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SIBO in patients with Crohn’s disease is not only associated with a more severe disease, but is also marked by dramatic changes in the gut microbiome

kiny

Well-known member
What is interesting about the SIBO-Crohn's connection is that now that SIBO is recognized, the diets that are used for crohn's like EN, are just as effective for SIBO.

Researchers used to come up with lots of ridiculous explanations as to why EN works for crohn's disease. Vitamins, low particle antigens, lactose intolerances, etc.

What EN actually does is simply bring down bacterial load in the intestine, this has been confirmed with multiple studies. It doesn't matter what type of EN it is, what vitamins it contains, it simply works due to the high bioavailability of the maltodextrin and proteins that have such high bioavailability that they get taken up high in the intestine, depriving bacteria of nutrients. This results in a rapid decrease in of bacterial load which means less bacterial antigen, a lowered immune response and a drop in inflammation.
 

kiny

Well-known member
EN causes severe dysbiosis, but yet it lowers inflammation dramatically in crohn's patients and SIBO patients. This idea that there are "good" and "bad" microbiomes seems increasingly a bunch of baloney. It is based on the idea that a diverse microbiome is somehow better.

But what studies show is that the pathobionts and pathogens in crohn's disease are behind the inflammatory cascade, not the dysbiosis. If one is able to lower bacterial load, with EN, with feeds, by simply removing the fecal stream (see Rutgeerts studies), the intestine heals.

Crohn's is maintained by the presence of bacteria, crohn's can not exist without the presence of bacteria that interact with the intestinal lining, peyer's patches and lamina propria. If one is able to decrease bacterial load, the inflammation subsides.
 

kiny

Well-known member
Fusobacteria and E Coli are once again implicated in this study. It is clear that pathogens are behind the inflammation.

The reaction is not directed at commensals, and why would it be, surface TLR4 and peyer's patches are more than capable to distinguish commensals from pathogens. This idea that the immune system that has been trained to create tolerance to commensals since we were still babies, would somehow one day decide to mount a chronic immune response to commensales is the most ridiculous explanation for crohn's disease ever suggested. The inflammation is directed at pathohgens, our immune system knows very well what it's doing, it is trying to prevent pathogens from entering tissue.
 
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