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Researchers from Weill Cornell Medical College have added to the growing body of evidence that multiple sclerosis may be triggered by a toxin produced by common foodborne bacteria. The presented their research at the 2014 ASM Biodefense and Emerging Diseases Research Meeting.

Multiple sclerosis (MS) is an inflammatory disease of the central nervous system characterized by blood brain (BBB) permeability and demyelination, a process in which the insulating myelin sheaths of neurons are damaged. The disease is thought to be triggered in a genetically susceptible individual by a combination of one or more environmental factors. The environmental trigger of MS, however, is still unknown. According to the National Multiple Sclerosis Society, the condition affects approximately 400,000 Americans and is, with the exception of trauma, the most frequent cause of neurological disability beginning in early to middle adulthood.......Read More - http://www.ms-uk.org/bacteria

very important

further explanation on http://www.thisisms.com/forum/general-d ... 8-495.html

1975
Effect of Clostridium perfringens epsilon toxin on the blood brain barrier of mice.
http://www.ncbi.nlm.nih.gov/pubmed/171606

Abstract
It was shown that Clostridium perfringens epsilon toxin has the effect of allowing the passage of 125I polyvinyl-pyrrolidone and 125I human serum albumin into mouse brain. These substances did not enter the brains of normal control mice. The passage of albumin into the brains of mice poisoned with epsilon toxin was extremely rapid. When large doses of toxin (+/-4 000 MLD) were given death ensued within 2-3 min at which stage 1,5% of the injected albumin had already entered the brain. In cases where smaller doses were given and the time interval between injection and death was longer the figure was increased to 2-2 1/2% of the injected plasma albumin.

It is important to understand these bacterial toxins are present in our teeth if we have root canals.

I think this would be connected to missing enzymes called protease. These enzymes digest dietary proteins. I posted a great deal of information on the association to these missing enzymes and MS on this thread. http://www.thisisms.com/forum/general-d ... 22806.html

Researchers have already determined that in animals a lack of protease leads to the proliferation of C. perfringens. For instance, the following information states that ingestion of a protein-rich diet in a protease-deficient intestinal tract allows for "rapid growth" of C. perfringens. Pathogenic bacteria, such as C. perfringens, feed and proliferate on the undigested protein fragments.

Managing Clostridial Diseases in Cattle
Sheila M. McGuirk, DVM, PhD

"Possible risk factors for calves... Ingestion of C. perfringens in the first few days of colostrum feeding...Ingestion of protein-rich diet in a protease-deficient intestinal tract allows rapid growth of C. perfringens organisms"

The following information from Wiki states that trypsin (trypsin is a protease) shortages in the digestive system of experimental animals has been used to "induce" Clostridium perfringens.

"Clostridium perfringens beta toxin one of the four major lethal toxins produced by Clostridium perfringens Type B and Type C strains...C. perfringens beta toxin is susceptible to breakdown by proteolytic enzymes, particularly trypsin. Beta toxin is therefore highly lethal to infant mammals because of trypsin inhibitors present in the colostrum...It is primarily fatal to animals 1–3 days old, whose digestive enzymes may not be sufficiently active to break down beta toxin. It has been experimentally shown that trypsin may normally break down beta toxin and trypsin shortages in the digestive system of experimental animals has been used to induce type C disease."
http://en.wikipedia.org/wiki/Clostridiu ... beta_toxin

So, as we can see, pathogenic organisms such as C. perfringens would proliferate in the absence of protease.

You can find more links between epsylon toxin and trypsin in this paper: http://www.mdpi.com/2072-6651/5/11/2138/pdf

"2.2. Beta Toxin

Originally purified in 1977, beta toxin is a 35 kDa protein that shares sequence similarity with the alpha and gamma hemolysins of Staphylococcus aureus [23,24]. The toxin is responsible for fatal necrotic enteritis in animals and humans involving intestinal necrosis and bloody stools. In humans, diseases such as pigbel (Papua, New Guinea) or Darmbrand (post-World War II Germany) follow consumption of meat by individuals on a minimal protein diet with a low-basal level of pancreatic trypsin [25]. For some pigbel cases, individuals may have consumed trypsin inhibitor via sweet potatoes (a staple component of the normal diet) and/or be infected by round worms (Ascaris lubricoides) that release trypsin inhibitor into the intestinal lumen. Unusually high concentrations of protein in the intestinal tract facilitate C. perfringens types B (animal) or C (human) overgrowth, leading to lethal levels of beta toxin, which forms cation-selective channels in lipid membranes [26]. Tachykinin (neuropeptide) receptors play a role in beta-toxin induced fluid release from the circulatory system into tissue, suggesting involvement of the sensory nervous system [27]. This particular study in murine dermis reveals that beta intoxication is inhibited by tachykinin NK1 antagonists, capsaicin and an omega conotoxin (Conus magus MVIIA) that specifically blocks N-type calcium-channels."