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The wasting lands - The CWD epidemic in deer

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The WASTING LANDS - Page 3

Infrasonic shock waves, high manganese, low copper; what’s the connection with CWD ?

Whilst there seems to be a correlation between the presence of this package of environmental toxic denominators and  the timing and distribution of CWD outbreaks in the USA, how can all of these factors prove relevant to the cause of these mystery spongiform lesions found in the brains of the victims of these diseases?.

An alteration in the normal molecular shape of a specific brain protein, known as the prion protein, has been shown to be a critical deciding factor in the development of TSEs; since a deformed prion protein hallmarks the brains of all those mammals who have died of TSEs, perhaps indicating that some loss of function of this protein is all part and parcel of the TSE disease process.  Intriguingly, the prion protein has been shown to bond up with copper in the normal healthy brain, and I have hypothesised that the copper found attached to the prion protein plays a role in conducting the electromagnetic energy that is received from incoming sources of  ultraviolet, geomagnetic, infrasonic radiations, etc, form the external environment. These energies are utilised for the bodies own balanced metabolism; for regulating circadian mediated functions such as immune defence, growth and repair of cells, sleep/wake cycles, etc.

But when copper is in short supply in the brain, due to certain environmental influences, the prion protein is capable of bonding onto certain alternative metals, such as manganese, bismuth or silver. But these foreign substitutes may not act in the overall best interests of the organism. For instance, manganese will store up electro energy instead of conducting it like copper; thereby blocking the flow of electromagnetic energy that is required for regulating certain vital body functions.

But one of the specific characteristics of manganese is that it can absorb the energy of sound – such as the high intensities of ‘phonon’ energy that are insidiously radiated with the inaudible low frequency range of sound, known as infrasound. But manganese can only absorb this energy when found in its specific ‘trivalent’ manganese form; whereupon the sound energy actually metamorphoses the atomic structure of the manganese so that it can become permanently magnetised. So whenever an individual who is carrying excessive levels of this freaky form of trivalent manganese in their brains enters into an external magnetic field, the manganese bonded prion proteins become permanently magnetised to explosive flash point levels; whereby self perpetuating, chain reactions of free radical mediated neurodegeneration burst forth, and TSE pathogenesis ensues.

Whilst high intensities of trivalent manganese may be ‘manufactured’ in the living brain via an ‘oxidative transformation’ of manganese 2+ in the retina by incoming ultraviolet radiation or other eco-oxidants, etc, it is also possible that an exclusive source of trivalent manganese has got into the food chains in TSE endemic areas; via its incorporation into animal feeds or mineral licks, etc, or via their natural presence in the indigenous geological bedrock of the TSE region. Such a scenario may explain why hunters who are feasting off deer shot in CWD regions who have thrived off mineral licks/pine needles containing trivalent manganese, will, in turn, become contaminated with trivalent manganese themselves; and thereafter rendered hyper susceptible to the low frequency infrasonic shocks in their hunting environment (eg; natural infrasound, rifle shots, etc ).The same eco-prerequisites that caused CWD in the deer are now primed and present in the human hunter. CJD could result. 

Not only has this abnormal mineral imbalance been consistently identified in all of the ecosystems blighted by clusters of TSE, but studies on the brains of CJD casualties by Case Western University’s US Prion Disease Surveillance Unit have identified a 10 fold higher level of manganese and 50% reduction of copper in relation to control brains. Furthermore, Dr David Brown at Cambridge University in the UK has produced the TSE-like malformed prion protein in cell culture experiments after adding manganese to copper deprived cells.

Despite publication of all of these complementary field and laboratory studies in prestigious scientific journals, the various European health authorities and their key TSE advisors are blindly ignoring these findings. Not only are they discarding such an important fresh direction in TSE research, but they are doing their utmost to  publicly marginalize those of us who are trying to pursue this line; and using public money to implement their tactics of suppression into the bargain!

The Genetic Connection.

Whilst it is true that all types of TSE require components of genetic susceptibility in their causal interplay, the TSE susceptible individual still very much requires the additional exposure to these toxic environmental factors before the disease can ever begin to manifest itself; Witness, the large number of scrapie susceptible sheep that live in scrapie-free Australia but never develop the outward symptoms of scrapie. Yet whenever Aussie sheep are exported to countries where scrapie is endemic, symptoms of scrapie invariably break out - presumably because the environmental causal factors are absent in their native Australian terrain, yet fully present in the importing countries.

The same scenario is duplicated in respect of a CJD susceptible Greek-Italian population that lives in many regions across southern Italy. But CJD has only ever erupted (at an excessive incidence rate) in just one of the many hamlets where these people live - a hamlet that is exclusively exposed to the specific environmental prerequisites that initiate TSE.

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Last updated 02-Apr-2007