Insecticides Cause Mad Cow Disease
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 UK surge of ‘Mad Cow’ disease.
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 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 neurological degeneration seen in BSE. According to the specialists, by a similar process 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.
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.
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.
Purdey has been consistently denied even exploratory funding to extend his privately supported research. Yet the Purdey/Brown chemical poisoning model matches with the epidemiological 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 noninfectious, 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.
Why does CJD degeneration in humans begin in the retina, and why are CJD disease clusters found in high altitude locations?
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.
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.
EIONews.com December, 13 2000
Recent Comments