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Medical Mystery ME/CFS solved To day May 28th at 11 A.M., the members of the press are invited at a press conference, which will be held at the Ritz Hotel in London. Belgian scientists (Brussels) have identified causes and mechanisms of the medical mystery Myalgic Encephalomyelits (ME)/Chronic Fatigue Syndrome (CFS). In light of the nature of the discoveries and its consequences for public health, the scientists who will be present at this press conference felt obliged to inform the public prior to publication of the results in a medical journal. Professor Kenny de Meirleir MD, PhD, (Professor at the Vrije Universiteit Brussels and Director HIMMUNITAS Foundation Brussels) ........sent me his speech for this press conference, named: ME: End of an Era of Medical Negation But there were some changes in the last days and they will use slides now; instead of the address, I'm allowed to post now an ‘uncorrected’ abstract of the study: *Research on extremely disabled ME patients reveals the true nature of the disorder* He will also speak about this subject at the 4th Invest in ME International ME/CFS Conference in London on 29th May. If I remember well, the ME/CFS urine test, of which is spoken below, will come on the market as a "do it yourself test". So you know in a few minutes, if you are an ME/CFS patient or not. Jan van Roijen ```````` Kenny De Meirleir(1), Chris Roelant(2), Marc Fremont(2), Kristin Metzger(2), Henry Butt(3) Research on extremely disabled M.E. patients reveals the true nature of the disorder (1) Vrije Universiteit Brussel & HIMMUNITAS foundation, Brussels, Belgium (2) Protea Biopharma, Brussels, Belgium (3) Bioscreen & Bio 21, University of Melbourne,Melbourne, Australia In this study we compared totally bedridden patients (Karnofski score 20-30) with less ill ME patients (Karnofski score 60-70), family controls, contact controls and non-contact controls. EBV, HHV6 and Borna virus titers were not different in the three groups. Plasma LPS distinguished the groups, with the highest values in the bedridden patients. LPS is a strong activator of the immune system and high plasma concentrations suggest a hyperper- meable gut. There are many possible causes for this, but a lack of ‘local’ energy production is one of them. In a separate study (In Vivo, in press) we observed intestinal overgrowth of Gram positive D/L lactate producing bacteria which are also known to produce H2S in presence of certain heavy metals as a survival defence mechanism. We therefore hypothesized that the urine of the bedridden ME patients would contain more H2S derived metabolites than the less ill and the controls. Using a proprietary simple color change urine test this hypothesis was confirmed. In the extremely ill, urine added to the yellow color reagent immediately turns dark blue, whereas in the less ill the reaction is slower and in the controls no reaction occurs. Being a potent neurotoxin, H2S induces photophobia, intolerance to noise, mitochondrial dysfunction by inhibition of cytochrome oxidase and depresses the cellular immune system and induces neutropenia and low numbers of CD8+ lymphocytes. Its effects, at least in part explain the clinical condition of the severely disabled ME patients. Furthermore the effects of the bacterial H2S induces increased ROS production by the liver and retaining of heavy metals particularly mercury in the body. The latter is also neurotoxic, induces apoptosis and interferes with the aerobic metabolism. Chronic increased production of H2S by intestinal bacteria leads to build-up of mercury in the body as proven by a Zn DTPA/DMPS challenge test. Finally in 20% of the ME patients (in the severely ill) we found using a special luminescence technique aberrant prions which also interfere with the energy metabolism. These patients have gone on to develop A.P.D. (aberrant prion disease – patent pending). These aberrant prions give rise to a transmissible disorder. 10% of the A.P.D. patients have very high prion counts in their saliva and can directly transmit it to others. APD patients can transmit these proteins via blood and likely also through sexual contact which then can give rise to slowly developing aberrant prion disease. In a separate experiment 40 healthy blood donors were screened for A.P.D. One individual tested very positive, indicating that apparently healthy individuals can already be carriers and that blood transfusion carries the risk of transmitting A.P.D. In conclusion, ME is a disorder which is caused by increased endogenous H2S production. For the latter many factors can be present. Because of the effects of H2S in the body a chain of events will develop which have more and more negative effects on the aerobic metabolism and depression of the immune system leading to more and more infections and reactivation of endogenous viruses. In its final stage aberrant transmissible prions develop which put the patients in a total energy depleted state. ~~~~~~ ~~~~~~~~~~~~~~~~~~~~~~~ Send an Email for free membership ~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~: >>>>> Help ME Circle <<<< >>>> 28 May 2009 <<<< Editorship : [EMAIL PROTECTED] mail scanned by Comodo I. 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