Wednesday, June 17, 2009

Medical Mystery Solved

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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



````````


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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