British Cattle Veterinary Association journal
CATTLE PRACTICE VOL 10 PART 4, 2002
The Manganese Loaded Copper Depleted Bovine Brain Fails to Neutralise Incoming Shockbursts of Low Frequency Infrasound: The Origins of BSE?
Purdey M., Elworthy, Somerset, UK.
ABSTRACT
Intensive exposures to natural and artificial sources of infrasonic acoustic shockwaves (tectonic disturbances, supersonic turbojet aeroplanes. etc.) have been observed in ecosystems supporting mammalian populations that are blighted by clusters of traditional and new variant strains of transmissible spongiform encephalopathy (TSE). But TSEs will only emerge in those 'infrasound-rich ' environments which are simultaneously predisposed to specific environmental factors that induce a high manganese (Mn) /1ow Copper (Cu) /low zinc (Zn) ratio in brains of local mammalian populations. Cellular prion protein (PrPc) is a Cupro-protein expressed throughout the circadian - vestibular pathways of the body. It is proposed that PrP's Cu component performs a role in the conduction and distribution of electromagnetic energy that has been transduced from incoming ultraviolet, acoustic, geomagnetic, etc, sources of radiation. TSE pathogenesis is initiated once manganese replaces copper, whereupon the piezoelectric manganese atoms absorb and blockade that energy flow instead of conducting it. The epidemic of BSE in the UK resulted from the combined simultaneous exposure of the bovine to three environmental factors : Cu chelating insecticides, Mn inclusion in milk replacer / mineral blocks, and intense infrasonic shock waves from turbojet aircraft. Compulsory, exclusive high dose formulations of systemic phosmet warblecides penetrated the CNS and deprived PrP of its copper component, enabling the excesses of Mn to substitute at the vacant Cu domain on PrPc resulting in the formation of a non pathogenic, protease resistant, trivalent Mn3+ PrP isoform. The final stage of pathogenesis comes into play, once a low frequency wave of infrasonic shock metamorphoses the atomic structure of the Mn3+ component of the prion, thereby 'priming' the sleeping prion into its fully fledged, pathogenic TSE isoform - where the paramagnetic status of the Mn 3+ atom is transformed into a stable ferrimagnetic lattice work, due to the strong electron-phonon coupling, specific to the trivalent Mn species. The so called "infectivity" of the prion is a misnomer and should be correctly defined as the magnetic / "reactive" free radical generating capacity of the Mn3+ component of the prion, which remains active at all temperatures below the 550 degree "curie point". TSE can be likened to a solar charged battery on continuous charge where the Mn contaminated /Cu depleted circadian pathways absorb and pile up, rather than conducting the vital life force energies of incoming ultraviolet, acoustic and geomagnetic radiation. Instead of harnessing these energies for the body's own bio-rhythmic requirements, an infrasonic shock induced metamorphosis of the Mn atom intervenes, initiating an explosive free radical mediated pathogenesis that perverts the healthy, pathways of sound and light. Cu prions are replaced by 'hyperpolarized' Mn prions that seed self perpetuating 'cluster bombs' of radical mediated neurodegeneration. TSE ensues.