MAGICAL MEDICINE: HOW TO MAKE AN ILLNESS ... - Invest in ME

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158 often precedes the fully developed condition), NK cytotoxicity might be around 13 or 14 percent. (ME)CFS patients represent the lowest cytotoxicity of all populations we’ve studied” (Nancy Klimas, Professor of Medicine, University of Miami School of Medicine; Director of Immunology; Director of AIDS Research and Director of the Allergy Clinic at Miami. Presentation: Immunological Markers in (ME)CFS. The CFIDS Association Research Conference, November 1990, Charlotte, North Carolina. Reported in CFIDS Chronicle, Spring 1991; pp 47‐50). 1991 “Despite the broad divergence of opinion in the medical community, there is little doubt that classic allergy and atopy are inexplicably prevalent in (ME)CFS. In a recent study, a high proportion (50%) of patients were found to be reactive to a variety of inhalant or food allergens when inoculated epicutaneously in the classic manner. Certainly patients with (ME)CFS differ immunologically from their healthy counterparts and it is this observation, more than any other today, that is evoked in support of the organic hypothesis of disease causation” (Stephen E Straus. Review of Infectious Diseases 1991:13: Suppl 1: S2‐S7). 1992 A major study looking at neurological, immunological and virological aspects in 259 (ME)CFS patients found that neurological symptoms, MRI findings and lymphocyte phenotyping studies suggest that patients “may have been experiencing a chronic, immunologically mediated inflammatory process of the central nervous system” and that “ We think that this is probably a heterogeneous illness that can be triggered by different environmental factors (including stress, toxins and infectious agents), all of which can lead to immune dysfunction and the consequent reactivation of latent viruses” (D Buchwald, Paul Cheney, Daniel Peterson, Robert C Gallo, Anthony Komaroff et al. Ann Int Med 1992:116:2:103‐113). 1993 At the 1993 Los Angeles Conference on (ME)CFS, evidence was presented by Professor Nancy Klimas from the University of Miami that she and her team have been able to accurately predict 88% of (ME)CFS patients with a mathematical model of immunological parameters. This model combines levels of activated T cells and CD4 inducers of cytotoxic T cells with NK cell count and function: “In a normal population, 20% of lymphocytes are active at any given time. ‘In (ME)CFS, up to 80% of the cells are working’. These lymphocytes and cytokines are so up‐regulated that they cannot be driven any harder. It is as if they have been pushed as far as they can go and the immune system is completely exhausted” (CFIDS Chronicle: Summer 1993). 1993 “Using the immunophenotypic data presented, we were able to demonstrate that almost 50% of (ME)CFS patients, especially those with severe symptoms, showed signs of CD8 + cell activation and an abnormal suppressor / cytotoxic CD8 + cell ratio. Our observations strongly suggest that a large population of (ME)CFS patients have immunologic disorders and that their symptoms could be explained by a chronic immune activation state (and) that (ME)CFS represents a type of autoimmune disease in which a chronically activated immune system reacts against the host. The 3:1 female/male ratio would not be unexpected: autoimmune syndromes are more common in women. Because of the autoreactive nature of this condition, it might also lead to other immune disorders, such as well‐recognised autoimmune diseases and multiple sclerosis” (Jay A Levy et al. Contemp Issues Infec Dis 1993:10:127‐146). According to Dr Elizabeth Dowsett, former President of the ME Association, at least 13% of ME/CFS patients are indistinguishable from patients with multiple sclerosis (personal communication).
1994 159 “The chronic fatigue immune dysfunction syndrome (CFIDS) is a major subgroup of the chronic fatigue syndrome (CFS). We and other investigators have reported a strong association between immune dysfunction and a serological viral activation pattern among patients in this group. This finding appeared similar to that for a variety of conditions, such as chronic active hepatitis and systemic lupus erythematosus, in which a definite association between a particular HLA‐DR/DQ haplotype and increased disease frequency has been reported. We thus elected to examine a cohort of patients with CFIDS, with use of HLA‐ DR/DQ typing. A significant association between CFIDS and the presence of HLA‐DQ3 was noted. The association with HLA‐DQ3 could represent an additive effect for patients who also have HLA‐DR4 and/or HLA‐DR5. (Our) results are intriguing. DQ3 was significantly more prevalent in patients than controls. It is possible that DR4 and DR5 are also associated with an increased risk of developing CFIDS. These findings strongly suggest that further evaluation of persons with CFIDS, including an investigation of an HLA Class I linkage dysequilibrium, are warranted. The data presented herein suggest that CFIDS, together with a variety of immune‐ mediated diseases, may share similar sequences of pathogenic mechanisms (and) in a subpopulation (of CFIDS), a genetic predisposition may be triggered immunologically by any number of potential stimuli, resulting in a state of chronic immune dysequilibrium. This model could easily explain findings with regard to viral infection (and) allergies” (RH Keller, N Klimas et al. Clin Inf Dis 1994:18: (Suppl 1): S154‐156). 1994 “These data suggest a correlation between low levels of NK cell activity and severity of CFIDS. Compromised or absent natural immunity is associated with acute and chronic viral infections such as AIDS, CFIDS and various immunodeficiency syndromes. Stratification of patients with CFIDS into distinct groups according to the severity or duration of physical abnormalities might allow identification of laboratory abnormalities that are associated with severity. The fact that NK cell activity decreases with increased severity and duration of certain clinical variables suggests that measurement of NK cell function could be useful for stratification of patients and possibly for monitoring therapy for and / or the progression of CFIDS” (EA Ojo‐Amaize et al. Clin Inf Dis 1994:18: (Suppl 1):S157‐159). 1994 “The immune system is a readily accessible, sensitive indicator of environmental or internal changes, and studies conducted by different groups over the past few years have provided valuable evidence for changes in immune status among individuals with (ME)CFS. To gain insight into the nosology and aetiology of (ME)CFS, we assessed patterns of soluble immune mediator expression at the protein and mRNA levels in individuals with (ME)CFS. The data presented in this report are consistent with previous evidence of immune dysregulation among patients with (ME)CFS and point to a dysregulation of TNF (tumour necrosis factor) expression as a distinctive feature of this condition. Imbalances in TNF and associated changes in levels of other cytokines may underlie many of the characteristic features of (ME)CFS. In addition, TNF‐α can have deleterious effects on the central nervous system” (Roberto Patarca, Nancy G Klimas et al. Clin Inf Dis 1994:18: (Suppl 1):S147‐153). Tumour necrosis factor is a cytokine involved in systemic inflammation. Its primary role is in the regulation of immune cells. Increased TNF causes apoptosis, inflammation and tumorigenesis. 1994 “The up‐regulated 2‐5A pathway in (ME)CFS is consistent with an activated immune state and a role for persistent viral infection in the pathogenesis of (ME)CFS. The object of this study was to measure key parameters of the 2‐5A synthetase/RNase‐L antiviral pathway in order to evaluate possible viral involvement in (ME)CFS. The data presented suggest that 2‐5A synthetase/RNase L pathway is an important biochemical indicator of the anti‐viral state in (ME)CFS. Evidence that this pathway is activated in (ME)CFS was identified in this subset of severely disabled individuals as related to virological and immunologic status. This pathway phenotype could
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MAGICAL MEDICINE: HOW TO MAKE A DIS
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Section 3: Consideration of the MRC
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5 MYALGIC ENCEPHALOMYELITIS/CHRONIC
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Introduction MAGICAL MEDICINE: HOW
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9 associations purely in order to
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11 “It’s not an illness that pe
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13 release that is not found in hea
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15 “The second clinical implicati
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17 In January 2003 the wife of Rich
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19 biomedical aspects of ME/CFS wer
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“Social factors 21 “Several of
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23 Despite the substantial evidence
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25 as possessed by devils or spirit
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27 However, as Crombez G et al poin
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29 Professor Anthony David’s resp
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31 From these beliefs of the PACE T
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33 warning about dependence being e
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35 This is unequivocal: according t
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37 Those studies, however, have bee
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39 The answer may be found in the f
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41 than giving actual numbers of pa
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43 deconditioning caused their illn
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45 Legitimate access has been obtai
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47 Goldstein’s search took a litt
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49 says about GET: “GET will be b
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51 The whole concept of “a CBT mo
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53 International concern about the
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55 The CISSD project was the brainc
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57 are changed in IBS lends credibi
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59 (http://www.entretiens‐du‐ca
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61 As Jonathan Rutherford, now Prof
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63 There are many who would profoun
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65 The term “CFS/ME” was carefu
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67 ill‐health and disability is d
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69 “The sick role does have advan
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71 Such is the influence of the Wes
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73 Editors of broadsheet newspapers
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75 Collins J who found that the UK
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77 The “Invitation to join the PA
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79 On 10 June 1988 Wessely provided
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81 “There is a record of a confid
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83 (6) Another, more recent illustr
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85 psychological hypotheses of caus
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87 Of particular note are the follo
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89 • “Two forms of treatment…
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91 patients with chronic fatigue st
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93 • Another UNUM policyholder, A
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95 “Over the twenty years I have
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97 a functional somatic syndrome),
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99 protein and serum amyloid A (whi
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101 their cortisol response, in tha
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103 exposures. Responsibility for t
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105 illness (and) these biases have
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Page 129 and 130: 2005 129 On 10 th April 2005 Carol
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Page 193 and 194: 193 Moreover, recent research has s
Page 195 and 196: 195 In August 1991, together with c
Page 197 and 198: 197 “The data do not support the
Page 199 and 200: 199 Lerner Research Institute who i
Page 201 and 202: 201 It is regrettable that the UK M
Page 203 and 204: 203 Notably, Dr Stuart Le Grice, he
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209 They would do well to remember
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211 itself said at the time: “stu
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213 muscle, endocrine and lymphoid
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215 “ ‘I don’t take the Briti
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217 “This is a major concern give
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219 “The availability of sensitiv
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221 impinge upon medical decisions
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SECTION 3: Consideration of the MRC
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225 such as multiple sclerosis in w
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227 of 600 participants. Issue 3 of
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229 Dr Gabrielle Murphy is/was part
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231 trials…are open to the charge
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233 Given that the Oxford criteria
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235 maximised by the collaboration
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237 c) I had been told by Dr. X (th
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The Investigators’ Reasons for th
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241 In his presentation entitled
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243 Peter White, however, asserted
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245 To many people, it is incompreh
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247 In her communication of 16 th J
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249 a) emotional lability….b)…d
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Undue influence on the PACE Trial o
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253 Pensions) and copied to the PAC
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255 only one database. This will be
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257 Conflicts of interest of those
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259 • a copy of the original prop
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261 There is another curious aspect
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Fraudulent research (Cargo cult sci
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265 It seems that, in comparison wi
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267 Initially, the Trial Investigat
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269 Information on other abnormalit
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271 It is notable that advising exe
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273 “Outcome choice bias: Sometim
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275 say that they have physical sym
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277 consent requires that the parti
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279 If in the PACE Trial the Wessel
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281 “Enhanced negative‐feedback
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283 health problem. There is no des
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The Handbook continues: 285 “Main
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287 Mark Seddon, a member of Labour
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289 Section B covers “Basic princ
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291 To combine all states of “med
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293 PACE Trial includes those who d
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295 • “People who present with
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297 • have succeeded in making cl
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299 White treating this as a purely
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301 “ Attempting to come to a con
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303 “CFS/ME” on State benefits
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307 could he require Primary Care T
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309 The Judge said: “The ‘psych
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311 they so desperately need and de
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313 condition that is seen by many
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315 17 th July: 1‐8 (Epub ahead o
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317 The APT Manual for Participants
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319 defining feature of ME/CFS (the
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321 PACE Trial participants and the
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323 Despite the fact that this was
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325 was available even before the p
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327 Physical factors, such as infec
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329 someone to change their fundame
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331 “A purely physical attributio
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333 “Therapist: I can understand
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335 On page 12 the authors state:
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337 However, as Chief Investigator,
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339 • “In all individuals, musc
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341 consistent with the assumption
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343 “6. The ‘wrong’ kind of s
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Quotations from the Therapists’ M
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347 Bavinton, Clark and White discu
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349 In the section of the GET Manua
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351 to be a consequence “of too m
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353 Phase 3 (page 54 of the Manual)
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355 going viral infection); should
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359 increase in bone density; think
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361 The authors summarise their adv
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363 Next comes a section on the Bor
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365 Such advice seems culpable. It
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371 doing at the time); there must
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373 are the “solutions” that ar
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375 The section beginning on page 4
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377 Three months after the end of s
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379 Participants were to be given a
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“Budgeting Energy: � Evaluating
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Comments by participants in the PAC
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385 Page 5 of the SSMC Manual infor
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387 illness is non‐biological…
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389 • have the main symptom of fa
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391 dispute/negotiation of benefits
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393 Appendix 6: Summary of Therapie
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395 There can be no doubt that, for
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397 evidence for a specific persist
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399 To imply that patients can reco
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401 (8) The Investigators did not i
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403 (15) The Investigators and some
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405 ME/CFS have reduced blood volum
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407 PACE Trial is about “Health e
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409 APPENDIX I: Dr Tony Johnson, De
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411 “I have advised many clinical
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413 “Fibromyalgia patients are in
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415 who do not agree to take part i
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417 Appendix III: Dr Melvin Ramsay
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419 • “It is not only people in
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421 “It will be imperative that h
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423 “It is important to understan
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425 with what look like exhaustive
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427 To date, MPs’ postbags contin
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429 APPENDIX VI: The Wessely’ Sch
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431 They explain that historically,
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433 Why would two PACE Trial Princi
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435 • deniers engage in “comple
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APPENDIX VIII: Two FINE Trial Case
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439 After four months, Miss C’s h
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441 What an extraordinary claim: wh
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