Published at ProHealth today: At 11:00 AM London time on May 28, 2009, ME/CFS researcher Dr. Kenny De Meirleir, MD, PhD, spoke at a press conference unveiling his team's groundbreaking findings regarding the illness called Myalgic Encephalomyelitis / Chronic Fatigue Syndrome (ME/CFS). The presentation covered the team's conclusions regarding the complex mechanisms of ME/CFS pathogenesis, a diagnostic test, and directions for therapeutic strategies.
(Dr. De Meirleir, a Belgian scientist known for his cutting edge ME/CFS research, is a professor at the Vrije Universiteit Brussels and Director of HIMMUNITAS Foundation Brussels.)
• A link to slides used in the press conference (accompanying script to come soon, perhaps in a presentation Dr. De Meirlier will give Friday, May 29 at Invest in ME’s International ME/CFS Conference in London)
• The preliminary draft abstract of an upcoming journal article by the De Meirleir research team (“Research on Extremely Disabled M.E. Patients Reveals the True Nature of the Disorder”)
SLIDES USED IN PRESS CONFERENCE
To view the slides Dr. De Meirleir used in his press conference, go to http://www.mefmaction.net/Portals/0/docs//CFSDeMeirleir.pdf.
ABSTRACT OF UPCOMING JOURNAL ARTICLE – Preliminary Draft
The De Meirleir research team will also publish a journal article on their work. The following draft was disseminated via the CO-CURE listserv May 28 by ME research reporter Jan van Roijen (j.van.roijen@CHELLO.NL).
Research on Extremely Disabled M.E. Patients Reveals the True Nature of the Disorder
By Kenny De Meirleir(1), Chris Roelant(2), Marc Fremont(2), Kristin Metzger(2), Henry Butt(3)
(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 [lipopolysaccharide] is a strong activator of the immune system, and high plasma concentrations suggest a hyperpermeable 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 [hydrogen sulfide] 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 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.