New - ''Theory on the cause of BSE''

Originally from: Farmtalking
                        
Mark Purdey has just published his 'Theory on the cause of BSE' on his web site and you can see it here –

http://www.markpurdey.com/news_the_cause_of_bse.htm

Originally from: mark purdey
                        
Dear Bill,

I find it quite ironic that you should be telling me that it is the displacement of copper ions from the prion protein that is the core of TSE pathogenesis, when it was clearly my very own research and peer reviewed academic publications since 1994 that have first injected this whole concept into the scientific domain !! You yourself have probably read the "copper displacement" facet from my very own pages or papers in the first instance, but forgotten your original sources. You must get things right if you are going to launch off at me with such negative comments.

 The fact that my research on 'displaced copper' was a central theme of my BBC documentary on "the Correspondent" slot that went out around the world ( on both BBC 2 and BBC world ) in 2001 means that you can hardly turn the clocks back and deny that it was my own original 'hands on' research that was the first to instigate this proposal. I have presented this concept at numerous lectures that I have delivered around the world since; at Harvard, Cambridge, Turin, Tokyo and numerous other universities .

Since you are saying that my theory is not worth the paper that it is written on, then you are ironically saying that the copper displacement facet ( which you obviously support ) is not worth the paper it is written on.

I take great offence to the dismissive comments of armchair theorists ( or plagiarist theorists should I say ) such as yourself. I am sitting on real, hard analytical data that I have personally amassed from my global excursions around every significant cluster of TSE around the world, and it would be socially irresponsible of me to hide the fact that I have observed a very clear cut correlation between elevated levels of radioactive metals and each TSE cluster area that i have sampled. Furthermore, the various sources of the radioactive contamination are very evident in each area ( most are well documented in the literature too ). What is so unscientific about that, for god's sake ???????? The rudiments of my concept might be a commercially and politically uncomfortable fact, but it is not an unscientific fact. So why deny the hard reality of what is staring you in the face in the environment around every TSE cluster around the world ???

Furthermore, perhaps you could explain how you think that copper displacement from the prion protein ( which has 5 copper atoms ligated on by the way ) is ALL that is required to induce a pathogenic reaction that is sufficient to invoke the extreme spongiform encephalopathy that you see in TSE ? You must either have a microbiological or neurotoxic agent ( eg a radioactive metal ) that is capable of invoking the free radical mediated neurodegeneration that is central to TSE neuropathology. It is the combination of the two prerequisites – copper displacement and radioactive metal microcrystals – that is the cause of TSEs.

Since I have suffered severe personal losses as a result of my self financed global treks and analytical work around the world – work which has unearthed considerable insight and benefits for the public good – I do not take kindly to your superficial, unscientific, inaccurate, misconceived and misappropriated comments.

Best,

Mark Purdey.
                        

Originally from: Bill
                        
The core issue in BSE and other so-called TSE's is displacement of copper atoms. The healthy protein molecule quite literally hangs on four copper atoms, displace some or all of these atoms and the molecule collapses.

Mark is approaching the problem from the wrong end, from a scientific point of view his theories are not worth the paper they are written on.

Sorry Mark!

All the best,
Bill.
                        

Originally from: frances fish
                        
========================================
Message date : Aug 28 2004, 11:27 PM
From: ...

Originally from : "Peter Greenhill"
To : ...
Copy to : ..., ...
Subject : Re: [farmtalking] New – 'Theory on the cause of BSE'
It might help the interested onlookers (of which I am but one) if Mr. Snape gave us his qualifications for proposing that the Mark Purdey theory is "not worth the paper it is written on"

Originally from: Peter Greenhill
                        
It might help the interested onlookers (of which I am but one) if Mr. Snape gave us his qualifications for proposing that the Mark Purdey theory is "not worth the paper it is written on"

Peter Greenhill

Originally from: Bill
                        
Regarding microbiological agents there is currently a lot of interest in Borrelia bacteria that causes Lyme disease. By strange coincidence it is a CWD bacteria (cell wall deficient), transmitted by deer ticks and could well be involved in CWD (chronic wasting disease).

Originally from: Bill
                        
Dear Mark,

It has been known since the early 90's that the protein molecule has associate copper atoms, my information is there are four, but I am willing to be corrected if you will acquaint me with details.

I am not a TSE specialist but equally am not an "armchair" scientist, having discussed TSE's at length with Government Ministers.

From: ...

Originally from the Government's point of view every various theory from Kudu to Kamikaze merely further clouds the issue and reinforces the case for caution. "Whilst there is any element of doubt we cannot put lives at risk" as one Minister told me. We all know their hidden agenda is "rationalisation" of the farming industry, less farmers means less grant money to be paid out.

My opinion is the only way forward is to identify the mechanisms by which the healthy protein becomes the prion protein. Then it would be possible to demonstrate how various metals and compounds can bring about the changes.

Have you identified the function of the healthy molecule? I believe it is involved in the voltage gate mechanism of ion channels, a theory that I can assure you has not been "plagiarized"!!!

All the best,
Bill.
                        

Originally from: mark purdey
                        
Dear Bill ,

Yes, I am aware that the likes of Hornshaw M et al , and then later Brown D et al, had identified that the normal cellular form of prion protein binds to copper in the early 1990s. But our issue is not about this. It is about the issue of copper depletion / disruption as a TSE causal prerequisite which was first raised in the academic literature in my paper that reported the data from my 1995 – 1998 analytical studies of the foodchains where sporadic TSEs where clustering around the world. In this paper I combined the knowledge already brought to us by Hornshaw / Brown et al with that of my own environmental data, to hypothesise that the displacement or loss of copper from the prion protein molecule in conjunction with the substitution by a rogue replacement metal – eg; manganese or silver, etc – caused the malformed protease resistant form of prion protein to develop ( eg the abnormal form that is seen in the brains of TSE victims).

Whilst someone had proposed copper toxicity as a cause for TSE, nobody had proposed copper loss as a prerequisite before, which I found strange since the chemical cuprizone had been repeatedly used by the Compton labs during the 1970s to induce a chemical scrapie in mice ( albeit non-transmissible, since, according to my theory, there was no additional rogue metal microcrystal prerequisite involved in these tests that would have rendered the scrapie transmissible;). I guess that the researchers did not see the possible aetiological relevance of the fact that cuprizone is a copper chelator. This naturally interested me when I started to observe rock bottom levels copper in all of the TSE cluster foodchains I was visiting and sampling around the world ( eg; where the TSE affected populations were self sufficient off their local foodchain ), and lead to me generating this theory of copper loss from the prion protein.

Brown et al, then tested my hypothesis of high manganese / low copper in cell cultures and got a positive result. He produced the protease resistant prion using my hypothesis – and this elevated my theory several rungs up the ladder of respectability amongst the non political quarters of the purist scientific community. For no research team had ever produced protease resistant prion protein before – as a de novo transformation. This deserved alot more academic attention than it actually recieved.

This is why I take offence when you say that my theory is not worth the paper that it is written on, since, as I have just pointed out, in real scientific terms the track record of my research work to date has been highly successful. But sadly it is simply not viewed in its true positive light by the Establishment because the findings that I and the likes of David Brown have been making to date do not support the conventional theory. These findings are uncomfortable for the people who control the reigns; eg; the Prusiners, the senior scientific advisors and the multinational corporations of this world. The Ministers are deliberately mislead over the true validity of our work. It is very frustrating to have to live with this.

People such as myself who have been forced to research outside of the system
( for lack of grant funding ) have no power at all. The establishment totally criminalizes and marginalises you; which has the overall effect of disempowering you – regardless of the degree of strength of your scientific data . The more truth that you find out and publish , the worse it becomes !! It is a very pathetic and frustrating state of affairs.

On the function of the normal prion protein, your suggestions seem totally plausible to me, since some studies have shown that prion protein may play some role in regulating calcium channels. I have suggested that the copper on the prion protein may play a role in conducting electric signals that mediate the circadian ( daylight-darkness ) regulation of the biosystem – eg; the immune response, growth and repair, reproduction cycles, sleep-wake rhythms, behavious patterns, etc.

I also feel that there could be mileage in David Brown's proposal that prion protein acts as an antioxidant – since, in accord with my theory, the manufacture of the prion protein is switched on in the areas where these rogue metals / radioactive metals are accumulating in metal-protein crystal aggregates
– and in areas where you get a build up of these transition metals to elevated levels, you will get a cascade of oxidative free radical mediated damage ( eg; the spongiform neurodegenerative damage ) as a result. And the body is going to respond by calling up its respective antioxidant ( eg; the copper/zinc prion protein ) in defence.

Best,

Mark
                        

Originally from: mark purdey
                        
Thanks Frances,

it is good to know that I am communicating, since I sometmes find myself getting buried in too deeply into some of the research papers that I am reading. And as a result, I start to loose the position / orientation of my own research at times.

 I think that the scientific perspectives of life ( not that humans understand a great deal of that so far ) is something that needs to be circulated and shared by as many people on the planet as possible. Afterall, its often the grass roots people on the ground that have made the creative leaps in scientific thinking and discoveries, but this is all too often ignored for many decades after the initial flashburst of insight – until some socially recognised 'expert' stumbles on the same idea. Meanwhile society has been disadvantaged for all of those decades in that it has not derived any of the social benefits from that discovery – all due to the arrogant / bigoted elements of the scientific leadership that automatically reject any ideas flowing in from the non scientific quarters of the community – like Pavlov's salivating dogs .

So communication has to be the key – a crossflow of knowledge passing between academic and practical / hands-on earth based communities in the world. That sows the seeds for the growth of lateral based thinking which will inevitably result in positive scientific advancements.

 But one is not going to communicate to 99% of the population if you confine your communications to the elitist phraseology of the scientific world. As you say, some so called 'experts' hide their inadequacies behind that veil of scientific jargon, and they end up suffocating themselves in the realms of their meaningless phraseology; which, once you have decoded it, turns out to be saying absolutely nothing constructive at all – often wholly unscientific too !!

I always remember the paper that came out in the Veterinary Record that broke the news of the BSE in the Kudu antelopes that were kept at the London Zoo. Because, no meat and bone meal had been fed to these antelope in any guise at all – only dried grass / alfalfa pellets and minerals – and this was embarrassing to the official theory, the authors had launched into this ridiculously far fetched ramble of epidemiological jargon which was trying to suggest that in the history of the zoo, some cow incubating BSE might have actually walked across the paddock where the kudu were kept and deposited prions on the pasture in their dung. I could not believe such stupidity. Its beneath the level of schoolkids. Have they ever kept the domestic cow at the London zoo ? I would not pay the entry fee to the zoo to go and see a common Friesian !! Also how many runaway stray cows do you get in Regent's Park in the centre of London ?

Then the authors concocted some equally ridiculous hypothesis , how wild cats had access to the meat store which was the source of the Puma's / Cheetah's feed ( they had also developed BSE too ), so those cats might have cross contaminated the Kudu feed store with the infectious prion agent – where the wild cats also visited. It went on trying to squeeze blood out of a sinking stone......

If I had even submitted ( let alone got published ) such an unscientific hypothesis to the Vet record, I would have been discredited for life – debarred from getting published or even considered for publication ever again. But because the unscientific myth of these authors was supportive of the government theory, this "landmark" publication is still upheld as the unquestionable gospel according to the cause of BSE in the zoo animals , even today. This kind of junk science has thwarted the whole healthy evolution of scientific advancement in the world , and it must be brought to account immediately.

It is clear that BSE is not going to present us with the crisis of biblical proportions that the leading experts had forcast. But one day the ignorant, unilateral, self protecting approach that is currently adopted by Western governments into dealing with mystery epidemics might actually backfire on us and reap catastrophic repercussions – particularly if a real, all life threatening condition does actually rear its ugly head above the horizon one day. This could lead to the extermination of life on earth. So we need to change the way that governments approach and deal with these kind of crises NOW, before it is too late.

Best,

Mark
                        

Originally from: frances fish
                        
Dear Mark, Thank you for posting that. The thing I like about your postings is that I can follow your drift and understand to a large extent, what you say. I have only the scientific background of school A levels to help me out, so am grateful for your undoubted skill in this field. Perhaps it comes from trying to explain to government officials ( who don't want to know) about your work. You make it clear for me, and I would think, many others, who would otherwise be floundering in a sea of scientifica (just invented that word, I think !) So many,when challenged ,retreat to jargon which we lesser mortals haven't a hope of understanding, and that, of course, is deliberate. They are saying, ''Hey, you, I'm the expert, I know what I'm talking about, who do you think you are to question it ?'' So, as I said, a most refreshing change.
Best Wishes, Frances
P.S. Nearly fused the whole of the science block at school once, how's that for research !

========================================
Message date : Aug 29 2004, 08:20 PM
From: ...

Originally from : ...
To : ...
Copy to :
Subject : Re: [farmtalking] New – 'Theory on the cause of BSE'
Dear Bill ,

Yes, I am aware that the likes of Hornshaw M et al , and then later Brown D et al, had identified that the normal cellular form of prion protein binds to copper in the early 1990s. But our issue is not about this. It is about the issue of copper depletion / disruption as a TSE causal prerequisite which was first raised in the academic literature in my paper that reported the data from my 1995 – 1998 analytical studies of the foodchains where sporadic TSEs where clustering around the world. In this paper I combined the knowledge already brought to us by Hornshaw / Brown et al with that of my own environmental data, to hypothesise that the displacement or loss of copper from the prion protein molecule in conjunction with the substitution by a rogue replacement metal – eg; manganese or silver, etc – caused the malformed protease resistant form of prion protein to develop ( eg the abnormal form that is seen in the brains of TSE victims).

Whilst someone had proposed copper toxicity as a cause for TSE, nobody had proposed copper loss as a prerequisite before, which I found strange since the chemical cuprizone had been repeatedly used by the Compton labs during the 1970s to induce a chemical scrapie in mice ( albeit non-transmissible, since, according to my theory, there was no additional rogue metal microcrystal prerequisite involved in these tests that would have rendered the scrapie transmissible;). I guess that the researchers did not see the possible aetiological relevance of the fact that cuprizone is a copper chelator. This naturally interested me when I started to observe rock bottom levels copper in all of the TSE cluster foodchains I was visiting and sampling around the world ( eg; where the TSE affected populations were self sufficient off their local foodchain ), and lead to me generating this theory of copper loss from the prion protein.

Brown et al, then tested my hypothesis of high manganese / low copper in cell cultures and got a positive result. He produced the protease resistant prion using my hypothesis – and this elevated my theory several rungs up the ladder of respectability amongst the non political quarters of the purist scientific community. For no research team had ever produced protease resistant prion protein before – as a de novo transformation. This deserved alot more academic attention than it actually recieved.

This is why I take offence when you say that my theory is not worth the paper that it is written on, since, as I have just pointed out, in real scientific terms the track record of my research work to date has been highly successful. But sadly it is simply not viewed in its true positive light by the Establishment because the findings that I and the likes of David Brown have been making to date do not support the conventional theory. These findings are uncomfortable for the people who control the reigns; eg; the Prusiners, the senior scientific advisors and the multinational corporations of this world. The Ministers are deliberately mislead over the true validity of our work. It is very frustrating to have to live with this.

People such as myself who have been forced to research outside of the system
( for lack of grant funding ) have no power at all. The establishment totally criminalizes and marginalises you; which has the overall effect of disempowering you – regardless of the degree of strength of your scientific data . The more truth that you find out and publish , the worse it becomes !! It is a very pathetic and frustrating state of affairs.

On the function of the normal prion protein, your suggestions seem totally plausible to me, since some studies have shown that prion protein may play some role in regulating calcium channels. I have suggested that the copper on the prion protein may play a role in conducting electric signals that mediate the circadian ( daylight-darkness ) regulation of the biosystem – eg; the immune response, growth and repair, reproduction cycles, sleep-wake rhythms, behavious patterns, etc.

I also feel that there could be mileage in David Brown's proposal that prion protein acts as an antioxidant – since, in accord with my theory, the manufacture of the prion protein is switched on in the areas where these rogue metals / radioactive metals are accumulating in metal-protein crystal aggregates
– and in areas where you get a build up of these transition metals to elevated levels, you will get a cascade of oxidative free radical mediated damage ( eg; the spongiform neurodegenerative damage ) as a result. And the body is going to respond by calling up its respective antioxidant ( eg; the copper/zinc prion protein ) in defence.

Best,

Mark

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Originally from: Bill
                        
I agree, Mark, it is very frustrating, the Establishment are very good at closing ranks, and at closing doors, Prusiner is about as elusive as bin Laden!

Regarding our own Government's stance on involvment of metals allow me to quote an extract from a letter written by Elliot Morley;

(in reply to my suggestion of forensic testing of diseased animals for contaminents)
"Forensic studies of the type suggested would be difficult to interpret since it is likely that mineral and metal levels will vary depending on animal breed and geographical location as well as on a number of other physiological factors pertinent to a particular animal. It would therefore be necessary to first determine the correlation between mineral and metal levels and TSE disease status before meaningful interpretation of test results would be possible".

That's why I am of the opinion the problem should be tackled from the other end, by first determining the structure and function of the healthy molecule, together with an explanation of the role of the associated copper atoms.

As previously mentioned I believe the molecule to be involved in the voltage gates of ion channels. Eight molecules are arranged somewhat radially (imagine the iris of the eye or a camera), changes in voltage cause the copper atoms to shift position, consequently the gate (iris) is caused to open or close.

On the basis of four copper atoms per molecule I have constructed a model demonstrating I think it works, but I'll have to re-design the model if there are five atoms per molecule!

All the best,
Bill.
                        

Originally from: Peter Greenhill
                        
Mark,

 I have seen your correpondence with Frances and I fully understand your point of view. There are occasions in every walk of life where a comparative layman/woman says "I don`t know why, but this or that does not seem right". Isaac Newton did much the same as did John Harrison with his now-famous sea clocks proving that there was a mechanical answer to a desperately serious problem for marine navigators. The so-called "experts" pooh-poohed his ideas and it took forever for him to prove his point.

 I get very angry with the press over any whiff of BSE. Recently, Border tv (itv for the region) carried an item about the hint that a Holstein had gone down with BSE. The lady journalist who can be best described as an "airhead" banged on about the human form of mad cow disease and the horrible threat this posed to anyone eating beef tarahtarahtarah!!!!. I remonstrated with the tv company pointing out that there was absolutely no evidence that the cow had contracted BSE, in fact it was more likely that it was a bovine infection with some clinical similarities which could not be transmitted to humans. In any event – and this was well-know BEFORE the broadcast, the cow concerned was a dairy heiffer and in any event, the meat from such an animal would not enter the food chain. They responded by saying that the milk could be contaminated but failed to take any notice that the cow concerned was a heiffer and had never contributed to the national milk system.

 You may recall when you were here that we mentioned the four cases of CJD in Queneborough (Northants) This was only of interest to us in that a friend had lived there. One of the cases was a girl who had NEVER eaten meat having been a veggie from almost infant days. We had suggested that in view of this cluster it might be worthwhile looking at the medical records and in particular, any prescriptions where there could be some commonality. As you will know, there was some concern that preparations using bovine spinal fluids were still in store at pharmacies well after the outbreak of BSE. There was an absolute stonewall silence and I heard on my NHS grapevine that the subject was not to be taken up. How accurate this info was I cannot say but it makes you think.

 I have no scientific knowledge but I get very angry that many of those who have are prepared to sell their souls for the sake of their careers. Clear evidence for that was the BSE/CJD and FMD fiascos. Those in political power are quite prepared to repeat twaddle because with them it sounds fine – well it would wouldn`t it?

BR

Peter