By Mark Purdey

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.

What's 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.


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 Collins. 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 Phillip'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 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.


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.