THE MAGNETICS OF MADNESS: THE FIRST REPORTED CASE OF MAD COW IN THE USA

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THE MAGNETICS OF MADNESS: THE FIRST REPORTED CASE OF MAD COW IN THE USA

 

 

 

By RFD Columnist, Mark Purdey

 

www.markpurdey.com

 

tel; 00 44 1984 656832.

 

 

 

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 furore 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 neuropathological 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 geochemical 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

hotspot around the world. This has involved travelling 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, this conduction collapses since

the prion protein is unable to find its normal copper co-partner; and is

thereafter rendered susceptible to binding up with certain rogue ‘foreign’

metals that can only 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

following the contamination of atmospheres or food supplies, 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-proteoglycan 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 sulphurs locked onto copper in the

brains of 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 ferrimagnetic / 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 neurodegeneration – a well

recognised toxicological phenomena that is generated by the radioactive decay

and ferrimagnetic 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.

 

 

 

 

 

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