When looking for a cure, we encourage our researchers to explore and run studies.
Rifaximin has never been studied to treat AS. There is a high amount of conjecture. One persons unblinded results of two days of usage for a chronic condition is not something I would think any physician would recommend without more data.
I'm grateful that this forum is here for people to share experiences and ideas.
The studies I referred to did use Rifaximin to treat AS, but only in mice so far. There are also studies I supplied where symptoms of AS were severely reduced using moxifloxacin in human patients with GREAT results. This already puts another tick on the side of "treat bacteria, reduce AS symptoms." (LINK)
Generally regarding antibiotics and spondylitis:
Prolonged and even short-term use of antibiotics can alter one’s microbiota, and in particular gut microbiota. Gut microbiota are implicated in the pathogenesis of spondyloarthritis, but it remains to be determined whether there is a particular shift one way or another, that is ‘good’ or ‘bad’ for SpA. It is also unclear as to whether changes in gut microbiota can trigger SpA, or whether SpA triggers changes in gut microbiota (or both). Prolonged courses of antibiotics can lead to many gastrointestinal problems and could make someone’s SpA worse, OR could make their SpA better. It’s just not clear.
I hope that helps.
I am pretty sure it was the papers I mentioned, or others I can find if not, that the bacterial shifts pre-dated the SpA. This was not just one experiment, this is well-documented in multiple experiments. Please, search for these findings and you will find them. The direct link between microbiota affecting the interleukin pathways, which then upregulated the cytokine expression is well-documented in them. I didn't make that up. While you are stating these things to be safe, I think what is more accurate is that "mainstream medicine" has not "accepted" these things as the truth, but the data backs them up in multiple studies already and that is why they keep getting funded...because there is merit in the idea. What I mean is that there is "repeatable" experimentation being done...and these repeated experiments find the same thing and multiple organizations/institutions/people keep funding these repeated experiments.
Also, in reply to this alteration of gut microbiota by taking antibiotics...yes it is true. However, at least that is exactly the target of the drug and you are intending to affect what you are affecting. How about all the drugs every single person on this forum takes to manage pain, such as NSAIDS, or others that take diabetes medications, etc. These are not intended to affect gut microbiomes, yet are prescibred and supposedly help people. (LINK)
They have anti-microbial effects and even promote resistance to drugs. So, at least what I am proposing is EXACTLY the target it should be intending to affect. I'd suspect all these IL-17 and IL-6 drugs are also affecting the microbiome, since they modulate interleukin activity anyway.
Also, I am now on my 4th day and went to physical therapy. I have NEVER been able to sit in a seated position and do my exercises without frequent breaks because I am in so much pain. Today, I did all exercises without even needed to stand up and "shake it off." I walked into therapy without crutches today, and they said to me, "Who is this guy? You are like a completely different person." Again, anecdotal, but it lines up with what I'll reference next.
I am not the only person who has used Rifaximin, however, I am the only one to put all the pieces together for everyone. This person (LINK)
also had the same experience and was, and I quote, "afraid to stop taking Rifaximin," because of how her pain completely went away while on it. Her doc even called in and agreed to refill her script! (Dig deeper into that post and you will see that Rifaximin only stays in the intestines and is not well absorbed, as I discuss below. Also, another poster there talks about how amazing Rifaximin is in its ability to help with AS, and he claims it is "the best for AS." So, this brings the count from 1, now to 3, and these are people who have done more than my few days of dosing.)
I am not trying to be a pest, but medicine often moves slower than science, which often moves too slowly as well, when it need not and people get harmed or end up incurring "damage in wait." It is already accepted that "healthy people" have a VERY characteristic ratio of the different types of bacteria in their intestines performing similar tasks (though they may be different specific species, they are of the same class)...this is accepted and used as a clinical diagnostic standard. Ask companies that doctors use to assess their patients, like Genova Diagnostics...they will literally tell you what bacteria and what ratios are normal in healthy people because they are paid to know and collect this data. I can even provide my PDF's of my stool samples that show EXACTLY the same imbalance in firmicutes to bacteroidetes ratios that the mice in the first article I ever submitted for Rifaximin usage had. The mice transfected with HLA-B27 develop a disease progression which mirrors mine? This cannot just be due to coincidence. The chance of that being coincidence alone is astronomically low. It was also noted that Rifaximin alters gut microbiota towards ACCEPTED ratios of these bacteria, which is why it is now being prescribed for IBS, not just SIBO and HE. Rifaximin is also one of the safest of all antibiotics because it is not absorbed by the body. It only acts in the intestines because of this lack of absorption,(LINK)
, so for all the other people taking rounds of antibiotics anyway, this would still be safer than ALL of those in most cases (you are not allergic to Rifaximin.) I have taken antibiotics before and they all make me feel like garbage...this is THE ONLY ONE that I haven't felt really anything other than slightly elevated heart rate on day one. In fact, I am feeling so good I am smiling all day and becoming happier and more energetic.
I am just providing facts from papers that demonstrate, repeatedly, that gut microbiota shifts occur, and more recently they are reporting that it occurs BEFORE SpA. If it was the other way around then, "mice raised in germ-free environments don't develop SpA" (LINK)
wouldn't make sense. It is the introduction to bacteria that causes the disease progression. Even if it WERE the other way, then you still need to treat bacteria being out of whack, to begin with, because SpA's got them out of whack. So fixing them at least addresses a problem...
Also, yes now it's more than just me experiencing success with this course of action for treating AS. The other methods of treating (interrupting communication between your body and your interleukin signaling) are far more dangerous, which is why people get infections, cancer, or even die from those treatment methods. If altering gut microbiota was a huge huge risky deal, people would be reporting tons more issues with probiotic supplements than they do. I have not really heard of people dying from probiotic usage, but Humira directly lists death as a possible side-effect. I am being extremely reasonable in deciding to attack the bacterial aspect of this disease due to both its safety profile and the logic behind it.
Lastly, each of the people on the forum who have replied to my post so far, including me, have all stated that some sort of gut or oral thing had happened to them before their disease started, or occurred right as the disease started. Putting this many pieces together, that all fit well with scientific evidence and all point to the microbiome, it would literally be one chance in a billion that these relationships were due to chance. I definitely ended my first post by stating that these were my opinions and that if people chose to follow suit, they did so at their own risk. I even detailed and outlined the risks associated with Rifaximin usage and dosing. Given all that, it is still my opinion that this is the safest and most well-targeted option currently out there for management of this disease, as well as potentially the best.