If the results obtained from the sweet potatoes have anything to do with protease inhibition,
this small human study which I have posted before is interesting.
Protease inhibitor was the only med used,for complete remission from pan colitis.
Bowman Birk inhibitor has been tried in the USA in a small trial and worked pretty well.
Old Mike
https://www.jstage.jst.go.jp/article/internalmedicine1992/32/4/32_4_350/_pdf
here is a downside to trypsin inhibitors from sweet potatoes
Pigbel I think I see what is going on here,if you are on a low or very low protein diet the pancreas
trypsin activity is lower than normal,and if you also eat a large amount of sweet potatoes containing
trypsin inhibitor it makes things worse since trypsin destroys the toxin.
Editorial Note
The laboratory results, clinical course, and epidemiologic findings indicate that this outbreak was caused by C. perfringens type A. A related organism, C. perfringens type C, causes clostridial necrotizing enteritis or "pigbel," a type of foodborne illness characterized by necrotizing small bowel inflammation caused by the beta toxin. Necrotizing enteritis is caused when the normal trypsin-mediated degradation of beta toxin is impaired by a protein-poor diet or coingestion of foods such as sweet potatoes that contain trypsin inhibitors. Clostridial necrotizing enteritis has a mortality rate of 15%–25%, but it is rare in developed countries such as the United States (2) and was ruled out in this outbreak when samples tested negative for the beta-toxin gene
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
Post Edited (Old Mike) : 8/4/2014 9:20:09 AM (GMT-6)