FRESH RESEARCH REPORT OF A TRACE METAL-CWD STUDY AT SASKATOON UNIVERSITY IS BEING EXPLOITED TO DISCREDIT A MISREPRESENTED VERSION OF PURDEY’S THEORY

The following article authored by Professor Peter Flood’s team at Saskatoon Uni has been circulated widely in the public domain by the likes of the USDA / DNR personnel. The officials are exploiting the findings of this study as a means of discrediting the validity of my research into the involvement of trace minerals in the origins of TSE. However, this study fails to address the key tenets of my published theory on the origins of CWD (see below for full abstract ‘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?’).

Whilst the results of this study do in fact inject some interesting fresh insight into our understandings of the metal-protein chemistry of TSEs – which actually supports the observations of my own trace metal studies across North American TSE / TSE-free locations in 2002/2003 ( see; abstract below) – it is a great shame that the conclusion of this article has seemingly adopted a more politically orientated tact which rejects outright the viability of any trace metal imbalance in the aetiology of TSEs. The conclusion is largely based on a misinterpretation of my own and other researchers’ published studies.

It is also a shame that many government officials, who are clearly unaware of the tenets of my hypothesis, have taken it upon themselves to disseminate this un-reviewed paper widely throughout the public domain, using it as a means of discrediting a theory which ironically is not mine.

The conclusion of the Flood study rejects any role for trace element disturbances in the origins of CWD. Such an opinion is both unscientific and premature in that it fails to take account of my actual environmental analytical observations and the relevant pathogenic mechanisms that I have proposed in my published theory on the origins of the CWD.

In this respect it is the Saskatoon research study that is deficient, since they have only analysed for the levels of six trace elements in total, which excludes the majority of the key metals like silver, barium and strontium – which have shown up at high level in my analytical studies of CWD clusters across North America in 2002/2003, in relation to CWD-free control zones. The fact that these specific rogue metal pollutants have been identified, has been presented in both my published papers and at the specific lectures that these authors’ attended ( see; abstract below ). So why has this been ignored ?

The Saskatoon conclusion also fails to grasp the relevance of one of the central tenets of my theory which indicates that it is the loss of copper from the metal binding domains on the prion protein which is the pertinent prerequisite. In this respect, it appears that the authors have not read my initial publication ( Purdey M, Medical Hypotheses 54 (2) 278-306 ) on the role of metals in the pathogenesis of TSEs ( reprints were provided to the authors when we met ); since on page 281 of this article, it is clearly depicted that the ‘copper disturbance’ prerequisite can be achieved via several different routes that do not necessarily involve a primary copper deficiency in the external environment. This pathogenic cornerstone pivots upon the loss of the five copper atoms from the octapeptide repeat region of the cellular prion protein ( Brown D, trends in Neurosci, 2001 24 (2) 69-127 ) which can be achieved in the following ways;

a. Via a primary deficiency of copper in the external environment.

b. Via environmental exposure of the organism to copper chelating chemicals such as organo dithiophosphate insecticides, molybdenum, cuprizone (a well known copper chelator which induces scrapie in lab mice )

c. Via exposure to pollutant metals, like silver, which will preferentially bind to prion protein’s metallo ligands in relation to copper, thereby displacing the copper from binding to its native domains - irrespective of the levels of available copper within the organismand external environment.

d. via exposure to chemicals which could mutate the genes that encode for the synthesis of the metallo binding ligands on prion protein.

 

Since the authors’ study has focused exclusively on the single facet of environmental copper deficiency as the sole means of achieving copper depletion at the prion protein, then there is no basis on which to conclude that my hypothesis is incorrect.

On the contrary, my latest publication of data collected across North American / Canadian CWD clusters and CWD-free locations ( see abstract below ) clearly indicates that the high levels of silver ( identified in the hard tissues of the deer, as well as local vegetation/soil ) could preferentially bind to the prion protein metal-domains in place of copper. This could theoretically indicate that the all important loss of copper binding to the prion protein has been achieved via the mechanism of displacement of copper from its binding domain on the prion protein rather than as a result of a primary copper deficiency in the external environment.

If this turns out to be the case, then the levels of copper in the soil, pasture, liver, brain, etc, are irrelevant in respect of the pathogenesis of the CWD strain of TSE. Furthermore, there is evidence that silver intoxications will induce symptoms of copper deficiency (Ganther H, Annals NY Acad Sci 1980 212-225 ) probably via this mechanism of displacement of copper at the copper-binding domains on various key enzyme groups.

Peter Flood’s paper also makes totally unsupported statements over the viability of the conventional ‘infectious protein-only theory’; for instance the authors state that " the abnormal prion can be passed from one animal to another causing CWD ", yet they fail to give any references that demonstrate these outlandish, scientifically inept claims . To my knowledge, there is no research paper that supports these ideas.

The authors also fail to explain how the so called protein-only 'prion' can remain 'infectious' after being heated up to 800-1000 degrees, not to mention their failure to address the myriad of other major flaws in the protein-only theory.  This kind of Pavlovian-like allegiance to the current mindset, represents just another example of the scientific community assuming that the majority theory represents unquestionable 'gospel', without ever taking time out to assess the validity of the original research that initiated this misguided hypothesis in the first instance. 

A POINT BY POINT CRITIQUE OF THE ‘FLOOD PAPER’ AND ITS IRRELEVANCE TO MY PUBLISHED WORK IS AS FOLLOWS :

 

1. The authors fail to analyse their samples for silver, strontium, barium, selenium, sulphur, etc, which have been putatively implicated in TSE pathogenesis.
   
   
2. The authors exclusively focus on ‘environmental copper deficiency’ as a means of depriving prion protein of its copper co partner, whilst failing to recognise alternative pathogenic possibilities, such as a silver induced displacement of copper binding at the prion protein.
   
   
3. On the basis of the findings in this study, it seems that the contribution of environmental copper deficiency to CWD pathogenesis could still be plausible. For the authors concede that the two main farms involved in the sampling ( eg; those farms on which they held the most information ) did indeed produce a significant correlation between copper deficiency and CWD incidence. Despite this statement, the authors proceed to ‘water down’ the more reliable data of their project by introducing the results from farms which they declare they had little information about. They then use the overall results - drawn from both reliable and unreliable sample locations -  to discredit the whole trace mineral hypothesis.
   
   
4. No allowance has been made for the marked variation in the levels of copper and manganese that is normally invoked by either the oestrus or diurnal/nocturnal cycles (Morton DJ; J Pineal Res 1990 9 95-101 ) that operate in the healthy brain and biosystem. To bypass this problem, samples would need to be collected from deer / elk that have been slaughtered at the same stage of the oestrus cycle and daylight/darkness cycle to guarantee representative results. However, If the samples had been sourced from ‘hard’ as opposed to ‘soft’ tissues in these tests, then this potential complication of rhythmic alterations in cation levels would have been avoided. The more stable, static levels of cations in bone and antler tissue tend to offer a more reliable reflection of the overall levels of these metals in the deer’s environment.
   
   
5. The authors understate the potential importance of the results of the one brain sample in this study which had been sourced from a deer that was suffering from the clinical stages of CWD.  Whilst, the authors comment that this particular animal did indeed demonstrate lower levels of copper, it is strange that such a pertinent result was not given the prominence it deserved in the overall context of this paper.
   
   
6. The authors’ discussion also ignores the possibility that the malformed prion proteins could have been initiated months or even years before the samples were collected. Since we are looking at a protease resistant prion protein here ( eg; an undegradable protein ) that remains permanently fixed in the brains of animals suffering from TSEs like CWD, then it is perfectly possible that a short ephemeral period of copper deficiency ( eg; as experienced during drought periods that are common to the CWD regions ( Flynn A et al, J Nutrition, 1977 107 1182-1189)) in the history of the animal, could be all that is required to enable any rogue metal pollutants that are concurrently present to jump in and substitute the vacancies at the bonding sites on the prion protein. Once a rogue metal bonding has transformed the protein into its abnormal protease resistant form – as has been demonstrated experimentally ‘in vitro’ (Brown D et al. EMBO Journal 2000 19 (6) 1180-1186) - then the malformed proteins will simply sit there and accumulate over time. In this respect, the levels of copper and other metals that were recorded in the livers and brains at the time of this study, may be totally irrelevant to the levels of those metals that were present during the ‘misfolding’ period when these malformed proteins were first initiated. That is why it is interesting that the one clinical case of CWD that was involved in this study did indeed demonstrate low levels of copper.
   
   
7. The authors also do not consider the fact that elevated or normal levels of copper in liver may not necessarily reflect an overall state of elevated/normal copper in the animal's biosystem. It is well established that the levels of copper in the liver and blood may actually measure in the ‘elevated’ range in cases of sub clinical copper deficiency ; due to an increased demand upon the remaining stores of the metal in the liver, to mobilise the copper-transporter proteins via the blood, for delivery to the tissues that are experiencing copper deficiency.
   
   
8. This study is considerably weakened by the fact that it has drawn its samples from a non specific section across the entire brain - the left lobe of the cerebrum. A study of the literature on the precedent studies conducted on the levels of metals in TSE diseased brains indicates that the aberrant levels of cations ( high manganese, low copper, etc ) were actually identified in very specific regions of the CNS. For example, Case Western University's Prion disease surveillance centre, Cleveland, Ohio (Boon-Seng W, et al; J Neurochem 2001 78 1400-1408 ) found a ten fold increase in the levels of manganese  and a 50% reduction in copper in the frontal cortex of CJD affected brain, whilst another study by Kopp N et al (Proceedings of conference; BBRSC International workshop, Cambridge Uni, 6/8/01) identified a similar aberrant mineral profile in select regions of the CJD brain. In this respect, the analyses conducted by the Saskatoon team should have focused more selectively on regions like the brain stem, cortex , olfactory bulb or the other areas which are invariably implicated in the neuropathological profile of CWD - eg; the area where you would expect to find any mineral imbalances that are associated with the pathogenesis of the disease.
   Furthermore, mineral studies on the healthy brain have demonstrated marked variations in the levels of copper, manganese, etc, in the different regions ( Gooddy W, et al; Brain 1975 98 (1) 65-70 ) as well as in respect of the natural influences of the circadian and oestrus cycles, etc.
   

PERSONAL REPERCUSSIONS.

As an overworked, unsupported single handed international TSE researcher and lecturer, it is very tedious to be constantly forced to spend valuable time and energy countering these kind of publications - that employ irrelevant scientific arguments as a means of discrediting my work. This happens much too frequently, where scientific teams who are understandably eager to maintain a steady inflow of grant money, feel forced to compromise their good science by moulding their results to satisfy the agenda of their paymasters – the local government departments, etc.

But the problem is that the readers of these widely circulated government papers are invariably ill informed of the relevant details of the theory under attack. So one is left with little choice but to mount a substantial counter-defence in order to rectify the myths that are being circulated surrounding your work. Or, alternatively, if you choose to ignore the challenge, you are forced to face the risk of loosing your hard won credibility, along with any future income ( lecturing, grant support ) on account of a misrepresentation of your true position. This is totally unfair, because the ever increasing financial sacrifices that I am forced to make for my research make it hard for me to continue with these types of projects. I have to meet the needs of six children who are all wanting to go to university !

 

In the interests of positive progress and efficient use of resources in testing for potential roles of environmental factors in TSEs, it is also ‘out of order’ that my personal input has been continually excluded from the various official forums that have debated my work over the years ( save the UK’s BSE Inquiry ). My absence from these unilaterally orientated discussions has obviously left me powerless to rectify the blatant misconceptions that are repeatedly raised in the resulting statements about my work that are circulated throughout the public domain.

Over the years various protocols have been designed to challenge the environmental based theories on the cause of TSEs and this has represented a positive advance on each occasion. But the potential capacity of each research project that has actually got launched has been seriously compromised by the failure of the teams to consult with myself or other field researchers over the project’s design.
The technicians have launched an irrelevant challenge to a misrepresented version of my work which betrays the predetermined agenda to discredit rather than test the hypothesis in an impartial perceptive scientific manner.

In respect of the Saskatoon team who have been fortunate enough to acquire grant funding to pursue this interesting new line of environmental research into the causes of TSEs, their money would have been better spent if they had tested the relevant tissues for the full spectrum of metals ( 50 or so ) that could potentially be involved in the pathogenesis of these grotesque diseases – for little extra above the costs which they spent for screening for six elements .

It is only by working together as a unified group of lateral thinking, cross-discipline, trans-global researchers ( involving biochemists, geochemists, geophysicists, neuropathologists, veterinarians, livestock farmers, CJD victims’ relatives etc ), that we will be able to get to the root cause of these disturbing diseases as quickly as possible.

But I feel that before we can reach this somewhat idealistic position in the way that researchers co-operate and tackle disease research from a multidisciplinary perspective, the scientific community needs to wake up and recognise that the repeated identification of a specific toxic environmental agent/s in all of the key cluster areas of a given disease may actually provide us with some valuable intelligence that will help elucidate the primary causal pathways involved in that disease.

People such as myself need to be treated with respect, rather than misrepresented, plagiarised, discarded, insulted, criminalized and then ‘bullied’ into the backstreet gutterscapes of academia. Why does such an innocent pursuit as trying to find out the cause of a disease pose such a grave threat to the establishment ? Why has my existence warranted such a sustained bout of vitriolic and inappropriate treatment from the mainstream scientific community ?

Mark Purdey 26/3/04

Abstract ( a presentation of the contents of this ‘in press’ paper were delivered at the specific lectures which the Flood team had attended in Canada;)

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?

Mark Purdey, High Barn Farm, Elworthy, Taunton, Somerset, TA43PX, UK.

Tel; 00 44 1984 656832. Email; TSEPurdey@aol.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 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.