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?
High Barn Farm, Elworthy, Taunton, Somerset TA4 3PX, UK. email@example.com
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 practice 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 (Manganese) 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.
PMID: 15236778 [PubMed - indexed for MEDLINE]
Elevated levels of aluminium (Al), strontium (Sr), barium (Ba), iron (Fe), manganese (Mn) cations - combined with deficiencies of magnesium (Mg)/calcium (Ca) - have been observed in the food chains that traditionally support the Chamorro populations affected by high incidence clusters of Alzheimer (AD), Parkinson-like (PD), motor neurone diseases and multiple sclerosis on the island of Guam.
Soils drawn from the cluster region demonstrated an excessive fivefold increase in 'magnetic susceptibility' readings in relation to soils from disease free adjoining regions.
A multifactorial aetiological hypothesis is proposed that pivots upon the combined exposure to high levels of natural/industrial sources of ferrimagnetic / ferroelectric compounds incorporating Al, Fe, Mn, Sr, Ba (e.g., via yam/seafood consumption or exposure to world war 2 (WW2) munitions) and to low levels of Mg/Ca in all S. Pacific locations where these clusters of neurodegenerative disease have simultaneously erupted.
Once gut/blood brain barrier permeability is impaired, the increased uptake of Al, Fe, Sr, Ba, or Mn into the Mg/Ca depleted brain leads to rogue metal substitutions at the Mg/Ca vacated binding domains on various enzyme/proteoglycan groups, causing a broad ranging disruption in Mg/Ca dependent systems - such as the glutamine synthetase which prevents the accumulation of neurotoxic glutamate.
The rogue metals chelate sulphate, disrupting sulphated-proteoglycan mediated inhibition of crystal proliferation, as well as its regulation of the Fibroblast growth factor receptor complex which disturbs the molecular conformation of those receptors and their regulation of transphosphorylation between intracellular kinase domains; ultimately collapsing proteoglycan mediated cell-cell signalling pathways which maintain the growth and structural integrity of the neuronal networks.
The depression of Mg/Ca dependent systems in conjunction with the progressive ferrimagnetisation of the CNS due to an overload of rogue ferroelectric / ferrimagnetic metal contaminants, enables 'seeding' of metal-protein crystalline arrays that can proliferate in the proteoglycan depleted brain.
The resulting magnetic field emissions initiate a free radical mediated progressive pathogenesis of neurodegeneration.
The co-clustering of these various types of disease in select geographical pockets around the world suggests that all of these conditions share a common early life exposure to ferromagnetic metal nucleating agents in their multifactorial aetiology.
Factors such as individual genetics, the species of metal involved, etc., dictate which specific class of disease will emerge as a delayed neurotoxic response to these environmental insults.
PMID: 15488650 [PubMed - indexed for MEDLINE]
Source: http://www.ncbi.nlm.nih.gov/pubmed/15236778?ordinalpos=6&itool=EntrezSystem2.PEntrez.Pubmed. Pubmed_ResultsPanel.Pubmed_RVDocSum
Source: http://www.ncbi.nlm.nih.gov/pubmed/15488650?ordinalpos=5&itool=EntrezSystem2.PEntrez.Pubmed. Pubmed_ResultsPanel.Pubmed_RVDocSum