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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, 19 Jun 2007 13:36:27 -0400 From: "Bernice A. Melsky" <bernicemelsky VERIZON.NET> Subject: RES: Mindfulness training as an intervention for fibromyalgia: evidence of postintervention and 3-year follow-up benefits in well-being Mindfulness training as an intervention for fibromyalgia: evidence of postintervention and 3-year follow-up benefits in well-being. Psychother Psychosom. 2007;76(4):226-33. Grossman P, Tiefenthaler-Gilmer U, Raysz A, Kesper U. Division of Psychosomatic Medicine, Department of Internal Medicine, University of Basel Hospital, Basel, Switzerland. PMID: 17570961 Background: Mindfulness-based stress reduction (MBSR) proposes a systematic program for reduction of suffering associated with a wide range of medical conditions. Studies suggest improvements in general aspects of well-being, including quality of life (QoL), coping and positive affect, as well as decreased anxiety and depression. Methods: A quasi-experimental study examined effects of an 8-week MBSR intervention among 58 female patients with fibromyalgia (mean, 52 ± 8 years) who underwent MBSR or an active social support procedure. Participants were assigned to groups by date of entry, and 6 subjects dropped out during the study. Self-report measures were validated German inventories and included the following scales: visual analog pain, pain perception, coping with pain, a symptom checklist and QoL. Pre- and postintervention measurements were made. Additionally, a 3-year follow-up was carried out on a subgroup of 26 participants. Results: Pre- to postintervention analyses indicated MBSR to provide significantly greater benefits than the control intervention on most dimensions, including visual analog pain, QoL subscales, coping with pain, anxiety, depression and somatic complaints (Cohen d effect size, 0.40-1.10). Three-year follow-up analyses of MBSR participants indicated sustained benefits for these same measures (effect size, 0.50-0.65). Conclusions: Based upon a quasi-randomized trial and long-term observational follow-up, results indicate mindfulness intervention to be of potential long-term benefit for female fibromyalgia patients. Copyright (c) 2007 S. Karger AG, Basel. [Return to top] ------------------------------ Date: Wed, 20 Jun 2007 08:52:15 +0200 From: "Dr. Marc-Alexander Fluks" <fluks COMBIDOM.COM> Subject: RES: CFS/ME & FM papers, published since May 2007 Source: NCBI PubMed Date: June 20, 2007 URL: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi Topic=((chronic fatigue) OR (myalgic encephalomyelitis)) OR fibromyalgia Ref: In the update, you will only find journals that are indexed by Medline (PubMed). All scientific papers 1938-today, http://www.me-net.combidom.com/library/literature.htm#publications Search scientific papers, http://www.me-net.combidom.com/library/literature.htm#catalogue Figures computer analysis scientific papers, http://www.me-net.combidom.com/library/literature.htm#figure All popular papers 1900-today, http://www.me-net.combidom.com/library/literature.htm#popular CFS/ME & FM papers, published since May 2007 -------------------------------------------- ___ Sundgren PC, Petrou M, Harris RE, Fan X, Foerster B, Mehrotra N, Sen A, Clauw DJ, Welsh RC. Diffusion-weighted and diffusion tensor imaging in fibromyalgia patients: a prospective study of whole brain diffusivity, apparent diffusion coefficient, and fraction anisotropy in different regions of the brain and correlation with symptom severity. Acad Radiol. 2007 Jul;14(7):839-46. ___ Grossman P, Tiefenthaler-Gilmer U, Raysz A, Kesper U. Mindfulness training as an intervention for fibromyalgia: evidence of postintervention and 3-year follow-up benefits in well-being. Psychother Psychosom. 2007;76(4):226-33. ___ Balon R. Reflections on relevance: the fields of psychosomatics and psychotherapy in 2006. Psychother Psychosom. 2007;76(4):203-12. ___ Martinez-Lavin M, Infante O, Lerma C. Hypothesis: The Chaos and Complexity Theory May Help our Understanding of Fibromyalgia and Similar Maladies. Semin Arthritis Rheum. 2007 Jun 13. ___ Wallace DJ, Gotto J. Hypothesis: Bipolar Illness with Complaints of Chronic Musculoskeletal Pain Is a Form of Pseudofibromyalgia. Semin Arthritis Rheum. 2007 Jun 13. ___ Masuko K, Nakamura H. Functional somatic syndrome: how it could be relevant to rheumatologists. Mod Rheumatol. 2007;17(3):179-84. ___ Wyller VB, Saul JP, Amlie JP, Thaulow E. Sympathetic predominance of cardiovascular regulation during mild orthostatic stress in adolescents with chronic fatigue. Clin Physiol Funct Imaging. 2007 Jul;27(4):231-8. ___ Tomoda A. School phobia and childhood chronic fatigue syndrome (CFS) [Japanese]. Nippon Rinsho. 2007 Jun;65(6):1121-33. ___ Oki J, Okubo J. Usefulness of growth chart in children and adolescents with chronic fatigue syndrome [Japanese]. Nippon Rinsho. 2007 Jun;65(6):1113-9. ___ Tanaka H. The autonomic function and child chronic fatigue syndrome [Japanese]. Nippon Rinsho. 2007 Jun;65(6):1105-12. ___ Miike T. Childhood chronic fatigue syndrome [Japanese]. Nippon Rinsho. 2007 Jun;65(6):1099-104. ___ Masuda A, Munemoto T, Tei C. A new treatment: thermal therapy [Japanese]. Nippon Rinsho. 2007 Jun;65(6):1093-8. ___ Murakami M. Attentive consideration for the treatment of chronic fatigue syndrome [Japanese]. Nippon Rinsho. 2007 Jun;65(6):1089-92. ___ Yamadera W, Itoh H. Overview of psychiatric therapy for chronic fatigue syndrome [Japanese]. Nippon Rinsho. 2007 Jun;65(6):1082-6. ___ Yoshihara K, Kubo C. Overview of medical treatment and management of chronic fatigue syndrome [Japanese]. Nippon Rinsho. 2007 Jun;65(6):1077-81. ___ Hakariya Y, Kuratsune H. Chronic fatigue syndrome: biochemical examination of blood [Japanese]. Nippon Rinsho. 2007 Jun;65(6):1071-6. ___ Nishikai M. Antinuclear antibodies [Japanese]. Nippon Rinsho. 2007 Jun;65(6):1067-70 [Japanese]. ___ Tajima S, Kuratsune H, Yamaguti K, Takahashi A, Takashima S, Watanabe Y, Nishizawa Y. Estimation of fatigue state in patient with CFS using actigraph and R-R interval power spectrum analysis [Japanese] Nippon Rinsho. 2007 Jun;65(6):1057-64. ___ Sakudo A, Kuratsune H, Hakariya Y, Kobayashi T, Ikuta K. Spectroscopic diagnosis of chronic fatigue syndrome by multivariate analysis of visible and near-infrared spectra [Japanese]. Nippon Rinsho. 2007 Jun;65(6):1051-6. ___ Kondo K. Chronic fatigue syndrome and herpesvirus reactivation [Japanese]. Nippon Rinsho. 2007 Jun;65(6):1043-8. ___ Yamaguti K. The evaluation of fatigue by using acceleration plethysmography [Japanese]. Nippon Rinsho. 2007 Jun;65(6):1034-42. ___ Kawai T, Rokutan K. Identification and application of marker genes for differential diagnosis of chronic fatigue syndrome [Japanese]. Nippon Rinsho. 2007 Jun;65(6):1029-33. ___ Yoshiuchi K. Psychological symptoms in chronic fatigue syndrome [Japanese]. Nippon Rinsho. 2007 Jun;65(6):1023-7. ___ Kumano-go T, Adachi H, Sugita Y. Sleep disturbance [Japanese]. Nippon Rinsho. 2007 Jun;65(6):1017-22. ___ Ban N, Saiki T, Ko G, Kuwahata A. Clinical features of chronic fatigue syndrome-symptoms [Japanese]. Nippon Rinsho. 2007 Jun;65(6):1011-5. ___ Miwa S, Takikawa O. Chronic fatigue syndrome and neurotransmitters [Japanese]. Nippon Rinsho. 2007 Jun;65(6):1005-10. ___ Narita M, Narita N. Genetic background of chronic fatigue syndrome [Japanese]. Nippon Rinsho. 2007 Jun;65(6):997-1002. ___ Sairenji T, Nagata K. Viral infections in chronic fatigue syndrome [Japanese]. Nippon Rinsho. 2007 Jun;65(6):991-6. ___ Kuratsune H. Overview of chronic fatigue syndrome focusing around prevalence and diagnostic criteria [Japanese]. Nippon Rinsho. 2007 Jun;65(6):983-90. ___ Hashimoto N. History of chronic fatigue syndrome [Japanese] Nippon Rinsho. 2007 Jun;65(6):975-82. ___ White PD. How common is chronic fatigue syndrome; how long is a piece of string? Popul Health Metr. 2007 Jun 8;5(1):6. ___ Reeves WC, Jones JF, Maloney E, Heim C, Hoaglin DC, Boneva RS, Morrissey M, Devlin R. Prevalence of chronic fatigue syndrome in metropolitan, urban, and rural Georgia. Popul Health Metr. 2007 Jun 8;5(1):5. ___ Armitage R, Landis C, Hoffmann R, Lentz M, Watson NF, Goldberg J, Buchwald D. The impact of a 4-hour sleep delay on slow wave activity in twins discordant for chronic fatigue syndrome. Sleep. 2007 May 1;30(5):657-62. ___ Mease P, Arnold LM, Bennett R, Boonen A, Buskila D, Carville S, Chappell A, Choy E, Clauw D, Dadabhoy D, Gendreau M, Goldenberg D, Littlejohn G, Martin S, Perera P, Russell IJ, Simon L, Spaeth M, Williams D, Crofford L. Fibromyalgia syndrome. J Rheumatol. 2007 Jun;34(6):1415-25. ___ Hauser W. Self-assessed pain intensity and disability in subjects diagnosed with fibromyalgia claiming retirement pension [German]. Schmerz. 2007 Jun 6. ___ Forbes D, Chalmers A. Fibromyalgia: revisiting the literature. JCCA J Can Chiropr Assoc. 2004 Jun;48(2):119-31. ___ Torpy DJ, Ho JT. Corticosteroid-binding globulin gene polymorphisms: clinical implications and links to idiopathic chronic fatigue disorders. Clin Endocrinol (Oxf). 2007 Jun 4. ___ Ter Wolbeek M, van Doornen LJ, Kavelaars A, van de Putte EM, Schedlowski M, Heijnen CJ. Longitudinal analysis of pro- and anti-inflammatory cytokine production in severely fatigued adolescents. Brain Behav Immun. 2007 May 31. ___ Bennett B, Goldstein D, Friedlander M, Hickie I, Lloyd A. The Experience of Cancer-Related Fatigue and Chronic Fatigue Syndrome: A Qualitative and Comparative Study. J Pain Symptom Manage. 2007 May 31. ___ Bazzichi L, Rossi A, Massimetti G, Giannaccini G, Giuliano T, De Feo F, Ciapparelli A, Dell'osso L, Bombardieri S. Cytokine patterns in fibromyalgia and their correlation with clinical manifestations. Clin Exp Rheumatol. 2007 Mar-Apr;25(2):225-30. ___ Rossini M, Di Munno O, Valentini G, Bianchi G, Biasi G, Cacace E, Malesci D, La Montagna G, Viapiana O, Adami S. Double-blind, multicenter trial comparing acetyl l-carnitine with placebo in the treatment of fibromyalgia patients. Clin Exp Rheumatol. 2007 Mar-Apr;25(2):182-8. ___ Brown MM, Jason LA. Functioning in individuals with chronic fatigue syndrome: increased impairment with co-occurring multiple chemical sensitivity and fibromyalgia. Dyn Med. 2007 May 31;6:6. ___ White PD. What Causes Prolonged Fatigue after Infectious Mononucleosis - and Does It Tell Us Anything about Chronic Fatigue Syndrome? J Infect Dis. 2007 Jul 1;196(1):4-5. ___ Torres Mata X, Peri Nogues JM. Non pharmacologic and alternative treatments in fibromyalgia [Spanish]. Med Clin (Barc). 2007 May 5;128(17):679. ___ Faulkner S, Smith A. A longitudinal study of the relationship between psychological distress and recurrence of upper respiratory tract infections in chronic fatigue syndrome. Br J Health Psychol. 2006 Dec 18. ___ Thieme K, Turk DC, Flor H. Responder criteria for operant and cognitive-behavioral treatment of fibromyalgia syndrome. Arthritis Rheum. 2007 Jun 15;57(5):830-6. ___ Scheeres K, Wensing M, Mes C, Bleijenberg G. The impact of informational interventions about cognitive behavioral therapy for chronic fatigue syndrome on GPs referral behavior. Patient Educ Couns. 2007 May 21. ___ Fioravanti A, Perpignano G, Tirri G, Cardinale G, Gianniti C, Lanza CE, Loi A, Tirri E, Sfriso P, Cozzi F. Effects of mud-bath treatment on fibromyalgia patients: a randomized clinical trial. Rheumatol Int. 2007 May 23. ___ Wyller VB, Thaulow E, Amlie JP. Treatment of chronic fatigue and orthostatic intolerance with propranolol. J Pediatr. 2007 Jun;150(6):654-5. ___ Massey PB. Reduction of fibromyalgia symptoms through intravenous nutrient therapy: results of a pilot clinical trial. Altern Ther Health Med. 2007 May-Jun;13(3):32-4. -------- (c) 2007 NCBI PubMed [Return to top] ------------------------------ Date: Wed, 20 Jun 2007 13:14:10 -0700 From: "TVA12082208 aol.com" Subject: MED: Lyme and herpes in CFS It has been puzzling to me that every cancer patient I test for a Lyme infection turns out positive. My ongoing research on Lyme has focused in recent weeks on a mycoplasma that lies at the root of the disease. It appears to be the fundamental factor that severely depresses the immune system allowing the entire complex of pathogenic bacteria, fungi, parasites, and viruses to proliferate. A recent study shows that "chronic infection or colonization by mycoplasma(s) could gradually and significantly alter many biologic properties of mammalian host cells in culture, including induction of malignant transformation." Therefore, in those individuals with cancer, it is important to eliminate the Rife BX/BY "virus", the Gregory "cancer virus", the SV40 virus, and Lyme disease. Failing to do this sets the individual up for progression and/or recurrence of malignancy. Mycoplasma fermentans infection promotes immortalization of human peripheral blood mononuclear cells in culture. Zhang S, Tsai S, Wu TT, Li B, Shih JW, Lo SC Department of Infectious and Parasitic Diseases Pathology, American Registry of Pathology, Washington DC, USA. Blood. 2004 Dec 15;104(13):4252-9. Epub 2004 Aug 26 Chronic infection or colonization by mycoplasma(s) could gradually and significantly alter many biologic properties of mammalian host cells in culture, including induction of malignant transformation. We examined effects of Mycoplasma fermentans infection on the continuing survival and immortality of human peripheral blood mononuclear cells (PBMCs) from healthy blood donors. Without specific supplemental growth factors, human PBMCs normally die rapidly, with few cells other than macrophages/monocytes surviving after 2 weeks in cultures. Only occasional Epstein-Barr virus (EBV)-positive B lymphocytes would continue to proliferate and undergo spontaneous immortalization. Our present study revealed that infection of human PBMCs in culture with the incognitus and PG18 strains of M fermentans, but surprisingly not with some other strains tested in parallel, markedly enhanced the rate of EBV-positive B lymphocytes to undergo immortalization (74% vs 17%). Compared with spontaneously immortalized PBMCs, the PBMCs immortalized in cultures infected with the mycoplasmas often had prominent karyotype changes with chromosomal loss, gain, or translocations. Furthermore, many of these immortalized B lymphocytes were found to be monoclonal in nature. The in vitro findings would be of relevance to lymphoproliferative disorders that occurred in patients with immune suppression. The mycoplasma-mediated promotional effect in cell immortalization and its potential clinical implications warrant further study. Kind regards, Katharina Gutsche ~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~ Katharina Gutsche, M.A. Psycholinguistics, Dipl.-Psych.Clinical Psychology, State Licensured Naturopath (Psychotherapy) http://stores.lulu.com/katharinagutsche ~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~ [Return to top] ------------------------------ Date: Thu, 21 Jun 2007 11:33:19 +0200 From: "Dr. Marc-Alexander Fluks" <fluks COMBIDOM.COM> Subject: RES,NOT: CDC on CFS prevalence Source: Population Health Metrics Vol. 5, #1, p 5 Date: June 8, 2007 URL: http://www.pophealthmetrics.com/content/5/1/5 http://www.pophealthmetrics.com/content/pdf/1478-7954-5-5.pdf Prevalence of Chronic Fatigue Syndrome in Metropolitan, Urban, and Rural Georgia -------------------------------------------------------------------------------- William C. Reeves(1,*), James F. Jones(1), Elizabeth Maloney(1), Christine Heim(2), David C. Hoaglin(3), Roumiana S. Boneva(1), Marjorie Morrissey(4), Rebecca Devlin(4) 1 Chronic Viral Diseases Branch, Coordinating Center for Infectious Diseases, Centers for Disease Control and Prevention, Atlanta, GA, USA. 2 Department of Psychiatry & Behavioral Sciences, Emory University School of Medicine, Atlanta, GA, USA. 3 Abt Associates Inc, Cambridge, MA, USA, 4 Abt Associates Inc, Chicago, IL, USA. * Corresponding author Email: William C Reeves* - email@example.com; James F Jones - firstname.lastname@example.org; Elizabeth Maloney - email@example.com; Christine Heim - firstname.lastname@example.org; David C Hoaglin - email@example.com; Roumiana S Boneva - firstname.lastname@example.org; Marjorie Morrissey - Marjorie_Morrissey@abtassoc.com; Rebecca Devlin - Rebecca_Devlin@abtassoc.com Abstract Background Chronic fatigue syndrome (CFS) is a debilitating illness with no known cause or effective therapy. Population-based epidemiologic data on CFS prevalence are critical to put CFS in a realistic context for public health officials and others responsible for allocating resources. Methods Based on a random-digit dialing survey we ascertained CFS cases and controls to estimate the prevalence of CFS in metropolitan, urban, and rural populations of Georgia. This report focuses on the 5,623 of 19,381 respondents ages 18 to 59 years old. Fatigued (2,438), randomly selected unwell not fatigued (1,429) and randomly selected well (1,756) respondents completed telephone questionnaires concerning fatigue, other symptoms, and medical history. Subsets of those identified by interview as having CFS-like illness (292), chronic unwellness which was not CFS-like (268--randomly selected), and well subjects (223, matched to those with CFS-like illness on sex, race, and age) completed a clinical evaluation. Results We estimated that 2.54% of persons 18 to 59 years of age suffered from CFS. There were no significant differences in prevalence of CFS between metropolitan, urban or rural populations or between white and black residents of the three regions. However, there were significant differences in female-to-male ratios of prevalence across the strata (metropolitan female: male 11.2 : 1, urban 1.7 : 1, rural 0.8 : 1). Conclusions We estimated that 2.54% of the Georgia population suffers from CFS, which is 6- to 10-fold higher than previous population-based estimates in other geographic areas. These differences may reflect broader screening criteria and differences in the application of the case definition. However, we cannot exclude the possibility that CFS prevalence may be higher in Georgia than other areas where it has been measured. Although the study did not identify differences in overall prevalence between metropolitan, urban, and rural Georgia populations, it did suggest the need for additional stratified analyses by geographic strata. Background Chronic fatigue syndrome (CFS) is a complex medical and public health problem that is associated with severe personal suffering and loss. The median duration of illness is 7 years, a quarter of those with the illness are unemployed or receiving disability, and the average affected family forgoes approximately $20,000 in annual earnings and wages . Yet, fewer than 20 percent have received medical care for CFS [2, 3]. Despite more than 3,000 articles in the peer- reviewed medical literature, the pathophysiology of CFS is not well understood. There are no diagnostic laboratory abnormalities or clinical tests. There is no public health control or prevention strategy for CFS. An understanding of the prevalence and distribution of CFS in the general population is fundamental to focusing etiologic research, estimating the effects of CFS on quality of life and productivity, and devising control and prevention strategies. The few studies which have estimated the prevalence of CFS in defined populations [4, 5, 3, 6] reported prevalence estimates for CFS in adults to be between 0.24%  and 0.42% , and prevalence for CFS-like illness between 0.25%  and 1.67% . These studies used different sampling, screening, and evaluation strategies; so, their results are not strictly comparable. They also identified relatively small numbers of persons with CFS, and thus they lack statistical power. However, all four studies documented that CFS disproportionately affects women, is more common in the economically disadvantaged, and affects racial/ethnic minorities at rates equal to or greater than those of whites. We conducted the survey herein reported to estimate the prevalence of CFS in racial/ethnic groups representative of defined metropolitan, urban, and rural populations. The primary objective was to obtain information that could be used as a basis for the development and evaluation of a control strategy for CFS. The study also rectified two major weaknesses of previous studies. First, previous studies have screened the population for individuals with fatigue and then evaluated them for CFS. Although fatigue is central to CFS, focusing on fatigue ignores other important dimensions of the illness such as impaired memory or concentration, unrefreshing sleep, and bodily pain. For many persons who suffer from CFS, these symptoms, rather than fatigue, constitute the primary complaint. In addition, a household informant may not be familiar with specific symptoms but can identify whether someone is generally unwell or not. Thus, rather than limiting the initial screening stage to fatigued and non-fatigued persons, this survey cast a broader screening net, utilizing household informants to identify unwell (fatigue, problems with memory/concentration, unrefreshing sleep, or pain) members of these populations. We then conducted detailed evaluations of participants who were identified by a household informant as unwell to further identify those with CFS. Second, previous studies have not defined CFS in a rigorous reproducible manner (i.e., they did not use validated and standardized instruments to measure fatigue, impairment, and accompanying symptoms) . To address this deficit, we used validated and standardized instruments to define CFS according to criteria of the 1994 case definition . Methods The CDC Institutional Review Board, as required by Department of Health and Human Services regulations, approved the study. All participants were volunteers who gave informed consent. The study was conducted in English. Non-English speaking respondents were not included. Study Design Metropolitan, urban, rural. The definitions of metropolitan, urban and rural geographic strata are complex. The U.S. Office of Management and Budget defines several categories of metropolitan statistical areas according to specific standards. In general, metropolitan areas contain at least a million residents living in a core area (i.e., central city), together with adjacent communities that have a high degree of economic and social integration with that core. Atlanta, with approximately 4 million residents, is a metropolitan city. The Census Bureau defines urban and rural areas independently of OMB's classification. Urban and rural can occur inside of and outside of metropolitan areas. Typically, settled areas of 2,500 or more are considered to be urban and the remainder rural. Based on these definitions, we determined that the cities of Macon and Warner Robins (with populations of 300,000 and 48,000, respectively) were urban. For this study, we considered the counties surrounding Macon and Warner Robins to be rural. Survey in general. The survey was conducted between September 2004 and July 2005. It included residents of three areas of Georgia: metropolitan (Atlanta -- Fulton and DeKalb counties), urban (Macon -- Bibb County and Warner Robins in adjacent Houston County), and rural (10 counties surrounding Bibb County -- Houston -excluding Warner Robins, Baldwin, Bleckley, Crawford, Jones, Macon, Monroe, Peach, Twiggs, and Wilkinson). The survey used the same strategy as previously reported CDC population surveys of CFS [7, 6]. We used list- assisted random-digit dialing  and an advance letter  to contact households containing persons aged 18-59 years in the three population strata. Telephone screening interviews. In contrast to our previous studies, which screened households for fatigue, in this study we modified the initial screening interview to cover a broader range of CFS defining symptoms. In brief, the screening interview asked a household informant (=> 18 years) to report the age, sex, ethnicity and health status of each household member aged 18 and older and to identify unwell household members, who the informant noticed to have at least one of the CFS defining symptoms (fatigue, cognitive impairment, unrefreshing sleep, muscle pain, joint pain, sore throat, tender lymph nodes, or headache) for 1 month, and well residents, who had none of these problems for => 1 month. Detailed telephone interviews. Household residents between 18 and 59 years of age who were identified by the informant as unwell with fatigue, randomly selected persons identified as unwell without fatigue (i.e., identified with cognitive impairment, unrefreshing sleep, muscle pain, joint pain, sore throat, tender lymph nodes, or headache), and a random sample of people identified as well were asked to complete a detailed telephone interview. The detailed interview covered fatigue status and duration, other symptoms, race ("What race do you consider yourself to be? Please note that you may choose more than one option. White, black of African American, Asian, American Indian or Alaskan Native, native Hawaiian or other Pacific islander"), self-identified Hispanic/Latino or Spanish origin or descent, other demographic characteristics, and medical history. Based on their responses to the detailed interview, respondents were classified as: 1) having a medical or psychiatric condition considered exclusionary for CFS ; 2) having CFS- like illness if they reported severe fatigue lasting 6 months or longer that was not alleviated by rest, that caused substantial reduction in occupational, educational, social or personal activities, and that was accompanied by at least 4 of the CFS case defining symptoms ; 3) being chronically unwell (reporting any of the CFS defining symptoms) with or without fatigue);, 4) or being well. Clinical evaluation. All respondents between 18 and 59 years who had no exclusionary conditions per interview, and were classified as having a CFS-like illness were invited for a one- day clinical examination to further investigate exclusionary medical and psychiatric conditions. We also invited a similar number of randomly selected participants identified with chronic unwellness (at least six months of unwellness with or without fatigue but not CFS-like). Finally, we invited well participants, matched to the CFS-like on geographic stratum, sex, race/ethnicity and age (within 3 years), for a one-day clinical examination. Those from the urban or rural areas attended a clinic in Macon, and those from Atlanta attended a similar clinic in Atlanta. No more than 4 participants attended a clinic on any day, and appointments were staggered for optimal flow. Clinic staff with responsibilities for examinations was not aware of participants' telephone interview responses or classification. The authors and CDC CFS Research Program staff attended clinics on a regular basis to assess operations. Case definitions. Telephone interview. Study participants who underwent a detailed telephone interview and met criteria of the 1994 CFS case definition  were classified as CFS-like. In brief, criteria for classification as CFS-like on telephone included persistent or relapsing fatigue of at least 6 months' duration; the fatigue was not relieved by rest and caused substantial reduction in previous levels of occupational, educational, social, or personal activities. Exclusionary conditions included self-reported medical or psychiatric conditions that could cause the fatigue. Finally, the medically/psychiatrically unexplained fatigue must have been accompanied by at least 4 of the 8 CFS case defining symptoms : 1) unusual post-exertional malaise; 2) unrefreshing sleep; 3) impaired memory or concentration; 4) headaches; 5) muscle pain; 6) multi- joint paint without swelling or redness; 7) sore throat; 8) tender cervical/axillary lymph nodes. CFS-like subjects differ from CFS by not having been evaluated clinically in the study. Clinic. The objective of the clinical evaluation was to classify participants' clinical status and diagnose exclusionary medical and psychiatric conditions. As recommended by the International CFS Study Group , participants were classified as CFS, unexplained chronic illness not meeting criteria for CFS (termed ISF), or well by using standardized reproducible criteria for measuring specifics of the 1994 case definition . We used the Multidimensional Fatigue Inventory (MFI)  to assess fatigue status. For classification as CFS, those with a score => well-population medians on the general fatigue or reduced activity scales of the MFI were considered to meet fatigue criteria of the 1994 case definition. Functional impairment was assessed by the medical outcomes survey short form-36 (SF-36) . For classification as CFS, those with a score =< 25th percentile of population norms in the physical function or role physical, or social function, or role emotional subscales of the SF-36 were considered to have substantial reduction in activities as specified in the 1994 definition. Finally we used the CDC Symptom Inventory (SI)  to evaluate occurrence, frequency and severity of the 8 CFS- defining accompanying symptoms. The SF-36, MFI and SI domain scores require complete data for the subscales. We imputed a zero value in the case of one-item non-response for subscales contributing to the relevant domains. For classification as CFS, those reporting => 4 case defining symptoms and who scored > 25 on the SI concerning frequency and severity of the 8 case defining symptoms  were considered to meet accompanying symptom criteria of the 1994 case definition. Participants who fulfilled some, but not all of these criteria were classified as ISF. Those who met none of the criteria were considered to be well. The MFI, SF-36 and SI are self-administered paper and pencil forms. A trained clinic supervisor reviewed forms and helped subjects complete missing or misunderstood portions. To screen for medical conditions considered exclusionary for CFS [11, 7], participants completed past medical history questionnaires and were requested to bring all their medications and supplements to the clinic. A licensed nurse practitioner or physician assistant reviewed subjects' past medical histories and medications to clarify omissions or discrepancies and also catalogued all medications. Relevant information was brought to the attention of the study physicians. A specifically trained licensed physician then performed a standardized physical examination . The examination was expanded if there were any concerns. The examiner recorded a differential diagnosis. Blood and urine specimens were obtained for laboratory screening tests to identify possible underlying or contributing medical conditions as stipulated by the case definition [11, 7]. Laboratory tests included a complete blood count with differential, c-reactive protein, alanine aminotransferase (ALT), SGPT, albumin, alkaline phosphatase, asparatate aminotransferase (AST), SGOT, total bilirubin, calcium, carbon dioxide, chloride, creatinine, glucose, potassium, total protein, sodium, urea nitrogen BUN, antinuclear antibodies, rheumatoid factor, TSH, free T4, and urinalysis. To screen for psychiatric conditions considered exclusionary for CFS [11, 7], a trained and experienced licensed psychiatric social worker, clinical psychologist, psychiatric nurse practitioner or certified psychiatric research nurse administered the research version of the SCID . They underwent specific training for the SCID. Psychologists on the CDC CFS Research Program monitored their technique on a regular basis. The SCID included the screening module, mood episodes, psychotic symptoms, psychotic disorders, mood disorders, substance use disorders, anxiety disorders, somatoform disorders, eating disorders, and adjustment disorders. A review committee of CDC and Emory University physicians and psychologists reviewed medical and psychiatric evaluations to determine the presence of medical and psychiatric conditions exclusionary for CFS. Members of the review committee were not aware of subjects' classification either on phone interview or in the clinic. Weighting Prevalence estimates and statistical analyses utilized weighted data. The survey weights maintained (through the stages of the survey) the relation between the sample and the population in each geographic stratum, and they included several adjustments that are customarily employed to reduce bias. In the process of developing weights, one step adjusted for households that did not have telephones. To estimate the proportion of households that did not have a telephone in each of the three geographic strata, we analyzed data from the 5% public-use microdata samples (PUMS) of the 2000 Census. For the metropolitan stratum, the analysis used PUMS data from De Kalb and Fulton Counties. The other two strata, however, do not correspond exactly to geographic entities for which data are available in the PUMS. Thus, the analysis for the urban stratum used data from Bibb County; the rural stratum used data from a larger combination of counties that contained the counties of that stratum. The resulting estimates of the proportion of households that did not have a telephone were 1.68% in the metropolitan stratum, 3.66% in the urban stratum, and 6.35% in the rural stratum. Adjustments for nonresponse on the detailed telephone interview and nonresponse on the clinical evaluation kept the categories of illness separate; thus, to the extent possible, respondents accounted for nonrespondents who belonged to the same illness category (and shared other key characteristics). The adjustment factor, applied to the weight of each respondent, equaled the ratio of the sum of the weights (at that stage) of respondents and nonrespondents to the sum of the weights of respondents. Another adjustment, at the household level, used data on interruptions in telephone service to compensate for the inability of the telephone survey to reach households that did not have telephone service. Households completing the screening interview received a base sampling weight (64.4 in the metropolitan stratum, 6.4 in the urban stratum, and 4.9 in the rural Stratum) equal to the reciprocal of the probability that the household's telephone number was selected for the sample. Base weights were reduced for multiple residential telephone numbers in the household (either by a factor of 2 or a factor of 3) and adjusted for households that did not complete screening interviews (by a factor of 1.03 in each stratum), for numbers associated with undetermined residential status (by a factor of 2.4, 2.3, and 2.1, respectively), and for non-telephone households in the population (by a factor of 1.7, 2.2, and 2.3 for households that reported interruptions in telephone service and by a factor of 1.24, 1.38, and 1.04 for households that did not report interruptions) [16, 17]. (The household weights ranged from 66 to 268 in the metropolitan stratum, from 7 to 34 in the urban stratum, and from 4 to 24 in the rural stratum.) Subjects selected for detailed interviews received an initial interview weight equal to their household weight multiplied by the reciprocal of their probability of selection (the probability of selecting a household as a source of a subject ranged from 0.32 to 1.0 for unwell subjects and from 0.17 to 1.0 for well subjects; the probability of selecting an individual subject within the household was the reciprocal of the number of unwell, respectively well, persons in the household; subjects with prolonged fatigue were selected with certainty). Within each combination of stratum (metropolitan, urban, rural) and illness classification (fatigued, unwell, well), initial weights were adjusted for nonresponse on the detailed interview, within a total of 195 cells defined by sex, age, and race (the adjustment factors ranged from 1.05 to 2.25 and exceeded 2.0 in only 22 cells). A further adjustment in each stratum used an iterative form of post-stratification to bring the weighted totals into agreement with control totals from the 2000 Census on race and on the combination of sex and age. This process produced an interview weight for each subject who completed a detailed interview. (The interview weights ranged from 84 to 16,723 in the metropolitan stratum, from 5 to 822 in the urban stratum, and from 4 to 892 in the rural stratum.) Each CFS-like subject who completed a clinical evaluation received a clinical-evaluation weight, which incorporated an adjustment for nonresponse on the clinical evaluation within stratum- specific cells defined by sex and age (over the 19 cells the adjustment factor ranged from 1.11 to 2.71). For chronically unwell subjects the clinical-evaluation weights incorporated a parallel adjustment for nonresponse (over the 14 cells the adjustment factor ranged from 1.52 to 2.61), preceded by an adjustment for selection of the subsample (by a factor of 3.02, 3.88, and 2.89 in the respective strata). (The clinical-evaluation weights ranged from 193 to 32,354 in the metropolitan stratum, from 8 to 1,787 in the urban stratum, and from 10 to 1,358 in the rural stratum.) Because they were selected for clinical evaluation only as a result of being matched to a CFS-like subject, well subjects did not have their own clinical-evaluation weight. Prevalence estimates Within each stratum, prevalence was estimated using SUDAAN (SUDAAN: Research Triangle Institute, Research Triangle Park, NC)  software to calculate weighted percentages and obtain standard errors that reflected the sample design and survey weights. Prevalence estimates based on illness classifications derived from the detailed interviews used the data of all subjects who completed detailed interviews, and their respective interview weights. In order to maintain the relation to the population, prevalence estimates based on illness classifications derived from clinical data used a combination of clinical data and interview data. For CFS-like and chronically unwell subjects who completed clinical evaluations, the data obtained from the clinical evaluations were used along with their clinical-evaluation weights. For subjects classified as CFS-like and chronically unwell who were not eligible for clinical evaluations, and also for all well subjects, the data obtained from detailed interviews were used along with their interview weights. Because the matching process does not preserve a sampling-based connection with the population, clinical data from well subjects were not used in calculating prevalence estimates. Statistical analyses Weighted chi2 tests in SUDAAN were used to compare proportions of subjects diagnosed with CFS by demographic categories. P-values were calculated to evaluate the statistical significance of differences in CFS prevalence by age, sex, race, ethnicity, education and household income. Results Screening telephone interview Overall, 105,000 telephone numbers were selected for a screening interview; 66,295 (63%) were ineligible because they belonged to businesses, were not working, or were cellular phones. Residential status could not be determined for 24,594 (23%) of the numbers -- 2,136 (2%) because all attempts produced no contact, 4,258 (4%) because attempts reached only an answering machine, and 18,200 (17%) because of another outcome (primarily the person refused to participate before household status could be determined). A total of 2,864 numbers (3%) belonged to households where all residents were over the age of 59; these households were not eligible for the study. The remaining 11,247 numbers (11%) were residential and eligible for screening. We completed screening telephone interviews for 10,837 of the identified residential numbers (96% participation). Taking into account estimated numbers of age-eligible households among the telephone numbers for which residential status could not be determined and among the households for which screening was not completed, the response rate for the screening step was 79%. There were no important differences in response across the strata (range 76.1% to 81.4%). The screening interviews enumerated 19,381 residents. Of these, 10,834 (56%) were identified by the household informant as well, 5,122 (26%) as unwell for at least a month but not fatigued, and 3,425 (18%) as unwell and fatigued for at least a month. We attempted to conduct detailed telephone interviews on all those who were unwell with fatigue, and 2,438 (71%) completed the detailed interview. We randomly selected 2,134 of those who were unwell not fatigued, and 1,429 (67%) completed detailed interviews; similarly, 1,756 (56%) of 3,113 randomly selected household members identified as well completed detailed telephone interviews. There were no important differences in detailed interview completion across the strata (range 66.8% to 72.6%) Telephone interview sample Individuals' responses during the detailed telephone interview roughly mirrored the household informants' classification (Table 1). For example, 65% of those described as well by household informants during the screening interview, described themselves as `well' during the detailed interview. Similarly, 69% of those described as unwell not fatigued by household informants, described themselves as unwell not fatigued. A smaller proportion (49%) of those who were initially described as unwell fatigued by household informants described themselves as unwell with fatigue during the detailed interview. Following the detailed telephone interview 1,513 respondents were classified as well, 1,803 as unwell for at least a month but not fatigued, 1,400 as unwell with fatigue, and 907 as CFS-like, meaning that they fulfilled all criteria of the 1994 case definition  on telephone interview. Responses during the detailed telephone interview identified a self-reported medical or psychiatric explanation for the illness in 438 (48%) of CFS-like participants, 558 (40%) of those unwell with fatigue, and 429 (24%) of those who were unwell but not fatigued. Interestingly, 184 (12%) of participants classified as well reported medical and psychiatric conditions and these were in general the same as those reported by participants with CFS-like illness and those who were unwell. Clinic sample We invited all 469 individuals with CFS-like illness and no medical/psychiatric exclusions for a clinical evaluation, and 292 (62%) agreed to participate. Those who did not come for a clinical evaluation were similar to those who did with regard to age, sex, income, and duration of illness. We randomly selected 505 from the 1,763 identified as chronically unwell (=> 6 months duration with or without fatigue) and invited them to clinic; 268 (53%) participated. Finally, we selected 641 interview participants classified as well (n=481) or prolonged unwell, i.e. unwell for 1 to 6 months duration (n=160). These were matched to the CFS-like on sex, race, and age (within 3 years). A total of 163 participants classified as well and 60 who were classified as prolonged unwell completed clinical evaluations. As with telephone interviews, there were no important differences in clinical evaluation participation across the three strata, either overall or by classification status. Clinical evaluation identified a medical or psychiatric exclusion in 26 (16%) of those classified as well based on their detailed telephone interview responses, 24 (40%) of those with prolonged unwellness, 44 (30%) of the chronically unwell not fatigued, 45 (38%) of the chronically unwell fatigued, and 141 (48%) of the CFS-like. The most frequent medical exclusions included previously undiagnosed thyroid disease (24% of the total), anemia (18%), uncontrolled diabetes (14%), autoimmune disease (11%), inflammatory disease (8%), heart disease (7%), arthritis (3%) and pulmonary disease (3%). Psychiatric exclusions encompassed alcohol or substance abuse (43%), melancholic depression (26%), bipolar disorder (19%), psychosis (7%), and anorexia/bulimia (5%). One subject enrolled with chronic unwellness and one CFS-like subject had incomplete medical or psychiatric evaluations and could not be classified. Table 2 summarizes the relation between classification following detailed telephone interview and clinic classification among the 501 study subjects who did not have an exclusionary condition. One hundred-thirteen met criteria for CFS, 264 had an unexplained illness (ISF), and 124 were well. Interestingly, 53 (39%) of those who were classified as well based on their telephone interview data were classified as ISF (insufficient symptoms or fatigue for CFS) or CFS when evaluated in clinic, while 26 (15%) of those enrolled as chronically unwell based on telephone interview had no evidence of unwellness when evaluated in clinic. Prevalence estimates Table 3 summarizes prevalence of CFS in metropolitan, urban and rural populations according to demographic characteristics. Overall, 2.54% of the study populations had CFS; 83% reported gradual onset and 17% reported sudden onset of their illness. There were no statistically significant differences in prevalence of CFS among metropolitan, urban, and rural populations among women (p=.37). However, among men, CFS prevalence varied significantly among geographic strata, and was lowest in the metropolitan stratum (p=.038). In the metropolitan area, the CFS prevalence in women was 11.2 times that in men (p=.009), whereas in the urban and rural populations the female-to-male ratios of CFS prevalence were 1.7 and 0.8, respectively, and did not represent statistically significant differences. Overall, white and black adults had roughly similar rates (2.3% and 2.9%, respectively). Although Hispanic adults in metropolitan and rural populations had considerably higher prevalence than non-Hispanic, the numbers of Hispanics interviewed were low (23 in the metropolitan area, 38 urban, and 59 rural), and the differences were not statistically significant. Age-specific prevalence of CFS differed among age categories in urban and rural populations (p=.041 and p=.0001, respectively), but not in metropolitan (p=.224). The rate was lowest among urban and rural adults aged 18-29 and highest among rural adults aged 50-59. The prevalence of CFS was not significantly related to level of education in metropolitan, urban or rural strata (p=.129, p=.486, and p=.695, respectively). Similarly, CFS prevalence was not significantly related to household income in these strata (p=.741, p=.900, and p=.373, respectively). Discussion This is the first published study, of which we are aware, that screened defined populations for unwellness and then used standardized, validated instruments to define CFS, unwellness, and wellness based on functional impairment, characteristics of fatigue, and frequency/severity of the 8 case defining symptoms . Using this approach, we found 2.54% of the Georgia population to suffer from CFS, which was 10-fold higher than previous estimates in the population of Wichita (0.24%)  and 6-fold higher than estimated in the Chicago population (0.42%) . We are aware of no other published population-based surveys of CFS. However, several studies have published estimates of CFS prevalence; although they cannot be directly compared to the 2 U.S. studies, their prevalence estimates serve to put the present study into a more complete perspective. A well-conducted survey of the Group Health Cooperative of Puget Sound estimated that between 0.75 and 0.27% of that HMO population had CFS . A survey of primary care patients in England, published in 1997, estimated that 2.6% of that population met criteria for CFS . Finally, analysis of data from the Australian National survey of Mental Health and Wellbeing estimated that 1.5% of the Australian adult population suffers from chronic neurasthenia (defined similarly to CFS) . In part, the increased prevalence we estimated in Georgia reflects a difference in screening criteria. The Georgia survey screened for unwell (the core symptoms of CFS), whereas previous studies have screened only for fatigue. Our less restrictive approach allowed the inclusion of potential cases whom, although noted as unwell-not fatigued by a household informant, endorsed chronic fatigue upon detailed in-person interviewing. Sixty-nine people whom the household informant identified during the screening telephone interview as well or unwell without fatigue were classified as CFS-like based on their responses during detailed telephone interview (7.6% of all CFS-like). Further, 13 clinic participants classified as well or unwell without fatigue, based on their detailed telephone interview were diagnosed as CFS when evaluated clinically. In other words, 11.5% of subjects with CFS would not have been detected in previous studies that queried participants only for fatigue. The 6- to 10-fold greater prevalence estimates also reflect application of more sensitive and specific measures of the CFS diagnostic parameters specified by the 1994 case definition. Previous prevalence estimates from population surveys and those based on patients attending clinics did not use validated standardized instruments to define CFS; rather they simply queried as to the presence or absence of fatigue, accompanying symptoms, and impairment. In 2003, the International Chronic Fatigue Syndrome Study Group published recommendations concerning application of the case definition . They recommended the use of validated instruments to obtain standardized measures of the major symptom domains of the illness, and this study implemented those recommendations. The Study Group specifically recommended: 1) the SF-36, to measure functional impairment; 2) the Checklist Individual Strength or MFI, to obtain reproducible quantifiable measures of fatigue; 3) and the CDC Symptom Inventory to document toe occurrence, duration and severity of the symptom complex. The manner in which we applied the case definition in Georgia has been shown to detect about 3 times the number of CFS cases as verbatim application of the 1994 definition . Of course, we cannot exclude the possibility that CFS prevalence may be higher in Georgia than Wichita and Chicago. However, the manner in which we chose and applied subscales and their cutoffs from the SF-36 and MFI can be debated. We used the SF-36 physical function, role physical, social function and role emotional subscales to define an illness severe enough to "result in substantial reduction in previous levels of occupational, educational, social, or personal activities." . In particular, we included the role emotional subscale to capture the relation between functional emotional impairment and reduced social and personal activities. We ascertained the onset and duration of fatigue during interview (the case definition requires => 6 months of fatigue that is of new or definite onset) and utilized the MFI general fatigue and reduced activity scales to define severe fatigue. We used stringent (i.e., =< 25th percentile population norms on any of the 4 SF-36 scales) to define severe functional impairment. Numerous publications tabulate slightly different population norms and we chose those published by Quality Metric . We are not aware of published population norms for the MFI, so we used the cut-offs established in a previous CDC study (=> than the median determined in Wichita) , which is more sensitive and less specific than the 25th percentile SF-36 cutoff. There are no population norms for the Symptom Inventory, so we also used cutoffs applied in the previous study. Finally, population norms are not cast in iron and one might consider defining cut-offs specific to each population studied. In the end, we decided to use these cutoffs because we believe they make sense; because we used them in the Wichita study and can compare findings in similarly ill individuals; and, because others can replicate the findings if they use the same cutoffs and stratify their populations based on variations of the cutoffs.. The other important new finding is that, despite differences in demographic factors, CFS prevalence was similar in the metropolitan, urban, and rural populations we surveyed (about 2.5%). However, differences in sex-specific prevalence among the strata must be evaluated in more detail. The striking differences between female and male rates in the 3 strata may indicate risk effects of gender (a social construct) in distinction to sex (a biologic attribute). In addition, the high prevalence among those of Hispanic ethnicity in the metropolitan area bears further investigation in a study designed to include Spanish-speaking persons. The final major finding concerns the high proportion of study participants in whom the survey documented previously undiagnosed medical or psychiatric conditions. Overall 48% of persons recruited for clinical evaluation because CFS-like illness was identified on phone interview had exclusionary medical or psychiatric conditions, which is similar to the occurrence of such illness in other studies [2, 3]. Most of these exclusions are amenable to treatment if appropriately recognized. It is also important to note the relatively common occurrence of such conditions in people with other categories of unwellness identified during the phone interview. Indeed, 16% of respondents classified as well on the basis of interview had such exclusions identified. Further analyses will address whether the onset of psychiatric illness preceded or followed development of CFS-like illness. Interpretation of the findings must consider obvious study weaknesses. First, like other telephone surveys, we faced challenges of nonresponse. Potential respondents can be lost in the processes of determining whether telephone numbers belong to households, completing screening interviews with household respondents, and maintaining contact with selected subjects to complete detailed interviews. In addition, some people are reluctant to schedule a full-day clinical examination. A random-digit-dialing survey that subsamples some types of subjects does not have a standard, single-number response rate. Taking into account the resolution of sampled telephone numbers (as residential or not), completion of screening interviews, and completion of detailed interviews, we calculated a response rate of 47.8% through the detailed interview. A further calculation, including the completion of clinical evaluations by subjects with CFS-like illness and chronically unwell subjects, produced a response rate of 27.5% through the clinic stage. Although nonresponse is always an appropriate subject for concern, detailed adjustments in the sampling weights often are able to mitigate its adverse effects. Thus, the adjustment for nonresponse on the detailed interview used a total of 195 cells, taking into account stratum, illness classification, sex, age, and race; post-stratification aligned respondents' weights with population totals; and the adjustment for nonresponse on the clinical evaluation used a total of 33 cells based on stratum, illness classification, sex, and age. The second weakness concerns obtaining clinical information by telephone interview. Initial classification of subjects as well, unwell not fatigued, and unwell fatigued based on telephone interviews with household informants was confirmed by detailed interviews in 65%, 69% and 49% of subjects in those respective categories. Except for the unwell fatigued group, these levels of agreement between household informants and self-reports were similar to the 66% agreement detected in a study designed to examine concordance between self-reported health conditions and proxy information among adults => 65 years of age in the United Kingdom . This degree of agreement was considered reasonable. The lower level of agreement detected among the unwell fatigued may be due to the relative nonspecificity of fatigue, compared to other symptoms of unwellness, including problems with memory/concentration, unrefreshing sleep, or muscle/joint pain. Third, the study was conducted in standard 8th grade-level English, which may have led to an under-sampling of ethnic minority groups (e.g., Spanish speaking). Prevalence of CFS was unusually high among the metropolitan and rural Hispanic populations and unusually low among rural Hispanic residents. This may reflect important ethnic differences in risk  and we weighted the sample to allow for ethnic differences. Most likely it reflects language-related misunderstanding of the questions and weighting cannot address this. It will be important to further evaluate the occurrence of and risk factors for CFS in English and non-English speaking metropolitan, urban, and rural Hispanic populations . Fourth, the study utilized Atlanta (Fulton and DeKalb counties) to represent metropolitan Georgia, Macon and Warner Robins to represent urban Georgia, and the counties surrounding the urban area to represent rural Georgia. We did this for logistic reasons, and the results cannot a- priori be generalized to other populations. Indeed, populations of the 10 rural county seats varied from 587 to 19,000 (median 2,000), so several exceeded the Census Bureau definition of rural. Finally, in spite of a rigorous case definition, CFS has no diagnostic markers or characteristic physical signs. Thus, CFS diagnosis is based on self-reported symptoms, disability and exclusion of known diseases. Therefore, potential misclassification of study subjects remains a concern, as CFS is clinically heterogeneous and likely represents more than one entity [25, 26]. Conclusions In conclusion, this investigation suggests that 2.54% of the adult population of Georgia suffers from CFS. This figure is 6- to 10-fold higher than previous prevalence estimates and likely reflects improved screening methods and more sensitive and specific diagnostic criteria. However, this is the first study to measure CFS prevalence in Georgia, so we cannot rule out the possibility that CFS prevalence is higher in Georgia than other geographic areas where CFS prevalence has been reported. We did not find evidence for metropolitan, urban, rural differences in the prevalence of CFS, nor did we find differences in prevalence between white and black populations. These findings are important for public health officials, health care providers, and the public in general. The methodology and findings from this study should be of interest to those studying CFS and those with responsibilities for health care in other states in the US and in other countries. Competing interests The authors declare that they have no competing interests. Authors' Contributions WCR was Principal Investigator of the study. WCR, EM, CH, RB, JFJ designed the study and wrote the protocol. DCH was responsible for sampling strategy and statistical analysis. WCR, CH, EM, RSB, JFJ supervised fieldwork. MM and RD supervised technical aspects of the study and supervised daily phone interviews and clinic operations. All authors contributed to preparation of the manuscript. Acknowledgements This study was fully funded by the US Centers for Disease Control and Prevention. We acknowledge Dr. Jin-Mann Lin for her statistical review of this manuscript. The findings and conclusions in this report are those of the authors and do not necessarily represent the views of the funding agency. Tables Table 1. Screening Interview Classification ------------------------------------------------------------------------------ Detailed Interview Well Unwell not Unwell Fatigued Classification n=1,756 Fatigued n=2,438 n=1,429 Well (n=1,513) 1,141 (65%) 242 (17%) 130 (5%) Unwell not Fatigued (n=1,803) 545 (31%) 982 (69%) 276 (11%) Unwell Fatigued (n=1,400) 57 (3%) 149 (10%) 1,194 (49%) CFS-like (n=907) 13 (1%) 56 (4%) 838 (34%) ------------------------------------------------------------------------------ (%) indicates column percent Table 2. Clinic Classification of Participants with No Exclusionary Conditions ------------------------------------------------------------------------------ Clinic Classification ------------------------------------------ Detailed Interview Well ISF CFS Classification n=124 n=264 n=113 Well (n=137) 83 (61%) 53 (39%) 1 (1%) Prolonged Unwell (n=36) 15 (42%) 19 (53%) 2 (6%) Unwell not Fatigued (n=104) 20 (19%) 74 (71%) 10 (10%) Unwell Fatigued (n=74) 6 (8%) 52 (70%) 16 (22%) CFS-like (n=150) 0 (0%) 66 (44%) 84 (56%) ------------------------------------------------------------------------------ (%) indicates row percent Table 3. Prevalence of CFS (in percent) by Demographic Characteristics in the Three Populations ------------------------------------------------------------------------------ Metropolitan Urban Rural % (SE) % (SE) % (SE) ------------------------------------------------------------------------------ Overall prevalence 2.55 (0.85) 2.48 (0.67) 2.66 (0.58) Sex Female 4.70 (1.60) 3.10 (0.81) 2.40 (0.57) Male 0.42 (0.37) 1.82 (1.08) 2.89 (0.97) Race White 3.72 (1.71) 2.39 (0.70) 3.20 (0.72) Black 1.78 (0.63) 2.71 (1.27) 1.71 (1.00) Ethnicity Hispanic 21.21 (11.97) 7.02 (6.74) 0.70 (0.71) Non-Hispanic 2.25 (0.82) 2.30 (0.64) 2.72 (0.59) Age 18-29 4.15 (2.28) 0.54 (0.29) 0.00 30-39 0.74 (0.43) 5.59 (2.40) 2.68 (1.06) 40-49 2.64 (1.34) 2.38 (0.83) 2.08 (0.77) 50-59 2.11 (1.13) 1.74 (1.09) 6.88 (2.17) Education =< High School Graduation 0.00 1.02 (0.73) 2.48 (1.10) High School Graduate 1.60 (1.24) 2.54 (1.02) 3.80 (1.34) Technical or Some College 2.02 (1.01) 3.05 (1.60) 2.33 (1.15) => College Graduate 3.44 (1.47) 2.60 (1.25) 1.97 (0.72) Household Income =< $20,000 4.85 (4.01) 1.87 (1.06) 1.87 (0.83) $20,001-$40,000 3.43 (2.49) 2.89 (1.57) 4.72 (1.70) >$41,000 1.60 (0.61) 2.79 (1.19) 2.25 (0.80) Poverty Level =< $20,000 4.85 (4.01) 1.87 (1.06) 1.87 (0.83) > $20,001 2.09 (0.80) 2.82 (0.95) 3.09 (0.79) ------------------------------------------------------------------------------ References 1. 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An empirical delineation of the heterogeneity of chronic unexplained fatigue in women. Pharmacogenomics 2006, 7:355-364. 26. Broderick G, Craddock RC, Whistler T, Taylor R, Klimas N, Unger ER: Identifying illness parameters in fatiguing syndrome using classical projection methods. Pharmacogenomics 2006, 7:407-419. -------- (c) 2007 BioMed Central Ltd [Return to top] ------------------------------ Date: Thu, 21 Jun 2007 12:11:59 +0100 From: Tom Kindlon <tomkindlon OCEANFREE.NET> Subject: RES: More symptoms could be added to a CFS Symptom Inventory In response to: Psychometric properties of the CDC Symptom Inventory for assessment of Chronic Fatigue Syndrome Dieter Wagner, Rosane Nisenbaum, Christine Heim, James F Jones, Elizabeth R Unger and William C Reeves Population Health Metrics 2005, 3:8 doi:10.1186/1478-7954-3-8 http://www.pophealthmetrics.com/content/3/1/8 More symptoms could be added to a CFS Symptom Inventory http://www.pophealthmetrics.com/content/3/1/8/comments Tom Kindlon (21 June 2007) Many would feel that the 8 symptoms used in the CDC '94 definition  were chosen in a somewhat arbitrary fashion; so it is to be welcomed that the CDC itself has started to look beyond these symptoms with the CDC CFS Symptom Inventory. The idea of a Short Form of the CDC Symptom Inventory is also interesting. However, it is not clear to me where the extra symptoms that are on the CDC CFS Symptom Inventory came from. For example, I didn't see some of the symptoms listed in Reeves et al . In 2001, De Becker et al  published data on the symptoms found in over 2500 patients. They tried to improve on the 1988  and 1994 CDC criteria. They suggested a list of symptoms that could be used to strengthen the ability to select ME/CFS patients. Many of the symptoms they mentioned are not in the CDC CFS Symptom Inventory. So to claim that the "CDC Symptom Inventory assesses the full range of CFS associated symptoms" seems questionable. It would be interesting if in future these symptoms (that De Becker et al were suggesting) were added before statistical analyses are performed. The fatigue criteria and functional impairment criteria have become much less restrictive . For example, to satisfy the fatigue criteria, the fatigue is required to be greater than or equal to the medians of the MFI general fatigue (? 13) or reduced activity (? 10) scales. So it now seems particularly important that the symptom criteria have good sensitivity and specificity or one is going to end up with a definition that leads to very heterogeneous samples. Tom Kindlon  Fukuda K, Straus SE, Hickie I, Sharpe MC, Dobbins JG, Komaroff A: The chronic fatigue syndrome; a comprehensive approach to its definition and study. Ann Int Med 1994, 121:953-959.  Reeves WC, Lloyd A, Vernon SD, Klimas N, Jason LA, Bleijenberg G, Evengard B, White PD, Nisenbaum R, Unger ER, International Chronic Fatigue Syndrome Study Group: Identification of ambiguities in the 1994 chronic fatigue syndrome research case definition and recommendations for resolution. BMC Health Services Research 2003, 3:25. http://dx.doi.org/10.1186/1472-6963-3-25  A definition-based analysis of symptoms in a large cohort of patients with chronic fatigue syndrome, P. De Becker, N. McGregor, and K. De Meirleir. Journal of Internal Medicine 2001;250:234-240  Holmes GP, Kaplan JE, Gantz NM, Komaroff AL, Schonberger LB, Straus SE, et al.: Chronic fatigue syndrome: a working case definition. Ann Intern Med 1988, 108:387-389.  Reeves WC, Wagner D, Nisenbaum R, Jones JF, Gurbaxani B, Solomon L, Papanicolaou DA, Unger ER, Vernon SD, Heim C: Chronic fatigue syndrome - a clinically empirical approach to its definition and study. BMC Medicine 2005, 3:16. ----------------- The latest prevalence study only appears to use the 8 original CDC criteria. However perhaps in the future the CDC will use the 19-symptom scale used in this study or the Symptom Inventory Short Form (6 symptoms). This study suggests that the 8 symptoms currently being used correlate with the 19 symptoms score. However if different or more symptoms had been used, the correlation might have been weaker. Also if different symptoms had been used as part of the full inventory, the Short Form may have had different symptoms. My concern would be that any future CDC definition would not learn from the Canadian definition or the research that informed it. Here's an extract from the Canadian Guidelines with information on the De Becker study: "Since the development of our clinical criteria, we have had an opportunity to review the analysis of symptoms in over 2,500 patients by De Becker et al. (45). They found that the Holmes definition (42) of fatigue, swollen/tender lymph nodes, sore throat, muscle weakness, recurrent flu-like symptoms, post-exertional fatigue, myalgia, memory disturbance, nonrestorative sleep and replacing low-grade fever with hot flashes; and the addition of ten other symptoms (attention deficit, paralysis, new sensitivities to food/drugs, cold extremities, difficulties with words, urinary frequency, muscle fasciculations, lightheadedness, exertional dyspnea and gastrointestinal disturbance) strengthen the ability to select ME/CFS patients. Based on this study, we added exertional dyspnea and muscle fasciculations to our clinical definition. All the symptoms which the De Becker et al. study (45) recommended adding to strengthen the ability to select ME/CFS patients are in our definition except paralysis, which the panel did not consider prevalent enough for inclusion in a clinical definition. The clinical definition has additional symptoms, such as orthostatic intolerance, which we feel are important in a clinical setting." Tom Kindlon [Return to top] ------------------------------ Date: Fri, 22 Jun 2007 00:52:24 +0200 From: Jan van Roijen <j.van.roijen CHELLO.NL> Subject: med: Link Between Autism & Lyme Disease ~~~~~~~~~~~~~~~~~~~~~~~~~~~~ Send an Email for free membership ~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~ >>>> Help ME Circle <<<< >>>> 22 June 2007 <<<< Editorship : j.van.roijen chello.nl Outgoing mail scanned by Norton AV ~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~ See also: *Lyme & herpes in ME/CFS* Help ME Circle, 20 June 2007; at Co-Cure: http://listserv.nodak.edu/cgi-bin/wa.exe?A2=ind0706c&L=co-cure&T=0&P=9532 ~jvr ```````` http://www.prweb.com/releases/2007/6/prweb534519.htm PRWeb PRESS RELEASE NEWSWIRE 2007-06-21 New Data Supporting the Link ~~~~~~~~~~~~~~~~~~~~~~~~~~ Between Autism and Lyme Disease The LIA foundation plans to release new data at the Lyme-Autism Connection conference this weekend linking Autism and Lyme disease. "At this conference, we have presenters who will show that this connection is real" Corona, CA (PRWEB) June 20, 2007 -- News reports indicate a staggering number of Lyme disease cases going unreported. With autism rates rising each year, doctors are examining this new connection. With new CDC numbers showing one of the largest populations of Lyme disease sufferers being boys from the age of 5-14, this rings of déjB vu to parents of children with autism. Young boys are the largest category of victims of autism as well as Lyme disease, which is caused by a bacteria called Borrelia Burgdorferi. Interestingly, the symptoms of chronic Lyme disease when affecting the central nervous system are literally the same symptoms as autism spectrum disorder. The LIA Foundation will hold its first conference this week in Irvine, CA, in which new data will be released supporting this connection. "It's time that parents and doctors start looking outside the box as to why these children are so sick," comments co-founder of the LIA Foundation, Tami Duncan. "At this conference, we have presenters who will show that this connection is real." "The increasing incidence of autism spectrum disorder (560,000 in the US) is a serious threat to our children and in most cases the cause is still unknown. Some clinicians and parents have noted chronic infections, including tick-borne infections; including Lyme disease and the immune reactions to these infections are sometimes associated with autistic symptoms and autistic spectrum disorder. This meeting will review the data regarding this observation and possible explanations of this association with a goal to help reduce any preventable cases of autism spectrum disorder," states Robert Bransfield, M.D. of Red Bank, NJ. Doctors are beginning to support this link. Joseph Burrascano, M.D., the Vice President of ILADS (International Lyme and Associated Disease Society) states his position on Lyme disease and Autism. "It is my contention that Autism is an inflammatory encephalitis cause by a pathogen such as Bartonella or Mycoplasma. I share the view that Bartonella is a major infection that may eclipse Borrelia Burgdorferi as the ultimate cause of the morbidity in chronic Lyme disease. Mycoplasma too is a major concern of mine- in reviewing my 7000+ cases, those patients who were relentlessly chronic, all at one point or another in their illness, were positive for Mycoplasma." In fact, one speaker at the conference, Professor Garth Nicholson of the Institute for Molecular Medicine has found that 58% of children with Autism spectrum disorder are also harboring multiple-infections, specifically Mycoplasma. "Since these chronic infections like Borrelia, Mycoplasma and Bartonella are known to suppress the immune system, it is not a stretch to assume that when the child was injected with obscene amounts of mercury, that his fate of having an autism diagnosis, would become reality," Duncan states. Proof is on the way, with data to be released at the Lyme-Autism Connection Conference this weekend and studies in progress, parents and doctors can be sure to hear more about this in the coming months. Conference information is available online at www.liafoundation.org . It is going to be held at the Hyatt Regency in Irvine, CA, June 22 - 24th. Registration is available at the door. About Autism Autism is a disorder that currently affects 1 out of 150 children. Boys are the majority of those affected. The numbers of autism cases spiked in the mid-late 90's and continues to remain high. The exact cause of autism is still unknown, however, many theories exist. Most children do improve with some sort of bio-medical intervention. About Lyme disease Lyme disease is generally caused by a tick bite in which the tick transmits a bacteria called Borrelia Burgdorferi. Symptoms of Lyme disease include, achy joints, confusion, slurring words or word retrieval problems, brain fog, sensitivity to light and sound. Lyme disease in its late stage can be fatal, causing MS like symptoms and debilitating its victims. Treatment for Lyme disease consists of antibiotic therapy. About the LIA Foundation The foundation was started in September 2006 by parents of children with autism and Lyme disease. Kathy Blanco of Beaverton, OR and Tami Duncan of Corona, CA are the founders. The foundations' goals are to educate families and physicians on the link between Lyme and autism, bring physicians together to form a consensus for testing and treatment options and to provide funding for research studies related to autism and/or Lyme disease. Contact information: Tami Duncan LIA Foundation 1771 Honors Lane Corona, CA 92883 (951) 817-1173 ------------------------------ Date: Thu, 21 Jun 2007 22:24:14 -0400 From: "connie <connie.nelson@NTLWORLD.COM> [via Co-Cure Moderators]" Subject: ACT,NOT,MED:Cochrane on trial Margaret Williams notes that the "bible" of "evidence-based" medicine -- the Cochrane Collaboration -- has been exposed in this article as being corrupted by money and vested interests. It will be recalled that Professor Simon Wessely is responsible for Cochrane entries on ME/CFS. It will also be recalled that the York Systematic Review relied heavily on Cochrane data in its work upon which the NICE draft Guideline on "CFS/ME" is founded. --------------------------------- Commentaries Evidence-Based Medicine and the Cochrane Collaboration on Trial David K. Cundiff, MD Medscape General Medicine. 2007;9(2):56. ©2007 Medscape Posted 06/12/2007 The Cochrane Collaboration was founded in 1993 and was named for the British epidemiologist Archie Cochrane, MD (1908-1988). At the initiation of the National Health Service in the 1940s in the United Kingdom, Dr. Cochrane suggested that the free care in the National Health Service should be limited to interventions supported by evidence of their effectiveness. This was a very innovative thought in the 1940s. Dr. Ian Chalmers, the driving force behind the Cochrane Collaboration, was strongly influenced by the writings of Archie Cochrane. Most physicians perceive that "evidence-based medicine" means practicing medicine by using tests and treatments that have been vetted by randomized controlled clinical trials (RCTs) to prove that they work. Although the Cochrane Collaboration focuses mainly on systematic reviews of RCTs, it also addresses issues specific to reviewing other types of evidence when relevant. Bernadine Healy, MD, former Director of the National Institutes of Health, wrote an essay entitled "Who Says What's Best?"; the piece, critical of evidence-based medicine, appeared on September 11, 2006 in US News and World Report. Kay Dickersin, PhD, the Director of Cochrane's US Center for Clinical Trials, asked me and other Cochrane Collaboration evidence-based medicine reviewers to respond by sending op-ed pieces to the media. I agree with many of the points made by Dr. Healy. She writes that the rigid adherence to RCTs as the only valid form of scientific evidence about medical tests and treatments unfairly excludes other ways of determining what medical interventions will best serve an individual patient with a particular health problem. Dr. Healy put it succinctly: "The autonomy and authority of the doctor, and the subsequent variability in care, are the problems that evidence-based medicine wants to cure." While I concur with Dr. Healy that relying solely on evidence-based medicine to determine medical guidelines better suits the needs of governments and insurance companies for cost control than the needs of patients for optimal medical treatment, I agree for a different reason. While evidence-based medicine is absolutely essential to comprehensive healthcare reform, it has been profoundly corrupted by money. In 2001, I volunteered to help conduct a review for the Cochrane Collaboration of the evidence base for the use of anticoagulants (warfarin [Coumadin] and heparins) for blood clots in the lungs (pulmonary emboli, or PE) and legs (deep venous thromboses, or DVT), as recently affected Vice President Dick Cheney. Dr. Juliet Manyemba, a physician from England, and John Pezzullo, PhD, a retired biostatistician formally from Georgetown University School of Medicine, were my coauthors. I disclosed to the Cochrane editor that my research interest in anticoagulants for DVT and PE originated because of a malpractice case against me concerning a DVT patient that resulted in the loss of my medical license. Warfarin, heparin, and other anticoagulant drugs have been used to treat blood clots since the 1940s based on unscientific anecdotal evidence and observational studies with historical controls. Subsequently, countless RCTs involving blood thinners for venous thromboembolism (VTE) patients have included no un-anticoagulated control subjects. According to anticoagulation researchers contracted or employed by drug companies, the rationale is that it would be "unethical" not to give anticoagulants to clinical research subjects with blood clots in their legs or lungs. After reading over 1000 studies on the topic, I found 1 randomized and properly controlled trial of DVT patients. Patients in the study received either standard treatment (warfarin and heparin) or phenylbutazone (an anti-inflammatory drug like aspirin). From this single well-designed study of anticoagulants came a startling result: The anticoagulants did not prevent deaths.[3,4] Cochrane archivists turned up 2 other RCTs of anticoagulation therapy in DVT patients. Neither trial found any benefit due to anticoagulants. Summing the results of the 3 trials, 66 DVT patients received anticoagulants and 6 of them died; 60 DVT patients did not receive anticoagulants, and 1 of them died. None of the 3 trials had been referenced in any journal articles or reviews of anticoagulant therapy that I read. Although these 3 trials show a trend suggesting that warfarin and heparin do harm, there were too few patients to show with statistical significance that anticoagulants increase deaths. But they contain enough subjects to show that anticoagulants do not reduce mortality. Based on the complication rate of anticoagulation for DVT or PE in much larger observational studies, anticoagulants kill 1000-4000 Americans with VTE each year due to internal bleeding, mostly in the brain.[5-7] According to a recent population-based study of anticoagulation-related intracerebral bleeding (AAICB) rates in the greater Cincinnati area, AAICB occurred in 2000-2500 VTE American patients in 2004 (5.1-6.5 AAICB cases per 100,000 population; 12.9% of AAICB cases were related to anticoagulation of VTE patients). About 60% of AAICB patients die within 1 year. Most of the surviving 40% remain permanently disabled. Warfarin distribution in the United States quadrupled on a per-capita basis between 1988 and 1999. In Cincinnati, cases of AAICB rose 5.5-fold from 1988 to 1999. The Cochrane peer reviewers (at least 4 out of 7 of which had undisclosed financial ties to the drug companies that make anticoagulants) delayed four years over releasing this review for publication. When the only 3 RCTs discovered showed no benefit and possible harm from anticoagulants, the editor and peer reviewers directed us to include 8 additional lines of evidence supporting anticoagulation from about 50 other studies in the medical literature. When my critique of those 8 lines of evidence showed that they were all faulty, the peer reviewers did not rebut a single point. Instead, the editor demanded that we delete the additional lines of evidence from the review, because they were not from RCTs. The Cochrane editor also would not allow publication of the estimate of major and fatal bleeding from anticoagulants for VTE, because I derived those figures from large retrospective observational studies and not RCTs. When the author of one of the randomized trials discovered by the Cochrane archivists refused to cooperate and clarify to us his method of randomizing patients in his study, the Cochrane editor and/or peer reviewers invented a reason to disqualify the trial from inclusion in our review. The editor told us to accept the edits or the review wouldn't be published. The "authors' conclusions," written into our article by the Cochrane editor and peer reviewers, were these: "The limited evidence from randomized controlled trials of anticoagulants versus nonsteroidal anti-inflammatory drugs or placebo is inconclusive regarding the efficacy and safety of anticoagulants in venous thromboembolism (DVT and PE) treatment. The use of anticoagulants is widely accepted in clinical practice, so a further randomized trial comparing anticoagulants to placebo could not ethically be carried out." In our final draft of the review, we authors said that a placebo-controlled trial would be impractical and suggested a "noninferiority trial" with anticoagulants vs a nonsteroidal anti-inflammatory drug. One of the peer reviewers, with no conflict of interest that I could find, commented, "Note that it is ethically possible to conduct a study to determine if anticoagulation therapy is harmful. If nothing else, dose reduction studies could determine if lower doses or weaker therapies (aspirin or NSAIDS?) are equally effective" (ie, a noninferiority trial). Finally, in January 2006, The Cochrane Database of Systematic Reviews published our review -- completely altered by the peer reviewers and editor -- entitled, "Anticoagulants or Non-steroidal Anti-inflammatories or Placebo for Treatment of Venous Thromboembolism." At the suggestion of Dr. Dickersin, I issued a complaint to the Cochrane Collaboration publication arbitrator in September 2006. In the 7 months since I submitted the complaint, 580-2300 American VTE patients have bled to death from anticoagulants as estimated from observational studies.[5-7] This estimate is consistent with 1160-1450 deaths based on the above mentioned Cincinnati population-based AAICB study. Worldwide, at least twice as many have died. Dr. Dickersin recently told me that she cannot estimate when the Cochrane investigation will be completed. A recent similar investigation took 2 years. The publication arbitrator has resigned, and she has no guarantee of finding a replacement anytime soon. Options that they are considering include withdrawing the review from the Cochrane Database of Systematic Reviews and having new peer reviewers critique the review (except that she doesn't know when she can find new peer reviewers with expertise in anticoagulation). Options that are not under consideration include printing the review as we authors wrote it, having the Cochrane peer reviewers reply to my analysis of their 8 lines of evidence supposedly supporting anticoagulation, and asking the FDA Office of Surveillance and Epidemiology (formerly Office of Drug Safety) to examine the evidence and issue a report, as I suggested 7 months ago. Medscape General Medicine published my entire review, including the evidence from the 8 lines other than the 3 RCTs included in our Cochrane VTE review.[11-13] The Medscape VTE review concluded, "Anticoagulants have not been shown to be efficacious in reducing morbidity or mortality or safe in venous thromboembolism treatment." Medscape Chief Editor, George Lundberg, MD (former Chief Editor of JAMA), wrote the accompanying editorial, entitled "Is the Current Standard of Medical Practice for Treating Venous Thromboembolism Simply Wrong?" I sent the link to the review to several anticoagulation experts at the Food and Drug Administration. Warren Rumble, Ombudsman - FDA, Center for Drug Evaluation and Research, replied for them: "Thank you for asking FDA to provide an official response to your published article in Medscape General Medicine. I have consulted with officials in our Center for Drug Evaluation and Research regarding your request, and we will not have a response to your publication. We appreciate that you provided access to your article, and the chance to comment on it." Since anticoagulation researchers and FDA scientists chose not to rebut any of the data or conclusions of either review, the media was not interested, few physicians read the reviews, and no debate ensued. Researchers continue receiving lucrative contracts from drug companies for more anticoagulant trials. The medical establishment (drug companies, doctors, hospitals) keeps making money from the diagnosis and treatment of DVT and PE with anticoagulants (estimated total cost in 2007 will be $13 billion-$48 billion in the United States), and medical journals keep publishing more anticoagulation trials without proper controls, which are dutifully covered by a compliant media, while thousands of DVT and PE patients keep bleeding to death. To have a fair resolution concerning the interpretation of the scientific evidence about the efficacy and safety of anticoagulants for the treatment of VTE, I suggest that the reader call for the FDA Office of Surveillance and Epidemiology to investigate the issue and decide which of the 2 reviews of this topic published under my name[11,10] is valid (Office of Surveillance and Epidemiology Director Gerald Dal Pan, MD, email@example.com ; Ph: 301-796-2380; or go to http://www.fda.gov/cder/comment.htm Readers are encouraged to respond to the author at firstname.lastname@example.org or to Paul Blumenthal, MD, Deputy Editor of MedGenMed, for the editor's eyes only or for possible publication via email: email@example.com References Higgins JPT, Green S, eds. Cochrane Handbook for Systematic Reviews of Interventions 4.2.6 [updated September 2006]. Available at: http://www.cochrane.org/resources/handbook/hbook.htm Accessed January 16, 2007. Healy B. Who says what's best? US News & World Report. September 3, 2006. Available at: http://www.usnews.com/usnews/health/articles/060903/11healy.htm Accessed May 31, 2007. Nielsen HK, Husted SE, Krusell LR, Fasting H, Charles P, Hansen HH. Silent pulmonary embolism in patients with deep venous thrombosis. Incidence and fate in a randomized, controlled trial of anticoagulation versus no anticoagulation. J Intern Med. 1994;235:457-461. Abstract Nielsen HK, Husted SE, Krusell LR, et al. Anticoagulant therapy in deep venous thrombosis. A randomized controlled study. Thromb Res. 1994;73:215-226. Abstract van der Meer FJ, Rosendaal FR, Vandenbroucke JP, Briet E. Bleeding complications in oral anticoagulant therapy. An analysis of risk factors. Arch Intern Med. 1993;153:1557-1562. Abstract Fihn SD, McDonell M, Martin D, et al. Risk factors for complications of chronic anticoagulation. A multicenter study. Warfarin Optimized Outpatient Follow-up Study Group. Ann Intern Med. 1993;118:511-520. Abstract Landefeld CS, Beyth RJ. Anticoagulant-related bleeding: clinical epidemiology, prediction, and prevention. Am J Med. 1993;95:315-328. Abstract Flaherty ML, Haverbusch M, Sekar P, et al. Location and Outcome of Anticoagulant-Associated Intracerebral Hemorrhage. Neurocrit Care. 2006;5:197-201. Abstract Flaherty ML, Kissela B, Woo D, et al. The increasing incidence of anticoagulant-associated intracerebral hemorrhage. Neurology. 2007;68:116-121. Abstract Cundiff DK, Manyemba J, Pezzullo JC. Anticoagulants versus non-steroidal anti-inflammatories or placebo for treatment of venous thromboembolism. The Cochrane Database of Systematic Reviews. 2006; Issue 1. Art. No.: CD003746. DOI: 10.1002/14651858.CD003746.pub2. Cundiff DK. Anticoagulation therapy for venous thromboembolism. MedGenMed. 2004;6(3):5. Available at: http://www.medscape.com/viewarticle/487577 Accessed May 31, 2007. Cundiff DK. Letters to editor re "Anticoagulation therapy for venous thromboembolism." Medscape General Medicine. 2005;7(1):49. Available at: http://www.medscape.com/viewarticle/496148 Accessed May 31, 2007. Cundiff DK. Author's response to letters to the editor regarding the article entitled "Anticoagulation therapy for venous thromboembolism." Medscape General Medicine. 2005;7(1):48. Available at: http://www.medscape.com/viewarticle/496149 Accessed May 31, 2007. Lundberg GD. Is the current standard of medical practice for treating venous thromboembolism simply wrong? MedGenMed. September 9, 2004;6(3):36. Available at: http://www.medscape.com/viewarticle/488717 Accessed May 31, 2007. Cundiff DK. Money Driven Medicine--Tests and Treatments That Don't Work. 2006;:170-172. Available at: http://doctormanagedcare.com Accessed May 31, 2007. David K. Cundiff, MD, Los Angeles County and USC Medical Center (Retired) Author's email: firstname.lastname@example.org Disclosure: David K. Cundiff, MD, has disclosed no relevant financial relationships. [Return to top] ------------------------------ Date: Fri, 22 Jun 2007 06:13:42 +0200 From: Jan van Roijen <j.van.roijen CHELLO.NL> Subject: not,med: First Fibromyalgia Treatment ~~~~~~~~~~~~~~~~~~~~~~~~~~~~ Send an Email for free membership ~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~ >>>> Help ME Circle <<<< >>>> 22 June 2007 <<<< Editorship : j.van.roijen chello.nl Outgoing mail scanned by Norton AV ~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~ http://www.salon.com/wire/ap/archive.html?wire=D8PTEC8O2.html FDA OKs First Fibromyalgia Treatment ~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~ June 21,2007 | WASHINGTON -- A Pfizer Inc. drug won expanded federal approval Thursday as the first treatment for fibromyalgia, a mysterious syndrome marked by muscle pain and fatigue. The Food and Drug Administration action means Lyrica becomes the first drug that can be marketed specifically as a treatment for adults with fibromyalgia. Patients currently make so-called "off label" use of pain medications, antidepressants, muscle relaxants and sleep aids to treat the condition. Exercise and applying heat also can help. Fibromyalgia typically affects women, striking them with long-lasting or chronic pain, as well as muscle stiffness and tenderness, according to the FDA. An estimated 3 million to 6 million people in the United States are affected each year. Lyrica, known generically as pregabalin, previously won FDA approval to treat partial seizures, pain following the rash of shingles and pain associated with diabetes nerve damage. The FDA warned that common side effects of the drug included mild-to-moderate dizziness and sleepiness. Also, the agency said that Lyrica reduces pain and improves daily functions for some patients with fibromyalgia, but that not everyone derived benefit from the drug in studies. The cause of fibromyalgia is a mystery, though it may be linked to injury, emotional distress or viruses that change the way the brain perceives pain, the FDA said. `````````` On the Net: FDA information on fibromyalgia: http://www.fda.gov/consumer/updates/fibromyalgia062107.html ```````````````` Salon provides breaking news articles from the Associated Press as a service to its readers, but does not edit the AP articles it publishes. © 2007 The Associated Press. All rights reserved. The information contained in the AP News report may not be published, broadcast, rewritten or redistributed without the prior written authority of The Associated Press. ################## http://www.myfoxdc.com/myfox/pages/News/Detail?contentId=3562011&version=1&locale=EN-US&layoutCode=TSTY&pageId=3.2.1 Lyrica Medication Approved for Fibromyalgia ~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~ Last Edited: Thursday, 21 Jun 2007, 8:22 PM EDT Created: Thursday, 21 Jun 2007, 8:19 PM EDT Pfizer announced Thursday that the Food and Drug Administration approved Lyricacapsules CV for the management of fibromyalgia, the most common chronic, widespread pain condition in the U.S. The approval of Lyrica, which received a priority review, represents a breakthrough for the more than six million Americans who suffer from this debilitating condition and who previously had no FDA approved treatment options Characterized by chronic widespread pain that can be relentless, fibromyalgia is usually accompanied by poor sleep, stiffness and fatigue; patients also report experiencing deep tenderness, soreness and flu-like aching. Fibromyalgia can have devastating effects on a sufferer and engage in everyday activities, as well as their relationships with family, friends and employers. Fibromyalgia is thought to result from neurological changes in how patients perceive pain, specifically a heightened sensitivity to stimuli that are not normally painful. Although its exact mechanism of action in fibromyalgia is not known, Lyrica is thought to act in the central nervous system to reduce the level of perceived pain. In the clinical trials, Lyrica demonstrated rapid and sustained improvements in pain compared with placebo. In addition, patients taking Lyrica reported feeling better and improvements in physical function. ```` Copyright 2007 Fox Washington, D.C. (WTTG). All rights reserved. This material may not be published, broadcast, rewritten, or redistributed. AP contributed to this report. [Return to top] ------------------------------ Date: Fri, 22 Jun 2007 00:08:38 -0700 From: Jerry Campbell <jerrycamz YAHOO.COM> Subject: RES: Dendritic cells are replenished from blood Hi, Dendritic cells are the type of cell that is the first line of immune defense. Until a foreign cell is identified by a dendritic cell, it remains invisible to the immune system. Once a dendritic cell has tagged it as foreign, the dendritic cell then 'trains' T cells to attack it; the T cells can then go on to cause B cells that make antibodies against this foreign cell to multiply and make more antibodies. The following article finds that dendritic cells within the spleen - and presumably the digestive tract and liver - are continuously replenished from the bone marrow. Because the dendritic cells are continually dying off and being replenished, if one becomes infected it will not create a permanent line of infected cells; instead it will dy off and be replenished by new uninfected cells from the bone marrow. Jerry ----------------------------------- Posted: June 12, 2007 Dendritic cells are replenished from blood Dendritic cells help direct the body’s immune response by presenting invading antigens to T cells so they know what to attack. But an ongoing debate exists about where dendritic cells originate and how they multiply, especially in the spleen and lymph system. Now, in a paper published in this month’s issue of Nature Immunology, Rockefeller University scientists have come a step closer to understanding the origins of the spleen and lymph node dendritic cells, findings that are especially important for researchers developing immune-cell-targeted vaccines. Prior studies suggested that dendritic cells in the spleen either must continually divide and renew their population, or must be constantly replenished from precursor cells migrating from the bone marrow. Resolving the debate is important, says Kang Liu, postdoctoral associate and the study’s first author, because if dendritic cells divide endlessly then they could be acting as a reservoir for pathogens. "On the other hand, dividing could also allow them to present antigens to T cells for a longer period and prime the immune system to fight the pathogens off," Liu says. The study by Liu and Michel Nussenzweig, Sherman Fairchild Professor and head of the Laboratory of Molecular Immunology, appears to resolve the debate. According to their research, spleen and lymphoid dendritic cells migrate to these organs through the blood as "dendritic cell precursors," mature into dendritic cells, divide a few times and then die, leaving a void to be replenished by bone marrow precursors. By joining two mice together so that they shared the same bloodstream, a technique called parabiosis, the scientists found that even though the mice shared most of their immune cells equally, they only had about a 30 percent exchange rate in their spleen and lymph node dendritic cells. These dendritic cells were continually being replaced by precursors from the blood, precursors that were never evenly distributed between the two mice because they were removed from circulation too quickly to equilibrate. Liu and Nussenzweig, who’s also an HHMI investigator, found three main factors for the maintenance of a mouse’s population of spleen and lymph node dendritic cells: continuous replenishment of dendritic cell precursors from the blood at a rate of about 4,300 cells per hour, the limited division of differentiated dendritic cells and the dendritic cell death rate. "These dendritic cells can’t last longer than 14 days without being replenished, and the number of dendritic cells can be the rate-limiting factor of immune response," Liu says. "This is the first time that their division and self-renewal capacity has been directly measured." Nature Immunolgy 8(6): 578-583 (June 2007) Contact: Lauren Gravitz (212) 327-8977 email@example.com [Return to top] ------------------------------ Date: Fri, 22 Jun 2007 23:46:16 +0200 From: "Dr. Marc-Alexander Fluks" <fluks COMBIDOM.COM> Subject: RES,NOT: Members of European parliament support research into CFS The European parliament made a statement on CFS this week. Unfortunately, the text is not available in English, http://www.europarl.europa.eu/news/public/story_page/057-7909-169-06-25-909-20070615STO07874-2007-18-06-2007/default_en.htm but it is in the Dutch version of this page, http://www.europarl.europa.eu/news/public/story_page/057-7909-169-06-25-909-20070615STO07874-2007-18-06-2007/default_nl.htm The last line of the text says that a dozen of MPs will work on research into stam cells, CFS, astronomy and biotechnology. [Return to top] ------------------------------ Date: Sun, 24 Jun 2007 04:20:52 +0200 From: Jan van Roijen <j.van.roijen CHELLO.NL> Subject: res: ME/CFS -Metabolic & Neurocognitive Responses to Exercise Challenge ~~~~~~~~~~~~~~~~~~~~~~~~~~~~ Send an Email for free membership ~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~ >>>> Help ME Circle <<<< >>>> 24 June 2007 <<<< Editorship : j.van.roijen chello.nl Outgoing mail scanned by Norton AV ~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~ From: Frank Twisk <frank.twisk hetnet.nl> http://www.acsm-msse.org/pt/re/msse/fulltext.00005768-200705001-02582.htm Metabolic And Neurocognitive Responses To An Exercise Challenge In Chronic Fatigue Syndrome (CFS) ~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~ Medicine & Science in Sports & Exercise: Volume 39(5) Supplement, May 2007, p S445 VanNess, J. Mark; Snell, Christopher R.; Stevens, Staci R.; Stiles, Travis L. University of the Pacific, Stockton, CA. Email: firstname.lastname@example.org Supported by the CFIDS Association of America 2401: Board #80 June 1 3:30 PM - 5:00 PM [F-25 Free Communication/Poster - Clinical Exercise Physiology - Chronic Diseases and Conditions: JUNE 1, 2007 1:00 PM - 6:00PM ROOM: Hall E] A comprehensive view of CFS patients during conditions of post-exertional malaise can provide an integrated perspective on the pathophysiology the illness. PURPOSE: To compare the metabolic responses and neurocognitive consequences of a maximal exercise challenge between CFS and control subjects. METHODS: Twenty (n=20) women with CFS and twenty (n=20) sedentary control subjects performed a graded exercise test to maximal exertion. Cardiopulmonary analysis was performed during the exercise test. Blood samples for plasma lactate and glucose were collected before and after the test. Nasal acoustic rhinometry (NAR) was used to measure nasal cross-sectional area and volume on both nostrils before and after the exercise test. Neurocognitive function was measured before and after the exercise test using the CalCap computer program. RESULTS: Multivariate analysis of cardiopulmonary variables found a significant difference between groups; Wilks' ? = 0.053, F = 6.393 (7, 20), p>0.01. Follow-up univariate tests with alpha levels adjusted to account for inflation of the error term indicated that CFS patients scored significantly lower on measures of peak workload (116±19 vs. 176±26 Watts), peak ventilation (70±22 vs. 102±16 L), peak VO2 (23.4±6.4 vs. 32.0±4.5 ml/kg/min), and VO2 and workload at anaerobic threshold (9.7±2.3 vs. 17.3±3.9ml/kg/min and 42±12 vs. 75±21 Watts respectively). For the CalCap, a group by test (2X3) factorial MANOVA with dependent variables; simple reaction time (SRT) and three levels of choice reaction time (CRT), produced a significant main effect for group; Wilks Lambda = 0.85, F=4.76 (4, 105), p=0.001. Follow up discriminant function analysis indicated that the CRT measures were more important in differentiating CFS than was SRT. The CFS group was slower on all measures. CONCLUSION: These results indicate that exercise performance and neurocognitive abnorma¬lities exist in CFS. The lack of any significant differences in lactate, glucose or nasal rhinometry precludes clear explanation for these differences. © 2007 The American College of Sports Medicine [Return to top] ------------------------------ Date: Sun, 24 Jun 2007 04:45:28 +0200 From: Jan van Roijen <j.van.roijen CHELLO.NL> Subject: res: ME/CFS -post-exertional symptomology ~~~~~~~~~~~~~~~~~~~~~~~~~~~~ Send an Email for free membership ~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~ >>>> Help ME Circle <<<< >>>> 24 June 2007 <<<< Editorship : j.van.roijen chello.nl Outgoing mail scanned by Norton AV ~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~ From: Frank Twisk <frank.twisk hetnet.nl> http://www.acsm-msse.org/pt/re/msse/fulltext.00005768-200705001-02583.htm Post-exertional Symptomology In Chronic Fatigue Syndrome ~~~~~~~~~~~~~~~~~~~~~~~~~ (CFS Medicine & Science in Sports & Exercise: Volume 39(5) Supplement, May 2007, p S445 Stiles, Travis L.; Snell, Christopher R.; Stevens, Staci R.; Moran, Megan; VanNess, J. Mark University of the Pacific, Stockton, CA. Email: email@example.com Supported by the CFIDS Association of America Symptom exacerbation following physical stress has been documented in illnesses such as multiple sclerosis (MS), lupus and rheumatoid arthritis (RA). Similar phenomenology has been reported in CFS but is not well understood. PURPOSE: The purpose of this study was to explore symptom exacerbation following an exercise challenge in CFS patients relative to a sedentary control population. METHODS: Forty female subjects (n=40), 20 CFS and 20 matched sedentary controls served as subjects. All participants underwent a graded maximal cardiopulmonary exercise test (CPX). Two questionnaires, Short Form-36 (SF-36) and a series of open-ended questions, were completed 7 days after the exercise challenge to assess post-exertional differences between groups. The open-ended questions pertained to symptoms experienced following the test and time taken to recover from any testing effects. SF-36 data were analyzed using a multivariate analysis. Written questionnaire responses were evaluated by determining recovery time in days as well as number and type of symptoms experienced. RESULTS: SF-36 analysis found statistical significance across all 8 health domains measured between groups (p <.01), but no effects were found for the exercise test. Analysis of the open-ended questionnaires revealed that within 24 hours of the exercise challenge, 85% of controls indicated full recovery in contrast to 0% of CFS patients. The remaining 15% of controls recovered within 48 hours of the test as opposed to only one CFS patient. Clear differences in number and type of reported symptoms were also found between groups. CONCLUSIONS: The results of this study indicate that CFS patients suffer symptom exacerbation following physical stress. As with MS, lupus and RA, post-exertional symptom exacerbation appears to be both a real and incapacitating feature of the syndrome. The delayed recovery response evoked by a single bout of exercise stress is distinctly different from that of sedentary controls. The debilitating effects experienced by these patients help to explain activity avoidance, which should be considered when prescribing exercise and activity management programs for CFS patients. © 2007 The American College of Sports Medicine [Return to top] ------------------------------ Date: Mon, 25 Jun 2007 19:53:10 -0400 From: "Marly Silverman <beatcfsfms bellsouth.net> via Co-Cure Moderator" Subject: NOT,RES: Miami researchers are looking for patients for innovative CFS research study Miami researchers are looking for patients for innovative CFS research study The University of Miami-Behavioral Medicine Research Center is conducting research studies on chronic fatigue syndrome that allows patients to participate in the comfort of their homes. It is called the TeleHealth Study. FAQs What: The TeleHealth Study is a research project designed to help individuals with CFS understand and manage their condition. Participants will be provided with information about the nature and effects of stress reactions; how to cope and manage stress; and how to take better care of themselves via an innovative home-based program. The TeleHealth study is funded by the National Institutes of Health (NIH) in collaboration with the University of Miami Behavioral Medicine Research Center. Who is eligible: People who 1. Have a diagnosis of CFS 2. Are between the ages of 21-65 3. Speak, read and write English fluently 4. Have a telephone line 5. Live in Dade or Broward counties for the next 9 months. Payment: $50 for each completed assessment Contact: To participate or for more information, call 305-243-1434 or 305-355-9057 In Good Health and In Beauty, Marly C. Silverman Founder P.A.N.D.O.R.A. - Patient Alliance for Neuroendocrineimmune Disorders Organization for Research and Advocacy, Inc. -Volunteer Help Line : 954-783-6771 - Fax: 954-783-1098 www. pandoranet.info Built on Hope - Strong on Advocacy - Finding a Cure through Research Please support the I NEED A HERO! campaign for a Congressional Caucus for CFS/ME-FM-GWI-MCS and related illnesses. [Return to top] ------------------------------
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