Taking Back Our Stolen History
Mad Cow Disease
Mad Cow Disease

Mad Cow Disease

The common term for Bovine Spongiform Encepholopathy (BSE), a progressive neurological disorder of cattle which can be transmitted to other species, including humans. In humans, it is called Creutzfeldt-Jakob Disease, after the two doctors who first described the symptoms of the disease. Pharmaceutical interests in the UK ignored scientific research that shows the insecticide used in the UK government’s own warble-fly campaigns triggered the UK surge of ‘Mad Cow’ disease and is also linked to Alzheimer’s disease. Scientist and organic farmer Mark Purdey, who had sent evidence to a parliament inquiry committee on the insecticide, had his house burned to the ground, his lawyer and veterinarian were killed, and 2 scientist – Dr. C. Bruton, a specialist on the disease who died just before he could release his completed study, and leading Alzheimer’s and brain researcher Tsunao Saitoh and his daughter were both killed in a “very professionally done” shooting according to Reuters.

Just as he would later do in fear-mongering for the Covid fake pandemic, Neil Ferguson of Imperial College Modeling Center (funded by Bill Gates) predicted 136k deaths from mad cow, forcing the killing of 11M sheep. The actual number of deaths was 177.

The disease in cattle is called Bovine Spongiform Encepholopathy because this form of the disease occurs in cows (therefore, the term bovine), it causes a sponge-like destruction of the brain (therefore, the term spongiform encepholopathy – enceph means brain and pathy means pathology – meaning an abnormality).

Latest experiments by Cambridge University prion specialist, David R. Brown, have shown that manganese bonds with prions. Other researchers 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 led the prevailing theory at the time that an infectious prion in bonemeal fed to cattle causes bovine spongiform disease (BSE).

Infectious prions were also claimed to cause the 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 work proves that the prions can bond with manganese in animal feeds or mineral licks. These manganese prions cause the neurological 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 Alzheimer’s -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 marginalized research has devastating financial implications for ICI. It would provide a firm basis for litigants -who could include CJD sufferers, farmers across the world 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 licenses 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 fits neither.

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 Alzheimer’s 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 has recently conducted experiments on mice that confirm the organophosphate risk.

Not only is the EC beef slaughter campaign futile -because BSE 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 organophosphate insecticide.

Of greater concern is that some lotions for scabies and head lice are now priming children and adults, for CJD and Alzheimer’s 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 absorber of damaging energy from ultraviolet rays and other oxidizing agents.

Once this prion defense 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 pharmaceutical 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 favor 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 spongy thinking myopathy.

Do Not Use Systemic Organophosphate Insecticides

Do NOT treat children with OP head lice products – they may cause CJD and Alzheimer’s
Do NOT treat your pets with OP anti-flea products
Do NOT treat cattle or animals with OP products – they may cause BSE
Do NOT give manganese to cattle previously dosed with a systemic OP
The relative availability of the metals copper and manganese in you local environment is a major factor in BSE & CJD


Fascinating information about the truly horrible things that pesticides can do and the travesty of Mad Cow Disease. Be sure to read the other article in this week’s newsletter on this topic, which is entitled “Animal Pharm” and written by Mark Purdey himself, the originator of this theory.

Source: Mercola.com

Following are key dates in the mad cow crisis:1

1986 — First diagnosis of bovine spongiform encephalopathy (BSE), a new disease in cattle, is made.

1988 — Britain makes BSE a notifiable disease.

July 7, 1988 — Britain announces that all cows known to be infected with BSE will be destroyed as a precautionary measure.

1989 — Britain bans human consumption of certain offal, including brain, spinal cord, thymus, spleen and tonsils.

1990 — European Commission bans imports to the continent from Britain of cattle over six months old.

Sept. 25, 1990 — Ban is imposed on use of offal from cattle in animal feed.

1994 — European Union approves proposal to ban exports of meat containing bones from herds which had not been free of BSE for six years instead of two.

Dec. 7, 1994 — European Union agrees to ease export curbs on beef from British cattle born since January 1, 1992.

1996 — British government admits for the first time that BSE could be transmitted to humans in the new form of Creutzfeldt Jakob disease (vCJD).

March 23, 1996 — Fast food giant McDonald’s suspends the sale of British beef products in its restaurants in Britain.

March 27, 1996 — European Union ban on British beef and beef products is announced.

April 1, 1996 — Britain offers a range of actions including general and targeted culling of cows. It would involve killing all unproductive cows over the age of 30 months and destroying their carcasses.

April 24, 1996 — Britain offers to slaughter up to 40,000 cows in a bid to speed up elimination of mad cow disease. This offer is increased to 80,000 later.

May 21, 1996 — Prime Minister John Major says Britain will no longer cooperate in E.U. business until the ban on its beef exports had been eased and a framework for a complete lifting put in place.

May 24, 1996 — Britain issues proceedings in the European Court of Justice seeking the annulment of the beef ban.

June 11, 1996 — European Commission formally lifts export ban on British beef by-products.

June 19, 1996 — Framework deal for gradual lifting of ban includes Britain agreeing to cull up to 67,000 more older cattle.

June 21, 1996 — Deal agreed on lifting beef ban at Florence summit of E.U. leaders.

July 12, 1996 — The European Court of Justice rejects a bid by Britain for an immediate suspension of the European Union’s worldwide ban on British beef exports.

July 22, 1996 — E.U. scientists say BSE can infect sheep.

Aug. 1, 1996 — Britain’s agriculture ministry confirmed that mad cow disease can be passed from cow to calf.

Aug. 2, 1996 — A British scientist said that reports that cows can pass BSE on to their calves meant it was possible pregnant women with vCJD could infect their babies.

Aug. 19, 1996 — A British coroner ruled that Peter Hall, a 20-year-old vegetarian who died of mad cow disease, caught it from eating beef burgers as a child. The verdict is the first to legally link a human death to mad cow disease. Hmmm?

1997 — The European Parliament condemned European Commission President Jacques Santer and Britain for serious errors in the way they handled the mad cow crisis.

Dec. 3, 1997 — Britain banned the sale of boneless beef as a precautionary move to stop the risk of mad cow disease.

March 16, 1997 — E.U. farm ministers voted to ease the worldwide ban on British beef exports and allow a limited resumption in exports from Northern Ireland of beef from cattle in herds guaranteed to be free of mad cow disease for eight years.

Aug. 1, 1999 — An export ban on British beef following the mad cow disease scandal was lifted after 3½ years.

Sept. 22, 1999 — The British government’s chief medical adviser warned that the country could face a possible epidemic of human mad cow disease in the years ahead.

Oct. 29, 1999 — The European Commission’s top scientists gave British beef a clean bill of health.

June 29, 2000 — British Agriculture Minister Nick Brown announces that a cow, born after measures were introduced to eradicate mad cow disease, had been found to have BSE.

Oct. 2, 2000 — An independent British inquiry’s 16-volume report into “mad cow’s disease” and its human form is given to Health Secretary Alan Milburn and Agriculture Secretary Nick Brown.

Oct. 26, 2000 — Britain’s official report into BSE criticizes officials for consistently playing down the risk to humans and failing to properly coordinate a government response. British government announces compensation scheme for the victims of the human form of mad cow disease.

Nov. 7, 2000 — French farmers decide to no longer sell meat from cows born before mid-1996, the date when France introduced strict measures to fight the illness.

Nov. 8, 2000 — French Prime Minister Lionel Jospin tries to soothe spiraling fears about the safety of beef, urging calm and criticizing farmers for fueling general panic about deadly mad cow disease.

Nov. 10, 2000 — France bans sweetbreads, the Swiss Red Cross limits blood donations from people who spent time in Britain, and the European Union’s health and consumer protection commissioner urged EU member nations to go beyond a recent requirement that they randomly test their herds by January.

Nov. 14, 2000 — France bans the T-Bone steak and the use of animal feed made with meat, calls for a review of slaughterhouse practices and triples funds for studying the cause of BSE.

Nov. 17, 2000 — Italy bans most beef imports from France, hoping to prevent mad cow disease from speading in the country.

Nov. 18, 2000 — Greek butchers associations begin a boycott of French beef in a bid to stop a sharp decline in sales in the country, saying they would only sell Greek beef and pledging to set up blockades to stop the distribution of French imports.

Nov. 21, 2000 — European Union farm ministers order cattle over 30 months old deemed to be at higher risk from the brain-wasting disease to be tested for BSE as of Jan. 1, with all cattle categories over 30 months old to be tested as of July 1.

Nov. 22, 2000 — Spain confirms its first case of mad cow disease and investigates a second possible case. Farms where the cows lived are quarantined.

Nov. 24, 2000 — German Chancellor Gerhard Schroeder promises to get tough in fighting mad cow disease after two German cows test positive for BSE. Portugal’s Azores Islands report the first case of mad cow disease there, involving an animal imported two years earlier from Germany.

Dec. 4, 2000 — At a special meeting, EU agriculture ministers approve a six-month ban on the use of animal products in animal feed. Germany expresses concern that the ban is too short. The EU estimates the cost of a six-month ban at $1.3 billion.

Dec. 7, 2000 — Germany, arguing that a six-month ban is too short, pushes European Union leaders to agree to make the six-month-ban on the use of animal products in fodder permanent. Germany’s Chancellor Gerhard Schroeder announces a permanent ban has been ordered.

Dec. 8, 2000 — EU ministers end up supporting a six-month rather than a permanent ban on animal products in animal feed. The ministers agree to set up a food regulatory agency. They also agree to keep out of the food chain all cattle older than 30 months that have not been tested for the disease.

Dec. 19, 2000 — The French government announces it is banning blood donations of people who spent more than a year in Britain from 1980 to 1996, a precautionary measure against mad cow disease. German officials rush to reassure consumers that their sausages are safe after a European Union official hinted the country’s beloved bratwurst, currywurst or even weisswurst could also be considered suspect in the mad cow disease scare.

Dec. 20, 2000 — Germany’s health minister warns the public to stop eating some sausages made of meat from the backbones of cattle and calls on producers to take the products off the market, saying it was a precaution based on the recommendation of scientists.

Jan. 2, 2001 — France begins testing cattle aged 30 months and older, six months before such testing — mandated by the European Union — was required to begin. Spanish authorities announce two new cases of mad cow disease.

Jan. 5, 2001 — Hoping to fend off criticism of its reaction to the panic, the German government proposes lowering the age of cows to be tested for BE, implementing tougher food safety inspections and banning animal-based feeds and risky products. Spain reports three new cases of mad cow, while Australia and New Zealand announce they will ban all beef imports from Europe.

Jan. 9, 2001 — Germany’s agriculture and health ministers resign over their handling of the mad cow scare. The Belgian Federal Agency for Food Safety reports 161 cases of BSE in 2000, more than five times the number detected in 1999. French farmers block a slaughterhouse to protest the economic impact of the disease.

Jan. 16, 2001 — The European Union appeals to consumers to stay calm, despite the discovery of suspected mad cow cases in Austria, Spain, Bavaria, Belgium, and in an Italian slaughterhouse that has supplied beef for McDonald’s hamburgers. Some of the suspected cases were in areas previously believed to be in the clear. The EU says it’s only natural that new cases would be discovered, now that a mandatory beef testing policy is in place.

Jan. 18, 2001 — An FDA advisory panel votes to ban blood donations from anyone who lived in France, Ireland or Portugal for 10 or more years after 1980. A wider ban had been requested by the American Red Cross.

Jan. 25, 2001 — The U.S. Food and Drug Administration quarantines some cattle in Texas to investigate whether the animals ate feed made from carcasses of cows. Regulations meant to keep mad cow disease out of the United States prohibit that practice.

Jan. 26, 2001 — The U.N. Food and Agriculture Organization urged precautions worldwide against mad cow disease, saying that any country that imported cattle, meat or bone meal from Western Europe since the 1980s was at risk. Germany, meanwhile, dropped the testing age for cattle from 30 months to 24 months.

Jan. 31, 2001 — Germany said it would destroy about 400,000 cattle that may be infected with the disease. Spanish officials said they had detected three new cases of the disease, bringing to 12 the number discovered there so far.

Feb. 16, 2001 — France asks for aid for farmers affected by the mad cow scare, Germany passes a law increasing government’s powers to deal with the beef emergency and Italy confirms its second case of BSE.