Question re: the ICC Criteria and Ion Transport issues

[percyval577]

Yes. Unfortunately it was a very small study, though, with apparently only 5 patients and 5 controls (as suggested by Figure 1).

I searched then and found this sentence (page 7):

The selection of subjects
for inclusion into the gene expression pilot study,
focused on those without allergies, to whom an exercise challenge was given:
5 women with CFS and 5 female controls.

Why would they "focus" on those ones?? So, they cheated a bit, and dropped the ones with allergies. Maybe they did some other study at the same time, and here the ones with allergies might have displayed any significance??

Do you mean that the ICC Committee made up the "ion transport issues" as part of the criteria so it would have more weight (but there was nothing to back it up)? What would be the purpose of doing that?

In some sense well, nothing really conclusive for ME/CFS. It´s only that the suggested symptoms - which are by far not restricted to ME/CFS - have been found to have ion channels problems involved (I think this will be really sure enough).

This is the Review @Mary found linked in her second quote from the ME-pedia.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3935107/pdf/kjped-57-1.pdf 2014
I havn´t already read this very interesting looking article (but it seems that they even wouldn´t mention ME/CFS).

In the ICC from 2012 (here the primer for medical practitioners: Encephalomyelitis%20International%20Consensus%20Primer%20-2012-11-26.pdf)
one should find back some of the 2014 reviewed literature.

The question is, I think: What does it say that these symptoms have been found to have involved an ion channel problem? Is it a cause, or technical follow up from whatever? Do other diseases for sure not involve an ion channel problem? How are these more or less well known symptoms related to ME/CFS in its wholeness?

I really think they only made a quite narrow definition using/making an observation that patients who presumably suffer from this not-understood illness often display these widespread symptoms as well (saying "look, here are ion channel problems"); there is no special/important hint why ion transport issues (and in these special diseases/symptoms) would be an essential part of the ME/CFS (if at all).

How do you know that you occasionally meet criteria for an ion transport issue? Do you mean an autoantibody or a genetic issue (or something else)? Also, you did not have muscle weakness or fatiguability unless it was triggered by certain combinations of foods?

My temperature is generally low, especially in the extremities (only sometimes, though very seldom, it suddenly is normal). Then I have very seldom some asthma, but more regularly difficulties to breathe in a halfway comfortable manner. Honestly, I don´t know how my strange heartbeat would fit in. So, the last points are only occasionally, and the first point is occasionally absent.
I put my words not exactly, however, b/c of this occasionality, you might exclude me from the ICC. But reading through the forum, I am not sure if this would be a justified idea.


My muscle pain only arose from having drunken beer (0.9l) and then ca. 4-22 h later eating cheese or other calcium rich food. I have read that patients from the EBV subgroup would tend to suffer with leg pain, and this I have (it´s slowly vanishing, but has been very uncomfortable). Though I have not read that they especially would not suffer fro muscle pain.

Recently I had muscle aches obviously from tea, when I had started drinking tea again, after having discovered that I can drink tea without feeling worse and heavy if I only drink a sip of vitamin D before a sip of tea (and b/c I love tea, I obviously overdid it). Tea might be bad b/c of some manganese, and/or it´s influence on the thyroid (infomation from @PatJ).

When I detoriated, I had for a week a weakness in movements that tried to lift up things, it never came back so far. I generally can feel quite sluggish, but I could also ride bike a whole day. Movements had never disturbed me mentally, but now while improving (feeling rather good now) this happens quite soon and lasts for some hours (... and potentially for more).

That is my understanding @Inara (that Mg ions can block the voltage gated calcium channels which are already blocked for me by an autoantibody). This is as deep as my understanding goes though and I cannot tell you anything more!

I remember this also, I think also non-voltage gated ones, NMDAR´s(?)

 

[Inara]

I would love to understand (for real life) if Propofol (anesthesia) is safe for me since it technically is a calcium channel blocker

Interesting! It caused weakness and paralysis in me.

 

[Gingergrrl]

In some sense well, nothing really conclusive for ME/CFS. It´s only that the suggested symptoms - which are by far not restricted to ME/CFS - have been found to have ion channels problems involved (I think this will be really sure enough).

I agree that nothing is really conclusive for ME/CFS and that there are many illnesses in which ion channel problems are involved. I was just trying to figure out if they were finding solid proof of ion channelopathies when they wrote the ICC Criteria or if they threw that term in as more of a "guess" as to what was going on?

My temperature is generally low, especially in the extremities (only sometimes, though very seldom, it suddenly is normal). Then I have very seldom some asthma, but more regularly difficulties to breathe in a halfway comfortable manner. Honestly, I don´t know how my strange heartbeat would fit in. So, the last points are only occasionally, and the first point is occasionally absent.

So you were considering low temperature, asthma, and heart rate issues to be due to channelopathies? (I am not saying that they are not, I am just trying to understand this all better). I have never had asthma but I do have chronically low temperature (96 to 97F) and heart rate issues & POTS were one of the first major problems of my illness. In my case, I associated the calcium channelopathy with other symptoms (muscle weakness and fatiguability, breathing weakness of lungs and diaphragm, etc).

When I detoriated, I had for a week a weakness in movements that tried to lift up things, it never came back so far. I generally can feel quite sluggish, but I could also ride bike a whole day.

Do you mean at your worst you could still ride a bike for a whole day? Or do you mean now that you are better?

I remember this also, I think also non-voltage gated ones, NMDAR´s(?)

My understanding (which is still very minimal ) is that the anti NMDAR autoantibodies are paraneoplastic but I had not heard that they were voltage gated channelopathies like the calcium and potassium channel autoantibodies.

Interesting! It caused weakness and paralysis in me.

@Inara, do you mean that Propofol caused weakness & paralysis at the time that it was being used as an anesthesia for surgery (which is normal) ... or do you mean that these negative effects lasted much longer after the surgery was over and you had trouble regaining normal muscle strength AFTER having Propofol?

 

[percyval577]

So you were considering low temperature, asthma, and heart rate issues to be due to channelopathies? (I am not saying that they are not, I am just trying to understand this all better). I have never had asthma but I do have chronically low temperature (96 to 97F) and heart rate issues & POTS were one of the first major problems of my illness.

Well, the ICC do this interpretation, I think, following section D.

Do you mean at your worst you could still ride a bike for a whole day? Or do you mean now that you are better?

I felt so very bad, I could not answer in a sense-making manner for longer than a few minutes (though being adroit enough), when I started to walk it made soon "whuutch whuutch" in my already heavy ugly legs, but I went to work 2 times a day for two hours each time, and I still could ride bike without a crash two times a week for a whole day (though it was of course a thinking that it would be fun rather than it were fun).

Only now, while I am sill improving, and feel comparable very well - rather no pain, sleeping well, no problems to breathe, for some days able to do things mentally with at least some continuity - only now often unimportant movements destroy my well being, but it never gets into the bad area that I felt back then. When I now would ride bike it will be dangerous, two years ago I almost rode myself into a car.

I deteriorated from food, the new bad baseline was pretty stable, though I did pacing in respect of mental effort (also before deterioration though). Now the baseline is not stable at all (short termed), but I feel better and better (long termed).

My understanding (which is still very minimal ) is that the anti NMDAR autoantibodies are paraneoplastic but I had not heard that they were voltage gated channelopathies like the calcium and potassium channel autoantibodies.

I think, Mg blocks NMDAR channels and goes out when some Na ions have come into the cell through AMPAR´s. Probabaly no voltage gated channels with Mg (?) [I have forgotten the most things for now :/ probably even mixing things up(There was something with a ball on a kind of rope that would block something, but it rather couldn´t be a small ion). Ben94 = Ben Garside on you tube is a great teacher for such things.]

 

[Inara]

@Inara, do you mean that Propofol caused weakness & paralysis at the time that it was being used as an anesthesia for surgery (which is normal) ... or do you mean that these negative effects lasted much longer after the surgery was over and you had trouble regaining normal muscle strength AFTER having Propofol?

Ha, yes, I see my post is puzzling. I meant the latter: I had trouble getting awake and gaining consciousness, sitting up and everything. The right leg was paralyzed for 45min. The nurse was not friendly: She told me to try harder. At that time I didn't know what was happening, only that after a gut biopsy a few months before - also with propofol - I didn't have these problems, and there I got O2. But they ignored my demands for O2 at that 2nd biopsy. At that time the doctor looked at me as if I was a hysteric.

 

[Gingergrrl]

Well, the ICC do this interpretation, I think, following section D.

Thx @percyval577 and I was not sure if you had meant that you matched your symptoms to the ICC Section D (ion transport issues section) or if you had done some kind of test which showed ion transport issues. I understand what you meant now.

I deteriorated from food

Do you get allergic reactions to food?

I had trouble getting awake and gaining consciousness, sitting up and everything. The right leg was paralyzed for 45min.

Wow, I wonder if your reaction to the Propofol was b/c of your calcium channel issues? I know that you don't have LEMS but I read a journal article re: anesthesia in patients with MG, LEMS, channelopathies, etc, and certain anesthesias that are "neuromuscular blockers" can induce muscle weakness where the patient ends up on a ventilator after having the anesthesia .

Propofol is NOT a neuromuscular blocker but is a calcium channel blocker (of the L-type channels). I asked many months ago in the N-type CA+ Channel group I belong to if anyone had Propofol for a colonoscopy (or other procedure) and many people had used it and had no problems. So it is very unclear to me if it would be safe for me but I am choosing to avoid it unless no other option (and for my colonoscopy I had Versed & Fentanyl with no problem).

Can you remind me, Inara, do you have problems with Magnesium causing muscle weakness, breathing weakness, respiratory depression, sedation, etc.

The nurse was not friendly: She told me to try harder.

 

[percyval577]

Do you get allergic reactions to food?

I crashed three months after I had begun eating beans instead of meat, so the effect was delayed, and I didn´t notice that there was a relationship.

Only five years later I figured out that the high manganese in beans and some other pulses should have been the cause. I stopped eating high manganese food, and since then I am improving, slowly, and with additional symptoms as well though.

The story should roughly be: I got borrelia (perhaps from a couple of ticks during the spring/summer of ´75), and when they divided they released packages of high manganese into the blood. The Mn will have altered some pathways, but maybe the borrelia itself didn´t last for too long (although I got tested positive in 2016 with "compatible with late stage Lyme"). So, this impact was noticible in the late summer, and caused some subclinical changes in my life.
Then much later the catastrophy arose with EBV. One thing could be that it blocked the vitamin D receptor (also been shown for CMV), the Mn transporter ZnT10 would have become downregulated, the Mn could not get out of the cell, and whatever. Probably the synaptical structure in the basal ganglia and thalamus crashed, I think, (though general changes might have also been triggered).

So, Mn is in my case the main thing.

 

[Inara]

Wow, I wonder if your reaction to the Propofol was b/c of your calcium channel issues?

I can only speculate. An expert in known channelopathies (e.g. periodic paralysis) told me such a reaction would be typical for PP. Other substances like progesterone, cortisone or anesthesia trigger weakness/paralysis, too. Although oral cortisone did not trigger weakness/paralysis in me (so far; progesterone didn't at the beginning, too, this began 2 years later), cortisone i.v. did. In a few seconds I was paralyzed. It's pretty disgusting because I am conscious, I can open the eyes at times, but I can't move. Speaking is very difficult - but I can brabble single words.

What seems untypical, though, is that O2 helped me so far, i.e. Propofol and adminstering O2 prevented weakness and paralysis, giving O2 after the cortisone i.v. brought back my ability to move etc. - pretty fast btw.

I start to think that this might be an experiment/example that shows what @Pyrrhus meant, that all the channels "communicate" with each other, such that, for example, a ligand-gated calcium channel or another voltage-gated channel might change the voltage potential so that another voltage-gated channel gets temporarily dysfunctional.

Can you remind me, Inara, do you have problems with Magnesium causing muscle weakness, breathing weakness, respiratory depression, sedation, etc.

No, I'm taking lots of Mg every day. I do wonder, though, if there might be a connection (low Mg <-> calcium channel dysfunctions?).

 

[Gingergrrl]

Then much later the catastrophy arose with EBV. One thing could be that it blocked the vitamin D receptor

Do you mean that there is a connection between EBV and something blocking the Vit D receptors?

An expert in known channelopathies (e.g. periodic paralysis) told me such a reaction would be typical for PP.

So a reaction to Propofol (that causes muscle weakness, especially of the lungs/diaphragm or paralysis) would be typical for PP? The article that I read (and can post if helpful) was re: LEMS (Lambert Eaton Syndrome) and anesthesias that were neuromuscular blockers (which to my understanding Propofol is NOT a neuromuscular blocker but it is a calcium channel blocker).

Other substances like progesterone, cortisone or anesthesia trigger weakness/paralysis, too.

cortisone i.v. did. In a few seconds I was paralyzed.

Wow, that is very scary, Inara! I had never heard that before and I have never had a problem from oral Cortef or IV Solu-Cortef (hydrocortisone). My problems are with tapering off of Cortef (without triggering an adrenal crisis) which is why my taper will have taken about 2 yrs by the time it is over.

I start to think that this might be an experiment/example that shows what @Pyrrhus meant, that all the channels "communicate" with each other, such that, for example, a ligand-gated calcium channel or another voltage-gated channel might change the voltage potential so that another voltage-gated channel gets temporarily dysfunctional.

That makes more sense to me (that all of these calcium channels or other ion channels are interconnected and a change in one can affect the others).

No, I'm taking lots of Mg every day. I do wonder, though, if there might be a connection (low Mg <-> calcium channel dysfunctions?).

For some reason, I thought you had posted in another thread that you'd had a negative reaction to Mg. I will have to figure out which thread it was and maybe I am totally confused It also seems that there are some calcium channel dysfunctions in which calcium channel blockers are helpful vs. in mine in which they are dangerous and contraindicated.

 

[percyval577]

Do you mean that there is a connection between EBV and something blocking the Vit D receptors?

This has been shown for one time, see the first paper in this thread:
https://forums.phoenixrising.me/threads/vitamin-d-and-viruses-that-can-trigger-me-cfs.77284/

EBV has of course more properties but I wonder if a vitamin D thing could be a common issue in mecfs, though it´s of course also not very specific, so far.

For some reason, I thought you had posted in another thread that you'd had a negative reaction to Mg. I will have to figure out which thread it was and maybe I am totally confused It also seems that there are some calcium channel dysfunctions in which calcium channel blockers are helpful vs. in mine in which they are dangerous and contraindicated.

In my case its good to block them. I often wonder if PwME have the same things dysregulated but in opposite directions.

 

[Inara]

For some reason, I thought you had posted in another thread that you'd had a negative reaction to Mg.

Yes! I forgot. It's in the Mg poll thread. I once tried "Mg oil" on my lower arms with a surprising reaction - first, there was a reaction which I didn't expect because I put transdermal Mg into the quack box. Second, I developed weakness. I bought calcium tablets for a second try, having the idea that Mg and calcium are "counterplayers". After weakness developed again I took calcium orally, which helped a bit (but nothing moving). So I had to wait until the weakness went away, which actually was the next day. At that time I never had experienced such reactions and I was a bit scared. Today I know that I don't die from these "attacks" (well, not so far).

So a reaction to Propofol (that causes muscle weakness, especially of the lungs/diaphragm or paralysis) would be typical for PP?

He didn't say Propofol specifically, only that reactions to anesthetics was typical. And it seems in PP (but duncan would know better) that the breathing muscles most often remain unaffected; that was the case during my progesterone-triggered "attacks", although at the end it felt like breathing slightly changed. So who knows where it would have gone hadn't I understood where these "attacks" come from.

I have never had a problem from oral Cortef or IV Solu-Cortef (hydrocortisone)

I have side effects due to oral cortisone, but I never got an "attack". (But, again, who knows what would happen if I took it longterm.) It is scary because you don't know what happens and people around you don't get it and don't help and you can't explain. I could just brabble "oxygen" - then they said that my saturation was normal (actually it was not because it was larger than 100% which means hyperventilation; I read in a paper that this may happen due to tissue hypoxia - and in exercise), but I repeated again and again oxygen. I complained afterwards to the doctor because I had briefed them about oxygen and normal saturation and that they had to give me oxygen nonetheless.

 

[Gingergrrl]

This has been shown for one time, see the first paper in this thread:
https://forums.phoenixrising.me/threads/vitamin-d-and-viruses-that-can-trigger-me-cfs.77284/

Thx for linking me to that thread and I commented over there (but was not able to read all of the research papers that you cited).

Yes! I forgot. It's in the Mg poll thread. I once tried "Mg oil" on my lower arms with a surprising reaction - first, there was a reaction which I didn't expect because I put transdermal Mg into the quack box.

Transdermal Mg is definitely not in the quack box and can cause serious reactions.

Second, I developed weakness. I bought calcium tablets for a second try, having the idea that Mg and calcium are "counterplayers". After weakness developed again I took calcium orally, which helped a bit (but nothing moving). So I had to wait until the weakness went away, which actually was the next day. At that time I never had experienced such reactions and I was a bit scared.

You are now the fourth person from PR (plus myself) that has had significant muscle weakness from Mg. I had horrible reactions to IV Magnesium and an Epsom salt foot bath. It is interesting that you also have a calcium channelopathy (although it is different than mine). It makes me wonder if the others who had these reactions have one as well (but I do not know).

He didn't say Propofol specifically, only that reactions to anesthetics was typical.

I wish the anesthesiologist could have told you if it was Propofol or a neuromuscular blocker (or something else).

I have side effects due to oral cortisone, but I never got an "attack".

I have never had a side effect like that to hydrocortisone (which isn't a calcium channel blocker and shouldn't cause muscle weakness or respiratory depression -- that I know of)?! I wonder what it was doing in your case?

 

[Inara]

I wish the anesthesiologist could have told you if it was Propofol or a neuromuscular blocker (or something else).

I reacted to Propofol. The doctor (not an anesthiologist, but with knowledge in channelopathies) said anesthesias are typical triggers, so I guess he counted Propofol to anesthesia.
I've read elsewhere that in hypoPP there should be "Careful use of neuromuscular blocking agents and no depolarizing muscle relaxants" (https://www.ncbi.nlm.nih.gov/books/NBK1338/#!po=59.2857).

And about hyperPP (https://www.ncbi.nlm.nih.gov/books/NBK1496/#!po=40.5660):
"Opioids or depolarizing agents such as potassium, anticholinesterases, and succinylcholine can aggravate a myotonic reaction and induce masseter spasms and stiffness of respiratory muscles."

I have somehow the feeling that, when it comes to ion channels, "anything goes". And most of it is not understood.

I wonder what it was doing in your case?

I don't know the specifics. I remember that dexamethasone, e.g., is an inhibitor of the IP3 receptor type 3 (one of the endoplasmic reticulum calcium channels). In PP it is recommended to avoid glucocorticoids. Somewhere there might be a paper explaining it (or not ).

 

[Gingergrrl]

I reacted to Propofol. The doctor (not an anesthiologist, but with knowledge in channelopathies) said anesthesias are typical triggers, so I guess he counted Propofol to anesthesia.

Thx for clarifying that it was indeed Propofol and that is what I thought you had meant (but then was not sure)! I agree with the doctor that anesthesias are typical triggers but it really depends on the specific type of anesthesia. It is very interesting to me that you had that reaction to Propofol which is an L-type calcium channel blocker.

I've read elsewhere that in hypoPP there should be "Careful use of neuromuscular blocking agents and no depolarizing muscle relaxants" (https://www.ncbi.nlm.nih.gov/books/NBK1338/#!po=59.2857).

I totally agree with this and would not use those types of anesthesias.

And about hyperPP (https://www.ncbi.nlm.nih.gov/books/NBK1496/#!po=40.5660):
"Opioids or depolarizing agents such as potassium, anticholinesterases, and succinylcholine can aggravate a myotonic reaction and induce masseter spasms and stiffness of respiratory muscles."

I don't have hyperPP (vs. another kind of channelopathy) and I do well with opioids and Potassium. I am not sure about the other two things that were mentioned.

I have somehow the feeling that, when it comes to ion channels, "anything goes". And most of it is not understood.

Sadly, I agree with this

 

[Inara]

It is very interesting to me that you had that reaction to Propofol which is an L-type calcium channel blocker

It seems Propofol has some effect on IP3 receptors, too:
https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0197934

"It significantly increases peak and integrated calcium (Ca2+) responses..."

"Propofol protects rat cardiomyocytes and hippocampal neurons [6] against ischemia/reperfusion-induced autophagic cell death."

The authors looked at the effect of Propofol on autophagy. "In this study, we evaluated whether the effects of propofol on autophagy, if any, were associated with ER stress and Ca2+ homeostasis."
"Autophagy is an important regulatory mechanism, and its inhibition may either result in direct cell death or sensitize cells to stimuli-induced damage." It seems to be known that (some?) general anesthesia boosts autophagy in some organs.

"Collectively, these results indicated that propofol disrupted Ca2+ homeostasis and increased cytoplasmic Ca2+." And increased cytoplasmic Ca2+ may influence voltage-gated calcium channels.

"IP3R-mediated Ca2+ release from the ER is associated closely with increased levels of free cytoplasmic Ca2+, which activates autophagy... Taken together, the data implied that propofol disrupts Ca2+ homeostasis directly by regulating Beclin-1 and its interaction with IP3R, thereby inducing ER stress."

"Our results indicated that propofol provokes cellular autophagosome accumulation via ER stress and Ca2+ homeostasis disruption."

"In light of this, we consider it important to determine whether propofol promotes mitophagy. Additional research is needed to explore this issue, and to clarify whether propofol impacts mitophagy through IP3R, which physically links the ER and mitochondria."

"Some patients with skeletal muscle disorders, including dystrophies and myopathies, also exhibit dysregulated autophagy and are at risk for anesthesia-related complications..."

 

[Gingergrrl]

It seems Propofol has some effect on IP3 receptors, too:
https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0197934

"Some patients with skeletal muscle disorders, including dystrophies and myopathies, also exhibit dysregulated autophagy and are at risk for anesthesia-related complications..."

That is really interesting and thanks for finding/ posting it @Inara.

 

[Marylib]

I don't know that this helps at all, because it seems everyone has read the research out of Australia, detailed in this paper:

https://link.springer.com/article/10.1186/s10020-019-0083-4#Sec14

From those I speak with who are on calcium channel blockers, it seems the improvement basically involves blood flow. This could explain an improvement in POTS, for example. Also since the defect in the TRPM3 has been confirmed against healthy controls by the research group at Griffith University in Melbourne, they are having success in distinguishing M.E. (the ICC diagnoses this ) and ME/CFS (the CCC diagnoses this) from other neuroimmune or neurological illnesses.

The research lab website is here:

https://www.griffith.edu.au/menzies...unology/neuroimmunology-and-emerging-diseases

The Australian govt. has seen fit to give them some money - it is never enough - but it helps.

They use a clamp device, which may end up being a tool in terms of a creating a firm bio-marker - and when we have that, we can diagnose very early and thus people will have the best chance of recovery by going to bed and staying there, accepting their limitations instead of continually trying to push themselves. (They are enrolling patients who are severely affected by going to their homes to obtain samples. That would be a tough job because these people are so ill. )

Their findings so far link up the longstanding finding (originally by immunologist Mary Fletcher, I think) of the problems with the NK cells.

Who knows what this condition will be called once science understands more about it. My favorite name has always been "Ramsay's Disease." As far as I am aware, the hallmark of ME in terms of symptoms remains the delayed response "big crash" to activity or exercise beyond what the system can tolerate metabolically. The key word is "delayed" or PEM or PENE (post exertional neuro immune exhaustion.)

At the moment the research group in Melbourne are setting up trials of a calcium channel blocker. The way I think of it is kind of like an SSRI being used as an anti-depressant - a serotonin reuptake inhibitor. Perhaps the calcium channel blocker leaves more calcium available to the cells - in a sense prohibiting its reuptake, thus treating the genetic SNP of the TRMP3.

In other words, you could take all the calcium supplements in the world, but if the genetic defect gets in the way, the cells will not be able to communicate with each other in terms of the calcium ion channels. That is just my take on it

The finding of shortened telomeres is also interesting. So many of us feel like we are ninety years old when our chronological age may be much younger. Plenty of 90-year-old people can still take exercise without suffering post exertional crashes. They just eat well, go to sleep and get up the next day. That is a generalization, of course.

One other back-to-the-future moment is the observation about red blood cells not being "plastic" enough to flow properly through the circulatory system. Some decades ago, a researcher named Dr. Les Simpson in New Zealand identified abnormal red blood cells in ME patients. He probably followed up the work of Dr. Peter Snow with a set of patients who were identified as having the Tapanui Flu in Otago, NZ back in 1984 or so. The book by Dr. Simpson and Nancy Blake was written in 1988. Dr. Simpson passed away a few years ago. The title of his book says it all, in terms of names for the illness.

https://www.amazon.com/Ramsays-Dise...ate-Creation/dp/0957181728/#reader_B00875TLB4

The hopeful thing is that there are epigenetic changes happening all the time which have the possibility to alter the expression of the faulty genes we may have been born with.

In the meantime, we will have Jarred Younger reporting on his findings regarding glial cell activation and possible means of treating this beyond low-dose naltrexone. LDN is hit and miss for me, so I don't bother anymore. Apparently it's greatest success may be in treating pain in fibromyalgia, which is considered at this point to be co-morbid with ME. And it does help some people with sleep, apparently, in the style of an immune-modulator.

My diagnosis is M.E. by the international criteria or ICC, with prominent cognitive dysfunction. I might have been diagnosed with FM some years ago, (poor sleep and body myalgia or pain) but that all changed with a really bad case of the flu in 2004. That kind of pain disappeared, I suppose from a shift in my immune system which may have then gone into overdrive. Before that flu, I felt not too bad if I could drug myself enough for a decent night's sleep. I could catch colds very easily in those days.

Catching the common cold can be a good sign in ME. It would mean that the immune system is reverting back to more normal basis. Usually I get the "ME sore throat," which goes away without enabling me to run a fever. I am proud to say that I did catch a cold some weeks ago and even ran a fever for a couple of nights. I was pretty happy about that!

 

[pattismith]

Interesting! It caused weakness and paralysis in me.

Did you check for Myotonia Dystrophy? It is a multisystem/organ genetic disease that cause muscle ion channels dysfunction, fatigue, exercice intolerance, sensitivity to opioids and many drugs.

 

[Gingergrrl]

From those I speak with who are on calcium channel blockers, it seems the improvement basically involves blood flow. This could explain an improvement in POTS, for example. Also since the defect in the TRPM3 has been confirmed against healthy controls by the research group at Griffith University in Melbourne, they are having success in distinguishing M.E. (the ICC diagnoses this ) and ME/CFS (the CCC diagnoses this) from other neuroimmune or neurological illnesses.

Thank you for your detailed post @Marylib on this topic. Do you know why the ICC lists ion channelopathies in their criteria but none of the other criteria do? That is what I was so curious about when I started this thread. I have an autoimmune calcium channelopathy (confirmed by multiple tests) but in my case, I am NOT to take anything that blocks the calcium channel and mine seems to be in the opposite direction of what you are describing above (although I do have POTS and prior to treatment, the POTS was completely disabling for me).

In other words, you could take all the calcium supplements in the world, but if the genetic defect gets in the way, the cells will not be able to communicate with each other in terms of the calcium ion channels. That is just my take on it

The Neuros who originally diagnosed me (but are not my treating doctors) said that I could also take as much calcium as I wanted but it would not get into the cells b/c it was in the regular oral form of calcium and not the ion form that was being blocked by the autoantibody. I am certain that I did not explain that well in case it did not make sense! I actually do not supplement calcium (and just get it from food) but it would be fine in my case if I supplemented since it would be the opposite of a calcium channel blocker (which I am to avoid).

 

[Marylib]

@Gingergrrl
In regards to the inclusion of the ion channelopathies being listed in the ICC, I can only assume that there was further input about research and clinical reports in the latter document that was not included in the earlier CCC.
I wish I could understand much of what you have written regarding your own particular treatment of the autoimmune condition. Maybe all of us with POTS have the autoimmunity. I will have to go back and read what your treatment is. I want to understand the reasoning for not using a calcium channel blocker. This will take some time for me, as I tire quickly when using my brain to sort this stuff out.