More anecdotes, I was diagnosed with debilitating pulmonary sarcoidosis several years back and after 8 months of steroids and pain killers wrecking my stomach I found some research on the 'immuno-modulating' effects of some broad spectrum antibiotics, with minocycline in particular being successfully used as therapy. I printed out some pubmed articles and convinced my pulmonologist that it was a relatively low risk thing to try because I was hating the standard by-the-book therapy. Within a few days I was feeling better and after a couple weeks started waning down, so just about a month total to remission. I've only had the feeling of flare-ups returning a few times since after drinking or being stressed out.
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.
I've also got Sarcoidosis, some pulmonary involvement, but certainly not debilitating (as long as I remain on medication anyway). However, every time I get prescribed antibiotics for something unrelated, damn I feel so much better for a few weeks after taking them!
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.
My completely naive and unqualified opinion on why antibiotic therapy worked in my case is that some percentage of sarcoidosis and possibly other autoimmune disease like RA is caused by 'internal acne' of some tissues causing runaway inflammation. Minocycline is mostly used to treat skin/face acne but has fallen out of favor because of side effects. IIRC this is because it penetrates deeper into tissues and can cross the blood/brain barrier.
I'm putting this info here in case it helps anyone. I am not a doctor and not giving medical advice, just sharing my personal story.
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/
My Dad had IPF (scarring of lung tissue) which I believe can develop from pulmonary sarcoidosis. For my Dad it was frustrating to know what to do or who to ask about it. He was on Esbriet to slow the progression of IPF and it did work he got 10 more years instead of 3 years. But before he passed I had read metformin and low-dose nintedanib could reduce or reverse lung scarring. I'm not saying you'll get IPF from what I can read about it pulmonary sarcoidosis can reverse. But metformin/nintedanib info is good to be aware of. My Dad's doctor wouldn't even consider it.
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.
> But if the standard treatments aren't working for you, do your own research and ask your doctor to try something else.
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?
In a way, the entire differential diagnosis process and treatment planning is already based on data. Your doctor and insurance companies don't think you're special. Autoimmune problems are so varied, everything from testing to biopsy to diagnosis to treatment is based on a slow moving and incomplete body of knowledge and doctors are generally conservative when it comes to straying from the pack. It's why published research is so important for doctors to keep up with. Luckily these antibiotics are cheap so insurance didn't even come into the equation for me.
Yes. But as treatment goes on and there is a lack of change / progress why wouldn't the insurance companies look for ways to save? They have the data. There are millions of patients and doctors, etc.
1000% agree. I shudder to think what I would have done at the time if the non-standard treatment cost tens of thousands of dollars out of pocket because insurance wouldn't cover it. Through insurance coverages we're kinda locked into the meaty part of the curve when it comes to treatment options, unless you have money or your doctor really makes a good argument why something should be covered that goes against what insurance will cover for your condition.
It was over 10 years ago, iirc there were more case studies on skin vs pulmonary, but a quick search found this one https://pubmed.ncbi.nlm.nih.gov/18458989/ another search term would be the broader class of antibiotics tetracyclines
> Some people at risk for the disease have antibodies against this bacteria, and Subdoligranulum activation of T cells was more prevalent in people with RA than in healthy controls.
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.
And it's not unprecedented. It was in my lifetime that we found out that stomach ulcers could be caused by H. pylori infections. For many people, what'd previously been a chronic condition could be cured with a round of antibiotics.
I speculated last year that various known diseases could turn out to have some sort of microbe, or microbe-like cause that we're unaware of; things we haven't seen or noticed yet. And that we might occasionally find out, with new tools, that a difficult condition has an understandable, discrete, physical cause. Similar to how people discovered that the flu and strep-throat and meningitis etc were caused by the tiny living or life-like critters (are viruses alive?).
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
"Everyone you said it to" was probably the wrong audience? Because digging into potential infection/inflammation related precursors for a number of chronic conditions has been a thing for over a decade now.
> ...was probably the wrong audience? Because digging into...
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.
You should read "The Next Fifty Years" [1], specifically the essay named "Mastering Disease" by Paul W. Ewald.
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.
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.
Germ theory is not widely believed. Not really. We wash our hands because we've been trained since a young age to do so, and generally accept that touching stuff is unsanitary.
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.
> 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.
Funny you should mention that. The UK has avoid giving children the chick pox vaccine in order to keep up natural immunity. Thus ensuring shingles in later life.
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.
>I was insulted and mocked by everyone I said it to
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.
Lyme disease also causes symptoms that overlap with RA, due to the Borrelia burgdorferi bacteria. It is latent in some people and causes serious symptoms in others.
I truly wonder sometimes whether antibiotics are actually underused in medicine (while simultaneously being overused in the food supply chain).
> 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.
Once your microbiome is disrupted, I believe studies indicate that it's unlikely that adding probiotics in will fix it. I could see antibiotics followed by probiotics being an effective treatment for a microbiome gone haywire.
You still should consider collateral damage - we've been throwing broad spectrum antibiotics at damned near everything for decades.
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.
In the case of Chrons and Ulcerous colitis diet changes have big impact. There have been studies that show that high consumtion of processed food increase the likely hood of getting sick.
> I truly wonder sometimes whether antibiotics are actually underused in medicine
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.
Antibiotics are both overused and underused in medicine. We still see antibiotics being prescribed as a prophylactic measure even without a confirmed bacterial infection, or for minor bacterial infections that patients could probably clear on their own. People think of antibiotics as being benign but they come with significant risks and side effects, including disrupting the gut microbiome.
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.
>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.
Multiple superbugs have broken out and are killing thousands every year. The irresponsible overuse of antibiotics in places like Mexico is certainly part of the problem.
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.
Scientifically it's nearly impossible to prove things. However, scientific evidence supporting the antibiotic-driven increase in antibiotic resistant "superbugs" has been found.
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".
One of the biggest risk factors for a C. difficile infection is being treated with fluoroquinolones (ciprofloxacin, gemifloxacin, levofloxacin, moxifloxacin, norfloxacin, and ofloxacin), which are often used in outpatient settings.
> 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.
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.)
A word of caution for everyone talking about RA here. RA is just a simple name we give to a number of conditions that share similar symptoms but we dont really know if they are all related and if they share the same root causes or not. Its not a very specific disease that you can diagnose, so what may have worked for you does not carry much bearing on what would work on someone else with a condition labeled as RA
I was diagnosed with RA a few years ago when my left knee kept swelling to the size of a grapefruit. It was incredibly painful; I have a very high pain tolerance and it put me in tears and made me bed ridden or on crutches for multiple days at a time.
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.
I am sorry if this is insensitive, but thank God it is difficult to sue a doctor for misdiagnosis. If it were easy, there would be hardly any doctors in the world. Also, maybe I come from a different position but I get a second consult for just about any non-minor ailment I have ever had. Instead of suing doctors, "get second opinion" should be the thing! Every doctor tries their best, its years of toil and labor, and they can make mistakes. Please do not leave such important decision in the hand of one person under the assumption that they are an expert. I understand if you do not have money or time, but the consequence of a misdiagnosis are going to hurt you.
At the very least, if you get a second opinion that's different from the first, and it turns out to be the correct one, you should be able to get your money back from the first doctor.
I am not claiming to be all aware on the big picture, but based on my personal experience till now as an Australian, an even better solution is free Medicare.
under the free medicare are you able to go see a different doc for the same thing just to get a second opinion? Is it much hassle/paperwork to get approved?
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.
Sorry, its not exactly free like I described. When you are seeing experts (and when you really need second consult) you get back a small part of your money, but expert costs are high enough to deter most people from getting second opinion. But, no it is not a lot of hassle/paperwork for seeking second opinion.
Yeah this. I guess we all have some story, bigger or smaller, when doctor didn't do perfect diagnosis or treatment.
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.
How about if doctors were required to work for larger entities with deep pockets (e.g. HMOs, hospitals, the private partnerships backing plastic surgeries, etc), and we could easily sue those?
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!
> 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?
Obviously, because they can get sued, just not for a misdiagnosis in most cases. A surgeon who removed the wrong organ, for example, is liable to get sued.
After getting off methotrexate I never had that inflammation occur again. The only thing that changed is I stopped taking some B vitamins I'd been taking prior to the diagnosis. RA can be tested for by doing a synovial biopsy, if she hasn't had one I'd suggest asking her doctor about it. If she has and it came back abnormal she has RA or gout. The synovial biopsy is what I never got, they diagnosed me on symptoms alone.
I would argue that "professional judgement" should be taken out of the equation as much as possible. What would we lose by requiring any prescribed intervention to go through a rigorously-defined flowchart/checklist? A lot of doctors think they know better than the consensus best practice. They're almost universally wrong. Off-label prescription? Mostly horse crap, unless it's part of a serious clinical trial.
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.
I think someone more knowledgeable than me should reply to this, but my understanding is that most medicine is still too complex, with too little data to reliably make machine judgement. We don’t have the training data.
The comment is also uneccessarily confrontational. There are plenty of areas in medicine where checklist and sops have been widely adopted.
> [...] my understanding is that most medicine is still too complex, with too little data to reliably make machine judgement.
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. :)
This “flow chart” can exist now on the the back of well prompted large language models. Not that there isn’t potential for huge headaches for all parties (hallucination around medical topics will be really dangerous) but doctors should be prepared for far more sophisticated self diagnosis coming their way. I think the safest use might just be for lay users to get a third opinion and sanity check doctors.
Seropositive RA is a specific but variable condition. Seronegative RA... you are quite right. It's almost easier to group by a rational treatment approach for a chronic inflammatory polyarthritis that looks like RA clinically rather than one diagnostic entity.
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.
There's also psoriasis (and psoriatic arthritis), where it's been firmly established that one subtype — guttate psoriasis — is triggered by _Streptococcus pyogenes_, which also causes strep throat, which is very common.
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.
My mom has this had this disease for at least 40 years and I’d love to find something else for her to try. How can one tell if hers is triggered by this bacteria? Any tests?
There are treatments that are very effective for treating psoriasis, especially those based on monoclonal antibodies. I was treated for atopic dermatitis (which is a similar disease), and I have been in near remission for several years. However, the treatment is very expensive.
No, there's no such test. Doctors typically test for strep after you've had strep throat, but the test is only positive if you have strep bacteria in the throat.
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.
Came here to mention AS and the klebsiella hypothesis. Like you said, nothing conclusive has come out of it (and certainly no evidence of using antibacterial treatment successfully to treat AS), but I still find it super interesting considering the high comorbidity between AS and intestinal diseases like Crohn's and ulcerative colitis. IIRC some of the more recent "AS is a form of reactive arthritis" truthers have focused on gut infections specifically as the pathway.
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.
I started with a diagnosis of reactive arthritis (still called Reiter's Syndrome at the time), after an intestinal infection. After 10 years of feeling fine and unmedicated, but with occasional flare-ups, I suddenly went downhill and my diagnosis was changed to ankylosing spondylitis (modified New York criteria). To my knowledge, there is very little research on the separation or progression between reactive arthritis and ankylosing spondylitis.
I cannot really add anything useful, but my progression was so similar in all senses that I thought I should comment: it started after an intestinal infection I got in India, many different hypotheses until they settled on Reiter's syndrome/reactive arthritis. Then for 12 years I was without real symptoms or medication, though with almost chronic back pain.
A new bout 12 years later (knees like grapefruits etc), diagnosed now as ankylosing spondylitis.
In fact I had understood that this was a specific form of reactive arthritis (rather than something different), but probably you're right.
I have a sibling that has been diagnosed with AS, along with a handful of other related diseases, such as juvenile rheumatoid arthritis.
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 hesitate to give unprompted quasi-medical advice to a stranger online, but if the potentially harmful treatment you're referring to is biologic therapy, just know that millions of people have taken TNF inhibitors for decades to positive ends. There are risks, to be sure, but not necessarily greater than the risk of untreated autoimmune disease—runaway inflammation is linked to heart problems, for example, and untreated Crohn's/colitis massively increases your risk of colorectal cancer.
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.
Seconded. My father who also had AS 25 years ago, had to get on sulpha drugs to stop disease progression. In comparison, I consider biologics a walk in the park and truly consider myself lucky to have access to them. I luckily haven't had symptoms of AS (yet) but the auto-immune problems I've had include recurrent uveitis. I was similarly reluctant to get on biologics but having been on it a while now, I truly consider it a miracle drug - especially when the alternative is losing my eyesight.
Problem with biologics is that you can never really know how long you can take them. Some people who take them for years all of a sudden stop tolerating them and have to drop out of using them
It's true that biologics can wear off, but two counterpoints: (1) with the wealth of options available on the market today, you can generally hop to a new drug if a particular formulation starts losing its effectiveness, and (2) even if you only got Three Glorious Years of relief before all biologics stopped working for you forever, isn't that still a net gain versus not going on them at all?
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.
I've been on adalimumab since I was 19, I'm 34 now. Treatment for Crohn's disease. I've had the talk with my doctors multiple times about what we do if the treatment stops working, and they
always reassure me that there's multiple other options these days.
> many people don't develop resistance, or at least not for a loooong time
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 have AS. Diagnosed or rather verified on the sole basis of presence of HLAB27 antigen. Luckily it's peripheral, but it was detected pretty late in the cycle. The doctor was super helpful. I realize the how this is an evolving science when I shared the reports with a friend who studied medicine for 8 years, and her reaction was total surprise about the tests, medicines, and injections I was given. Only thing that has worked so far is Adalipca injections and they too need to be taken atleast once every year (two at a time). (Edit: The doctor told me pointblank that we dont know what could have triggered it)
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 know anecdotes aren't data, but I would not be surprised if this was hitting close to the truth.
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!
I experienced the same, although my gluten-induced inflammation is linked to something with my gut bacteria. If I take a certain antibiotic that targets the digestive tract, I can eat anything for 9 months, including gluten, without problems. After about 9 months, I can no longer eat gluten. And then about a year after that, I can't eat corn. This has repeated 3 times, and unfortunately, I'm with a gastro doc now who won't give me the antibiotics and wants to test me for celiac (which will be the 5th time - I've always been negative).
Very similar for me. Mid 30s, chronic arthritis in multiple joints. Lots of other issues as well. I had previously derided those on gluten free diets, but in desperation, I tried it. After two weeks my symptoms abated significantly. A year on and I feel like a million dollars. I have no idea if I had some kind of intolerance to gluten, or if some bacteria really liked that gluten, but it worked.
very similar experience with me. after frustration with medical treatment over many years into my mid-60s, i went gluten-free and symptoms cleared within weeks.
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.
Somewhat off topic. But I felt like this article was extreamly well written. It summarized the science while also not going overboard in trying to convince the reader that the bacteria referenced was 100% definitely the main culprit.
I really liked how the experiment was broken down so that a normal person could understand the high level logical steps between each section.
Had a major flare up of RA after a particularly stressful moment in life. Went to doctor who prescribed steroid lotion - a non starter.
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.
I use Carlson also; from everything I've read, that is the best. I eat fatty fish a few times a week too, but I saw no harm in adding a little extra oil.
Crohn's and several forms of arthritis are closely linked to the HLA-B27 gene. (And I should know, because I have the whole shebang :P)
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!
As someone that's been dealing with SIBO (small intestinal bacterial overgrowth), I'm confident that most diseases are the result of your gut microbiome.
Really looking forward to research in this field and I hope the US starts putting more focus on phage therapy.
I agree. The frustrating thing with a lot of this is that microbiota seem to follow the Anna Karenina principle: every healthy microbiota is alike, but every dysfunctional one is dysfunctional in its own way. FWIW, I have a friend whose SIBO spontaneously went into remission almost immediately after travelling to a tropical country. Of course, that probably wouldn't work for you.
Did you take rifaximin, and did it work? I'm currently on my fourth day, and am finding that all of my joint pain has disappeared. Could be coincidental, but now there's the coincidence of this story in Science.
Been dealing with it 3 years now, took the first 1.5 years to figure out what it was. So far took 2 rounds of rifaximin. The first round didn't do much, but the second round (with neomycin) got rid of my methane overgrowth. I still have a hydrogen overgrowth and waiting on insurance to improve another round of just rifaximin.
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 have been taking Candibactin-AR and Candibactin-BR with my meals and have seen an improvement in my stool consistency (I have recently diagnosed SIBO/Crohn's). I was given the metronidazole for one week and it helped as well, but symptoms came back.
I've been taking low dose herbals as maintenance since my last round while I wait for the next round
> 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...
That sounds alike a pain to have to wait. Out of interest: when people compare US medicine with socialised medicine like the NHS, does the time spend waiting for insurance paperwork get included in comparisons?
Probably not. People in the USA have been brainwashed to be terrified of social programs so they'll never give them a fair comparison. They just talk about the worst cases where it takes months to be seen by the doctor, which funnily enough is exactly how it is here if you're trying to see a specialist.
Similar sufferer of recurrent uveitis here (spent 10 years doing several tests none of which ever explained what I have, only excepting HLA-B27 which occurs with several of these auto-immune diseases). The only thing that helps me now is Humira.
I wonder if gut bacteria has anything to do with my condition and how I can even go about digging into this :/
Interesting. I have Crohn's, and I've gotten uveitis during really, really, really bad flare ups. I've had Crohn's for 40 years, and I wasn't even aware there was a link until my gastroenterologist told me about it.
>Antibiotic exposure was associated with an increased risk of IBD as compared with no antibiotic exposure for all age groups, although was greatest among individuals aged 40–60 years and ≥60 years (age 10–40 years, IRR 1.28, 95% CI 1.25 to 1.32; age 40–60 years, IRR 1.48, 95% CI 1.43 to 1.54; age ≥60 years, IRR 1.47, 95% CI 1.42 to 1.53). For all age groups a positive dose–response was observed, with similar results seen for both ulcerative colitis and Crohn’s disease. The highest risk of developing IBD was seen 1–2 years after antibiotic exposure, and after use of antibiotic classes often prescribed to treat gastrointestinal pathogens.
So people who were more likely to use antibiotics because there was a suspected infection were more likely to have Crohn's disease, possibly underlying at the time
I'd wager yes, for that very reason. Years ago I was in hospital and a registrar told me that guts are smelly but they're the next big frontier of medicine. I didn't immediately know what she meant, but having thought about it since, she was absolutely right. The biome has a lot to answer for.
I was diagnosed with RA, I ignored it forever until I was having issues functioning normally. I was prescribed prednisone for a week and then methotrexate/folic acid. The methotrexate helped me feel fine despite decimating my hairline.
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.
I’ve had mild psoriasis since I was a young teenager.
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.
The gut-brain axis is so important. It's only natural that commenters here would want to know when a treatment for RA is available based on these findings. Nothing's for certain, but it wouldn't hurt to improve your gut biome.
- 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.
Interesting, I new someone who had RA in her 20s, by the time she reached here mid 30s, it was gone. This was a long time ago but the doctors then were a bit surprised.
That really is interesting. I started developing it in my early 20s, and I still have it (mid 30s now), but in some ways it has improved quite a bit. I have no idea why or how. I'm grateful, though I assume it'll eventually get worse again rather than go away.
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.
No inhibitors or medications of any kind during the onset or most of the progression.
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).
did she have children? pregnancy suppresses the immune system, many women find that auto-immune conditions go away (temporarily usually) when they are pregnant.
I had psoriatic arthritis and it just went away after several years. The only thing that could keep it in check was comfrey ointment (I tried everything conventional medicine had to offer except biologics). But since about two years ago I am symptom free.
Although the title is definitive, it should really say "possible".
> 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.
I have same anecdotal evidence about my mood. I had some tooth infections and took some strong horse dose antibiotics couple times in my life and my mood and “adhd” symptoms got better.
A lot of people (me included) report this when they induce ketosis after eliminating carbs and sugar. It would seem reducing carbs and sugars would drastically change the biotic makeup of one's gut, so this is all seeming to be tied to ones gut... microbiota is very interesting.
That does not surprise me at all.
For depression there is the chronic inflammation hypothesis which states that depression is caused by subacute inflammation in the brain. Some antibiotics work as antiinflammatory agents. Although a recent study did not show significant evidence for the treatment of chronic depression with antibiotics.
Then there is something along the lines of underexpressed BDNF genes which get more expressed by butyrate which in turn is produced by gut bacteria.
And there have been some case studies for treatment resistant depression where they did a stool transplant which improved the symptoms considerably.
Anecdotally, I‘ve experienced these benefits after ca 9 months of strictly no sugar (not even fruit). But just a couple weeks of eTRF (stopping to eat at 3PM) gave the same results (normal IF did nothing of the kind for me).
Hope there will be advancement for RA. It took my father away, doctor, at 71 years old. RA led to lung fibrosis which ultimately gave him a heart attack.
Unfortunately, few months ago, my gf who is in her very early 30s, was diagnosed with RA. She was immediately placed on the very expensive medication - $5000/month (you read it right, a month). It helps a lot, but not 100% effective and we don't know how it will work long term. We are hoping, that some new treatment might be available in the future.
My sister had RA in her early twenties. For years no treatment was able to restore a reasonable quality of life. There were many side effects which needed treatment as well. She went from doctor to doctor, while she lost the best parts of her life.
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 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.
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.
My friend has RA, after being on medication for years where he would have nausea for at least a week every month. He stopped taking any medication altogether. He goes to Gym twice a day and keeps a strict diet (relaxed at times). He is way better since the last 4 years.
I also have RA and have the exact same experience. I really wish doctors would actually present lifestyle changes as an alternative treatment. Sure if flares every once in a while but my feet are super strong now with barefoot running & slacklining and I hardly even notice it anymore when I'm moving.
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.
I know I already posted in another comment but how active is she?
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.
It is true that it helped me when I went to gym, it hurt at first but got a lot better within 2 weeks. Could be just coincidence but now I've stopped the pain is coming back.
There're generic versions of the drug coming to market. Amjevita from Amgen is bio-similar to Humira and just got FDA approved. It costs about half at retail. As more generic versions of the anti-TNF biological drugs coming online, the price should be driven down.
very large molecules (proteins) can't be exactly replicated. It's not something like aspirin with a barely a few atoms bundled together, those are very complex structures with very long chains and 3D hyperstructures that have a clear impact on their effect.
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.
> what do you mean can't be replicated? that's how they manufacture the drug.
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.
Praying for generic adalimumab to finally hit the US market. People overseas have been getting this stuff for a hundred bucks a pop for years now, but AbbVie's done everything in their power to extend the US patent for as long as possible. They'd milk us forever if they could.
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).
My body created an antibody to infliximab after about 6 months of treatment and I had a bad reaction to it. 6 months of expensive treatment wasted.
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.
This does not invalidate my comment at all. It only shows that Fasting can be an effective way to reduce symptoms - but it won't cure RA. There is no known cure for RA.
My biologic (brand Xeljanz) prescription was $5000/month but was paid for 100% through a special program from my pharmacy/drug manufacturer (I'm still not 100% clear how). I had to stop because I was dealing with an infection, but I just wanted to share that because it's still new for you.
I feel for you. We're in the same boat. My wife is a similar age and also has to finaggle her way around these ludicrously expensive RA medications. I also really hope a new treatment will arrive before this one either stops working or we become incapable of affording it.
I know someone who has it. How lond does it usually take to go from a research like this to a medicine available to patients (if the hipothesis turns true)?
~8 years at best if everything goes well (rarely ever does), there are outliers like Polio took ~4 years, and Covid took ~1 year. But those are much different than RA.
I'm surprised to see an article on rheumatoid arthritis (RA) at the top of HN.
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).
Damn, do you work in rheumatology? I rarely see explanations this detailed (and well-communicated) about autoimmune conditions, even when I'm going out of my way to look for them. Color me impressed.
This reminds me of my GERD when it was bad and if I had the flu (yes I was vaccinated) my GERD symptoms disappeared. It was flu not a cold and I didn't have a runny nose if anyone is assuming it was post nasal drip causing a antacid effect.
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!
I also have relatively bad GERD and I've also noticed it getting better when I have flu or some other minor illness. I think this is just because I eat less and move less. Moving less helps because sometimes random movements in a wrong way can trigger the reflux.
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.
Also anecdotal, but I know a lot of people with autoimmune diseases report feeling "better" when they're sick. Might be because your immune system finally has a real target to set its sights on and takes a break from attacking your own tissues.
Actually also the recent Parkinson's breakthrough reminded me of when Fox and three crew of a TV show he was on as a young teen all developed Parkinson's disease.
I have been following RA for years now. There is a small public company (OMX:SYNACT) I found that are in its Phase 2b with a medication that looks very promising. They completed their Phase 2a with statistical significance in a couple of key indicators. It looks like to be on par with JAK inhibitors but with a cleaner safety profile and no need for injections.
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.
Aw, I'm sorry to hear that. AS can absolutely wreck your mobility over time. (And the reason I know is because I also have AS—I should've been more clear and gestured towards my username :P)
Not sure if it was the same thing, or just worn out hips, Osteoarthritis? But in retrospect, I've been thinking about it. A timer and getting up from the computer every half hour or wearing compression socks and maybe a foot massager would have helped. But I'm not sure if it would have been enough to prevent DVT.
HN doesn't have messaging features, does it? Feel free to shoot me a DM on Reddit then, I'm -ThisWasATriumph over there. (Just don't forget the leading hyphen in my username!)
For me it was electricity, make sure you're not exposed to high currents and strong electrical fields. Especially things like a modern macbook charger plugged in is capable of producing fields up to 1000v according to the emf meter I got on hand.
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.
That's not a strong counterargument because people use laptop chargers for hours at a time many days of every week, compared to rubbing balloons against their hair maybe ten minutes total spread out over a lifetime.
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.