Spongiform diseases occur in both animals and humans. The disease is given a different name according to the species, such as CJD in humans, Scrapie in sheep, BSE in cattle, and CWD (chronic wasting disease) in deer and elk. The disease occurs in elk and deer, yet these species have a vegetarian diet. Eating meat obviously does not cause the disease in vegetarian elk or deer. Therefore, eating meat cannot cause it in cows, sheep, humans, or any other species. Eating British beef cannot possibly cause a new variant or any other form of CJD.
We can also prove that BSE was never experimentally transmitted. What appeared to be transmitted was in reality induced putrid protein poisoning. Bio-accumulated neurotoxic residues that survived in the fat component of the newly introduced solvent-free fat extraction process triggered the British 1986 BSE epidemic.
Spongiform Encephalopathy is not a modern disease. It has been documented since 1750 occurring in sheep and is commonly known as Scrapie. CJD, a spongiform encephalopathy specific to humans, was first documented in the 1920's. Deaths caused by this disease prior were probably diagnosed as 'encephalitis.' The disease may have been misdiagnosed subsequently as encephalitis or Alzheimer's.
Bovine Spongiform Encephalopathy (BSE) was first documented as recently as 1985 and marked the beginning of an epidemic, which swept across the country resulting in almost 180,000 cases to date. We claim BSE always existed in older animals as a rare disease, but like CJD, it went unrecognized until the 1920s.
Another disease that went unrecognized was cot deaths. Over 1,500 babies died each year in Britain alone, yet it was not medically defined until 1969.
BSE is not spreading to Europe. They are just finding it!
Current Scientific Opinion
Gajdusek and Prusiner feel that the theoretical risk that BSE was transmissible to man was initially based on the assumption that the pathogen was transmissible and a virus. A Nobel Prize was awarded to (Gajdusek) for this proposal in 1976. The virus theory was eventually discarded but the concept of transmissibility remains, now enshrined with a Nobel Prize.
This is from a Daniel C Gajduseks 1976 press release:
"Ten percent of all cases of Creutzfeldt-Jakob's disease have a hereditary background. Also from these cases an infectious agent can be isolated. The finding that a hereditary disease had an infectious origin was completely new and unexpected."
This finding cannot be correct -- a genetic hereditary disease must be endogenous. We are being asked to believe the impossible.
Professor Stanley Prusiner won his Nobel Prize in October 1997 for his alternative prion hypothesis. Our March 1996 an Internet published discovery appeared in many ways, to be similar. He, however, attempted to explain how the infectious prion could replicate. He also claimed the disease is transmissible horizontally.
From Prusiner's 1997 press release quotes:
"The infectious prion particle forms within the body."
"Prions exist normally as innocuous cellular proteins."
"Prions are much smaller than viruses. The immune response does not react to prions since they are present as natural proteins from birth." http://www.nobel.se/medicine/laureates/1976/index.html
This quotation confirms our discovery.
The second Nobel Prize proves the first was wrong
It seems that once a disease is deemed transmissible it must always be transmissible. The well-established textbooks were never altered. Yet, both opposing theories cannot be right. The 1976 award was clearly wrong. As the transmissible element of the first Nobel Prize award was wrong, it logically follows that the same element was wrong in both awards. The second Nobel Prize award actually proves that the first was wrong.
Numerous experiments were conducted to prove that SEs were transmissible. These involved injecting or feeding healthy animals diseased tissue. The healthy animals went on to show symptoms of the disease. This was provided as evidence of transmissibility of the disease. However, this conclusion is incorrect -- the disease was never transmitted at all. The disease cannot under normal conditions breach the species barrier. It is the incorrect use of this word transmission to describe induction which forms the basis of our discovery proposal. This presumes and implies transmission when no true transmission has taken place.
The different ages of onset for Scrapie, BSE, Kuru, and CJD in the elderly are consistent and fit with the times of poisonings proposed by this discovery.
Changes in the feed rendering process
Animal meat and bone meal (MBM) processing was widely used for many decades without problems. In 1981-2, a new non-solvent-fat-removing-process was introduced. The government was correct in establishing this crucial causative factor but they are unable to determine the illusive pathogen responsible.
The epidemic can be explained by understanding the rendering process. MBM is a by-product of waste animal carcasses mainly from abattoirs. To remove excess fat from this ground-up compound it was subjected to a solvent wash. This solvent fat removing process was discontinued mainly in England because the price for tallow had dropped. The new process increased the final fat content which now also contained the previously removed toxic residues. These were in the form of bio-accumulated free radicals i.e. dioxins and insecticide. The final stage of the solvent extraction process was a high temperature solvent blow-off which also assisted in the removal of the other toxic residues mentioned.
The cattle then chronically ingested the insidious poisonous residue. This triggered the 1986 BSE epidemic. Other toxic farm practices probably contributed and may still be promoting the disease today. The pathogenesis and pathology of the British BSE epidemic was different from old age related spongiform diseases because the toxins were transported by blood from cow to calf in the womb (teratogenesis), and then again via the feed. MAFF and SEAC have secretly acknowledged this discovery because cows are now slaughtered before reaching the age of thirty months, proving our claim that this disease of old age has begun to affect the young.
"Dioxins" refer to a group of chemical compounds that share certain similar chemical structures and biological characteristics. Dioxins are present in the environment all over the world. Dioxins are released into the air from combustion processes such as waste incineration and from burning fuels.
Dioxins can also be formed when household trash is burned and during forest fires. Animals can take up dioxins deposited on plants and concentrated in the food chain. Those animals then have higher concentrations than plants. Dioxins tend to accumulate in fat. About 95% of exposure to dioxins occur through consumption of food, especially food containing animal fat.
Organophosphorus pesticides used to treat cows with warble fly infestations are still in use and are implicated as an additional BSE promoter.
Many American elk and deer, like sheep, can also become infested with ticks.
The best example of BSE/CJD incorrect reasoning is the destruction of surgical implements without any evidence of a pathogen. This is the only infection known that is supposed to survive sterilization. This is really because the phantom transmissible agent simply does not exist. The tools are even being blamed for direct brain, cadaver extracted, dura mater graft surgery.
The phantom strikes again
The following is a report of the deaths of five young people in the village of Queniborough from vCJD.
"Traditional butchery practices are the most likely cause of Britain's first variant CJD cluster," say experts.
Clearly, we disagree. This blunder alone should be sufficient to demonstrate to the world the truth of our discovery. If you - the reader - cannot grasp this flagrant example, I will quote an American expression: "If you are not part of the solution, then you are part of the problem".
Similarity of SEs with Alzheimer's
Now Professor Chi Ming Yang, of Nankai University in Tianjin, China, has discovered that Alzheimer's amyloid proteins and prions have very similar structures. Alzheimer's disease, we propose, is spongiform disease without the parasite infection. The infection may independently produce CJD and the spongiform effect.
Researchers in Washington D.C. have discovered that a high-fat diet during early and mid-adulthood may be associated with an increased risk of developing Alzheimer's disease. When this research is combined with this proposal, the 1996 discovery is yet again clearly proven because independently each study reaches the same polyunsaturated fat, free radical damage conclusion. This we claim was the British BSE epidemic pathogen and trigger factor.
Our proposition could again be tested and proven by conducting a simple experiment which would involve treating two samples of organs from a cow. Dry clean and process one sample with a solvent used in the feed manufacturing process i.e. trichloroethylene, and compare the toxic residues of each. Only the non-solvent treated sample will contain the predicted neurotoxic residue.
We have proven the disease is not transmissible. A poisoning is not a transmissible disease, but an injury. The prion is a symptom, not the cause!
Two Nobel Prizes have been awarded, both claiming the disease is transmissible.
We affirm again our 1996 discovery that Spongiform encephalopathies are not transmissible to man or beast, unless aided by the intervention of man.
For more evidence go to: http://www.onshop.co.uk/bse/us_bse.htm
Wilesmith J.W., RYAN J.B.M, & Atkinson M.J. (1991) Bovine Spongiform Encephalopathy: Epidemiological Studies on the Origin, The Veterinary Record, 2 March 1991, 128, pp 199-203.
Bradley R. (1996) Experimental Transmission of Bovine Spongiform Encephalopathy, Prion Diseases, Elsevier: Paris, 1996, pp 51-56.
Transmissible Spongiform Encephalopathies. SEAC. London HMSO. September 1994.
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