Old Mike said...
Funnyplay: I am just a small part of what I call the internet brain,I research info,others may supply alternative treatment methods,of which I have tried many. Others research in different directions than I do,or have different takes on the same info,or may dig deeper into things I find,such as Canada Mark. I try and cover as much as I can find on IBD,but seem to find something new everyday that I did not know about,such as intestinal alkaline phosphatase. A 100 plus years of some of the best medical brains, have been trying to solve IBD,perhaps we might find something they missed,or new data may lead to a solution. Way too many colons have been lost.
I've been reading pretty much all day about
the genes associated with UC and how gut bacteria modulate the immune system. One of the papers I've found seem to indicate that UC may not have just one trigger and instead is created by a series of factors in some sequence, which may be different in everyone, which is why it is difficult to figure out what exactly is causing the disease. www.ncbi.nlm.nih.gov/pmc/articles/PMC4143199/
But then I read another paper that said that the genes involved in UC account for less than 30% susceptibility to it, and thus a much larger factor is the environmental contribution, especially gut bacteria. There is so much going on with the gut bacteria and how it directly influences the immune system, the mucus barrier, our genes, and so on. www.sciencedirect.com.ezproxy1.lib.asu.edu/science/article/pii/S1075996413000607
It's clear that the general thinking about
this disease is much more in the mucus barrier defect/bad immune response to gut bacteria line of thinking than a loss of tolerance to some sort of colon autoantigen. When I searched for "colon autoantibodies" on PubMed, most of the studies are from 20 years ago...seems to indicate that research is not really concerned with that direction anymore, if I am interpreting that correctly.
Something i'd like to see in the near future is a probiotic treatment that would allow anti-inflammatory/immune modulating bacteria to not just pass through the colon like they do now, but actually colonize the colon and begin modulating the immune response. With the various different genes possibly involved and the huge variations from person to person in which types of microbes are colonizing our guts, I suspect that targeted, individualized treatment of the microbiome might be necessary to overcome unique differences in each case of the disease, but an underlying dysbiosis causing uncontrolled immune response that also breaks down the mucus barrier may be a common factor in all of us with UC.
In short, I feel it's plausible that all of us could have broken/weak mucus barriers and dysbiosis, but correcting that may require individualized approaches to account for the wide genetic and bacterial variety. I believe this would account for the mixed responses to probiotics/FMT/antibiotics, and doesn't simplify the disease unnecessarily.
Fun fact I also learned recently: In DSS colitis, DSS doesn't actually cause inflammation itself, but simply works by eroding away the mucus barrier. The inflammatory response is actually in response to gut bacteria. DSS models may be more accurate than I thought.
But I am but a humble, amateur, internet researcher. I could be totally off the mark.
Post Edited (Tunnelvisionary) : 9/12/2014 8:27:17 PM (GMT-6)