Some would question how the toxic manganese theory of TSE origins can account for the well recognised ‘iatrogenic’ forms of TSE, where growth hormone treatment of humans - which utilises pituitary tissue as the pharmacological inoculant - can lead to a form of CJD.

But intriguingly, tissues such as pituitary and retina which transmit TSE in the lab most efficiently, are the same tissues in which manganese is recognised to concentrate most intensively in the body. So once an individual is contaminated with a rogue source of ferrimagnetic manganese, any subsequent use of their pituitary tissues in pharmaceuticals for ‘growth hormone therapy’ could spread the so called ‘infectious’ toxic agent, and initiate CJD.

Others would question how this theory can account for the outbreak of the kuru strain of TSE that exclusively erupted in an isolated tribe in the Fore region of the New Guinea Highlands. The conventional dogma blames this outbreak upon the Fore tribe’s traditional practice of cannibalism. Whilst cannibalism may have played a role in the bio-accumulation of manganese - particularly if the pituitary tissues were ingested in these cannibalistic binges – the fact that virtually every tribe across New Guinea had adhered to a cannibalistic lifestyle, whilst remaining free of Kuru, needs to be addressed by those who promote this theory. And furthermore, considering that cannibalism had been traditionally practiced for centuries across New Guinea, why did kuru fail to erupt until a few years after world war two?

My investigations suggest that the cause of Kuru stems from the same template of eco-factors; the Fore tribe’s self sufficient lifestyle on copper deficient soils, coupled to their scavenging of manganese-aluminium sheet metal from the fuselages of several Japanese bomber aircraft which had crashed in their area of the highlands during world war two. The Fore folk moulded the salvaged metal to make tools, cooking pans and bowels. This consequently contaminated their foods. They also accidentally exploded some of the bombs that were still on board the crashed aircraft. These infamous explosions - well remembered by the surviving Fore folk - infra-sonically irradiated their local environment.

This story goes on. At the mouth of the Fuji river valley in Japan lies a manganese-aluminium alloy factory that had manufactured these metal aircraft panels since the late 1930s. During this period, the manganese enriched chimney emissions dispersed downwind, permeating the entire length of the valley. Intriguingly, a cluster of CJD has blighted the residents of the Fuji river basin for 50 years.

The role of prion protein genetics is also entirely compatable with the environmental facets as part of the overall multi-factorial aetiology of TSEs. It is well established that prion protein genetics plays a major role in dictating which individuals are most susceptible to TSEs – where susceptibility hinges upon the expression of a defective prion protein that can only bind two or three atoms of copper, instead of the usual five. But the sole focus of TSE susceptibility studies to date has almost exclusively concentrated upon the role of prion protein genotypes. Yet my own studies have revealed that fair skinned/white or yellow/red pigmented individuals are at much greater risk of developing TSE. This suggests that the genetics of melanin expression may also perform a genetic role in the cause of TSE – N.B. Melanin is involved in cushioning the toxic side effects of light and sound absorption. Some support for this observation was amassed when misfortunate lab mice were genetically engineered to express a mutant form of melanin; they consequently developed spongiform encephalopathy.

Despite publication of the hard evidence in support of this theory in prestigious scientific journals (see references below), the various UK authorities and their incestuous clique of ‘minder’ advisors are blindly ignoring these findings. 

What is more, they are doing their utmost to publicly marginalise those of us who are trying to persue this alternative research line; and using public money to implement their tactics of suppression into the bargain.

For 18 years now, I have found my work and personal integrity subjected to a steady derisory trickle of ridicule and dirty tricks. During the 1980s my farm and family became the victims of a raft of ‘once in a lifetime’ type physical disasters; arson, firearm intimidation, vandalization of my research library/communications, and an insidious infiltration by a bizarre array of bogus greens, phoney free lance journalists. Not to mention the seductive approach by a scantily clad pseudo student from the Leeds Tech college who was supposedly doing her dissertation on my theory. After becoming suspicious, my investigations revealed that she was not even registered at the college where she was purportedly studying!

It invariably transpired that the true objectives of these ‘agent provocateurs’ was to subtly set about discrediting my social and scientific esteem, whilst finding out the current state of play of my research investigations. Once my work gained support from the likes of the former Minister of Defence, Tom King, and HRH Prince of Wales, the physical aspects of this harassment abruptly ceased.

A recent demand to the UK Government Departments for my personal data revealed much of what had been going on behind the scenes. Repeated requests by Environment Minister Michael Meacher to personally meet with me had been deliberately stymied by his own officials. When the Minister eventually broke through his barrage of officials to make direct arrangements with me for the meeting, it was postponed on five separate occasions and then completely fizzled out. Other documents revealed how The British Agrochemical Association had been organising a ‘joint initiative’ with the Ministry of Agriculture’s own grant funding department to channel public funds into a live animal trial that had been deliberately designed to refute my theory.

Since the BSE Inquiry had rejected the official scrapie-BSE hypothesis and found in favour of some aspects of my own hypothesis, the UK Government responded by setting up a further mini Inquiry to re-look at the origins of BSE. The resulting publication known as the ‘Gabriel Horn report’ employed a judicious selection of misrepresentation and outright bogus disinformation in order to discredit the validity of my theory. 

For example, they had stated that the use of OP warblecides had ceased in the UK by 1982, and that warblecides had been routinely used on Jersey island. So, according to the Horne Report, if OPs were the cause of BSE, why were all of the cows that developed BSE born after 1982, and why were BSE rates so low on Jersey?

But ironically, the truthful picture of the UK’s compulsory 2x annual OP warblecide treatment programme was that it was first introduced in 1982, whilst only one cow on Jersey was ever subjected to the compulsory ‘formal’ OP warblecide treatment.

When I attempted to sue the government for defamation/loss of income resulting from the bogus statements in this globally circulated publication, they pleaded ‘qualified privilege’ of the expert committee, and then spun out the legal communications beyond the one year post publication mark; thereby exempting themselves from my claim.

And after broadcasting of the BBC Correspondent film ‘Mad Cows and An Englishman’ which chartered my investigations, the government tried to appease the mounting public interest by inviting me to resubmit an application to them for funding. After sitting on my application for a year and a half, they homed in on the most fastidious, nit picking comments in the peer review appraisal; trumping them up as a sound scientific basis for their rejection. Immediately after, the author of the most irrational, irrelevant critique found himself promoted to the government’s expert ‘TSE surveillence steering committee’; presumably as a reward!

The UK government’s tactics have thwarted the whole healthy evolution of this new scientific perspective on TSEs.

A multi-national masterplan?

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. 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. Another reason must undoubtedly stem from the fear of massive compensation claims, should government mandated use of ‘OP warblecides’ or licensing of ‘manganese additives’ be held accountable at the end of the day.

But delving a bit deeper; who are the key culprits that are currently capitalising on the fashionable scare stories which maintain that "BSE prions will exterminate us all" ?    Who are spinning out the propaganda myths that beef, lamb, venison, game and organic food (grown from animal manure) are contaminated with prions; and are therefore unfit for human consumption?

The key scaremongers can invariably be traced back to a mere handful of socio-pathic pseudo-scientists who move between the upper echelons of government and corporation controlled institutions. These incestuous experts are singing for their supper. They are on the payroll of the multi-national chemical consortiums; corporations who have invested billions of bucks in researching and developing their GM arable protein crops and the complementary package of pesticides to go with them. They have bought up oceans of acres of dirt cheap arable land across Eastern Europe, the Third World and North/South America and they are clearly attempting to destroy anyone competing for "their" global protein market - Prime targets are the small mixed livestock farming sectors of agriculture who have traditionally maintained the mainstay of meat and milk protein production around the world.

The multi-nationals’ preference for a mono arable cropping land use is easily understood; since each acre of grassland that is devoted to meat and milk production requires negligible inputs of pesticide/GM seeds in relation to each acre of farmland that is devoted to agrochemical-intensive arable protein production.

Despite the scare-mongering over the ‘hyperinfectious’ nature of the prion, a basic study of the epidemiological history of TSE 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 ‘experts’ blatantly refuse to consult the ‘down to earth’ wisdom of the Icelandic farmers and vets who have been living and breathing with scrapie/TSE for light years. When the first hint of scrapie symptoms emerge in their sheep, it is customary practise to slaughter the affected animal instantly, eating the flesh (brains and all!) before the poor animal has had time to waste away.

So if scrapie or CWD can be passed onto humans via consumption - as the scientific authorities would have us believe - why have no cases of CJD erupted in these Icelandic sheep farmers? In fact, Iceland has only ever witnessed two cases of CJD in its entire medical history, and these victims had both hailed from the scrapie-free district in the far south of the country.

Despite the repeated failure of attempts to eradicate long established TSE hotspot regions in Colorado and Iceland by wholesale livestock slaughter/fallowing regimes enacted across the cluster zones, governments are still adopting this same slaughter strategy as a first choice means of control. 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, irrespective of the slaughter programmes.

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).

Despite these simple observations, a manic mindset has recently gripped the global authorities who have jumped to the assumption that TSEs stem solely from hyper-infectious origins.

For example, the recent discovery of new clusters of CWD in US deer has invoked an official over-reaction of unprecedented proportion – a wholesale slaughter policy of indigenous deer herds has been enacted throughout all CWD regions across the USA, leaving many of the Native American tribes without their traditional source of dietary protein. Whilst studying in Wisconsin recently, I heard the story of a deer rancher who had retained some body tissues from one of their CWD affected deer - for reasons of independent post mortem - only to find himself subjected to a gunpoint raid by wildlife officials.

These draconian slaughter measures are invariably promoted by the same hardcore cell of ‘expert’ global advisors - the hysterics who dreamt up the hyper-infectious hypothesis in the first instance. By burying or incinerating the evidence of their own control measures – eg the thousands of slaughtered animal carcases – and then fallowing the land, the experts are placing themselves in a fool-proof position where the success or failure of their control measures can never be properly assessed. In this respect, they can guarantee keeping their professional reputations afloat for the remaining lifespan of their careers.

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 control programmes being enacted after 1% or more animals in a flock prove positive to the TSE genotype test – an endemic phenomena that has existed for light years without ill effect. Annihilation of a herd of water-buffalo in Vancouver, sheep flocks from Vermont, 400,000 cows slaughtered in Germany, plus thousands of scrapie susceptible traditional sheep and goat herds erased from the European hillsides – all healthy animals.

Along with the sad threat to the survival of some indigenous wild and domestic animal breeds, we shall also loose their valuable outputs of manure - the heartbeat of humus supply which protects the soil against the erosive forces of nature, and, more importantly, feeds the fertility of the earth that ultimately sustains all life on the planet.

Furthermore, these slaughter measures are imposing the death knell on the survival of traditional peasant cultures - lifestyles which have evolved to be symbiotically dependent upon the income generated from their livestock enterprises. We are saying farewell to one of the last bastions of our cultural identity; a holistic charm that flavours the landscapes that have been etched out by centuries of occupation under peasant family farms. That delicate ethereal relationship that flows between the soil, crops, livestock and landscape is under threat, along with the aesthetically pleasing array of idiosyncrasies that go hand in hand with peasant lifestyles; the architecture, craft skills, folklore and dialects that have divided the rich rustic out backs apart from the homogenised, synthetica of the city.

The ‘all out’ slaughter tactic betrays a total lack of interest in the cause, prevention or cure of this grotesque disease. The Establishment’s current global agenda to depopulate livestock numbers at whatever the cost (Agenda 2000), is for reasons that have nothing whatsoever to do with illusory health risks to the human race, but more to do with envisioned profits from multinational GM proteins .

I cannot help but feel that the global leaders have sold out to the multinational carrot. PR tactics used to promote "important" government policy increasingly capitalises upon some emotive scare story as a means of manipulating public mentality into conforming with the overall global agenda of the corporations. In much the same way as a war for Iraqi oil has been presented under the pretext of a morally justified war to rid Iraq of weapons of mass destruction, so the corporations’ war to rid the world of livestock protein has been presented under the guise of ridding the world of the ‘health risks’ posed by hyper-infectious prions.

The BSE debacle represents the mere tip of an iceberg of establishment ineptitude and socio-eco-irresponsibility. It displays a clear cut example of the far reaching extent to which the ‘talons’ of multi-national monopolies can stretch to protect their global master plan on the fast expanding ‘Health and Food chain Industry’. Can we afford to allow this insidious mode of food chain control to continue unregulated and unabated ?

There is an increasing groundswell of public unease concerning the unknown effects that our polluted environment is exerting on our health and long term survival. Public suspicion is mounting towards the transparent array of so called independent scientific experts and medical spin doctors who are called to advise governments and address the public on all aspects of the impact of chemical, metal, radioactive or electromagnetic pollutants upon our food chain.

This story returns us to the lessons that can be learnt from the intuitive wisdoms of the people on the "ground" . At the same time it alerts us to the insidious and unscientific techniques which the incestuous clique of official experts employ to marginalize and discredit those who dissent from the totalitarian line. It shows us the ill conceived basis on which the positions of the Establishment are truly based, along with the woeful degree of administrative complacency over issues which, in most cases, are matters of life and death for normal people.

My most recent eco-detective adventures across Japan, USA, Sardinia and the UK’s vCJD clusters have prospected for a broader range of metals in the TSE cluster environments than previously undertaken. In this respect, the analytical results have thrown up some exciting new possibilities in the quest for the true cause of TSEs. They have unearthed high levels of the ferrimagnetic metal ‘strontium’ as well as the usual high levels of manganese in the TSE environments. The levels returned to normal in the adjoining TSE-free areas.

Much like manganese, strontium is emitted as a significant contaminant from volcanos, steel/glass/dye/explosive/paint/metal refining/firework factories. It is used in surgery/ dentistry, and as a bone/antler promoter in mineral supplements for humans and deer, etc. Strontium will also compete and replace vacant calcium, magnesium, copper sites on proteins in the bio-system, so tests are currently in place to see if this metal can bind to copper deprived prion protein like manganese .

The Strontium facet offers an exciting new theoretical possibility that can be generated without disturbing the basic pathogenic template of this TSE causal theory – where the rogue ferrimagnetic ‘strontium’ substitutes at the copper depleted metal bonds on the prion protein, thereby impairing the protein’s ability to conduct the vital ‘life force’ electromagnetic energies derived from incoming light and sound.

It naturally follows that exposure to high levels of naturally occurring strontium could have triggered off the traditional strains of TSE, whereas exposures to the more reactive, radioactive ‘strontium 90’ could have caused the more aggressive new variant strains of TSE in younger mammals.

Perhaps the ‘strontium 90’ emissions from the Chernobyl nuclear disaster in April 1996 – the bulk of which were deposited by the substantial rainstorms over North Western Europe (eg UK, Ireland, Brittany) at that time – were responsible for setting up susceptibility for mad cow disease in any cattle, humans or cats who had been simultaneously exposed to the copper-chelating, organo-dithio-phosphate warble fly/head-lice insecticides. The first reported case of BSE erupted in October 1986, whereas the almighty BSE epidemic that followed was largely contained within the key Chernobyl fall out zone.

It seems that several species of rogue ferrimagnetic metal - be it manganese, strontium or barium – may individually carry the potential to act as the TSE trigger in the copper depleted brain. The resulting mineral imbalance compromises the brain’s ability to deal with low frequency infrasonic shocks.

Governments and Corporations have deliberately conspired to manipulate what the public get to hear surrounding the causes of TSE - not to mention the causes of so many other modern ailments. Their concealment of the whole truth is betrayed by the fact that the UK’s BSE Inquiry team was debarred from accessing 30% of the government’s data on BSE - since it was ‘classified’ under the Official Secret’s Act.

BIBLIOGRAPHY

• Website - www.markpurdey.com
• Purdey M. Ecosystems supporting clusters of sporadic TSEs demonstrate excesses of the radical generating divalent cation, manganese, and deficiencies of antioxidant co factors Cu, Se, Fe, Zn. Does a foreign cation substitution at Prp’s Cu domain initiate TSE. Medical Hypotheses 2000 54 (2) 278-306.
• Purdey M. Does an ultra violet photoxidization of the manganese loaded/ copper depleted prion protein in the retina initiate the pathogenesis of TSE. Medical Hypotheses 2001 57 (1) 29-45.
• Purdey M. The Mn loaded/Cu depleted bovine brain fails to neutralise incoming shock bursts of low frequency infrasound ; The origins of BSE?
  Cattle Practise; October 2002 10 (4) 311-325.
• Brown D, Hafiz F, Glassmith L, et al. Consequences of manganese replacement of copper for prion protein function and proteinase resistance. EMBO J. 2000 19 (6) 1180-1186.
• Wong BS, Chen SG, Colucci M, Xie Z, Pan T, Liu T, Sy MS, Gambetti P, Brown DR.Aberrant metal binding by prion protein in human prion disease. J Neurochem 2001 78 1400-1408.
• Gordon I, Abdulla EM, Campbell IC, Whatley SA. Phosmet induces up-regulation of surface levels of cellular prion protein. Neuroreport 1998 9 (7) 1391-1395.