Kickas.org Forums Treatments, Drugs and Alternatives NSD and diet-related; bovine spongiform encephalopathy

But what's your opinion? hehe. Have heard the hardest thing about eating a vegtable was the wheel chair, but what do I know, hehe.
I need to look into organic, perhaps Sun Harvest's meat supply is. Doesn't undo the last ten years though.
I'd be really ticked if after getting this diet working I found out my brain was taking a leave of absence. Well, more so.

Soylent Green Baby!

Allan

Ebringer is correct about AS so HE CAN'T also be right about BSE, can he? What are the odds?

copied here for those interested is a portion of the BSE handout he prepared for the kickas meeting in Las Vegas last June. [highlights mine]

bon apetit



Page one
Kick AS” Meeting - LAS VEGAS - June 2003
BSE could be an autoimmune disease of cattle caused by Acinetobacters
which are microbes found in soil and muddy waters.
Alan Ebringer B.Sc,MD,FRCP,FRACP,FRCPath.
Professor of Immunology, Division of Life Sciences, King’s College
(University of London), 150 Stamford Street, London SE1 8WA.

ABSTRACT
Bovine spongiform encvephalopathy (BSE) could be an autoimmune disease caused by exposure to Acinetobacter bacteria which are found in soil and muddy waters. A study sponsored by the Department of Agriculture (U.K.) involving 218 BSE affected animals and compared to 290 control cows has shown that elevated levels of antibodies to Acinetobacter bacteria but not to 6 other microbes are present in such animals. Elevated levels of antibodies to Acinetobacter are also present in patients with “multiple sclerosis”(MS). The working hypothesis is proposed that BSE is MS in cows.
KEYWORDS: BSE, Acinetobacter, autoimmune disease, multiple sclerosis.

INTRODUCTION
“Bovine spongiform encephalopathy” (BSE) is a neurological disease, that appeared in the U.K., in cattle following the introduction of a new form of “winter feed”, based on abattoir materials obtained from brain, spinal cord, pancreas and guts with their contents.

The unresolved question is:
What component of the winter feed material or “meat-and bone-meal” (MBM) component could have been responsible for this disastrous development in British Agriculture ?
Could it have been due to exposure to a common microbe present in soil and muddy waters ?
By 1988, some 60,000 cows had been identified as suffering from BSE and “Ministry of Agriculture, Fisheries and Food” (MAFF) scientists suggested that “brains” in the “winter feed” could have been contaminated by “prions” from sheep having had “scrapie” and thereby probably caused BSE in cows.
The use of the “winter feed” preparations was banned in 1988 and since then the incidence of BSE in British herds has drastically fallen, although not to zero levels.
Concern has been expressed that consumption of beef containing “prions” could cause “Creutzfeldt-Jakob disease” (CJD) or a “new variant” form of CJD.
Page 2

NO EVIDENCE LINKING MEAT CONSUMPTION TO v-CJD

However no scientific evidence exists linking meat consumption to the development of neurological diseases such as CJD.
This was illustrated by the recent report from the "National CJD Surveillance Unit" in Edinburgh, who in their "Eighth Annual Report 1999" described a study involving 51 vCJD patients and compared their dietary habits to 27 hospital controls.
The consumption of beef in the vCJD patients was 98% compared to 96% in the controls, 88% of the CJD patients had sausages compared to 93% of the controls and 88% of subjects in both groups enjoyed burgers.

Furthermore 86% ofvCJD patients consumed meat pies compared to 87% of controls, 18% of CJD patients had veal compared to 35% of controls and none of the patients had consumed brain tissue compared to one control subject (4%).
The occupational background was also examined but there was no relative increase in people employed in livestock farming or the veterinary profession.

The final conclusion of the report reads: "We have found no evidence of any dietary, iatrogenic or occupational risk for vCJD".

So why was extensive culling of cattle carried out in the U.K. over the last ten years if there is no evidence that meat consumption leads to the disease?

The answer to this question involves the debate as to what causes BSE.


THEORIES ABOUT ORIGIN OF "BSE"

There are now in the literature two main theories trying to explain the origin of BSE:

The first one is the "prion theory" and the second one is the "autoimmune theory" which suggests that cattle were exposed to bacteria containing molecules resembling brain tissue.

Although the "prion theory" has wide acceptance it also has several serious limitations.

How do vegetarians develop vCJD and why should prions cause ONLY neurological diseases, since prions are present in all nucleated cells ?

"Prions" as independent, infectious particles have not been demonstrated in nature but are generally recognised as being sialoglycoproteins encoded by the DNA of the host and present in most nucleated cells, except red blood cells.

Professor Prusiner from San Francisco, has proposed that abnormal prions can convert normal prions into infectious particles which then cause BSE in cows, scrapie in sheep, Kuru in New Guinea natives and CJD in man.
However the mechanism by which this process occurs has not been explained and it raises serious questions in molecular biology.

In view of the molecular biology problems associated with prions, an autoimmune theory of BSE has been proposed, whereby it is suggested that the “winter feed” materials contained bacteria or bacterial fragments which showed molecular mimicry with brain tissues.

AUTOIMMUNE DISEASES
Exposure to such bacteria would lead to the development of autoimmune responses, similar to the situation of Streptococcus in rheumatic fever, Klebsiella in ankylosing spondylitis and Proteus in rheumatoid arthritis.
The classical model of an autoimmune disease caused by a microbe is rheumatic fever.
The microbe Streptococcus has in its coat molecular sequences which resemble human heart tissue.
When someone develops tonsillitis caused by Streptococcus, the antibodies produced by the patient will not only have anti-streptococcal activity but will also attack the heart because of this molecular similarity.
Thus the anti-streptococcal antibodies are acting as autoantibodies and producing
“rheumatic fever”.
“Rheumatic fever” is no longer a problem in the Western World because the widespread use of antibiotics has drastically reduced the incidence of streptococci tonsillitis.
However in many parts of the Third World, “rheumatic fever” is still a serious problem because of the financial difficulties in obtaining access to antibiotics which could reduce the frequency of streptococcal infections.
Thus “rheumatic fever” is an autoimmune disease produced by an infection.
“Rheumatoid arthritis” is another autoimmune disease caused by a bacterial infection.
There are 1 to 2 million individuals in the U.K. who suffer from “rheumatoid arthritis” and it is three to four times commoner in women than men.
The microbe Proteus mirabilis has in its coat molecular sequences which resemble hyaline cartilage, a component of the small joints of the hands and feet.
“Rheumatoid arthritis” usually affects the small joints of the hands and feet. Page 4
When a person develops an upper urinary tract infection with Proteus mirabilis, the antibodies produced will attack the hyaline cartilage of the small joints of the hands and feet and over a period of time a destructive, inflammatory arthritis will develop which we call “rheumatoid arthritis”.
Thus “rheumatoid arthritis” is another autoimmune disease caused by an environmental microbe. (Wilson et al., 2000)
The question arises: “Which bacteria possess molecular sequences resembling brain tissues ?”
A computer search for bacteria having molecular mimicry with bovine myelin and neurofilaments showed that Acinetobacter, a common microbe found in the soil, water supplies and on skin, has such sequences. (Ebringer et al., 1997)
Such a microbe could have been incorporated in the MBM preparations when rendering conditions had been changed in the early 1980’s - clearly the MBM preparations were involved, since the ban on their use led to the virtual disappearance of BSE in the U.K.
Although a microbe had been identified it did not mean that BSE cows had been exposed to it.

FIRST MAFF STUDY (MAFF=Ministry of Agriculture, Food & Fisheries)
MAFF were approached with this new hypothesis and Dr. David Shannon, Chief Scientist at the Ministry, authorized a pilot study involving 29 BSE cows, which were compared to 18 animals which did not have BSE.
The majority of BSE-positive cows came from dairy Friesian herds from different parts of England.
In addition, sera were obtained from an additional 58 healthy animals: 30 serum
samples from animals aged less than 30 months (8 Friesians and 21 Hereford-Friesian and 1 Charolais-Friesian crossbreeds, the crossbreeds being raised for meat production) and 28 serum samples from animals aged more than 30 months, all of which were dairy Friesians.
The animals were raised on a farm kept under organic farming conditions, where no case of BSE had been reported and winter feeds consisting of hay and grains, but no MBM supplements.
The results carried out under coded conditions showed that cows affected by BSE had elevated levels of antibodies to Acinetobacter, but not to E.coli or Agrobacterium when compared to cows suffering from other diseases or sera from cows raised under “organic farming” conditions (=No “winter feed” supplements). (Tiwana et al., 1999)


Furthermore, Gajdusek’s group at the National Institutes of Health in Washington, had shown some twenty years previously that patients with CJD or kuru and sheep with scrapie possessed autoantibodies against neurofilaments located in the gray matter of the brain.(Sotello et al., 1980)
So our group also measured autoantibodies to both bovine myelin (white matter) and bovine neurofilaments (gray matter) in the 29 BSE affected cows: High titre of autoantibodies were found thereby strongly suggesting that BSE is an autoimmune disease.
A composite index of Myelin-Acinetobacter-Neurofilaments (M.A.N.) antibodies has been developed which provides an ante-mortem test for BSE.
This simple test that can be carried out on 1 cc of blood and can determine whether a cow has BSE or not before it is sent to a slaughterhouse.

SECOND MAFF STUDY
Following the successful results obtained with the pilot study, which were published in the United States (Tiwana et al.,1999) a second study was commissioned in 1999, involving 128 BSE affected animals and 127 controls.
The results confirmed the original study that elevated levels of antibodies to Acinetobacter were present in BSE affected animals but not when tested against 6 different microbes.

Furthermore, investigations on 189 BSE positive animals and compared to 214 healthy controls showed elevated levels of antibodies to Acinetobacter peptides as well as autoantibodies to peptides of myelin basic protein and brain neurofilaments.


POSSIBLE LINK BETWEEN MULTIPLE SCLEROSIS, CJD and BSE

When the first case of BSE was shown on television, the affected animal was standing on it forelegs but falling in the mud by its hindquarters and this resembled the clinical features of “multiple sclerosis” (MS).
Lower limb paralysis is a characteristic feature of MS a disease which affects approximately 80,000 individuals in the U.K. and over 400,000 individuals in the U.S.A.
Approximately 750 people die per year in England and Wales from MS, which is about 2 persons per day.
Furthermore 7% of these MS patients die below the age of 40 years.
Since v-CJD patients are usually aged below 40 years, the question arises whether v-CJD is a severe form of MS

In view of this clinical similarity between BSE and MS, and the demonstration that 6 BSE animals had elevated levels of antibodies to Acinetobacter a skin saprophyte, the National Hospital for Nervous Diseases in Queen Square London, was approached in an endeavour to study patients with MS and CJD.
Sera from patients with MS and CJD have been compared to blood donors and found to also have elevated levels of antibodies to Acinetobacter but not to E.coli (Hughes et al, 2001)

Some 50% of MS patients suffer from sinusitis whilst only 5% of the general population has this condition: chronic biological material in the respiratory and nasal tract could be an ideal growth medium for a saprophytic microbe like Acinetobacter.
The autoimmune theory suggests that MS, CJD and BSE are caused by Acinetobacter infections but the actual mechanism remains to be elucidated.


CONCLUSIONS ARISING FROM THE PROPOSAL THAT “BSE” IS AN AUTOIMMUNE DISEASE:
(1) The working hypothesis is proposed that “BSE is MS in cows”.
(2) Meat is safe to eat and has always been safe to eat.
(3) The cattle cull was unnecessary.
(4) There will be no epidemic of CJD.
(5) The M.A.N. assay provides a simple ante-mortem test of BSE and should be evaluated in prospective studies.
(6) Scrapie affected animals should be tested for antibodies to Acinetobacter, as well as deer, elk and moose animals suffering from “chronic wasting disease”.
Page 7
REFERENCES
Ebringer A., Pirt J., Wilson C., Cunningham P., Thorpe C., Ettelaie C. (1997) Bovine spongiform encephalopathy: Is it an autoimmune disease due to bacteria showing molecular mimicry with brain antigens ? Environmental Health Perspectives 105: 1172-1174.

Hughes L.E., BoneII S., Natt R.S., Wilson C., Tiwana H., Ebringer A., Cunningham, P., Chamoun V., Thompson E.J., Croker J., Vowles J. (2001) Antibody responses to Acinetobacter spp. and Pseudomonas aeruginosa in multiple sclerosis: Prospects for diagnosis using the Mye\m-Acmetobacter-Newofilamen\. antibody index. Clinical and Diagnostic Laboratory Immunology 8: 1181-1188.

Sotello J., Gibbs C.J., Gajdusek D.C. (1980) Autoantibodies against axonal neurofilaments in patients wuth Kuru and Creutzfeldt-Jakob disease. Science 210: 190-193.

Tiwana H., Wilson C., Pirt J., Cartmell W., Ebringer A. (1999) Autoantibodies to brain components and antibodies to Acinetobacter calcoaceticus are present in bovine spongiform encephalopathy. Infection and Immunity 67: 6591-6595.

Wilson C., Tiwana H., Ebringer A. (2000) Molecular mimicry between HLA-DR
alleles associated with rheumatoid arthritis and Proteus mirabilis as the aetiological basis for autoimmunity. Microbes and Infection 2: 1489-1496.






"Last winter blew so cold no lies, And my fire smoke would not rise;
Soon as the smoke tried to depart, It'd be froze up harder than a landlord's heart"
Robin Williamson, 'Smoke Shovelling Song'

John,

I just don't like the theories of the universe that have one proponent, who is the sole repository of all the truth
and is never wrong...don't believe in jesus, don't believe in beatles.
alohaben

Allan,
we brits had this panic back in '96; we had already been scoffing mad cows for 10 years! All the friggin government advisers forecast the possibility of all the beef eaters like me going toes up, 100s of thousands could be infected, big panic. Well I'm still here, whether mad I leave to your better judgement. After a while people stopped worrying and the butchers' shops started ignoring the ban on beef on the bone and I was able to get my T bones and foreribs again. And those 'experts' now just say 'we just don't know....we don't don't know...' like cracked gramaphone records. Indeed they do not.

This we prescribe though no physician . . .
Our doctors say this is no month to bleed. (Rich. II)

Hey Tink,

Cute link with a serious message, this site has really taken off!

http://www.themeatrix.com/

Take care,

Jan

There are no ordinary cats

- Collette

Cute Cartoon, Jan. I started buying my hamburger at Sun Harvest. All organic fed, but they still kill'em to get'em to market....Moosiest can't free'em all.


Allan