The Magnetics of Madness - The first reported case of BSE in the USA.
<http://www.markpurdey.com/news_the_magnetics_of_madness.htm>See also: <http://www.mercola.com/2000/dec/17/bovine_spongiform_disease.htm>
 A brief statement by Mark Purdey - UK TSE researcher and lecturer. 

Despite increasing evidence that the 'mad cow' group of diseases stem from environmental as opposed to infectious origins, the first reported case of BSE in the USA has been met with a furor of hyper-infectious hysteria. Whilst the arrival of the disease in North America should not be treated lightly, the epidemiological track record of the BSE outbreaks in Europe suggests that there is no need for the panic.
One of the key neuro-pathological markers that have enabled researchers to diagnose BSE, has focused upon the presence of a malformed version of the prion protein - a native brain protein which is present in all healthy mammals, and performs a functional role in mediating the circadian rhythm.
 
Various researchers have established a hypothesis on the origins of TSEs (the BSE group of diseases) which is based on the unproven assumption that this malformed 'prion' serves as the infectious agent that is responsible for the cause of BSE. Furthermore, it has been suggested that the feeding of the ground down remains of TSE affected sheep to cattle served as the vehicle for transmitting these infectious prions into the European cattle herd, and causing BSE. But many major flaws have arisen in the established theory, such as the exportation of thousands of tons of the UK's BSE incriminated cattle feeds to countries all over the world. Despite those countries receiving this feed throughout the 1960s, 70s, 80s and 90s, their cattle populations have remained BSE-free to date. So how can micro doses of the feed cause BSE?
 
Furthermore, why have tens of thousands of BSE outbreaks continued to emerge in European cattle that have been born after their respective bans on the meat and bone meal going into cattle feeds?
 
Recent UK lab research has demonstrated that an intermediate toxic factor - which causes the normal prion protein to transform into its abnormal prion form - is the actual causal agent; thereby indicating that the malformed prion represents little more than a 'tombstone' legacy that is a 'hang over' from the toxic TSE disease process.
 
The Metal Detective.
 
For fifteen years I have carried out geo-chemical analyses of the ecosystems (soil, water, vegetation, etc) to gauge the levels of 46 metals and their radioactive/magnetic susceptibility status in every sizeable TSE cluster hot spot around the world. This has involved traveling to Japan, New Guinea, Canada, USA, Europe, Iceland, etc, in order to pinpoint the common toxic denominator that is exclusively shared
by all of these isolated cluster locations.
 
This work has identified that a package of toxic environmental factors underpins the pathogenesis of TSEs, where the simultaneous exposure to a copper deficient food chain and rogue radioactive metal pollutants brings about the malformation of the prion protein , with a consequent break down in the way that the brain deals with incoming surges of electromagnetic radiation - eg; light and sound waves, etc.
 
The normal prion protein actually binds up with copper in the healthy brain, where this metal performs a role in the conduction of incoming electromagnetic energy along the circadian circuits - in order to
regulate various essential physiological processes under daylight/darkness control. But once the problem of copper deficiency surfaces via the food chain, then the prion protein is unable to find its normal copper co partner and is rendered susceptible to binding up with certain rogue 'foreign' metals that serve as undesirable substitutes at the protein's vacant copper bonds.
 
My studies have shown that TSEs will develop in environments where metals such as manganese and silver are at high level - as a result of various natural or artificial sources of pollution. These can get taken up into the animal via contaminated foods or atmospheres, and , under certain circumstances, can flood past the blood/ brain barrier where they are free to bind onto any copper depleted prion proteins. This triggers off the progressive chain of events that leads to the development of the so called sporadic, traditional strain of TSE which usually surfaces in the susceptible members of the local mammalian populations during the later stages of middle age.
 
Mad Cow Melt Down.
 
But my research has further identified the presence of the more virulent radioactive metals, such as strontium 90 and barium, in the ecosystems where the clusters of the more aggressive modern strains of TSE, like BSE and vCJD, have emerged in younger mammals. Lab studies have shown that these radioactive metals can also bind into the prion protein-ferritin complexes in the brain.
 
In this respect, it can be explained why the 1986 outbreak of BSE in Europe - largely confined to the UK - emerged in those areas where exclusively high doses of a systemic acting organo-dithiophosphate
insecticide had been compulsorily used for the treatment of warble fly since the early 1980s. This chemical acts as a copper chelator, where its two free sulfurs locked onto copper in the brains treated cows, thereby starving the prion proteins of their crucial copper co-partners. And once the radioactive metals rained down over the pastures of NW Europe after the Chernobyl blow out in April 1986, the prion proteins of those copper depleted cattle were vulnerable to bonding up with these rogue radioactive substitutes.
 
When the prion protein has attached itself to a radioactive metal in place of copper , it is easy to envision how the brain is subjected to a steady, self perpetuating state of 'melt down'. These foreign substitute
metals will fail to act in the overall best interests of the organism, particularly since the invasive metal is in ferri-magnetic/radioactive form. In this respect, the prion protein becomes much like a Trojan horse which trucks around the circadian circuits of the brain carrying its lethal radioactive cargo of metallic missiles on board - a fire power capacity that is potentially capable of detonating a deleterious chain reaction of free radical mediated neuro-degeneration - a well recognized toxicological phenomena that results from the radioactive decay and ferri-magnetic fields that are emitted by any radioactive metal that gets lodged into biological tissue. TSE ensues.
 
The US Wasting Lands.
 
During the autumn and spring of 2002/2003, I carried out a series of analyses in the ecosystems supporting the clusters of TSE that had emerged across the USA and Canada. My resulting data indicated that all of these clusters are located in areas where copper is virtually absent in the food chain. Furthermore, I identified the presence of high levels of certain radioactive metal species in those environments, which had invariably resulted from toxic discharges vented out of the military munitions production/testing ranges or oil/gas well sites that were centrally located within all of these cluster environments.
 
In this respect, the lone case of BSE that has emerged in Washington state, has probably stemmed from the fact that this cow had been imported from the copper deficient pastures of Alberta Canada into an area where the most intensive radioactive metal pollution has occurred in the USA - around the Hanford plutonium nuclear processing plant.
 
For further details see the Articles on this website. Mark Purdey - 30th December 2003