Medical Mystery ME/CFS solved

To day May 28th at 11 A.M., the members

of the press are invited at a press

conference, which will be held at the Ritz

Hotel in London.

Belgian scientists (Brussels) have

identified causes and mechanisms of the

medical mystery Myalgic Encephalomyelits

(ME)/Chronic Fatigue Syndrome (CFS).

In light of the nature of the discoveries and

its consequences for public health, the

scientists who will be present at this press

conference felt obliged to inform the public

prior to publication of the results in a

medical journal.

Professor Kenny de Meirleir MD, PhD,

(Professor at the Vrije Universiteit Brussels and

Director HIMMUNITAS Foundation Brussels)

would send me his speech for this press conference,

named:

ME: End of an Era of Medical Negation

But there were some changes in the last days and

they will use slides now; instead of the address, I'm

allowed to post now an 'uncorrected' abstract of the

study:

*Research on extremely disabled ME patients

reveals the true nature of the disorder*

He will also speak about this subject at the 4th

Invest in ME International ME/CFS Conference in

London on 29th May.

If I remember well, the ME/CFS urine test, of

which is spoken below, will come on the market as a

"do it yourself test".

So you know in a few minutes, if you are an ME/CFS

patient or not.

Jan van Roijen

````````

Kenny De Meirleir(1), Chris Roelant(2), Marc

Fremont(2), Kristin Metzger(2), Henry Butt(3)

Research on extremely disabled

M.E. patients reveals the true

nature of the disorder

(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 hyperper-

meable 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 ˆ 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.