The WorldWide Threat: TSE Disease
January 19, 2001
January 23, 2001
January 31,
2001
March 5,
2001
|
| What is "Mad Cow" Disease? |
BSE (Bovine
Spongiform Encephalopathy - mad cow disease) is a specific term which refers to
the bovine form of a mind-wasting prion disease, or a generic term for
prion-induced disease passed between sheep, cattle, humans and other mammals,
now more appropriately referred to as TSE (Transmissible Spongiform
Encephalopathy). Some of TSE's threat was identified by the year 1988, at which
time the United States began measures to keep infected cattle from being
brought into the country, specifically from the U.K. and other isolated parts
of Europe. TSE incubation in humans results in the symptomatic
Creutzfeldt-Jakob Disease (CJD; pronounced Kruts-felt Yok-ob Disease) of the
same TSE prion, with a 100% fatality rate. Once symptomatic, all TSE
manifestations in all animals are fatal following extended and horrid effects
of neural degeneration.
As of January 2001,
the epidemic of the prion's spread through Europe is being realized as Germany,
and Belgium, formerly free of BSE, have been cut off from beef exportation to
most of the European Union since November, 2000, joining 30 other countries
with known BSE infection. It was not realized early on that scrapie or mad
sheep disease, afflicting sheep even during the 18th century, and in many parts
of the world including North America, is also a TSE disease, nor did anyone
imagine the extent that this disease would spread throughout the world during
the late 20th century, nor its implications for our world as it spreads.
In North America, mad sheep disease (scrapie), mad deer disease
(wasting disease) and mad elk disease have been endemic throughout regions of
Canada, the U.S. states of Wyoming, Colorado and Montana, and sheep production
facilities in the eastern U.S. During January, 2001, it was announced that the
first deer death from wasting disease had been discovered in the U.S. beef
producing heartland of Nebraska, USA.
All these diseases
are variant manifestations of the same TSE prion. TSE prions attack nervous
tissue, eventually causing death by brain damage as neuronal brain cytoplasm
transforms into spongy, diseased tissue full of fluid-filled holes, like swiss
cheese. TSE has killed 80 people in Europe to
date, while 15+ million cattle have been
slaughtered and burned in attempts to prevent its spread.
(See Updates at the bottom of this page.)
As of
New Year's, 2001, the United States, Australia and Argentina, of the major beef
producing countries, have not reported BSE within their cattle industry nor CJD
in humans *(See update, Jan 23). Unfortunately, that does not guarantee that
TSE is excluded from these countries.
Where did it come
from?
(Contempt for Nature) |
Cattle were
designed by Nature to convert nearly pure cellulose into sugars, amino acids
and proteins to support the production of muscle and fat, bone, milk, and baby
cattle, of course, who would carry on the original design specifications for
each model into new generations.
Cattle are true herbivores. These
"primary grazers" are plant-matter cellulose conversion machines at the lower
end of a planetary food chain which includes predators, like humans, "higher"
on the chain. Humans are not capable of ingesting clumps of grass or other pure
plant cellulose into nutrients to sustain life. True herbivores include
rabbits, sheep, deer, elk, cattle, horses, and other primary
grazers.
During the 1950s, dairy farmers began to pump massive amounts
of proteins into cattle feed. Cattle, that can mow grass effectively without
killing it, aren't as ruthlessly efficient as sheep that rip grass and roots
from soil and metabolize the whole plant. The 20th Century solution was to put
sheep on leased grazing land until the land had been denuded of edible
vegetation, then slaughter the sheep, grind them into high-protein feed and
shovel it into cattle to make cattle bodies to do things that Nature had not
intended.
A conservative dairy farm allows cattle to graze, with dairy
cows returning (happily) during early mornings and late afternoons to be
milked. Under these conditions, dairy cows produce milk for about ten years.
Many of today's large, commercial, high-production
dairy operations do not allow dairy cows to walk around or graze. Dairy cattle
remain penned during their productive life, which is as short as two years.
They are crammed full of protein-enriched feed and milked four times each day.
After two years, the animals simply burn-out and are discarded for harvesting
as meat.
Bovine gastrointestinal systems use symbiotic bacterial
digesters to break down cellulose into sugars that can produce energy and
tissues for growth. The breakdown is a slow process, requiring all the stomachs
cattle have to do this gradual but effective conversion properly. Cattle do not
have the same acids and enzymes that exist within predator intestines to
process food. Consequently, a bovine gut cannot effectively render animal
proteins into constituent building blocks for absorption and reuse like a
carnivore gut can, since cattle were not engineered for that sort of lifestyle.
Ground sheep contains ground-up sheep cell structure which includes
sheep DNA. The DNA, inside a bovine gastrointestinal system, ineffectually
decays into billions of variously-sized protein fragments. In at least one out
of a million humans, sheep and cattle, a naturally-occurring genetic defect
produces "beta sheet" folding structures with production of infectious, deadly
protein fragments. At least one of those fragments has now found a new
environmental niche in which to propagate itself as a significant, new type of
organic entity on our planet, called a TSE prion, which propagated through the
20th Century farming practice of feeding animals the tissues of other animals.
The infectious prion's nearly insignificant appearance in past history is now a
major source of concern and alarm in Europe and the world.
Mammalian DNA
contains specific protein groups coded as "prion," as part of the normal DNA
sequence. Forty two prion sites along human DNA have been postulated as
potential sites for spontaneous mutation of normal prion between bonding sites
in DNA structure. One of these, human PrP(C)117, has been the subject of most
tests and speculation regarding lethal CJD in humans. In the presence of
infectious proteins under low pH conditions (~4.5 or lower within the cell
solutions surrounding the prion area), PrP(C)117 can mutate to PrP(Sc) - a
small but deadly substitution of hydrogen-bonded lysene to glutamate. Once the
substitution occurs, a helix'es prion site whips into unstable coils and loops
which can apparently break and rebond repeatedly, popping off more copies of
the infectious prion. The mutation is not compatible with continued integrity
of affected tissue. Cell membranes, the membrane itself being coded by the
altered DNA site, cannot be maintained by the faulty genetic program. Affected
tissue turns to fluids, without membranes to differentiate cell tissue
boundaries. "Prion," in relation to TSE, means infectious, altered prion
PrP(Sc). It is believed that TSE prion was created by feeding high-protein food
to cattle that contained sheep DNA. Sheep protein fragments provided the
necessary source of proteins for replication of the infectious, mutated prion
from within small populations of normally-benign but mutated, bovine cells. The
World Health Organization now reports that studies of feed shipment records
show that ground-sheep feed has been distributed worldwide since the 1950s.
This high-protein feed not only contained the constituent proteins to encourage
random, mutated cells to begin pumping out infectious prions instead of just
disappearing within a healthy body, it also carried infectious prion from
diseased sheep. If this mechanism of mad cow disease spread is correctly
understood, the current world BSE crisis was inevitable as cattle were fed with
sheep protein. This feed was shipped worldwide until only a few months
ago.
Now
what?
(What can we do?) |
BSE has
spread to over thirty countries, effectively destroying dairy production of
each country as many millions of cattle have been slaughtered and burned in
attempts to control the spread of BSE. Britain, Ireland and France are among
these countries. Germany joined them in November, 2000. Italy discovered
positive BSE cases in January, 2001. The US and most other "BSE-free" countries
ban beef product imports from much of Europe including all of the 30+ countries
with known BSE, however the disease appears to be unstoppable and mad sheep,
mad deer and mad elk are evidence that the prion is firmly entrenched in the
United States and Canada, even though the public has not been notified of any
incidence of BSE in domestic herds of cattle.
In the U.K. and Germany,
known government cover-ups of BSE allowed BSE infected foods to reach the food
shelves in other countries. This is causing massive political turmoil as
politicians are sued and expelled from office over their cover-ups and
inaction. But after tracking as many details of the BSE issue as possible for
the past two years, it now seems unlikely that much of the human population has
not been exposed to at least some prion infection.
This tiny monster
has a tremendous incubation period, possibly up to ten and even fifty years,
making sources of the infection difficult to identify. Also, it's possible that
the prion is spreading through many sources of food in human populations that
have not identified vCJD yet.
In one of the early lab tests of the
prion, viable prion was discovered by one scientist in his flower planter
outside a laboratory window. After autoclaving surgical instruments, the
scientist would pour autoclave ash into his flower planter. His discovery
resulted in further testing to learn that autoclaving was not adequate to
destroy the prion.
Nothing compatible with any other life-form has been
found to destroy this prion. It has no natural enemies, inoculations or
barriers, and mammalian immune systems cannot recognize it or fight it. BSE is
terrorizing the world except for the U.S., where it's politically incorrect for
news media to upset Americans with bad news.
Higher risks of prion
infection to humans may occur from "mechanically-separated meat by-products;"
sausage, bratwurst, lunchmeat, and other by-products produced by machines that
remove meat, including nervous tissue, from bones. Prions can apparently be
absorbed by plant life and passed to grazing mammals. Huge Canadian elk herds,
condemmed due to infection during December, 2000, were probably contaminated by
scrapie-infected sheep tissue sent to a wastewater plant for disposal, with the
sludge later spread on forest grasslands.
Scientists believe that
people are infected by their food, although there is one case in the U.K. being
analyzed right now where a man may have been infected by casual contact with
another man who later developed vCJD. The contact was non-sexual and the
mechanism of infection is currently a mystery. One of the men was an avowed
vegetarian while the other rarely ate red meat of any kind. Food is primarily
considered to be the vector of infection, although experiments where fly larvae
consumed infected brain tissue successfully transferred TSE to hamsters through
oral consumption. Establishing an insect as a possible vector of disease spread
was important, but hardly surprising. In any case where DNA proteins can be
communicated as prion fragments, some infectious prion will remain
viable.
In January, 2001,
some scientists suggested that space debris brought the prion to earth.
Although the suggestion may have been honestly proposed, it seems rather
absurd. Such suggestions are not likely to allow an escape for British
politicians who are being pursued via litigation, as they are accused of
criminal incompetence for allowing BSE-contaminated meat to reach store shelves
in France. The idea is mentioned here in an attempt to be condescendingly
supportive of even the stupidest contributions of science. More realistically,
the massive (and insipid) agricultural use of slaughtered animal tissues and
blood, fed to cattle, is a known to have contributed heavily to the current BSE
crisis.
Prions may now be in our food, our pet food, our pets, our lawns
and ourselves.
The first symptom of vCJD in humans has included
overnight personality changes. "She woke up as a different person." Initial
symptoms seem to resemble stroke as the disease disconnects portions of the
brain that accomplish the unique traits of Self. Memory is quickly
destroyed. -Confusion, regression of developmental thought, defensive behavior,
rage. -Staggering, loss of feeling and loss of control. Speech is impared. The
ability to think clearly is rapidly destroyed. Human death after symptoms first
appear normally requires 1 - 2 years while the quickest documented case (a
fourteen year-old girl) resulted in death five months after symptoms first
appeared. Victims often spend their final year as screaming vegetables.
To date, a test to detect infectious prion in a living creatures does
not exist *(See Jan 23 Update), with the exception of costly DNA sequencing
tests. Human and bovine brains are examined for spongiform vacuolization after
death. For humans, diagnosis is only confirmed after autopsy. Only cattle
younger than 30 months old are not inspected, but that's because the EFFECT of
the prion has never been observed in a young brain. It may take up to ten years
for the prion to incubate into symptomatic stages, although it may be
reasonable to suggest that prions may already be present in many more of
earth's mammalian populations than we would like to know about. Original
studies by Dr. Creutzfeldt and Dr. Jakob, independantly, were centered on
manifestations of senility, including premature dementia and Alzheimer's
disease. During their studies, both doctors reported vacuolization on brain
tissue after death of patients as well as disorientation, mental regression and
loss of coordination. Very obviously, both doctors worked with TSE prion
victims and the human variant was later named after these two scientists. It
may be staggering to determine how much senseless violence and how many
diagnosis of Alzheimer's disease are actually CJD.
John Stauber and
Sheldon Rampton, authors of Mad Cow USA: Could the Nightmare Happen Here?
are highly critical of efforts in the U.S. to limit the spread of prions.
"They [people] should be very angry that the U.S. government is covering up the
risks of mad deer and mad elk disease to hunters and to those who eat venison
products," Stauber said. "And also that our regulations in the U.S., with
regard to feeding slaughterhouse waste to animals, are
inadequate."
It is our nature to push the extreme edge of
productivity, constantly. But trying to circumvent natural contraints may be
our undoing. We play with powers we cannot fathom and if we haven't already
created the monster of our own destruction, we will probably do so through
other genetic manipulation of plants and animals, or genetic creation of other
diseases which we cannot control; forms of life we artificially create which
were not selected into coexistence within our carefully-balanced environment of
planetary ecosystems through millions of years of tweaking to environmental
stresses. In this matter, we agree with Michael Crichton: "Genetic engineering
is the most powerful force on the planet. You play with it like a kid who has
just found his dad's gun."
No one seems willing to face the
responsibility for thinking through the implications of incredible corruptions
of natural effrontery before releasing the latest toys for maximum, commercial
exploitation. -That's assuming that we have anything near the wisdom required
to evaluate such implications in the first place. While some groups protest
G.M. (Genetically Modified) crops, our ignorance of the possible effects of
this science may have already created other monsters that have just begun to
breathe their first, stinking breaths of terror into the future of world
agriculture. Ecological justice is absolute and inescapable. Our planet's
balance of the ecosystem is not only required, but it will be enforced by our
world at the cost of our own extermination, if necessary.
It's
important to note the differences between selective breeding of plants and
animals, including hybrid pollenation, to that of genetic modification of crops
which produces traits previously unknown. As an example, the former has
exemplified desirable traits in crops and animals that were already inherent,
but not new. The latter science has produced creatures and crops with
completely new genetic traits that did not evolve within our ecosystem, such as
traits that are genetically resistant to certain chemicals so that the
chemicals can be produced as pesticides to destroy target insects and blight.
Farmers not planting the GM crops often cannot compete with the
genetically-enhanced crops that can produce massive, short-term advantages. To
create new wonders is seductive science; to be an individual farmer against the
trend is economic suicide. But often, other plagues appear within a few years
to wipe out not only the GM crops but many others besides. Such plagues include
previously benign insects that become agricultural terrors when the original
pests are wiped out and no longer compete to control populations of the new
parasitic threat. The potential to create monumental horrors between
genetically modified lifeforms and indigenous life is staggering to
contemplate. Individual agriculturists do not have the option to refuse GM
products. That is up to us - world opinion can direct the
future.
Greed is a good
thing. Greed fuels economies in the quest for technology, development and
wealth, without which progress would stagnate and return human life to the era
of sticks and stones, But ignorance, untempered greed and highly-advanced
science without ethical constraints are a dangerous combination that may
threaten all of our futures, if it continues to run
amok.
* UPDATE:
January 23, 2001
Not only has more
information about CJD deaths in the United States and Australia shown that
numerous cases have occurred, but the numbers are shocking.
Remember that the effects of this prion has many
different names, but misdiagnosis is very, very common. It's nearly impossible
to positively identify except through genetic tests or autopsy after death, and
the horror of dealing with victims of CJD leaves others in shock, having
themselves suffered through the tragedy of this cruel disease. So incorrect
diagnosis are usually not followed up with corrections. Regions are also not
anxious to advertise that someone has died of prion disease which requires
super-extraordinary measures to control contagion, striking terror in medical
professionals and hospitals who use incredible biological containment rooms to
handle anyone suspected of CJD. Meanwhile, governments irresponsibly babble
about no evidence of contagion while TSE sweeps through our planet. (See new
informational links at the end of this article.) After Britian, France,
Germany, Italy, and some thirty EU countries have already played the idiotic
game of TSE denial while prion spreads outward to the world, why are
politicians in other countries still unwilling to support justified measures to
identify and control this contagion before entire populations are exposed and
well on their way to a future of horror as the insidious prion inclubates into
CJD? The prion defies all political denials of its existence, and is firmly
establishing itself worldwide. Ignorance is this monster's friend.
There is evidence that TSE has not only claimed 80
lives in recent history, (recent history is the period of time from now back to
the last, major elections,) but has killed thousands of people since the
1950s. In the jungles of New Guinea, TSE is called kuru. Rituals of
death, abominable agricultural practices, organ transplants (including corneal
transplants), fertility hormone injections, innoculations made from bovine
products, reuse of surgical instruments, blind ignorance of the disease and its
incredibly, contagious nature, plus the long incubation period (two to fifty
years) and irresponsible politics have all ensured widespread prion
contamination throughout the world.
Regarding the
political aspect, enormous pressure applied by agricultural interests to
suppress evidence of contamination merely defeats any hope of containment,
while politicians can usually expect their terms to expire before TSE's long
incubation period ignites the truth of how far the disease has spread.
Meanwhile, TSE scientists and researchers have been snubbed for the evidence
they've obtained before their results are published, and politicians buckle to
special interests, even though ignorance promoted by the special interest
coverups may kill the politicians and "us" and "them" (who knows how many?) in
the future.
More confusion: "Sporadic CJD occurs at a rate of one
per million..." Responsible reporting tends toward conservative calculations of
issues like TSE, but more data has identified families in some areas with
inherited E200K or A117V prion mutations found in 10 family members out of 10
subjects. Human E200K mutation is a result of inbreeding within a limited
genetic population, and it causes physical weaknesses when the E200K mutation
is present, with nearly 100% lethal CJD within 50 years of life. Entire closed
populations can predominantly carry the mutation when close family
intermarriages are common. The rate at which either A117V or E200K point
mutations become clinical CJD can be predicted by laboratory results, where
concentrations of prion (from food sources) under low cell pH conditions
conspire to produce geometric translations from DNA normal helix cross-linked
structure to a beta-sheet oligomer structure (this can occur in milliseconds of
the occurrence of lysene>glutamate or alanine>valine mutations). With
proteins to feed looping within DNA structure near the mutation site, mutant
prion production becomes a runaway condition. While prion is associated with
cell membrane formation, mutant (contagious) prion prevents mammal DNA coding
for effective cell membranes, from mammal 90-231 inclusive of points 117
(within prion prior to a doppel gene) and 200 (also within prion-doppel) as
well as attaching directly to existing membranes and causing those membranes to
hemorrhage and dissolve where mutant prion attaches. It's not surprising that
mutant prion is capable of the observed spongiform destruction. Other DNA
prion-doppel sites exist. Research has concentrated on genetic effects of TSE
alteration of 90-231 coding due to the obvious effects of spongiform in
cellular tissue, but production of TSE prion may also involve DNA prion
mutations at any prion protein structure.
As it
attacks cells, contagious prion can break down healthy cell membranes, thereby
eliminating the cell's protective barrier and exposing DNA for mutation by the
contagious prion.
Several assay
techniques have now been developed to detect marker proteins for communicable
prion mutations. These range from poor (40%) to excellent with nearly 100%
effictivity. The assays are being used for blood analysis. Blood donations by
persons ever visiting, living or getting very close to Britian and other
European areas are now refused by American hospitals. All other blood donations
are tested with TSE marker assays now included with other batteries of
tests.
Inherited prion mutation is simply a race between
other attrition factors, or the prion's eventual contributions to alternate
body wasting effects, or CJD itself. Animal prion availability feeds mutant
prion production and contagious prion assures that both carriers of inherited
mutant prion and, eventually, persons with normal prion, will develop CJD with
faster incubation of clinical effects as prion concentration increases in the
blood.
Known mammalian
carriers of TSE now include mice, mink, cats, hamsters, sheep, pigs, cattle,
deer, elk and humans. It may be vital for us to set aside short-term political
objectives at this time and engage the maximum scientific resources at our
disposal to offset potential epidemics of TSE, which evidence suggests may
occur within the near future.
A number of additional links to world wide web TSE information
have been added to this document.
Update, January 26, 2001
A
British official has stated that Asia's TSE outbreaks are expected to begin
appearing within two to three years. (Minimum incubation time.) China, Taiwan,
Korea and other Asian countries have imported substantial amounts of suspect,
infected feed. It's also common practice in these countries to grind up dead
carcasses to recycle into feed for living animals.
Update, January 31, 2001
QUESTION: Scientists recognized "new variant" prion
effects in U.K. CJD victims since 1997. Why do you say it is not a new
variant?
ANSWER: As British CJD cases began to appear, medical
experts were surprised that incubation times seemed to be faster (two years)
than previous expectations of symptomatic CJD appearance after infectious
exposure (five to ten years). An alternative explanation is that expected mean
distribution of CJD will appear as a statistical curve peaking at the "normal"
incubation times, and that the current 87 European deaths are simply the early
responders at the very beginning of an epidemic. (We hope this is not the
case.) Genetically, no "variant" of the infectious prion has been identified,
although mutation sites within individuals (and probably individual cells) do
vary.
It should be noted that inherited prion mutations,
and how long it takes for symptoms to occur, depend on where mutations occur
within DNA. Some inherited mutations have prion disease manifestations that
appear up to fifty years later in life, with different names given to the
different presentations of these mutations.
In the presence of
infectious BSE prion, A117V mutation seems to be inevitable within humans.
Chaperone proteins which protect other DNA struture from mutation don't seem to
be able to control beta-sheet geometric mutation of normal prion when infective
prion is present.
QUESTION: Does the
amount of contaminated beef consumed matter?
ANSWER: In lab
tests, the percentage of mutated prion present in cells, as well as cell pH,
affected the rate of DNA damage. However, cell membrane barriers may introduce
a time-rate control for attacking prion to gain access to DNA structure. That
limitation may be responsible for TSE's long incubation periods.
In general, such populations grow exponentially
beginning with the initial population of pathogenic agents. With very small
initial populations, integration of the early part of population curves will
begin slowly with respect to time, yet inevitably toward symptomatic prion
populations without intervention by some sort of controlling mechanism. No
laboratory evidence out of many reams of research has provided any results
which might suggest that a single, infectious prion cannot begin the
destruction an entire animal or human being. But more exposure to BSE should
cause CJD to become symptomatic sooner.
QUESTION: How many
cattle have actually been positive for BSE in the U.K?
ANSWER: Testing for BSE has been based on inspection
of cattle brain tissue until recently, meaning that only cattle in the
symptomatic stages of mad cow disease were listed as "positive." Tests have
improved during the past months through laboratory development to look for
protein markers for infectious prion, vastly improving detection. To date, over
170,000 British cattle have been declared "positive" for
BSE.
One of the best, dedicated sites for TSE information is
http://www.mad-cow.org/, with
comprehensive coverage of this subject matter. BSE, originally identified in
the U.K. is also reported in frequent
BBC
stories. Wired News also reports
occasional, but excellent, stories on this subject. Search for "BSE."
Additional information may be found in the American Medical Association's Journal
publications and from the World Health
Organization's website.
MORE LINKS TO TSE INFORMATION
(WorldWide)
Alzheimer's Society - CDJ
Support Network
Australian
Support Network
Blood
Recall
BSE - CJD Home
Page
CJD
Foundation
CJD Support
Network
CJD
Voice
CJD U.K.
Department of Health
CJD
Harvard
CJD Foundation,
Inc.
UK Creutzfeldt-Jakob Disease
Surveillance Unit
Faces of
CJD
Australian CJD HomePage [This page pops opens multiple browser windows for
advertising. Since this violates our own policy, we've included this
notice. The site is informal but does have some interesting information. Click
here for the
link.]
We've located about 2,700 web links to CJD to date. The obvious
scope of this disease is becoming a staggering statistic of the 21st
century.
Update, March 5, 2001
Within two weeks
time, Hoof & Mouth Disease has appeared in Britian and spread to France,
Wales, Belgium, Northern Ireland, Denmark and Scotland. The wild outbreak of
Hoof & Mouth virus has already resulted in an additional 45,000 animals in
the U.K. and 50,000 animals in France being destroyed to contain outbreaks.
The agricultural death toll from TSE in Europe has
now reached 200,000 animals, with 94 human deaths from CJD.
The March 12th issue of Newsweek Magazine estimates
that "millions" of human cases may be incubating at this time. See Newsweek's
story, Cannibals to Cows: The
Path of a Deadly Disease.
Q: Besides food, what kinds of products may be
infected with TSE?
A:
Innoculations, hormone supplements, any vitamins & supplements produced
from animal tissues, herbs (or food) grown in organic fertilizer, food and
extracts grown on soil occupied within two years by infected animals, all food
sold for carnivorous pets including fish, soap made from animal fats (almost
all soap), facial and skin creams, protein enricheners for hair, lip balm,
shampoo, many cosmetics. Also, chicken, farm-raised fish and pets. It's
reasonable to expect that short-lived animals like chickens and fish can carry
prion disease from food enriched with animal proteins, even though they
probably will not exhibit symptoms during their lifespans. Infectious prion has
now been verified in cats.
Q: Is there
something we should do?
A: As far
as already-infected populations are concerned, fatal mutation occurs at the
molecular-genetic level. There's no hope of specific antigens that could
recognize such an insigificant difference in genetic structure between normal
and damaged cells, much less the prion fragment itself. But various chaparrone
proteins supervise and often correct genetic defects, although research has
indicated that the beta-sheet defect is not reversible, so far. Continued
research is important. Since the start of Y2001, a reliable (96%) lab test has
improved TSE detection. Success against TSE demands heros, like Professor
RIchard Lacey, who tried to warn the world of this danger years ago, and new
heros to carry on against TSE.
We must completely
halt the practice of feeding any agricultural livestock feedstocks containing
other mammalian proteins. It's not adequate to maintain this practice with
livestock that doesn't show symptoms and call that good enough. Any animal
meant to graze should only feed on grass, grain, corn, and other non-animal
feed, including domestic and wild herds of deer, elk and sheep. Animal residues
must not be scattered on the earth where plants can absorb and propagate prion
infection. |
|
|
