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HALF LIVES, WARBLE FLIES AND GOVERNMENT LIES -
THE DIRTY THREE PREREQUISITES THAT CAUSED BSE?
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.
The Official Hypothesis on the cause of TSEs.
The official hypothesis decrees that the transmissible spongiform encephalopathy (TSE) group of diseases are caused by various modes of exposure to brain material sourced from animals that have become contaminated by an infectious protein-only agent known as the prion - a malformed version of the native prion protein that is found in all healthy mammalian brain. The route of the supposed infection can be via prion contaminated feeding stuffs, injections of prion contaminated tissues (e.g.; involving blood/growth hormone), cranial implantation with prion contaminated depth electrodes, etc. or merely through body to body contact (via saliva, etc.)
In this respect, the BSE outbreak in cattle was blamed on the feeding of the rendered remains of prion contaminated scrapie affected sheep brains (that was added into cattle concentrated feeds) once the temperatures were relaxed from 150 degrees in the rendering factories during the early 1980s. The 'infectious' fraction of the concentrated cattle feed has therefore become associated with the meat and bone meal (MBM) ingredient which was used to boost the protein content of concentrated feeds for cattle – a lucrative replacement for the more expensive arable crop proteins that can also be used for this purpose.
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 – radioactive metal micro-crystals 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 and introduced to 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 dithiophosphorus (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-dithiophosphate insecticide for the control of warbles on UK cattle. Amongst a myriad of toxicological effects, the systemic types of dithiophosphate can disrupt copper and sulphur binding sites in the bio system, as well as opening up the blood brain barrier; thereby disturbing the overall crucial balance of metals in the brain.
In this respect, it is interesting to know that the normal prion protein has been shown to bond up with copper in the healthy brain. This led me to theorize that the copper component of the protein plays a role in conducting electrical signals into the areas of the brain that are mediated by the circadian (daylight – darkness) rhythm. But once the availability of copper for bonding to the protein is curtailed in any way, then the protein will cease to fulfil its metabolic function of conduction. The disruption of the copper supply to the protein could therefore have something to do with the primary cause of TSEs.
I therefore considered that the ability of these OP insecticides to disturb the metabolism of copper and sulphur within the bio system was associated with the origins of BSE. I was not surprised to witness the first cases of BSE rearing their ugly head in the UK cattle herd in November 1986; which, in my opinion, was a legacy of the UK government's compulsory 'high dose' warble fly campaign. The few other European countries who instigated warble fly campaigns (e.g.; France, Switzerland, Ireland, etc) used lower doses of insecticide, and, not surprisingly, developed proportionately fewer cases of BSE as a result.
The Flaws in the Official Theory.
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 lead 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, albeit in the artificial laboratory context, via injections of massive doses of TSE diseased brain tissues into misfortunate laboratory animals. Yet, various other disease, 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 key Flaws in the Conventional Hypothesis are as follows -
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 whose cattle populations have remained BSE-free to date. - e.g., 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. However, none of these alterations were exclusive to the UK rendering plants, since 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 has been shown to remain active after heating to temperatures up to 800 degrees C – way above the 150 degree C 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.
4. Forty thousand plus cows that were born after the UK's 1988 ban on MBM incorporation into cattle or other ruminant feed have still developed BSE.
5. These 40,000 misfit cases of BSE were partly blamed upon vertical transmission – e.g.; transmission of the infectious prion from mother to calf. But no cases of BSE could be induced in the studies involving nearly 1000 calves / embryos that were experimentally incubated/reared by mother cows maintained under high risk BSE conditions (according to the MBM theory) on a Dept of Agriculture farm at High Mowbray in Yorkshire, UK.
6. 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.
7. 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.
8. Four of the original five kudu antelope that developed BSE at the London zoo had not had any possible access to MBM containing feeds.
9. 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.
10. 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 of CJD in the Icelandic population at large.
11. 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.
12. BSE fails to fulfil ' Koch's postulates'- the yardstick for gauging whether a given disease (e.g. BSE) stems from infectious origins (e.g. the scrapie agent). One example of this failure involves the 10 to 30% of cattle that were slaughtered each month under the BSE slaughter order, where the presence of the 'infectious' prions (the supposed causal agent) could not be identified in the post mortem analyses of their brainstem samples. The identical symptoms and space/time distribution of these so called "BSE Negative" cases with the BSE positive cases suggests that the "negative" cases were all part and parcel of the same disease. The fact that the hypothetical causal agent, e.g.; the prion, could not be identified in up to 30 % of the cattle killed each week under the BSE order throughout the BSE crisis indicates that the official theory fails to fulfil the most fundamental of Koch's postulates.
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.
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 lobbies 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
Cluster Buster – the crystallization of an alternative theory that attempts to explain the true cause of TSEs.
As a TSE field scientist, my observations and research findings lead 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 OP warble fly insecticides which disturbed the balance of copper and sulphur in the bio-system , could play a primary role in the cause of TSEs. 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, food chains and hard tissues (bone, etc,) in various ecosystems of Japan, Slovakia, Italy, Sardinia, Sicily, Iceland, Colorado, Wisconsin, Alberta, 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 metal micro-crystals such as manganese, strontium, barium or silver, in combination with deficiencies of copper, zinc, natural sulphur, selenium, etc, constituted an abnormal mineral imbalance that was common to every TSE cluster region that I have analysed to date. 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 intoxication of the brain with these metal nano-crystals was compromising the ability of nervous system to protect itself against the deleterious effects of incoming sonic shocks from the external environment. In fact, the millions of alien micro-crystals that have invaded the TSE affected brain actually enhance the impact of incoming sound waves, by acting much like the crystals found in microphones or radio receivers.
I therefore concluded that BSE, as well as other TSEs, are primarily caused by environmental exposure to one or other of a select group of metal micro-crystals – Barium, Strontium, Manganese or Silver. Each rogue micro-crystal has the potential to act as a nucleator once it successfully establishes itself within the brain. It seeds off an aberrant "cluster bomb" of hyper-crystallization within the tissues – that do not normally require this mode of hyper-mineralisation for their maintenance or function.
The specific species of metal crystal involved in the intoxication determines factors such as the length of incubation period (e.g.; which represents the period of growth of the resulting metal-protein crystal contaminant), the distribution of lesions within the brain, etc. - factors which all combine to determine which specific strain of TSE prion disease will emerge at the end of the day.
My analytical research has found that wherever the key clusters of TSE have emerged around the world , there is a significant source of metal contamination in the local environment which can precisely explain the origins of the outbreak. The rogue metals are either emitted into the atmosphere from naturally occurring sources- via volcanic eruptions or quarrying/extraction of certain rock, coal or oil which are naturally rich in barium/strontium. Or from man made activities that implicate the use of these metals in the steel, glass, ceramic, welding, oil drilling or most importantly, the military munitions industries – also from personal exposures to dental amalgams, surgical instruments (re; the silver in depth electrodes, etc), use of barium swallow in radiographic investigations or silver in water purification, etc.
Use of Barium/Strontium and Silver crystal sprays that are discharged into the upper atmosphere for cloud seeding rainmaking operations, refraction of incoming ultra violet rays or as a radar/radio refraction technique employed by the military during warfare (e.g.; Gulf war 1) or practice operations should also be born in mind as a significant source of potential environmental contamination by these metal nano-crystals .
The Half Lives.
It was my recent research in the USA that has brought me much closer to a clear cut conclusion on the precise causes of TSEs – particularly after I uncovered the fact that deer from the Fort Collins wildlife research facility in Colorado had been deliberately used in experiments to monitor the biological effects of the atmospheric leak of plutonium and other radioactive metals from the infamous Rocky Flats nuclear trigger/weapon factory during the 1960s. By 1967, The first ever recorded case of TSE in a deer had emerged in the same deer facility that was being subjected to this raft of nuclear experiments.
Wherever these radioactive metal components were used – in the missile production factory at Tucson in Arizona, in the missile silos that have impregnated the plains of NE Colorado/SE Wyoming/SW Nebraska , or in the missiles that have been test fired across the White Sands Missile range in New Mexico or Cold Lake air weapons range/Camp Wainwright in Alberta/Saskatchewan, TSEs have invariably broken out in those local deer, sheep or human populations that have been exposed to the atmospheric fall out of these metal micro-crystals. It is a very clear cut correlation.
I have subsequently identified this same correlation between exposure to these munition metals and the vast majority of the outbreaks of TSE around the world. For instance, the largest cluster of new variant CJD in humans is located at Queniborough village in Leicestershire in the UK. This tiny village is sited one mile away from what was the largest munitions factory for the manufacture of detonators, triggers and chemical warfare agents in the UK – at East Goscote. Aerial photos indicate that during the 1950s, the munitions were actually stored along the edge of the lanes around Queniborough itself.
In Italy, I came across a cluster of CJD in humans who were all employed or connected to a munitions factory in the Po valley in Italy during the 1970s; as well as another cluster of 20 cases of CJD in a remote Calabrian village which had resulted from the contamination of the local water source by illegally dumped radioactive metals.
I unearthed another mysterious cluster of scrapie TSE that had emerged in sheep that were kept upon a block of common land at Ashoro in Hokkaido in Northern Japan – land which was formerly occupied by the Japanese military during world war two; where, according to the local farmers, many covert tests were carried out with "munitions". Sheep can no longer be pastured in this region, because they invariably contract scrapie. The correlations between TSEs and exposure to munitions are just too close for comfort.
Rogue Metal Micro-crystals – the seeds of Mad cow Madness.
These observations have lead me to believe that TSEs are caused by exposure to these various metal micro-crystal pollutants. Once these metal crystals are able to leak across the blood brain barrier (facilitated by the presence of other abnormal eco-influences) and penetrate their way into brain cells that are depleted in certain essential minerals (like copper and sulphur), the micro-crystals are then free to opportunistically bond up with certain brain proteins in place of their normal copper/sulphur co-partners, whereupon they subsequently 'seed' the growth of substantial sized metal-protein crystal arrays.
Since the prion protein is a copper bonding protein, it represents one of the proteins that can be successfully targeted and occupied by these invading micro-crystals – but this can only happen at a time when the supply of free copper is disrupted within the brain.
Once the alien micro-crystals become lodged and bonded into the nerve membranes. It is here that they start to multi-replicate themselves, growing into substantial metal-protein crystal structures that form the characteristic aberrant fibril-like features that are seen to hallmark the TSE diseased brain.
I believe that these crystals are 'piezoelectric' in nature; that is to say that they work much like the crystals that are used in microphones. They convert the energy of incoming acoustic sound waves into electrical energy. Thus, once an individual's brain has become contaminated by these rogue crystals, the brain is no longer able to conduct/dissipate the high energy shock-bursts of sound and light that radiate in from the external environment (NB. the presence of these shock-bursts are well evident in the TSE cluster environments).
The incoming energy ends up being absorbed into the rogue crystals, which subsequently convert it into electrical shock bursts, which generate magnetic fields around the crystals, which, in turn, initiate chain reactions of deleterious free radical damage in the surrounding tissues.
The additional impact of the radioactive decay emitted from the metal component of these crystals serves to compound the intensity of the free radical chain reactions. Spongiform neuro-degeneration of the brain ensues – represented by the so called 'halos' or holes of spongiform damage that surround these aberrant fibril structures in the TSE diseased brain.
The piezoelectric crystal facet of this theory is well supported by the classic hypersensitive response of the BSE affected cow to the veterinarians' hand clap test – the customary field test that is applied for diagnosing clinical BSE when a government vet enters the farm to examine a BSE suspect cow. If the cow is genuinely suffering from BSE, the modest shock waves of the hand clap will invariably cause the poor beast to collapse to the floor quivering and bellowing out in writhing agony – just as though the clap had detonated an electric shock-burst inside the cow's brain.
My hypothesis therefore asserts that the rogue metal micro-crystal represents the transmissible, pathogenic agent that underpins the primary cause of TSE diseases. This theory explains many of the missing links in our understanding of the pathogenesis of TSEs. For instance, nobody yet understands why TSE can still be invoked in misfortunate healthy lab animals after they have been injected with the inorganic ash that results from the heating of TSE affected brain material up to temperatures as high as 800 degrees C. How can the various protein-only/microbiological agents that have been ascribed to the cause of TSEs begin to survive these kind of elevated temperatures; and then retain their so called hyper-infectious property thereafter?
But in accord with my theory; the metal crystal nucleator, along with its piezoelectric pathogenic capacity, is well capable of surviving these kind of elevated temperatures, and then being artificially transmitted back into a healthy animal, where they are free to reseed the multi-replication of a pathogenic metal-protein crystal (the fibril) all over again. For the magnetic charge that is permanently captured within these ferrimagnetically ordered crystals will not be drained until temperatures are raised above the respective 'curie point' threshold of the specific metal involved – around the 600 degrees C for manganese. Furthermore, the actual structure of the crystals themselves is retained until temperatures exceed their melting point - which can be as high as 1000 degrees C for some crystal species.
In this respect, my thesis also explains how TSEs can sometimes be successfully transmitted in the real world via blood transfusions or injections of pituitary growth hormone treatments; where the rogue micro-crystals contaminants are transmitted via these injections of TSE affected tissues into the healthy human; whereupon the crystals are free to multi-replicate themselves all over again, ultimately building up substantial sized 'fibril' arrays of metal protein crystal in the fresh host.
It is interesting that metals such as Barium and Strontium are actually exploited in therapeutics for 'seeding' the process of crystallisation in the bone matrix as a means of reversing the wasting of the bones in those who are suffering from osteoporosis. But under conditions of good health, the process of mineralzation within the organism is under delicate bio-regulation; whereby any aberrant crystal growth that starts to run away with itself within the tissues is kept in check. But once this delicate regulatory system is disrupted, then diseases like rheumatoid arthritis, Alzheimer's disease and TSEs are able to proliferate.
The long incubation period experienced in these diseases, can be explained by the protracted period that the metal-protein crystal takes to grow in the brain. Once grown to full size, any subsequent exposure to sonic shocks from the external environmental will jettison the contaminated individual out of the dormancy period, by triggering off the deadly chain reaction of electro-magneto induced radical reactions that create the classic spongiform type of neuro-degeneration that is seen in the TSE diseased brain.
The particular species of rogue metal crystal contaminant that is involved will dictate which specific strain of TSE will emerge at the end of the day.
Other eco-genetic influences must play a role. Besides the exposure to the metal micro-crystal pollutant itself, there must be other abnormal environmental or genetic influences at work in the TSE hotspot locations which compromise the abilities of the local mammalian populations to defend themselves against the uptake and binding of these rogue metals into their brain tissues. In this respect, any healthy, well nourished, mineral balanced individual should be able to mount a viable metabolic defence that prevents both the uptake and binding of these alien micro crystals into their brain
The origins of the UK's BSE epidemic.
In respect of the cause of the massive epidemic of BSE in the UK, I became interested in the possible contributory role posed by the compulsory use of exclusively high doses of systemic acting organo phosphate (OP) insecticides that were used for the control of warble fly during the 1980s/1990s.
It appeared that the all important use of this specific insecticide during the 1980s had increased the permeability of the blood brain barriers of treated cows, thereby disrupting the "front line" of defence that protects the brain against the uptake of alien toxic metals. Furthermore, the chemical structure of the particular dithio-phosphate type of OP used in the UK indicates that it would also act as a chelator of copper (e.g.; would lock up available copper in the tissues), as well as competing for sulphur bonding sites in some of the key proteins - like the copper bonding prion protein and the sulphated proteoglycans - that are implicated in the pathogenesis of TSEs.
All in all, the simultaneous exposure of UK cattle to these OP insecticides during the 1980s would have enabled any rogue metal micro-crystals that contaminated the UK environment at that time to enter the brain and then bind up with these specific proteins in place of their correct metal co partners; thereby initiating the TSE disease process.
The most likely metal micro-crystal candidate that could be held responsible for kicking off the UK's BSE epidemic in November 1986, could stem from the UK's contamination with the radioactive strontium 90 that was showered down in the massive rainstorms that covered North Western Europe shortly after the Chernobyl power station accident in April 1986. In this respect, BSE could have been triggered off in any cow that was simultaneously treated with the high dose OP warblecide whilst it was consuming strontium 90 contaminated pastures.
The OP treatment enabled the strontium 90 to literally flood into the bovine brain; where it subsequently coupled up with the prion and ferritin proteins, which all conjugated together to build the characteristic fibril crystal structures that represent the key abnormal hallmark of the BSE diseased brain.
Countries like France, Ireland, Switzerland, Germany, Portugal, Holland, etc, used much lower doses of a less concentrated OP formulation for warble fly control on their cattle, and, correspondingly, suffered much lower incidence rates of BSE as a result – probably due to the fact that their blood brain barrier function was not so disrupted by the lower doses of OP which they were exposed to.
Likewise, it is interesting that all countries in the southern Hemisphere, like Australia and New Zealand, have not been blighted by any BSE. Perhaps this is because they were not exposed to the Chernobyl fall out , nor has their different climate ever favoured the establishment of any warble fly infestation in their cattle - thereby exempting them from any need to use the systemic OP warble fly treatments.
Much like the cows, humans and cats were also exposed to the systemic acting types of OP which were voluntarily used as head lice and flea shampoos during the hottest period of the Chernobyl contamination. OPs were also used extensively on all food crops. This cocktail of OP contamination would have rendered humans and cats more vulnerable to the uptake of the Chernobyl metals (locked into the proteins within the food-chain) into their brains; thereby explaining the outbreaks of vCJD and BSE in humans and cats across Europe.
According to my research, the substantial drop off in the incidence rate of BSE during the late 1990s is due to a combination of dynamic environmental factors;
The virtual eradication of the warble fly - with a corresponding cessation of use of the OP warble fly insecticides over this 1990s period .
The gradual decay in the radioactive half life of the metals emitted from the 1986 Chernobyl atmospheric leak.
Furthermore, cows that are more susceptible to these environmental challenges, and are therefore more susceptible to developing BSE, will have been killed out by the BSE epidemic itself ; leaving the less susceptible animals alive that are less likely to succumb to BSE in the future.
The supportive data.
Apart from the academic publication of my own environmental analytical data on the elevation of manganese, barium, strontium or silver/deficiencies of copper ,etc, in the TSE cluster ecosystems and more recently in the antlers of TSE affected deer, some follow up laboratory studies were conducted which also provided positive support for my hypothesis.
For example, cell culture experiments were performed at Cambridge Uni by Dr David Brown who showed that the prion protein deformed into its abnormal shaped, protease resistant conformation (the form that hallmarks the brains of those who have died of TSEs) after the cells were loaded with manganese (one of the metals that I observed at high level in some of the TSE cluster zones) and starved of copper. The actual aberrant bonding of manganese onto the prion protein - in place of copper - was considered responsible for misfolding the protein into its abnormal conformation. This work was published in the journal of the European molecular biology association.
Another study at the US Prion disease surveillance centre at Case western Uni, Ohio, demonstrated that CJD affected brain material contained a ten fold elevation in manganese and a 50% reduction in copper in relation to the brains of those who had died of non-neurological disorders. This work was published in the Journal of Biochem.
Further work was conducted in Japan at Kobe Uni, where exposure of manganese bonded prion protein to specific wavelengths of light had caused the metal proteins to aggregate into the aberrant fibril structures that hallmark the brains of TSE victims.
And finally, a catalogue of Government Lies...
Sadly, in choosing to ignore the true causes of these grotesque diseases, the British government remains blatantly negligent in its duty to safeguard the health of its own people and environment. Furthermore, whilst remaining fully aware of the major flaws in their own official theory, the government remains criminally negligent in trying to deceive the rest of the world over the so called 'viability' of their deeply flawed and failed hypothesis.
Mark Purdey - August 27th 2004
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REFERENCES;
Purdey M; Elevated silver, barium and strontium in antlers, vegetation and soils sourced from CWD cluster areas; Do Ag/Ba/Sr piezoelectric crystals represent the transmissible pathogenic agent in TSEs ? Medical Hypotheses 2004 63: 211-225
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; 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.
HALF LIVES, WARBLE FLIES AND GOVERNMENT LIES -
THE DIRTY THREE PREREQUISITES THAT CAUSED BSE?
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.
The Official Hypothesis on the cause of TSEs.
The official hypothesis decrees that the transmissible spongiform encephalopathy (TSE) group of diseases are caused by various modes of exposure to brain material sourced from animals that have become contaminated by an infectious protein-only agent known as the prion - a malformed version of the native prion protein that is found in all healthy mammalian brain. The route of the supposed infection can be via prion contaminated feeding stuffs, injections of prion contaminated tissues (e.g.; involving blood/growth hormone), cranial implantation with prion contaminated depth electrodes, etc. or merely through body to body contact (via saliva, etc.)
In this respect, the BSE outbreak in cattle was blamed on the feeding of the rendered remains of prion contaminated scrapie affected sheep brains (that was added into cattle concentrated feeds) once the temperatures were relaxed from 150 degrees in the rendering factories during the early 1980s. The 'infectious' fraction of the concentrated cattle feed has therefore become associated with the meat and bone meal (MBM) ingredient which was used to boost the protein content of concentrated feeds for cattle – a lucrative replacement for the more expensive arable crop proteins that can also be used for this purpose.
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 – radioactive metal micro-crystals 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 and introduced to 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 dithiophosphorus (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-dithiophosphate insecticide for the control of warbles on UK cattle. Amongst a myriad of toxicological effects, the systemic types of dithiophosphate can disrupt copper and sulphur binding sites in the bio system, as well as opening up the blood brain barrier; thereby disturbing the overall crucial balance of metals in the brain.
In this respect, it is interesting to know that the normal prion protein has been shown to bond up with copper in the healthy brain. This led me to theorize that the copper component of the protein plays a role in conducting electrical signals into the areas of the brain that are mediated by the circadian (daylight – darkness) rhythm. But once the availability of copper for bonding to the protein is curtailed in any way, then the protein will cease to fulfil its metabolic function of conduction. The disruption of the copper supply to the protein could therefore have something to do with the primary cause of TSEs.
I therefore considered that the ability of these OP insecticides to disturb the metabolism of copper and sulphur within the bio system was associated with the origins of BSE. I was not surprised to witness the first cases of BSE rearing their ugly head in the UK cattle herd in November 1986; which, in my opinion, was a legacy of the UK government's compulsory 'high dose' warble fly campaign. The few other European countries who instigated warble fly campaigns (e.g.; France, Switzerland, Ireland, etc) used lower doses of insecticide, and, not surprisingly, developed proportionately fewer cases of BSE as a result.
The Flaws in the Official Theory.
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 lead 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, albeit in the artificial laboratory context, via injections of massive doses of TSE diseased brain tissues into misfortunate laboratory animals. Yet, various other disease, 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 key Flaws in the Conventional Hypothesis are as follows -
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 whose cattle populations have remained BSE-free to date. - e.g., 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. However, none of these alterations were exclusive to the UK rendering plants, since 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 has been shown to remain active after heating to temperatures up to 800 degrees C – way above the 150 degree C 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.
4. Forty thousand plus cows that were born after the UK's 1988 ban on MBM incorporation into cattle or other ruminant feed have still developed BSE.
5. These 40,000 misfit cases of BSE were partly blamed upon vertical transmission – e.g.; transmission of the infectious prion from mother to calf. But no cases of BSE could be induced in the studies involving nearly 1000 calves / embryos that were experimentally incubated/reared by mother cows maintained under high risk BSE conditions (according to the MBM theory) on a Dept of Agriculture farm at High Mowbray in Yorkshire, UK.
6. 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.
7. 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.
8. Four of the original five kudu antelope that developed BSE at the London zoo had not had any possible access to MBM containing feeds.
9. 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.
10. 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 of CJD in the Icelandic population at large.
11. 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.
12. BSE fails to fulfil ' Koch's postulates'- the yardstick for gauging whether a given disease (e.g. BSE) stems from infectious origins (e.g. the scrapie agent). One example of this failure involves the 10 to 30% of cattle that were slaughtered each month under the BSE slaughter order, where the presence of the 'infectious' prions (the supposed causal agent) could not be identified in the post mortem analyses of their brainstem samples. The identical symptoms and space/time distribution of these so called "BSE Negative" cases with the BSE positive cases suggests that the "negative" cases were all part and parcel of the same disease. The fact that the hypothetical causal agent, e.g.; the prion, could not be identified in up to 30 % of the cattle killed each week under the BSE order throughout the BSE crisis indicates that the official theory fails to fulfil the most fundamental of Koch's postulates.
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.
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 lobbies 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
Cluster Buster – the crystallization of an alternative theory that attempts to explain the true cause of TSEs.
As a TSE field scientist, my observations and research findings lead 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 OP warble fly insecticides which disturbed the balance of copper and sulphur in the bio-system , could play a primary role in the cause of TSEs. 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, food chains and hard tissues (bone, etc,) in various ecosystems of Japan, Slovakia, Italy, Sardinia, Sicily, Iceland, Colorado, Wisconsin, Alberta, 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 metal micro-crystals such as manganese, strontium, barium or silver, in combination with deficiencies of copper, zinc, natural sulphur, selenium, etc, constituted an abnormal mineral imbalance that was common to every TSE cluster region that I have analysed to date. 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 intoxication of the brain with these metal nano-crystals was compromising the ability of nervous system to protect itself against the deleterious effects of incoming sonic shocks from the external environment. In fact, the millions of alien micro-crystals that have invaded the TSE affected brain actually enhance the impact of incoming sound waves, by acting much like the crystals found in microphones or radio receivers.
I therefore concluded that BSE, as well as other TSEs, are primarily caused by environmental exposure to one or other of a select group of metal micro-crystals – Barium, Strontium, Manganese or Silver. Each rogue micro-crystal has the potential to act as a nucleator once it successfully establishes itself within the brain. It seeds off an aberrant "cluster bomb" of hyper-crystallization within the tissues – that do not normally require this mode of hyper-mineralisation for their maintenance or function.
The specific species of metal crystal involved in the intoxication determines factors such as the length of incubation period (e.g.; which represents the period of growth of the resulting metal-protein crystal contaminant), the distribution of lesions within the brain, etc. - factors which all combine to determine which specific strain of TSE prion disease will emerge at the end of the day.
My analytical research has found that wherever the key clusters of TSE have emerged around the world , there is a significant source of metal contamination in the local environment which can precisely explain the origins of the outbreak. The rogue metals are either emitted into the atmosphere from naturally occurring sources- via volcanic eruptions or quarrying/extraction of certain rock, coal or oil which are naturally rich in barium/strontium. Or from man made activities that implicate the use of these metals in the steel, glass, ceramic, welding, oil drilling or most importantly, the military munitions industries – also from personal exposures to dental amalgams, surgical instruments (re; the silver in depth electrodes, etc), use of barium swallow in radiographic investigations or silver in water purification, etc.
Use of Barium/Strontium and Silver crystal sprays that are discharged into the upper atmosphere for cloud seeding rainmaking operations, refraction of incoming ultra violet rays or as a radar/radio refraction technique employed by the military during warfare (e.g.; Gulf war 1) or practice operations should also be born in mind as a significant source of potential environmental contamination by these metal nano-crystals .
The Half Lives.
It was my recent research in the USA that has brought me much closer to a clear cut conclusion on the precise causes of TSEs – particularly after I uncovered the fact that deer from the Fort Collins wildlife research facility in Colorado had been deliberately used in experiments to monitor the biological effects of the atmospheric leak of plutonium and other radioactive metals from the infamous Rocky Flats nuclear trigger/weapon factory during the 1960s. By 1967, The first ever recorded case of TSE in a deer had emerged in the same deer facility that was being subjected to this raft of nuclear experiments.
Wherever these radioactive metal components were used – in the missile production factory at Tucson in Arizona, in the missile silos that have impregnated the plains of NE Colorado/SE Wyoming/SW Nebraska , or in the missiles that have been test fired across the White Sands Missile range in New Mexico or Cold Lake air weapons range/Camp Wainwright in Alberta/Saskatchewan, TSEs have invariably broken out in those local deer, sheep or human populations that have been exposed to the atmospheric fall out of these metal micro-crystals. It is a very clear cut correlation.
I have subsequently identified this same correlation between exposure to these munition metals and the vast majority of the outbreaks of TSE around the world. For instance, the largest cluster of new variant CJD in humans is located at Queniborough village in Leicestershire in the UK. This tiny village is sited one mile away from what was the largest munitions factory for the manufacture of detonators, triggers and chemical warfare agents in the UK – at East Goscote. Aerial photos indicate that during the 1950s, the munitions were actually stored along the edge of the lanes around Queniborough itself.
In Italy, I came across a cluster of CJD in humans who were all employed or connected to a munitions factory in the Po valley in Italy during the 1970s; as well as another cluster of 20 cases of CJD in a remote Calabrian village which had resulted from the contamination of the local water source by illegally dumped radioactive metals.
I unearthed another mysterious cluster of scrapie TSE that had emerged in sheep that were kept upon a block of common land at Ashoro in Hokkaido in Northern Japan – land which was formerly occupied by the Japanese military during world war two; where, according to the local farmers, many covert tests were carried out with "munitions". Sheep can no longer be pastured in this region, because they invariably contract scrapie. The correlations between TSEs and exposure to munitions are just too close for comfort.
Rogue Metal Micro-crystals – the seeds of Mad cow Madness.
These observations have lead me to believe that TSEs are caused by exposure to these various metal micro-crystal pollutants. Once these metal crystals are able to leak across the blood brain barrier (facilitated by the presence of other abnormal eco-influences) and penetrate their way into brain cells that are depleted in certain essential minerals (like copper and sulphur), the micro-crystals are then free to opportunistically bond up with certain brain proteins in place of their normal copper/sulphur co-partners, whereupon they subsequently 'seed' the growth of substantial sized metal-protein crystal arrays.
Since the prion protein is a copper bonding protein, it represents one of the proteins that can be successfully targeted and occupied by these invading micro-crystals – but this can only happen at a time when the supply of free copper is disrupted within the brain.
Once the alien micro-crystals become lodged and bonded into the nerve membranes. It is here that they start to multi-replicate themselves, growing into substantial metal-protein crystal structures that form the characteristic aberrant fibril-like features that are seen to hallmark the TSE diseased brain.
I believe that these crystals are 'piezoelectric' in nature; that is to say that they work much like the crystals that are used in microphones. They convert the energy of incoming acoustic sound waves into electrical energy. Thus, once an individual's brain has become contaminated by these rogue crystals, the brain is no longer able to conduct/dissipate the high energy shock-bursts of sound and light that radiate in from the external environment (NB. the presence of these shock-bursts are well evident in the TSE cluster environments).
The incoming energy ends up being absorbed into the rogue crystals, which subsequently convert it into electrical shock bursts, which generate magnetic fields around the crystals, which, in turn, initiate chain reactions of deleterious free radical damage in the surrounding tissues.
The additional impact of the radioactive decay emitted from the metal component of these crystals serves to compound the intensity of the free radical chain reactions. Spongiform neuro-degeneration of the brain ensues – represented by the so called 'halos' or holes of spongiform damage that surround these aberrant fibril structures in the TSE diseased brain.
The piezoelectric crystal facet of this theory is well supported by the classic hypersensitive response of the BSE affected cow to the veterinarians' hand clap test – the customary field test that is applied for diagnosing clinical BSE when a government vet enters the farm to examine a BSE suspect cow. If the cow is genuinely suffering from BSE, the modest shock waves of the hand clap will invariably cause the poor beast to collapse to the floor quivering and bellowing out in writhing agony – just as though the clap had detonated an electric shock-burst inside the cow's brain.
My hypothesis therefore asserts that the rogue metal micro-crystal represents the transmissible, pathogenic agent that underpins the primary cause of TSE diseases. This theory explains many of the missing links in our understanding of the pathogenesis of TSEs. For instance, nobody yet understands why TSE can still be invoked in misfortunate healthy lab animals after they have been injected with the inorganic ash that results from the heating of TSE affected brain material up to temperatures as high as 800 degrees C. How can the various protein-only/microbiological agents that have been ascribed to the cause of TSEs begin to survive these kind of elevated temperatures; and then retain their so called hyper-infectious property thereafter?
But in accord with my theory; the metal crystal nucleator, along with its piezoelectric pathogenic capacity, is well capable of surviving these kind of elevated temperatures, and then being artificially transmitted back into a healthy animal, where they are free to reseed the multi-replication of a pathogenic metal-protein crystal (the fibril) all over again. For the magnetic charge that is permanently captured within these ferrimagnetically ordered crystals will not be drained until temperatures are raised above the respective 'curie point' threshold of the specific metal involved – around the 600 degrees C for manganese. Furthermore, the actual structure of the crystals themselves is retained until temperatures exceed their melting point - which can be as high as 1000 degrees C for some crystal species.
In this respect, my thesis also explains how TSEs can sometimes be successfully transmitted in the real world via blood transfusions or injections of pituitary growth hormone treatments; where the rogue micro-crystals contaminants are transmitted via these injections of TSE affected tissues into the healthy human; whereupon the crystals are free to multi-replicate themselves all over again, ultimately building up substantial sized 'fibril' arrays of metal protein crystal in the fresh host.
It is interesting that metals such as Barium and Strontium are actually exploited in therapeutics for 'seeding' the process of crystallisation in the bone matrix as a means of reversing the wasting of the bones in those who are suffering from osteoporosis. But under conditions of good health, the process of mineralzation within the organism is under delicate bio-regulation; whereby any aberrant crystal growth that starts to run away with itself within the tissues is kept in check. But once this delicate regulatory system is disrupted, then diseases like rheumatoid arthritis, Alzheimer's disease and TSEs are able to proliferate.
The long incubation period experienced in these diseases, can be explained by the protracted period that the metal-protein crystal takes to grow in the brain. Once grown to full size, any subsequent exposure to sonic shocks from the external environmental will jettison the contaminated individual out of the dormancy period, by triggering off the deadly chain reaction of electro-magneto induced radical reactions that create the classic spongiform type of neuro-degeneration that is seen in the TSE diseased brain.
The particular species of rogue metal crystal contaminant that is involved will dictate which specific strain of TSE will emerge at the end of the day.
Other eco-genetic influences must play a role. Besides the exposure to the metal micro-crystal pollutant itself, there must be other abnormal environmental or genetic influences at work in the TSE hotspot locations which compromise the abilities of the local mammalian populations to defend themselves against the uptake and binding of these rogue metals into their brain tissues. In this respect, any healthy, well nourished, mineral balanced individual should be able to mount a viable metabolic defence that prevents both the uptake and binding of these alien micro crystals into their brain
The origins of the UK's BSE epidemic.
In respect of the cause of the massive epidemic of BSE in the UK, I became interested in the possible contributory role posed by the compulsory use of exclusively high doses of systemic acting organo phosphate (OP) insecticides that were used for the control of warble fly during the 1980s/1990s.
It appeared that the all important use of this specific insecticide during the 1980s had increased the permeability of the blood brain barriers of treated cows, thereby disrupting the "front line" of defence that protects the brain against the uptake of alien toxic metals. Furthermore, the chemical structure of the particular dithio-phosphate type of OP used in the UK indicates that it would also act as a chelator of copper (e.g.; would lock up available copper in the tissues), as well as competing for sulphur bonding sites in some of the key proteins - like the copper bonding prion protein and the sulphated proteoglycans - that are implicated in the pathogenesis of TSEs.
All in all, the simultaneous exposure of UK cattle to these OP insecticides during the 1980s would have enabled any rogue metal micro-crystals that contaminated the UK environment at that time to enter the brain and then bind up with these specific proteins in place of their correct metal co partners; thereby initiating the TSE disease process.
The most likely metal micro-crystal candidate that could be held responsible for kicking off the UK's BSE epidemic in November 1986, could stem from the UK's contamination with the radioactive strontium 90 that was showered down in the massive rainstorms that covered North Western Europe shortly after the Chernobyl power station accident in April 1986. In this respect, BSE could have been triggered off in any cow that was simultaneously treated with the high dose OP warblecide whilst it was consuming strontium 90 contaminated pastures.
The OP treatment enabled the strontium 90 to literally flood into the bovine brain; where it subsequently coupled up with the prion and ferritin proteins, which all conjugated together to build the characteristic fibril crystal structures that represent the key abnormal hallmark of the BSE diseased brain.
Countries like France, Ireland, Switzerland, Germany, Portugal, Holland, etc, used much lower doses of a less concentrated OP formulation for warble fly control on their cattle, and, correspondingly, suffered much lower incidence rates of BSE as a result – probably due to the fact that their blood brain barrier function was not so disrupted by the lower doses of OP which they were exposed to.
Likewise, it is interesting that all countries in the southern Hemisphere, like Australia and New Zealand, have not been blighted by any BSE. Perhaps this is because they were not exposed to the Chernobyl fall out , nor has their different climate ever favoured the establishment of any warble fly infestation in their cattle - thereby exempting them from any need to use the systemic OP warble fly treatments.
Much like the cows, humans and cats were also exposed to the systemic acting types of OP which were voluntarily used as head lice and flea shampoos during the hottest period of the Chernobyl contamination. OPs were also used extensively on all food crops. This cocktail of OP contamination would have rendered humans and cats more vulnerable to the uptake of the Chernobyl metals (locked into the proteins within the food-chain) into their brains; thereby explaining the outbreaks of vCJD and BSE in humans and cats across Europe.
According to my research, the substantial drop off in the incidence rate of BSE during the late 1990s is due to a combination of dynamic environmental factors;
The virtual eradication of the warble fly - with a corresponding cessation of use of the OP warble fly insecticides over this 1990s period .
The gradual decay in the radioactive half life of the metals emitted from the 1986 Chernobyl atmospheric leak.
Furthermore, cows that are more susceptible to these environmental challenges, and are therefore more susceptible to developing BSE, will have been killed out by the BSE epidemic itself ; leaving the less susceptible animals alive that are less likely to succumb to BSE in the future.
The supportive data.
Apart from the academic publication of my own environmental analytical data on the elevation of manganese, barium, strontium or silver/deficiencies of copper ,etc, in the TSE cluster ecosystems and more recently in the antlers of TSE affected deer, some follow up laboratory studies were conducted which also provided positive support for my hypothesis.
For example, cell culture experiments were performed at Cambridge Uni by Dr David Brown who showed that the prion protein deformed into its abnormal shaped, protease resistant conformation (the form that hallmarks the brains of those who have died of TSEs) after the cells were loaded with manganese (one of the metals that I observed at high level in some of the TSE cluster zones) and starved of copper. The actual aberrant bonding of manganese onto the prion protein - in place of copper - was considered responsible for misfolding the protein into its abnormal conformation. This work was published in the journal of the European molecular biology association.
Another study at the US Prion disease surveillance centre at Case western Uni, Ohio, demonstrated that CJD affected brain material contained a ten fold elevation in manganese and a 50% reduction in copper in relation to the brains of those who had died of non-neurological disorders. This work was published in the Journal of Biochem.
Further work was conducted in Japan at Kobe Uni, where exposure of manganese bonded prion protein to specific wavelengths of light had caused the metal proteins to aggregate into the aberrant fibril structures that hallmark the brains of TSE victims.
And finally, a catalogue of Government Lies...
Sadly, in choosing to ignore the true causes of these grotesque diseases, the British government remains blatantly negligent in its duty to safeguard the health of its own people and environment. Furthermore, whilst remaining fully aware of the major flaws in their own official theory, the government remains criminally negligent in trying to deceive the rest of the world over the so called 'viability' of their deeply flawed and failed hypothesis.
Mark Purdey - August 27th 2004
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REFERENCES;
Purdey M; Elevated silver, barium and strontium in antlers, vegetation and soils sourced from CWD cluster areas; Do Ag/Ba/Sr piezoelectric crystals represent the transmissible pathogenic agent in TSEs ? Medical Hypotheses 2004 63: 211-225
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; 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.
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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.
