Mad Cow: long article- "food for thought"

About Mad Cow Disease (The Crisis That Never Was - Part 1 by Mark
Purdey)
westonaprice.org ^ | Fall, 2000 | Mark Purdey


Posted on 12/26/2003 1:56:15 PM PST by Pubbie


Note: 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
paralysed 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 is 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 was 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 pounds 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 were 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 is 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 fulfil
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 programme 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 epidemiology—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 circles, 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 tax payer 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 shudder 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?

Mad Cow Update Those in charge of public health policy in the US do
not really understand what I am demonstrating about bovine spongiform
encephalopathy (BSA) and Creutzfeld-Jakob Disease (CJD). They get the
main linchpin of the work wrong by stating “manganese deficiency”
instead of “manganese excess.” Then they seem to marginalize my
position in the BSE debate by falsely suggesting that I am at odds
with Stanley Prisiner’s prion concept that has now been accepted as
mainstream.

Ironically, both my own studies and those of Dr. David Brown largely
open up the final door of evidence in support of Prisiner’s concept.
We have shown what causes the prion protein to transform into its
protease-resistant form (the disease-associated form). Prisiner first
identified the abnormal prion as the hallmark of the BSE-diseased
brain and he hypothesized that his abnormal protein somehow caused the
disease. Where I do differ from the Prisiner brigade is only in one
point—I don’t believe that the “prion” is highly infectious as they
are suggesting; that is, I don’t believe that it can infect those who
eat prion-contaminated meat. I believe that it is the manganese 3+
attached to the prion that is the infectious agent and only when it is
transmitted by injection, etc., into susceptible genotypes. Prisiner
himself is skeptical of “the-BSE-feed-caused-new-variant-CJD”
hypotheses. He was the only person (apart from myself) who suggested
this to the BSE inquiry!

I just hope that the beef industry in America realizes that we’re not
as “way out” as has been suggested. The industry is shooting itself in
the foot by rejecting the link to toxic mineral excess and
organophosphate pesticides. We have accumulated so much hard evidence
now—more than all other theories.

I have been to Calabria in Southern Italy looking at the case of 20
CJD victims in a hamlet of 150 population since 1995. Intriguing
stuff! But I was warned that the Mafia controls the property market
and meat market in this part of Italy and would be hostile to me. So I
was unable to get soil samples at that time.

Things are so desperate in farming in Europe at present. We are so
concerned by the totalitarian, global control that is molding the
direction of agriculture into complete ecological and economic crisis.
The “arable aid payments scheme” has caused acres of former livestock
grassland to be ploughed up. The global warming flash flood storms
have caused an unprecedented degree of soil erosion, with its
attendant self-perpetuating drain on human reserves.