My current trial of VSL#3 - mle_ii

[tex]

Could be. I don't know offhand if the enteric encapsulation used for Entocort requires any "assistance" from bacteria in order for it to become active, or not, and I don't have the time to research it, right now.

Re: your thought - Asacol does become active in the small intestine, (the ileum, where SIBO is the greatest threat). It's designed to do that, (so is Entocort, of course). If Asacol were to become activated further up the GI tract, the 5-ASA active ingredient might lose it's potential for benefiting the distal colon, but that shouldn't cause any adverse event in the SI, in and of itself.

Actually, though, the idea that activation further up the GI tract leads to poorer treatment coverage of the colon, (as Dr. Lewey and most other researchers have maintained), sort of flies in the face of the premise that inflammation is greatest at the proximal end of the colon, and diminishes toward the distal end. In fact, if that distribution pattern is accurate, then that viewpoint suggests that inflammation might possibly be greater in the SI than it is in the colon, (in the absence of data to the contrary. Researchers never seem to check the lymphocyte infiltration in the ileum, (in regards to MC), they always stop short of the cecum. Perhaps MC involves just as much SI inflammation as celiac disease, but this possibility has just been overlooked or ignored, simply because MC normally does not present with villous atrophy, the way that celiac disease does.

Tex