My observations of high manganese/low copper in TSE cluster areas lead to my connecting with the pioneering laboratory investigations of Dr David Brown at Cambridge University in the UK; a widely published biochemical expert who had pursued ground breaking studies which had elucidated interesting new facets of the elusive prion protein.

So David Brown ran the necessary cell culture experiments where he introduced manganese into copper depleted prion protein cell cultures. Amazingly, his experiments produced the key deformation of the prion protein which the earlier tests using OPs at the Institute of Psychiatry had failed to create. These experiments represented the first time that malformed prion protein had been created experimentally as a ‘de novo’ transformation.

Furthermore, follow up trials by the USA’s Prion Surveillance Centre at Case Western University (Cleveland) looked at post mortem tissue samples taken from CJD brains. Their analyses revealed the same abnormal mineral ratio as identified in the TSE cluster environments; a tenfold higher level of manganese and 50% reduced levels of copper in relation to control brains. Interestingly, the manganese was bonded to the abnormal prions in these CJD tissues.

It seemed that the basic cornerstone of the environmental theory was beginning to establish itself, and an overall picture of the pathogenesis of this disease was panning out. That a high manganese/low copper imbalance somehow compromised the brain’s ability to deal with acute shock bursts of sound and light – the other common characteristics of TSE ecosystems.

My investigations indicated that the traditional forms of TSEs - which tend to surface in elder mammals - represent a less intensive mode of exposure to naturally occurring environmental influences which bring about a high manganese/low copper ratio in the mammalian brain. Whereas, the more aggressive ‘rapid attack’ modern strains of TSE, BSE, vCJD , can be explained by the current trend of increased mammalian exposure to a modern cocktail of man made pollutants involving manganese compounds and copper chelating chemicals (the warble fly and head lice OP insecticides). These penetrate into the central nerves and give rise to the more virulent, accelerated version of TSE, where full blown symptoms of TSE erupt in much younger mammals than normal.

But unfortunately the abnormal shaped prions, which Brown’s high manganese/low copper experiments had created, had failed to demonstrate the bizarre ‘infectious’ multi-replicating property that has been associated with the fully fledged prion in the TSE diseased brain. Could the further infrasonic shock factor that I had identified in the TSE cluster regions fulfil this final missing piece in the causal jigsaw? Perhaps some ‘shock-induced’ quantum facet of the manganese atom may provide that final clue.

Modern health authorities could learn a lesson from the alchemists of the Byzantine era who regarded manganese as the black magic metal; whereby the quantum capacity of manganese to absorb light and sound energy, can induce a lethal ‘Jekyll and Hyde’ style conversion of this metal from innocuous to toxic form.

Interestingly, the initial pathological damage of TSE is manifested within the retina, eyelid, skin, auditory and optic nerve endings of the diseased mammal - areas that perform a front line role in neutralising the deleterious effects of incoming sound and light from the external environment. Furthermore, the normal copper bound prion protein is exclusively manufactured in these same tissues; the retina, spleen, lymphatic, tonsils, gut membranes, growth/repair cells, myocardium, pineal, visual cortex, pituitary, sympathetic neurones, etc – tissues whose metabolism is regulated by the circadian daylight/darkness rhythm.

Lab animals cruelly subjected to GM prion protein ‘knock out’ experiments, have demonstrated that they are no longer able to regulate their sleep, sex and immune cycles – a sick way of demonstrating the role of the prion protein in mediating the circadian rhythm.

The simple fact that copper is employed in electric cables for conduction of electrical energy, whereas manganese is employed in batteries for storing up electrical energy, offers a feasible explanation for both the function/dysfunction of the prion protein, as well as the cause of TSEs;

Perhaps the copper element of the normal healthy prion protein plays a role in the conduction of electromagnetic energy along the circadian/auditory pathways of magnetic super-exchange; where a linear chain of paramagnetic copper atoms (bonded to prion proteins) provides a ‘metal to metal to meta’ motorway which distributes the energy of light and sound around the body for energizing the cycles of sleep, sex, behaviour, heart beat, cell growth/repair and immune response.

Whereas the abnormal manganese prion serves to block these pathways of electromagnetic super-exchange; by storing up that electromagnetic energy to a level where the critical threshold of ‘flash point’ is exceeded; thereby detonating off neuro-pathogenic cluster bombs of free radical chain reactions that progressively degenerate the circadian pathways of the brain – and cause TSE.

In this respect, the blockage of the electromagnetic energy flow by such a manganese replacement of copper can precisely account for the clinical and pathological profiles of the TSE disease process.

It could be said that the discovery of the function of the prion protein may turn out to give further scientific substance to the existence of the electromagnetic meridians recognised by Chinese medicine - where the healthy copper prion performs a regulatory role in maintaining the electro-homeostatis along the acupuncture meridians and nodes.

Whilst David Brown’s manganese experiments had created the infamous deformed prion protein, they had failed to produce the all important pathogenic, ‘infectious’ prion. Furthermore, manganese is a paramagnetic metal (eg; a metal that can be temporarily magnetised) just like copper, so to some extent you would expect the manganese to effectively substitute for the electromagnetic conduction function of copper without too much negative repercussion. Perhaps some further modification of the manganese atom initiates a pathogenic capacity that is capable of kicking off the full blown pathogenesis of TSE?

So if atmospheres or soils containing manganese 3+ atoms are exposed to high intensities of infrasonic shock energy, the low frequency vibrations are capable of metamorphosing the actual atomic structure of the manganese atom itself, creating a kind of ‘Jekyll and Hyde’ like transformation of manganese from its normal paramagnetic to rogue ferri-magnetic form; eg from a temporary to permanently magnetiseable form.

Once an ecosystem has been infra-sonically adulterated, any manganese 3+ minerals that have been exposed to the full force of infrasonic shock – from military explosions, supersonic over-flights, volcanic and tectonic eruptions, etc - would leave a permanent legacy of rogue ferri-magnetic manganese atoms that are free to infiltrate the food chain; thereby contaminating any mammalian population that is self sufficient upon the local ecosystem in the years to come. If these adulterated food chains are simultaneously short of copper, then the mammalian population is put at high risk of developing TSE.