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The Origins of BSE - 

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Scientific papers - The origins of BSE?




Mark Purdey  

Journal of Cattle Practise (Journal of the British Cattle Veterinary Association)
2002, Vol 10 , Part 4, p 311-335.


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.


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;

1. BSE has failed to surface in the cattle populations of the Middle East, India, Africa, North America, Third World countries, etc, despite these countries receiving substantial tonnages of the BSE incriminated meat and bone meal (MBM) imported from the UK from the 1960s onwards (7). UK MBM was exported either in its straight feed form or as an inclusion in cattle concentrate feeds (7).

2. 40,000 + cases of BSE have erupted in UK cows that were born after the 1988 ban on MBM entering cattle feed, and more recently, 22 cases of BSE have erupted in cows born after the 1996 ban on MBM going into animal feeding stuffs designated for all types of domestic animal (8). Furthermore, some BSE endemic countries have experienced a greater total number of BSE cases in cattle born after their respective MBM bans than in cows born before.

3. There have been no reported cases of BSE in TSE susceptible species, such as  sheep and goats (8), despite the customary inclusion of an MBM protein source in  their concentrated feeds.

4. Four of the original five Kudu antelopes which contracted BSE at the London Zoo  had no possible access to feeds containing MBM (9).

5. BSE erupted in four cattle that were raised on MAFF’s  former Liscombe  experimental farm on Exmoor – a beef suckler farm which was designed to raise  beef from an all grass/silage system without any resort to purchased in concentrate  feeds (personal communication; M. Stanbury, formerly ADAS, Quantock House, Taunton, UK.)

6. Alterations in the rendering of MBM (cessation of solvent extraction, lower temperatures) from the batch to the continuous flow system had purportedly  enabled the survival of scrapie agent in UK MBM, thus initiating the outbreak of BSE (10). However several scrapie endemic countries, such as the USA and Scandinavia, had also adopted these same BSE-causing prerequisites into their  rendering systems (11), yet these countries remain BSE-free to date (8). 

7. Several US trials failed to invoke BSE in cattle after feeding or injecting massive doses of scrapie-contaminated brain homogenate (12)(13).

8. The UK’s mechanically recovered/processed beef products and baby foods –  blamed for causing vCJD in humans – were exported worldwide to countries where  the practise of “skull splitting” in small rural vCJD has never erupted. Likewise, butchers were offered as an explanation for the growing number of vCJD clusters in  rural areas. But this practise had been adopted universally by rural/urban butchers across the UK.  

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