Journal of IiME Volume 6 Issue 1 (June 2012) upregulation leads to oligodendrocyte excitotoxicity in MS, whilst glutamate downregulation in ME/CFS impairs hypothalamic CRH secretion. These results suggest that ME/CFS and MS are extremes of an array of dysfunctions in the 2-5A/RNaseL/PKR pathways into which other autoimmune diseases such as lupus erythematosus might fit. Dr Pascale de Becker (Belgium) presented a poster showing that a number of different stressors and consequent immunological and neuro-endocrinological changes can contribute to the onset of ME/CFS. C.H. Little (Mt Waveney, Victoria, Australia) said that their laboratory has identified a separate class of immune products (T cell antigen binding molecules) which may be the basis for adverse reactions experienced by some patients to foods. Research indicates that an appropriate immune response to ingested food proteins is an absence of both Th1 and Th2 immune responses. This outcome (i.e. no response) may depend on antigen-specific regulatory cells whose function is to maintain tolerance to food proteins. The presence or absence of an immune response depends critically on signals delivered by special antigen-presenting cells (dendritic cells). This process can be potentially disrupted by environmental influences. (With grateful acknowledgement to Dr Rosamund Vallings from New Zealand). 2002 In an article entitled “CFS Research: The Need for Better Standards”, Professor Nancy Klimas was unequivocal: “Research effort is hampered by poorly conceived, constantly changing – even non-existent – standards….Authors of the 1988 case definition set out to identify a group of patients sharing similar symptoms and clinical signs, but problems using the definition quickly became apparent. A revision in 1994 (i.e. the Fukuda CDC definition, with which the Wessely School was involved) …attempted to address some of the difficulties, but the resulting guidelines are rife with ambiguity and vagueness. Symptoms are counted as either present or absent, without regard to severity or frequency….The use by some groups of outdated Invest in ME (Charity Nr. 1114035) case criteria developed in England (the Wessely School’s Oxford criteria) and Australia obscures comparability….A stronger research effort will enhance credibility for the illness….Overcoming the methodological challenges of studying (ME)CFS is essential to making progress in understanding this complex illness and to uncovering more direct means of diagnosis and effective treatments” (The CFS Research Review 2002:3:2:5-7). It is worth recalling that, eight years earlier, the Report of The UK The National Task Force (see above) stated exactly what Professor Klimas needed to repeat in 2002: the Task Force Report was unequivocal in concluding that progress in understanding (ME)CFS is hampered by the use of heterogeneous study groups and definitions of CFS; by the lack of adequate comparison groups; by the lack of standardised laboratory tests, and by the invalid comparison of contradictory research findings stemming from these factors. Research has shown that using the Holmes et al CDC 1988 criteria, 80% may have (ME)CFS; using the Fukuda et al CDC 1994 criteria, 40% may have (ME)CFS, and using the 1991 Oxford (Wessely School) criteria, 10% may have (ME)CFS; the Australian criteria give roughly the same results as the Oxford criteria (Co-Cure RES.MED, 3rd December 2002: New Canadian clinical definition – ME/CFS). It is also worth recalling Professor Wessely’s published view that “It is usual to try to discover the causes of an illness before thinking about treatments. Some illnesses are treated without knowledge of the cause…examples include… chronic fatigue syndrome” (New Research Ideas in Chronic Fatigue. Ed: Richard Frackowiak and Simon Wessely for The Linbury Trust; pub: The Royal Society of Medicine, 2000). This is in direct contradiction to Professor Klimas’ (and other biomedical researchers’) call for progress in understanding such a complex illness in order to find effective treatments. 2002 “The present review examines the cytokine response to acute exercise stress. The magnitude www.investinme.org Page 63 of 108
64 Publizr Home