BREAKING NEWS -Dr Kenny De Meirleir

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The slides, used in the London Press Conference, may be of interest for

many people.

They can be found at: _http://bit.ly/15fr3o_ (http://bit.ly/15fr3o)

 

 

~jvr

 

``````

ProHealt Library

 

 

BREAKING NEWS: Dr. Kenny De Meirleir Announces He has Revealed the True

Nature of ME/CFS (Myalgic Encephalo- myelitis/Chronic Fatigue Syndrome) in

London Press Conference titled: **ME: End of an Era of Medical Negation**

_http://bit.ly/FnhCe_ (http://bit.ly/FnhCe)

May 28, 2009

 

 

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 concerning the complex mechanisms of ME/CFS pathogenesis, a

diagnostic

test they have developed " for a major cause of ME, " and possible 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.)

 

 

FOLLOWING ARE:

 

-- 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 Disorderâ€)

 

 

SLIDES USED IN PRESS CONFERENCE

 

To view the slides Dr. De Meirleir used in his press conference, go to:

_http://bit.ly/15fr3o_ (http://bit.ly/15fr3o)

(Note: The urine test Dr. De Meirleir mentions will be offered for sale as

a home testing kit via his company - Protea Biopharma. To read more about

the test, go to: _http://bit.ly/yjFF0_ (http://bit.ly/yjFF0)

 

 

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_

(j.van.roijen) ).

 

 

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.

 

 

 

 

 

 

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~jvr

 

 

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Send an Email for free membership

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>>>> 29 May 2009 <<<<

Editorship : j.van.roijen

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