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

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168 cell associated cytotoxic deficit in (ME)CFS. Because perforin is important in immune surveillance and homeostatis of the immune system, its deficiency may prove to be an important factor in the pathogenesis of (ME)CFS and its analysis may prove useful as a biomarker in the study of (ME)CFS” (Maher KJ, Klimas NG, Fletcher MA. Clin Exp Immunol 2005:142(3):505‐511). 2005 “Previous research has shown that patients with (ME)CFS present with an abnormal exercise response and exacerbations of symptoms after physical activity. The highly heterogeneous nature of the CFS population and the lack of uniformity in both diagnostic criteria and exercise testing protocols preclude pooling of data. Still, we conclude that at least a subgroup of CFS patients present with an abnormal response to exercise. Importantly, the exacerbation of symptoms after exercise is seen only in the (ME)CFS population and not in fatigue‐associated disorders such as depression. Earlier (studies) revealed that in (ME)CFS patients, irrational fear of movement is not related to exercise performance. The aim of this study was to examine the interactions between several intracellular immune variables and exercise performance in (ME)CFS. These data add to the body of literature showing impairment of intracellular immunity in patients with (ME)CFS. The results provide evidence for an association between intracellular immune dysregulation and exercise performance in patients with (ME)CFS” (J Nijs, N McGregor, K De Meirleir et al. Medicine & Science in Sports & Exercise 2005:Exercise Immunology in CFS:1647‐1654). 2005 “The hypothesis of the present study is that the appearance of cell‐specific autoimmune antibodies may define subsets of (ME)CFS. (ME)CFS is clinically similar to several autoimmune disorders that can be diagnosed and characterised by autoantibody profiles. For this reason, we conducted an exhaustive evaluation of 11 ubiquitous nuclear and cellular autoantigens in addition to two neuronal specific antigens. Very few studies have evaluated the presence of autoantibodies in people with (ME)CFS. The findings of this study hint that evaluation of certain autoantibodies may give clues to on‐going pathology in subsets of (ME)CFS subjects. Among (ME)CFS subjects, those who had been sick longer had higher rates of autoantibodies” (S Vernon et al. Journal of Autoimmune Diseases May 25 th , 2005:2:5). 2006 “The diagnostic criteria of CFS define a heterogeneous population composed of several subgroups. This study was designed to examine NK cell activity as a potential subgroup biomarker. The results (provide) evidence in support of using NK cell activity as an immunological subgroup marker in (ME)CFS. Improved treatment options will only come with better understanding of the syndrome’s underlying pathophysiology. The present study specifically investigated the existence of an immunological subgroup of CFS patients. Reduced NK cell activity may contribute to enhanced cytokine production. Given the role that NK cells play in targeting virally infected cells, a clinically significant reduction in NK cell activity may lead to activation of latent viruses and new viral infections. (ME)CFS is a misunderstood condition. Research in the last two decades has produced little advancement in the understanding of the pathophysiology of (ME)CFS. Unfortunately, this lack of progress seems to have further contributed to the belief among some members of the medical community that (ME)CFS is not an actual organic condition” (Scott D Siegel, Mary Ann Fletcher, Nancy Klimas et al. J Psychosom Res 2006:60:6:559‐566). 2006 “(ME)CFS is a poorly defined medical condition which involves inflammatory and immune activation. The Type I interferon antiviral pathway has been repeatedly shown to be activated in the most afflicted patients. An abnormal truncated form of ribonuclease L (37‐kDa RNase L) is also found in (ME)CFS patients and this protein has been proposed as a biological marker for (ME)CFS (M Fremont, K De Meirleir et al. JCFS 2006:13(4):17‐28).
2007 169 “For decades, (ME)CFS patients were – and still are – dismissed as lazybones or hypochondriacs. Many medical doctors and insurance companies still assert that (ME)CFS is a mental condition. The mainstream treatment for (ME)CFS is CBT, which means that patients with (ME)CFS are being treated as having a mental illness with ‘treatments’ that do not treat any underlying cause. Doctors who treat (ME)CFS patients as suffering from an organic disorder and scientists who examine the biological causes of (ME) are often considered quacks by their colleagues (and) insurance companies, which are sometimes even officially supported by governments in their attempts to eliminate the scientific view that (ME)CFS is an organic disorder. The official acceptance of the latter obviously would mean that the national health care systems are obliged to financially support those patients who are now considered hypochondriacs and, therefore, may easily be suspended from the national health care systems. There is, however, evidence that (ME)CFS is a severe immune disorder with inflammatory reactions and increased oxidative stress. Maes et al show that patients with (ME)CFS show very high levels of nuclear factor kappa beta in their immune cells. NFkβ is the major mechanism which regulates inflammation and oxidative stress. Thus, the increased production of NFkβ in the white blood cells of patients with (ME)CFS is the cause of the inflammation and oxidative stress (seen) in (ME)CFS” (Maes et al. Neuroendocrinology Letters, 2007. http://www.michaelmaes.com/ ). 2007 “Recent research has evaluated genetic signatures, described biologic subgroups, and suggested potential targeted treatments. Acute viral infection studies found that initial infection severity was the single best predictor of persistent fatigue. Studies of immune dysfunction (have) extended observations of natural killer cytotoxic cell dysfunction of the cytotoxic T cell through quantitative evaluation of intracellular perforins and granzymes. Other research has focused on a subgroup of patients with reactivated viral infection. Our expanded understanding of the genomics of (ME)CFS has reinforced the evidence that the illness is rooted in a biologic pathogenesis that involves cellular dysfunction and interactions between the physiologic stress response and inflammation. A large body of evidence links (ME)CFS to a persistent viral infection. (ME)CFS patients exhibited a distinct immune profile compared with fatigued and non‐fatigued individuals. These patients displayed increased anti‐inflammatory cytokines. Investigators noted the tropism with brain and muscle and suggested that the neuroinflammation seen in neuroimaging studies of a subgroup of CFS patients may result from enteroviral infection. The clinical implications are consistent with an immune system that may allow viral reactivation and raises a concern for tumour surveillance as well. The preponderance of available research confirms that immune dysregulation is a primary characteristic of (ME)CFS. These advances should result in targeted therapies that impact immune function, hypothalamic‐pituitary‐adrenal axis regulation, and persistent viral reactivation” (Nancy G Klimas et al. Current Rheumatology Reports 2007:9:6:482‐487). 2009 In “Contemporary Challenges in Autoimmunity”, the Annals of the New York Academy of Sciences published several articles looking at autoimmunity in (ME)CFS. One such paper by Ortego‐Hernandez et al states: “In association with (ME)CFS physiopathology, immune imbalance, abnormal cytokine profile or cytokine genes, and decreased serum concentrations of complement components have been reported…Many studies have shown the presence of several autoantibodies in (ME)CFS patients. Antibodies to diverse cell nuclear components, phospholipids, neuronal components, neurotransmitters, as well as antibodies against some neurotransmitter receptors of the central nervous system have been described”. The authors consider the different types of antibodies that have been reported in (ME)CFS patients and consider in particular antibodies to nuclear components (52% of (ME)CFS patients are reported as having autoantibodies to components of the nuclear envelope, particularly to lamin B1 molecule); to neurotransmitters and receptors (especially to neurotransmitters such as serotonin (5H‐T), adrenals, ACTH and to receptors such as muscarinic cholinergic receptor I and μ‐opioid receptor 1), and to diverse microorganisms, noting that serum levels of IgA were significantly correlated to the severity of illness. The authors state that the results showed that enterobacteria might be involved in the
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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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107 diagnoses before (ME)CFS onset,
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109 He noted that: “The most extr
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111 According to Professor Nancy Kl
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113 95% have abnormal cognitive‐e
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115 In 2003 a UK study of skeletal
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Page 123 and 124: 1995 123 “The use of cardiopulmon
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Page 129 and 130: 2005 129 On 10 th April 2005 Carol
Page 131 and 132: 131 The next system to be compromis
Page 133 and 134: 2005 133 Researchers at the US Cent
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Page 143 and 144: 2000 143 In 2000, the CFIDS Associa
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Page 147 and 148: 2003 147 German researchers Siessme
Page 149 and 150: 149 producing any evidence of damag
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Page 153 and 154: 2006 153 “(ME)CFS is a poorly def
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Page 157 and 158: 1990 157 “In order to characteris
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Page 163 and 164: 1999 163 An article from researcher
Page 165 and 166: 2003 165 “(ME)CFS is an increasin
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Page 171 and 172: 171 Documented abnormalities in the
Page 173 and 174: 1996 173 De Lorenzo et al noted tha
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Page 179 and 180: 1955 179 Acheson described and comp
Page 181 and 182: 181 (In the light of the discovery
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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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Page 207 and 208: 207 “Just because one is blessed
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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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305 segments of the medical establi
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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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Quotations from the Participants’
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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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Comments from someone who has under
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Quotations from the Therapists’ M
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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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