alywest
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- Joined
- Apr 19, 2017
- Messages
- 1,028
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I found charcoal to be constipating and I suffer from ibs-C so constipation is a no no.
But I did feel good and at ease from taking it. It got rid of a lot of angst and anxiety I didn't even know I had and I felt like a different person.
TMI warming: The bathroom movement the next day was difficult and painful and put me off it
you will find less issues with constipation if you take your AC with sugar and lots of liquid
ie. I will take a 50 gram dose with 12 ounces of OJ and 2-3 Tbs sugar before bed
and bm will be completely normal (other than its black ;-)
I will take a 10 gram dose with say a few ounces of water before bed and it will delay transit times for up to 36 hours
I thought taking it with other things made it less functional. Do you get 5x the good effects from the 50g dose as u do the 10g dose
how do you test for the pathogen by labs any labs out there?
Perhaps it's still an infection just no longer of bacterial origin that's sustaining disorder and inflammation
I have been under the impression that antibiotics can clear endotoxin temporarily but only as long as the course of antibiotics lasts, then it tends to return.
To the poster who used cyproheptadine for IBD.
Did you try Benadryl? -- Since it is readily available, compared to cyproheptadine.
I have Crohns, and the only thing that has helped me is Cyproheptadine. And I've tried prog, dhea, preg, charcoal, R5, carrots, mushrooms, phages, tetracycline, and many other things. A lot of these make it worse. Lysine can help temporarily but with side effects.
My metabolism is very resistant to increase. I can take 150 mcg t3 a day (do not try this) but I eventually get side effects. Anyways, lately I've normalized my body temp with high dose thiamine, about 1 g a day. This is detailed in another @haidut post that I wouldn't have known about without you so thank you.
Not sure how many people on the forum know that Chron's disease, which is a type of an inflammatory bowel disease (IBD), has recently been reclassified in some countries as infectious of origin and not as an autoimmune disease. The causative pathogen of Chron's is thought to be a type of Mycobacterium
Mycobacterium avium subspecies paratuberculosis - Wikipedia
The change in disease type designation has only occurred in some European and Asian countries, but the FDA is also considering adding the above bacteria as a "possible cause" to its official guidelines on Chron's. Anyways, the more important implication is that the studies which identified this bacteria as a possible cause of IBD hinted that it was not the bacteria per se which caused the damage to the colon wall but a byproduct associated with the bacteria. To my knowledge, none of the studies pointed the finger directly at endotoxin (LPS) but there aren't that many other byproducts of bacterial metabolism that can be the culprit.
This new study points the finger directly at endotoxin (LPS) and its activity through the TLR4 receptor as a causative factor in IBD. The more important finding is that this inflammatory damage occurs as a result of recurring infections that have been resolved completely. Thus, treating the infections with antibiotics would likely not have much benefit. However, the study found that it was the endotoxin-driven decrease in intestinal alkaline phosphatase (IAP) which was the direct cause of intestinal damage and that raising the levels of IAP was highly therapeutic. Injections with IAP are not very practical and to my knowledge are not approved anywhere as treatment. However, one of the most potent inducers of IAP is progesterone, which Peat has actually recommended in the past to a few people with IBD. In combination with charcoal, fiber or other dietary measures that reduce endotoxin load in the colon and the blood, progesterone could be a much safer option for treating IBD than the current immunosuppressive therapies, which have a very high risk of causing cancer or a deadly infection such as PML (Progressive multifocal leukoencephalopathy - Wikipedia).
Recurrent infection progressively disables host protection against intestinal inflammation
"...Pathogenic infection has been implicated in the chronic inflammation seen in inflammatory bowel diseases (IBDs) such as ulcerative colitis and Crohn's disease. Yang et al. show that recurrent, low-level, and fully resolving Salmonella enterica Typhimurium (ST) infections can precipitate severe colonic inflammation in mice. ST-induced TLR4 activation resulted in increased neuraminidase 3 (Neu3) production and activity in the duodenum. This led to intestinal alkaline phosphatase (IAP) desialylation and degradation. IAP deficiency caused a marked increase in commensal bacteria-generated lipopolysaccharide-phosphate in the colon, provoking inflammation. Treatment with calf IAP or the antiviral drug zanamivir (which inhibits Neu3 activity) prevented this inflammatory cascade. This pathway may serve as an effective target for future human IBD therapies."
Lactoferrin up-regulates intestinal gene expression of brain-derived neurotrophic factors BDNF, UCHL1 and alkaline phosphatase activity to alleviate early weaning diarrhea in postnatal piglets.
Lactoferrin up-regulates intestinal gene expression of brain-derived neurotrophic factors BDNF, UCHL1 and alkaline phosphatase activity to alleviat... - PubMed - NCBI
In addition, Lf increased intestinal alkaline phosphatase activity (P<.05) and delayed the onset of food transitional diarrhea, reducing its frequency and duration (P<.05). The incidence of diarrhea in the high and low Lf groups was decreased 54% and 15%, respectively, compared with the control group (P=.035). In summary, these findings provide new evidence that dietary Lf supplementation up-regulated gene expression of BDNF and UCHL1, decreased the colon microbiota of E. coli, improved gut maturation and reduced early weaning diarrhea in piglets. The molecular basis underlying these findings suggests that Lf may enhance gut development and immune function by providing new insight into the gut-brain-microbe axis that has not been previously reported.
as a former crohn's sufferer
Lactoferrin up-regulates intestinal gene expression of brain-derived neurotrophic factors BDNF, UCHL1 and alkaline phosphatase activity to alleviate early weaning diarrhea in postnatal piglets.
Lactoferrin up-regulates intestinal gene expression of brain-derived neurotrophic factors BDNF, UCHL1 and alkaline phosphatase activity to alleviat... - PubMed - NCBI
In addition, Lf increased intestinal alkaline phosphatase activity (P<.05) and delayed the onset of food transitional diarrhea, reducing its frequency and duration (P<.05). The incidence of diarrhea in the high and low Lf groups was decreased 54% and 15%, respectively, compared with the control group (P=.035). In summary, these findings provide new evidence that dietary Lf supplementation up-regulated gene expression of BDNF and UCHL1, decreased the colon microbiota of E. coli, improved gut maturation and reduced early weaning diarrhea in piglets. The molecular basis underlying these findings suggests that Lf may enhance gut development and immune function by providing new insight into the gut-brain-microbe axis that has not been previously reported.
i have read forum posts on people healing crohns by doing a fecal transplant.. although it's only regulated in australia i think as a treatment option
Are you sure it was for Chron's and not for C. Difficile infection? If it was indeed Chron's I think it is the most direct human evidence so far for it being of bacterial origin.