Elevated silver, barium and strontium in antlers, vegetation and soils sourced from CWD cluster areas: Do Ag/Ba/Sr piezoelectric crystals represent the transmissible pathogenic agent in TSEs?

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Abstract

High levels of Silver (Ag), Barium (Ba) and Strontium (Sr) and low levels of copper (Cu) have been measured in the antlers, soils and pastures of the deer that are thriving in the chronic wasting disease (CWD) cluster zones in North America in relation to the areas where CWD and other transmissible spongiform encephalopathies (TSEs) have not been reported. The elevations of Ag, Ba and Sr were thought to originate from both natural geochemical and artificial pollutant sources – stemming from the common practise of aerial spraying with `cloud seeding' Ag or Ba crystal nuclei for rain making in these drought prone areas of North America, the atmospheric spraying with Ba based aerosols for enhancing/refracting radar and radio signal communications as well as the spreading of waste Ba drilling mud from the local oil/gas well industry across pastureland. These metals have subsequently bioconcentrated up the foodchain and into the mammals who are dependent upon the local Cu deficient ecosystems. A dual eco-prerequisite theory is proposed on the aetiology of TSEs which is based upon an Ag, Ba, Sr or Mn replacement binding at the vacant Cu/Zn domains on the cellular prion protein (PrP)/sulphated proteoglycan molecules which impairs the capacities of the brain to protect itself against incoming shockbursts of sound and light energy. Ag/Ba/Sr chelation of free sulphur within the biosystem inhibits the viable synthesis of the sulphur dependent proteoglycans, which results in the overall collapse of the Cu mediated conduction of electric signals along the PrP-proteoglycan signalling pathways; ultimately disrupting GABA type inhibitory currents at the synapses/end plates of the auditory/circadian regulated circuitry, as well as disrupting proteoglycan co-regulation of the growth factor signalling systems which maintain the structural integrity of the nervous system. The resulting Ag, Ba, Sr or Mn based compounds seed piezoelectric crystals which incorporate PrP and ferritin into their structure. These ferrimagnetically ordered crystals multireplicate and choke up the PrP-proteoglycan conduits of electrical conduction throughout the CNS. The second stage of pathogenesis comes into play when the pressure energy from incoming shock bursts of low frequency acoustic waves from low fly jets, explosions, earthquakes, etc. (a key eco-characteristic of TSE cluster environments) are absorbed by the rogue `piezoelectric' crystals, which duly convert the mechanical pressure energy into an electrical energy which accumulates in the crystal-PrP-ferritin aggregates (the fibrils) until a point of `saturation polarization' is reached. Magnetic fields are generated on the crystal surface, which initiate chain reactions of deleterious free radical mediated spongiform neurodegeneration in surrounding tissues. Since Ag, Ba, Sr or Mn based piezoelectric crystals are heat resistant and carry a magnetic field inducing pathogenic capacity, it is proposed that these ferroelectric crystal pollutants represent the transmissible, pathogenic agents that initiate TSE.

Introduction

Exceptionally high levels of Ag, Sr and Ba were measured in deer antlers, vegetation, soils sourced from chronic wasting disease (CWD) cluster areas in Colorado, Wisconsin, Saskatchewan, whilst levels were 3-fold, 2.5-fold and 3-fold less (for Ag, Sr, Ba, respectively) in CWD-free areas of Alberta/UK. Ag was virtually undetectable in antlers sampled from CWD-free deer herds in the UK.

These observations were recorded as part of an extensive comparative analytical study of the levels of 46 metals in the soils, water and vegetation of CWD cluster and CWD-free regions conducted across North America. This work represented the North American perspective of a three year globally orientated project designed to establish whether any abnormal mineral profile or abnormal magnetic/radioactive/oxidative capacity is a common characteristic of transmissible spongiform encephalopathie (TSE) cluster ecosystems around the world, and, if so, whether that abnormality plays a primary role in the pathogenesis of TSEs.

Since the primary origins of TSEs are unknown, this study was designed to challenge the theory based upon previously amassed data [1], [2], [3] that high levels of specific metals, such as manganese (Mn) or Ag, in combination with low levels of Cu in the environment may bring about a rogue metal replacement at vacant Cu ligands on the cellular prion protein (PrPc) – a Cu binding protein [4] whose misfolded isoforms hallmark the TSE diseased brain [5].

Section snippets

Does a network of Cu–PrP–Cu-proteoglycan conduits conduct a relay of electric signals that regulate the auditory/circadian associated circuitry of the biosystem?

Since PrPc `knock out' mice develop symptoms (sleep disorders, abnormal EEG, etc.) that indicate an underlying disturbance in the regulation of the nocturnal–diurnal rhythm [6], [7] and GABA inhibitory currents at synapses [4], [5], it has been suggested that PrPc performs some metabolic role in mediating the circadian diurnal–nocturnal rhythm and other external stimuli. In this respect, it has been proposed that the paramagnetic Cu [8] component of the PrP molecule [4] performs a role as a

Ag, Ba, Sr or Mn nucleated crystal-PrP-ferritin complexes disrupt these conduits of electrical signalling throughout the CNS. A primary prerequisite for the pathogenesis of TSEs? (see Fig. 1)

In this respect, the pathogenesis of TSE could be initiated by a disruption at any point along these putative PrP-proteoglycan `conduits' of electrical conduction; ultimately resulting in the overall collapse in both the GABA mediated modulation of neuronal response at the synapses [4] and the proteoglycan regulated anti-oxidant/growth factor signalling systems [21], [28].

Environmental analytical observations in TSE cluster zones suggest that a foreign metal replacement binding on the native

Soil sample collection/analysis method

Each soil sample comprised a 300 g sample drawn from a mix of 20 columns of dry soil bored with a stainless steel auger; each column having been bored at equidistant spaces along a W shape spanning an area of ≈10 acres, the area being representative of the region grazed by the CWD affected deer under study. Each column was drawn from the top soil to a depth of 6 in. having taken care to avoid inclusion of root material/surface organic matter and collection of samples near to gateways,

High silver, possible environmental sources and modes of uptake

High levels of Ag and low levels of Cu were recorded in the antler material, soils and deer browse vegetation drawn from CWD affected zones (see Table 1, Table 2, Graph 1, Graph 2). These results represent the first time that Ag has been detected in antlers, whilst adding some support to the proposal [2], [3] that high Ag and low Cu in the environment may bring about an Ag replacement of vacant Cu ligands on the cellular prion protein (PrPc).

Particularly interesting is the fact that Ag was

Conclusion and future research

Irrespective of any role that elevated levels of Ag, Ba and Sr may play in the pathogenesis of TSEs, the novel observation of Ag in antler might suggest that the antler acts as a hitherto unrecognised toxic `sink' for storing excess intakes of Ag, Ba, Sr and other metals in cervidae who are thriving off foodchains that have bioconcentrated these metals. The toxic load is conveniently shed along with the antler on an annual basis. Or, alternatively, Ag and/or Ba could perform some metabolic role

Acknowledgements

The Fats and Protein Research Foundation, USA, Allan and Judith Pincus, the Fred Foundation, JM and MD Purdey for funding of this project. Thanks to Sarah Simpson for collection of TSE-free Vermont samples, and to Judy Cabay, Kay Sinclair, Shirley Parrish, Mark and Linda Kessenich, Gene Flees, Ken Dolores and the Ruell family for assisting with antler/soil collection. Thanks to Dr. David Grant (Aberdeen) and Dr. Thad Mauney (Billings, Montana) for enlightening education over the biochemistry of

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