Fibromyalgia syndrome—am I an autoimmune condition?, 2025, Goebel

V

voner

Senior Member (Voting Rights)
This is disapointing…

…"This implies that experience of trauma and distress might elicit a specific immune-biological response in genetically or otherwise (eg, past infection, toxicity, trauma) vulnerable individuals, which includes the production of harmful noninflammatory autoantibodies." …

Fibromyalgia syndrome—am I an autoimmune condition? - PMC

Either the majority or all patients with severe fibromyalgia syndrome harbour proalgetic serum-immunoglobulin G autoantibodies; their possible relevance for patients must now be established through clinical trials. Keywords: Fibromyalgia syndrome, ...
pmc.ncbi.nlm.nih.gov pmc.ncbi.nlm.nih.gov
 
I think it’s worth pasting the entire section (line breaks added). I’m putting it in plain text to make it easier to quote.

4.4. Triggers and the biopsychosocial dimension
If FMS is autoimmune, then it has “special” features. The recognition of biopsychosocial triggers to the onset of FMS59 implies that a substantial group of patients, although not all and perhaps not the majority, have experienced severe distress before FMS onset. The sensitive nature of such a link, which can and commonly does lead to misunderstanding and stigmatisation, has been discussed.12

Clearly, FMS does not develop in everybody who experiences severe distress, so that other factors must also play a role. At the same time, more fundamentally the recognition of a likely trauma/distress-trigger in a subgroup of patients with FMS, together with the described autoantibody findings now positions any distress-FMS relation into a new context.

This implies that experience of trauma and distress might elicit a specific immune-biological response in genetically or otherwise (eg, past infection, toxicity, trauma) vulnerable individuals, which includes the production of harmful noninflammatory autoantibodies. More studies are needed to confirm this.

Similar sequences from distress experience to disease phenotype are of course known from other autoimmune disorders,2,24 but in FMS, this phenomenon might be particularly common; in addition, FMS is also a much more common condition than “classical” autoimmune disorders; hence, any such relation should perhaps more acutely lead to considerations of preventative approaches.

Alternative primary triggers for the immune reaction leading to FMS might include infection, such as after COVID19 exposure26,36 or toxicity, such as after fluroquinolone medication.3 Other patients may develop the condition spontaneously, without any trigger.

Understanding autoimmunity in FMS should help us to better understand our human nature and how profoundly, truly biopsychosocial we in fact are. A debate about the additional importance of preventing toxic distress and how early preventative interventions might be designed and implemented would be welcome.
 
Utsikt said:
I do not understand why there even is a focus on severe distress. Surely, it would be more productive to focus on the factors that seem to always be involved, and what can be done to fix it?
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I agree. It looks as if this is a review prompted by a journal special issue. It does not seem to raise anything very new.

They suggest that psychosocial aspects apply to other autoimmune conditions but the two examples are unconvincing. One is alopecia areata, which is pretty much on the fringe of autoimmunity I think. The other is lupus, where there is a paper suggesting an increased coincidence with 'PTSD'. That doesn;t mean there is a link between trauma and lupus. It just means that fed up ill people with lupus probably score enough on diagnostic criteria for PTSD a bit more often = unsurprisingly.

I have been very sceptical about antibodies mediating "fibromyalgia" but I admit that it is a possibility, if perhaps in a subtle way (maybe analogous to the story we have suggested for ME/CFS). Unfortunately, I don't think passive transfer experiments are the best way to pin this down.
 
Study results are out for the auto antibody study.

ClinicalTrials.gov

www.clinicaltrials.gov www.clinicaltrials.gov

Couldn't find an associated paper.
Seems FIQR was the significant outcome the press release of UCB spoke about?

Not significant in a useful way though, but statistics was also very low.
And it's questionable if 12 weeks are enough to see an effect depending on the causing mechanism.

I think this is one of the studies where a negative or close to negative outcome doesn't really tell us anything about the probability of the theory behind being true. especially considering the mechanism behind the drug which only reduces igg down to about 20 percent I think.

Sorry for the spelling I need to use voice input.
 
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Absolutely zero attempt at making sense of what the pieces of the puzzle are. This is basically the equivalent of a baby chewing on one of the pieces and drooling on the others.

It basically just reads as some attempt to promote biopsychosocial ideology, with fibromyalgia tucked in as an afterthought.

I don't get it, what is even the point of paying for this expensive process, then paying for employment, when this is the nonsense they do with it?
 
rvallee said:
Absolutely zero attempt at making sense of what the pieces of the puzzle are. This is basically the equivalent of a baby chewing on one of the pieces and drooling on the others.

It basically just reads as some attempt to promote biopsychosocial ideology, with fibromyalgia tucked in as an afterthought.

I don't get it, what is even the point of paying for this expensive process, then paying for employment, when this is the nonsense they do with it?
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In my opinion, the author is a really helpful ally to fms sufferers.
He could very well be one of the key persons in the Hunt for medication that will finally bring relief to patients.

Considering the track record of the author, I think it's really not fair to put him as a promoter of non scientific BPS ideology.
It's quite the opposite, he's one of the few people searching for a biomedical cure.
And with the UCB Trial and the auto antibody studies, he has achieved more for the patients than almost all other people in the field.
 
Kronos said:
In my opinion, the author is a really helpful ally to fms sufferers.
He could very well be one of the key persons in the Hunt for medication that will finally bring relief to patients.

Considering the track record of the author, I think it's really not fair to put him as a promoter of non scientific BPS ideology.
It's quite the opposite, he's one of the few people searching for a biomedical cure.
And with the UCB Trial and the auto antibody studies, he has achieved more for the patients than almost all other people in the field.
Click to expand...
I think we should take the actions for what they are: the current article contains completely unevidenced speculation about psychosocial factors. Therefore, he is currently promoting non-scientific BPS ideology, and he should be critiqued for it just as everyone else that does it.

It could also be argued that it’s even worse when it’s endorsed by them, because it normalises and legitimises it.
 
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