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Could chronic fatigue syndrome be caused by hydrogen sulfide produced by gut bacteria?

 

 

 

Researchers say that hydrogen sulfide produced by certain species of gut bacteria found in chronic fatigue syndrome could be a possible cause for the disease and have developed a cheap and simple diagnostic test based on their work.

On May 28, 2009, chronic fatigue syndrome (ME/CFS) researcher Dr. Kenny De Meirleir, MD, PhD, spoke at a press conference in London unveiling his team's groundbreaking findings regarding the illness. Dr. De Meirleir is a Belgian scientist known for his "outside the box" ME/CFS thinking and research; he is a professor at the Vrije Universiteit, Brussels and Director of HIMMUNITAS Foundation, Brussels.

Dr. De Meirleir's presentation described the team's conclusions concerning the complex mechanisms of ME/CFS pathogenesis, a diagnostic test they have developed "for a major cause of ME," and possible therapeutic strategies.

Below is a preliminary draft of the abstract of a journal article Dr. De Meirleir and his research team will publish on their work. The draft was disseminated through the CO-CURE listserv May 28 by ME research reporter Jan van Roijen (This email address is being protected from spambots. You need JavaScript enabled to view it. ).


Research on Extremely Disabled M.E. Patients Reveals the True Nature of the Disorder

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.


The Presentation - slides used by Dr. De Meirleir in his presentation of May 29th at Invest in ME’s International ME/CFS Conference in London entitled "Unravelling the Origin of Myalgic Encephalomyelitis: Gastrointesinal Dysfunction, Production of Neurotoxins and Environmental Exposure," posted on the Co-Cure Listserv Monday, June 1 on behalf of Tate Mitchell: http://www.steungroep.nl/index.php/component/content/article/195

The Urine Test - The test mentioned by Dr. De Meirleir is available as a home testing kit via his company - Protea Biopharma. To read more about the test and order, visit the Protea Biopharma website: www.proteabiopharma.com/page/diagnostics.php


 

 

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