THE PATHOLOGY AND PATHOGENESIS OF SPONGIFORM ENCEPHALOPATHY

THE PATHOLOGY AND PATHOGENESIS OF SPONGIFORM ENCEPHALOPATHY

From: http://www.gerryparish.co.uk/research/bse/

Researchers: Anthony Parish PhD. & Ben Parish MSc.

(1) BSE is not a transmissible disease

(2) The endogenous origins of spongiform encephalopathy

(3) BSE epidemic trigger factor

Contact details

Other documents:

British BSE epidemic: Caused by three poisons

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(1)

 BSE is not a transmissible disease

Researchers: Anthony Parish PhD. Benjamin Parish MSc.

It has been scientifically determined that various forms of spongiform brain diseases such as BSE are transmissible. We claim this analysis was reached as a result of incorrect interpretation of the evidence. We have discovered that all forms of spongiform encephalopathies are endogenous similar to Alzheimer's disease,and are not transmissible even under abnormal experimental conditions (1). When researchers claim that BSE is being transmitted, it is of course being intentionally induced (2). The incorrect use of the word transmission to describe induction can be seen clearly by examining the dictionary definition of the two words. It is also incorrectly described as an infection. There can be  no infection without a virus or bacteria, as there are neither  it is clearly a poisoning. A poisoning cannot produce a  transmissible disease but it can be transplanted from one animal to another and made to appear transmissible.(3) (4) One can induce a broken leg but it would not then be described as being transmissible.

Transmission is an illusion.

Proof that all spongiform diseases are produced endogenously has been confirmed by animal research.

When cats,mice,sheep,pigs,goats,monkeys,etc.,are experimentally inoculated with BSE, they die of BSE (2), yet all naturally occurring forms of spongiform disease when microscopically examined have a species specific recognisable  pattern. When a different genotype is used to donate the feed or inoculums it produces what is referred to by SEAC as the "Donor species effect" (2) a mouse  with induced BSE for example (2) produced a mutant form of BSE as the induced poison is simply being transplanted from the donor to the recipient as these articles (3) (4) clearly demonstrate. 

To successfully reproduce the true disease the induced genetic material  must come from same species as the recipient.

This "Donor species effect" (2) visibly demonstrates  the disease cannot be transmitted to other species. New variant CJD was never new and never variant. It has always been simply CJD. If a new disease was immerging in Britain related to eating British beef the "species effect" would reveal from what animal the disease originated. The missing 'Donor species effect", in all forms of spongiform encephalopathy not induced by scientists, proves the disease did not breech the species barrier.

Conclusion

All forms of spongiform disease currently categorised as transmissible (2) are in fact, rock solid, fixed to each species. The whole theoretical transmissible risk to man was based on this unfortunate major scientific blunder. All research interpretations based upon it are flawed, null and void. A poisoning is not a transmissible disease.

(1) Bradley R., Experimental Transmission of Bovine Spongiform Encephalopathy, 1996, Elsevier, Paris.

(2) Transmissible Spongiform Encephalopathies. SEAC. London HMSO. September 1994.p 62

(3) http://www.asahi.com/english/op-ed/K2001111700276.html

(4) Brown P., Carleton Gajdusek D., Gibbs C.J Jr., & Asher D.M. (1985) Potential Epidemic of Creutzfeldt Jakob Disease from Human Growth Hormone Therapy, The New England Journal of Medicine, Sept 19, 1985, p728

Elk and  deer spongiform disase existed in America before the British epidemic

http://www.producer.com/articles/20010118/special_report/20010118cwd202.html

CJD is the young USA: http://www.usatoday.com/news/healthscience/health/mental/2002-04-29-hnb.htm

World © Copyright 2000 A R Parish ProtectRite Registration #: R692-5607

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(2)

The endogenous origins of spongiform encephalopathy

Summary

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 new variant or any other form of CJD. We can also prove that it 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.

Background

Spongiform Encephalopathies

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 until the 1920s it went unrecognised. Another disease that went unrecognised 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 around the world they are just finding a very rare disease.

Current Scientific Opinion

Gajdusek and Prusiner

Gajdusek and Prusiner 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 Daniel C Gajduseks 1976 Press Release:

"Ten percent of all cases of Creutzfeldt-Jakob's disease have a hereditary background. Also from these cases can an infectious agent 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 Oct 1997 for his alternative prion hypothesis. Our March 1996 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.

Transmission Studies

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.

Kuru

The different age's 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 this 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 to 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 effect the young.

Endogenous Origins of SEs

Dioxins

"Dioxins" for just one example refers 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 so those animals 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."

Organophosphate pesticides

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.

An Illusion

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 sterilisation. 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

Conclusions

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 prove the disease is not transmissible. A poisoning is not a transmissible disease it is 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..

Authors

Benjamin Parish M.Sc.

Anthony Parish PhD.

References

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. p. 62

For more evidence goto: http://www.onshop.co.uk/bse/us_bse.htm

World © Copyright 2000 A R Parish ProtectRite Registration #: R692-5607

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(3)

BSE epidemic trigger factor

Researchers: Anthony & Benjamin Parish 

The British BSE epidemic was caused  by cows eating  recycled waste meat and bone meal (MBM) The MBM content within the feed was doubled in the early 1980s to help boost milk yields.(1) 

Prior to this around  the 1970s a  new solvent free MBM feed process was  introduced (2) this we claim allowed bio-accumulated dioxins and other free radicals to survive  within the MBM (3). Previously the full  solvent cleaning method had efficiently removed them.

The third toxic synergistic factor responsible  was the governments  compulsory prophylactic warble fly eradication campaigns 1978 and  1982, England and Wales (4) (5). These three main toxic events when combined synergistically produced the BSE epidemic "trigger factor" that caused  the  epidemic. The double portion of the inherently unnatural MBM together with the double dose of free radicals, produced the main poisoning. The illusive infectious agent was not an infection or any other living organism. The MBM was poisonous.

The discovery facts:

(a) The neurotoxic free radicals still exist in cows today: http://www.ejnet.org/dioxin/ 

(b): The animal feed solvent process is still being used around the world today.The solvents are the same as those used in dry-cleaning establishments. These chlorinated hydrocarbon solvents would remove  synthetic  chemicals as they are solvent soluble.

(c) The  organophosphate toxic payload was increased by the warble fly eradication campaign 1978-82 England and Wales.  (Very low incidence of BSE in Scotland)

(d)The calculated date of origin (2) including the  period of incubation, coincide with the actual date of the epidemic (2) (3)

 Alzheimer's link

Alzheimer's disease and free radical damage (7) (8) (9)

The fat laced milk in the suckling feed is implicated as it came from the same source:

http://www.alz.org/media/news/current/071200highfatdiet.htm

Note:BSE is not spreading from Britain to around the world. The rare disease is just being found.

Summary and conclusions

The epidemic was caused by the double helping of  MBM introduced in the early 80s prior to this the solvent free process allowed dioxin free radicals to survive in the fat component of the MBM,  The double helping of recycled cannibalistic MBM also provided a double helping of free radicals.This together with the known neurotoxic damage caused by organophosphates enhanced the  protein poisoning disease process. A very rare disease of old age began affect the young.

The trigger factor responsible for the British BSE epidemic has been scientifically determined as "unknown" we propose that we have clearly identified that  "unknown" factor.

References

(1) BSE inquiry looks at animal feed:

 http://news6.thdo.bbc.co.uk/low/english/uk/newsid_84000/84064.stm

(2) 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.

Extract from (2)

"the results of further epidemiological studies of bovine spongiform encephalopathy (BSE) support the previous findings that the onset of exposure of the cattle population to a scrapie like agent, sufficient to result in clinical disease occurred in 1981/82. The onset of this exposure to the cessation. in all but two rendering plants, of the hydrocarbon solvent extraction of fat from meat and bone meal. A further possible explanation, related to the graphical variation in the processing of greaves to produce meat and bone meal, was identified for the geographical variation in the incidences of BSE".

(3)  http://www.bse.org.uk/report/volume12/annex1.htm#786376

(4) Free radicals defined:  http://www.karlloren.com/biopsy/p61.htm       

(4 +)  http://telomeres.virtualave.net/radical.html

(5) Purdy, M. (1994) Are organophosphate pesticides involved in the causation of Bovine Spongiform Encephalopathy? Journal of Nutritional Medicine 4, 43-82.

(6)  Current hypotheses: http://sparc.airtime.co.uk/bse/hypoth.htm#29.

(7) BSE and Alzheimer's disease:  http://www.rgs.uky.edu/ca/digest/alzheimers/freeradicals.html

(8) Harman Denham. Alzheimer's Disease. A hypothesis on pathogenesis. Annals of the New Academy of Sciences. Vol 854, p515, 1998.

(9) An interview with Denham Harman: http://www.lef.org/magazine/mag98/jan-interview98.html

The above is presented  as  discovery, we also  present as hypothesis:  that the same poisoning damaged the bovine immune system and as a consequence it may have promoted  two more disease epidemics.  (1) Foot and mouth disease and (2) bovine tuberculosis

This discovery proves the free radical theory of ageing (9) Spongiform disease is probably an accelerated rapid onset form of Alzheimer's disease.

”All truth goes through three stages. First it is ridiculed. Then it is violently opposed. Finally, it is accepted as self-evident.” (Schoepenhouer)

World © Copyright 2000 A R Parish Protect Rite Registration #: R692-5607

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14 November 2000

Note: My father Anthony 'Gerry' R. Parish passed away December 16th 2002. He dedicated the last 15 years of his life to helping others through medical research. This website is maintained as a lasting tribute to him.

Email: Ben Parish

Last updated 17/06/2002

THE PATHOLOGY AND PATHOGENESIS OF SPONGIFORM ENCEPHALOPATHY

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