Journal of IiME Volume 6 Issue 1 (June 2012) we’ve talked about all these years is really fleshing out into a real picture”. She concluded by conveying her own enthusiasm, saying that due to new techniques that were not available even five years ago, “there’s been tremendous progress” and that both patients and investigators should be heartened. In the Question & Answer session, in response to a question from the floor, Professor Klimas said “What subgroup do people fit in? What we’re down to now is looking for the biological markers that put people in the proper group to give us targeted treatment approaches that make sense for that individual – certainly that’s the way, thank goodness, the field is finally moving”. (It must be stressed that this is in direct contrast to the Wessely School, who are intent on collating all states of medically unexplained “fatigue” and rolling out “cognitive restructuring” across the board of “fatigue”). 2007 “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 Invest in ME (Charity Nr. 1114035) kappa beta in their immune cells. NFk is the major mechanism which regulates inflammation and oxidative stress. Thus, the increased production of NFk 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 perforin 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 (IL-10, decreased IFN-/IL-10 ratio) and reductions in pro-inflammatory cytokines (IL-6, tumour necrosis factor-)…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. Advances in the field should result in targeted therapies that impact immune function, hypothalamic-pituitary-adrenal axis regulation, and persistent viral reactivation in (ME)CFS patients” (Nancy G Klimas et al. Current Rheumatology Reports 2007:9:6:482-487). www.investinme.org Page 79 of 108

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