Canada Mark said...
@Tunnel -
I keep thinking about FMT now that I am in some sort of remission. Even though I poop perfectly 95% of the time I still feel as though something is off still... something's not quite right. At night I always sit back and wonder if FMT would take root better and change things being in a stable remission versus being super inflamed.
Honestly, I would really consider trying it. From everything I've read, it seems many people turn to home FMT when they've exhausted all other options, and likely have ongoing (possibly severe) inflammation. While it seems there are at least plenty of short term successes and improvements with FMT, the longer cases of seemingly more stable and robust remissions attempted to quell inflammation simultaneously along with performing FMTs. So it might actually be more effective to try out FMT while you are already in remission from meds, and not using it as a last resort, even though you're more likely to be motivated to do it as a last resort.
I think the argument for FMT as an effective treatment for Crohn's is stronger at the moment than FMT for UC imo, considering we can say for sure that the populations are screwed up at even the phylum level and then those small scale studies and case reports of great remission rates after just a single mid-gut transplant.
On the other hand, I do wonder about
whether it's a good idea to mess with your condition if you're finding something that is already working great. The potential payoff of FMT could be awesome, but you never know...there are a few who have gotten worse. If you're not on biologics yet, and find you need to go on them and reach remission quickly, then maybe that would be a good time to attempt it (wellbutrin is also an option...anti-depressant with anti-tnf properties you could use for the duration of FMT [others have found this really helpful]).
I think the latter option is better, to be honest. The evidence is promising but I'd wait till we have more info on Crohn's and FMT if you are in a really good remission right now. Sorry for the brief derail, but those are just my thoughts...i hope they are useful in some way.
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On topic...
I was thinking about
this study and a previous one you posted a few months back about
how certain types of bacteria drive inflammation significantly in mouse models of colitis. Do you remember that paper, Mark? They took specific species of bacteria linked to drivers of inflammation from humans, and microbes from healthy colons I think, and they found that implanting the inflammation driving bacteria gave much more severe colitis.
But simply implanting the bacteria didn't cause colitis, they had to break down the mucus barrier.
In the discussion of the paper on this original post, there is a note about
how different types of mice result in different kinds of changes in the mucus composition, and the need for standardization to study this further.
That makes me wonder whether the mice in the drivers of inflammation paper would have seen their mucus barrier break down further if perhaps they had the same sort of mucus as the person/people they came from.
I dunno if that makes sense...but there seems like there might be some sort of connection there.