A bacterial culprit for rheumatoid arthritis?
the-scientist.com
the-scientist.com
I have no doubt antibiotic therapy helped me. There are so many biological pathways with everyone being different so for at least some people, bacterial problems upstream could be the initial conditions that put your system into chaos downstream.
A lot of autoimmune diseases are just fancy words for 'unexplained inflammation' and doctors (who are trying their best), use a differential diagnostic funnel based on what's likely and what's worked as treatment for others. But if the standard treatments aren't working for you, do your own research and ask your doctor to try something else.
A few months back I had an infection that required fairly high dose antibiotics and my Sarcoidosis has been noticeably better since, despite a significant increase in other things that usually cause flare-ups e.g. stress and lack of sleep. I am still on Hydroxychloroquine, but in the past I required Methotrexate (which was horrid).
There's been a heap of studies regarding Mycobacterium and Sarcoidosis. Doesn't seem to be the cause for everyone. As another poster pointed out — Sarcoidosis, Rheumatoid Arthritis; these are basically catch all names for conditions of unknown cause that exhibit similar symptoms. That said I'm pretty optimistic about all this research into bacterial involvement.
I haven't thought about this stuff in over 10 years, but there seems to be a lot of evidence now supporting this theory of bacterial acnes causing runaway inflammation. I can't believe that steroids plus pain killers are still the standard treatment for autoimmune diseases without any investigation into root causes. https://pubmed.ncbi.nlm.nih.gov/14620162/
Furthermore, there is evidence in discs https://pubmed.ncbi.nlm.nih.gov/28369127/ a common flare-up point for people with RA
Sad. But true. That said, why don't the insurance companies know about successful alternatives? After paying out X, isn't it in their best interest - and the patients' best interest - to say, "Our data shows that these alternatives have been successful is similar cases. Perhaps there are somethings here to consider."
It's not a diagnosis, just data / possibilities. This might also encourage insurance companies to be less tight fisted about what they'll cover. That is, they're not blindly paying for fringe "experiment" but investing in solutions that will mitigate future payouts.
Smarter use of the data would means more choices and better care for patients, and more profits for insurance companies. Is that not a win win?
I was debating whether to even write this comment. Like Dad it was a constant search for something new or some hope of a new drug next year. He had rheumatoid arthritis too it developed about the same time so maybe the bacteria and IPF were all connected.
Very important to qualify (through studies) whether this is the cause of rheumatoid arthritis, or just one of a number of precipitating things. The answer will tell us whether treating/preventing Subdoligranulum is a silver bullet, or whether, like cancer, we have a lot more work to do.
> “It's hard to know how big of a player this specific isolate is,” he said. “It could be the dominant player, and that's why they came across it first. But it could be that if they went back and did larger screens, that they would come up with more — that [Subdoligranulum] would be just one of many.”
> In keeping with this, the researchers only found this Subdoligranulum strain in 16.7 percent of people at risk or with early-stage RA, indicating that this strain is likely not the sole driver of disease.
Regardless, given the results mentioned here, I would bet that "infection" with this strain would exacerbate RA through increased production of antibodies. So it seems a good target to reduce severe RA.
I truly wonder sometimes whether antibiotics are actually underused in medicine (while simultaneously being overused in the food supply chain).
In the US, this is basically a given. You don't have to look past the lobbying numbers to understand why.
I'm curious outside the US, how often antibiotics are given out. From my buddies telling me stories about Mexico + the fear mongering with US Physicians, you'd expect a superbug to have broken out by now.
There is no mention on your page, or the wiki, that antibiotics are the cause the resistant bacteria.
I can logically see why we would believe this, but you'd expect given the use of antibiotics on the farm and in non US pharmacies; we'd have such a superbug scientifically proven by now.
https://www.theguardian.com/environment/2019/sep/19/superbug...
Antibiotics, and antibiotic resistance genes, have existed for an uncountable number of megayears. Antibiotic use by humans is probably not creating many new antibiotic resistance genes, if any at all. But is is driving the increase in bacteria that contain these genes, as well as encouraging the horizontal transmission of antibiotic resistance genes and the accumulation of multiple such genes in so-called "superbugs".
https://www.nature.com/articles/s41467-021-22757-1
https://pubmed.ncbi.nlm.nih.gov/30248271/
https://genomemedicine.biomedcentral.com/articles/10.1186/s1...
You'd expect it, and it has.
https://en.wikipedia.org/wiki/Methicillin-resistant_Staphylo...
At the same time we lack evidence-based medicine guidelines for treating most low-grade chronic bacterial infections. In many cases there aren't even reliable diagnostic tests for such conditions, so it's not clear what the root cause of a patient's symptoms are and physicians have to try treatments at random in an attempt to find something that works. More basic research is needed in this area.
Killing gut microbiota is also being increasingly linked to diseases, so it's likely a very complicated balancing act where we need to maintain the correct bacterial flora.
This could just mean that diseases trigger same pathways. Overlap doesn’t mean a common etiology.
I think we underestimate the extent to which pathogens thrive in niches carved out by the absence of symbiotic bacteria required by our microbiomes.
Fecal transplants have shown significant results in some diseases (such as Crohn's): https://academic.oup.com/ibdjournal/article/21/3/556/4602907
> Based on [Pediatric Crohn's Disease Activity Index], 7 of 9 patients were in remission at 2 weeks and 5 of 9 patients who did not receive additional medical therapy were in remission at 6 and 12 weeks.
> No or modest improvement was seen in patients who did not engraft or whose microbiome was most similar to their donor.
So I think it's either a case of pathogens that fit in with the established microbiome or that the microbiome is missing vital components.
We've started an arms race with a staggeringly dynamic enemy, and our solution thus far has been to attack them with static munitions, until those munitions stop working.
You can mitigate the issue with combination antibiotic therapy (it's harder to evolve resistance on multiple fronts simultaneously), but in general (when we use them) we need to move towards targeted antibiotics.
The difficulty being that you actually need to diagnose the specific problem before treatment, not just that it's bacterial in nature.
This requires pathogen detection and recognition: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4941824/
This adds significant complexity (though I don't think that knowing what you're doing is a bad idea).
We've been using nukes for a long time now, we need to move to scalpels.
I was insulted and mocked by everyone I said it to
But if nobody looks, we'll never find out. It looks like somebody looked in the case of ulcers and arthritis
I mean, it’s not a fringe theory. MS could be one example.
But that's about it. Witness the reaction to aerosol spread of disease despite literal videos that can capture and show aerosols being spread around a room. People simply don't believe it.
They likewise don't believe in any kind of long run response to an infection. We associate the symptoms of acute immune response to be the virus itself, and the entirety of the virus.
I believe that car accidents cost lives, that power tools can take off my fingers, that illnesses like coronavirus can kill me or give me chronic lung conditions.
I also believe that it's worth driving, woodworking, and interacting with people in public despite those risks.
Most people, excluding the rare nutjobs, are like that. If you force them on an issue and don't accept variants of "I don't care" as an answer, they might come up with a bizarre explanation, sure.
It's hard for a lot of people to simply be honest and say - yes, sure, but I think it's worth it, instead of trying to deflect.
Anyone who had shingles would think otherwise.
I spoke flippantly. There are specific diseases people do recognize cause specific issues.
But even in a case like shingles a society like the UK calculates it knows all the consequences. For instance I’m not sure anyone can say whether fighting shingles for decades makes our immune response less flexible in targeting other pathogens.
What matters is that there’s more and more evidence for microbiota in the gut having impact on seemingly unrelated systems like CNS. I think we’ll find many more surprises of how disregulated host-microbiome interactions lead to some kind of diseases.
There’s a lot of conditional situations the protocol sets up that are hard to achieve and measure.
If the Protocol doesn’t work, it seems like the explanation given by the “practitioner” will be something akin to “you didn’t believe hard enough”.
edit: I am now wondering whether that section is a honeypot to get rid of "non-believers" before they commit any further.
In a nutshell he argues that the current batch of scientists should either die or retire before the new generation can start investigating alternative theories:
> A sufficient proportion of the old guard will have to retire or expire, and a sufficient number of young people entering the arena without these vested interests must mature into positions of influence, to tip the balance of expert opinion.
It's been 20+ years since that essay was written, so it looks like it is slowly becoming a reality.
[1] https://ia601004.us.archive.org/26/items/nextfiftyyears/%5BJ...
There's the problem. People don't need to die off; the hierarchy of influence (especially as it pertains to funding, and secondarily as it pertains to publication) has to level out and be evidence-based.
> My guess is that this point will have been reached by 2015 for atherosclerosis and Alzheimer’s disease.
For AD the point was reached because of evidence of past research misconduct, and inability to replicate. Not because of new evidence per se. Or at least that's what I gather.
Quit, trying to tell anyone. You really would end up making a fool in most cases of yourself if you tried. The world is not kind to people who go against the narrative, even if you are provably correct.
Look up the Marshall Protocol, it's old news in some circles.
I think the casm separates testers from non-testers.
I've noticed that there are either doctors who will order ALL of the blood tests (all at once, and a few times to track trends), or doctors who will not order any, even if it's clear that tests are absolutely necessary.
A LOT of stories I've read on HN, or heard from others I've spoken with about this subject mention that somewhere along their journey to recovery, they (the patient):
- Did some research,
- Requested their doctor order a few labs,
- Were denied by their doctor (not for insurance reasons),
- Ordered the tests on their own from jasonhealth / ultalabtests etc.,
- Received high/low results as predicted.
...and only then did their doctors respond appropriately.
The fact that we can order our own tests is the difference -- I think -- because it's very similar to the difference between GenZ and Boomers with respect to being tech-native.
From my own experience, younger doctors, generally, order as many tests as possible and want as much data as possible (since data and testing are now cheaper, faster, and more available -- and this is native to their experience, now), whereas older doctors are less likely to behave that way (since tests used to be more expensive, slower, and generally not covered by insurance).
-HOWEVER-
Looking from the other side of the table, sometimes it might not be best to order lots of tests all the time for certain patients, since some (possibly acute or false-positive) results might just stress them out...
Especially when most patients are happy with the current standard. Patient has a rash. Doctor prescribes steroid. Rash goes away, and the patient is happy. No need to dig into the root cause of the rash, and if that cause might lead to cancer 10 years down the line, if ...for 99% of people... it won't.
That said... for the patients who do show an interest in debugging, I think some accommodations should be made that don't involve the frustrating "self-ordered tests process" listed above.
A subsequent study[0]—albeit with a very small sample size—“proves the causative relation between … periodontal pathogens and RA.” (Or at least flares thereof.)
https://www.drugdiscoverynews.com/mouth-bacteria-trigger-rhe...
Here is kind of a fun prospective study that illustrates your point well: https://pubmed.ncbi.nlm.nih.gov/29998832/ . The investors assessed what patients in their centre were reclassified into 10 years after a diagnosis of seronegative RA.
"13 (13/435 [3%]) could be reclassified as seropositive or erosive RA: 4 turned seropositive (2 for ACPA and 2 for RF [> 2x reference level]) and 9 developed erosions typical for RA. " ... "Reclassification revealed 68 (16%) cases of polymyalgia rheumatica, 46 (11%) psoriatic arthritis, 45 (10%) osteoarthritis, 38 (8.7%) spondyloarthritis, 15 (3.4%) plausible reactive arthritis, 10 (2.3%) gout, 17 (3.9%) pseudogout, 6 (1.4%) paraneoplastic arthritis, 6 (1.4%) juvenile arthritis, 2 (0.5%) haemochromatosis, 3 (0.7%) ankylosing spondylitis, 2 (0.5%) giant cell arteritis, and 8 miscellaneous diagnoses. The other 140 patients (32%) could not be reclassified in any clear-cut diagnosis "
Caveat: A big limitation is we don't know how many patients were diagnosed with seropositive RA in that time frame: I'd wager it's over an order of magnitude higher. These were probably less clear cut cases.
Doctors were unable to find anything in the fluid of my knee and the only thing that seemed to work was corticosteroids. Prior to that I was given the diagnosis of pseudo-gout. I took methotrexate in my twenties and thirties for years, my hair fell out, and I couldn't drink. When I moved I went to reup my prescription at a Rheumatologist who ran a research clinic and as she went over my paperwork she looked in shock as she read through it and asked me, "Have you actually ever had site testing for RA or did they just look for markers?" Turns out, all they'd ever looked for was markers, tried methotrexate, and my symptoms stopped. Doctors at Baylor Scott & White thought that was good enough. At the time, I was told repeatedly that we know "a lot" about RA and that I could trust the diagnosis. I was slowly weened off of methotrexate and we waited to see if I would have a flare-up. The flare-up never came and she told me not to come back after telling me more or less what you've said here.
I also learned it's incredibly difficult to sue a doctor for a misdiagnosis, even if they put you on a drug like methotrexate and took years of normalcy from your life.
This seems so frustrating to me. A big factor in the high healthcare prices in the US is that doctors need to pay heavy premiums for their malpractice insurance. If they can't get sued anyway then why are we all paying them to pay for the insurance?
It's not "free" (unless bulk-billed), depends on what specialist and what type of appointment is involved but will range from $20-100
You can go for as many as you like
I've been seeing a specialist for six years under this system, and he has had to close his books for the past two years
There are genuine shortages for a lot of specialists - they personally seem very over worked to me (well paid though)
If a disease is as extreme as the OP though I'm sure the ~$400 max isn't a life altering barrier to entry to a second opinion though
You’d go back to your regular non-specialist doctor, your GP, and ask for a new referral to a specialist, explain that you want a different one, and why… the GP would give you the referral.
You might end up seeing a “private” specialist - Medicare would pay some money toward it, but the gap, the extra bit, you pay yourself (or if you have medical insurance, your insurer pays it). The insurer doesn’t waste time checking before hand whether you are or are not “approved” - and the “gap” for seeing a specialist might be $200, not much more than that.
If you don’t want to pay any money, then you wait longer for a “public” specialist to be available. It might be the same actual specialist btw, as the public hospitals are good hospitals.
Does not exist for a growing number of Australians. No clinic in practical range of me bulk bills any more.
Take a look form different perspective - if you do software, have you ever created a bug? Imagine if your employer wanted to vengefully sue you for every other bug you ever did - that's what many doctors are facing with various patients. Maybe you yourself are perfectly stable well balanced individual, but our of those 2000 other patients some are bipolar, schizophrenic, sociopathic etc. without proper diagnosis and treatment.
We outsiders often tend to have this image of medicine being a solved problem, when reality is so far from this.
Or we could just cut out a step, and have those entities put a warranty on the treatments doctors working for them provide. Not satisfied with a treatment? "Return it" and get your money back!
This could not be more false. The bell curve also applies to doctors.
a great doctor who phones it in because he's got Sixers tickets that evening can still get you killed.
Unfortunately, it would be damn near impossible to get most doctors to give up any of their powers of discretion. It's all too tied up with the prestige of the role, so anything that challenges it is seen as a personal attack. For example, see how doctors in general react to pretty much any technology that automates part of their job, like reading an ECG. You can prove that the machine does a better job than the human, and they'll still reject it.
Indeed! I should have been clearer: I'm not suggesting any kind of AI / ML stuff — rather, only that where there is an established and uncontroversial best practice process for, e.g., diagnosing and treating X (which there often is), then I would hope for there to be a requirement to make a record of the path a doctor took to the conclusion, including a record any deviations like not ordering some standard test that most doctors would before starting a patient on Y. It could literally be a printed flowchart with check boxes on it and room for comments. The goal is to make the cowboys out there a little more accountable (incentivise doing things by the book), and to stop treating vague notions of "professional judgement" (a common protest against doing things by the book, I hear) as sufficient reason for ignoring the consensus best practice or simply forgetting important steps.
> The comment is also uneccessarily confrontational.
Fair call. I suppose ranting and raving doesn't really help anything. But I sincerely believe that a significant part of the problem is the defensiveness that tends to arise when a person is told (or it is implied): you are fallible. This tool will help to catch your mistakes, and make you more effective. I'm sure this happens in every industry, and I see working with that as 90÷ of the challenge.
> There are plenty of areas in medicine where checklist and sops have been widely adopted.
Yep, I agree wholeheartedly. And it saves lives. Hospitals in particular have made huge improvements to patient care/survival in this way, and continue to do so every year with new initiatives. I just think there are still a lot of, uh, exciting opportunities for future excellence. :)
I ask because my sister is diagnosed with RA, and is on methotrexate, with her hair falling out.
I read your comment with literally bated breath hoping there was a new diagnosis or treatment at the bottom so we could try it.
I also take methotrexate for my RA - does she take folic acid?
There is no specialty in medicine for treating undiagnosed diseases. You just bounce around between doctors until you give up.
There is 30 years of contradictory research on the association of the disease with the bacteria Klebsiella pneumoniae. So far, it has come to nothing.
Big grain of salt, of course. Thankfully even if we can't pinpoint its exact etiology we still have a million proven drugs to throw at this thing.
This is a strain of bacteria that can also cause rheumatic fever, which has an autoimmune component; it's capable of molecular mimicry, which causes the body to develop antibodies against itself. So the thinking goes that many strep bacteria can linger in the body and cause autoimmunity.
The idea behind the streptococcal hypothesis is that you have a sub-clinical infection. There's a lot of uncertainty about whether strep bacteria merely act as a trigger — confusing the immune system into developing autoimmunity, but then disappearing — or whether bacteria remain in the body, hiding in places like the tonsils and in biofilms and periodically coming out to reinfect the host.
About molecular mimicry, Helgi Valdimarsson and his colleagues at the university of Reykjavik has written several papers [1] [2]. The same team has also experimented with whether a tonsillectomy can improve psoriasis, something we actually have a lot of evidence for [3]. The biofilm hypothesis has some clinical evidence (e.g. [4]).
Regarding things your mom can do that's actually supported by studies:
* A recent study on the probiotic Streptococcus salivarius K12 against S. pyogenes saw incredible (many too incredible) results [5].
* We have some support for other probiotics [6].
* There's decent evidence that large doses (10K–30K IU daily) of vitamin D2 and D3 may help psoriasis [7]. Psoriatics are, pretty consistently, vitamin D-deficient. It's very hard to achieve hypervitaminosis, but it's a good idea to monitor your serum levels while doing this. It's important to take vitamin K2 to increase bioavailability and avoid bone loss.
* Psoriasis severity is linked to being overweight, to alcohol consumption, and to smoking.
* There's anecdotal evidence that a radical diet change can significantly improve psoriasis; for example, going vegetarian. I don't have any proof, however.
[1] https://pubmed.ncbi.nlm.nih.gov/19781993/
[2] https://pubmed.ncbi.nlm.nih.gov/15373909/
[3] https://pubmed.ncbi.nlm.nih.gov/22491250/
[4] https://www.walshmedicalmedia.com/open-access/psoriasis-a-se...
[5] https://www.researchgate.net/publication/359856583_Improveme...
[6] https://www.medicaljournals.se/acta/content/html/10.2340/000...
The specialists can’t concur with their own conclusions, let alone the conclusions of others. Diagnosis changes every few years. It’s a confusing situation for the patient and their family.
One treatment that is used for a specific condition might have harmful - even carcinogenic -side effects. It’s difficult
I mainly mention this because I was terrified of starting Humira when I got diagnosed with AS years ago—those black box warnings are legit scary. But I had to weigh the risk of maybe developing a rare side effect versus the guarantee of my spine permanently fusing and my immune system burning everything else to the ground out of spite, and ultimately went for the Humira. And I'm glad I did, because my quality of life has improved massively.
Which is all to say that I hope your sibling's doing okay and found a treatment that works for them. It's scary out here, but there's hope, I promise.
For what it's worth, though, many people don't develop resistance, or at least not for a loooong time. My gastro told me one patient of his has been on Remicade for 15+ years and it's put them in happy remission the whole time.
Not everyone's a success story, but the success stories are very very good.
Yes, but I have also seen people who used biologics for 10 years without issue, and out of the blue they started to have severe side effects that made them move drop off (or move to another one). You just never know.
I read somewhere that a startup was working on controlling Immune system response via some brain waves. I have never rooted so strong for any startup as I am rooting for them.
I had a friend who had RA starting in her teens and was on very heavy medication for it, with no real hope of improvement. In her mid-20s she changed her diet significantly -- I think she went gluten free, maybe it was some other restriction. I thought it was silly TBH, why would changing what you eat affect arthritis?
After about 6 months her RA was entirely in remission and she was off all of her medication. As far as I know has not recurred. I can very easily imagine that dramatic diet changes affect the gut biome and could have tipped the scales to make her gut less hospitable for specific causes of RA. I hope so!
My autoimmune condition Sjogrens (similar to RA)was initially diagnosed (later confirmed) specifically because symptoms always improved on antibiotics. Was an old optha-neurologist doctor who had noticed this trend over his life time.
I later found the marshal protocol. But modern doctors have no interest in bacteria as a cause of problems.
I really liked how the experiment was broken down so that a normal person could understand the high level logical steps between each section.
After research and some trial and error what solved it fairly quickly were high doses of extremely high quality fish oil (DHA & EPA) and an overall cleaner diet with less low quality gluten.
As for the "spots" sunlight seemed to be the best disinfectant to the point where now if there is any flare up I just get a nice tan and they go away.
I have no scientific basis for any of this so DYOR.
How much fish oil are you taking? I think the normal dose is a tablespoon, how much did you have to increase the dose?
Have you tried Cod Liver oil instead?
Are you taking any other vitamins regularly?
I would suggest focusing less on the "how much volume" and rather more on the "how much DHA & EPA". Dr. Rhonda Patrick suggest 4g per day though.
Personally I was doing 2 teaspoons during that time and continue to do so today - liquid version (they also make capsules).
As for Cod - it looks like Carlson Cod has DHA and EPA but I personally use the "Very finest fish oil" one.
The one thing according to Dr. Patrick is that the plant based versions just don't work the same.
I'm wondering this because there is a large crossover in the biologic "TNF Blocker" drugs that treat RA, Crohn's and UC (Humira, Remicade, etc).
Really looking forward to research in this field and I hope the US starts putting more focus on phage therapy.
Do you have a methane or hydrogen overgrowth?
Herbal Therapy Is Equivalent to Rifaximin for the Treatment of Small Intestinal Bacterial Overgrowth https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4030608/
Subjects with newly diagnosed SIBO by lactulose breath testing (LBT) were given two open-label treatment choices based upon individualized treatment preference; either two 200 mg rifaximin tablets three times daily (TID) or 2 capsules twice daily of the following commercial herbal preparations; Dysbiocide and FC Cidal (Biotics Research Laboratories, Rosenberg, Texas) or Candibactin-AR and Candibactin-BR (Metagenics, Inc, Aliso Viejo, California) for 4 consecutive weeks immediately followed by a repeat LBT.
> I was given the metronidazole for one week and it helped as well, but symptoms came back.
Make sure you focus on gut motility. A lot of people have it come back due to poor MMC which causes the food to sit for longer, ferment, foster the overgrowth, and cause inflammation. Here's a good thread with some options: https://www.reddit.com/r/SIBO/comments/11ac3ic/list_of_possi...
There have been some (tenuous) hypotheses suggesting that certain types of otherwise-benign gut infections in HLA-B27+ people basically short-circuit your immune system and teach it to attack its own tissues. So if you're HLA-B27+ you're not guaranteed to have an autoimmune disease, but you're potentially one bad stomach bug away from developing one.
Which, to be fair, all of this is still highly speculative, and it seems like even the hypotheses treat the resulting arthritis/IBD as an immune condition rather than a bacterial condition—Remicade et al are our best bet either way. But I'd love to one day unravel how a single gene can singlehandedly mess up your spine and your gut and your eyes and your skin!
After about a year into the pandemic I just stopped taking the methotrexate/folic acid after a couple of years of using it regularly, and I haven't had an RA issue since. I had tried this way in the past, but I would get flair ups, but this time around no symptoms.
One day it disappeared. Then about 15 years later it came back. In one particularly stressful time of my life it progressed to psoriatic arthritis. Then that went away when the stressful situation was resolved.
I’m now trying to retrace my steps to try to make it go away again. Low inflammation diet, lots of sleep, low stress.
- Take a probiotic and prebiotic daily. Swanson sells a bunch of cheap and high-quality ones. - Some people have had luck improving their gut health with supplementing collagen peptides. YMMV.
Obviously, the gold standard is a double-blind study that proves the effectiveness at eliminating rheumatoid arthritis through intervention. Both of the above suggestions are well-tolerated in the general populace.
It has been useful in motivating me to use my hands before I can't, which is bitter sweet I guess. Certainly sweet in that I've appreciated my hands in ways I likely wouldn't have known I should otherwise.
Here's hoping that it continues to fade!
I find exercise useful too. Not much can keep the cold and wet conditions from making my hands scream, but when I climb and deadlift it has the odd effect of reducing pain after a half hour or so, and keeping it at bay for hours.
People have told me this means it can't be arthritis, but I've met others with a diagnosis who have the same experience. So long as the activity doesn't involve impact or to much opening and clenching of my hand while under stress, it's very relieving (though painful at first).
> In keeping with this, the researchers only found this Subdoligranulum strain in 16.7 percent of people at risk or with early-stage RA, indicating that this strain is likely not the sole driver of disease.
Still, exciting work. The gut-brain axis is so important.
Family member is on Remicade. It's administered in two doses (IV infusions) every 4 months, so 6 treatments/year. And retails for something like $12k/treatment. And many insurance companies have removed it from their list of preferred drugs due to the cost, leaving patients to fight for medically necessary treatment.
It's a fucking nightmare (as if RA on it's own isn't bad enough).
Doc replaced it with Azathioprine, a cheap generic, and I've had no major flare-ups of UC in 6 years.
If I have minor symptoms (usually triggered by certain foods), I also take mesalazine, but once I am in remission I can do without the mesalazine. If I withdraw from AZA when I am in remission, minor symptoms typically return after around 3 months, but subside after I resume taking the AZA for a couple of months. I can retain remission doing 3 months on, 3 months off.
Use of Azathioprine is still controversial for treatment of UC: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7034525/
I have no noticeable side-effects from taking Azathioprine.
An unexpected path led her to a tropical diseases doctor who had positive results with RA patients by using an unconventional treatment not supported by mainstream medicine at the time: He tested the patients blood for bacteria (by cultivation in a lab) and prescribed an antibiotic course that matched the detected bacteria. This treatment (testing + prescribing antibiotic)was repeated in regular intervals over the course of a whole year.
Her RA flare-ups stopped and recurred only in ever longer intervals which were arrested by this treatment. After a year the progression of the RA had stopped.
This treatment is controversial because it is considered bad practice to prescribe antibiotics liberally, for several good reasons. Mainstream medicine did not have a theoretical foundation to justify this treatment path.
The tropical disease doctor founded his treatment on the empirical research by some research factions that the “auto-immune” theory of RA was not showing the full picture.
This doesn't seem like prescribing antibiotics liberally to me? Having symptoms, test for bacterial infection, prescribe antibiotics seems reasonable to me with no medical training. I would consider liberal prescription to be something like prescribing antibiotics based on symptoms that align with viral infection, without doing any labs to determine the type of infection and hoping for the best.
Interesting. Can antibiotics be matched to that level of specific targeting?
I was diagnosed in my 20s and at first it was a real atruggle to get out of bed. After initial rounds of steroids/TNF blockers, I really started to focus on strengthening my affected joints and it has quite literally been a miracle cure for me.
Nothing too crazy at first either, mine is in my feet so just lots of yoga and walking a couple miles or so a day did it for me.
Both groups observed significant decrease in disease activity score (DAS) (p < 0.001). Significantly higher decrease in pain in fasting group on seventh day (p = 0.049). No significant difference was observed in total fatty acid profile, butyrate and propionate but acetate increased significantly (p = 0.044) in fasting group and decreased significantly in MD group.
So it's not easy to replicate exactly the protein done by another company, so what a biosimilar is, is an attempt at making proteins that have similar kind of folding and efficacy while not being strictly identical.
That's why they are not generics.
or do you mean cannot be made legally in the usa absurd copyright law where a company can simply deny licensing for medication?
because manufacturing is much more complex, depends on genetic modification of bacteria or things like that, and there are trade secrets involved in the manufacturing process - so you won't be able to replicate it even if you know the final structure.
RA is a complicated disease. This is interesting but there is already data implicating infections like P. gingevalis, EBV, Parvovirus B19 with plausible mechanisms like citrullination of proteins, molecular mimicry contributing but there is no direct evidence and issues with these being prevalent in the general population.
The question to ask when reading this are: Does this antibody/evidence of prior infection raise or decrease the probably of developing pre-RA? clinical-RA? Is it pathogenic or just an interesting finding? What's the prevalence of these antibodies in first degree relatives without disease or healthy controls in the general population e.g. can you reasonably use it for screening? I'd say the answer is no / we don't know to all of these and they it needs more research before this is clinically interesting.
RA is a complicated disease but ultimately a clinical (/imaging) diagnosis based on synovitis and extraarticular features supported by investigations. There are mouse models of arthritis e.g. collagen induced but sometimes hard to translate to humans.
If you are interested in the topic. Think of RA in terms of a susceptible host progressing to benign autoimmunity, subclinical disease, then clinical disease. Factors like HLA-DR4/DRB1*0401/0404 increases an individual's lifetime risk but are seen in 20-30% of population vs 0.5-2% of the population having disease so aren't helpful from a screening point of view. Environmental exposures like smoking (the data says in shared epitope + individuals) raise that risk significantly. Other exposures like microbiome are clearly important and they interact with the immune system (e.g. via TLRs) so they probably make a difference but aren't well studied (this work would fit in here trying to address it). There is good cohort data that many patients develop detectable autoantibodies years ('benign autoimmunity) before becoming patients with clinical disease. But even with everything Ive said this is still a two-way street: some of these individuals don't develop disease and can even lose their autoantibodies. In at least one real world cohort I'm aware it's been shown of you can be very high risk with ethnicity, CCP+, RF+, have a family member with RA (in some sense controlling for genetics, environmental exposures) and you still have even odds of progressing to disease vs. losing your double seropositive status and not developing disease. So what do you do with that? (It comes down a clinical diagnosis with prompt recognition, treatment to target of remission.) The (very important) trials so far for treating/preventing preclinical RA in ~similar high-risk individuals have been sadly negative or at best may delay onset slightly (abatacept, hydroxychloroquine).
I developed hypothyroidism a few years later too. I know people can develop type 1 diabetes from influenza I had a first aid instructor tell me of a local incidence of such a thing after a block party. The pancreas and thyroid both being part of the endocrine system it's tempting to guess of wild things going on inside me.
So GERD and hypothyroidism and viruses who knows what is going on. It's hard to not sound like a nut telling stories that are just anecdotal!
GERD is also one of those ailments that seems to be sometimes cured by weird random lifestyle changes. Low/no carbohydrate diet is something some people swear by. I also know someone whose GERD was completely cured after an antibiotics treatment to an unrelated disease.
For GERD there seems to be one clear structural factor that has something to do with its development: hiatal hernia. However, the link is not perfect so it's possible other factors (such as some microbial imbalance) affect it too.
However it’s hard to think of an alternative that doesn’t end up with things like coerced adults or poorly consented paid volunteers.
Unlike the JAK inhibitors that suppresses the immune system, their pill instead resolves the inflammation by activating receptor 1 and 3 in the melanocortin system. Phase 2b completes this summer and I am personally super excited to see the results.
My own experience is very consistent confirms it as well.
Check how can a two hour session where you get your body voltage close to 0 can reduce inflammation. Imagine the opposite effect, possibly multiples. https://yewtu.be/44ddtR0XDVU?t=1667
You can also check this lecture by Dr Jerry Tennant which may give you a better understanding overall. Hope this helps someone.