Mark Purdey - The BSE Theory


Radioactive metals, Sonic shock bursts and the Ferrimagneto-Prion theory on the origins of TSEs. by Mark Purdey  - August 2003

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The White Sands Missile Range is an extensive spread of US military controlled cacti country that perimeter fence. One of the wildlife officers gets out and walks to security, seemingly oblivious to the distant thump of a missile exploding across the range. He is clearly preoccupied with the more important task of slaughtering animals who have succumbed to this so called "hyper-infectious" disease. The truck is soon on its way, loosing itself within the thousands of acres of parched up military compound.

They've come to investigate yet another new eruption of chronic wasting disease (CWD) in the USA -- the deer equivalent of 'mad cow disease'. This outbreak is particularly significant, in that it represents the first cases of a transmissible spongiform encephalopathy (TSE) disease recorded in a deer herd within the state of New Mexico. Furthermore, the affected herd has been confined within the perimeters of this missile range for several decades.

This latest epidemiological aberration delivers a serious challenge to the viability of the conventional consensus on the origins of CWD. It has rumbled the cornerstones of institutionalised 'expertise', bringing into question those veterinarians who have plumped for the assumption that some unconventional "hyper-infectious" agent is spreading via body to body contact through the deer populations.

So how did the 'infectious agent' jump the 500 mile gap between the long standing CWD hotspot zone in Colorado and the CWD-free deer residing within the White Sands Missile Range? The 'experts' were baffled. But, true to form, this latest challenge to the official theory was conveniently obfuscated into oblivion; outcast as some illusory mirage that just happened one day in the New Mexico desert.

But the answer is only evident to those who care to scratch a bit deeper than the dust. For they cannot help but notice some overt environmental features that exclusively predominate this unique location. A package of factors which are invariably shared by every single TSE cluster location around the world;

Before the military came, White Sands was an industrial centre for the mining of wulfenite ores (NB; wulfenite contains the copper chelating molybdenum metal). And since the military have occupied the range, there has been the ongoing issue of the accumulation of rogue radioactive metals -- the chilly legacy of detonating so many various munitions. Furthermore, White Sands has become a leading world centre for monitoring infrasonic shock bursts from around the globe - not least for monitoring the unique intensity of bursts that are radiated by the explosions of their own missiles. The poor deer herd has played guinea pig to an unwitting experiment that has cracked the causal riddle of spongiform disease.

"The atomic fawns"

But a series of well planned experiments had been designed and carried out back in the 1960s/70s, where the US atomic energy agency and government had funded the Colorado department of wildlife and Colorado State University's (CSU) Department of radiology and radiation biology at Fort Collins to monitor the exposure of deer to plutonium, strontium 90 and cesium 134 at every level. I recently stumbled upon these sinister studies whilst browsing through the vaults of PHD theses stored in the basement of the CSU library.

One of the trials involved transporting deer fawns back and forth between the deer pens at the Department's Foothills facility at Fort Collins and the plutonium contaminated pastures of the Rocky Flats Nuclear Weapons Factory at Boulder 60 kilometres away. The objective was to monitor the effects and eco-dynamics of leaked plutonium (and its daughter radio-nuclides) through the bio-system of the deer and within the general ecosystem.

A series of radioactive leaks from rusting barrels that stored plutonium contaminated oil at the Rocky Flats Plant (combined with a fire) had enabled plutonium and its daughter radio-nuclides to become airborne, contaminating a wide area of the Colorado section of the Front Range -- an area that has become the CWD endemic area today. The peak of contamination was during the 1967-1969 seasons when the air sampler detected Plu as high as .35 pCi/M3. A program of environmental monitoring had picked up significant levels of plutonium as far afield as the Pawnee Butt plains NE of Fort Collins and Roxy Ann mountain. Disturbingly, the levels of plutonium were higher in the livers of the wild deer that roamed the Cache le Poudre canyon at .042 dpm/gm than in the deer that roamed near to Rocky Flats itself (.033 dpm/gm).

This whole problem was probably exacerbated by the emissions from the kiln chimneys of the local cement factory at Lyons; where, according to a 16/12/92 report in the South West Sage by John Dougherty, the EPA's Division of solid waste made an emergency response on cement kiln dust, stating that they had found radioactive plutonium and cesium in the kiln dust at Lyons, and at two other plants near to weapon's factories in the USA. The Lyon's contamination was presumed to be the result of utilising low level nuclear waste material from the nearby Rocky Flats Weapons plant as fuel for the cement kiln.

During the 1960s/70s, it seems that the entire operation of the Fort Collins wildlife facility was geared towards a raft of radiation experiments - including the direct injection of strontium 90 and cesium 134 into the deer - in order to monitor the biological effects of these potentially lethal 'cold war' compounds.

But it seems that one of the major biological repercussions of these unique experiments was neither reported nor published until 13 years later, when a 1980 paper by Williams and Young reported on the first ever recorded case of TSE in a deer (eg CWD) in 1967. The delay before publication is mysterious, since most scientists would normally be tripping over themselves to get important novel discoveries into the academic press. Whilst the authors made no mention of possible causal factors, they merely stated that the TSE affected deer were resident at the Fort Collins facility -- eg; in the very same deer pens that had been involved in these radioactive experiments. Putting two and two together, it is unlikely that the space/time correlation between these unique radioactive experiments and the emergence of a novel neuro-degenerative disease is a mere coincidence.

The subsequent emergence of CWD in the various other wildlife facilities within the plutonium contaminated region, was probably assisted by the fact that there was frequent importation of wild deer into these other captive facilities from Fort Collins. It is also well known that deer frequently escaped from these facilities into the wild.

And then I stumbled upon a study by Dr Randolph Crom on a CJD cluster amongst the workforce of a factory engaged in the assembly of missiles -- who had no doubt had been working with some of these same radioactive metals -- at the former Hughes Missile Plant at Tucson in Arizona. In this respect, It is also relevant that CWD has erupted in deer grazing across the White Sands desert scapes of New Mexico, the tundra terrain of NATO's Cold Lake air weapons range and the sand hills of Camp Wainwright on the Alberta and Saskatchewan, borders -- areas where similar types of missile and munitions are test fired.

In fact, exposure to both naturally occurring and man made radioactive metals seems to explain the emergence of every cluster of TSE that has reared its ugly head around the world -- like the tiny Aspromonte mountain village in Calabria that was abruptly evacuated for no 'apparent' reason during the 1980s. Since 1995, twenty five cases of CJD have subsequently erupted amongst the former inhabitants of this village. When I trekked up that rocky road to their former village, I got to hear of an illegal dumping of radioactive waste on the mountain slopes immediately above the old houses. I instantly knew that I had a feasible explanation for this CJD outbreak.

Back to the Beginnings of the BSE debacle.

Since 1986, the infamous novel neuro-degenerative syndrome , BSE and vCJD , has insidiously blighted the heartbeat of British rural life. The disease has annihilated thousands of cattle and a growing number of young people, as well as creating a fierce battleground between nations, vested interests, political parties, farmers, victim support groups and consumers. More recently, the shock waves of the BSE debacle have ricocheted around the entire world, reaching as far afield as Japan and North America.

Yet despite the severity of the mad cow legacy, little genuine attempt has been made to crack the causal riddle of these diseases; thereby leaving us devoid of insight into measures that would best cure, control and better still, prevent this disease.

But hard scientific evidence is being amassed which indicates that vCJD and BSE could both result from separate exposure of bovines and humans to the same package of toxic environmental factors -- ferrimagnetic metals and low frequency sonic shock - and not from the ingestion of the one species by the other. If such a polemic hypothesis continues to accumulate momentum, a radical upheaval of the status quo mindset can be expected.

As a working livestock farmer and TSE researcher with first hand experience of BSE erupting in cattle that had been purchased into my organic farm, I was struck by the fact that no cases of BSE had ever emerged in cows that had been born and raised on fully converted organic farms, despite those cattle having been permitted access to the feed that contained the incriminated meat and bone meal (MBM) ingredient - as part of their 20% conventional feeding stuff allowance decreed in the organic standards at that time.

In this respect, I developed a 'hunch' that the total absence of BSE in organic cattle could be explained by the resistance of organic livestock farmers to comply with the UK government's compulsory warble eradication programme using systemic organo dithio-phosphorus (OP) insecticides - toxic chemicals derived from the OP military nerve agents.

In 1982 measures were passed that enforced twice annual application of a uniquely concentrated dose (20 mg/kg bodyweight) of a systemic acting organo-dithio-phosphate insecticide for the control of warbles on UK cattle. Amongst a myriad of toxicological effects, the systemic types of dithio-phosphate can chelate copper and open up the blood brain barrier; thereby disturbing the overall crucial balance of metals in the brain. I therefore considered that the copper depleting capacity of these OP insecticides had something to do with the origins of BSE, and had therefore been unsurprised to witness BSE rearing its ugly head in the UK cattle herd in 1986; which, in my opinion, was partly a direct legacy of the UK government's compulsory 'high dose' warble fly campaign. The few other European countries who instigated warble fly campaigns (eg; France, Switzerland, Ireland, etc) used lower doses of insecticide, and, not surprisingly, developed proportionately fewer cases of BSE as a result.

From then on, I became deeply sceptical of the conventional consensus on the origins of BSE and its human equivalent vCJD. There were just too many radical flaws blighting the hypothesis that bovine ingestion of micro doses of scrapie contaminated MBM led to BSE. Equally flawed was the follow up theory that human ingestion of BSE contaminated beef caused vCJD.

The hyper-infectious hypothesis was based upon a single strand of evidence - that TSEs could be transmitted via injections of TSE diseased brain tissues into misfortunate laboratory animals. Yet, various other diseases , such as familial alzheimer's disease, thyroiditis, some cancers and toxic metal encephalopathies have been transmitted in this way. So why aren't the health authorities freaking out about the supposed 'hyperinfectious' capacities of these other diseases ?

The Flaws in the Conventional Hypothesis ;

1. Thousands of tons of the BSE incriminated meat and bone meal (MBM) feed were exported as cattle feed during the 1970s/1980s/1990s to countries that have remained BSE-free to date. - eg, South Africa, Sweden, Eastern Europe, Middle East, India, Third World, etc.

2. Relaxation in the temperature/manufacturing techniques of the MBM rendering process in the UK were blamed for permitting the survival of the scrapie agent in the sheep brain material; thereby enabling the "agent" to jump across into cattle, producing BSE. But none of these alterations were exclusive to the UK rendering plants. For instance, other scrapie endemic countries such as USA and Scandinavia had adopted the same continuous flow system of rendering five years before the UK, yet these countries have remained BSE-free. Furthermore, the pathogenic, 'infectious' capacity of the scrapie agent remains active after heating to temperatures up to 700 degrees -- way above the 150 degree temperatures employed in the supposedly 'safe' rendering processes operating in pre BSE days.

3. Several live animal trials in the USA failed to induce BSE in cattle after feeding/injecting them with massive doses of scrapie contaminated brain tissue. Furthermore, no cases of BSE have developed in the feeding studies involving 1000 cows that were experimentally challenged with high doses of MBM feed/innoculant on a Dept of Agriculture farm at High Mowbray in Yorkshire, UK.

4. Forty thousand plus cows that were born after the UK's 1988 ban on MBM incorporation into cattle feed have still developed BSE.

5. Several countries such as Ireland, Portugal and France have witnessed a greater number of BSE cases in cows born after their respective bans on MBM than in cows born before their bans.

6. There have been no cases of BSE in other TSE-susceptible ruminants in the UK, such as goats and sheep, despite the customary inclusion of the same BSE-incriminated MBM protein source in their feeds.

7. Four of the original five kudu antelope that developed BSE at the London zoo had not had any possible access to MBM containing feeds.

8. The UK government's former experimental farm at Liscombe on Exmoor was designed to raise suckler beef cattle on a pure grass/silage system - without resort to feeding any MBM containing concentrated feeds at all. Yet BSE struck down four animals on this holding.

9. It is customary for Icelandic sheep farmers to slaughter and eat their scrapie affected sheep (brains included) immediately the first symptoms of this rapid wasting disease are recognised. Yet, no cases of CJD have ever been recorded in Icelandic sheep farmers, and only two cases in the Icelandic population at large.

10. The infamous mechanically retrieved meat products/baby foods blamed for causing vCJD in the UK were exported all over the world to countries where vCJD has not erupted to date.

11. BSE fails to fulfil 'Koch's postulates' - the yardstick for gauging whether a given disease (eg BSE) stems from infectious origins (eg the scrapie agent).

Hyper-infectious Hysteria takes a hold.

Despite the myriad of epidemiological flaws and millions of pounds worth of research failing to ascertain any association between the origin of these diseases and the scrapie agent, the whole propaganda myth that BSE was caused by scrapie became impregnated as 'gospel' into mainstream public/professional mentality.

But It is easy to see how the momentum of such a reductionist mindset took a hold; The media loved the theory because they could drum up a viral holocaust-horror scoop. The farming industry could get their beef sales back on the road by deluding consumers that the causal agent had been eliminated. The vegetarian lobby found themselves landed with a powerful propaganda weapon on their plate, whilst the scientific institutions could carry on drawing generous funding for their hyper-infectious witch hunt without the embarrassment of having to account for years of barking up the wrong tree. And the government could conveniently offload the blame onto the vagaries of some naturally occurring 'nasty' for which no vested interest or official directive could ever be held accountable.

Governments of the BSE affected countries rapidly found themselves cornered into providing 'quick fix ' remedies to appease the mounting intensity of political and economic pressures levied on them by their BSE-free neighbours.

Sound scientific reasoning has been forced to give way to the panic response ; where wholesale slaughter regimes are enacted across the TSE affected regions, despite well documented historical evidence that these measures have repeatedly failed to eradicate TSEs in the long standing scrapie and CWD hotspot regions across Iceland and Colorado--at great expense to the taxpayer, the farmer and animal life.

Cluster Buster.

As a TSE field scientist, my observations and research findings led me to question the scientific validity of the conventional consensus on the origins of TSE. I felt convinced that some key package of environmental factors, such as the copper chelating OP warble fly insecticides or molybdenum, played a primary role in the cause of TSEs, and so I embarked on a global investigation in search of the etiological needles in the causal haystack.

I carried out a total environmental analyses of the soil, water and foodchains in various ecosystems of Japan, Slovakia, Italy, Sardinia, Sicily, Iceland, Colorado, Wisconsin, etc, where long term clusters of TSE have emerged in mammalian populations who are largely self sufficient upon the local food chain. I also sampled the adjoining TSE-free areas as controls.

My results indicated that high levels of specific metals such as manganese, strontium, uranium, barium, in combination with deficiencies of copper, constituted an abnormal mineral imbalance that was common to every TSE cluster region that I had analysed. The levels returned to normal in TSE-free adjoining areas.

I also identified the co-presence of high intensities of low frequency sonic shock bursts in all of these TSE cluster environments, which stemmed from a variety of prominent sources; such as low flying military or concorde jets, quarry and military/gun explosions, volcanic/earthquake tectonic rift lines, thunder and electric storms, etc.

I compiled and published a hypothesis which proposed that this abnormal mineral imbalance compromised the ability of the brain to protect itself against the neuro-toxic effects of incoming sonic shocks from the external environment.

Copper prion proteins as the 'conductors' and Manganese/strontium prion proteins as the 'blockers' of electromagnetic energy flow.

Whilst endorsing the well established view that a malformed version of a native brain protein, known as the prion protein, plays a pivotal role in the pathogenesis of TSEs, I was unable to subscribe to the more 'way out' facet of this theory, that the proteinaceous particle of the prion acted as the hyper-infectious TSE agent.

Given the mystery surrounding the healthy function of this elusive protein, I became interested in the work of Dr David Brown who had had to move mountains of "prions and prejudice" in order to get the world to listen to the fact that the normal prion protein had been shown to bond onto copper in the healthy brain and that this copper-bonding property of the prion protein had something to do with its function. Around this time, other scientists had shown that the healthy prion protein performs a role in the mediation of the circadian rhythm .

I proposed that the copper component of the normal healthy prion protein plays a role in the conduction of electromagnetic energy along the circadian/auditory pathways of magnetic super-exchange. In this respect, Electromagnetic energy is picked up from the melanin reception/transducer stations in the retina, skin and cochlear, whence the energy is conducted via a linear chain of paramagnetic copper atoms (bonded to prion and other proteins) that provides a 'metal to metal to metal' motorway for distributing the electromagnetic energy of light and sound around the tissues for activating the calcium channels, which, in turn, mediates the circadian regulation of sleep, sex, behaviour, heart beat, cell growth/ repair and immune response -- locations where the prion protein is intensively expressed.

So once the crucial supply of copper is curtailed in the brain, due to straight forward environmental copper deficiency or exposure to copper chelating OP insecticides, molybdenum etc, the prion protein's metal bonds become vacant, rendering the protein vulnerable to bonding up with certain alternative replacement metals, such as manganese, uranium or strontium; eg specific metals which have binding affinity for the vacant copper domains on prion protein under certain physiological conditions. Once these metals begin to overload the bio-system, it is interesting that they are scavenged by the ferritin protein -- a metal storage protein that represents one of the key proteins (along with the misfolded prion protein) comprised in the proteinaceous 'cocktail stick' aggregations (the so called 'prion rods') which hallmark the brain tissues of all TSE diseased mammals.

It should also be considered that excesses of rogue metals such as manganese, strontium or barium in the bio-system, will readily conjugate with free sulphur atoms before the resulting sulphate compounds are capable of 'chelating' copper in their own right. But the subsequent starvation of free sulphur within the bio-system can also cause metabolic upheaval, in that it can deprive the army of endogenous heparin (glyco-aminoglycans - GAGs) molecules of their sulphur co partners -- a disruption that could account for one of the key pathogenic mechanisms in the pathogenesis of TSEs, since many studies have shown that endogenous GAGs need to be sulphated before they can perform their crucial role in protecting cellular prion protein from aggregating into its crystalline, 'prion rod' tombstone structure in the TSE diseased brain. Perhaps this is why therapy with the sulphated heparin molecules is exerting such a positive, life prolonging effect in animals/ humans that are suffering from TSE.

But these foreign substitute metals that are attached to these proteins in place of copper may not be acting in the overall best interests of the organism, particularly if the invasive metal is in 'ferrimagnetic' and/ or in 'radioactive' form. In this respect, the malformed prion protein becomes much like a trojan horse that trucks around the circadian circuits of the brain carrying its lethal radioactive/ferrimagnetic cargo of metallic missiles on board -- a fire power capacity that is potentially capable of detonating a chain reaction of free radical mediated neuro-degeneration whenever physiological circumstances permit.

So once a ferrimagnetic manganese 3+ or strontium 90 atom substitutes at the vacant copper bonds on prion protein, the field inducing influence of the ferrimagnetically ordered atoms will progressively corrupt the circadian mediated pathways of electromagnetic super-exchange throughout the brain; whereby a state of permanent magnetic saturation is spread much like a domino-style, contagious corruption, jumping from metal bond to metal bond, from prion to prion. This phenomena is well

Diagram; A rogue ferrimagnetic ordering of Mn3+ prions progressively corrupt the CNS circadian pathways of magnetic super-exchange. A contiguous, domino-like aggregation of PrP fibrils result, and TSE pathogenesis ensues.

Illustrated by the classic college physics experiment, where a magnet is placed alongside a steel nail and the force field of the magnet rapidly magnetises the adjoining nail.

So once an individual's brain is contaminated by this 'freaky' form of ferrimagnetic manganese or strontium, any subsequent exposure to external electromagnetic fields (eg, UV, sound waves, radar, cell phones, etc) will permanently charge up the ferrimagnetically ordered manganese prions to saturation point.

In this respect the TSE diseased brain can be likened to a solar powered battery on continuous charge; where the manganese loaded/copper depleted brain is no longer equipped to deal with the incoming surges of electromagnetic energy from the external environment. Instead of utilising this energy for the body's own vital requirements, its conduction is blocked and perverted into a potent force field for neuronal suicide; whereby the magnetically saturated atoms emit intensive magnetic fields, which, in turn, generate self perpetuating 'cluster bombs' of free radical mediated spongiform neuro-degeneration. TSE ensues.

Does the rogue ferrimagnetic metal co partner of the mis-folded prion protein serve as the infectious/transmissible component in TSEs?

This theory explains why the so called 'hyperinfectious' property of the prion is a misnomer. It is the toxic ferrimagnetic metal component of the prion that serves as the so called 'infectious' pathogenic agent in TSEs. So whenever scientists inoculate misfortunate lab animals with TSE brain tissues (eg: tissues contaminated with this rogue type of manganese or strontium atom) and effectively transmit TSE, they are actually transmitting 'a magnetic field inducing/radioactive capacity' that is carried along with the ferrimagnetically ordered metal contaminant into the recipient animals, who, in turn, develop TSE.

Furthermore, the concept of the rogue ferrimagnetic manganese atom as the 'TSE agent' also explains why the so called 'infectious' pathogenic capacity of the prion can survive heating to temperatures in excess of 500 degrees -- since ferrimagnetic metals will hold onto their magnetic charge until they are heated to temperatures beyond their respective 'curie point' temperature. (eg: 550 degrees for manganese 3+) - whence its magnetic energy (eg: its pathogenic capacity) is instantly drained.

The various strains of TSE disease could be explained by the different prion protein phenotypes and their different metal binding affinities for the various combinations of rogue replacement metals that could be involved in the aetiology of TSEs. In this respect, a raft of specific metal valencies, magnetic states and radioactive counts on the candidate replacement metals could determine the particular strain of TSE that emerges at the end of the day. Such factors as the length of incubation, aggressiveness of the disease process is determined by such factors as the radioactive, magnetic field inducing capacity of the rogue replacement atoms.

Laboratory support for the TSE environmental origin theory.

Several laboratory studies have come out in strong support of the mainstay of these environmental observations, suggesting that the abnormal mineral template common to TSE ecosystems represents more than an incidental finding. For instance, David Brown at Cambridge University demonstrated that the prion protein adopts its TSE deformed shape after manganese has been added to copper depleted prion protein cell cultures, whilst the US Prion Surveillance Centre at Case Western University in Cleveland observed a ten fold increase in manganese levels and 50% reduction of copper in sCJD diseased brain tissues.

From the soil to the brain; the environmental eco-dynamics of TSE pathogenesis .

Rogue metal intake.

Interestingly, neuro-pathologists working on post mortem TSE diagnosis in Sardinia, Iceland and Colorado, report worn down, soil stained incisor teeth as well as an excessive deposition of grit/soil in the gastro tracts of the carcasses of scrapie and CWD casualties that are sent in for TSE analyses. These unusual phenomena could be explained by the fact that both CWD and scrapie have a tendency to erupt in overpopulated ruminant populations who are overgrazing short-cropped pastures in drought stricken areas; indicating that these hard pressed, grazing animals would be taking in significantly larger amounts of top soil than normal.

Likewise, CJD has a tendency to erupt in self sufficient and/or rural based human populations whose work and lifestyles infer closer contact with the soil.

My studies have observed that TSE clusters arise in mammalian populations who are dependent upon soils that are both copper deficient and contaminated by certain rogue ferrimagnetic metal species - eg; where a ferrimagnetic manganese 3+, uranium or strontium species of metal is at high level. Thus any intake of top soil into the guts of grazing ruminants is likely to result in the increased uptake of these rogue metals into their biosystems, and, in certain circumstances, into their brain. Furthermore, the overpopulation of cervids in the CWD areas, has also led to increased browsing of juniper/pine and to 'break ins' into locally farmed alfalfa crops as a means of bolstering up their impoverished diet -- These plants bio-concentrate metals such as uranium, strontium and manganese to excessively high levels. (Author's latest unpublished analytical observations 2002/2003), so could represent another route of intensive exposure to these rogue metals in conjunction with the more direct route of exposure via soil ingestion .

It is interesting that certain species of ruminant, like the Pronghorn antelope, that have evolved to conserve copper levels very efficiently, have never succumbed to TSE despite roaming the same Front Range foothills around Fort Collins where CWD is so rife.

Sonic shock waves.

Once these rogue metals are attached to the copper depleted prion proteins in the living brains, it seems that the contribution of the 'sonic shock blast' from the external environment might come into the pathogenic interplay at this particular stage of the game.

The bombardment of the biological system by shock waves invokes an intensive burst of 'molecular motion' in the tissues, where proteins, for instance, are actually jiggled around by the heat energy resulting from the actual pressure of the incoming shock wave pulse. In more extreme circumstances, the protein molecules adopt an abnormal conformational shape as a result of the pressure stimuli, but will rapidly return to their normal shape in the healthy 'mineral balanced' individual. But in the individual whose metallo proteins are contaminated by these rogue metals, the change could be permanent (personal communications; Thad Mauney).

Use of certain metals like chromium and manganese 3+ in the manufacture of music audio tape material shows us that various ferrimagnetically ordered metal species will efficiently absorb and store up the energy of sound in a permanent magnetic form. It is this quantum capacity of the specific rogue metals implicated in the TSE affected bio-system that could hold the clue to what is going on in respect of the final transformation of the prion protein into its fully fledged, pathogenic TSE isoform.

The various intensive sources of infrasonic vibrational shock that I have observed in the TSE cluster environments could be sufficient to trigger off an actual atomic transmutation; where a metamagnetic transition of certain iron 3+, manganese 3+, uranium, strontium atoms is induced by the acoustic-vibration shock pulse, whereby the energy successfully metamorphoses the octahedral crystalline lattice of some of these metal compounds - inducing a metamagnetic transmutation of the atom from its paramagnetic to ferrimagnetic form. This phenomena is well recognised by magneto-physicists and referred to as the 'Jahn-Teller' distortion effect.

A good example of this phenomena is illustrated in the context of the racing pigeons who had flown into the 100 km shock wave boom carpet left in the wake of the Concorde supersonic aircraft. This had permanently disrupted their magnetite-mediated sense of magnetic orientation as a result.

Furthermore, cell culture studies have also shown that a sound wave challenge will proliferate the mysterious multi-replicating property of the prion protein.

Summing up.

It is proposed that the long standing, less aggressive, traditional strains of TSE are largely caused by exposure of grazing animals to food chains that are contaminated by naturally occurring sources of toxic ferrimagnetic metals (manganese, thorium, strontium from volcanic emissions, etc) and deficiencies of copper; along with their simultaneous exposure to intensive shock bursts of naturally occurring sources of low frequency acoustic waves which emanate from the movement of tectonic fault lines (during earthquake, volcanic activities) or from thunder/lightning storms.

Whereas, the more aggressive, accelerated version of new strain TSEs (BSE/vCJD) that has emerged more recently in younger mammals, are caused by exposure to the more intensive artificial sources of these same eco-factors. In this respect, it is proposed that the UK's BSE and vCJD 1986 -- 2000 epidemics were caused by the simultaneous exposure of cattle, cats, humans and zoo animals to;

1; The soils/atmospheres that were contaminated with radioactive strontium 90 after the toxic cloud of emissions from the April 1986 Chernobyl atomic leak were rained down over North Western Europe (UK, and to a lesser extent Brittany, Ireland, the Alps, etc) -- the precise region which shortly after became the first ever BSE hotspot region in the world.

2. The systemic acting 'copper chelating' types of organo-dithio-phosphate insecticide that were intensively used for warble fly/head lice/flea/food crop treatment around this time; thereby starving the prion protein of its copper co partner, subsequently rendering the protein's vacant metal domains to binding up with any replacement metals that are at high levels within the brain; eg; the rogue radioactive strontium 90.

The resulting mineral imbalance impairs the ability of the mammalian brain to deal with the ever increasing challenge of sonic shocks from the external environment. The sheer intensity of low flying military and Concorde jet aircraft over flights all over the UK bears testimony to the fact that the UK represents the most intensive 'noise' challenged country in the world. In this respect it may be no coincidence that the UK has hosted by far the highest incidence rate of BSE/vCJD in the world.

2003 - North America joins the cattle-battle .

Since no possible linkage can be made between exposure to 'contaminated feed' and North America's first declared case of BSE, the Canadian authorities should start to make a concerted attempt to identify the true origins of their TSE cases.

My own preliminary survey has identified some of the key TSE eco-risk phenomena in the environments where TSE has erupted in Alberta and Saskatchewan to date. The two farmed deer diagnosed with CWD were both raised on a farm that was directly under the take off flight path out of the Nameo military air base on the northern side of Edmonton.

The 'nidus' of both the new variant and traditional TSE cases that have erupted in Canada so far, have involved a single human, single cow and herds of wild/captive deer that have all originated from around the Lloydminster district of the Saskatchewan/Alberta borders.

Identical to the other TSE hotspot regions across North America, the soil is copper deficient and of the drought prone sandy type. It is also becoming increasingly contaminated by thorium, radium, barium uranium, strontium and other radio-nuclides that are being unleashed into the ecosystem by the fast expanding oil and gas well industry in that part of the world. I visited one elk farm that had suffered forty CWD positives and noticed that its fields lay amidst a cluster of gas wells. There is also a major refinery on the edge of the main town of Lloydminster itself.

The vegetation is also predominated by the juniper bush that is characteristic of the TSE ecosystem. After years of continuous browsing by the local deer herd, the juniper has evolved into a kind of close cropped carpet across whole tracts of the uncultivated Sandhills region.

Interestingly, the largest military tank test shelling range in North America, Camp Wainwright, is also located immediately to the West of this area, where the low frequency acoustic shock bursts from the tank shelling reverberate throughout the summer period. In fact, the first case of CWD was purportedly observed in a wild deer that was picked up staggering around in dazed condition on the edge of one of these shooting ranges.

To the North of Lloydminster lies the Cold Lake air weapons range. Intriguingly, the BSE cow was reared on one of the few farms that is uniquely exposed to the shock blasts of low flying military jets from the Cold Lake base. A neighbour told me that their farm happened to lie at the end of one of the test flight tracks; where several jets would mock 'dog fight' circling around and around before returning to the base. The local farmers around this intensive 'acoustic shock spot' had understandably had to complain to the airbase on several occasions .

It reminded me of my investigations into the single cases of BSE that have suddenly erupted in Sardinia and then Sicily, plus the six cases that had appeared in cattle reared along the Northern Coastal belt of Japan. These all involved cows (and one human with vCJD) that were reared beneath intensive jet practice areas involving aeroplanes from the Decimomannu, Sigonella and Northern Hokkaido bases (flown along the north coast for the 'North korea' patrol) respectively.

Given the potential financial losses that could be incurred by the Canadian/North American economy as a result of the recent outbreaks of TSEs in deer and cattle herds, it would seem wise for the appropriate authorities to break ranks with the mainstream reductionist mindset on the origins of TSE and adopt an alternative foolproof strategy for getting to the root of this problem - rather than 'cuckooing' out the same old stereotype protocol of control measures that have invariably failed to control a single outbreak of TSE to date .

Understanding the true causes of TSEs provides the best insight into measures that would best cure, control and, more importantly, prevent these grotesque diseases. If the key tenets of this theory should ever turn out to be correct, then it does not take much intelligence to envision the use of de-magnetising or chelation therapies as a possible means of arresting the TSE disease process.

Wholesale slaughter measures; the final farcical solution?

The epidemiological and experimental evidence amassed to date points to the fact that TSEs are caused by a clear cut combination of genetic and toxic environmental factors. And, despite the universal scare mongering over the 'hyperinfectious' nature of the prion, an impartial study of the epidemiological history of TSEs clearly demonstrates that this disease does NOT originate from animal to animal contact or through ingestion of feeds contaminated with TSE brain material. So why do the authorities continue to treat these diseases as if they solely stem from hyper-infectious origins?

The reasons for such an irrational, Pavlovian-like stance of the Establishment towards the environmental perspectives of TSEs probably hangs upon issues that are more to do with protecting academic egos, professional reputations and the vested interests of the TSE institutions/key advisors, than with promoting sound scientific argument. But the main reason must undoubtedly stem from the fear of massive compensation claims, should issues such as government mandated use of copper chelating 'OP warblecides' (re; the massive BSE epidemic in the UK) or leakage of radioactive metals from power or military facilities ever prove to be partially accountable for TSE causation at the end of the day.

Despite the repeated failure of wholesale livestock slaughter/fallowing regimes to eradicate long established TSE hotspot regions in Colorado and Iceland since the 1970s, governments are still adopting this same slaughter strategy as a first choice means of control today. But history has shown that TSEs will invariably re-erupt as soon as fresh livestock are introduced back into the slaughtered out areas; supporting the idea that the environmental causes of TSE are still well and truly wedded to the local food chain.

Such extreme mammalio-geddon measures do little more than remove the superficial evidence of the disease. They merely mislead the public into the illusory notion that TSE has been controlled (a good vote catching policy for any government).

But who is questioning the scientific reasoning for executing this final farcical solution on these poor creatures. For the unilateral adoption of a policy of 'totalitarian overkill' of a few million healthy animals across the world has been received with almost complacent acceptance. Such perverse and senseless 'carry ons' have sadly become the daily 'non-stories' of our modern times. Reports pop up with ever increasing frequency of so called TSE precautionary slaughter control programmes being enacted after 3% or more animals in a flock prove positive to the TSE genotype test; an innocuous, endemic phenomena that has existed in the sheep flocks across countries like Australia for light years -- eg; in countries where clinical scrapie has never emerged, presumably because the environmental TSE triggers are simply not present in those locations.

Nonetheless, despite the total absence of any sound scientific requirement, the prophylactic annihilation of livestock still carries on - a herd of water buffalo in Vancouver, deer herds across North America, sheep flocks from Vermont, hundreds of cows slaughtered in Germany, plus thousands of scrapie susceptible traditional sheep and goat herds erased from the European hillsides - all healthy animals. And hand in hand with the annihilation of our livestock runs the attendant demise of our small farmer/peasant cultures that have flamboyantly flavoured our fields and forests for centuries; that heartbeat of our hills that has given us the cultural identity that is so important to the survival of our psychological and spiritual sanity on this earth.

Regardless of the common sense approach, the authorities would appear to be capitalising from this so called 'crisis' rather than wishing to deal with it in a rational scientific manner. Having trumped up a scare story surrounding every aspect of the prionic 'nasties' that are lurking in our natural protein based foods, governments and multinational corporations seem hell bent on selling us the enormous 'risk-free' benefits of a brave new world of genetically modified soya protein -- a billion dollar global monopoly which they can design and control to suit the expansion of their own commercial empires.

Meanwhile, with 30% of the BSE data held behind the veil of the UK's Official Secret's Act, it is more than likely that we will never get to hear about the true cause of BSE- well, as far as the official clique of 'expertise' goes.

My thanks are extended to the many truly independent thinking individuals scattered across the TSE quarters of the globe who have housed, fed, transported, entertained and advised me whilst carrying out my analytical field surveys. Also to those who have donated towards the substantial laboratory analyses costs that my research has incurred.