Insecticide linked to BSE, CJD and Alzheimer's.
by Fintan Dunne.
Tel: +353-87-681-4133
Editor, http://www.aidsmyth.com/
Research Kathy Mc Mahon
7th December 2000.

«The media loved the BSE theory because they could drum up a viral holocaust-horror scoop. The vegetarian and green lobbies found themselves landed with a powerful propaganda weapon on their plate- turning cows into cannibals. The UK scientific establishment could go on drawing generous grant funding for their viral witch-hunt without the embarrassment of having to account for years of barking up the wrong tree. And the government could foist the BSE blame onto a naturally occurring agent for which no significant vested interest or official body could be held accountable». Scientist, Mark Purdey.

Mark Purdey.

New scientific research indicates pharmaceutical interests and the UK government have been leading the European public on a BSE wild goose chase to conceal it was the British government's own phosmet warble fly dosing which triggered BSE in British cattle.

The Europeans are already mad at the British over BSE, they will go balistic when they find out they have been decimating the European beef industry-based on a junk science designed to cover up a straightforward chemical poisoning scandal.

Cambridge University prion specialist David R. Brown has shown that prions are damaged by ICI's phosmet organophosphate insecticide and they can interact with manganese in animal feeds, then turn 'rogue' and directly cause BSE.

The very well-connected British pharmaceuticals group ICI, is the parent company of phosmet supplier Zeneca. Phosmet was used in the British warble fly campaign. In 1996, the phosmet patent was sold to a PO Box company in Arizona called Gowan -one week before the UK government admitted to a link between BSE and nvCJD. The US Environmental Protection Agency is now reviewing phosmet safety.

As Europe prepares to mass-sacrifice cattle on the altar of consumer protection -convinced that ingestion of prions from BSE-infected cows causes new variant CJD in humans- the marginalised scientists have clear evidence that both diseases are instead induced by organophosphate insecticides -not infected bonemeal or hamburgers.

Pharmaceutical determination to hide the chemical source of BSE and CJD is high. Awareness of the true cause would expose the role the insecticides play in Alzheimer's disease. British BSE management and research bodies are under pharmaceutical control. A number of leading brain researchers have died in suspicious circumstances in recent years.

But the current BSE debacle in Europe now threatens to uncover all this to public view.

The alternative theory matches with the epidermiological spread of clusters of CJD in humans and the incidence of BSE-type diseases in animals. If the research is right, then not only is the EC action futile, but lotions for scabies and head lice could be priming children for CJD and even Alzheimer's disease later in life.

Bending the prion.

Cambridge University prion biochemist, David R. Brown is dismissive of the science underlying the infectious model of BSE -what he terms «a very limited amount of science by a few assumed-reputable scientists». He insists there is «no evidence an infectious agent is present in either meat or milk».

«Simple tests on udder walls of cows -which could easily detect an infectious prion- have not been done, why I don't understand».

His latest published study examined how organophosphate (OP) in systemic warble fly insecticide can deform the prion molecule, rendering it ineffective at buffering free radical effects in the body. Worse still, the prion is then partial to bond with manganese and become a 'rogue' prion. A chain reaction whereby rogue prions turn others to rogues also, can explain the bovine spongiform disease mechanism.

He showed how prion protein bonds benignly with copper, but lethally with magnesium when the prion is degraded by OP effects. Even natural variations in relative environmental availability of manganese versus copper can trigger prion degradation.

The CJD and BSE symptoms mirror 'manganese madness', an irreversible fatal neuro-psychiatric degenerative syndrome that plagued manganese miners in the first half of the XIXth century.

Shining a light.

Organic dairy farmer and peer-published independent scientist, Mark Purdey, says the accepted theory of transmission from BSE-infected cattle to human CJD by bonemeal or meat is dependent on a mutant prion that has never been isolated under the scientific protocol called Koch's postulates.

Purdey's insistence on sticking to the letter of this scientific law earned him the condemnation of UK officialdom when he first mooted his theory. But Purdey pointed to CJD clusters downwind of a British Phosmet production plant to back his case.

He gave evidence to the UK Government BSE inquiry and was supported by Conservative MP, Thessa Gorman. His views were discounted, but his subsequent research and the new Cambridge prion work have confirmed the alternative theory. Despite this, and the backing of a British peer, he is denied even exploratory funding.

Speaking from his rural English Somerset farm today, as plans for the European cattle cull forge ahead, Purdey asks: «why does CJD degeneration in humans begin in the retina, and why are CJD disease clusters found in high altitude locations?».

The question is rhetorical, and Purdey has an eye-opening answer. He argues that the prion molecule has a known natural role as a shock adsorber of damaging energy from ultraviolet rays and other oxidizing agents.

Once this prion defence system is rendered ineffective by organophosphates - for example in human head lice lotions, these oxidizing effects have an unmediated impact on tissues. Eventually, UV radiation damages the retina and oxidative stress destroys the brain tissues of CJD patients. This theory would expect to find higher CJD incidence in mountain regions -where UV radiation levels are elevated. That prediction holds true.

A similar but accelerated mechanism could be driving BSE. ICI's Phosmet organophosphate warble fly insecticide -applied on the backs of animals along the spinal column, similarly degrades prions. "Systemic versions of the insecticide are designed to make the entire cow carcass toxic to warble fly," explains Purdey. «Unfortunately it's toxic to prions too -especially those prions located just millimeters from the point of application».

The damaged prions are then ready to react with manganese in animal feed, or manganese sprayed on land or in mineral licks -to become the driving force of BSE neurodegeneration. Purdey says manganese-tipped prions set off lethal chain reactions that neurologically burn through the animal.

Chickens notoriously excrete most of the supplements fed to them -including manganese. And their manganese-rich excreta have been blended into cattle feed in the UK. Natural variations in the relative environmental availability of copper and manganese can also spur prion degeneration says Purdey.

If these disease mechanisms are valid then there is a significant risk attaching to the use of organophosphate in humans. Preparations for head lice and scabies are known to be overused in practice and might be priming users for CJ disease.

Purdey believes his bias for field work is the key to his success. He bemoans the «reductionism» of much lab-centered science. «I have traveled the world to investigate known clusters of spongiform disease -something mainstream researchers don't seem remotely interested in doing».

Since first postulating an environmental -rather than infectious- theory of spongiform diseases, Purdey has built evidence from around the world that explains and predicts the incidence in humans and animals: a cluster of CJD in Slovakia, Eastern Europe -around a manganese plant; Icelandic reindeer with BSE, who were found to be eating pine needles rich in manganese; the futile slaughter of sheep in Cyprus -only for BSE to reemerge within years.

«The reappearance of BSE in Cyprus obviously points to an environmental cause», says Purdey, who is sanguine when reflecting on the condemnation of him by mainstream scientists.

«I suppose they have mortgages and kids who need to go to university», he muses. «Privately, some were agreeing with me, but then they would denounce me publicly. It was quite strange really».

The money trail.

Critical scientists like Purdey are unlikely to prevail in this argument. The pharmaceutical industry holds most research purse strings and would hardly energetically explore an avenue of research that could expose them to litigation as the prime cause of BSE. The official theory is lavishly funded, alternative theories rarely, if at all.

There are even more explosive implications to the new work. Purdey says similar OP-induced protein deformation could also underlie Alzheimer's disease. If that were true, the litigation fallout would destroy some pharmaceutical giants, and a lot of very influential noses would be out of joint.

Disturbingly, Purdey and other brain researchers seem to have had an undue share of unfortunate accidents. Purdey's house was burned down and his lawyer who was working with him on Mad Cow Disease was driven off the road by another vehicle and subsequently died. The veterinarian on the case also died in a car crash, locally reported as: 'Mystery Vet Death Riddle'.

Dr. C. Bruton, a CJD specialist -who had just produced a paper on a new strain of CJD- was killed in a car crash before his work was announced to the public. Purdey speculates that Bruton might have known more than what was revealed in his last scientific paper.

In 1996, leading Alzheimer's researcher Tsunao Saitoh, 46 and his 13 -year-old daughter were killed in La Jolla, California, in what a Reuters report described as a "very professionally done" shooting.

What Alzheimer's Disease, Mad Cow Disease, and CJ Disease have in common, is abnormal brain proteins and a putative link to organophosphates. Even Gulf War syndrome among returning veterans has been attributed, in part to the insecticide. But the sidelined scientists' suspicions are still largely ignored.

In their favour at the moment, is a growing unease on the part of the public. As BSE forges on and Governments panic, Science may be out to lunch on BSE, compromised by bovine spongythinking myopathy.

Mark Purdey funds his own research, testing/labs/travel to cluster sites. Donations to his research fund will help him carry on his work. Send to: Mark Purdey Research Fund, High Barn Farm, Elworthy, Nr Taunton, Somerset TA4 3PX, UK. Copyright © 2000.

http://www.aidsmyth.com/

Supplemental information:

Edited Introduction to the Purdey hypothesis on Spongiform Encephalopathy (SE).

The main problem we have with the meat and bonemeal (Mbm) hypothesis of either MAFF or the Royal Society is the amount of scientific contra evidence that exists to them. Any hypothesis that can’t demonstrate Koch’s postulates after 15 years of international multimillion pound research should be jettisoned.

Mbm fed to experimental animals does not produce SE Millions of tons of Mbm exported abroad, when mutant prion material was at its highest, did not produce any BSE. Mutant prion has been drastically reduced (to presumably nil) in Mbm over the last 14 years and yet BSE has been starting, with a continued trend upwards, in a number of EU countries ie Ireland, Portugal, Belgium, Brittany, Switzerland.

The hypothesis in summary:

In prion disease there is an error in the manufacture of the prion protein caused by an abnormal configuration and or binding of two key metals Copper (Cu) and Manganese (Mn). Mn substitutes for Cu when the latter is low or fails to bind to the histadine sites of the octapeptide repeat region of the protein. This substitution results in eventual conformational change/ protease resistance. In addition the host would be exposed to a free radical trigger that generates excessive oxidative stress and up regulates the prion protein as a defense.

The most important function of the Prion is to resist oxidative stress by acting as a Super Oxide Dismutase (SOD). On conformational change the prion cannot function as a SOD and protect cells, and consequently a pro oxidative status quo is established at a location in the host. This pathology spreads through the host during the incubation period, with neurones eventually being destroyed by the build up of toxic by products such as hydrogen peroxide, quinones or peroxynitrite.

Finally the metal species bound by the prion is more highly oxidised ie Mn 3+ or 4+ and this may explain strain difference and difference in incubation times. Environmental factors that affect the levels of metals, their species and protein 'sinks' cause the disease. Oral infectivity via food products is secondary and we think is rare in vivo. The often quoted transmission experiments are not reliable predictors of the situation in life - even oral homogenate studies are unreliable because reactive metals are freed from protein sinks in the process.

Further reading: Mark Purdey 'Ecosystems supporting TSEs demonstrate excesses of the pro-oxidant Manganese' Medical Hypotheses (2000) 54 (2) I’m hoping to get this online soon. D.R Brown et al «Consequences of Manganese replacement of Copper for prion protein function and proteinase resistance». EMBO journal vol 19 no.6 p 1180 - 1186 Useful background New Scientist 26 august 2000 article 'Metal Heads' by Jonathan Knight

FAQ; Organophoshates (OPs) and TSEs: The OP Phosmet used at 4 times the recommended max dose on cows in Britain in the 80s to control warble fly is a di thiophosphate systemic OP. The 2 sulphurs bind to copper forming a mercaptide ring. The Institute of Psychiatry conducted trials adding this OP to living cell cultures at very low dose. Off the record we were told that phosmet had created a conformational change in prion protein. This part of the work was suppressed by SEAC and not published or presented to the BSE inqiry.

Some OPs contain Mn - Mancozeb, Maneb. Mn is often sprayed on farmland where Mn levels are low. OP residues increased in Mbm in the early 80s.

Our current studies: Scrapie in Sardinia, TSEs in Calabria , vCJD (Kent, Queniborough, Armthorpe) - We receive no funding for these.

Past studies: Rida in Iceland, CWD in Colorado, CJD in Slovakia, Scrapie in Somerset/ N.Devon

Urgenttly needed, but straightforward, Lab research: Identify what is bound to the histadine sites of the octapeptide repeat in BSE, CJD and Scrapie prion material. Phosmet + live cell culture, transmit the result Maneb + live cell culture, transmit result. High Mn and low cu in transgenic mice. Transmit.

Trial therapeutic strategies:

1. Desferrioxamine.
2. Porphyrins.
3. Atropine/oxime.