Journal of IiME Volume 3 Issue 1 www.investinme.org P PRROOFFIILLEESS ooff PPRREESSEENNTTEERRSS aatt tthhee IINNVVEESSTT iinn MMEE I INNTTEERRNNAATTIIOONNAALL MMEE//CCFFSS CCOONNFFEERREENNCCEE bacteria which are also known to produce H2S in presence of certain heavy metals as a survival defense 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 colorimetric 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, 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 bacterial H2S induces increased ROS production by the liver and retaining of heavy metals, particularly mercury, in the body. Mercury 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. In about 20% of the ME patients (the most severely ill) we observed using a special luminescence technique the formation of proteins with aberrant conformation which interfere with the energy metabolism. In conclusion, ME is a disorder which is caused by increased endogenous H2S production. H2S initiates a chain of events in the body, with more and more negative effects on the aerobic metabolism and depression of the immune system leading to higher rates of infections and reactivation of endogenous viruses. In the most severe cases of the disease proteins with aberrant conformation may develop which put the patients in a total energy depleted state. Examples of other papers from Professor De Meirleir include – Lower frequency of IL-17F sequence variant (His161Arg) in chronic fatigue syndrome patients. Metzger K, Frémont M, Roelant C, De Meirleir K. Biochem Biophys Res Commun. 2008 Nov 7;376(1):231-3. Epub 2008 Sep 5. PMID: 18774769 [PubMed - indexed for MEDLINE] Unravelling intracellular immune dysfunctions in chronic fatigue syndrome: interactions between protein kinase R activity, RNase L cleavage and elastase activity, and their clinical relevance. Meeus M, Nijs J, McGregor N, Meeusen R, De Schutter G, Truijen S, Frémont M, Van Hoof E, De Meirleir K. In Vivo. 2008 Jan-Feb;22(1):115-21. PMID: 18396793 [PubMed - indexed for MEDLINE] Dr. Daniel Peterson MD Daniel Peterson is a graduate Magna cum Laude, Phi Beta Kappa of Carleton College in Northfield, Minnesota. He graduated from the University of Rochester School of Medicine in Rochester, New York, in 1976. Dr. Peterson served his internship and residency at the University of Utah Medical Center from 1976-1979 and became a Diplomat of the American Board of Internal Medicine in 1979. He has been caring for patients with Myalgic Encephalomyelitis/ Chronic Fatigue Syndrome (ME/CFS), for two decades, and his clinical work is complimented by a strong commitment to research as evidenced by his participation in more than 17 research studies, numerous drug trials and his foresight to collect and maintain the world's single largest repository of ME/CFS patient samples. Dr. Peterson was on the founding board of the IACFS. Among the numerous awards that he has received, in 2007 he was awarded the prestigious Nelson Gantz Clinician Award. Invest in ME (Charity Nr. 1114035) Page 69/76
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