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| * ] Added mention of a common pitfall in this opening, with game and diagram. | * ] Added mention of a common pitfall in this opening, with game and diagram. | ||
| Regards, ] (], ]) 16:55, 26 May 2009 (UTC) | Regards, ] (], ]) 16:55, 26 May 2009 (UTC) | ||
| == Mystery of ME solved? == | |||
| <div style="border:1px solid black; background:#FFEE99;">'''Research on extremely disabled M.E. patients reveals the true nature of the disorder''' | |||
| :''ahead of publication'' | |||
| ''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 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 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. ] (], ]) 11:08, 28 May 2009 (UTC)</div> | |||
Revision as of 11:08, 28 May 2009
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| Prof. Malcolm Hooper (2007): "The simplest test for M.E. is just to say to the patient ‘stand over there for ten minutes’." |
Hey, I'm glad your back
Thanks for the complement. I have some other stuff going on in my life right now and don't know how much time I can give to Misplaced Pages, but I will monitor my watchlist as best I can. Ward20 (talk) 01:08, 24 May 2009 (UTC)
- Well, there is really nothing left for me to do here. Misplaced Pages is dead, I won't waste any more energy on it. Guido den Broeder (talk, visit) 15:20, 26 May 2009 (UTC)
My contributions
As various users are currently suggesting that my account should be blocked because of my contributions, here is a complete overview for easy reference.
- Basic income in the Netherlands Removed 'welfare' that was incorrectly put forward as an example, improved layout and corrected a link description
- Chess World Cup Added a mention of the earlier GMA Grand prix.
- Geoengineering Reworded the lead where there was some confusion between definition and application
- Global Cooling Changed an anon's addition of 'today' (the infamous moving target) into 'beginning of the 21st century' in accordance with source and info at Global Warming
- Owen's Defense Added mention of a common pitfall in this opening, with game and diagram.
Regards, Guido den Broeder (talk, visit) 16:55, 26 May 2009 (UTC)
Mystery of ME solved?
Research on extremely disabled M.E. patients reveals the true nature of the disorder- ahead of publication
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 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 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. Guido den Broeder (talk, visit) 11:08, 28 May 2009 (UTC)