Dr. Kenny De Meirleir Announces He has Revealed the True Nature of ME/CFS

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BREAKING NEWS:

Dr. Kenny De Meirleir Announces He has Revealed the True Nature of ME/CFS

(Myalgic Encephalomyelitis / Chronic Fatigue Syndrome) in London Press

Conference titled “ME: End of an Era of Medical Negation "

http://www.greatfal lstribune. com/article/ 20090529/ NEWS01/905290318

/1002/U.S. +Supreme+ Court+won+ t+hear+Blackfeet +mold+caseMay 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://www.mefmacti on.net/Portals/ 0/docs//CFSDeMei rleir.pdf.)

(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 www.proteabiopharma .com/page/ diagnostics. php

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), Roelant(2), Marc Fremont(2),

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.