A Different Take on Mad Cow Disease

[Guest guest]

It is time to dispel the erroneous information about Mad Cow Disease which

has people feeling helpless and in a panic without there being adequate scrutiny

of the official explanantion of the cause of " Mad Cow " . The actual remedy may

well be to challenge the use of organophosphate chemicals which are

profoundly damaging to the neurons of all mammals. When coupled with other

nutritional

deficiencies (mineral) and atmospheric conditions... a new explanation

deserves our consideration.

 

ANIMAL PHARM

 

by Mark Purdey

 

> 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.

Mark Purdey

Somerset, UK

Fall, 2000

 

 

 

[Guest guest]

---

Hi,

it's pointless to argue that organo-phosphates are not dangerous to

anyones health they are and it has been a proven medical fact for a

long, long time

the part that most people miss is that usually there is also some

type of bacterium/virus that also plays a part in the mechanics of

disease causation in that these compounds mutate the bacterium/virus

thus making the pathogen even more virulent/transmissable, we hear

all the time in mainstream media that such and such disease has

mutated and is now even more virulent/transmissable, but to blame it

totally on organo-phosphates/ minerals would leave known/proven anti-

toxicity remedies on the table which simply do not work in the case

of TSE's although it would be worth testing and we definitely would

have nothing to lose by it

each organo-phosphate has an MSDS which lists the symtomology of

overdose and some symtoms do resemble other diseases but

unfortunately these overdose symtoms have as of yet not been proven

to be transmissable unless accompanied by a pathogen

karl

 

 

In , celeis1@a... wrote:

>

>

> It is time to dispel the erroneous information about Mad Cow

Disease which

> has people feeling helpless and in a panic without there being

adequate scrutiny

> of the official explanantion of the cause of " Mad Cow " . The actual

remedy may

> well be to challenge the use of organophosphate chemicals which

are

> profoundly damaging to the neurons of all mammals. When coupled

with other nutritional

> deficiencies (mineral) and atmospheric conditions... a new

explanation

> deserves our consideration.

>

 

> ANIMAL PHARM

>