Dear Dr. Siff,
Thanks for the scary info. Do you have a date for that Pittsburgh study?
Thanks. Sarah Fern Striffler, PT
----- Original Message -----
From: <[log in to unmask]>
To: <[log in to unmask]>
Sent: Friday, February 02, 2001 1:02 PM
Subject: Brain Eroding Diseases
Most of us will now have been made aware by the media of an horrific brain
eroding disease called Mad Cow or Creutzfeld-Jakob Disease. The following
selections of readings provide some interesting insights into the nature of
this unique disease.
< http://www.sightings.com/health/madcowinfridge.htm>
Mad Cow Disease causes no antibody response. The damage to the brain is done
by infectious prions or rogue proteins which become part of the cell walls
in
the infected host. When infection enters any animal, the victim's immune
system shows no sign of fighting the infection as it does with bacteria,
germs, and viruses. This means the immune system can neither detect nor
fight it, nor can scientists use the antibody-search method to see if
someone
is sick, as we do with AIDS. CJD (Creutzfeld-Jakob Disease) disease takes
10 months to 50 years to eat away human brain.
Mad Cow, or BSE, (Bovine Spongiform Encephalopathy) causes transmissable
genetic mutation which means that if you have it, all your children will be
born with it. Sheep and cows pass it to offspring, too, and chickens to
their
eggs. If it weren't transmissable, why for decades has the FDA demanded that
all donors to the blood supply answer the question 'has anyone in your
family
died of CJD? That disease is entirely inherited and one drop of blood of a
descendant of a CJD victims can infect the rest of your line. PRION
diseases
are well known to be genetic in that they bond with with DNA and are passed
on.
No scientist can tell if a cow or human is in an incubating phase. Except
for
brain biopsies, there are no tests, no genetic markers. Prions are not
reliably found in urine. You can see prions in brain tissue but you cannot
open the skull of a live mammal to scoop them out. If a cow whose milk you
are drinking has it, her calf, sent to be a veal chop last Winter, also had
it when you ate it. A long incubation period means that the farmer cannot
see that the animal is ill.
Consider the link which scientists are now following. Alzheimer's is
rampant
in America and yet few people talk about how these scientists think that it
could also be a prion or protein-borne disease associated with the
consumption of tainted meat and dairy products. This research began in
earnest when Pittsburgh Veterans hospital autopsied 53 SEQUENTIAL
Alzheimer's
victims. Sample A showed 5.5% had died of Mad-Cow; Sample B showed that 6.3
Percent died of Mad-Cow. Alzheimer's death tolls are doubling and tripling,
which is not characteristic of a normal genetic disease. It appears as if
some statistics for Mad Cow and CJD are being obscured by Alzheimer’s
statistics.
Pasteurization or even radiation cannot destroy prions which can tolerate
these adverse conditions because they are not living infectious agents. Mad
Cow prions can't be killed the way we fought the plague or fight cholera
epidemics, or Ebola, by burning bodies. Prions are, for all practical
purposes, indestructible. These rogue proteins will only begin to degrade at
800 degrees fahrenheit, way above the temperature that would reduce them to
ash! In fact, burning is a bad idea, as prion molecules will rise up in the
smoke, become airborne and fall back on the land.
No laboratory will accept a Mad Cow autopsy as the laboratory cannot be
sterilized afterwards. You canot kill prions with fire or disinfecting
agents. Those are the facts. Remember, beef and sheep farmers have been
sending livestock to factories to be made into 'protein powder' for
livestock
for the last 26 years. Mad Cow prions could be in every ounce of meat,
milk, pork, chicken, egg, cheese, or butter you eat today and in gelatin
caps, animal glandular supplements, and in the glue on every postage stamp.
Until all slaughterhouses have brain autopsy labs, until no animal we eat is
fed another animal's dead body, under penalty of law, and not just leaving
it
to farmers' discretion, nobody can feel safe eating meat, butter, eggs or
drinking milk any longer.
Chickens and turkeys are also high risk because cattle blood is sprayed onto
their feed! The FDA recommended a ban on feeding dead cows to live ones, but
has said nothing about the practice of using the blood of cattle as food for
cattle or any other livestock or poultry. Any good doctor will tell you that
the blood is a carrier of virtually all diseases present in a sick animal.
So, remember the next time you are in line at the fast food restaurant, or
heading out to your favourite steak house, you might be about to eat your
way
to a prion eroded brain in a few years' time, especially if the prions are
found to be the missing link in the Alezheimer’s riddle.
------------------------------------------------------
Here are some sites with plenty of information on Creutzfeld-Jakob (CJD) and
Mad Cow Disease:
<http://www.cjdfoundation.org/CJDInfo.html>
<http://www.mad-cow.org/>
----------------------
One of the theories explaining these types of disease maintains that special
infectious proteins called "prions" (proteinaceous infectious particle)
cause
"Mad Cow" disease. The following websites discuss this topic:
<http://www.sciam.com/askexpert/medicine/medicine14.html>
"The term 'prion' was coined by Stanley B. Prusiner of the University of
California School of Medicine at San
Francisco in 1982 to distinguish the infectious agent that causes scrapie in
sheep, Creutzfeldt-Jakob disease
(CJD) in humans and bovine spongiform encephalopathy (BSE) in cattle from
other, more typical infectious
agents. The prion hypothesis postulates that these diseases are caused not
by
a conventional virus or bacterium
but by a protein that has adopted an abnormal form.
Here is an article by Dr Prusiner himself reporting in "The Scientific
American" on the nature of prions:
<http://www.sciam.com/0896issue/prion.html>
"Fifteen years ago I evoked a good deal of skepticism when I proposed that
the infectious agents causing certain degenerative disorders of the central
nervous system in animals and, more rarely, in humans might consist of
protein and nothing else. At the time, the notion was heretical. Dogma held
that the conveyers of transmissible diseases required genetic material,
composed of nucleic acid (DNA or RNA), in order to establish an infection in
a host. Even viruses, among the simplest microbes, rely on such material to
direct synthesis of the proteins needed for survival and replication.
Later, many scientists were similarly dubious when my colleagues and I
suggested that these "proteinaceous infectious particles"-or "prions," as I
called the disease-causing agents-could underlie inherited, as well as
communicable, diseases. Such dual behavior was then unknown to medical
science. And we met resistance again when we concluded that prions
(pronounced "pree-ons") multiply in an incredible way; they convert normal
protein molecules into dangerous ones simply by inducing the benign
molecules
to change their shape.
Today, however, a wealth of experimental and clinical data has made a
convincing case that we are correct on all three counts. Prions are indeed
responsible for transmissible and inherited disorders of protein
conformation. They can also cause sporadic disease, in which neither
transmission between individuals nor inheritance is evident. Moreover, there
are hints that the prions causing the diseases explored thus far may not be
the only ones. Prions made of rather different proteins may contribute to
other neurodegenerative diseases that are quite prevalent in humans. They
might even participate in illnesses that attack muscles."
-------------------------------------------
This article discusses potential risks from vaccines and cultures made from
cattle:
<http://www.mad-cow.org/00/01jan_news.html>
-------------------------------------------
This article discusses similarities between Mad Cow and Alzheimer's Proteins
<http://www.cnn.com/2000/HEALTH/08/24/bc.health.madcow.reut/>
WASHINGTON (Reuters) August 24, 2000 -- Proteins linked with Alzheimer's and
the human version of mad cow disease have some striking similarities -- and
thus might be susceptible to similar treatments, a researcher said. Both
diseases are marked by a gradual deterioration of the brain and both are
associated with rogue proteins. Both are always fatal.
Chi Ming Yang, a professor of chemistry at Nankai University in Tianjin,
China, said he used a computer model to map the prion protein associated
with
Creutzfeldt-Jakob disease (CJD), the human equivalent of mad cow disease,
and
the amyloid precursor protein associated with Alzheimer's.
Proteins are made up of amino acids, and Yang told a meeting of the American
Chemical Society in Washington that he found a similar pattern of amino
acids
in the two proteins -- a reductive amino acid followed by three
non-reductive
amino acids. "This suggests a common molecular mechanism underlying the
initiation stages of sporadic Alzheimer's disease and both sporadic and
genetic prion diseases," he said in a statement.
------------------------------------------
The Mystery of Mad Cow Disease:
<http://www.msnbc.com/news/439861.asp?cp1=1&cp1=1#BODY>
"THE CULPRIT behind the so-called transmissible spongiform encephalopathies
(TSEs), such as mad cow disease or the human version, Creutzfeldt-Jakob
disease, is thought by many to be a misfolded protein called a prion. These
misshapen molecules also have been linked to more common, non-infectious
brain diseases such as Alzheimer’s, Parkinson’s, Huntington’s and Lou
Gehrig’s. If prions truly are the culprits behind these diseases, their
existence flies in the face of the conventional wisdom that only organisms
with a genome (such as viruses or bacteria) can spread disease or perpetuate
themselves in living cells."
--------------------------------------
What USA Authorities may not be admitting about CJD:
A cover-up style of article citing instances of where CJD was first spread
among cattle in the USA, and only later to the UK. You will have to check
through various references to extract what is fact and what is not:
<http://home.earthlink.net/~astrology/udder.htm>
"....From the Pittsburgh sampling we realize that there are hundreds if not
thousands of CJD deaths in America but they are passed off as Alzheimer's.
BSE (Bovine Spongiform Encephalopathy) is entrenched in American beef
regardless of what the US Government wants you to believe, and boy, there
seems to be an effort to control what you believe.
Ted Koppel interviewed BSE and CJD expert, Dr. Richard Marsh, on the
Nightline TV program in 1996. The interview went like this:
Koppel: But we (USA) don't feed sheep brains to cows, do we?"
Dr Marsh blinked. "I don't know where your information comes from, but we
do."
He was instantly cut off by a commercial and did not reappear that night.
(Capitol Cities which owns ABC was founded by William Casey of the CIA. It
is
as close to being an official mouthpiece of the oligarchy as exists....
The truth is, Virologist Veteran Marsh knows of what he speaks. All those
BSE
cow bodies he saw in Wisconsin 1981-1989 had been fed dead sheep, yet the
cows became 'feeder cattle' to feed thousands of other cows who have bred
thousands of animals. Papuan prions have been spread to herds from Maine to
Hawaii. Knowing the genetic mode of transmission of the disease is to all
offspring, it is reasonable to suspect that there is sponge brain infection
slowly crawling up the brain stem of every cow in America as well as all the
humans who have eaten them as well as all the offspring of both species.
And
to pigs, chickens who were also fattened with the deadly Soylent Green. As a
poultry farmer told a prion researcher, "rendering salesmen brought us bags
of this powder saying it was wonderful stuff and had ever so many uses: we
could use it for fertilizer or to feed our chickens."
As so many CJD deaths are misclassified as Alzheimer and private labs won't
let CJD tissue in the door to be examined, it is certain the American public
will not be informed of the disease that is in our food, our kitchens and
our
bodies. We are scheduled to be 'downers' and Ted Koppel doesn't want us to
know it.
Dr. Richard Deandrea, a Los Angeles physician who has studied CJD and BSE
extensively, tells of his first CJD patient. After her death, which
featured
frills atypical of Alzheimer's (fingers numb, blindness, slurred speech,
weak
knees), Deandrea dogged the Center for Disease Control for a pathologist
who'd give him an autopsy to see if it might be CJD. CDC evaded 3 weeks of
his calls. Finally, a female CDC staffer told him that off the record -
she'd deny it later -"CJD is an issue no pathologist will deal with, a
virtual death sentence to a lab. A well trained pathologist knows the
quarantine would never be lifted. You couldn't sterilize the lab to OSHA
protocols. It would have to be gutted, incinerated. Forget it. Your patient
died of Alzheimer's." So, there may be CJD deaths but there sure aren't
going
to be CJD death certificates. ......>
----------------------------------
Scientific articles on a possible prion role in CJD and Alzheimer's:
<http://www.alzforum.org/members/research/news/index.html#molecularClue>
The process by which a normal prion protein (provoked by an abnormal prion)
undergoes a conformational change to the abnormal form, and the hypothesized
resulting neuropathology, is of particular interest to researchers of other
neurodegenerative diseases that also feature abnormal buildup of toxic
proteins. Because the presence of abnormal prion alone does not lead to
neurodegeneration, it is assumed that the protein must work via other
molecules. Aguzzi and colleagues in Switzerland and Austria determined that
plasminogen - a plasma component that serves as the proenzyme for the
protease plasmin - binds selectively to the prion protein in its abnormal
form, probably via lysine residues on the prion. They found this to be true
with mouse prion protein, as well as with prion protein from the brains of
human Creutzfeldt-Jakob disease patients.
Normal Prion Protein Signals With Fyn (14 September 2000).
The intracellular protein Fyn, a suspect in the formation of neurofibrillary
tangles because of its associations with tau protein--has now popped up in
conjunction with prion diseases. Researchers in France report in tomorrow's
Science that Fyn couples with the normal form of prion protein, an
interaction that also involves the protein caveolin-1.
There is still no demonstrated function for the normal form of prion protein
(as opposed to the abnormal form thought to cause transmissible spongiform
encephalopathies such as mad-cow disease and scrapie). The fact that it is
localized in particularly high concentrations in the cell membranes of
neurons has led to speculation that it is involved in signal transduction
across the membrane. The current Science report adds fuel to that idea,
finding that the normal prion protein is involved in an interactions with
the
intracellular tyrosine kinase Fyn. Because the two proteins are localized in
different compartments, the researchers searched for an intermediate that
might be able to link the two and found caveolin-1 involved in this cascade.
(The protein clathrin, included as a control, also had some effect on the
interaction, suggesting that it too may be involved.)
The researchers also noted that Fyn was not activated until the cultured
cells had differentiated into neurons and that the signaling cascade seemed
to only involve prion molecules located on neurites, and not on the cell
body. Implicit in these results is the idea that an extracellular messenger
must somehow be involved. (See William Klein's comment below on whether
there
might be some common factor in signal cascades in prion disease and in
Alzheimer's.)
( Mouillet-Richard S, et al. Science. 15 Sept 2000; 289: 1925-8.
Comment by William Klein:
Coupling of cellular prion proteins to Fyn is a real surprise, but maybe it
shouldn't be. Fyn keeps popping up. Shirazi and Wood showed that
tangle-bearing neurons in AD have a hefty overload of Fyn. Gloria
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