Scientists have developed a home-testing kit which they claim will help identify people suffering from myalgic encephalopathy (ME). The urine test is based on the theory that the illness is strongly linked to certain bacteria and a build up of toxins in the body. Experts are divided on what exactly causes ME, which was dismissed as "yuppie flu" in the 1980s. At a conference in London, Professor Kenny deMeirleir, who works at the University of Brussels, discussed his theory. He and fellow scientists have developed a simple urine test which they say identifies the presence of high levels of the chemical hydrogen sulphate. This chemical builds up after antibiotic use or exposure to salmonella infection, and can occur when there is too much exposure to mercury, he said. Prof de Meirleir's research has shown that around 90% of patients with ME also have an excess of the bacteria enterococcus and streptococcus, which he believes interacts with exposure to metals to produce hydrogen sulphate. Prof de Meirleir, who treats between 3,000 and4,000 ME patients a year, said his patients had been shown to excrete high quantities of the metals copper, mercury and nickel, possibly contracted through the environment or food. Prof de Meirleir said his new test, produced by his company Protea Biopharma and available via its website from Monday, accurately shows whether an ME patient has high levels of hydrogen sulphate. The patient's urine turns a dark colour when mixed with a chemical agent in the test. "This is a test for a major cause of ME," he said. "Anyone with a positive result should talk about it with their GP and get referred to a specialist."
reprint courtesy of www.co-cure.org
Friday, May 29, 2009
Medical Mystery ME/CFS solved
ME: End of an Era of Medical Negation
Belgian scientists (Brussels) have
identified causes and mechanisms of the
medical mystery Myalgic Encephalomyelits
(ME)/Chronic Fatigue Syndrome (CFS).
Professor Kenny de Meirleir MD, PhD,
(Professor at the Vrije Universiteit Brussels and
Director HIMMUNITAS Foundation Brussels)
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.
Article courtesy of www.co-cure.org
Belgian scientists (Brussels) have
identified causes and mechanisms of the
medical mystery Myalgic Encephalomyelits
(ME)/Chronic Fatigue Syndrome (CFS).
Professor Kenny de Meirleir MD, PhD,
(Professor at the Vrije Universiteit Brussels and
Director HIMMUNITAS Foundation Brussels)
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.
Article courtesy of www.co-cure.org
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