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Re: Bird Flu hits North.K 100000birds destroyed! Whats Up 2Tuff??
 
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Published: 19 y
 
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Re: Bird Flu hits North.K 100000birds destroyed! Whats Up 2Tuff??


i am sorry. i said mike but i meant mark. check out his website:

http://www.purdeyenvironment.com/Index.htm

then there is an article on rense:

BSE (Bovine Spongiform Encephalopathy), or Mad Cow Disease, and its human form, nvCJD (New Variant Creutzfeldt-Jacob Disease), are incurable brain disorders. Holes appear in victims' brains, then they become demented and die. The diseases are not caused by a virus or a bacterium, but by a mysterious type of twisted protein, known as a "prion". The prion can propagate itself by causing other proteins to twist into the same shape. Prions can be passed on by eating the flesh of another animal, and are resistant to cooking and digestion.

A theory about how prions are formed suggests that organophosphate pesticides could be partly to blame. Two people have already died defending this theory, apparently at the hands of professional assassins working either for the British government or the chemical industry. So the theory needs to be taken seriously.

BSE first appeared in the UK in 1985. Since then, the disease has affected half of the cow herds in the country. New Variant CJD also first appeared in the UK, ten years later: to date, around 90 people have died from it. Both BSE and CDJ are beginning to spread throughout the rest of Europe; today, 30 European countries have had exports of their cattle banned. The diseases have the potential to destroy the entire European cattle industry, and kill thousands of people. The death toll from nvCJD is increasing by 35% per year, and the disease has a gestation period of twenty years. Some projections suggest that hundreds of thousands of people could eventually die from it.

Given the huge amount at stake, one might expect that any credible theory would be welcomed. Yet Mark Purdey, a British farmer from Somerset, has suffered constant harassment and has had to support his research from his own pocket. Purdey has a theory which might explain the mystery of why BSE and new variant nvCJD started in the UK, and why they are so much more serious there. However, since he went public with his ideas, some rather unfortunate things have happened:

1. Both his vet and the lawyer defending his case died in suspicious road accidents. His second lawyer also had a car crash, but survived.

2. When an article about his work appeared in the "Independent", a national British newspaper, his telephone lines were cut. He was therefore unable to take follow up calls from other papers and television stations.

3. His farm house was burnt down just before he was about to move in.

4. His Science library was destroyed by a collapsing barn.

5. When he travels around the country to talk about his theory, he is constantly trailed. Purdey believes that the root cause of BSE is an imbalance of magnesium and copper, exacerbated, in the case of the UK, by the use of a highly toxic pesticide known as phosmet. Phosphet is an organophosphate nerve toxin, originally developed by the Nazis. It is also related to the drug Thalidamide, which causes birth defects.

Phosmet is made by Zeneca, a subdivision of the British chemical giant ICI. A week after the British government first announced the link between BSE and nvCJD, Zeneca sold the patent for phosmet to a PO Box company in Arizona, apparently to avoid potential legal action.

The theory started when Purdey noticed that his cows, unlike those of his neighbours, were not getting BSE. Cows often suffer from a parasitic infection known as warble fly. Since Purdey is an organic farmer, he treated his herd with derris root powder, a natural remedy. Other farmers were using phosmet, which was later made compulsory throughout the UK. When Purdey bought an infected cow from another herd, he was able to reduce the symptoms of BSE by injecting oxime, which is an antidote to pesticide poisoning. However, officials from MAFF (the Ministry for Agriculture, Fisheries and Food) turned up to kill the cow before the experiment could be completed.

As well as the link to phosmet use, Purdey discovered that brain diseases such as BSE and nvCJD appear in clusters in many places around the world. The link seems to be a lack of copper and an excess of manganese.

For example, in some areas of Colorado and Wyoming, 4-6% of deer and elk suffer from CWD (Chronic Wasting Disease), which is related to nvCJD. These animals live in areas where the soils are very high in manganese. In Slovakia, where the incidence of nvCJD is a thousand times higher than normal, most of the victims live near a glass making plant (where manganese is used) or else down-wind of one of two large ferro-manganese factories.

In the UK, two factors have increased the amount of manganese which cows consume. Until 1988, cows were fed chicken manure. The chicken had been fed manganese to strengthen their eggs, but 98% of it ended up in the manure. In addition, a fungicide rich in manganese was used on crops at that time.

According to Purdey, a lack of copper and an excess of manganese causes proteins in the nervous system of foetal cattle to change into the abnormal prion forms found in BSE and nvCJD. Phosmet facilitates this process by binding to copper, and therefore reducing the amount available to brain tissues.

Recently, Dr David Brown, a chemist at Cambridge University, showed that manganese can replace copper in brain proteins, thereby transforming them into prions. Dr Brown lost his funding, and was not able to continue the research.

The BSE crisis started in the UK, and that country still has the highest rate of the disease. Purdey believes that this was because the British government was the only one to enforce systemic phosmet at such a high dose. Phosmet is used elsewhere, but either on a voluntary basis, or at a much lower dose, or non-systemically.

However, there is a long lag between the peak of phosmet use and the incidence of BSE. Purdey says that this is for two reasons. First, cows are most susceptible to phosmet damage when they are in the womb. Second, phosmet has to reach a certain concentration in the food-chain before it has an effect.

Quite apart from the direct attacks on Mr Purdey, the chemical industry have launched a media campaign to discredit his research. Although MAFF claims that any credible theories for BSE will receive funding, Purdey has received nothing.

The effort that the chemical industry has apparently gone to to discredit Mark Purdey mirrors the experiences of Alice Stewart, the scientist who first showed the link between radiation and cancer. Scientists who supported her had their cars rammed. Maybe in this case as well, the truth will come out in the end.


_____

Dr. Paul Kail has a Ph.D. in nueroscience from Cambridge University and is founder and Director of the Animal Consciousness Foundation, which can be reached via www.animals.org.


Did An Insecticide Trigger
Mad Cow/BSE In UK?
By Fintan Dunne
Research, Kathy Mc Mahon
From eionews.addr.com/organop.htm
12-16-00




Pharmaceutical interests in the UK are ignoring new scientific research that shows the insecticide used in the UK government's own warble-fly campaigns triggered the surge of 'Mad Cow' disease.

Latest experiments by Cambridge University prion specialist, David R. Brown, have shown that manganese bonds with prions to cause BSE. Other researchers unpublished work shows that prions in the bovine spine -along which insecticides are applied- can be damaged by ICI's Phosmet organophosphate(OP) insecticide -causing the disease.

British scientists have led the current theory that an infectious prion in bonemeal fed to cattle causes bovine spongiform disease (BSE). Infectious prions are also claimed to cause new variant Creutzfeld-Jakob Disease (CJD) in humans -from ingesting beef. But the infectious prion theory serves to obscure a tragic chemical poisoning scandal behind the majority of BSE cases.

The new work proves that the prions can bond with manganese in animal feeds or mineral licks. These manganese prions cause the eurological degeneration seen in BSE. By a similar process, prions in human brains are damaged by lice lotions containing organophosphate. This can result in neurological diseases like CJD and Alzheimers -later in life.

Many might be surprised to hear that organophosphates were developed by Nazi chemists during the course World War Two, as a chemical weapon nerve agent. One formulation of the insecticide -Maneb, or Mancozeb- actually contains manganese in addition to organophosphate.

The marginalised research has devestating financial implications for ICI. It would provide a firm basis for litigants -who could include CJD sufferers, farmers across the world, and the spouses and families of the many British farmers who committed suicide during this BSE debacle.

Phosmet organophosphate has been used at high doses in British warble fly campaigns. In 1996, ICI subsidiary Zeneca sold the phosmet patent to a PO Box company in Arizona called Gowan -just one week before the UK government admitted to a link between BSE and nvCJD.

The politically well-connected British pharmaceuticals group, ICI has the financial and political clout to block research into any cause other than the infective model. Indeed no substantive alternative research has been done. British BSE disease management and research bodies have taken decisions that do not seem guided by spirited scientific enquiry. Mysterious prions that jump species is the preferred research arena.

Scientist and organic farmer, Mark Purdey gave evidence to the UK BSE inquiry, that warble fly insecticide was the cause of the disease. The scientist wheeled out to rubbish Purdy's evidence -Dr. David Ray, later turned out to have been receiving funding from the insecticide manufacturer ICI.

A lobby group that includes Bayer, Monsanto, Novartis, Pfizer, Roche and Schering-Plough was behind the effort to discredit Purdey. In December 1999, the same David Ray was appointed to the UK Veterinary Products Committee (VPC) -a government body that licences animal medicines.

Purdey has been consistently denied even exploratory funding to extend his privately supported research. Yet, the Purdey/Brown chemical poisoning model matches with the epidermiological spread of CJD clusters in humans. It also predicts the incidence of BSE-type diseases in animals. The accepted infectious model does not fit either.

The pharmaceutical industry is all the more determined to hide the chemical source of BSE and CJD, because a spotlight on chemicals would expose the role the insecticides in Alzheimer's -another neurodegenerative disease. That might lead to claims which would dwarf those from BSE and CJD litigants. In fact, two leading brain researchers into CJD and Alzheimers have died in suspicious circumstances in recent years.

In the United States, the Environmental Protection Agency is already reviewing Phosmet's safety. The Centers for Disease control in the US have recently conducted experiments on mice that confirm the organophosphate risk.

Not only is the EC beef slaughter campaign futile, because the disease is mostly non-infectious, but unless the underlying chemical cause is addressed, BSE will simply reappear from chemical causes. A new warble fly campaign is already underway in France using the same organophosphate insecticide.

Of greater concern is that some lotions for scabies and head lice are now priming children and adults, for CJD and Alzheimers in later life.

BONDING THE PRION

Cambridge University prion biochemist, David R. Brown is dismissive of the Science behind the infectious model of BSE. He terms it "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."

A number of researchers have found that 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.

Brown showed how prion protein bonds benignly with copper, but lethally with manganese. 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 last century

SHINING A LIGHT ON SPONGIFORM

Organic dairy farmer and peer-review-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 yesterday -as plans forge ahead for the European cattle cull, he 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.

From this research, any prudent person would conclude 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; Rocky Mountain deer with Chronic Wasting Disease (CWD), 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. The pharma industry holds most research purse strings, and would hardly energetically explore an avenue of research that could expose them to litigation for causing BSE. The official theory is lavishly funded, alternative theories rarely, if at all.

There are more explosive implications to his -and other's latest research. Purdey says similar organophosphate-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. Mark Purdey Research Fund, High Barn Farm, Elworthy, Nr Taunton, Somerset TA4 3PX, UK.

and then he has another link:


http://www.markpurdey.com/

check him out.

http://www.markpurdey.com/

 

 
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