hyde of the Nightingale Research Foundation, Ottawa, Canada * Dr. Jonathan Kerr - Sir Joseph Hotung Senior Lecturer in Inflammation, St George's University of London * Dr. Kenny de Meirleir - Professor of Physiology and Internal Medicine at Free University of Brussels in Belgium * Dr. Vance Spence Chairman ME Research UK * Dr. Neil Abbot ME Research UK * Dr. Abhijit Chaudhuri - Consultant Neurologist at Essex Centre of Neurological Science * Dr. Sarah Myhill - GP and Secretary of the British Society of Allergy, Environmental and Nutritional Medicine * Dr. Nigel Speight Consultant Paediatrician at University Hospital of North Durham and member of Chief Medical Officer's Working Group on ME/CFS * Professor Basant Puri Consultant at Hammersmith Hospital * Professor Martin Pall Washington State University * Annette Whittemore HHV-6 Foundation, Nevada, USA * Ellen Piro President of Norwegian ME Association * Dr. Derek Pheby Director Unit of Applied Epidemiology, faculty of Applied Sciences, Univ. Western England Conference Registration: We welcome everyone who may be interested to attend this major international conference on ME/CFS. Bookings may also be made by using the internet web-site at - http://www.investinme.org/IIME%20International%20ME%20Conference%202007%20Registration.htm Full details of the conference can be found at ? http://www.investinme.org/IIME%20International%20ME%20Conference%202007%20Home.htm Should you have any further questions relating to the conference please contact us at email@example.com. We look forward to welcoming you to the conference, Yours sincerely, Invest in ME UK Registered Charity Nr. 1114035 Tel: 01603 701980 or 02392 252365 http://www.investinme.org/ [Return to top] ------------------------------ Date: Thu, 15 Mar 2007 14:34:20 -0700 From: Steven Du Pre <isaiah40 SONIC.NET> Subject: NOT, ACT, MED: Compounded medications in danger of prohibitive legislation from Congress Hello, A number of you in the US are taking compounded medications, whether Nexavir, bio-identical hormones, glutathione or vitamin B12 or you are a medical practitioner prescribing compounded medications.. I learned of this from a member of the Nexavir (Kutapressin) newsgroup. "Now the gel form of Nexavir at least might not be available for long. I just got an email from a compounder. I looked for more information. This sentence is from www.iacprx.org -- (go there for more info) "Senators Kennedy (D-MA), Burr (R-NC) and Roberts (R-MO) have circulated a copy of proposed draft legislation that would greatly restrict access to compounded medications. Read more and take action to prevent this legislation from gaining traction on Capitol Hill!" It would be helpful for us to do is write or call our senators, briefly telling why this is a personal threat to our well-being. There are links at the website for filling out email forms to your Senators. I wrote to both of mine. Please do not copy this person's letter - use your own - but here is the meat of her letter - "Two medicines that help me much are under threat by this bill. One of them is something I really cannot live without. The drug is obscure and the big pharmas, in cooperation with the FDA, are never going to let it have special privileges. It is more effective, with less waste, in the compounded form. As it is compounded for me, I can apply the drug to my skin, instead of injecting it intramuscularly. I can apply smaller doses as needed over the course of the day. Expensive--it is our family's largest personal expense, but it is necessary. It is good to use it well." Thanks for your help, Steven Du Pre Poetry website: http://www.angelfire.com/poetry/soareagle/index.html "By words the mind is winged." Aristophanes Website for National Alliance for Myalgic Encephalomyelitis: http://www.name-us.org [Return to top] ------------------------------ Date: Fri, 16 Mar 2007 11:51:32 -0400 From: Fred Springfield <fredspringfield VERIZON.NET> Subject: RES: Exercise Testing in Children and Adolescents with Chronic Fatigue Syndrome Exercise Testing in Children and Adolescents with Chronic Fatigue Syndrome. Journal: Int J Sports Med. 2007 Mar 15; [Epub ahead of print] Authors: Takken T, Henneken T, van de Putte E, Helders P, Engelbert R. Affiliation: Pediatric Physical Therapy and Exercise Physiology, UMC Utrecht, Utrecht, Netherlands. NLM Citation: PMID: 17357961 The objective of this study was to evaluate exercise capacity in children and adolescents diagnosed with Chronic Fatigue Syndrome (CFS). We examined 20 patients (12 girls and 8 boys; mean age 14.9 ± 3.7 years) diagnosed with CFS. Exercise capacity was measured using a maximal exercise test on a bicycle ergometer and an expired gas analysis system. Fatigue was assessed using a questionnaire and a daily activity diary was used to describe activities for three days. Z-scores were calculated using age- and sex-matched reference values. Z-scores in children and adolescents with CFS were - 0.33 ± 1.0 (p = 0.17) for peak oxygen uptake, - 1.13 ± 1.41 (p = 0.002) for relative peak oxygen uptake [ml/kg/min] and - 0.93 ± 1.29 (p = 0.07) for maximal work load. Both heart rate and blood pressure at peak performance were significantly reduced compared to reference values. Fatigue levels were significantly positively associated with age and negatively with blood pressure at peak exercise (p < 0.05). In conclusion maximum exercise testing was feasible in young people with CFS. Maximal exercise capacity was only reduced in a minority of the patients and was related to current physical activity levels. [Return to top] ------------------------------ Date: Fri, 16 Mar 2007 01:50:27 +0100 From: Jan van Roijen <j.van.roijen CHELLO.NL> Subject: med: New Human Cell-Produced Treatment for Anaemia [Please note comments from Nancy Klimas, M.D. after the footnotes to this post.] ~~~~~~~~~~~~~~~~~~~~~~~~~~~~ Send an Email for free membership ~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~ >>>> Help ME Circle <<<< >>>> 15 March 2007 <<<< Editorship : j.van.roijen chello.nl Outgoing mail scanned by Norton AV ~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~ In Help ME Circle, 10 March 2007, the article *Anemia drugs increase death risk* was posted, because these common anaemia drugs can increase the risk of death and other serious problems. Procrit, Epogen and Aranesp are used by some ME/CFS patients (mostly in research) in connection with low red blood cell volume). See Co-Cure http://listserv.nodak.edu/cgi-bin/wa.exe?A2=ind0703b&L=co-cure&T=0&P=2499 This new human cell-produced treatment for anaemia seems to be much saver. ~jvr ```````````` http://www.medadnews.com/News/index.cfm?articleid=423882# TODAY ON PHARMALIVE.COM New Human Cell-Produced Treatment for Anaemia Associated with Chronic Kidney Disease Now Available ~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~ Shire's launch of DYNEPO (epoetin delta) begins across Europe LONDON, 15 Mar 2007 - Today, Shire plc (LSE: SHP, NASDAQ: SHPGY, TSX:SHQ) launched DYNEPO(R)(epoetin delta) in Germany, completing the initial step of a launch programme planned for Europe over the coming months. DYNEPO is a unique erythropoiesis-stimulating agent (ESA), as it is the only ESA produced in human cells. ESAs are agents used in the treatment of anaemia to increase the production of red blood cells. DYNEPO is produced by activating the erythropoietin (EPO) gene in human cells . All other commercially available ESAs are presently made in animal cells. DYNEPO's entry to the market provides a new, effective and well-tolerated choice for both physicians and a wide range of patients who suffer from anaemia as a result of chronic renal failure (CRF).(i) It is approved for use in patients not yet requiring dialysis as well as those with end-stage renal disease (ESRD) on dialysis.(1) DYNEPO will be available in other European markets in the coming months. DYNEPO is supported by a comprehensive clinical efficacy and safety programme and competitive pricing structures designed to reduce the existing economic burden of healthcare to providers treating renal anaemia with ESAs. "This new and different treatment with its proven efficacy and tolerability is a welcome addition to the options available for physicians treating anaemia in chronic kidney disease (CKD) patients," commented Dr Markus Ketteler, Division of Nephrology, Academic Teaching Hospital, Coburg, Germany. "Anaemia can be a very compromising condition for patients suffering with CKD and successfully treating it can improve their quality of life and may reduce the risk of further complications. With the growing numbers of patients with kidney failure, we face a significant challenge to detect, diagnose and treat CKD across Europe," he added. Anaemia is a common and serious complication in patients with CKD, estimated to affect over 180, 000 people in Germany alone.(2,3) Research has shown that anaemia correction improves patients' quality of life by reducing fatigue and increasing both appetite and work capacity.(4) In addition, a study has shown that treatment with an ESA can reduce the crude relative risk of mortality by up to 30%.(4) International and national medical guidelines clearly emphasise the need for correcting haemoglobin levels in patients with anaemia and then maintaining them within a pre-specified range.(5,6,7) Two large-scale Phase III studies have shown that treatment with DYNEPO can effectively increase and maintain mean average haemoglobin at target levels (10-12 g/dL) over a period of up to 52 weeks by either subcutaneous or intravenous administration.(8,9,10) DYNEPO offers flexibility and ease of use for both healthcare practitioners and patients. DYNEPO may be administered intravenously or subcutaneously. It is packaged in pre-filled syringes for subcutaneous, self administration injection and is currently available in five presentations. The syringe is designed for ease of use by patients after training by a medical professional and features a needle safety guard to reduce needle stick injury. DYNEPO should be kept in a refrigerator, but it can be used after a single period of un-refrigerated storage at 25 degrees C or less for up to five days, after which it should be discarded. "The launch of DYNEPO is another milestone in Shire's continuing efforts to focus on improving health outcomes for patients with renal disease and servicing renal units with speciality pharmaceuticals," said Mike Cola, President of Shire's Specialty Pharmaceuticals Business. "DYNEPO's unique human gene activation origin and comprehensive clinical efficacy and safety programme provide physicians with an alternative choice in the management of anaemia. To continue building on these efforts and supporting DYNEPO's entry into the market, we have developed pricing structures that are intended to reduce the economic burden of treating renal anaemia by reducing the total renal healthcare costs currently consumed by ESA treatments," he added. About ERYTHROPOIETIN Erythropoietin is a glycoprotein hormone; the protein core is a sequence of 165 amino acids with four attached carbohydrate residues that make up approximately 40% of the molecular mass.(11) These carbohydrate residues are important for its biological activity within the body.(12) Erythropoietin is normally produced in the kidneys and stimulates the bone marrow to produce red blood cells. Red blood cells contain haemoglobin and are vital for oxygen transportation around the body. If the kidney starts to fail, natural production of erythropoietin declines leading to lower levels of haemoglobin(anaemia). About DYNEPO DYNEPO is the first ESA produced in human cells. This is accomplished by activating the endogenous human erythropoietin gene in a human cell line using specialised gene activating DNA sequences. All other commercially available ESAs are produced in animal cell lines derived from Chinese Hamster Ovary cells or Baby Hamster Kidney cells. Anaemic patients with CKD require treatment with an ESA such as DYNEPO in order to increase red blood cell production. DYNEPO is a registered trademark of Sanofi-Aventis. i) While common terminology is now chronic kidney disease (CKD), some regulatory agencies have not adopted this terminology, instead they refer to chronic renal failure (CRF); these terms are essentially interchangeable. DYNEPO (epoetin delta) is indicated for the treatment of anaemia in patients with CRF and may be used in patients on dialysis and in patients not on dialysis. Notes to Editors SHIRE plc Shire's strategic goal is to become the leading specialty pharmaceutical company that focuses on meeting the needs of the specialist physician. Shire focuses its business on attention deficit and hyperactivity disorder (ADHD), human genetic therapies (HGT), gastrointestinal (GI) and renal diseases. The structure is sufficiently flexible to allow Shire to target new therapeutic areas to the extent opportunities arise through acquisitions. Shire believes that a carefully selected portfolio of products with a strategically alignedand relatively small-scale sales force will deliver strong results. Shire's focused strategy is to develop and market products for specialty physicians. Shire's in-licensing and merger and acquisition efforts are focused on products in niche markets with strong intellectual property protection either in the US or Europe. For further information on Shire, please visit the Company's website: www.shire.com. "SAFE HARBOR" STATEMENT UNDER THE PRIVATE SECURITIES LITIGATION REFORM ACT OF 1995 Statements included herein that are not historical facts are forward-looking statements. Such forward-looking statements involve a number of risks and uncertainties and are subject to change at any time. In the event such risks or uncertainties materialize, Shire's results could be materially affected. The risks and uncertainties include, but are not limited to, risks associated with: the inherent uncertainty of pharmaceutical research, product development, manufacturing and commercialization; the impact of competitive products, including, but not limited to the impact of those on Shire's Attention Deficit and Hyperactivity Disorder (ADHD) franchise; patents, including but not limited to, legal challenges relating to Shire's ADHD franchise; government regulation and approval, including but not limited to the expected product approval dates of SPD503 (guanfacine extended release) (ADHD), SPD465 (extended release triple-bead mixed amphetamine salts) (ADHD); Shire's ability to secure new products for commercialization and/or development; Shire's planned acquisition of New River Pharmaceuticals announced February 20, 2007; and other risks and uncertainties detailed from time to time in Shire's and its predecessor registrant Shire Pharmaceuticals Group plc's filings with the Securities and Exchange Commission, particularly Shire plc's Annual Report on Form 10-K for the year ended December 31, 2006. References 1 DYNEPO, Summary of Product Characteristics, December 2006. 2 The World Factbook. http://www.cia.gov/cia/publications/factbook/print/gm.html Accessed 14 March 2007. 3 National Institute for Health and Clinical Excellence. Anaemia management in people with chronic kidney disease. Costing report. Implementing NICE guidance in England. September 2006. p15. 4 JFE Mann. What are the short-term and long-term consequences of anaemia in CRF patients? Nephrol Dial Transplant 1999; 14 (Suppl 2): 29-36. 5 Kidney Disease Outcomes Quality Initiative. KDOQI Clinical practice guidelines and clinical practice recommendations for anemia in chronic kidney disease. Am J Kid Dis 2006: 47(5): Suppl 3. 6 F Locatelli, P Aljama, P Barany, et al. Revised European best practice guidelines for the management of anaemia in patients with chronic renal failure. Nephrol Dial Transplant 2004; 19 Suppl 2: 6-15. 7 National Collaborating Centre for Chronic Conditions. Published by RCP. Anaemia management in chronic kidney disease. National clinical guideline for management in adults and children. 2006. p19. 8 M Smyth, KJ Martin, RD Pratt. Epoetin delta (Dynepo(R)), erythropoietin produced in a human cell line, is as effective as epoetin alfa in patients with renal anaemia, including those with diabetic nephropathy. Poster presented at the 42nd Annual Meeting of the European Association for the Study of Diabetes (EASD), 14-17 September 2006, Copenhagen-Malmoe, Denmark-Sweden. 9 JTC Kwan, RD Pratt on behalf of the Epoetin Delta 3002 Study Group. Epoetin delta, erythropoietin produced in a human cell line, in the management of anaemia in predialysis chronic kidney disease patients. Curr Med Res Opin 2007; 23(2): 307-311. 10 JTC Kwan. Subcutaneous epoetin delta for the management of anaemia in patients with CKD: safety and efficacy in a one-year study. Poster presented at the American Society of Nephrology (ASN) Renal Week, 14-19 November 2006, San Diego, CA. 11 R Deicher and W Horl. Differentiating factors between erythropoiesis-stimulating agents. Drugs 2004; 64(5): 499-509. 12 V Skibeli, G Nissen-Lie, P Torjesen. Sugar profiling proves that human serum erythropoietin differs from recombinant human erythropoietin. Blood 2001; 98(13): 3626-3634. ********** Date: Fri, 16 Mar 2007 15:09:56 -0400 From: Nancy Klimas MD via Co-Cure Moderator <ray CO-CURE.ORG> Subject: Re: med: New Human Cell-Produced Treatment for Anaemia From Nancy Klimas, MD: [I] would like to comment on the recent email on erythropoietin products. I would appreciate if you would widely disseminate this reply, as I believe CFS patients can be at real risk. [ ... ] If you know of other widely read group mails, feel free to send it on. Erythropoietin warning: As you know there has been a black box warning added to all of the erythropoietin products (Procrit, Epogen, and Aranesp), due to two forms of risk: 1) The potential for products that stimulate red cell production to stimulate tumor growth in patients with breast cancer and head and neck cancer. 2) The need to monitor very carefully when using red cell production stimulants in other conditions (including the anemia induced by cancer, renal failure and HIV medications) due to a risk of blood clots that could lead to stroke, heart attacks, deep vein thrombosis, and pulmonary embolism. The deep vein thrombosis risk and pulmonary embolism risk was also seen in healthy patients receiving the products to control post operative anemia. As you know, the University of Miami CFS research team recently completed a study of erythropoietin, using Procrit, in a phase 2 double blind placebo control study. While we did not have any of these complications in our study, patients were monitored very closely and the drug was titered to very low levels when the red cell expansion exceeded the plasma volume expansion and caused the blood to thicken. This happened very frequently, and doses were dropped in many subjects. Doses anywhere close to the doses suggested in the PDR would be very dangerous and even life threatening. The study's principal investigator, Dr. Barry Hurwitz recently reported the results of this phase 2 study at the 8th International IACFS Conference in Ft Lauderdale. He noted that we were unable to increase the red cell mass to mid-normal levels with erythropoietin and salt alone, restricted by safety concerns. At these lower than projected levels of RBC mass increase, the tilt table test did show a longer time until the onset or orthostatic hypotension. However, the patients' overall function and quality of life was not significantly improved. The results from this phase 2 study are not sufficient to suggest the use of erythropoietin in CFS patients. Should the pharmaceutical world like to review our data, and allow us to design a study that increased the plasma volume in addition to the RBC mass, we would consider another clinical trial. However, I think our data can be viewed in another way, as it would appear the inflammatory cytokines play a role in erythropoiesis suppression. In the future, our studies of immunomodulators that attempt to quiet the inflammatory cytokines will also look at the markers of red cell production. Finally, beware of the new erythropoietin drug, Dynepo, available currently in Europe. My reading of the literature suggests that the problem with the EPO drugs currently on the market is that they do their jobs too well. In the end, it is the act of red blood cell stimulation that induced the tumor growth, or the over production of red cells in relation to the plasma. Anything that pushes that button, should, in theory, hold the same risk. While the new product is derived from human cell lines, I don't see why the inherent risk would be different. As it took many patient years for this risk to become evident with the current products, I would not assume that the lack of vast amounts of safety data is the same as an all out "don't worry this one is safe" reassurance. Just my take on a complicated situation! Sincerely, Nancy Klimas, MD Professor of Medicine and Director CFS/GWI Research Center University of Miami Miller School of Medicine and the Miami VA Medical Center Co-PI NIH RO1 HL65668 (the EPO study) [Return to top] ------------------------------ Date: Fri, 16 Mar 2007 14:37:05 -0400 From: "Bernice A. Melsky" <bernicemelsky VERIZON.NET> Subject: RES: Neuroendocrine Implications of Opioid Therapy Neuroendocrine Implications of Opioid Therapy Current Pain and Headache Reports 2007, 11:89-92 B. Eliot Cole, MD, MPA, American Society of Pain Educators, 7 Oak Place, Suite 7, Montclair, NJ 07042, USA. Email: drcole paineducators.org Opioid analgesics are given to people with pain. These medications are highly effective for relieving pain and are generally considered to have little or no end-organ toxicities. Although they are generally feared because of their potential for abuse, diversion, and psychological dependence, little attention is given to their neuroendocrine consequences. They are known to have central nervous systems effects and are now understood to impact the regulation of gonadotropic hormones. Providing meaningful informed consent requires disclosure about the risks associated with lowered gonadotropic hormone levels. Copyright © 2007 by Current Science, Inc. [Return to top] ------------------------------ Date: Fri, 16 Mar 2007 14:40:29 -0400 From: "Bernice A. Melsky" <bernicemelsky VERIZON.NET> Subject: RES: Does Aerobic Exercise Improve Pain Perception and Mood? A Review of the Evidence Related to Healthy and Chronic Pain Subjects Does Aerobic Exercise Improve Pain Perception and Mood? A Review of the Evidence Related to Healthy and Chronic Pain Subjects Current Pain and Headache Reports 2007, 11:93-97 Martin D. Hoffman, MD and Debi Rufi Hoffman, MA Corresponding author: Martin D. Hoffman, MD Department of Physical Medicine and Rehabilitation (117), Sacramento VA Medical Center, 10535 Hospital Way, Mather, CA 95655, USA. Email: martin.hoffman va.gov Aerobic exercise can cause an acute improvement in mood as well as a reduction in the perception of pain from a painful stimulus. Regular exercise training also may offer some protection from depression, is clinically useful in treating certain psychiatric and chronic pain conditions, and may allow for an enhancement of the acute improvements in mood from a single exercise session. The utility of aerobic exercise training for improving mood disturbances and pain perception among patients with chronic pain requires further investigation. Copyright © 2007 by Current Science, Inc. [Return to top] ------------------------------ Date: Fri, 16 Mar 2007 19:37:56 -0400 From: "Richard Usher <websolutions2 hotmail.com> via Co-Cure Moderator" Subject: NOT,MED: Potential new pain killer drug developed by scientists at Leicester and Italy Potential new pain killer drug developed by scientists at Leicester and Italy Contact: David Lambert dgl3 le.ac.uk 44-011-625-85291 University of Leicester A potential new pain-killing drug developed by medical scientists at the University of Leicester and Ferrara in Italy is to be discussed at a public lecture on 20th March. Professor David Lambert, who has been involved in the development the drug in collaboration with Dr Girolamo Calo in Ferrara Italy, believes the new drug called UFP-101 - avoids many of the side effects of morphine, currently the ‘gold standard’ in pain reduction. Read the complete press release at http://fmsglobalnews.wordpress.com/2007/03/16/potential-new-pain-killer-drug-developed-by-scientists-at-leicester-and-italy/ [Return to top] ------------------------------ Date: Sat, 17 Mar 2007 14:38:32 -0400 From: Fred Springfield <fredspringfield VERIZON.NET> Subject: RES: Infection and vaccination in chronic fatigue syndrome: Myth or reality? Infection and vaccination in chronic fatigue syndrome: Myth or reality? Autoimmunity. 2007 Feb;40(1):48-53. Authors: Appel S, Chapman J, Shoenfeld Y. Affiliation: Department of Neurology, Sheba Medical Center. hashomer. Israel. NLM Citation: PMID: 17364497 Abstract Chronic fatigue syndrome (CFS) is characterized by severe disabling fatigue lasting for more than 6 months associated with physical and mental disturbances such as headache, arthralgia, myalgia, memory impairment, sore throat and tender lymph nodes. The exact pathogenesis is still unknown. Several models were proposed to explain its etiology including chronic infection, endocrine dysfunction, autonomic imbalance, depression, decreased immunity states and an aberrant reaction to infection. No convincing evidence was found to support any of the suggested pathogenic mechanisms. The current concept is that CFS pathogenesis is a multi factorial condition in which an infective agent cause an aberrant immune response characterized by a shift to Th-2 dominant response. When the response fails to be switched-off, a chronic immune activation occurs and clinically expressed as the symptomatology of CFS. Vaccinations are used in order to stimulate the immune system to induce a persistent immunity against the favorable antigens. Several syndromes that contain chronic fatigue as one of their symptoms, such as "Gulf war syndrome" and macrophagic myofasciitis were related to vaccinations. Can vaccinations induce the aberrant immune response of CFS? Little is known about this issue. There are some reports on CFS occurring after vaccination, but few prospective and retrospective studies failed to find such an association. A working group of the Canadian Laboratory Center for Disease Control (LCDC) that was founded in order to examine the suspected association between CFS and vaccinations concluded that there is no evidence that relates CFS to vaccination. Further studies are requested to examine this issue since it is very conceivable that if infection can lead to CFS, vaccination may also lead to it in the same immune-mediated pathogenesis. Keywords Chronic fatigue syndrome, infection, vaccination, Th-2 immune response References Steele, L and Dobbins, JG and Fukuda, K and Reyes, M and Randall, B and Koppel man, M and Reeves, WC. (1998) The epidemiology of chronic fatigue in San Francisco Am J Med, 105, pp. 83S - 90S. Straus, SE. (1988) The chronic mononucleosis syndrome J Infect Dis, 157, pp. 405 - 412. Fukuda, K and Straus, S and Hickie, I and Sharpe, M and Dobbins, J and Komaroff, A. (1994) The chronic fatigue syndrome: A comprehensive approach to its definition and study Ann Intern Med, 121, pp. 953 - 959. Sharpe, M and Archard, LC and Banatvala, JE. (1991) A report chronic fatigue syndrome: Guidelines for research J R Soc Med, 84, pp. 118 - 121. Poteliakhoff, A. (1981) Adrenocortical activity and some clinical findings in chronic fatigue J Psychosom Res, 25, pp. 91 - 95. Moorkens, G and Berwaerts, J and Wynants, H and Abs, R. (2000) Characterization of pituitary function with emphasis on GH secretion in the chronic fatigue syndrome Clin Endocrinol (Oxf), 53, pp. 99 - 106. Cleare, AJ and Blair, D and Chambers, S and Wessely, S. (2001) Urinary free cortisol in chronic fatigue syndrome Am J Psychiatry, 158, pp. 641 - 643. Cleare, AJ and Miell, J and Heap, E and Sookdeo, S and Young, L and Malhi, GS and O'Keane, V. (2001) Hypothalamopituitaryadrenal axis function in chronic fatigue syndrome, and the effects of low-dose hydrocortisone therapy J Clin Endocrinol Metab, 86, pp. 3545 - 3554. Cleare, AJ and Heap, E and Malhi, GS and Wessely, S and O'Keane, V and Miell, J. (1999) Low-dose hydrocortisonee in chronic fatigue syndrome: A randomised crossover trial Lancet, 353(6), pp. 455 - 458. Scott, LV and Svec, F and Dinan, T. (2000) A preliminary study of dehydroepiandrosterone response to low-dose ACTH in chronic fatigue syndrome and in healthy subjects Psychiatry Res, 97, pp. 21 - 28. Kuratsune, H and Yamaguti, K and Sawada, M and Kodate, S and Machii, T and Kanakura, Y and Kitani, T. (1998) Dehydroepiandrosterone sulfate deficiency in chronic fatigue syndrome Int J Mol Med, 1, pp. 143 - 146. Moorkens, G and Wynants, H and Abs, R. (1998) Effect of growth hormone treatment in patients with chronic fatigue syndrome: A preliminary study Growth Horm IGF Res, 8, pp. 131 - 133. Kennedy, G and Spence, V and Underwood, C and Belch, JJ. (2004) Increased neutrophil apoptosis in chronic fatigue syndrome J Clin Pathol, 57, pp. 891 - 893. Patarca, R. (2001) Cytokines and chronic fatigue syndrome Ann N Y Acad Sci, 933, pp. 185 - 200. Gerrity, TR and Bates, J and Bell, DS and Chrousos, G and Furst, G and Hedrick, T and Hurwitz, B and Kula, RW and Levine, SM and Moore, RC and Schondorf, R. (2002/2003) Chronic fatigue syndrome: What role does the autonomic nervous system play in the pathophysiology of this complex illness? Neuroimmunomodulation, 10, pp. 134 - 141. Naschitz, JE and Yeshurun, D and Rosner, I. (2004) Dysautonomia in chronic fatigue syndrome: Facts, hypotheses, implications Med Hypotheses, 62, pp. 203 - 206. Zachrisson, O and Colque-Navarro, P and Gottfries, CG and Regland, B and Mollby, R. (2004) Immune modulation with a staphylococcal preparation in fibromyalgia/chronic fatigue syndrome: Relation between antibody levels and clinical improvement Eur J Clin Microbiol Infect Dis, 23, pp. 98 - 105. Epub 2004 January 20 Prins, JB and Bleijenberg, G and Bazelmans, E and Elving, LD and de Boo, TM and Severens, JL and van der Wilt, GJ and Spinhoven, P and van der Meer, JW. (2001) Cognitive behaviour therapy for chronic fatigue syndrome: A multicentre randomised controlled trial Lancet, 357(9259), pp. 841 - 847. 17 Gold, D and Bowden, R and Sixbey, J and Riggs, R and Katon, WJ and Ashley, R and Obrigewitch, R and Corey, L. (1990) Chronic fatigue: A prospective clinical and virologic study JAMA, 264, pp. 48 - 53. Natelson, BH and Haghighi, MH and Ponzio, NM. (2002) A review of the evidence on the presence of immune dysfunction in chronic fatigue syndrome Clin Diagn Lab Immunol, 9, pp. 747 - 752. Lerner, AM and Dworkin, HJ and Sayyed, T and Chang, CH and Fitzgerald, JT and Beqaj, S and Deeter, RG and Goldstein, J and Gottipolu, P and O'Neill, W. (2004) Prevalence of abnormal cardiac wall motion in the cardiomyopathy associated with incomplete multiplication of Epstein-barr virus and/or cytomegalovirus in patients with chronic fatigue syndrome In Vivo, 18, pp. 417 - 424. Ablashi, DV and Eastman, HB and Owen, CB and Roman, MM and Friedman, J and Zabriskie, JB and Peterson, DL and Pearson, GR and Whitman, JE. (2000) Frequent HHV-6 reactivation in multiple sclerosis (MS) and chronic fatigue syndrome (CFS) patients J Clin Virol, 16, pp. 179 - 191. Soto, NE and Straus, SE. (2000) Chronic fatigue syndrome and herpesviruses: The fading evidence Herpes, 7, pp. 46 - 50. Lane, RJ and Soteriou, BA and Zhang, H and Archard, LC. (2003) Enterovirus related metabolic myopathy: A postviral fatigue syndrome J Neurol Neurosurg Psychiatry, 74, pp. 1382 - 1386. Galbraith, DN and Nairn, C and Clements, GB. (1997) Evidence for enteroviral persistence in humans J Gen Virol, 78, pp. 307 - 312. Straus, SE. (1996) Chronic fatigue syndrome BMJ, 313(5), pp. 831 - 832. Swanink, CM and Melchers, WJ and van der Meer, JW and Vercoulen, JH and Bleijenberg, G and Fennis, JF and Galama, JM. (1994) Enteroviruses and the chronic fatigue syndrome Clin Infect Dis, 19, pp. 860 - 864. Kerr, JR and Bracewell, J and Laing, I and Mattey, DL and Bernstein, RM and Bruce, IN and Tyrrell, DA. (2002) Chronic fatigue syndrome and arthralgia following parvovirus B19 infection J Rheumatol, 29, pp. 595 - 602. McGhee, SA and Kaska, B and Liebhaber, M and Stiehm, ER. (2005) Persistent parvovirus-associated chronic fatigue treated with high dose intravenous immunoglobulin Pediatr Infect Dis J, 24, pp. 272 - 274. Nijs, J and Nicolson, GL and De Becker, P and Coomans, D and De Meirleir, K. (2002) High prevalence of Mycoplasma infections among European chronic fatigue syndrome patients. Examination of four Mycoplasma species in blood of chronic fatigue syndrome patients FEMS Immunol Med Microbiol, 34(15), pp. 209 - 214. Endresen, GK. (2003) Mycoplasma blood infection in chronic fatigue and fibromyalgia syndromes Rheumatol Int, 23, pp. 211 - 215. Epub 2003 July 16 MacDonald, KL and Osterholm, MT and LeDell, KH and White, KE and Schenck, CH and Chao, CC and Persing, DH and Johnson, RC and Barker, JM and Peterson, PK. (1996) A case-control study to assess possible triggers and cofactors in chronic fatigue syndrome Am J Med, 100, pp. 548 - 554. Schutzer, SE and Natelson, BH. (1999) Absence of Borrelia burgdorferi-specific immune complexes in chronic fatigue syndrome Neurology, 53(6), pp. 1340 - 1341. October 12 Gustaw, K. (2003) Chronic fatigue syndrome following tick-borne diseases Neurol Neurochir Pol, 37, pp. 1211 - 1221. NovemberDecember Grayston, JT and Grayston, JT. (1992) Infections caused by Chlamydia pneumoniae strain TWAR Clin Infect Dis, 15(5), pp. 757 - 761. November Chia, JK and Chia, LY. (1999) Chronic Chlamydia pneumoniae infection: A treatable cause of chronic fatigue syndrome Clin Infect Dis, 29, pp. 452 - 453. Nicolson, GL and Gan, R and Haier, J. (2003) Multiple co-infections (Mycoplasma, Chlamydia, human herpes virus-6) in blood of chronic fatigue syndrome patients: Association with signs and symptoms APMIS, 111, pp. 557 - 566. Komaroff, AL and Wang, SP and Lee, J and Grayston, JT. (1992) No association of chronic Chlamydia pneumoniae infection with chronic fatigue syndrome J Infect Dis, 165, pp. 184. Rottem, M and Shoenfeld, Y. (2004) Vaccination and allergy Curr Opin Otolaryngol Head Neck Surg, 12, pp. 223 - 231. Molina, V and Shoenfeld, Y. (2005) Infection, vaccines and other environmental triggers of autoimmunity Autoimmunity, 38, pp. 235 - 245. Schattner, A. (2005) Consequence or coincidence? The occurrence, pathogenesis and significance of autoimmune manifestations after viral vaccines Vaccine, 23(10), pp. 3876 - 3886. Haley, R and Kurt, T. (1997) Self-reported exposure to neurotoxic chemical combinations in Gulf war JAMA, 277, pp. 231 - 237. [CrossRef] Rook, G and Zumla, A. (1997) Gulf war syndrome: Is it due to a systemic shift in the cytokine balance towards a Th 2profile? Lancet, 349, pp. 1831 - 1833. Hotopf, M and David, A and Hull, L and Ismail, K and Unwin, C and Wessely, S. (2000) Role of vaccinations as risk factor for ill health in veterans of the Gulf war: Cross sectional study BMJ(320), pp. 1363 - 1367. Gherardi, RK and Authier, FJ. (2003) Aluminum inclusion macrophagic myofasciitis: A recently identified condition Immunol Allergy Clin North Am, 23, pp. 699 - 712. Alleged link between hepatitis B vaccine and chronic fatigue syndrome CMAJ, 1461 1992. p 1145. Duclos, P. (2003) Safety of immunisation and adverse events following vaccination against hepatitis B Expert Opin Drug Saf, 2, pp. 225 - 231. Zuckerman, JN. (2006) Protective efficacy, immunotherapeutic potential, and safety of hepatitis B vaccines J Med Virol, 78, pp. 169 - 177. Sleigh, KM and Marra, FH and Stiver, HG. (2002) Influenza vaccination: Is it appropriate in chronic fatigue syndrome? Am J Respir Med, 1, pp. 3 - 9. Copyright ©2007, Taylor & Francis Group. All Rights Reserved. [Return to top] ------------------------------ Date: Sat, 17 Mar 2007 22:05:50 -0400 From: "Bernice A. Melsky" <bernicemelsky VERIZON.NET> Subject: RES: Use of mind-body therapies in psychiatry and family medicine faculty and residents: attitudes, barriers, and gender differences Use of mind-body therapies in psychiatry and family medicine faculty and residents: attitudes, barriers, and gender differences. Explore (NY). 2007 Mar-Apr;3(2):129-35. Sierpina V, Levine R, Astin J, Tan A. University of Texas Medical Branch, Galveston, TX. PMID: 17362848 BACKGROUND: Mind-body medicine (MBM) approaches to many health problems have been well documented in the literature, including through multiple meta-analyses. Efficacy has been well demonstrated in conditions such as headache, irritable bowel syndrome, anxiety, fibromyalgia, hypertension, low back pain, depression, cancer symptoms, and postmyocardial infarction. However, an apparent disconnect (ie, translational block) prevents more widespread adoption of such therapies into practice. Biofeedback, relaxation therapy, hypnosis, guided imagery, cognitive behavioral therapy, and psychoeducational approaches are the domain of MBM we examined in assessing physician attitudes, beliefs, and practices. METHODS: Using a Web-based survey, we obtained responses from 74 faculty and resident physicians in the Department of Family Medicine and the Department of Psychiatry. Our response rate was 69%. We conducted descriptive statistics, bivariate analysis, and multivariate analysis using a logistic regression model. Various statistics were chosen depending on the nature of analyzed variables. Synoptic tables are presented. RESULTS: Comparing these cohorts, we found little difference between physicians in the two specialties, but substantial reports that barriers to the use of MBM were largely based on lack of training, inadequate expertise, and insufficient clinic time. Lack of expertise and insufficient clinic time were higher among family physicians than among psychiatrists. There was a high interest in both groups in learning relaxation techniques and meditation and lower interest in biofeedback and hypnosis. Female physicians were significantly more likely to use MBM, both with patients and for their own self-care, and were less likely to be concerned that recommending these therapies would make patients feel that their symptoms were being discounted. Female physicians also had significantly higher beliefs about the benefits of MBM on health disorders in several of the conditions examined, with a consistent though nonsignificant trend in others. [Return to top] ------------------------------ Date: Sun, 18 Mar 2007 11:19:15 -0400 From: "ME/CFS" <me_cfs glocalnet.net> [via Co-Cure Moderators] Subject: RES:Speculative theory for ME Speculative theory for ME Here a speculative theory for an explanation of myalgic enecephalomyelitis (ME) will be presented. The text will be presented as if everything is true, but it is all speculation. The text or the ideas may be used, but only if the author is cited and credited. Speculative understanding of human body: When a healthy individual (person without ME) get an infection it protects itself by several physiological actions. The immune system releases cytokines that influences the CNS in order to change the behaviour of the person. The person shall optimally lie down and rest during an infection. How is this achieved? The person get orthostatic intolerance, so he will feel discomfort when standing up. He looses motivation and so on. This is achieved by an interaction between immune system and CNS. Probably basic mechanisms at several levels collaborate to achieve this change of behaviour. Also pain occurs in order to give the individual discomfort and motivate to rest. The brain is important to protect, therefore the "gates are closed" to the CNS compartment. The CNS compartment is protected by dura mater, but the brain is highly perfused with capillary blood vessels, and this is a "weak point" of the CNS compartment protection. In order to counter this "entry" for pathogens to the CNS compartment, the body has a strategy. The brain has to be highly perfused and nourished during normal function, so it adopts a strategy to "close the gates" when there is a threat. When the immune system signals that there is an infection, the capillaries in the CNS decreases its permeability. This means for example that the brains receives less blood during infection. Certain regions of the brain have their metabolism highly decreased, this can be in order to change the behaviour of the person and/or because some regions are particularly important to keep intact. Speculative theory of ME: The immune system is locked in a dysfunctional mode. This could be due to a combination of effects as for example: inheritance, gene expression (epigenetics), pathogens, toxins and stress. The immune system communicates with the CNS with cytokines and other signals. The CNS changes its mode of function in order to change the behaviour of the individual. Also the blood capillaries of the brain reacts to the immune system response, and they become less permeable. Kasper Ezelius [Return to top] ------------------------------ Date: Sun, 18 Mar 2007 16:50:19 +0100 From: ME/CFS <me_cfs@GLOCALNET.NET> Subject: RES: Hypothesis based research on "the speculative theory for ME" Hypothesis based research on "the speculative theory for ME" Earlier, 2007-03-16, a speculative theory for ME was presented in Co-Cure (http://listserv.nodak.edu/cgi-bin/wa.exe?A2=ind0703c&L=co-cure&T=0&O=D&P=24 49). Here a design of hypothesis based research will be presented with that theory as basis. Compare cerebral blood flow, activity and metabolism for healthy individuals (controls) in their healthy condition and in a condition with infection. Compare this with ME patients. Do controls with infection show any similarities in brain state with ME patients? Check with brain imaging, if any cytokines, interleukines, interferons or other signal from immune system injected in an healthy human or other mammal provoke any change in brain state (cerebral blood flow, activity and metabolism). Observe that the effects may be time dependent and therefore data should be collected as a function of time. Check if capillaries in the brain react (change of dilatation or change of permeability) to any cytokines, interleukines, interferons or other signal from immune system. The permeability should be checked to different molecules and cells. Could be performed in vivo and/or in vitro for humans and other mammals. The ideas and text in this message may be used under the condition that the author is mentioned. /Kasper Ezelius [Return to top] ------------------------------ Date: Sun, 18 Mar 2007 13:32:17 -0400 From: Fred Springfield <fredspringfield VERIZON.NET> Subject: RES: Sense of effort during a fatiguing exercise protocol in chronic fatigue syndrome Sense of effort during a fatiguing exercise protocol in chronic fatigue syndrome. Journal: Res Sports Med. 2007 Jan-Mar;15(1):47-59. Authors: Karen E. Wallman [a]; Paul Sacco [b] Affiliations: [a] School of Human Movement & Exercise Science, The University of Western Australia. Crawley. Western Australia [b] Rehabilitation Neurosciences, University of East London. London. England NLM Citation: PMID: 17365951 The purpose of this study was to determine whether chronic fatigue syndrome (CFS) subjects would produce greater force production in their matching limb during a fatiguing contralateral limb-matching task of the elbow flexors, compared with healthy, matched controls. Eight CFS subjects and 8 healthy, matched control subjects participated in a fatiguing task that consisted of intermittent submaximal contractions (30% maximal voluntary contraction) of the nondominant arm performed over a 45 min duration. Each minute, the subject attempted to match the force of the nondominant arm with their dominant arm (without visual feedback for the dominant arm). Results showed that average matching force and ratings of perceived effort values were significantly higher in the CFS group during the fatiguing task (P = 0.04, P = 0.02, respectively). This study demonstrated objectively that CFS subjects experienced a greater sense of effort in the elbow flexors while performing a fatiguing task. [All costs associated with this study were incurred by Edith Cowan University.] Keywords: contralateral limb matching task; fatigue; matching force [Return to top] ------------------------------ Date: Mon, 19 Mar 2007 00:34:25 +0100 From: Jan van Roijen <j.van.roijen CHELLO.NL> Subject: not,med: Lost to Lyme ~~~~~~~~~~~~~~~~~~~~~~~~~~~~ Send an Email for free membership ~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~ >>>> Help ME Circle <<<< >>>> 19 March 2007 <<<< Editorship : j.van.roijen chello.nl Outgoing mail scanned by Norton AV ~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~ Quote from below: *....Lyme can mirror other illnesses and is sometimes misdiagnosed as arthritis, Lou Gehrig's disease (ALS), fibromyalgia, chronic fatigue syndrome and multiple sclerosis....* ~jvr ```````` http://www.sunjournal.com/story/203796-3/MaineNews/Lost_to_Lyme/ Sun Journal Lost to Lyme ~~~~~~~~~~ By Lindsay Tice, Staff Writer Sunday, March 18, 200 Bill Chinnock's suicide means Maine's Lyme disease community has lost a champion ... and so much more. But they hope his death will bring help and maybe a cure. When Jodi Ireland heard last week that Bill Chinnock had died, she was stunned. When she learned he'd killed himself, she was devastated. As neighbors in Fairfield, Chinnock had helped her find a diagnosis - Lyme disease - for the crushing fatigue, headaches and numbness that plagued her. Chinnock, a well-known Maine rock musician, an Emmy-award-winning composer and a founding member of what became Bruce Springsteen's E Street Band, was waging his own battle with Lyme. The little-understood tick-borne illness can leave patients debilitated, in pain, confused and forgetful. Still, he encouraged Ireland. He was hopeful. "I don't know how he did it, but he always stayed so positive," Ireland said. Like many Lyme patients, Chinnock - a husband and father - had his ups and downs. But he always seemed eager to help others, eager to tell them they'd be all right. In Maine, he was the Lyme disease community's champion. He was its rock. And then, late last week, police were called to Chinnock's home. His manager said he committed suicide. In the press, his sister blamed it on the disease. The news sent the Lyme community reeling. "I just lost it. I kept saying 'I can't believe he did that,'" said Ireland, a dance teacher now struggling with a Lyme relapse. "I can't believe he gave up." 'Survive and rise above' Over 23,000 new cases of Lyme disease were reported in the U.S. in 2005, nearly 250 of those in Maine, according to the National Centers for Disease Control. But because testing isn't always accurate and because Lyme can mirror other diseases, experts say there were likely many more new cases than that. Lyme can cause myriad symptoms, including exhaustion, joint pain and a generally "foggy" feeling. If caught early, experts say, the disease can be cured with antibiotics. But some people aren't diagnosed for years. When that happens, despite long-term antibiotics, their symptoms are chronic and severe, turning them from healthy to bed-ridden without warning. "It's almost like a death every time you get sick again," Ireland said. Many Lyme patients go from doctor to doctor, getting diagnosed with every disease but Lyme. Some lose their jobs because they can't keep up with the workload. Others lose relationships because friends and family don't understand the illness. In Maine, the Lyme disease community is particularly close. A handful of support groups meet every month, trading help and advice. An online Yahoo group has 175 members who post hundreds of messages each month. For some, it's the only place they can find real understanding. "Other people say 'Well, you look good.' I hate that expression. Never mind that it took me all day to take a shower. Maybe I can put on mascara by the time my husband gets home," said Gail Richard, a former special education teacher who lives in Livermore Falls. Chinnock and Ireland both became sick in the late 1990s. They lived down the road from each other and he worked out at a gym she owned with her husband, she said. "We realized we were both having a lot of the same symptoms," Ireland said. Exhaustion. Headaches. Heart palpitations. Numbness. They checked for chemicals in the water. He went to doctors out of state. She went to doctors locally. "Basically his doctors told him he was crazy and mine told me I had fibromyalgia and to go home and cope," Ireland said. Chinnock eventually saw a doctor in Connecticut, where Lyme was named (after the town of Lyme, Conn.) and diagnosed in the 1970s. He called Ireland, excited, urging her to be tested for Lyme disease, too. They both had it. "I will always feel that I owe him so much. He helped save my life," Ireland said. Chinnock and Ireland went through treatment, including antibiotics, but some symptoms persisted. After Chinnock moved to Yarmouth several years ago, the pair kept in touch. They each had their ups and downs. Sometimes Chinnock felt well enough to put in a 17-hour day producing a new album. Sometimes he couldn't work at all. But no matter what was going on with his own health, Chinnock sought out others to help. "So many people are so sick and so few doctors know enough," Ireland said. He advocated for greater Lyme disease public education. He met with Lyme sufferers, recommending doctors and suggested treatments. Sometimes he simply commiserated, a blessing to patients who felt unheard for so long. He was constantly upbeat, unfailingly positive. Already a music legend as a songwriter and guitarist, Chinnock soon became a legend in the Lyme community as well. "A lot of people knew Bill. He helped a lot of people get diagnosed," said Constance Dickey of Hampden, founder of the MaineLymeDisease support group on Yahoo and chairwoman of the International Lyme and Associated Diseases Society. Stacey Cimino, a southern Maine resident, met Chinnock after learning she had Lyme. She'd been dealing with the symptoms - headaches, seizures, tremors, breathing and heart problems - for a decade. Doctors told her she had everything from Lou Gehrig's disease to stress. By the time Cimino was diagnosed with Lyme, she was sick and tired of being sick and tired. Chinnock sent her an e-mail. "He said 'God has a plan for people. You'll get through this,'" she said. He offered advice in his letters, telling her about his own experience with a new treatment. He encouraged her, like he encouraged so many people, to keep fighting. "You will survive and rise above," he wrote. Grief and hope In 2004 and 2005, Chinnock seemed to be doing well. He'd found an herbal supplement that helped and he was working long hours on a new album, the first in years. But when Chinnock called to check in with Ireland last year, he told her he wasn't feeling well again. That was the last time she heard from him. On March 2, Chinnock's live-in caretaker called police to his Yarmouth home. His manager said he committed suicide. Chinnock was 59. "This has been a huge emotional blow," said Dickey, the support group founder. "It has rocked the community." Some now wonder how they can possibly be strong enough to handle the waves of pain and fatigue if Chinnock, their champion, couldn't. "It broke my heart because I know what he goes through, I know what he went through," said Richard, the former special education teacher. "There are some days you don't want anyone to talk to you or touch you, the pain is so bad. I walk from window to window and look outside. I'm 52 years old and I feel 80." For a week, online message boards have buzzed with news of Chinnock's death. "I'm sure many of us here have had thoughts similar on our very worst days. How bad must he have been to take that last final step? My heart breaks for him," wrote one person on Lymenet.org. "I pray that he has found peace at last," wrote another. LymeMemorial.org now lists Chinnock among 230 people who have died from Lyme or other tick-borne diseases. But even as they grieve, Lyme patients say they also have hope: that Chinnock's death will not be in vain. "I hope someone in Augusta is paying attention," said Dickey. They want publicity. They want Lyme disease education for doctors and the public. They want passage of a federal bill earmarking $100 million for Lyme disease research and prevention. They want passage of a state bill that forces insurance companies to cover Lyme patients, requires employers to educate workers about Lyme if they work in a high risk area and creates a study of Lyme disease issues. It's all been missing, they say. And maybe now, with Chinnock's death, it will come. "I bet that's what he would have wanted, too," Ireland said. Lyme disease facts ~~~~~~~~~~~~~~~~~~ * Nearly 250 new cases were reported in Maine in 2005, the last year data is available. * Disease comes from deer ticks. * Symptoms often begin within days or weeks and sometimes come with a red rash that can look like a bull's-eye. * More severe symptoms include joint pain, fatigue, muscle aches, headaches, nervous system problems, facial paralysis and a general "foggy" feeling. * Lyme can mirror other illnesses and is sometimes misdiagnosed as arthritis, Lou Gehrig's disease (ALS), fibromyalgia, chronic fatigue syndrome and multiple sclerosis. * Treatment is a course of antibiotics, although doctors debate how long treatment should last. Deer tick facts * Both baby deer ticks and adult deer ticks can transmit Lyme disease. * Baby deer ticks are about the size of a pinhead. * Adult deer ticks are often shiny, reddish brown with black heads. * Deer ticks favor trees and leaves, although they can be found on the coast or in grass. * They must feed on someone for 24 to 48 hours in order to transmit Lyme disease. * They can also transmit ehrlichiosis, a rare disease with flu-like symptoms, and babesiosis, a malaria-like disease that affects red blood cells. * Use insect repellents with DEET and protective clothing to prevent tick bites. For pets, use only repellents OK'd by a vet. * To remove a tick, grasp it with fine tweezers as close to the skin as possible. Pull gently but firmly. It could take several minutes. Do not handle ticks with your bare hands. What you can do * Several U.S. centers test ticks for Lyme disease, including those listed below. Contact each for information on price, response time and proper procedure for mailing. North American Laboratory New Britain, CT (203) 826-1140 800-866-NALG New Jersey Laboratories New Brunswick, NJ (732) 249-0148 IgeneX Palo Alto, California http://www.igenex.com/ (415)424-1191 800-832-3200 Tick Research Laboratory Kingston, Rhode Island (401)874-2650 * The Vector-borne Disease Laboratory at Maine Medical Center identifies ticks and can tell whether they have fed long enough to transmit Lyme. It is free. Ask your doctor or veterinarian to send the tick or do it yourself by sealing the tick in a small, crush-proof container with alcohol. Include the form found at www.mmcri.org/lyme/lymehome.html and mail it to: Vector-Borne Disease Laboratory Maine Medical Center Research Institute 75 John Roberts Road, Suite 9B South Portland, ME 04106 Sources: Maine CDC, the Vector-Borne Disease Laboratory, Lymenet.org, International Lyme and Associated Diseases Society [Return to top] ------------------------------ Date: Mon, 19 Mar 2007 15:23:06 -0400 From: "Bernice A. Melsky" <bernicemelsky VERIZON.NET> Subject: RES: The Relationship between Psychological Factors and Health Care-Seeking Behavior in Fibromyalgia Patients [The Relationship between Psychological Factors and Health Care-Seeking Behavior in Fibromyalgia Patients.] [Article in Turkish] Turk Psikiyatri Derg. 2007 Spring;18(1):22-30. Gulec H, Sayar K, Yazici Gulec M. PMID: 17364265 OBJECTIVE: The aim of this study was to examine whether cognitive factors, such as attributions, expectations, and anger management style, contribute to the decision to seek medical care for fibromyalgia syndrome (FMS). METHOD: We recruited 3 groups of subjects; patients from a FMS tertiary care setting, community residents with FMS who had not sought medical care for their FMS symptoms (nonpatients), and healthy controls. In all, 38 FMS nonpatients were compared to 37 FMS patients and 41 healthy controls on measures of anxiety, depression, anger, locus of control (LOC), attributions, pain intensity, and disability, as well as demographic characteristics. RESULTS: The prevalence of FMS non-patients was 2%. There was a significant difference between the 3 groups on the measures of anxiety, depression, LOC, and somatic and normalizing subscale scores of the symptom interpretation questionnaire (SIQ). FMS nonpatients, relative to FMS patients and healthy controls, were characterized by a significantly higher measure of both LOC and normalizing subscale score on the SIQ. There were no differences between the 2 FMS groups in demographical percentage and other psychometric measures. A hierarchical logistic regression model showed that the number of tender points, normalizing attribution style, and depression were independent predictors of help-seeking behavior. CONCLUSION: The rate of psychiatric and medical history is not related to the FMS syndrome. Expectations and a normalizing attribution style may contribute to help-seeking behavior for FMS. [Return to top] ------------------------------ Date: Mon, 19 Mar 2007 04:31:53 +0100 From: Jan van Roijen <j.van.roijen CHELLO.NL> Subject: res: Infection & vaccination in ME/CFS - Myth or reality? ~~~~~~~~~~~~~~~~~~~~~~~~~~~~ Send an Email for free membership ~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~ >>>> Help ME Circle <<<< >>>> 19 March 2007 <<<< Editorship : firstname.lastname@example.org Outgoing mail scanned by Norton AV ~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~ Sat, 17 Mar 2007 Fred Springfield posted the abstract of *Infection and vaccination in chronic fatigue syndrome: Myth or reality?* - Appel S, Chapman J, Shoenfeld Y - Autoimmunity. 2007 Feb;40(1):48-53. - at Co-cure: http://listserv.nodak.edu/cgi-bin/wa.exe?A2=ind0703c&L=co-cure&T=0&P=2067 -------------------------------------------------------------- ~jvr: as fair use I add the *discussion* (*Can vaccinations induce CFS?* section of this article -------------------------------------------------------------- Can vaccinations induce CFS? As discussed above, the exact pathogen of CFS in unknown, but the leading theory is that an aberrant immunological response to infection causes a chronic activation biased toward a Th-2 dominant reaction. This theory raises the suspicion that vaccinations that are given in order to trigger an immunological defense reaction, may cause in distinct cases an aberrant reaction that will be expressed as CFS by the mechanism discussed above. The main adverse reactions to vaccinations are usually local at the site of injection (erhythema and pruritus) but systemic flue-like reaction (fever, myalgia, fatigue and lymph nodes tenderness) and allergy may occur . Those adverse reactions are usually mild and self-limited. Several reports associate distinct vaccinations with the induction of autoimmune disease [40,41]. Rheumatoid arthritis, reactive arthritis, vasculitis, encephalitis, thrombocytopenia and multiple sclerosis relapse have been documented after hepatitis B virus (HBV) vaccination. Acute arthritis or arthralgia, chronic arthritis and thrombocytopenia appeared after mumps and rubella vaccine (MMR). Guillain–Barre syndrome (GBS) and vasculitis after influenza, and GBS that appeared after polio-immunization. Several syndromes that are related to vaccinations contain chronic fatigue as a part of the syndrome. The Gulf war syndrome was described in 4–8% of the soldiers who participated in the Gulf war and few months–years later suffered from illness that included impaired cognition (distractibility, memory problems), fatigue, arthromyoneuropahy (joints and muscle pains) and post-traumatic stress disorder . The syndrome was related to chronic Th-2 biased immune response. Rook and Zumla  raised the hypothesis that the multiple vaccinations given to the troops during their deployment induced a systemic Th-1 to Th-2 switched immune response and cause to the symptoms above. Four features of the vaccination protocol used in this war led them to this theory: (1) The vaccination against anthrax that was given to the soldiers used Pertussis derivate as an adjuvant agent, which is known to induce a Th-2 dominant response. (2) The soldiers were exposed to large burden of vaccinations which tend to shift the immune response to a Th-2 dominant response. (3) The vaccinations were given after the deployment of the troops, while being in stressful condition. Under this condition the cortisol level is reduced, the DHEA level is increased and the immune response is shifted to Th-2 dominant profile. (4) The troops were exposed to carbamate and organophosphate insecticides which inhibits IL- 2—a pivot cytokine of Th-1 response. Support for this theory came from a cross sectional study of 923 UK Gulf war veterans who still had their vaccinations records . The study found an association between multiple vaccinations given during the conflict and later evolution of Gulf war syndrome. Another syndrome that was related to vaccinations is macrophagic myofasciitis. This syndrome is a postvaccination disorder characterized by stereotypic lesion on the deltoid muscle (site of injection) associated with prominent fatigue that fulfills the CFS criteria. Electron microscopy and experimental studies show that the lesion is due to persistent immune reaction to aluminum hydroxyl used in different vaccination as an adjuvant agent including HAV, HBV and toxoid vaccinations. The aluminum hydroxyl is known to induce a shift of the immune response toward a Th-2 profile reaction and if it persists—a chronic inflammatory activation may occur. The persistent elevated levels of the Th-2 cytokines induce the systemic symptoms of chronic fatigue, muscle and joints pain . An association between vaccination and CFS is much less documented. In 1992 several reports claimed that CFS was evolved after immunization to HBV was published in Canada. A working group of the Laboratory Center for Disease Control (LCDC) of the Canadian National Health andWelfare (NHW) was founded in order to examine the suspected association between anti-HBV vaccination and CFS. The working group gathered 30 cases of patients with CFS that appeared within 3 month after immunization against HBV—the great majority after the first dose of the vaccine .The working group examined several studies dill with this question. A retrospective study on 134 CFS patients found that 2.2% of them received anti-HBV vaccine within the 3 month before the beginning of the disease. When they compared this figure to the occurrence of anti-HBV vaccination in the matched Canadian population (1.9%), no significant different was found. A prospective study followed after 700 students who were vaccinated with anti-HBV vaccine. About 12% of the students complained on tiredness that was self limited and none of them evolved to CFS. Those studies brought the members of the working group to a conclusion that there is no evidence that show an association between CFS and anti-HBV vaccine. Updated studies that checked the relationship between CFS and vaccination came to the same conclusion [47,48]. The use of vaccinations in CFS patients did not exacerbate their symptoms. A study that examined CFS patients vaccinated with anti-influenza vaccination found no significant difference between the CFS patients and the control healthy group. Although CFS patients reported on adverse affects four times more then the healthy vaccines, those adverse effects were related to common post-influenza vaccination symptoms and to constitutional CFS symptoms . We can summarize carefully that except for several case-reports, there is no study that found induction of CFS by vaccination, but only few studies concerning this issue have been published. Further studies examining this question should be carried out and the physician's index of suspicion should be raised because this possibility of vaccination-induced CFS is reasonable in view of the ability of vaccinations to cause Th-2 dominant response. [Return to top] ------------------------------ Date: Mon, 19 Mar 2007 20:05:48 -0400 From: "Bernice A. Melsky" <bernicemelsky VERIZON.NET> Subject: RES: The Relationship Between Cytokines and Pain/Depression: A Review and Current Status The Relationship Between Cytokines and Pain/Depression: A Review and Current Status Current Pain and Headache Reports 2007, 11:98-103 Thomas B. Strouse, MD, UCLA Department of Psychiatry and Biobehavioral Sciences, Outpatient Cancer Center at the Samuel Oschin Comprehensive Cancer Institute, UCLA and Cedars-Sinai Medical Centers, 8700 Beverly Boulevard, Los Angeles, CA 90048, USA. Email: email@example.com Cytokines are small protein molecules secreted in response to immune stimuli. Recent research has outlined important roles for proinflammatory cytokines in the cascade of normal physiologic responses to environmental stresses, encompassing so-called sickness behavior that is thought to be an adaptive response to infection and other illnesses. Cytokines are involved in signaling that activates central nervous system glial cells. This activation is part of a poorly understood interaction between immune challenge or injury and host that can lead to the development or facilitation of persistent mood symptoms or pathologic pain. This article reviews evidence that may enhance our understanding of how pathologic symptoms, such as mood disorders and neuropathic pain, may emerge from proinflammatory cytokine activation. Possible conceptualizations of these illnesses and potential treatment implications are explored. Copyright © 2007 by Current Science, Inc. [Return to top] ------------------------------ Date: Mon, 19 Mar 2007 20:18:47 -0400 From: "Bernice A. Melsky" <bernicemelsky VERIZON.NET> Subject: RES: Evidence for a Mismatch Between the Brains Movement Control System and Sensory System As an Explanation for Some Pain-related Disorders Evidence for a Mismatch Between the Brain's Movement Control System and Sensory System As an Explanation for Some Pain-related Disorders Current Pain and Headache Reports 2007, 11:104-108 Candida S. McCabe, PhD, RGN and David R. Blake, MB, FRCP Corresponding author:Candida S. McCabe, PhD, RGN, The Royal National Hospital for Rheumatic Diseases and School for Health, University of Bath, Upper Borough Walls, Bath BA1 1RL, United Kingdom. Email: candy.mccabe rnhrd-tr.swest.nhs.uk The motor-control system usually operates below our conscious level, and we only become aware of the complex interaction between desired movements and actual movements when an irregularity in the system occurs. Recently, it has been proposed that such discordances in sensorimotor function may generate pain and other somaesthetic disturbances. This article describes this model of pain and determines how it may be applied to a range of chronic pain conditions in which there is a lack of obvious causal pathology, including complex regional pain syndrome. In addition, we discuss the clinical implications of such a theory and examine how enhancing sensory feedback may reduce chronic pain. Copyright © 2007 by Current Science, Inc. [Return to top] ------------------------------
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