Infrasonic Discussion

One of the superficial difficulties surrounding the viability of the ‘supersonic’ facet of this nvTSE origin hypothesis, is the approximate 10 year delayed lag period between the start of the first routine Concorde flights to JFK in 1976 (130) and the onset of the first reported cases of BSE in 1986 (1).

There are obviously many theoretical scenarios that could be generated involving the possible aetiological involvement of an infrasonic shock induced mutation in some cell line or other which did not manifest itself in a clinical capacity until the succeeding generation; as is the case with ionising radiation. But, relative to this theory, the delayed lag could be explained by the fact that the ‘infrasonic’ seeding of the first metamorphosed Mn rogue prions took place during the susceptible ‘in utero’ period, where the ‘infrasonic’ seeded bovine/human embryos would fail to develop the full blown clinical phase of the disease until adult life – after a protracted, so called ‘incubation period’ of free radical mediated neurodegeneration had gathered sufficient pathogenic momentum to enable the clinical phase of TSE to emerge.

However, It seems more plausible to suggest that additional causal prerequisites which increase mammalian sensitivity to infrasonic shock need to simultaneously come into play before TSE pathogenesis is initiated. In respect of the theory under discussion, the compulsory ‘high dose’ usage of the copper chelating warble fly insecticides which did not get underway until the start of the 1980s in the UK (6) (in combination with Mn supplementation in feeds), rendered the brains of cattle more susceptible to this class of infrasonic shock from the external environment.

A more nightmarish scenario could envision that the intense energy of infrasonic shock vibrations from jet over-flights had actually modified the atomic structure of trivalent Mn compounds in the open environment (in top soil, vegetation, etc), transforming these into their rogue ferrimagnetic form; thereafter rendering any Cu deficient livestock/human susceptible to TSE after ingestion/inhalation of these rogue Mn atoms from the infrasonically adulterated ecosystems.

A SPATIAL CORRELATION BETWEEN THE TECTONIC PLATE RIFT LINES AND CLUSTER LOCATIONS OF SPORADIC / FAMILIAL TSEs

(See map 3)

Clusters of sporadic/familial TSEs investigated in N Iceland, NE Colorado, Mt Horeb (Wisconsin), Fuji (Japan), Slovakia, Calabria, Sicily, New Quinea,etc. (4)(5)(142)(112)(113)(114) all lie over major seismic belt/tectonic plate rift lines in common. (108)(115). In fact, the offshoots from major plate margins, such as the infamous “ring of fire” and the mid Atlantic rift, seem to demarcate locations of traditional TSE clusters with remarkable fidelity. See map 1. Furthermore, the clusters often appear at specific locations on the plate boundaries where tectonic activity has historically given rise to intensive bursts of geomagnetic energy and seismic waves which radiate infrasonic energy (104)(99) via volcanic eruptions, (106), earthquakes, (107), geothermal extrusions, (99), thunder and lightning storms, etc.(102) See chart 1. Significant Earthquake activity has been recorded at every traditional TSE cluster location over the years.

Such a correlation gives credibility to the age old shepherds’ anecdote which decrees that sheep will contract clinical scrapie after they have been exposed to a thunder and lightning storm! (1) As mentioned previously, these TSE locations are all sited in the key topographical landforms- such as parabole mountain valleys – which can serve as acoustic radiators or beacons; where amplification of infrasonic radiation results from incoming prevailing waves converging through ‘wind tunnel’ type locations. (109)

FUTURE RESEARCH.

Insight into the primary causal mechanisms underpinning the pathogenesis of TSE would enable the development of the most effective means of prevention, control and pharmaceutical cure for these diseases.

In this respect, a major extensive research programme needs to be executed into re-testing/expanding the pilot observations cited in this paper. Furthermore, research that assesses the straightforward application of copper, selenium and zinc as a preventative treatment for TSEs should be put to test on domestic/wild livestock grazing in TSE risk cluster areas; where Cu and Zn would serve as a means of protecting PrP’s Cu domain (20)(21) against invasion by foreign cations, as well as ensuring an optimum supply of antioxidant activators in animals who would otherwise find their CNS unable to defend itself against the hyperoxidative assault by external environmental oxidants.

Furthermore, electrophilic-electron acceptor pharmaceuticals, such as the porphyrin molecules (57), could be employed to target manganese bonded to PrP’s histidine ligands and act as an electron acceptor; thereby reducing the potentially pathogenic Mn3+ prion back to its sleeping, innocuous Mn2+ prion form. Pharmaceutical chelators that are specific to Mn, etc, could also be tested as a means of reducing the load of Mn in the CNS.

Factors such as the polarisable susceptibility and resonance of the ‘metamorphosed’ Mn atoms bonded to prions in TSE is of critical importance when considering factors controlling ‘the duration of incubation period’ and ‘severity of symptoms’ in the TSE disease process. Therapies which could somehow depolarise or destabilise the magnetic charge of the foreign metal species bonded to pathogenic prions could be developed as a means of treating TSE .

Above all, surveillance programmes should be instigated which conduct analyses for the full range of metals present in TSE affected brain material as a matter of urgency. Such a programme could quickly identify the precise metal species that serves as the critical co-partner on the pathogenic prions in the different strains of TSE.

Comparative spectroscopy studies of the magnetic status of specific metals drawn from top-soils exposed to infrasonic shock vibration and metals drawn from top-soils in supersonic turbojet-free regions would make an interesting study. Furthermore, Mn 3+ prion cell cultures could be exposed to infrasonic shock waves to gauge whether infectious pathogenic prions are generated as a result.

Preventative treatment could be put to good effect at the basic level of farm/soil husbandry, where leaching of copper, zinc and selenium from soils could be stemmed by reducing irrigation and maintaining sufficient levels of humus and organic matter in soils. Also reduction of soil acidifying artificial nitrogen fertiliser applications, sewage spreading and mechanical compaction of soils could stem the build up of ‘available’ Mn and molybdenum (Cu conjugating) in the soils.

Removal of the types of systemic insecticide which directly chelate Cu or disrupt Cu binding to proteins could be instigated. More importantly, removal of Mn inclusions from calf milk replacer powders, free access mineral licks and concentrate feeds, etc, could virtually eliminate BSE.

Curtailment of low flying military/concorde over-flights over livestock/human populated regions would also assist in the reduction of TSEs, along with modifications to the design of their afterburner turbojets so that the, as yet unrecognised, specific ‘Mn3+ resonating’ toxic frequency of infrasound can be eliminated.

In consideration of the growing number of positive results of ‘in vitro’ laboratory trials that have confirmed the high Mn3+/low Cu/oxidant aspects of this TSE environmental origin theory (41)(43) (44)(45), as well as the positive recommendations made by the BSE Inquiry in respect of supporting this theory (7), the continued refusal of the various UK government departments to award grant support, let alone encourage research/debate into the environmental perspectives of TSEs is little short of gross negligence.

Mark Purdey - 2002

ACKNOWLEDGEMENTS - to Holly Purdey for secretarial assistance.

REFRERENCES -

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