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from the London Evening Standard 7/2/03 This brief article only mentions OPs and BSE but Mark will be discussing the full gamut of his research with Michael Meacher. - Phosmet, Maganese, Copper, and Infra sound and their role in causing the disease.

 

Spring 2002. CFS/ME is a genuine disease. I f you suffer from CFS as I do, boy you would have been celebrating last week with no alc.low allergen champagne, wicked stuff! on hearing the news that the 'real experts', after years of research have decided that you are really ill -I never knew it - so GPs cross out the heartsink diagnoses. But why haven't they a clue what's going on ! The core of the disease is not difficult - usual stuff -ie high intra cellular calcium (has anyone ever looked or understood the devastating implications of this marker) raised oxidative stress/phospho inositide 2nd messenger signal transduction, conformational changed proteins, anaerobic threshold reached early, usually immediately - poor oygen transport, not surprising because the red cells act as last ditch sacrificial anti oxidants, high apoptosis ( Ive got 50%). You can go on and on with the abnormalities and of course they make sense and form a coherent picture. So pesticides, pesticide compromised immune modulation -mycoplasma/candida/virus on the ascendant. So why all the tedious vacuous debate about what to call the condition and is it real. OK so the real experts are not really creative or any good at understanding diseases like this - but there are enough clues around. What are they waiting for.


4/01/02 Mark is now back from Germany with renewed vigour to mount an imminent legal assault on DEFRA's publication on the origins of BSE - as prepared by the Gabriel Horne Committee - which is considered to be defamatory towards his work (See New Links).
Having been awarded the "Acres USA Annual Eco-award" for his presentation at Minneapolis last December, he has now been invited for research and /or lectures in Vermont, Japan, Washington DC, Montana, Texas and Australia for the first half of 2002.
But despite his growing recognition abroad, the UK' government's reductionist mindset on the cause of TSEs has still frozen him out of TSE research in the UK. Their media and medical spin doctors have successfully indoctrinated the entire nation onto the Meat and bone meal theory. Not surprisingly, Mark's only opponent in the audience at the Fats and Protein Research Foundation symposium in Florida was an Englishman who, ironically , was chairman of the UK Renderers Association - an organisation who should know better than to misappropriate blame onto their very own products (MBM) which they had exported for cattle feed to BSE-free countries all over the world for half a century !
Even Mark's grant proposal to DEFRA for TSE field studies was rejected out of hand - despite recommendations from the Phillips BSE Inquiry that his work should be financially assisted.
Furthermore, the main basis for DEFRA's rejection was almost entirely based on the ineptitude of one of the five reviewers who had misread the standard W soil sampling protocol that Mark had proposed. The upshot of this error resulted in the whole DEFRA grant assessment team misconceiving the total number of samples to be drawn in each TSE cluster location by a 20 fold less amount than the number actually proposed. Despite Mark pointing this aberration out to DEFRA staff - that "20" soil / "20" plant samples had actually been proposed for each cluster location instead of the "one" / "one" samples misconceived by the reviewer - DEFRA have still rigidly held to their most senior "expert" reviewer's radical balls up.
The Horne committee report for DEFRA exhibits how shambling oversimplification, errors and judicious selection of data leaves us none the wiser on BSE or TSEs. Until we listen to scientists who understand the environment and oxidative biology nothing will change. BSE will continue to spread, as it has for 20 years - Its now in Slovakia and Japan. Read Mark's rebuttal of this work in relation to his research. Rebuttal of Prof. Gabriel Horne's committee publication on the origins of BSE.


Prince Charles and funding.
The results of Prince Charles's most encouraging private meeting with Mark at Highgrove last summer 2001 has ended up negative. That same old handful of incestuous experts who advise the Uk and Euro governments on anything to do with BSE, got their oars in there yet again, advising Prince Charles's King's Fund not to finance Mark.

  • I’ve been contacted by journalists and writers from Canada, Ireland, the States, Honolulu, Australia. Mark has been doing radio and TV interviews for Germany, France, the Netherlands, the States. He also spent a few days in early Feb 2001 in Montpelier in France where he appeared as an expert witness in a GM crop case and spoke at their ‘Mad Cow day’ conference.
    •

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    The British Medical Journal 7/4/01 -
    CLINICAL REVIEW on BSE and vCJD by Paul Brown

    There were many things in this article that made me fume. It gives the impression of being authoritative but is full of enormous assumptions, illogic and unsophisticated observations. I sent a detailed response to the BMJ but they didn't print it (or acknowledge it) Below are some of his statements but please go to Full text of article by Paul Brown.

    'It is sometimes forgotten that in the story of bovine spongiform encephalopathy and variant Creutzfeldt-Jakob disease there is but one incontestable fact, that bovine spongiform encephalopathy is the cause of variant Creutzfeldt-Jakob disease.'
    'The infectious agent that causes scrapie in sheep crossed the species barrier to bovines to cause bovine spongiform encephalopathy.'
    Summary Points :
    Changes in the rendering of livestock carcases allowed infectivity to survive and contaminate meat and bone meal in livestock feed, amplifying infection to epidemic proportions
    Export of contaminated meat and bone meal and live cattle incubating the disease caused the spread of bovine spongiform encephalopathy to other countries
    Bovine spongiform encephalopathy caused variant Creutzfeldt-Jakob disease, most probably through adulteration of cooked meat products with mechanically recovered meat contaminated by compressed spinal cord and paraspinal ganglia .
    International regulatory measures are limiting the further spread of bovine spongiform encephalopathy, its entry into the human food chain, and potential secondary human to human spread of variant Creutzfeldt-Jakob disease, so that both diseases should gradually disappear.'
    'Other theories about the origins of bovine spongiform encephalopathy are rather too fanciful to credit seriously. For example, the idea that bovine spongiform encephalopathy results from exposure to organophosphates fails to account for experimental transmissibility of the disease and for the absence of bovine spongiform encephalopathy in countries that use organophosphates extensively, such as Japan. The riposte that organophosphates originally induced a toxic disease in UK cattle that then became infectious simply has no biological (or logical) precedent.'

    CLINICAL REVIEW
    Regular review: Bovine spongiform encephalopathy and variant Creutzfeldt-Jakob disease

    Paul Brown
    BMJ 2001; 322: 841-844 [Full text]

    My comments:

    The theory of Paul Brown and MAFF is a long way from demonstrating Koch’s postulates for BSE or vCJD, which given the millions of pounds in research over 15 years, strongly suggests that it’s not correct.

    Summary points

  • As Paul Brown notes the experiments to investigate how effective the chemical extractor, acetone, had been at inactivating PrPsc showed it was very poor. This process did however result in higher residues of pesticides ending up in Mbm.

    • Brown starts his article ‘The one incontestable fact is that BSE is the cause of vCJD.’ It certainly is contestable - Products from the human food chain have not transmitted BSE experimentally. Mbm containing PrPsc doesn’t transmit BSE, but bovine homogenate fed orally does ( Humans and cattle don’t of course eat homogenate). This suggests food processing provides protection against PrPsc infectivity. The aggressive process of homogenisation causes a proliferation of free radical chain reactions by separating reactive metals like Iron and Manganese from their protein ‘sinks’: this is a risk factor in prion disease and this is likely to be the explanation for transmission by homogenate. Science must be precise and homogenate is not a reliable predictor of disease pathogenesis in vivo and so Koch’s postulates aren’t yet demonstrated for this hypothesis.

    You can’t demonstrate a cause and effect from BSE to vCJD, as Brown implies, simply because the pathology of vCJD and BSE is very similar.– If you discovered a pathology of lead poisoning in a cow and it’s herdsman would this prove that the cow had transmitted the pathology to the herdsman or vica versa or could they both have been exposed to a common trigger.

    The epidemiology of vCJD and sporadic CJD very strongly suggests that environmental factors common to victims are at work, because many of the cases are very close together, 200 metres in some cases. Bovine PrPsc must have been so common in the late 80s in a wide variety of processed foods consumed all over the UK, that virtually the whole population has been exposed. It’s thus very difficult to understand why ubiquitous PrPsc should concentrate CJD in precise topographical foci. In Queniborough, for example, there has been one case of classical CJD (12 years ago ) and 2 recent cases of vCJD in the same road, and 3 further vCJD cases in the area and a case of Feline Spongiform Encephalopathy. The recent observations by Dr Philip Monk are irrelevant because the practise of bovine skull splitting was widespread and brain and spinal cord would have ended up, in high dose, in foods consumed throughout the UK – burgers, gravies, meat pies etc. as Brown points out.

    Brown says ‘its fanciful to credit seriously that organophosphates could have initiated BSE’ whilst failing to grasp the most basic points of the theory. Obviously OPs per se don’t cause TSEs as they’ve been used all over the world for decades. There is enormous variation within OP compounds and how they are used: dose and interval between treatment; formulation - systemic or non-systemic, oil or water based; exposure route; means of application; additional ingredients and impurities are often present; neuropathic or non neuropathic; LD 50. Some OPs and treatment protocols would pose more risk than others.

    In the 70s I.H Pattison and others found that a non transmissible S.E was produced by treating animals with a copper chelator, cuprizone.

    About 5 years before BSE started a copper chelating di-thiophosphate, Phosmet, was poured along the spine of cattle in the UK, at 4x the maximum recommended dose, to eradicate warble fly. This was an intensive, compulsory campaign restricted to specific zones. The compound, Phosmet, also happened to be an OP and it was systemic and in an oil based formulation. This is the only country in the world that followed this procedure. Phosmet was also used, on a voluntary basis, as a lice powder at 2x max dose. There is a correlation between Phosmet usage and the rise and fall of BSE, but this is not the whole story.

    We think that there is another factor involved in TSEs based on our studies in several cluster zones. This is high levels of the trace metal Manganese (Mn).

    Broadly speaking we’ve found 3 main environmental pre requisites for sporadic prion disease to occur: High Mn levels, low Copper(Cu) /anti oxidants and an oxidising agent – in BSE Phosmet fulfils the latter 2 of these. These conditions can invoke an abnormal cellular chemistry in the host that gives rise to an error in the manufacture of the prion protein- when Cu is low the prion binds a second choice metal, Mn at the histadine sites of the octapeptide repeat region. An oxidative trigger, such as a pesticide, would encourage higher oxidative species of Mn, ( 3+ or 4+) and this change in field charge results in eventual conformational change/ protease resistance which is synonymous with the disease state. This has been tested in cell culture by Dr David Brown at Cambridge University. He found Mn bound to the prion in a low Cu cell , and on aging for 14 days, a protease resistant, conformationally changed prion developed in the culture – without the addition of exogenous PrPsc. He has also now found Mn to be elevated 10 fold in CJD brain samples.

    This scenario can explain most of the TSE we have studied. The support from lab work is limited because only 2 trials have been conducted into the hypothesis : we urgently need to do more .

    Nigel Purdey.

     

    INTERVENTION AT THE BBC FROM THE OP INFORMATION NETWORK


    A Mrs E. Sigmund, of an organisation known as the Organophosphate Information Network, phoned a number of the BBC staff who made the Correspondent programme shown on 25/3/01 and generally ‘pissing’ (their words) them off, according to director/producer Leo Telling. If you deconstruct the waffle you are left with her perceptive observation, (there only seems to have been one) goes like this ‘My OP victims are being treated with Manganese so how come they haven’t got CJD?’
    Well, well did she really mean this or has she got something a little bit wrong here – OP and other pesticide induced CFS/ME/MCS are frequently treated with intra muscular injection of Magnesium Sulphate and/or Magnesium supplements – quite a few papers on this. As it happens I’ve suffered with such a CFS for 12 years, induced by high levels of fat bound Mevinphos/+ OCs Lindane/DDT and others, and have had the Magnesium injections myself + supplements. I’ve never come across a single ref. to Manganese as a therapy for OP linked conditions : indeed it would be contra indicated in these conditions. Surely she couldn’t condone the use of Manganese for ‘her’ victims.
    The other explanation is she got it wrong - I suppose the first 2 letters are the same Ma… um, so easy mistake to make, after all she’s only in charge of a large number of OP victims’ campaigns- Gulf War vets, Sheep dip affected farmers.
    I can’t help thinking her time would be better spent in going back to biochemistry kindergarten to learn the basics rather than unleashing the tedious verbal diatribe against Mark’s work and wasting BBC time.
    Glad she doesn’t represent me.
    Nigel Purdey.27/3/01

    My response to the answers given by the Dutch Minister of Agriculture to questions from Joop Atsma MP, Dutch Parliament Jan 2001.

    I would like to respond to the questions and answers concerning my brother Mark Purdey in your Parliament. I have worked closely with Mark for many years and we have travelled to many places to study the environments where Spongiform Encephalopathy (SE) diseases are clustering.

    I will begin by making clear that your Minister of Agriculture is not familiar with Mark’s published work judging by his comments. Briefly Mark’s theory is that when Environmental factors give rise to particular abnormal conditions in the host’s cells then this leads to an error in the manufacture of a copper carrying protein, known as the prion. This is a normal anti oxidant protein that animals are constantly manufacturing in their bodies. We think there are 3 basic requirements to produce the abnormal form of this protein and the Spongiform type of disease that ensues when it is created: low Copper, high Manganese and a source of oxidative stress – such as produced by pesticides or Ultra violet light. These conditions are the primary cause of the disease.

    The abnormal prion also has a secondary infectious capability, well known from laboratory work. However there’s much Scientific evidence to suggest that this is rarely the cause of the disease in life and I think that the simple ‘infectious agent’ idea that has totally dominated orthodox research is a ‘red herring’.

    The basic requirements could be fulfilled by many combinations of Environmental factors.

    If we consider the case of BSE. In the UK we used a lipophilic systemic di thiophosphate OP pour on at 4x the recommended maximum dose to eradicate the warble fly in the eighties. This dosage was unique to the UK. There were also many other ways in which our cattle were being exposed to OPs ie. Phosmet was used as a lice powder at a high dose. The point about the di thiophosphate class of OP is they fulfil two of our criteria – they bind up and effectively lower available copper and they act as an oxidative stressor. Other OPs would serve as oxidative stressors only, whilst another class of OP that contain manganese, Maneb, Mancozeb would pose an added risk factor.

    I hope it is clear from this that we do not think that OPs per se cause BSE, this is obviously too simplistic as OPs have been used all over the world for decades.

    You have to consider the cumulative affect of pesticides: the way they are used, the dosage and formulation, their inert ingredients and then set this in the context of the nutritional status of the cattle with particular respect to anti oxidants.

    The levels of trace metals like Copper and Manganese are going to be affected by a number of factors – soil/herbage and water, levels in Meat and bone meal feed (Mbm), supplements and fertilisers, industrial pollutants as well as pesticides. You have to study all these things to reach an understanding of why the disease is occurring.

    The Minister states that this hypothesis is not based on Scientific evidence and that Scientists and Politicians consequently ignore it. Let’s just turn this around and consider the Scientific evidence for the official hypotheses.

    The Mbm theories ( there are 2 or 3 main ones) are not based on sound scientific evidence, and this is in spite of £140 million of research over 16 years : Mbm fed to experimental animals does not produce the disease ; Mbm exported in millions of tons to many countries other than UK produced no BSE ; No Scrapie strain innoculated into cattle has produced BSE ; The implicated mutant prion content of Mbm has been reduced to virtually nil over 14 years and yet BSE is starting, and shows an upward trend in many countries; Cattle are getting BSE in the UK who have not been fed Mbm or whose parents didn’t have BSE ; Cattle have fed on Mbm containing sheep remains since the 1850s without getting BSE ; on testing none of the changes in the rendering plants ( lowering temperature, cessation of solvent extraction) often blamed for triggering BSE, affected the mutant prion at all, hence they are irelevant.

    In contrast only about £25,000 over 12 years has been spent in directly researching Mark’s theory. I’ll summarise some of the key points.

    He’s published 6 papers in peer reviewed journals.

    The peer reviewed fieldwork studies of SE cluster zones, conducted in several countries, demonstrate high Manganese and low Copper in the environment. Preliminary cell culture studies with low dose OP Phosmet demonstrated a number of key changes in the prion protein associated with SE pathology (Institute of Psychiatry). Studies with high Manganese and low Copper in cell culture caused full conformational change in the prion protein – SE in a test tube without any infectious agents. ( Cambridge University).

    Professor Malcolm Ferguson, Scientific advisor to The UK BSE Inquiry, said after Mark’s presentation to the Inquiry that we need more research on OP/BSE links.

    I quote two passages from the published results of the Inquiry – ‘Although the full significance of these results (cell culture work with OPs) in relation to BSE is not clear, such effects do indicate that OPs, and other chemicals, could potentially be involved.’

    ‘However, the finding that PrP can be modified in vitro by appropriate chemistry raises the possibility that similar reactions might be induced by environmental factors ‘in vivo.’

    Professor Michel Bounias, Director of Research INRA-DSPE, Avignon University has been studying the links between ‘varron’ ( type of Warble fly) pesticide treatment and the incidence of BSE in France and his conclusion is that there is a strong correlation between the two ( yet to be submitted for peer review). He has asked Mark to collaborate with him on further research into the links.

    The British Government are on the point of funding, according to the Rt Hon.Tom King MP, Mark’s latest research project.

    Abroad we have had encouragement and help from highly distinguished researchers in the field such as Dr Eva Mitrova of Bratislava University and from Professor Maurizio Pocchiari ( an advisor to Franz Fischler) who asked to be part of our ongoing study in Italy, Sicily and Sardinia.

    I hope this goes someway to dispel the myth that what we are doing has no Scientific basis and is a waste of time .

    We do not have all the answers by any means. All we have ever wanted is to have our ideas subjected to rigorous Scientific scrutiny in the Lab. BSE and CJD are complex diseases much more similar to Alzheimer’s disease than to TB. Unless Scientists stop trying to force BSE and CJD into the simplistic model of a disease perpetrated by a single, DNA driven infectious agent, they, and the world at large will continue to be totally baffled as the disease spreads.

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    ©Nigel Purdey March 2002