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Animal Pharm
by Mark Purdey
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 far
ming 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 though
t 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 officaldom
.
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 afterb
irth 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.” Interesting
ly, 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 spongifor
m 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 no
w, 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 BS
E 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 “microorgani
sm” 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 far
ms 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 l
eakage 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-f
ree.
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 ju
st “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 cou
ld 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 compens
ation 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), desp
ite 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, acc
ording 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 particular
ly 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 progra
mme 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 environmen
t. 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-equivale
nt 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 pe
ts 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 penetra
te 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 epi
demics 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 th
e 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 mu
tant 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 scien
tists 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 prote
in 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 attack
s 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 h
omogenizing 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 pro
tein 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 p
rime 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 support
ed.
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 th
e 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?


End<{{
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The only real voyage of discovery consists not in seeking
new landscapes but in having new eyes. -Marcel Proust
~~~~~~~~~~~~~~~~~~~~
The libertarian therefore considers one of his prime educational
tasks is to spread the demystification and desanctification of the
State among its hapless subjects.  His task is to demonstrate
repeatedly and in depth that not only the emperor but even the
"democratic" State has no clothes; that all governments subsist
by exploitive rule over the public; and that such rule is the reverse
of objective necessity.  He strives to show that the existence of
taxation and the State necessarily sets up a class division between
the exploiting rulers and the exploited ruled.  He seeks to show that
the task of the court intellectuals who have always supported the State
has ever been to weave mystification in order to induce the public to
accept State rule and that these intellectuals obtain, in return, a
share in the power and pelf extracted by the rulers from their deluded
subjects.
[[For a New Liberty:  The Libertarian Manifesto, Murray N. Rothbard,
Fox & Wilkes, 1973, 1978, p. 25]]

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