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— MANGANESE & INFRASOUND — THE LINK TO MAD Cow DISEASE — MANGANESE INFRASOUND — Cow THE LINK TO MAD DISEASE Politicians and scientists have erred in claiming that BSE is hyperinfectious and can only be managed by the wholesale slaughter of livestock, while the corporations have profited at the expense of small farmers. Part 2 of 2 by Mark Purdey © 2002, 2003 High Barn Farm Elworthy, Taunton, Somerset TA43PX United Kingdom Email: MadCowPurdey@aol.com Website: http://www.markpurdey.com Is Rogue Ferrimagnetic Manganese the "Infectious" TSE Agent? nce the crucial supply of copper is curtailed in the brain, due to straightforward environmental copper deficiency or exposure to copper-chelating organophosphate (OP) insecticides, etc., the prion protein's metal bonds become vacant, rendering the protein vulnerable to bonding up with certain alternative metals such as manganese, strontium, silver or lithium. But these foreign substitutes may not act in the overall best interests of the organism, particularly if the invasive metal is in "ferrimagnetic" form. So when ferrimagnetic manganese substitutes at the vacant copper bonds on the prion protein, the field-inducing influence of its ferrimagnetically ordered atoms will progressively corrupt the circadian-mediated pathways of electromagnetic superexchange throughout the brain, whereby a status of permanent magnetic charge is spread via a domino-style of contagious corruption which jumps from metal bond to metal bond, from prion to prion. This phenomenon is well illustrated by the classic college physics experiment, where a magnet is placed alongside a steel nail and the force field of the magnet rapidly magnetises the adjoining nail. Once an individual's brain is contaminated by this freaky form of metamorphosed manganese, any subsequent exposure to external electromagnetic fields (e.g., UV, sound waves, radar, cell- phones, etc.) will permanently charge up the ferrimagnetically ordered manganese prions. The metals rapidly become permanently saturated with magnetic charge, generating intensive mag- netic fields which, in turn, generate self-perpetuating "cluster bombs" of free-radical-mediated spongiform neurodegeneration. TSE ensues. In this respect, the TSE-diseased brain can be likened to a solar-powered battery on continuous charge, where the manganese-loaded/copper-depleted brain is no longer equipped to deal with the incoming surges of electromagnetic energy from the external environment. Instead of utilis- ing this energy for the body's own vital requirements, it becomes perverted into a potent force for neuronal suicide. This theory explains why the so-called "hyperinfectious" property of the prion is a misnomer. It is the toxic ferrimagnetic metal component of the prion that serves as the so- called 'infectious" pathogenic agent in TSEs (transmissable spongiform encephalopathies). So whenever scientists inoculate unfortunate laboratory animals with TSE brain tissues (e.g., tissues contaminated with this rogue manganese atom) and effectively transmit TSE, they are actually transmitting "a mag- netic field—inducing capacity" that is carried along with the ferrimagnetically ordered manganese contaminant into the recipient animals which, in turn, develop TSE. Furthermore, the concept of the rogue ferrimagnetic manganese atom as the "TSE agent" also explains why the "infectious" pathogenic capacity of the prion can survive heating to tempera- tures in excess of 500 degrees Celsius—since ferrimagnetic metals will hold onto their magnetic charge until they are heated to temperatures beyond their respective "curie point" temperature (e.g., 550°C for manganese 3+). A Theory that Addresses All the Missing Links in TSE Science Some would question how the toxic manganese theory of TSE origins can account for the well-recognised "iatrogenic" form of TSE, where growth hormone treatment of humans—which utilises pituitary tissue as the pharmacological inoculant—can lead to a form of CJD (Creutzfeldt—Jakob disease). But intriguingly, ies such as pituitary and retina, which transmit TSE in the lab most efficiently, are the same tissues in which manganese is recognised to concen- trate most intensively in the body. So once an individual is contaminated with a rogue source of ferrimagnetic manganese, any subsequent use of their pituitary tissues in pharmaceuticals for growth hormone therapy could spread the so-called "infectious" toxic agent and initiate CJD. JUNE — JULY 2003 NEXUS +33 www.nexusmagazi ne.com