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"This is an Excellent piece by Craig Maupin:\r\n\r\n(Reposted with permission)\r\n\r\nhttp://www.cfidsreport.com/News/10_Reeves_History_CFS.html\r\n\r\n\r\nCFS, Reeves, and the CDC:\r\nA Rich History but A Poor Past\r\n\r\nCraig Maupin (www.cfidsreport.com)\r\n\r\nHistory relies on more than the past. History also relies on the present, on current perceptions and interpretations. A historians beliefs, experiences, and hopes form half of the story. \r\n\r\nThe history of this CFS (chronic fatigue syndrome) is as rich as its past has been poor. It is a history worth protecting and honoring, and I have no doubt that someday it will offer lessons to future generations. But recently, I have been concerned that myths are replacing our history, particularly in regard to the CDC (Centers for Disease Control and Prevention). What are those myths? \r\n\r\nMyth 1. William Reeves was, until recently, a bold innovator. His objectivity was lost in recent years, when he suddenly decided CFS was a stress disorder. \r\n\r\nFirst, William Reeves was extremely cautious with regard to his public statements about CFS. Despite his tact, he offered his thoughts when asked by an advisory committee in 1995 what he thought caused CFS. He said that the risk factor that we are finding most highly associated with chronic fatigue syndrome are multiple major lifetime stresses in the year before one becomes ill (1). This stress-predominant view toward CFS did not change throughout his tenure in the CDCs CFS program. \r\n\r\nSecondly, evidence of Reeves predilection toward CFS goes beyond his 1995 comment. Reeves (a) spent no money searching for a novel viruses, (b) he showed little interest in following up on distinct, previously published immune findings. By 2001, he began to invest the larger portion of his budget in the psychiatry department at Emory. The precise targeting of those investments within the psychiatry department at Emory is even more important. Psychiatrists at Emory, such as Christine Heim and Andrew Miller, specialized in post-traumatic stress response and anxiety. \r\n\r\nThird, three of Reeves most frequent collaborators (Andrew Lloyd, Wessely/Cleare at Kings College, and James Jones) propose very similar models for the illness, models that emphasize a viral/lifestyle/emotional stress as the precipitating factor, with brain/behavior as the primary perpetuator. \r\n\r\n　\r\n\r\n　Myth 2. For years, sufferers have accused Reeves of thinking ME/CFS was a psychological disorder but his open-ended attempt to merge gene expression, gene polymorphism and laboratory and clinical data suggested he was open, at least at that point, to various interpretations of the disease. \r\n\r\n　\r\n\r\nThis statement is based on the belief that biological research and genetic research belong to biomedical fields, not psychiatry. While that belief is understandable from a laymans perspective, it is not accurate. Current models of psychiatric disorders are multidimensional: stress trigger, genetic predisposition, lead to biological effects and behavioral perpetuation. Today, depression, stress disorders, and anxiety disorders are researched with an emphasis on genetics, behavioral interventions, neuroendocrine imbalances, and mild immune alterations. (2). \r\n\r\n　\r\n\r\nMyth 3. The CDCs Dubbo Infections Outcomes contract with Dr. Andrew Lloyd, a virologist, shows openness to looking viral models of causation. \r\n\r\n　Lloyd and his collaborators were far more forthcoming with speculation about CFS than Reeves. Long before Reeves chose Lloyd as a collaborator, Lloyds published work failed to reveal any signs of predilection toward a viral model for CFS: Current evidence suggests disruption of fundamental central nervous system mechanisms, such as the sleep-wake cycle and the hypothalamic-pituitary-adrenal axis, may underpin the clinical features of this disorder. (3) One of his most widely covered papers in 1994 stated: Psychological factors such as illness attitudes and coping style seem more important predictors of long term outcome than immunological or demographic variables (4). The list goes on. \r\n\r\nHistory will judge virologists involved in CFS, such as Andrew Lloyd, Stephen Strauss, William Reeves, NOT by how well those virologists were able to detect XMRV, Epstein-Barre, or any other virus. History will judge them on how accurately they interpreted their own viral research. History will also evaluate whether their beliefs/attributions influenced their sample selection. Until a biomarker for any disease is found, the attributions and feelings of the researcher toward those who suffer from the disease has a much greater bearing on their conclusions than tests. The clinical beliefs and observations are the foundation of their input. \r\n\r\n　\r\n\r\n　Myth 4. Regarding the 2006 CDC Press Conference, there are several stories floating around. A common account goes something like this: ME/CFS enjoys greatly increased credibility in the medical world and the CDC program played a large part in that. The teams innovative, cutting-edge techniques and its willingness to collaborate resulted in a signature event in ME/CFS history: the simultaneous publication of 14 papers in the Pharmacogenomics journal in 2006. Coincident with that the head of the CDC proclaimed, at a national press conference, that ME/CFS is a serious and legitimate disorder. Those events got the medical community to sit up and begin to pay attention.\r\n\r\nScience Magazine has currently gained recognition for their publication on XMRV. However, many forget that it was a Science article by Jocelyn Kaiser that raised serious concerns about the research methods, assumptions, and conclusions of the CDCs 2006 Pharmacogenomics study. So, Science Magazine has published progressive articles in regards to this illness more than once. \r\n\r\nIn Kaisers article, the Pharmacogenomics study design was not only closely examined, but concerns were voiced about the CDCs conclusions. Concerns about the small sample size and the lack of validation with PCR were aired. Most importantly, the implication that the conclusions of the CDC team were significantly exaggerated was raised by a variety of researchers from diverse fields.\r\n\r\nFurthermore, some severe flaws of the study were not included in the Science article, perhaps due to space constraints. First, the study limited its results only to those genes involved in the HPA axis. Even worse, the conclusion of the studys authors that three genes  serotonin, glucocorticoid, and tryptophan  immediately extrapolate to an illness caused by an accumulation of lifetime stresses required, at minimum, an extremely robust imagination. And the authors of the study never bothered to support such a large leap of faith with sources or citations. \r\n\r\nDespite these flaws, the leadership at the CDC and the studys authors decided that the study merited a shift in the conceptualization of the illness to a disorder of accumulated stress, and a press conference was called to proclaim that shift. For many, this decision was deeply discouraging and damaged the CDCs credibility as an objective research entity. \r\n\r\nIt is true that some of our most visible advocates, organizations, and clinicians participated in that press conference. Researchers and clinicians such as Nancy Klimas and Anthony Komaroff hailed Reeves findings. Understandably, this participation damaged the CFS communitys confidence in many. That damage was intensified as Reeves unveiled more details of how the Pharmocogenomics study was to inform clinical guidelines of his five year plan. \r\n\r\nMy concern is that many who participated in the CDCs efforts to shift the conceptualization of CFS believe that revising history  particularly the history of William Reeves and his views toward CFS  is a suitable way to recapture the CFS communitys confidence. The CFS community wants to move on. It wants healing. But it also wants its history to remain intact. \r\n\r\n　\r\n\r\nIn Conclusion 　\r\n\r\nThe findings of the Whittemore-Peterson-Institute (WPI) research team stepped onto a field of discouragement in October. The CFS community is well-aware that these preliminary findings may have one of many different conclusions. That said, the WPIs commitment and goals to those with this illness are unquestioned. \r\n\r\nGiven the climate following the CDCs 2006 press conference, the WPI had no option but to speak publicly on their findings. It was a historically-aware attempt to encourage fresh expertise to enter CFS research with a new perspective. \r\n\r\nThe WPI has been sharply criticized for that decision by some in the scientific community who seem more enthusiastic about conclusions of the Pharmacogenomics study (including Lloyd, Reeves, and Kings College). However, the decision of the WPI reflects a solid understanding of the historical difficulties of funding certain types of CFS research, as well as an understanding of the traditional, tightly-managed CFS research establishment. It is a solid understanding of history that causes a people over protocol decision to seem sensible and necessary. And that is why our history, our true history, is so important.\r\n\r\n(1) Reeves, W. Presidential Advisory Committee on Gulf War Illnesses. November 7,1995. \r\n\r\n\r\n(2) Several resources are available that are use for laypeople who want to become more informed about the types of genetics and biology that are emphasized in modern psychiatry.  Below are posted a few books with large previews available (Google books).  These texts can give anyone a general sense of what areas of biology are emphasized in PTSD. A brief skimming with the question \"What areas of biology are emphasized?\" is all that is required to become more educated on the subject.  \r\n\r\nVasterling and Brewin's 'Neuropsychology of PTSD: biological, cognitive, and clinical Perspectives' (2005) is an excellent place to skim. \r\n\r\nThe Psychobiology of Trauma and Resilience Across the Lifespan (2008) by Douglas Delanty explores genetic susceptibility and current genetic research. \r\n\r\n　　\r\n(3) Hickie I, Lloyd A, Wakefield D, Ricci C (1996). Is there a post-infection fatigue syndrome? Aust Fam Physician Dec;25(12): pg. 1847-1852. \r\n\r\n(4) Wilson A, Hickie I, Lloyd A, Hadzi-Pavlovic D, Boughton C, Dwyer J, Wakefield D. (1994) Longitudinal study of outcome of chronic fatigue syndrome. BMJ Mar 19;308(6931):756-759. \r\n\r\n(5) Kaiser, J. Jocelyn Kaiser. Genes and Chronic Fatigue: How Strong Is the Evidence? Science 2006; 312: 669-671"
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