MAD COW DISEASE AND THE MAD AND USELESS GLOBAL SLAUGHTER OF ANIMALS

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MAD COW DISEASE AND THE MAD AND USELESS GLOBAL SLAUGHTER OF ANIMALS

By Red Flags Columnist, Mark Purdey

High Barn Farm, Elworthy, Taunton, TA43PX, UK.

Tel; 00 44 1984 656832.

MadCowPurdey@...

An 86-year-old English farmer, Pamela Ainslee, is

poised to challenge the legal right of UK Dept of

Agriculture (DEFRA) vets to slaughter her healthy

prize-winning Jersey bull, Cooden Hamlet.

Precariously perched along the cliff tops that

span the ancient Sussex section of the English

coastline, lies Mrs Ainslee's weather-beaten

farm. It is a spectacular patchwork of farmland

that represent one of the foremost ‘first

glimpses' of England experienced by many a

transatlantic passenger on descent into London.

Furthermore, her hard-worked fields lie defiantly

beneath one of the key spots where World War II

Spitfires prevented the Nazis from taking English soil.

But this elderly lady is no stranger to the front

line ­ she has stood up to a lifetime of

battering by the winds and rain that relentlessly

sweep across her cliff top farm. So, if DEFRA

vets try to enforce the slaughter, it looks as

though this famous front line fortification for

England could witness action once again.

In fact, Pamela Ainslee is threatening a

grandmother of a battle on behalf of British

livestock and her lifetime's work as a

traditional cattle breeder; a battle which she

will fight with the full intention of

annihilating recently introduced Euro-backed

legislation that dictates the slaughter of both

male and female progeny of any cattle who have tested positive for BSE.

Pamela Ainslee is the proud owner and breeder of

one of the most noted traditional, well bred

jersey milking herds that is alive in the UK

today. Her 100-strong pedigree ‘Cooden' herd has

never witnessed a single case of BSE, until one

of her prize 18-year- old cows ­ the mother of

Hamlet - was sadly sent for slaughter the other week.

The problem first emerged when DEFRA inspectors

carried out one of their routine post mortem

examinations on the brain of Mrs Ainslee's cull

cow, where they identified the tell tale ‘prion'

hallmarks of mad cow disease ­ a surprise for

Pamela Ainslee, since this cow had never shown

the slightest clinical hint of BSE during its lifetime on her farm.

Mrs Ainslee summoned my help as a TSE research

scientist / farmer last week; since she

understandably needed help to marshal the

scientific evidence to bring a case against DEFRA

to block the slaughter of her prize bull - scheduled for early next week.

But softly spoken Mrs Ainslee struggles for

breath, and speaks in a highly distressed tone

about this up and coming fracas; an event which

she describes as the most “ghastly” ordeal to

taint her farming career. Her words seemed to

resonate with the clarity of the coastal horizon

that pans out behind her cliff-top farm.

I would guess that it is Mrs Ainslee's down to

earth approach to life that has caused her to run

with my own thesis on the environmental origins

of BSE rather than run with that of the Ministry

of Agriculture's ideas. For in Britain, every

farmer could not help but know about such

‘secrets' as the 40,000 cows that still developed

BSE that were born after the 1988 ban on the ‘infected' feed.

I have always stated that the simultaneous

exposure of cattle to copper

deficiency (exacerbated by systemic organo

phosphate insecticide treatments) and rogue

metals is to blame, rather than the

‘hyperinfectious' proteinaceous scrapie agent

that had purportedly contaminated the feed.

Whats more, Mrs Ainslee's case of ‘silent' BSE is

particularly interesting in respect of my own

theory, in that her herd has been officially

monitored over the years for its well known

problems associated with chronic copper

deficiency, and yet the other TSE causal

prerequisite appears to be absent on her farm.

THE ‘SCIENCE' OF THE SLAUGHTER.

Despite mounting evidence in support of the

environmental theory from noted academic

institutions around the world - not to mention a

firm endorsement from the UK's BSE Inquiry

- DEFRA have continued to treat the cause of

the TSE group of diseases as though they stem

from an infectious proteinaceous agent. Their

mindset suggests that governments have plumped

for this assumption since they can conveniently

capitalise upon this theory (which exempts them

from any blame ) as a means of persuading the

public that there is a sound scientific basis for

launching a spree of officially sanctioned

genocides on the ‘natural genetics' of the UK livestock industry .

The most recent ‘final farcical solution' adopted

by the UK government involves the ‘National

Scrapie Plan'. Widely detested by the farming

community, this scheme plans to slaughter

thousands of healthy traditional sheep flocks for

the crime of carrying one or two individual sheep

that are blighted by prion protein phenotypes

that encode for susceptibility to scrapie

disease. But we must not forget that

susceptibility to scrapie is a far cry from the

actual development of full blown clinical scrapie.

Witness the fact that the scrapie susceptible

gene is rife amongst sheep flocks right across

Australia where no actual cases of clinical

scrapie occur. Yet whenever these sheep have been

exported to foreign regions that demonstrate the

classic TSE environmental prerequisites, then

clinical scrapie does indeed emerge in the

susceptible genotypes. Likewise susceptibility to

CJD is high amongst certain Slovak and

Greek-Italian populations, yet clinical cases of

CJD have only erupted in a tiny portion of the

regions where these susceptible genotypes reside.

The outbreaks often involve a single isolated

village or some other ‘hot spot' location where

the existence of the relevant eco-idiosyncratic trigger factors all coincide.

But what is the point in running such

unscientifically misguided slaughter

programmes? For the history of control measures

applied in TSE endemic areas such as Iceland and

Colorado have shown that the wholesale slaughter

programmes enacted to date have invariably

failed, and TSE simply re-emerges after the

re-introduction of fresh livestock. This provides

further evidence of an environmental cause.

But the blanket slaughter programmes achieve

little more than masking the superficial evidence

of TSE, since they are merely taking out those

susceptible populations that are at high risk of

developing TSE. Meanwhile, the causal

prerequisites remain well and truly cemented as

‘endemic' into the bedrock of the TSE cluster

environment. A good example of this is

illustrated by the Colorado Division of

Wildlife's failed attempts to annihilate

so-called “Chronic Wasting Disease” (CWD) when

they bulldozed the top six inches of soil from

their CWD endemic deer facility at Fort . CWD still returned.

Since it is the TSE susceptible genotypes that

are the first in line to clinically manifest this

type of environmentally induced disease, we

should be taking notice of the ‘early warnings'

that these bucolic barometers are providing for

us; not merely burning or burying entire

populations in mass graves, and then ignoring the root of the problem.

There are other issues at stake, such as the

woeful waste of animal life and public

expenditure involved in these mass executions.

Equally ridiculous is the fact that the British

public have already coughed up 25 million pounds

in taxes to fund the Lord 's BSE Inquiry ­

a two-year hearing which reached the decisive

conclusion that sheep scrapie had nothing

whatsoever to do with the cause of bovine BSE. So

why have the UK government chosen to blatantly

ignore this widely gathered piece of scientific

advice, and then autocratically launch themselves

off with a further few million of taxpayer's

funds to enact their latest slaughter strategy ­ the National Scrapie Plan.

Since the so called scientific basis for the UK

government's latest plan of action hinges on the

notion that scrapie was the cause of BSE, then

their current directive clearly represents the

total opposite of what they were told to do by the BSE Inquiry!

But this wholesale slaughter policy is not only

confined to England's ungreen and unpleasant

lands. Hyperinfectious hysteria has gone global.

Witness the traditional sheep and goat flocks ­

the lifeblood of our peasant cultures - that are

being taken out right across Europe. Cattle

populations are being reduced likewise, whilst

entire districts across North America are loosing

their indigenous deer and elk populations that

have evolved for centuries. Such unscientific

annihilations are being carried out under the

name of safeguarding human populations against this illusory ‘prion' agent.

Yet Icelandic and Sardinian sheep farmers have

traditionally feasted off their sheep as soon as

they show the early stages of scrapie ( this

involves the consumption of the brains and all )

because they know from experience that the poor

beast will rapidly waste away to skin and bone.

Yet these farmers have not demonstrated any

incidence of CJD as a result. This kind of

epidemiological data is strangely ignored.

Whilst I certainly would not recommend taking any

risks that might be involved in the consumption

of a TSE affected animal, and likewise feel that

slaughter and quick lime burial is the best means

of disposal of these diseased animals, I do draw

the line at the current malpractice of wholesale

slaughter of 100% clinically healthy herds and

flocks. This is a grave disservice to the best

interests of agriculture, the environment and the food supply.

Many of the sheep flocks that carry scrapie

susceptibility are as old as the hills that they

are pastured upon. These sheep have evolved over

the centuries to produce the most hardy strains

that are geared to survive the toughest of fell

side conditions ­ rough mountain pastures that

can be used for little else in agricultural

terms. So if you artificially intervene by

slaughtering out thousands of years of natural

evolution at one mass execution, what on earth do you have to replace them?

THE GM PRION PROTEIN ‘KNOCK OUT' COW.

The corporate solution to this corporately

engineered global ‘crisis' was probably

premeditated long before mad cow disease first

began. It seems that the North American

authorities are as severely infected with ‘Dolly

the Sheep' mentality as we are in Europe. For

example, recent developments suggest that the US

tax payer will be sharing the same fate as their British counterparts.

The brain child of the widely discredited ‘Dolly

the Sheep' project has already been summoned to

North America to develop the concept of a prion

protein ‘knock out' GM cow as the best means of

solving the ‘horrendous' health crisis that has

gripped the US continent since the single case of

BSE was discovered on a Washington State farm

last Christmas. The idea is to genetically

manipulate the prion protein out of the domestic

cow in order to guarantee 100% freedom from BSE.

But we have obviously failed to learn from the

experiences of those corporations who have been

‘peddling' GM arable crop seed onto the already

hard-pressed farming communities across the

developed / undeveloped worlds. In the long term,

farmers have been unable to afford the premium

price required to purchase any GM seed be able to

make any profit at the end of the season. Such a

precedent hardly bodes well for the exorbitant

prices that will be commanded in the sale of GM

manipulated cows. With such an excessively hefty

capital outlay on livestock purchase at the

outset, farmers would simply not be able to

continue farming economically. Much like the

consumer lobbies, farmers do not want GM anyway.

So why is it being forced into the marketplace in this way?

The scandalous cruelty involved in unleashing

such a self-centred and vulgar industrial

procedure upon the animal kingdom goes without

saying. But we must also consider the fact that

the ‘knock out' of the prion protein is an

extremely ignorant and unscientific approach for

these GM Institutes to be taking. For the prion

protein naturally performs an essential metabolic

function in the mammalian biosystem; otherwise

the protein would have never evolved.

In this respect, I have always considered that

the prion protein's copper component performs a

contributory role in the conduction of the

electrical signals that mediate the circadian

daylight / darkness rhythm throughout the

biological system. Witness the misfortunate prion

protein ‘knock out' lab mice whose sleep rhythms,

breeding cycles and stress responses were

seriously disturbed. So naturally, if you remove

the prion protein from the cow, you will be left

with a severely dysfunctional animal that will

have a short lifespan and therefore be of no economic use to the farmer.

Furthermore, it is totally unproven that the

malformed prion performs the sole role - let

alone any role - in the pathogenesis of TSEs.

More recent research has shown that a dysfunction

of the proteoglycan molecules are equally, if not

more, important in the cause of TSE than the

prion protein itself. It may even turn out that

the malformed version of the prion (heralded as

the infectious agent in TSEs ) represents little

more than a secondary ‘tombstone' pathological

feature that is purely the resultant legacy of a primary toxic cause.

Furthermore, the idea of the proteinaceous prion

particle as the cause of TSE does not fulfil all

four of Koch's postulates ­ the yardstick for

gauging whether a particular disease stems from

exposure to a specific infectious agent or not.

For instance, 15% to 25% of cows that have been

slaughtered for displaying clinical BSE each

month under the UK's BSE order, have failed to

demonstrate the presence of malformed prions in

their brains at post mortem. This clearly

contravenes one of the Koch's postulates which

decrees that the causal agent needs to be

identified in every victim of the disease. The

fact that these prion negative cows share the

same clinical and spatial-temporal

epidemiological profile as the prion positive

cows suggests that both prion positive and

negative cows are part and parcel of the same

disorder. The UK government, however, tries to

argue that prion positive and prion negative

cases represent two totally separate diseases

and its put down to a mere coincidence that they both surfaced simultaneously.

My theory decrees that the copper depleted prion

protein merely acts as a vehicle for conveying

the rogue toxic metal agent that has successfully

substituted itself at its vacant copper bonds.

The pollutant metals that I have identified at

high level in the TSE cluster ecosystems - such

as manganese, barium , silver and strontium -

will seed the crystallisation process by acting

as crystal nuclei. The crystals propagate

themselves after combining with sulphates,

silicates, etc, and the prion / ferritin proteins

to form the characteristic ‘fibril' aggregates

that represent the characteristic hallmark of the TSE diseased brain.

The resulting crystals are piezoelectric, and

generate electric signals and magnetic fields

each time they are bombarded by incoming pressure

waves of sound from the external environment.

It's a bit like having a million microphone

crystals lodged in your brain without any loud

speaker systems to dissipate the transduced energy.

In this respect, it is the rogue metal crystal

that represents the ‘infectious' transmissible

agent in TSEs; a ‘seeding' agent that remains

stable even after heating up to temperatures as

high as 1000 degrees, and can be transmitted

whenever TSE affected brain or blood material is

injected into a misfortunate healthy lab animal

(or via blood transfusions into humans, etc).

These piezoelectric crystals lodge within the

fresh host, where they, in turn, start to

multireplicate all over again, subsequently

converting incoming acoustic radiations into

electrical signals and magnetic fields which

initiate free radical chain reactions and

spongiform mediated neurodegeneration.

ANIMAL PHARMACIDE.

Meanwhile back at Cooden farm, the ever so

English Mrs Ainslee is a dogged and determined

elderly lady. She shares the unanimous feelings

of her colleague livestock farmers across the UK,

if not across the entire world, that government

policies of livestock slaughter have gone several

steps too far. She says “enough is enough”, and

is rightly furious with the fascist-like diktats

of the UK government veterinary service ­ not to

mention her anger at those at the forefront of

the brave new world of genetic order. For they

have every intention of annihilating the fruits

of her life's work with a single shot.

Mrs Ainslee intends to challenge the legality of

DEFRA's powers to slaughter her bull, and will

demand that government vets produce the evidence

which demonstrates that her bull poses a real risk to public or animal health.

The official view surrounding the illusory threat

of infection with ‘prions' is based upon various

theoretical routes of exposure to the prion

agent; involving transmission via the

consumption of BSE tainted meat / blood / milk,

as well as transmission into the next generation

via placental transport. Even if the ‘protein

only' prion agent had been proved to be

infectious in this way ­ which it never has ­

then one could argue that the only conceivable

threat posed by ‘BSE transmission' is exclusively

related to the female and not the male of the species.

In this respect, the health risks posed by Mrs

Ainslee's bull, - even if it were affected with

BSE - are nonexistent. For bulls do not give

birth to calves, give milk or blood, or even need

to be consumed at the end of their lifespan.

Since body to body contact has long been

discounted as a mode of transmitting BSE, the

only possible way in which a BSE affected bull

could transmit BSE is through its genetic

material. And since this counters the official

theory anyway, plus the fact that there is no

evidence to suggest that BSE can be transmitted

to succeeding generations via a mutation in the

genes, then the UK's vet department will be

forced to brace themselves for one hell of a

cattle battle and challenge to their legal instrument.

Although the authorities will no doubt succeed in

obfuscating this seemingly insignificant ‘little'

event down on Pamela Ainslee's farm into

oblivion, it seems unfair that the responsibility

for such a broad ranging globalized

battlefield - involving the corporate take over

of genetics, the entire foodchain, etc, - has

been left up to the dogged determination and

kitchen-sink tactics of one single, very English, elderly lady.