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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)/low 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 ferromagnetic 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 ultra violet, 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.
INTRODUCTION
Flaws
in the conventional consensus on the origins of BSE.
The
conventional consensus on the origins of TSEs maintains that these
diseases are caused by “hyperinfectious” malformed PrP that is
capable of converting healthy PrPc into abnormal, protease resistant
prions in the mammalian brain (1). Advocates of this theory propose that
these so called ‘prions’ can be transmitted horizontally in the
external environment via animal to animal contact or via ingestion of
TSE diseased/prion contaminated brain tissue. But no evidence exists to
substantiate this speculative, yet universally held belief.
Environmental
perspectives of TSEs have been entirely excluded by research programmes
to date. Such a mindset dismissal has largely been based on the fact
that TSEs can be transmitted via injection of TSE affected brain
homogenate into TSE-free healthy laboratory animals (1). But in the
light of the fact that certain other neurodegenerative diseases, (eg;
familial Alzheimer’s) can be transmitted in this way (2), why don’t
we view these other conditions with the same degree of
‘hyperinfectious’ paranoia that has been misattributed to TSEs?
Furthermore,
BSE fails to fulfil Koch’s postulates(3) – the yardstick for
determining whether an ‘infectious’ agent underpins the aetiology of
a given disease. Despite these major discrepancies, the notion that
Bovine Spongiform Encephalopathy (BSE) was caused by scrapie infection
became cemented as ‘gospel’ into mainstream professional and public
mentality.
An
impartial study of the epidemiology of BSE/vCJD suggests that the
conventional consensus on the origins of BSE/vCJD is severely flawed
(4)(5)(6) for the following reasons;
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Scientific
papers - The origins of BSE?
