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Do MEs cause CFS?

Jonathan Edwards

"Gibberish"
Messages
5,256
@ Jonathan Edwards I had anti-thyroglobulin antibodies of 19 UI/mL, with normal value being < 4.1 according to the lab. I've heard different opinions on whether this is significant. What do you think?
Also adrenalin below the detection limit in two separate 24 hour urine catecholamine tests, low insulin, reactive hypoglycemia, low FH and FSH.

Different labs have different ways of deciding what is the upper limit of 'normal' and as for ANA it is not really clear even what that means. The reality is that nobody knows how significant these results are, but my guess is that it may be something to do with the ME. Most doctors will say not because there is no proven link, but they may be because nobody has studied it properly.

The hormone tests I would not comment on as I do not know enough endocrinology.
 

Jonathan Edwards

"Gibberish"
Messages
5,256
Somebody asked about separating people on the basis of infective triggers. Sorry I can't remember who. To some extent that is implied in the groups. ME2 would be post-infective. The others may not be but we have this problem that, as I think I discussed with Ninan, it may not be so easy to tell the cart from the horse. The sudden onset with a viral infection does not necessarily mean the viral infection started things - the ME may have been lying in wait to overreact to the virus. Lupus often presents as infection because it makes you susceptible to infection, not because it is caused by infection. So yes, infective trigger will be relevant, but it may not be simple to tell its role. A sudden onset is not necessarily due to a causal trigger at that time.
 

Jonathan Edwards

"Gibberish"
Messages
5,256
And in response to Marco, thanks for the rambles, which I very much like. In fact my last post is sort of saying what you are saying at the end I think. One thing I might add is that the 'detailed programming' of the brain's immune response is probably kept elsewhere in the lymph nodes, bone marrow and spleen. The exception to this is multiple sclerosis in which adaptive immune cells actually live in the CSF. Although the neural dynamics of brain are ideal for strange attractors the microglia themselves ought to be standard issue monocyte derived cells. If they are primed one might expect that to be due to a programme held elsewhere - in bone marrow plasma cell stocks for instance - feeding particular antibodies to be picked up by FcRI to pre-arm. On the other hand I guess that there might be local perpetuation of microglial misbehaviour through microanatomical changes - a bit like that mosquito bite that you keep scratching and making worse even though the mosquito proteins are long gone. I need to think about that a bit more.
 

wastwater

Senior Member
Messages
1,267
Location
uk
I think I may have a COL4A1 mutation,I think its to do with collagen would this be described as a connective tissue disorder
 

wastwater

Senior Member
Messages
1,267
Location
uk
I wonder if ME is a side effects type illness due to increased cytokine signalling not a targeted attack as in antibodies.The side effects being thyroid dysfunction depression and mitochondria problems.I have hypothyroidism without antibodies and normal ANA.
 

Legendrew

Senior Member
Messages
541
Location
UK
3. ME3 is not really a subgroup, but a causal component. It may ‘gang up’ with other MEs so that they feed off each other through regulatory pathways. ME3 is a resetting of brain sensitivity to all sorts of ‘noxious’ stimuli. It may well operate through feedback involving the autonomic nervous system. In some cases it may be reduced by the sort of voluntary strategies encouraged by ‘talking therapies’ but very often I suspect it is completely impervious. My own analogy is my tinnitus. Sometimes it seems unbearable and stops me sleeping or enjoying the quiet countryside and at other times I forget I ever had it. When it is there I cannot tell myself to not have it.

. ME5 is a speculation rather than something I have evidence for, but the specific autoimmune types I have given so far will not cover the majority. There is at least one more type needed and this is my guess. ME5 involves a sensitisation of the immune signalling mechanisms triggered by viruses. As part of an immune response to a virus the system produces antibodies that sensitise the ‘virus alarm system’ to the extent that even when there is no virus around it may trigger, just with exercise or stress. Two molecules might be particularly important here: gamma interferon and the immunoglobulin receptor FcRI (CD64) which is used to ‘pre-arm’ phagocytes with antibody even before any foreign pathogens have arrived.

I suspect I have a combination of both of these. I seem to be fine at times: almost normal but then I seem to flare up from viruses, stress (to which I am now very sensitive) or just doing a little too much physically or mentally. Strangely sometimes I can do all of these things and not flare but at other times I seem to be very sensitive to a flare up as I am right now: with symptoms appearing to be triggered even by a 1% hydrocortisone cream I'm using for a mild rash (funnily enough, at times this month the rash has been a more pressing medical concern to me than this ME/CFS business which shows just how much I seem to be fluctuating now...).

I do seem to be getting these periods more and more infrequently and can do more and more when they're not present so I'm optimistic of improvement but the symptoms are still incredibly unpleasant when they're with me. The most disconcerting has to be the internal tremors I feel when trying to sleep at times: almost like a strong adrenaline rush. Whenever I'm in this flaring stage my lymph nodes always seem to be swollen in my neck and behind my ears so make of that what you will. That said my lymph nodes seem to have gone down and I haven't suffered with the acid reflux that was so common for me last year in quite a while now. Hopefully this oversensitiveness is abating slowly.

Strangely I seem to feel at my worst while lying in bed in the morning: all my muscles seem to ache and at times I feel like I haven't the energy to even move a finger yet once I'm up and about I feel much better and can partake in most activity. I certainly seem to suffer from the strangest sensations and symptoms... It just sucks that I seem to be so sensitive to things now; that coupled with my migraines of which I've always suffered makes me feel like I'm having to avoid that many things it's getting silly.

My triggering event still stands in my memory as strange as it was both acute and somewhat drawn out... Immediately following the vaccination I experienced graying of vision and almost fainted on the way back home: having to sit down for 10 minutes before being able to continue (having a migraine later that day) but then over the next couple of days all my lymph nodes came up and I slowly deteriorated from there onward; not helped by the antibiotics I received which really hit me hard and no doubt the stress of the illness. I still wonder whether I may have autonomic problems, POTS or something to that effect but the trouble is that ME, CFS, dysautonomia and even POTS are still all in their infancy and diagnosis is just so difficult.
 
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Mij

Messages
2,353
I believe the intial sudden viral onset put me in a vulnerable postition and the added vaccine/stressors 2 months later put me on a path to ME down the road.

I feel as though I would have gotten over the virus eventually.
 

rosie26

Senior Member
Messages
2,446
Location
NZ
Somebody asked about separating people on the basis of infective triggers. Sorry I can't remember who. To some extent that is implied in the groups. ME2 would be post-infective. The others may not be but we have this problem that, as I think I discussed with Ninan, it may not be so easy to tell the cart from the horse. The sudden onset with a viral infection does not necessarily mean the viral infection started things - the ME may have been lying in wait to overreact to the virus. Lupus often presents as infection because it makes you susceptible to infection, not because it is caused by infection. So yes, infective trigger will be relevant, but it may not be simple to tell its role. A sudden onset is not necessarily due to a causal trigger at that time.

"ME may be lying in wait to overreact to the virus". Quote Jonathan Edwards.

That's how it was for me. I feel quite positive about that. I had ME 'light' for years - getting increasingly worse before the flu severe onset.
 
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Marco

Grrrrrrr!
Messages
2,386
Location
Near Cognac, France
@Jonathan Edwards

Thanks. Glad to hear I wasn't too off he wall with my musings.

Due to my lake of knowledge of biology I had assumed that when they referred to 'brain resident macrophages' that they were 'brain resident'.

I don't think though that an autoimmune loop needs to directly affect microglia, astroglia or oligodendrocytes directly. Activated glia (neuroinflammation) results in the usual inflammatory cycle of increased pro-inflammatory cytokines, oxidative stress and mitochondrial dysfunction. Autoimmunity that affects any part of this cycle could result in an exaggerated or sustained immune response.

One example is that certain TNF-a modulating SNPs have been associated with sickness behaviour (fatigue and mood problems) in primary biliary cirrhosis (one of Prof Newton's specialities). Autoimmunity could also impact on cytokine production or any other part of the cycle leading to elevated and sustained neuroinflammmation.

It could be a different part of the cycle for any individual who displays the symptom complex that leads to a diagnosis of ME/CFS.
 

rosie26

Senior Member
Messages
2,446
Location
NZ
After sudden severe onset I was able to recognize my 'light' years symptoms of ME. I had a 'lighter' kind of ME for about 10 years before severe onset.
 
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Scarecrow

Revolting Peasant
Messages
1,904
Location
Scotland
After sudden severe onset I was able to recognize my 'light' years symptoms of ME. I had a different 'lighter' kind of ME for about 10-17 years before severe onset.
Same with me, more or less. Well, definitely less. I had about five years of 'light' following sudden and severe IBS. But was the IBS the start or the first manifestation?
1. ME1 is due to antibodies to certain nuclear proteins that can enter cells and disturb function on a body-wide basis. ANA is positive and usually speckled in pattern. (The proteins are likely to come under what are called ENA antigens, which are not always strictly nuclear but no matter.) The fatigue of ME1 is basically the same as in primary Sjögren’s syndrome and other ANA-linked illnesses that have names. I have met many people in this group. Some might suggest that they are well enough described to take them out of the ‘unknown causes’ that are MEs but a lot of these people end up labelled as ‘CFS with an ANA’. The fatigue may be a bit different from other groups.
@Jonathan Edwards, are you able to expand on what you mean about the fatigue being different from the other groups? I think that most PWME would be able to describe many different kinds of fatigue. Do you mean that the fatigue associated with ME1 is more uniform?

Also, would you expect PEM to be a possibility in all six of your MEs or would the presence / absence of PEM rule some in or out?
 

Marco

Grrrrrrr!
Messages
2,386
Location
Near Cognac, France
After sudden severe onset I was able to recognize my 'light' years symptoms of ME. I had a different 'lighter' kind of ME for about 10 years before severe onset.

I've suggested several times that some may have had 'prodromal' symptoms not necessarily related to ME/CFS.
 

Scarecrow

Revolting Peasant
Messages
1,904
Location
Scotland
I've suggested several times that some may have had 'prodromal' symptoms not necessarily related to ME/CFS.
By 'prodromal' (i.e. the use of inverted commas) and the fact that you state 'not necessarily related', do you mean coincidental?
 

Jonathan Edwards

"Gibberish"
Messages
5,256
@Jonathan Edwards, are you able to expand on what you mean about the fatigue being different from the other groups? I think that most PWME would be able to describe many different kinds of fatigue. Do you mean that the fatigue associated with ME1 is more uniform?

Also, would you expect PEM to be a possibility in all six of your MEs or would the presence / absence of PEM rule some in or out?

I don't think I can be more specific. I guess I was thinking that although all these different processes might produce indistinguishable symptoms once it is clear how subgroups separate out it might also become clear that there are differences that people haven't really thought how to describe yet. I guess you are right that I might expect fatigue to be more uniform in ME1 since speckled ANA antibodies tend not to change much once they are there. But that presumes a simple analysis ...
 

alex3619

Senior Member
Messages
13,810
Location
Logan, Queensland, Australia
I've suggested several times that some may have had 'prodromal' symptoms not necessarily related to ME/CFS.

In the past this has led to the discussion of a third type of ME onset, staged onset. Its like there are steps to getting ME, including stages in severity. In some though a major trigger will suddenly push those who already have some of these steps into the "final" stage, though given how ME can morph I am not sure there is a single final stage.

This is speculative of course.
 

rosie26

Senior Member
Messages
2,446
Location
NZ
In the past this has led to the discussion of a third type of ME onset, staged onset. Its like there are steps to getting ME, including stages in severity. In some though a major trigger will suddenly push those who already have some of these steps into the "final" stage, though given how ME can morph I am not sure there is a single final stage.

This is speculative of course.

Yes, staged set up for me. I can count 3 stages. But I will have to think more carefully on it to make sure I haven't missed anything out.
 
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Kati

Patient in training
Messages
5,497
How about the contribution of the sex hormones, perhaps menopause since this disease (s) affects women quite predominantly ? Case or effects?

And I will repeat my question for @Jonathan Edwards can ANA pattern switch from speckled to homogenous?
 

voner

Senior Member
Messages
592
What I like about the immune system is that we are just beginning to know enough to build detailed systems analysis that one can actually make predictions about new metastable states from. That is what we did for RA. The analysis had 55 steps in the system, four positive feedback loops and lots of negative ones (less interesting). That then led to a generalised version with a key positive feedback loop that actually required only a minuscule perturbation - in theory a single B cell.......

@ Jonathan Edwards,

Is it possible for you to direct us to some references (preferably not behind a pay wall) that graphical show the steps in the RA system, feedback loops etc? I think it might be helpful (to at least me and probably others) to be able to visually see some of these interactions and loops, etc.
 
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