Myths
& Truths About Mad Cow Disease
by Mark Purdey
Reprinted
from the website of the The Weston A. Price Foundation
As an organic farmer,
Mark Purdey resisted the order to spray his cattle with organophosphates
for warble fly and went to court for a judicial review; he won
and was exempted from using the spray. No cows born in his herd
developed BSE (mad cow disease). He has contributed numerous articles
on the subject of BSE to scientific journals. He farms in Somerset,
UK. This article appeared in Wise Traditions in Food, Farming
and the Healing Arts, the quarterly magazine of the Weston A.
Price Foundation, Spring 2000.
As the first snowstorm
of winter hit the isolated hill where I farm, I pitched out the
last forkfuls of hay to my cattle before nightfall. Much like
the whirlwinds of snow surging all around me, my brain was turning
over and over the catalogue of injustices that successive governments
had levied onto the farming community over BSE. I felt paralyzed
and powerless in the encroaching snowstorm.
My confidence to carry
on was battered to pieces by the recent ban on beef-on-the-bone.
The announcement-based on the whims of a mere handful of government
"experts"-renders my hard graft over the last twenty
years in farming into pathetic insignificance.
But how can there
be any true "experts" from academia when the most basic
facets of the Bovine Spongiform Encephalitis (BSE) disease process
remain a total mystery? One would have thought that all of those
farmers and independent vets living and working in the front line
with BSE cattle would have been the first to be consulted. But
strangely, their observations have been completely ignored by
officialdom.
Cows frequently partake
in the bizarre habit of eating their colleagues' afterbirths after
calving, and I was particularly intrigued to watch my own home-reared,
BSE-free cows positively relishing the delicacies of afterbirth
tissues derived from a group of pedigree cows that I purchased
into my farm in 1989.
As the majority of
these imported cows went on to develop BSE, it is interesting
that BSE has not surfaced in my home-reared cows, despite their
overzealous exposure to the allegedly "infectious" blood
and lymph found in the afterbirths of the BSE cows. Other farmers
sharing the same experience report the same outcome.
Another anecdote hails
from the farming community of Shetland, where the island folk
are free of Creutzfeld-Jakob disease (the human form of BSE),
despite their ancient custom of eating "potted sheep's brain."
Interestingly, the equivalent of BSE in sheep, called scrapie,
has been rife in the sheep flock on Shetland for centuries.
The anecdotes are
ever flowing, and all point to a hypothesis based upon some environmental
causal factor that falls a long way short of the current government's
nightmare infectious "ingestion" scenario. If the spongiform
agent were as infectious as the authorities would have us believe,
why has chronic wasting disease (the BSE equivalent in deer) remained
uniquely confined to a small cluster zone in the Rocky Mountains
for thirty years now, without spreading across to the neighboring
deer herds roaming the rest of the Rockies? Why has no spongiform
developed in the various predators of those affected deer?
From the very beginning
of the crisis, the farming community has been the unfortunate
victim of the whole BSE campaign. Yet, ironically, the same presiding
authorities who are responsible for foisting off the burden of
BSE are, no doubt, totally oblivious to the fact that more farmers
have committed suicide as a result of official BSE blunderings
than people have died of new variant Creutzfeld-Jakob disease
(nvCJD).
A body of government
experts was quick to take exclusive control of BSE research, and
very rapidly the cause of the disease was attributed to the feeding
of scrapie-diseased sheep brains to cattle. In other words, scrapie
was said to jump from sheep to cattle by virtue of some sort of
infectious agent. And it naturally followed that this same assumption
of disease cause was extrapolated into the human CJD context-the
presumed "microorganism" had now jumped from cows into
humans. But this was no more than unproven hypothesis, and it
still remains that way today.
Not surprisingly,
only a handful of folk had insight into the unsavory world of
the meat and bone meal (MBM) rendering business. But for anyone
who had scratched the mere surface of the global distribution
of British MBM products, it became strikingly obvious that the
very mainstay of the official hypothesis was radically flawed.
For instance, during the 1980s thousands of tons of this very
same incriminated MBM were exported to cattle farms in BSE-free
countries such as the Middle East, Malta and South Africa.
Officials have always
brushed this challenge aside, arguing that the cattle in these
countries did not receive sufficiently large doses of scrapie
to contract BSE. But this contradicts their current official explanation
for the 30,000-plus cases of BSE that have developed in cattle
born after the 1988-ban on MBM, where government scientists conveniently
claim that leakage of micro amounts of MBM (destined for pig and
poultry feed) into the cattle rations, caused the 30,000 cases.
Furthermore, USA and
Scandinavian rendering systems duplicated exactly the same prerequisites
that were supposed to kick off BSE in Britain-scrapie affected
brains being milled into feed-yet their livestock remained BSE-free.
Nor were we told of
the numerous unsuccessful attempts by US scientists to induce
BSE in cattle that had been experimentally fed or injected with
massive amounts of scrapie brain material. Apparently, the cattle
either just "got fat" or went down with a sickness more
akin to motor neurons disease than BSE.
Despite millions of
dollars worth of scientific research failing to ascertain a link
between BSE and scrapie, the whole propaganda myth that BSE was
caused by scrapie became gospel in mainstream public mentality.
The media loved the
theory because they could drum up a viral holocaust-horror scoop.
The vegetarian and green lobbies found themselves landed with
a powerful propaganda weapon on their plate- turning cows into
cannibals. And the UK scientific establishment could go on drawing
generous grant funding for their viral witch-hunt without the
embarrassment of having to account for years of barking up the
wrong tree. And then the government could foist the blame of BSE
onto a naturally occurring agent for which no significant vested
interest or official body could be held accountable.
Whilst the maligned
renderers and feed merchants got the full brunt of blame for BSE,
it surprises me that neither was held accountable for the financial
damages of the crisis. Instead, they all received generous compensation
payments to the tune of millions.
Almost on a weekly
basis we are now finding ourselves listening to the same experts
regurgitating the same stereotype claims of how BSE has now jumped
from cattle into humans. On Channel 4 Dispatches (last December),
despite no reported cases of BSE in the British sheep flock, it
was assumed that sheep must be affected with BSE because they
had eaten meat and bone meal. We are now warned of the danger
of eating sheep.
Professor Blakemore
summed up the programme by saying that we should all eat chicken
and avoid beef and mutton. But as poultry received their fair
share of meat and bone meal as well, should we not be cutting
chicken out of our diet too, according the dictates of the official
theory?
These spokespeople
would do better to start questioning the entire foundation of
their hypothesis, rather than squeezing the last drop of "infected"
blood out of the sinking stone.
What is more, the
conventional consensus on BSE is ignoring that well-recognized
academic yardstick, Koch's postulates, which are employed for
assessing the cause of disease. The first postulate dictates that
a theory begins to carry weight once the hypothetical causal agent
can be identified in every victim of the disease in question.
The conventional hypothesis on scrapie/BSE/CJD certainly fails
to fulfill this basic postulate on several counts.
In this respect it
is particularly interesting that spongiform disease has been experimentally
induced in animals after receiving injections of brain tissue
derived from people who have died of Alzheimer's and Parkinson's
disease. Why is nobody freaking out about Alzheimer's disease?
In the case of BSE
where no viral cause has been identified, it is illogical to assume
that one animal has to eat another in order to catch the same
disease. Initially, the direction of any epidemiological research
program should follow elementary logic and investigate the most
likely assumption that the various different species of mammals
suffering from the same disease have all been exposed to the same
causal factor in the environment. But it seems that nobody has
investigated this route.
Sheep did not cannibalize
each other in order to catch scrapie, nor did wild deer in the
Rocky Mountains cannibalize each other in order to catch their
BSE-equivalent disease, chronic wasting disease.
The reductionist mindset
of government scientists is betrayed by the narrow scope of questions
that have been put to the relatives of the new variant Creutzfeld-Jakob
disease victims. The questionnaire is almost entirely focused
on the carnivorous perspective of the victims' diets, and therefore
tailored to suit their own hypothesis from the outset.
The Establishment's
assessment of nvCJD etiology seem to have completely ignored the
fact that adolescent CJD was recorded well before the 1980s. And
why do they move the goal posts every time a new challenge confronts
their theory-like extending nvCJD's incubation period to tally
with the long-term vegetarian victim from Kent? Take note that
they have completely ignored the case of the lifelong vegetarian
nvCJD victim from France.
The British government's
Spongiform Encephalitis Advisory Committee (SEAC), seems to have
thrown aside one of its most relevant long standing observations
on CJD epidemiological-people who are occupationally involved
with pets and farm animals are at greater risk of developing CJD.
And it is this observation that may well hold the key to the true
cause of these diseases.
During the 1980s and
early 1990s, cattle and cats (the species of animals that have
developed BSE) were exclusively treated with systemically acting
types of Organophosphate (OP) insecticide which were designed
to penetrate the entire physiological system of the animal, transforming
the bloodstream into a toxic medium so as to kill off any unwanted
parasites present.
In the context of
cattle, the use of these systemic OP's was subject to a compulsory
government order for the eradication of warble fly. The UK government
was unique in compelling a substantially higher biannual dose
of this OP by comparison with the few other countries around the
world that were following similar, less intensive measures to
control this fly. Interestingly, these other countries, including
Switzerland, France and Ireland, comprise the few other countries
that are suffering from very small epidemics of BSE in their home-reared
cows.
The National Farmers
Union, the Meat and Livestock Commission and The British Veterinary
Association formed a united front with MAFF (Ministry of Agriculture,
Fish and Forestry) to ensure that all farmers complied with the
law and treated their cattle.
Systemic OP's are
recognized as exerting their toxic effect by entering the central
nervous system and deforming the molecular shape of various nerve
proteins.
These chemically mutilated
mutant proteins are subsequently rendered incapable of performing
their proper function in the nerves.
The known toxic effects
of OP's lead me to wonder whether the use of systemic OP's on
British cattle have caused the malformation of another newly discovered
brain protein called prion protein-the phenomenon that US scientists
have proposed as the cause of spongiform encephalopathies.
Whilst some types
of spongiform disease have been attributed to genetically acquired
damage to the shape of the prion protein, the underlying cause
of protein damage in the BSE and new variant CJD strain of the
disease remains a mystery-amongst "open-minded" scientific
circle, at any rate.
OP's are known to
generate a highly reactive type of "free radical" in
the tissues that they intoxicate.
And it is this free
radical legacy of OP poisoning which is capable of instigating
a chain reaction of lethal attacks on nerve membranes and proteins
in the central nerves of susceptible individuals.
Once tissues become
'infected' with free radical chain reactions, the introduction
of freezing, heat or radioactive conditions to the affected cells
does not arrest such an 'infection.' In fact, irradiation, heating
and homogenizing of such tissue (brain tissue from spongiform
affected animals is homogenized before it is inoculated into healthy
animals in transmission trials) actually proliferates the free
radical phenomena. This suggests that these free radicals may
constitute the as yet unidentified "infectious" transmissible
agent of these diseases.
Concerned members
of the public helped me to fund a £14,000 experimental research
project at the Department of Neuroscience, Institute of Psychiatry
in London, where living tissue culture cells which express the
prion protein were exposed to low doses of the OP chemical; so
as to stimulate the context of a living cow undergoing OP treatment.
Significantly some of the recognized changes of the prion protein,
which appear in the early stages of spongiform disease, were induced
in these OP-treated cells.
Clearly, these results
go some way towards proving that OP's represent a primary or partial
cause of BSE. Yet it was this very same simple test that the government
had always assured me was too expensive for the taxpayer to fund
and, besides, impossible to set up anyway, even with the most
updated lab technology.
In December 1996 Lord
Lucas, MAFF's spokesman in the House of Lords, gave a written
answer stating that the government had asked the SEAC committee
to revisit the OP-BSE theory as a result of the recent research
findings conducted at the Institute of Psychiatry.
After being invited
to deliver my thesis to a SEAC meeting in April 1997, I was disturbed
that at no stage during the protracted enquiry that followed was
the experimental evidence of the Institute's work addressed-the
prime purpose behind this hearing. The committee dismissed the
evidence that I presented, which had been drawn from independent
peer-reviewed, published science literature.
I was not surprised
to learn that the outcome of this enquiry-the proceedings of which
were described as "confidential" to any enquiring journalist-was
a recommendation to government that any applications for funding
research into the OP-BSE theory should not be supported.
I still shutter each
time I visit our local farm stores and see the canisters of systemic
OP products up for sale. Although the warble fly is eradicated
and BSE is on the wane, farmers can still apply these chemicals
in a voluntary capacity for controlling lice and other pests.
I shudder further
when I see the bottles of OP head lice shampoo and OP systemics
for pets and gardens still in the shops for human use.
The real madness of
the mad cow fracas would seem to lie with the deadlock that has
kept these products on the open market for a full year since experimental
evidence first linked their use to the cause of BSE.
Perhaps the government
is so scared of compensation claims that it employs everything
at its disposal to prevent any degree of acceptance of the idea
that their compulsory warble fly programme caused the biggest
catastrophe in the history of British agriculture.
The brave new SEAC
committee appears to be totally preoccupied with effect"
rather than "cause." Such a back-to-front approach betrays
their sensitivity with anything to do with "cause."
But how can any government
programme seriously hope to eradicate BSE or nvCJD if it has failed
to eradicate, let alone recognize, the disease's true cause?
Commenting further,
Dr. Stephen Byrnes, discusses 2 other diseases, thought by most
to be in the same family:
"Kuru" was
a fabricated disease concocted to support the "Slow Virus"
theory of Carlton Gadjusek. Anthropologists who had studied the
same New Guinea tribes as Dr. Gadjusek openly contested his claims
of cannibalism and brain disease, as they had lived among these
tribes and witnessed no unusual disease called Kuru or any Cannibalism
(Science 1986; 232: 1497-1500).
Dr. Gadjusek ignored
all other possible causes for "Kuru" and could not isolate
any virus from the brain tissue of Kuru victims. These things
were fully discussed in "Inventing the AIDS Virus" by
Duesberg and Ellison (Regnery Publishing 1995), pp. 76-77.
Concerning Scrapie,
Potted sheep's brain is a national dish in Scotland, where scrapie
has existed for a long time. Isn't it odd that there have been
no human cases of scrapie ever reported in Scotland among people
who regularly eat sheep's brain?
Dr. Mercola's
Comment:
Thanks
to Dr. Byrnes for bringing this issue to my attention and also
for the comments. It would certainly come as no great surprise
to me if Mad Cow Disease (aka, BSE) really were caused by pesticide
use.
These are terrible
poisons that very likely cause much more harm than most people
realize. In addition, it would not surprise me if the prevailing
medical theory on BSE were totally wrong, as this certainly wouldn't
be the first
nor the last time that conventional medicine completely misses
the mark.
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