Journal of IiME Volume 6 Issue 1 (June 2012) and increased corticotrophin releasing factor (CRF). Professor Klimas said (ME)CFS was an excellent model of neuroendocrine-immune interaction and re-stated the PNI (psychoneuroimmunological) paradigm as a basis for understanding the complex relationships which underlie the extensive changes occurring in (ME)CFS patients. She concluded by confirming that immune abnormalities play an integral role in the pathogenesis of (ME)CFS and that they contribute to the symptom complex, and that they interact with the autonomic and endocrine systems; the pattern and type of immune activation are equal to “cause and effect”. Following this conference, on 19th October 1999 The Medical Post (volume 35, number 35) published an article pointing out that, according to a US study by Professor Paul Levine from George Washington University that was presented at the Second World Congress on CFS and Related Disorders, patients with (ME)CFS who show signs of recent immunosuppression should be monitored for certain types of cancer: “This study suggests that immune dysfunction is an important aspect of at least one CFS subgroup….according to Dr Levine, the types of cancer reported included B-cell lymphoma, brain tumours, adenoid cystic carcinoma of the breast, transitional carcinomas of the bladder, uterine cancer, basal cell carcinoma… and non-Hodgkin’s lymphoma. Two (patients) reported multiple primaries. ‘These weren’t the type of cancers you’d see in a typical population’ (said Dr Levine)….The mechanism for this effect might involve natural killer cell activity, Dr Levine said. People with (ME)CFS have decreased (NK) activity, which is associated with cancer”. 2000 “The purpose of the present study was to investigate the relationship between immunologic status and physical symptoms in (ME)CFS. (Results) revealed significant associations between a number of immunologic measures and severity of illness. Specifically, elevations of Thelper/inducer cells, activated T cells, activated cytotoxic/suppressor T cells, and CD4/CD8 ratio Invest in ME (Charity Nr. 1114035) were associated with greater severity of several symptoms. Furthermore, reductions in Tsuppressor/cytotoxic cells also appeared related to greater severity of some (ME)CFS-related physical symptoms and illness burden” (SE Cruess, Nancy Klimas et al. JCFS 2000:7(1):39-52). 2000 “Most long-term sufferers (ill an average of 16 years)…showed a higher percentage of infection with viral and immune-related illnesses including allergies” (Friedberg F et al. J Psychosomatic Res 2000:48:59-68). 2000 “Over the past 15 years, scientists have identified numerous biological abnormalities that provide evidence for the reality and seriousness of (ME)CFS….In particular, they have provided evidence that the illness involves both the brain and the immune system….The leading model of (ME)CFS pathogenesis is rooted in scientifically identified abnormalities in the brain (central nervous system) and the immune system….Low levels of circulating cortisol, identified in several (ME)CFS research studies, can increase immune activation, which is also a key feature of (ME)CFS….Several immune system patterns are seen more often in patients with (ME)CFS. The identified abnormalities mimic the immune pattern of a body fighting a virus….(and include) low NK cell function (and) elevated immune complexes. The most intriguing recent immunological finding in (ME)CFS is the discovery of a novel low molecular weight protein in an antiviral pathway called the RNase-L pathway. This novel protein is found much more often in (ME)CFS patients than in healthy controls” (Anthony L Komaroff. The CFS Research Review, Spring 2000:1: 1-3). 2000 In 2000 Professor Anthony Komaroff from Harvard wrote about Professor Kenny De Meirleir’s work on RNase L in an Editorial in the American Journal of Medicine: “What is this research telling us? It is another piece of evidence that the immune system is affected in chronic fatigue syndrome and it reproduces and extends the work of www.investinme.org Page 58 of 108
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