Metal microcrystal pollutants; the heat resistant, transmissible nucleating agents that initiate the pathogenesis of TSEs?

This paper exposes the flaws in the conventional consensus on the origins of transmissible spongiform encephatopathies (TSEs) which decrees that the protein-only misfolded 'prion' represents the primary aetiological transmissible agent, and then reviews/ presents the emerging data which indicates that environmental exposure to metal microcrystal pollutants (sourced from munitions, etc.) represents the heat resistant, transmissible nucleating agents which seed the metal-prion protein (PrP)-ferritin fibril crystals that cause TSE. Fresh analytical data is presented on the levels of metals in ecosystems which support populations affected by clusters of variant Creutzfeldt-Jacob disease (vCJD), sporadic/familiat CJD, and the scrapie types of TSE that have emerged in the UK, Sicily, Sardinia, Calabria and Japan. This data further substantiates the abnormal geochemical template (e.g., elevated strontium (Sr), barium (Ba) and silver (Ag)) which was observed as a common hallmark of the TSE cluster ecosystems across North America, thereby supporting the hypothesis that these microcrystals serve as the piezoelectrion nucleators which seed the growth/multireptication of the aberrant metat-PrP-ferritin fibrit features which characterise the neuropathotogy of the TSE diseased brain. A secondary pathogenic mechanism entails the inactivation of the sutphated proteogtycans which normally regulate the mineratisation process. This can be induced by a rogue metal mediated chelation of free sulphur, or by contamination with organo-sutphur pollutants that substitute at natural sulphur bonds, or via a mutation to the S-proteoglycan cell tine; thereby enabling the aberrant overgrowth of rogue fibrit crystal formations that possess a piezoelectric capacity which compromises the ability of the contaminated individual to process incoming acoustic/ tactile pressure waves in the normal way. The crystals transduce incoming sonic energy into electrical energy, which, in turn, generates magnetic fields on the crystal surfaces that initiate chain reactions of free radical mediated spongiform neurodegeneration. Metal microcrystal nucleating agents provide a group of plausible aetiotogical candidates that explain the unique properties of the TSE causal agent - such as heat resistance, transmissibility, etc. which the protein-only prion model faits to fulfill. This paper also discusses the possible nutritional measures that could best be adopted by populations living in high risk TSE ecosystems; as a means of preventing the successful implantation of these rogue microcrystats and their consequent hypermineratisation of the soft tissues within the CNS. (c) 2005 Elsevier Ltd. All rights reserved.