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Created in 2008, Phoenix Rising is the largest and oldest forum dedicated to furthering the understanding of and finding treatments for complex chronic illnesses such as chronic fatigue syndrome (ME/CFS), fibromyalgia (FM), long COVID, postural orthostatic tachycardia syndrome (POTS), mast cell activation syndrome (MCAS), and allied diseases.
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Of course that would just be by symptoms since most of us can't check for stuff like ANA:s.
@Jonathan Edwards Assuming your groups are correct, do you think there would be a big difference in symptoms between the groups? There are some quite obvious differences between us:
Onset: Symptoms started with infection or not
Infections: Impaired immune system (catches every cold there is) / Over active immune system (never gets a virus)
Course of illness: Relapsing form / non-relapsing form / gets worse over time / constant over time
Symptoms: Gut, sensory sensitivity, pain, developing new allergies, orthostatic problems -- Don't have it / smaller issue / huge issue
How relevant do you think these differences are for determining what subgroup someone belongs to? Are any of them more interesting than the others?
Could someone expand the abbreviation 'ANA' for me please?
I'm not sure how to say this respectfully, but I think you may have the cart before the horse. PEM is a defining feature of this illness and autonomic dysfunction in the form of POTS, etc. is prevalent in a very significant subset of patients. I think that if you are trying to discuss possible triggers or causes for this illness, at least some of the causes should taken to account autonomic dysfunction and probably all the causes should take into account PEM. I remember hearing Dr. Suzanne Vernon say that when they did in-depth surveys of CFS patients she was surprised to find how common significant muscular pain was also.
I personally think vascular dysfunction could take into account these three symptoms (PEM, autonomic dysfunction, muscular pain) and also "Fatigue", "brain fog", etc.. then the question is - What are the core causes that would trigger this vascular dysfunction?
I have trouble running a fever. If I get an incidental infection I typically feel worse (e.g. aches, malaise, possibly trembles, chills, cough) but don't have all the signs and symptoms unless it's a flu, but still not even moderately high fever. I have low NK cell function like those with infections. Is all this explained by autoimmune (or other expected immune) problems?
How does muscle dysfunction fit into everything? I can't paste studies from this device and honestly some (all?) of the studies are very small, but Yves Jammes and Kieren Hollingsworth are finding a neurological muscle problem in both smooth and skeletal muscle. Could the body be attacking the ion channels (if I understand it correctly) that work the muscles in some cases? I have a test result that would support this kind of muscle problem in my case (but no MG, MS, etc.). Also, if I walk too far, particularly if I've not been getting enough rest in general, my legs drag.
If autoimmune disease similar to Sjogren's were attacking the GI system, would it necessarily look bad on various scopes and image testing? Could this cause severe problems like malabsorption and maldigestion while looking relatively unimpressive and unidentifiable to a thoughtful GI doctor, or would that be a different problem? Second thought, I searched and I see it's not uncommon for Sjogren's patients to be diagnosed with IBS. They have some similar and some opposite problems to me, but this is intriguing.
How do you find a new autoantibody?
Yes, I agree that the autonomic nervous system is one arm of the spaghetti loop. It is definitely in there. My thought is just that its malfunction is secondary to some immune error - rather as you suggest.Dear professor Edwards,
Is it possible that the ANS problems like 'overdirve' can be 'driven' by the immune system? I think the problems of ME can be due to the ANS. There is a kind of an abnormal 'stressrepsons' going on. This respons can be the cause or can be a sort of compensation like by diabetic. I won't rule the ANS out at this moment. I think there can be several reasons for the ANS dysfunction: 1. compensation (low bloodflow?), 2. defect of the parasympathetic nervous system, 3. autoimmunity against acetylcholine- or bèta receptor..... etc...
BTW, although my (mild) clinical hypothyroidism caused fatigue/exhaustion, the symptoms and course of the illness were very different from the subjective experience of ME. There was an overlap in symptoms, but they felt like entirely different illnesses. I could distinguish the two concurrent illnesses quite easily even before I'd got a hypothyroidism diagnosis.
Is a 'cluster' of antibodies common for autoimmune disorders?I just wonder whether your ME is based on autoantibodies, maybe a cluster, including ones that led to the thyroid underactivity, but which predominantly produce this other effect of 'CFS'.
Anti-thyroid antibodies crop up in people with RA for no reason we can understand and RA itself seems to involve two processes that can feed off each other – one for anti-CCP antibodies and one for rheumatoid factor.
Is a 'cluster' of antibodies common for autoimmune disorders?
FYI, the symptoms of my hypothyroidism and the symptoms of ME did not wax and wane together. (i.e. the thyroid symptoms did not get worse when the ME symptoms got worse.)
Fascinating discussion. Just lately on another thread I'd posted some references to 'exercise intolerance' in post concussion syndrome (by definition occuring long after the acute inflammatory response to traumatic brain injury) where it's proposed that exercise intolerance (as evidenced by symptom exacerbation/new symptoms) results from an 'uncoupling' of the autonomic and cardiovascular systems.
Chronic neuroinflammation has been proposed as the 'cause' of post concussion syndrome which only (like ME/CFS) affects a minority of those exposed to concussion. Which makes you wonder of they were 'predisposed'?
My dad gets this (PCS) and I've noted that the cognitive dyfunction experiences appears to be very similar to mine..
Most autoimmune disorders have traditionally been associated with one autoantibody. RA had rheumatoid factor. Hypothyroidism had anti-thyroglobulin, pernicious anaemia had anti-intrinsic factor etc. But in the last twenty years it has become increasingly clear that autoantibodies come in bunches. We have always known that lupus tends to have several autoantibodies, including quite often rheumatoid factor. We have also known that 40% of RA patients have anti-thyroid antibodies. Now we know that most RA patients have both rheumatoid factor and anti-citrullinated protein antibodies. In Graves' disease decades ago it was suggested that the thyroid antibodies were different from some other antibodies, sometimes called EPF (exophthalmos producing factor).
So there do seem to be clusters of autoantibodies. Interestingly, what you do not get is two antibodies that look as if they can do the same job. Thus in scleroderma anti-topoisomerase, anti-centromere and anti RNA polymerase all seem to be able to lead to much the same tissue pathology. But patients only ever have one or other of these.
In Graves' disease the course of the eye problem does not necessarily follow the course of the thyroid problem. Similarly, in lupus different antibodies come and go in different ways. Anti-DNA jumps up and down with acute episodes but anti-Sm just sits there for years unchanged. My idea is that the loop that keeps these antibodies going may in some cases be a bit like a Swiss watch. Some antibodies are more like the second hand, some more like the hour hand, but they all mesh together in those little cogwheels inside the back.
I don't know for sure if psoriasis is caused by antibodies or not and hence not if this is relevant, but, speaking of the connection between different autoimmune (?) diseases in the same person: As you probably know, the PWME:s who had preexisting psoriasis and responded to rituximab in the Fluge/Mella study experienced a worsening of their psoriasis symptoms as they got better. I know someone who got better from Remicade and experienced the same thing. It happens to me too: When I take LDN or Doxycycline (I think they are both immunomodulators, right? At least they both give me energy after 24 hours, that lasts for a couple of weeks.) I get a lot more energy but my usually pretty mild psoriasis gets much, much worse too. It seems that when ME gets better, PSO gets worse. Do you have any idea what that means?