Mike
Well-known member
But, but, but, what does that have to do with cows, reader? :wink:
Sound familiar?
Sound familiar?
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Vertical Transmission of BSE Research
- Thread starter Mike
- Start date
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SASH
Well-known member
Yeah, good thing I'm not raising mice for a living. :roll:
Mike
Well-known member
SASH said:Yeah, good thing I'm not raising mice for a living. :roll:
Sash, there is a lab mouse grower just across the river from me! One of the Mayo's of the Mayo Clinic owns it.
Wonder if he sells them by the pound? :???:
They are not all white, they got some angus and holsteins too. :wink:
SASH
Well-known member
Mike said:SASH said:Yeah, good thing I'm not raising mice for a living. :roll:
Sash, there is a lab mouse grower just across the river from me! One of the Mayo's of the Mayo Clinic owns it.
Wonder if he sells them by the pound? :???:
They are not all white, they got some angus and holsteins too. :wink:
Well, I can see a few problems with that. If the mother rejected them, they'd be a heck of a thing to bottle feed and I wonder what you'd use if you had to tube feed them. I also imagine when it came time to castrate, that would be quite a chore, too. :lol:
rkaiser
Well-known member
:roll: Well reader, you're so bound and determined to show that BSE is infective; why don't you donate your dog for experimental purposes? One step closer to a cow than a mouse. Step this thing up a notch; maybe you can have proof before you're 6 feet under.
Sandhusker
Well-known member
SASH said:Mike said:SASH said:Yeah, good thing I'm not raising mice for a living. :roll:
Sash, there is a lab mouse grower just across the river from me! One of the Mayo's of the Mayo Clinic owns it.
Wonder if he sells them by the pound? :???:
They are not all white, they got some angus and holsteins too. :wink:
Well, I can see a few problems with that. If the mother rejected them, they'd be a heck of a thing to bottle feed and I wonder what you'd use if you had to tube feed them. I also imagine when it came time to castrate, that would be quite a chore, too. :lol:
You could brand with a bic lighter and a paperclip, though. :lol:
SASH
Well-known member
Sandhusker said:SASH said:Mike said:Sash, there is a lab mouse grower just across the river from me! One of the Mayo's of the Mayo Clinic owns it.
Wonder if he sells them by the pound? :???:
They are not all white, they got some angus and holsteins too. :wink:
Well, I can see a few problems with that. If the mother rejected them, they'd be a heck of a thing to bottle feed and I wonder what you'd use if you had to tube feed them. I also imagine when it came time to castrate, that would be quite a chore, too. :lol:
You could brand with a bic lighter and a paperclip, though. :lol:
:lol: :lol: :lol:
Kathy
Well-known member
In Dr. David Brown's research (with mice) called, "Metal Imbalance and compromised antioxidant function are early changes in prion disease",
The doc shows how after intracranial inoculation with prions, the level of manganese in the brain, liver, muscle and blood, all increase compared to control mice. A representative group of mice (5) were killed every 30 days and tested.
In the brain manganese levels peak at 105 days,
" " liver " " at 90 days, and again at 160 days
" " muscle " " at 150 days, and
in the blood manganese levels peaked at 60 days.
"Visible clinical signs became apparent from 125 days post-inoculation and continued until 160 days, when all remaining mice were killed at the terminal stage of the disease."
During the experiment, copper levels in the brains of the inoculated mice dropped well below the controls and reached the maximum lowest measurement at 150 days.
Quote, "Our findings in the present study are the first report of a neurodegenerative disease in which there is a systemic change in manganese."
Superoxide dismutase activity was also measured. This enzyme acts as an antioxidant and protects cells from free radicals.
SOD1 - a copper/zinc SOD activity
SOD - a manganese-SOD activity
Quote, "...copper/zinc SOD activity was significantly reduced compared with controls, whereas manganese-SOD activity in prion infected brains was increased. Collectively, these data show that whereas protein expression levels of both copper/zinc-SOD and manganese-SOD are not altered by prion disease, the activity of these enzymes is affected."
As for maternal tranmission.... What is being transmitted via the placenta to the unborn animal is not identified as prions, as prions include the glyco-anchor which permanently attaches them to the cell membrane in order to cause cell death.
There appears to be carrier proteins, or portions of proteins (markers) which transport manganese to the brain and later other parts of the body. Simultaneously copper levels in the brain are dramatically reduced. Prions are not carrying these metals in the blood. Prions are attached to the nerve cell membrane.
Metal ions can attach to amino acids, or they can disperse in the body in their most basic ionic form.
If you read Dr. David Brown's study you will learn alot about the importance of copper to our brains, and its role as an anti-oxidant within various enzymes, etc.
There is a very strong probability that these findings above, can explain what it happening during maternal transmission of intracranially inoculated lab mice.
The doc shows how after intracranial inoculation with prions, the level of manganese in the brain, liver, muscle and blood, all increase compared to control mice. A representative group of mice (5) were killed every 30 days and tested.
In the brain manganese levels peak at 105 days,
" " liver " " at 90 days, and again at 160 days
" " muscle " " at 150 days, and
in the blood manganese levels peaked at 60 days.
"Visible clinical signs became apparent from 125 days post-inoculation and continued until 160 days, when all remaining mice were killed at the terminal stage of the disease."
During the experiment, copper levels in the brains of the inoculated mice dropped well below the controls and reached the maximum lowest measurement at 150 days.
Quote, "Our findings in the present study are the first report of a neurodegenerative disease in which there is a systemic change in manganese."
Superoxide dismutase activity was also measured. This enzyme acts as an antioxidant and protects cells from free radicals.
SOD1 - a copper/zinc SOD activity
SOD - a manganese-SOD activity
Quote, "...copper/zinc SOD activity was significantly reduced compared with controls, whereas manganese-SOD activity in prion infected brains was increased. Collectively, these data show that whereas protein expression levels of both copper/zinc-SOD and manganese-SOD are not altered by prion disease, the activity of these enzymes is affected."
As for maternal tranmission.... What is being transmitted via the placenta to the unborn animal is not identified as prions, as prions include the glyco-anchor which permanently attaches them to the cell membrane in order to cause cell death.
There appears to be carrier proteins, or portions of proteins (markers) which transport manganese to the brain and later other parts of the body. Simultaneously copper levels in the brain are dramatically reduced. Prions are not carrying these metals in the blood. Prions are attached to the nerve cell membrane.
Metal ions can attach to amino acids, or they can disperse in the body in their most basic ionic form.
If you read Dr. David Brown's study you will learn alot about the importance of copper to our brains, and its role as an anti-oxidant within various enzymes, etc.
There is a very strong probability that these findings above, can explain what it happening during maternal transmission of intracranially inoculated lab mice.
rkaiser
Well-known member
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
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
