So once the crucial supply of copper is curtailed in the brain - due to straight forward environmental copper deficiency or exposure to copper chelating 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.

For instance, once ferrimagnetic manganese substitutes at the vacant copper bonds on prion protein, the field inducing influence of its ferrimagnetically ordered atoms will progressively corrupt the circadian mediated pathways of electromagnetic super exchange throughout the brain; whereby a status of permanent magnetic charge is spread like a domino-style of contagious corruption which jumps across from metal bond to metal bond, from prion to prion (see diagram 3). 

Diagram 3

This phenomena 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.

So once an individual’s brain is contaminated by this freaky form of metamorphosed manganese, any subsequent exposure to external electromagnetic fields (eg, 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 magnetic fields, which in turn, generate self perpetuating ‘cluster bombs’ of free radical mediated spongiform neuro-degeneration. 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 utilising 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. So whenever scientists inoculate misfortunate lab animals with TSE brain tissues (eg tissues contaminated with this rogue manganese atom) and effectively transmit TSE, they are actually transmitting ‘a magnetic field inducing capacity’ that is carried along with the ferrimagnetically ordered manganese contaminant into the recipient animals, who, in turn, develop TSE.

Furthermore, the concept of the rogue ferrimagnetic manganese atom as the ‘TSE agent’ also explains why the so called ‘infectious’ pathogenic capacity of the prion can survive heating to temperatures in excess of 500 degrees – since ferrimagnetic metals will hold onto their magnetic charge until they are heated to temperatures beyond their respective ‘curie point’ temperature. (eg, 550 degrees for manganese 3+).