The authors of this hypothesis do not believe that the prion is an infectious agent, but rather that the disease is caused directly by the organophosphate-damaged prions binding with manganese. This combination would then produce the chain reaction leading to disease. It is suggested that the transmissible 'infective agent' observed in laboratory tests may be the free radicals from the pesticide.
A similar view is supported by other researchers who propose a link to dioxins, accompanied by a change in procedures for rendering animal carcasses to produce the meat and bone meal for animal and pet feed (39, 40). In the past, excess fat was removed from this ground-up compound by subjecting it to a solvent wash. The solvent then underwent high temperature solvent blow-off, which also helped remove the toxic residues. This solvent fat-removing process was discontinued in England, and the new process increased the final fat content, which now also contained the previously removed toxic residues. These were in the form of bioaccumulated free radicals, such as dioxins and insecticide. Now, cattle are chronically ingesting this poisonous residue through eating feed containing other animals, and this may have triggered the BSE epidemic in Britain. Fat-laced milk in the suckling feed is also implicated as it comes from the same source. The major sources of dioxin are in our diet. Since dioxin is fat-soluble, it bioaccumulates in humans and in animals, climbing up the food chain, and it is mainly (97.5%) found in meat and dairy products (beef, dairy products, milk, chicken, pork, fish and eggs) in that order. (41, 53)
