Medical Mystery ME/CFS solved

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>>>> 28 May 2009 <<<<

Editorship : j.van.roijen

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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

 

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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 –

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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Editorship : j.van.roijen

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