Daylight on TSEs - the deadly oxidative connection unleashed.
But each time Purdey's trek took him to a newTSE hotspot, he found himself face to face with the same type of high altitude, snow covered terrain. But this common geographical association with TSEclusters continued to baffle him; each time recounting the memory of his first glimpse of chronic wasting countryside of deer and elk - the snow peaked Rocky Mountains sawtoothing the july skyline beyond the Denver Plain. But after arriving at the Calabrian village where 20 cases of CJD have emerged since 1995, the relevance of this geographical connection to TSE finally gelled. The houses in this village were newly constructed out of hideous bright white concrete sections - unusual for this area. All were couched within a parched, glaring landscape of bare white sandstone, producing all the criteria required for a most intensive ultra violet (UV) hotspot location; immediately connecting Purdey to the well recognised ëhigh UVí nature of high altitude, snow covered terrain which he found in common in the Icelandic, Colorado, Slovak clusters, etc, that he had surveyed. The UV prerequisite also explained other missing links in the science of traditional TSEs - such as the way in which initial pathological damage of TSE manifests itself within the retina or the eyelid or skin. Plus the fact that the normal , healthy form of copper bound prion protein is located in the pathways which coduct the electromagnetic energy of ultraviolet light around the brain - eg , the retina, pineal gland , visual cortex, hypothalamus, pituitary, brain stem, etc. Prion protein is also found in other areas of the body which are involved in the conduction of electromagnetic energy; for instance around glial cells and proliferating cells involved in the growth and repair of some tissues. In this respect, it could be said that the discovery of the prion protein may turn out to give scientific substance to the existance of the electromagnetic meridians recognised by Chinese medicine - where the healthy copper prion maintains the electro-homeostatis along the meridians. The fact that copper has an industrial use for conducting electricity in wiring and manganese has a use for storing electricity in batteries / Light bulb filaments elucidates a possible explanation for the cause of prion diseases; whereby the healthy copper prion continues to conduct the vital energy of sunlight along the circadian pathways in the brain to propel the sleep. sex, behavioural cycles,etc., whilst the unhealthy manganese contaminated prion serves to blockade and store up that UV energy to a critical flash point level ; where cluster bombs of free radical neurodegerative chain reactions are forced to burst forth . Could the oxidizing impact of UV at the retina convert the accumulated store of manganese ( both manganese and prion protein tend to accumulate in the retina ) from its innocuous manganese 2+ antioxidant form into its lethal manganese 3+ prooxidant form ? So any manganese that is abnormally attached to the prion protein in the retina finds itself switched from a safe to lethal form. Does the oxidising effects of UV therefore serve to unleash a lethal ë Dr jekyll and hydeí like property of the prion protein, which, in turn, kicks off a whole chain reaction of free radical mediated assault on the central nerves ? A neurodegenerative ëmelt downí of neurones proliferates, and TSE ensues. This has explained the genesis of the traditional strains of TSE, but what about the causes of the much more aggressive modern day strains of TSE ( BSE, vCJD ) surfacing in younger mammals. Perhaps these could result from our increased modern day exposure to the more potent oxidizing effects of a cocktail of man made agents which penetrate the central nerves - such as the systemic organophosphates (head lice shampoos, warblecides, etc ), radar, ozone, increasing UV due to stratospheric ozone depletion, microwave mobile phones, Concordeís supersonic waves-,thereby serving as the lethal oxidative triggers which produce a more virulent, accelerated version of TSE with full blown symptoms erupting in much younger mammals than normal. TSEs could therefore be viewed as diseases that result from a breakdown of oxidative homeostatis within the organism ; where TSE susceptible mammals living in environments characterised by high intensities of manganese and oxidising agents and by low levels of antioxidant metals (Copper/ selenium/ zinc ) combine to create circumstances where the central nerves are hyperoxidized - thereby kicking off a free radical chain reaction that can proliferate in the absence of antioxidant defence The pattern of emergence of traditional and new variant CJD clusters in rural/coastal as opposed to urban areas substantiates this idea, as well as helping to dispel the myth that vCJD arises from ingestion of BSE affected beef products - products that are consumed equally by urban and rural populations alike. Rural / coastal areas have become increasingly exposed to a toxic cocktail of oxidizing agents such as UV, ozone or systemic crop sprays in recent years; whereas town environments have ironically been spared. This is largely due to the shield of smog which envelopes the majority of urban airspace and scatters and absorbs the incoming UV rays; thereby preventing the deadly UV - exhaust gas interaction, which yields the deadly oxidative ozone gas. Furthermore, the well renowned chronic exposure of village communities to the oxidative assault of agrichemical spray drift, manganese based fungicide and fertiliser sprays, etc, all serves to place the English village community at the top of the league as far as toxic oxidant exposure goes.; thereby placing rural residents amongst the highest risk group for developing CJD - according to this theory. It is perhaps no surprise that the oxidative environs of Staten island and Long island in the USA ( enduring an oxidative cocktail of Concorde take offs, radar, coastal UV and ozone, microwaves, etc ) has served to host by far the highest incidence cluster of CJD in the USA . Some would question how the toxic manganese-oxidant theory can account for the well recognised ëiatrogenicí forms of TSE, where growth hormone treatment of humans ( which utilises pituitary tissue ), etc, can lead to a form of CJD. But intriguingly, tissues such as pituitary and retina that are considered to transmit TSE most efficiently, are the exact same tissues where manganese is recognised to concentrate most intensively. Could the high manganese levels contained within these tissues act as the so called infectious agent ? particularly once the metal has been oxidized into its lethal prooxidant 3+ form ? Future Pathways. Despite the apparent reluctance of Establishment bodies to overtly address the works of David Brown and Mark Purdey, both individuals independently strive to take this theory to its final conclusive stages. But funding has not been forthcoming, despite recommendations by the Ukís BSE Inquiry report, etc, as well as MAFFís subsequent invite to Purdey to resubmit proposals for research along these lines. Such a negative dismissal has thwarted the whole healthy evolution of this important new perspective on TSEs. Furthermore it has blocked the development of a possible cure for new variant CJD, a study that David Brown tried to launch last year. In the light of recent Frence and other Euro threats to sue the UK for allegedly giving them BSE- vCJD, it is puzzling to witness a continuation of the dismissive mindset of UK authorities towards any evidence that backs environmental involvement in TSEs; unbelievable , in fact, after studying Professor Bouniasís work which highlights the exact same spatial-temporal correlation between warble fly insecticide use and BSE emergence in France, as observed in the UK . Nonetheless, David Brown strives to run several further crucial experiments to test and explore the various facets of the theory; 1. To test whether the manganese loaded/copper depleted malformed prion protein ( as produced in cell culture studies ) can invoke TSE syndrome after injection into healthy animals. 2. To see whether monitoring for any abnormal changes in manganese levels/valencies in the blood, brain, etc, could act as a diagnostic tool in TSEs. For instance, the application of MRI scans on suspect vCJD victims may assist in this respect. 3. To see whether ëinfectiousí prions can be generated after introducing a combination of manganese and OP oxidizing agents into prion protein cell cultures. 4. To see whether TSE can be cured or diminished in diseased animals who have been treated with pharmaceuticals such as EDTA - a molecule which acts as a chelator of manganese, which locks up and expels available supplies of manganese from the central nerves, etc. To the Ends of the Earth. Meanwhile, despite lack of any formal funding, Mark Purdey continues to expand his field investigations. He has designed a full scale environmental surveillance programme( metal and oxidant analyses, etc ) of relevant water, soil, vegetation, atmosphere, blood / tissues that will be exercised in the variant CJD and BSE clusters that have recently erupted in the UK and Europe. He has also been invited to study a cluster of mystery progressive, fatal neurodegenerative disease ( known as Birds disease ) that has erupted amongst Aboriginal and Caucasian people thriving on a remote island ecosystem off the Northern Australian Coast - Groote Eylandt. The problem first developed after a mining corporation started the open cast mining of manganese on the island in the 1970s. A fine black manganese dust has reportedly coated the entire island. True to form, the local authorities have seemingly scapegoated the emergence of this syndrome - which manifests as a motor neurone disease or a mystery dementia - onto a rare virus that was introduced by a Portugese miner who came to work on the island three decades ago. With permission from the local Aboriginal society, Purdey hopes to acquire brain sections from those who have died of the TSE-like ëdementiaí strain of this disease and see if TSE prion tombstone features can be detected. Purdey has also been instrumental in persuading a local GP to treat some of the early stage victims of ëBird diseaseí with the manganese chelating drug; EDTA ; Up until now, victims of this grotesque disease have been kept in total dark regarding the existence of a possible cure, and, more importantly, an escape from what has always been considered to be an inevitable death. But today, the treatment has just begun. copyright 2002 by Mark Purdey All Rights Reserved
