CIDPUSA.ORG Autoimmune

Autoimmune Mad Cow disease

God Our Guide

Main Links

Home page

Autoimmune Diseases Guide

F.A.Q. Autoimmune


Help page

services contact page

Treatment Page

Encephilitis as Mad COW

Search Cidpusa web

Mad Cow is autoimmune

MAD COW IS AUTOIMMUNE THE LION-KING PATHOGEN part-2 Historically, mad cow has never been reported in cattle which are totally grass fed.  The outbreak in Britain and Europe which occurred 15 years ago has been linked to the practice of using animal by-products in feeding.  Providing cattle with their God designed diet of grass and forage results in the safest beef for families.

What Is Mad Cow Disease?

Bovine Spongiform Encephalopathy (BSE), known in vernacular as Mad Cow Disease, is one of a group of transmissible spongiform encephalopathies (TSE).  These transmissible, slowly progressive, degenerative, fatal diseases affect the central nervous system of many animals including man and cause neurological symptoms.  These diseases include BSE in cattle, Scrapie in sheep, Chronic Wasting Disease (CWD) in elk and deer, and Creutzfeldt-Jakob Disease (CJD) in humans among others.

What Causes Mad Cow Disease?

The causative agent for these diseases have not been proven exactly, however, numerous theories exist.  The leading and most accepted theory is that the diseases are caused by a prion (a protein particle).  Other theories involve a virus, Spiroplasma bacteria, organophosphates, magnesium, aluminum, and the autoimmune system.  

The greatest attention has been given to BSE when evidence in the 1990ís linked it to nvCJD (new variant Creutzfeldt-Jakob Disease).  CJD has been recognized with worldwide distribution for at least 80 years and usually has an onset in 60-70 year olds.  New variant CJD (nvCJD) was only recognized in the last decade and has been the form linked to BSE.  It has been seen in young people and even children.

Though not proven how, BSE may be spread to humans.  Evidence indicates that nvCJD has occurred after consuming BSE-contaminated cattle products.  Evidence has also indicated that the transmission of BSE to humans is only possible with the consumption of brain, eyes, lymph nodes or spinal tissue.  

The outbreak of BSE in cattle, which occurred in Britain, is believed to have started from the feeding of Scrapie-contaminated sheep meat and bone meal to cattle.  This outbreak was then made worse by the practice of feeding rendered bovine meat and bone meal to young calves. Just by going back to grass feeding all the Mad cow issue can be resolved.

Below is a research study

"" Ann N Y Acad Sci. ,2005 Jun;1050:417-28.

Bovine spongiform encephalopathy, multiple sclerosis, and creutzfeldt-jakob disease are  autoimmune diseases evoked by Acinetobacter bacteria.

Wilson C.

Bovine spongiform encephalopathy (BSE)

belongs to a group of conditions named together as transmissible spongiform encephalopathies (TSE). They are fatal neurodegenerative diseases that include "scrapie" in sheep, Creutzfeldt-Jakob disease (CJD) and kuru in humans, and chronic wasting disease in deers. BSE-affected animals suffer from "hindquarters" paralysis, which is also one of the main features of "experimental allergic encephalomyelitis" (EAE). EAE is considered an animal model of multiple sclerosis (MS) and lower limb ataxia is often observed in MS patients. The presence of clinical and histopathological similarities in these diseases suggests a common pathology. Specific brain peptides, which produce EAE, were shown to have "molecular mimicry" with the soil and skin saprophytic microbe, Acinetobacter. BSE-affected animals and patients suffering from MS have been found to have elevated levels of antibodies to both Acinetobacter and Pseudomonas bacteria, as well as autoantibodies to both white and gray matter brain components. The hypothesis is proposed that Acinetobacter/Pseudomonas bacteria may have evoked both BSE and MS through the mechanism of "molecular mimicry" and autoimmunity in a similar way to Streptococcus microbes producing rheumatic fever and Sydenham's chorea. The possibility that CJD patients may show similar features remains to be determined.