Question re: the ICC Criteria and Ion Transport issues

[Hip]

why are you so against the ICC? wouldn't you meet the ICC?

I think all of these criteria have their purpose. The CCC are certainly the most rigorous, and the ICC are more or less the same as the CCC. But Fukuda has it's place also, because there are patients who satisfy the Fukuda, but do not satisfy the CCC. Without the Fukuda, those patients would lose their diagnosis.

 

[Gingergrrl]

Thank you all for the new posts re: my question about ion transport being listed in the ICC criteria and I apologize for my slow reply! I wanted to add that I am very interested in ion channelopathies but I have absolutely no political agenda re: these different ME/CFS criteria and it was not the purpose of my question (just to clarify).

The ICC is the evolution of the CCC, and the ICC Primer is the largest and most detailed document on ME. Therefore, it is still incomprehensible to me why it is not used.

Thank you for explaining and I did not know the sequence of the different criteria or that the ICC was the largest or the most recent of the bunch. Upon learning that, it is interesting to me as well why it is not the criteria that is used. I think (but am not certain without checking) that the CCC criteria was used to select patients for the Rituximab studies and am now wondering why the ICC criteria was not used?

but you can see for decades, as the health authorities to dilute the ME diagnosis. first with the euphemism "CFS" and most recently with SEID. Strangely enough, this doesn't bother anyone on phoenixrising. Why?

I can only speak for myself but I do not know the history of the different criteria. I was given an ME/CFS diagnosis in 2013 and 2014 by about six different doctors and whole-heartedly believed it to be my diagnosis which is how I found PR.

As of 2016, my ME/CFS specialist did not feel that it was my diagnosis after all and I agree w/this. However, he said that I was one of the sickest patients that he had (at that time prior to my treatments) and it turned out from several blood panels done by Mayo's Lab that I have an (autoimmune) ion calcium channelopathy (among several other problems). It was not until last week that someone told me that the ICC lists "ion transport issues" which shocked me and made me want to learn the origin of how this symptom came to be included in the ICC.

It reads as if it isn't necessary to show evidence of an ion transport impairment; just at least one symptom of such (and the symptoms, of course, are common to a number of conditions and can have multiple causes.) I don't know whether it's deliberately vaguely worded or not, though.

First @Moof, I love your new avatar ... Now back on topic, I understand what you mean re: that it isn't necessary to show evidence of an ion transport impairment (like I have with the Mayo Panels) but if that is the case, why are those words included at all? Why not just list the symptoms (cardiac, respiratory, temperature regulation, etc)? I am so confused by how those words came to be included by a panel of so many ME/CFS experts?

Similarly regarding the topic of this thread: the ICC section entitled Energy Metabolism/Ion Transportation Impairments: I don't think there is any solid evidence to indicate that the symptoms and conditions listed in this section are caused by either energy metabolism or ion transport dysfunction.

But if they are not caused by either energy metabolism and/or ion transport dysfunction, why is that the title of the section?

Incidentally, in the original ICC paper, that section is labelled not Energy Metabolism/Ion Transportation Impairments, but Energy Metabolism/Transportation Impairments.

So if you remove the word "ion" and just call it "transportation impairments", what kind of transportation do they mean if not "ion"? (I am asking for real because I don't understand their intention).

Also, I met (almost) every single criteria in that section prior to my successful treatments (orthostatic intolerance, hypotension, POTS, palpitations, dizziness, air hunger, labored breathing, fatigue of chest wall muscles, subnormal body temperature, cold extremities, and intolerance of extremes of temperature).

There were only three symptoms in that section that I did not meet: light-headedness, sweating episodes (and I had the opposite which was a lack of ability to sweat), and feverishness.

I am mentioning this b/c whatever illness I had was a near perfect match for the section of the ICC titled "ion transport issues" and I have a proven ion transport issue. (I also have MCAS, POTS, Hashimoto's Disease, severe chronic neck pain, and other stuff that is probably not related).

Generally speaking, many ME/CFS symptoms can be exhibited by patients of channelopathies. In fact, it can be devilishly hard sometimes to distinguish the two.

That is really interesting and I belonged to a private medical group on FB in which everyone has a (proven) calcium channelopathy and almost 100% of the people in the group also have POTS. I cannot explain why this is the case. Many had been given an ME/CFS diagnosis at some point in their medical history as well.

Sure matches what I have seen and learned. POTS, for instance, is surprisingly (?) common in PP.

@duncan, so most people with PP (periodic paralysis), which please correct me if I am wrong, is a Potassium ion channelopathy also have POTS?

I'm out of the discussion. no energy to constantly discuss such nonsense. I sometimes get the feeling that some people in this forum are taking preventive action so as not to push ME research forward. ICC are the evolution of the CCC and the CCC are from 2003. 16 years old. many studies are not included there. we would have been far more advanced in research if every researcher were to take on the ICC. instead, researchers use fukuda or SEID to recruit people with depression. so we will never find a treatment if not even the patients manage to pull together!

I don't think that you should leave the discussion but I did want to reassure you that my purpose for starting this thread and posing the question re: the history of "ion transport" issues in the ICC was NOT for political reasons re: which criteria was superior or what things should be named, etc.

I think we are on the same page that I would also LOVE for ME/CFS to be solved because it does not help for anyone to be misdiagnosed (in either direction) meaning someone with ME/CFS is told they have something else or someone who truly has something else is told that they have ME/CFS. No one gets the right treatment when that happens and it also confounds the results of research studies.

I am confused myself why the most recent criteria (ICC) would not be used for the research studies? Also do you know (Peter Pain) why they included "ion transport" issues in the ICC but not in the other criteria? Was it b/c of the research on calcium channelopathies being done by the ME/CFS team in Australia?

 

[Sushi]

I understand what you mean re: that it isn't necessary to show evidence of an ion transport impairment (like I have with the Mayo Panels) but if that is the case, why are those words included at all?

An ME/CFS specialist told me that I had a problem with the calcium channel ion transport but I don’t know how that was determined (it was a long time ago). I was told not to supplement calcium—though I have taken calcium channel blockers with no problems. Wish I understood this better.

 

[duncan]

That is really interesting and I belonged to a private medical group on FB in which everyone has a (proven) calcium channelopathy and almost 100% of the people in the group also have POTS. I cannot explain why this is the case. Many had been given an ME/CFS diagnosis at some point in their medical history as well.

Through my wife, I belong to a private channleopathy "club" of sorts. It's not a forum, but rather a private email service that only vetted members can belong, or their spouses or caregivers. You literally have to provide documentation that you have a channelopathy, so stringent are their bylaws. This can be a calcium channelopathy, a potassium channelopthy...I can't remember if there is a sodium one at the moment, But it's pretty much all patients, and they talk like we do, and they talk doctors, about which are really worthwhile (which are not). More to the point, they talk about commonalities, including symptoms, that may or may not have been captured in any nascent research. POTS is one such. Another that leaps to mind is a general intolerance to statins - which leading neurologists versed in channelopathies would claim there is no evidence for. But the patients know, and in fact it is true for my wife. Many of these patients have been diagnosed with ME/CFS, many with a FND...you know the deal.

so most people with PP (periodic paralysis), which please correct me if I am wrong, is a Potassium ion channelopathy also have POTS?

PP is shorthand for periodic paralysis., and stands for any channelopathy, including calcium channelopatjies. You don't have to have bouts of paralysis. It's just called that due to the import to muscle weakness (sometimes profound enough to induce paralysis) among many other symptoms and manifestations - just like some with CFS don't have fatigue as the prominent symptom. But, yes, many potassium channeloptahies, and by extension many PP sufferers including calcium PP sufferers, have POTS. My wife has severe cardiac issues, but she has never been checked for POTS, while I have a good heart and have lab-confirmed POTS. So go figure.

An ME/CFS specialist told me that I had a problem with the calcium channel ion transport but I don’t know how that was determined (it was a long time ago). I was told not to supplement calcium—though I have taken calcium channel blockers with no problems. Wish I understood this better.

Curious. A significant portion of people with channelopathies test normal for calcium or potassium or whatever their ion transport issue is with. My wife, for instance, is normakalemic even though she has a severe genetic form of potassium channelopathy. You'd think they'd tinker with her diet, but I think they are afraid to provoke an episode for fear of the cardiac ramifications. But her heart meds by default are hyperkalemic, so they roll the dice with her PP daily with those meds.

Medicine takes liberties at times that are scary.

 

[Inara]

@duncan, would you be willing to specify the symptoms you come across in channelopathies? I didn't know, for instance, that POTS seems to be typical (?); I gave POTS.

I have a mutation in a calcium channel, although it remains to be proven it's dysfunctional. I fulfill CCC, but I always felt a bit closer to the ICC (that's just personal, not political or so). I actually find @Gingergrrl's question pretty good. I always wondered why ion channel issues are mentioned in the context of ME and what the basis of this is. I want to look into one of the references, "Ion Channels and Disease", which seems to be online available. When the calcium channel mutation was found, I was quite flabbergasted to be honest. Is ME (or a subset of it) a channelopathy, or are people with (yet unknown) channelopathies misdiagnosed with ME?

IF ion channels play a role in ME, which role and how? I.e. what causes these problems, and what is happening? Is it external, inherited, both? I know that viruses address ion channels (especially calcium channels, too) to get their DNA/RNA into a cell. So there might be a connection to an infectious onset.

Ion channel mutations, though are - as far as I know - rarer than ME. And I think ion channel autoimmunity is pretty rare, too?

PP is shorthand for periodic paralysis., and stands for any channelopathy, including calcium channelopatjies.

I never heard this before - it's quite interesting. Do you maybe have more info at hand?

 

[Gingergrrl]

An ME/CFS specialist told me that I had a problem with the calcium channel ion transport but I don’t know how that was determined (it was a long time ago).

@Sushi, Do you happen to remember if that specialist was using the ICC criteria, which lists ion transport issues in it, and therefore assumed that you had a calcium channel ion transport issue by default (since you have ME/CFS and this was part of the criteria) or did he run a blood test on you which showed that you had this issue?

I was told not to supplement calcium—though I have taken calcium channel blockers with no problems. Wish I understood this better.

The Neuro who first found that I have the autoantibody to the N-type Calcium Channel (which has now been confirmed on three separate tests between 2016 and 2019), actually told me the opposite: that it was absolutely fine for me to supplement dietary calcium BUT that I should NOT take any meds that were calcium channel blockers.

This makes me wonder if the ICC criteria are referring to the opposite issue that I was diagnosed with, or if they are referring to both types of issues, or if they are referring to something else all together?!

Through my wife, I belong to a private channleopathy "club" of sorts. It's not a forum, but rather a private email service that only vetted members can belong, or their spouses or caregivers. You literally have to provide documentation that you have a channelopathy, so stringent are their bylaws.

That is interesting and the private group that I am in on FB does not require any documentation or proof but every new member ends up explaining their story and which tests (usually Mayo panels) found that they have the N-type calcium channel autoantibody. Some have the corresponding diagnoses of LEMS or small cell lung cancer (in which case, it is often a paraneoplastic syndrome) but MANY do not have cancer or LEMS and have been given a long series of incorrect diagnoses or have been told that their symptoms are psychosomatic, etc.

This can be a calcium channelopathy, a potassium channelopthy...I can't remember if there is a sodium one at the moment

I assume that there is a sodium channelopathy but do not know this for sure. I had no idea that "PP" referred to anything but "periodic paralysis from a potassium channelopathy". No one in the group that I belong to has ever used this term. Some have other autoantibodies (like the P/Q calcium channel autoantibody) or completely random ones (like I have anti GAD65) but I don't know of anyone in the group who potassium channel autoantibodies.

More to the point, they talk about commonalities, including symptoms, that may or may not have been captured in any nascent research. POTS is one such.

That is so interesting that they also have POTS. Do they know what the connection is? (I do not understand it myself). I was diagnosed with POTS in early 2013 and did not discover that I had the calcium channel autoantibody until early 2016. I may have had it before but never tested for it so I will never know.

Another that leaps to mind is a general intolerance to statins - which leading neurologists versed in channelopathies would claim there is no evidence for.

I will NEVER take a statin for as long as I live but this is really good info to have (that they are extra dangerous for people with channelopathies) and really appreciate the info @duncan.

But the patients know, and in fact it is true for my wife. Many of these patients have been diagnosed with ME/CFS, many with a FND...you know the deal.

Yep... I know the deal.

PP is shorthand for periodic paralysis., and stands for any channelopathy, including calcium channelopatjies. You don't have to have bouts of paralysis.

I did not realize that. I have never had paralysis at any point in my illness but there was a point (prior to my treatments) that my breathing was so weak that it felt as if my lungs and diaphragm were partially paralyzed (but I don't think that they actually were).

It's just called that due to the import to muscle weakness (sometimes profound enough to induce paralysis)

Thanks for explaining and muscle weakness was a big problem for me prior to my treatments. I am assuming though that the treatments in your wife's case would be totally different since her illness is genetic vs. autoimmune?

But, yes, many potassium channeloptahies, and by extension many PP sufferers including calcium PP sufferers, have POTS. My wife has severe cardiac issues, but she has never been checked for POTS

Is there a reason that she has never been checked for POTS? Do her doctors feel that doing a TTT would be too dangerous?

A significant portion of people with channelopathies test normal for calcium or potassium or whatever their ion transport issue is with

In my case, I was told by Neuros that tests for actual calcium would be normal and it was the ion transport of calcium that was messed up and not the amount of regular calcium in the blood. (I know that "regular" is not the proper word but am not sure what is the opposite of "ion")?!

You'd think they'd tinker with her diet, but I think they are afraid to provoke an episode for fear of the cardiac ramifications. But her heart meds by default are hyperkalemic, so they roll the dice with her PP daily with those meds. Medicine takes liberties at times that are scary.

I was also told by Neuros that dietary issues did not play a role in my case BUT that meds or anesthesias that were calcium channel blockers could play a big role and to avoid them. (I had extreme dietary issues/ allergic reactions from MCAS in 2015 & 2016 but this, to the best of my knowledge, was a separate issue).

@duncan, would you be willing to specify the symptoms you come across in channelopathies? I didn't know, for instance, that POTS seems to be typical (?); I gave POTS.

I would be very curious as well

I have a mutation in a calcium channel, although it remains to be proven it's dysfunctional.

We are assuming that mine is dysfunctional b/c the autoantibody blocks the calcium channel, and I achieved such improvement from autoimmune treatments, but I still do not fully understand all of the specifics.

I fulfill CCC, but I always felt a bit closer to the ICC (that's just personal, not political or so).

I need to compare the two sets of criteria (CCC and ICC) b/c I am still unclear what the differences are (besides the ICC having a section titled "ion transport issues").

I actually find @Gingergrrl's question pretty good.

Yay! That made me happy @Inara since you are a true scientist and I am.... not

I always wondered why ion channel issues are mentioned in the context of ME and what the basis of this is. I want to look into one of the references, "Ion Channels and Disease", which seems to be online available.

I never wondered b/c until last week I did not even know that there was any connection between the two (except for the current research by the Australian ME/CFS team). I did not know that they were already listed in the ICC criteria. I am still curious if the Australian research came first (leading to the new criteria) or vice versa?

If you look into the references, please let me know what you find out!

When the calcium channel mutation was found, I was quite flabbergasted to be honest. Is ME (or a subset of it) a channelopathy, or are people with (yet unknown) channelopathies misdiagnosed with ME?

I am now wondering this as well.

IF ion channels play a role in ME, which role and how? I.e. what causes these problems, and what is happening? Is it external, inherited, both? I know that viruses address ion channels (especially calcium channels, too) to get their DNA/RNA into a cell. So there might be a connection to an infectious onset.

I was told by my doctors that in my case the chronic reactivation of the EBV virus (I was IgM+ for EBV for about 3-4 years post Mono) ultimately flipped into autoimmunity. My illness definitely had an infectious onset with severe Mono from EBV and then a second virus ten months later which immediately resulted in POTS.

Ion channel mutations, though are - as far as I know - rarer than ME. And I think ion channel autoimmunity is pretty rare, too?

I assume that they are pretty rare but I think that so few people are tested that it is hard to really know.

 

[Sushi]

@Sushi, Do you happen to remember if that specialist was using the ICC criteria, which lists ion transport issues in it, and therefore assumed that you had a calcium channel ion transport issue by default (since you have ME/CFS and this was part of the criteria) or did he run a blood test on you which showed that you had this issue?

This specialist uses the ICC but he also did a zillion blood tests so I don’t know what he based his assessment that I had calcium ion channel problems on.

This makes me wonder if the ICC criteria are referring to the opposite issue that I was diagnosed with, or if they are referring to both types of issues, or if they are referring to something else all together?!

This is something we would need to ask the authors about! In any case, for me, there are several reasons to avoid calcium supplementation—so I will do that—and also occasions where I need to take calcium channel blockers. I actually was given one IV in the ER on two occasions and it did the needed job. So the mystery continues.

 

[Hip]

But if they are not caused by either energy metabolism and/or ion transport dysfunction, why is that the title of the section?

I am not saying they are not caused by energy metabolism issues; just saying that there's not really any solid evidence for this. So it's premature to suggest these ME/CFS symptoms are due to energy metabolism dysfunction.

So if you remove the word "ion" and just call it "transportation impairments", what kind of transportation do they mean if not "ion"? (I am asking for real because I don't understand their intention).

Transportation of energy, ie, movement of the ATP molecule out of the mitochondria and into the rest of the cell.

 

[duncan]

would you be willing to specify the symptoms you come across in channelopathies? I didn't know, for instance, that POTS seems to be typical (?); I gave POTS.

I'm not sure any formal study qualifying channelopathies as an umbrella diagnostic symptomatically has been done. But I might be focused on the trees vs the forest because of my wife's rare potassium channelopathy.

Ok, so the one uncontested common feature would be episodes of profound muscle weakness. This can be more or less constant, and it can fluctuate in intensity and duration. In some, it can result in pararlysis. Muscle weakness is to channelopathies or periodic paralysis what "fatigue"(sorry!!) is to ME/CFS.

Because coherent studies investigating channelopathies as a group and individually are a relatively new phenomenon, I don't think you'll see much literature tying everything together. But this is my take on fairly "common symptoms" after about five years on the periodic paralysis forum - which does indeed include sodium and calcium and potassium channleopathy sufferers.

Cardiac arrythmias and the like.
Sleep problems
Cognitive problems
Pain, sometimes migrating
Fatigue
Digestive problems
Balance problems
Peripheral neuropathies
POTS
Symptom cluster worsening after exertion.
Food and chemical sensitivities

That's just my very informal layman's take. I've participated in the email exchange, but not alot because it's not me, but I read every single post and have for five or so years. The ignorance among neurologists and cardiologists and every other ist is appalling and dangerous and intolerable.

I have a mutation in a calcium channel, although it remains to be proven it's dysfunctional. I fulfill CCC, but I always felt a bit closer to the ICC (that's just personal, not political or so). I actually find @Gingergrrl's question pretty good. I always wondered why ion channel issues are mentioned in the context of ME and what the basis of this is. I want to look into one of the references, "Ion Channels and Disease", which seems to be online available. When the calcium channel mutation was found, I was quite flabbergasted to be honest. Is ME (or a subset of it) a channelopathy, or are people with (yet unknown) channelopathies misdiagnosed with ME?

I strongly suspect many people diagnosed with ME/CFS have a channelopathy, just as I suspect many diagnosed with ME/CFS have Lyme, at least in the US. But if you define ME/CFS as a symptom cluster, then that is understandable. Still, it's problematic vis-a-vis treatment protocols, at least eventually.

 

[duncan]

Sorry, I have to break up these replies.

IF ion channels play a role in ME, which role and how? I.e. what causes these problems, and what is happening? Is it external, inherited, both? I know that viruses address ion channels (especially calcium channels, too) to get their DNA/RNA into a cell. So there might be a connection to an infectious onset.

Ion channel mutations, though are - as far as I know - rarer than ME. And I think ion channel autoimmunity is pretty rare, too?

Depends on what channelopathy we are talking about, but as of right now, yes, channelopathies are pretty rare. I have a feeling, though, they are not as rare as we think. As we parse down, a lot more will be found to have a form of PP, and I would not be too surprised to see the ranks of ME/CFS diminished somewhat accordingly.

I never heard this before - it's quite interesting. Do you maybe have more info at hand?

Here's a link to the periodic paralysis association:
https://www.periodicparalysis.org/site/

 

[duncan]

I assume that there is a sodium channelopathy but do not know this for sure. I had no idea that "PP" referred to anything but "periodic paralysis from a potassium channelopathy". No one in the group that I belong to has ever used this term. Some have other autoantibodies (like the P/Q calcium channel autoantibody) or completely random ones (like I have anti GAD65) but I don't know of anyone in the group who potassium channel autoantibodies.

Yes, there are sodium channelopathies. Interesting, some channelopathies like my wife's are genetic. Her mutation is the KCNJ2 gene mutation. It results in ATS. But, there is something in PP circles referred to as ATS2 which appears to be an acquired form of ATS without the KCNJ2 mutation. Fascinating stuff.

That is so interesting that they also have POTS. Do they know what the connection is? (I do not understand it myself). I was diagnosed with POTS in early 2013 and did not discover that I had the calcium channel autoantibody until early 2016. I may have had it before but never tested for it so I will never know.

I will NEVER take a statin for as long as I live but this is really good info to have (that they are extra dangerous for people with channelopathies) and really appreciate the info @duncan.

I do not think they know what the connection is with POTS, but I could be wrong, and I'm sure a couple prominent neurologist like Lewis or Tawil could speculate on it. As for statins - this is patient-research at its finest. It simply came out over the years in conversations amongst PP patients that statins caused profound problems in many of them. Neurologists cannot explain it and many in fact disagree with patient reports - which strikes me as brazenly arrogant on the neurologists part.

 

[duncan]

I did not realize that. I have never had paralysis at any point in my illness but there was a point (prior to my treatments) that my breathing was so weak that it felt as if my lungs and diaphragm were partially paralyzed (but I don't think that they actually were).

Thanks for explaining and muscle weakness was a big problem for me prior to my treatments. I am assuming though that the treatments in your wife's case would be totally different since her illness is genetic vs. autoimmune?

Is there a reason that she has never been checked for POTS? Do her doctors feel that doing a TTT would be too dangerous?

My wife has never been paralyzed either. But she gets pretty weak. She has no treatment for her ATS. None. Her treatments are all for her downstream heart problems. As for POTS, I think she is almost indifferent because of the severity of her other heart issues which include heart failure and Long QT. She hates doctors and she steers clear of research because it distresses her. I am the family default research mechanism.

In my case, I was told by Neuros that tests for actual calcium would be normal and it was the ion transport of calcium that was messed up and not the amount of regular calcium in the blood. (I know that "regular" is not the proper word but am not sure what is the opposite of "ion")?!

I was also told by Neuros that dietary issues did not play a role in my case BUT that meds or anesthesias that were calcium channel blockers could play a big role and to avoid them. (I had extreme dietary issues/ allergic reactions from MCAS in 2015 & 2016 but this, to the best of my knowledge, was a separate issue).

That's interesting. Some people have to watch their diet. I do not know why it should matter if the cause were genetic vs autoimmune...But, hey, my wife doesn't watch her diet except as it pertains to her heart, despite my misgivings. Part of that is because we don't know if she's hypo vs hyper.

I think when the testing is perfected and the prices come down, we are going to see the ranks of channelopathy victims swell.

 

[Inara]

like I have anti GAD65

Aren't GAD65 antibodies elevated in Diabetes Type 1? Mine were elevated last time, and I'll get checked for Type 1. But an endocrinologist already told me (with a small grin) that I don't have Diabetes. Is GAD65 also connected to calcium channels?

I was told by my doctors that in my case the chronic reactivation of the EBV virus (I was IgM+ for EBV for about 3-4 years post Mono) ultimately flipped into autoimmunity.

I don't know what's the validity of these tests, but in my case EBV "titers" (I don't know what it's called in this case - it was a different test than IgM) were pretty high, and it cannot be proven (because no German doctor checks whether you have a virus - and which one - or a bacterium, unless you're dying), but it is quite possible the infection that triggered my disease was caused by EBV.

@duncan, thanks for all the info you posted. Very interesting, and I learned a lot! Really fascinating.

Muscle weakness is to channelopathies or periodic paralysis what "fatigue"(sorry!!) is to ME/CFS.

Would you find any noticeable lab parameters mirroring the muscle weakness? Is the muscle weakness always profound, or are there people that can lead a nearly normal life wrt. muscle weakness (like they can take some steps, do some walks, i.e easy stuff)?
And if you say that muscle weakness it to channelopathies what fatigue is to ME/CFS, do you mean that muscle weakness is not the center of channelopathies, but is made the center by doctors?

Cardiac arrythmias and the like.
Sleep problems
Cognitive problems
Pain, sometimes migrating
Fatigue
Digestive problems
Balance problems
Peripheral neuropathies
POTS
Symptom cluster worsening after exertion.
Food and chemical sensitivities

I have all the symptoms you listed (and more...).

Do you know of a channelopathy forum or is there a way to get into that email group you mentioned? If I wanted to dive deeper into that topic, how could I do it?

 

[duncan]

the info you posted. Very interesting, and I learned a lot! Really fascinating.

Would you find any noticeable lab parameters mirroring the muscle weakness? Is the muscle weakness always profound, or are there people that can lead a nearly normal life wrt. muscle weakness (like they can take some steps, do some walks, i.e easy stuff)?
And if you say that muscle weakness it to channelopathies what fatigue is to ME/CFS, do you mean that muscle weakness is not the center of channelopathies, but is made the center by doctors?

I have all the symptoms you listed (and more...).

Do you know of a channelopathy forum or is there a way to get into that email group you mentioned? If I wanted to dive deeper into that topic, how could I do it?

You're quite welcome.

I cannot think of any labs that look at muscle weakness per se. That doesn't mean they aren't out there. I just cannot remember off the top of my head. I'm sorry. I don't recall them testing my wife muscle-wise, but her diagnosis was backed into due to Long QT - they just did a genetic test that was remotely relevant to Long QT and Bam!, they got the KCNJ2 hit. Of course, technically it was a weak muscle, the heart, that led to the discovery of a channelopathy in her as the root cause of most if not all her symptoms.

The overall muscle weakness can be intermittent. It often is. Depends. My wife's is intermittent - although that may not be fair to her. I notice it as intermittent, but as I have learned to manage my symptom cluster better, so too has she, so I know somethings are transparent to me.. I'm sure she might say it's always there , just in varying degrees. As for what I meant by it's like "fatigue" is to ME/CFS: I guess I was trying to say it is central to the diagnosis, but it varies in degree based on the person, and maybe the type of channelopathy, but I don't know that re: Type.

Check out Periodic Paralysis International to get to their application to their email service which is listserve. I THINK they will be trying to go to a true forum format, but eh, I don't think they're quite ready yet. Go and get on the email. They will introduce you once you're approved and it's global and ALL types of channelopathies - still, not a huge population....

One of the things I find cool is the number of channelopathies that are "acquired" vs genetic. Autoimmune channelopathies are wide open for interpretation - the new wild west.

 

[Gingergrrl]

I'm breaking my reply into two parts

I am not saying they are not caused by energy metabolism issues; just saying that there's not really any solid evidence for this. So it's premature to suggest these ME/CFS symptoms are due to energy metabolism dysfunction.

That is interesting and I guess I had always assumed that there were proven energy metabolism issues in ME/CFS (vs. the possible ion transport issues being included in the ICC criteria which was new info to me).

Transportation of energy, ie, movement of the ATP molecule out of the mitochondria and into the rest of the cell.

Thank you and that makes sense. In your opinion @Hip, do you think that the creators of the ICC Criteria had proven info re: "ion transport issues" and this is why they used those words in the title of that Section, or that they were just "guessing" that it "might" be due to ion transport issues, or do you think it was simply an error and they did not mean to title that section "ion transport issues"?

I'm not sure any formal study qualifying channelopathies as an umbrella diagnostic symptomatically has been done.

That is my guess as well. At this point, I am given a LEMS (Lambert Eaton Syndrome) diagnosis b/c it is a closer match than ME/CFS but it is not a match in many key criteria. I am not positive for the P/Q type calcium channel autoantibody (the most common in LEMS) and am only positive for the N type. Also most cases of LEMS begin with profound leg weakness which I never had (and the upper body and lung/diaphragm weakness that I had pre-treatment is MUCH more rare in LEMS).

Also, the criteria states that people w/LEMS gain muscle strength with muscle exertion but I was the complete opposite and the more I tried to use my muscles (pre-treatment), the weaker and more fatigued they got. I asked about this in LEMS groups and most people were the same and their muscles got weaker with use (not stronger) so I question where that piece of the criteria even came from ?! It was only after successful treatment with IVIG & Rituximab that I was able to increase my muscle strength with PT & Pilates. Prior to treatment this literally was not possible and I could not turn on a shower faucet, open a bottle, or open my patio door by myself.

Ok, so the one uncontested common feature would be episodes of profound muscle weakness.

I agree with this but it seems to vary greatly whether the profound weakness is the legs, upper body, lungs/ breathing, etc.

I strongly suspect many people diagnosed with ME/CFS have a channelopathy, just as I suspect many diagnosed with ME/CFS have Lyme, at least in the US. But if you define ME/CFS as a symptom cluster, then that is understandable. Still, it's problematic vis-a-vis treatment protocols, at least eventually.

I agree with all of this.

Here's a link to the periodic paralysis association:
https://www.periodicparalysis.org/site/

Thank you and I am definitely going to look at this.

I do not think they know what the connection is with POTS, but I could be wrong

I also suspect that they do not know the connection with POTS. My doctor feels that I have "Autoimmune POTS" (viral trigger that shifted into autoimmunity) and I also test positive for the POTS autoantibodies on Cell Trend Panels. So I am not certain that POTS is related to the channelopathy in my case (although all of it is autoimmune based so it seems very likely to me that they are connected).

As for statins - this is patient-research at its finest. It simply came out over the years in conversations amongst PP patients that statins caused profound problems in many of them. Neurologists cannot explain it and many in fact disagree with patient reports - which strikes me as brazenly arrogant on the neurologists part.

This makes sense since statins can trigger profound muscle injuries even in totally healthy people (let alone people with channelopathies). It is a disgrace that Neuros do not recognize the connection but many also do not acknowledge the connection between tendon/muscle injuries with Fluoroquinolone antibiotics (which happened to me before I was sick). I have never taken a statin and never will.

 

[Sushi]

Thank you and that makes sense. In your opinion @Hip, do you think that the creators of the ICC Criteria had proven info re: "ion transport issues" and this is why they used those words in the title of that Section, or that they were just "guessing" that it "might" be due to ion transport issues, or do you think it was simply an error and they did not mean to title that section "ion transport issues"?

Having known the lead author, I’m sure they had evidence but I don’t know what it is. If you look at the authors, they would not be likely to write this unless they had research to back it up:

Bruce Carruthers, Marjorie van de Sande, Kenny de Meirleir, Nancy Klimas, Gordon Broderick, Terry Mitchell, Donald Staines, A C Peter Powles, Nigel Speight, Rosamund Vallings, Lucinda Bateman, Barbara Baumgarten-Austrheim, David Bell, Nicoletta Carlo-Stella, John Chia, Austin Darragh, Daehyun Jo, Donald Lewis, Alan Light, Sonya Marshall-Gradisnik, Ismael Mena, Judy Mikovits, Kunihisa Miwa, Modra Murovska, Martin Pall, and Staci Stevens

 

[Gingergrrl]

Part 2:

As for POTS, I think she is almost indifferent because of the severity of her other heart issues which include heart failure and Long QT. She hates doctors and she steers clear of research because it distresses her. I am the family default research mechanism.

I can't blame her for not wanting to see more doctors and I am glad that you are on top of the research! I wonder if any of her meds for heart failure or Long QT would also be helping with POTS symptoms?

Some people have to watch their diet. I do not know why it should matter if the cause were genetic vs autoimmune...But, hey, my wife doesn't watch her diet except as it pertains to her heart, despite my misgivings. Part of that is because we don't know if she's hypo vs hyper.

In my case, the calcium channel autoantibodies are not related to diet, but I am not supposed to have meds or anesthesia that block the calcium channel.

I think when the testing is perfected and the prices come down, we are going to see the ranks of channelopathy victims swell.

Do you mean for the Mayo autoantibody panels or genetic testing?

Aren't GAD65 antibodies elevated in Diabetes Type 1? Mine were elevated last time, and I'll get checked for Type 1. But an endocrinologist already told me (with a small grin) that I don't have Diabetes. Is GAD65 also connected to calcium channels?

Anti GAD65 autoantibodies are linked w/several different issues including Diabetes, Stiff Person Syndrome (SPS), and general autoimmunity (even to Hashimoto's Disease which I have). My Endo tested me on every diabetes test known to man, including some obscure ones, and I am completely negative on every single one.

We briefly wondered if I had some kind of atypical version of Stiff Person Syndrome (b/c I had an extremely exaggerated startle response and one possible "startle seizure" prior to my treatments, all of which caused tightness, shaking, and some dystonia to my muscles). But all of this 100% disappeared when I started IVIG in 2016 and has never returned.

No doctor thinks that I had SPS vs. that the GAD65 autoantibodies were another sign of my general "autoimmune chaos" prior to treatment. I don't know of a connection between GAD65 and calcium channels but that doesn't mean that there isn't one. GAD65 autoantibodies interfere with the process that converts glutamate to GABA.

I don't know what's the validity of these tests, but in my case EBV "titers" (I don't know what it's called in this case - it was a different test than IgM) were pretty high, and it cannot be proven (because no German doctor checks whether you have a virus - and which one - or a bacterium, unless you're dying), but it is quite possible the infection that triggered my disease was caused by EBV.

In my case, I had not been exposed to EBV until I got a severe case of Mono at age 41 following surgery (b/c I had been tested for EBV several times and was always IgM and IgG negative until Mono when I became IgM+ for EBV). So in my case, we were able to match the labs with when I had severe Mono with all of the classic symptoms. How I evaded EBV for 41 yrs prior to that is a mystery.

Would you find any noticeable lab parameters mirroring the muscle weakness? Is the muscle weakness always profound, or are there people that can lead a nearly normal life wrt. muscle weakness (like they can take some steps, do some walks, i.e easy stuff)?

In my case, I showed severe "pulmonary restriction" from muscle weakness on all spirometry and PFT tests for several years and nothing improved this until I started IVIG. My muscle weakness was profound and was also progressive. It did not fluctuate and was constant and worsening until I began IVIG. It did not go into "remission" until I had been on Rituximab for about 6-9 months. I was not able to stand, walk without wheelchair, or drive for 4 yrs until this "remission". But until it maintains itself without Rituximab, I will never call it anything more than "remission" and my next maintenance infusion is in about two months.

Do you know of a channelopathy forum or is there a way to get into that email group you mentioned? If I wanted to dive deeper into that topic, how could I do it?

I am curious, too, although if most people in the group have Anderson-Tawill Syndrome and Potassium channelopathy (vs. calcium), then I probably would not be a good match!

The overall muscle weakness can be intermittent. It often is. Depends. My wife's is intermittent - although that may not be fair to her. I notice it as intermittent, but as I have learned to manage my symptom cluster better, so too has she, so I know somethings are transparent to me.. I'm sure she might say it's always there , just in varying degrees.

Mine was not intermittent and once it started, it was progressive until I began IVIG. But I suspect that is b/c it was autoimmune in my case vs. genetic?

One of the things I find cool is the number of channelopathies that are "acquired" vs genetic. Autoimmune channelopathies are wide open for interpretation - the new wild west.

I agree this is a no-mans land and 99% of doctors know nothing about this. I spoke in great detail w/the GI doc & anesthesiologist who I will be doing a procedure with next week b/c I was so unclear if Propofol is considered a calcium channel blocker. Luckily, they were both amazing and we will not be using Propofol for my procedure so it is a non-issue. But everything that I do requires extensive research on my part (in addition to having MCAS and the potential for anaphylaxis).

 

[Gingergrrl]

I missed a few things that I wanted to reply to

This specialist uses the ICC but he also did a zillion blood tests so I don’t know what he based his assessment that I had calcium ion channel problems on.

That is interesting that your specialist uses the ICC Criteria and felt that you had calcium ion channel problems. I am so curious which blood test helped him to determine this?!

This is something we would need to ask the authors about! In any case, for me, there are several reasons to avoid calcium supplementation—so I will do that—and also occasions where I need to take calcium channel blockers. I actually was given one IV in the ER on two occasions and it did the needed job. So the mystery continues.

It definitely sounds like your case is the opposite of mine (re: calcium) and that you should avoid calcium and take CCB's. There must be many different types of calcium ion transport issues (not just autoimmune) and some are helped by taking CCB's vs. the type that I have, I am instructed to avoid them.

Having known the lead author, I’m sure they had evidence but I don’t know what it is. If you look at the authors, they would not be likely to write this unless they had research to back it up:

I agree and looking at that list of authors, I cannot imagine that they would just randomly include "ion transport issues" as the title of a section of the ICC for no reason! The list you posted included Donald Staines and Sonya Marshall-Gradisnik (who I believe are part of the Australian ME/CFS team studying calcium channel issues) so maybe they are the reason that it is included in the ICC criteria?

 

[Hip]

do you think that the creators of the ICC Criteria had proven info re: "ion transport issues" and this is why they used those words in the title of that Section, or that they were just "guessing" that it "might" be due to ion transport issues, or do you think it was simply an error and they did not mean to title that section "ion transport issues"?

I remember seeing at least one paper showing an ion channelopathy in ME/CFS. But it is one thing observing a pathophysiology like this, but quite another to connect it to specific symptoms.

They do mention ion channel issues in ME/CFS in the original ICC published paper, but the original published paper does not mention ions in the title of section D. So it could be a mistake, but I am not sure.

 

[Sidny]

and by the way: in the most severe cases of ME, dorsal root ganglionitis were found in autopsies. Who is looking for it? nobody. The researchers prefer to invest millions in microbiome research. ridiculous.

Good point although I wouldn’t be surprised that the same pathogens involved in microbiome dysregulation are also driving the gangliopathies. I find it hard to believe any of the reasearchers in this field can pretend to know anything about what’s going on if they avoid looking into the very obvious sigificant tissue pathologies.

I think the explanations about what’s going on are way too obscure. Occam’s razor- ME is an infectious, inflammatory nervous system disease.