Could there be an on/off switch for ME/CFS and if there is, what would that tell us??

Hopefully Audrey and Charlie will have some results to report next year.

 

I have not seen any studies on deep relaxation and can only comment from my own experience. Because of the relapse on exertion problem, deep relaxation only makes the glass cage a little clearer as long as you rest, as you put it "a few more spoons", which is better than nothing. That is all pacing can do. There does not seem to be an empirical reason for assuming there is a qualitative difference between that and waking from anaesthetic feeling normal then crashing in half an hour of trying to act as if you are. That is business as usual in ME.

We all long to feel normal and from time to time, in hiatus between immune episodes, I do but it doesn't last as the process reasserts itself and if I try to act normal because I feel normal I cause a crash.

We all know sleep is not relaxing. Unrefreshing sleep is one of the symptoms commonly reported in relation to ME. The mind is very active in sleep and not as quiet as conscious relaxation, once you get beyond the fidget barrier. Ever since onset I have had febrile dreams, still do every night, wake up feeling like I have had two games of rugby and a bout of mudwrestling with a surprisingly agile hippopotamus.

I get that you are suggesting anaesthesia can switch off some aspect of the neuroimmune interface which temporarily suspends ME's affect on the nervous system and make people feel normal even though it does not last long.

I dont know how anaesthetics impact the neuroimmune interface so cannot comment. Maybe it acts like a painkiller, or maybe it is just an extreme version of the same glass cage phenomenon as deep relaxation. However, the same logic applies to that idea as to the idea of one central control switch for the chronic immune response, if the problem causing the experience of ME persists underlying the affect on cognition switched off by anaesthetic, would it be safe to act as if it did not exist? It might be like taking neurofen for a broken leg. Quality of life maybe but only as long as you dont try to use the leg, i.e. not a cure just a painkiller.

But we would need to find evidence there was a qualitative difference between post anaesthetic remission and deep rest due to a form of anaesthetised unconsciousness which stills the activity of the mind in a way which far exceeds the unrestfulness of sleep, to encourage further experiments along that line.

 

Wasn't it Dr Paul Cheney who decades ago put out a video on one of his lectures that he had come across pwME who had remissions after general anesthesia? His hypothesis at the time and treatment goals was to shift towards a coma state to 'repair' the nervous system. I can't remember the exact details.

My doctor at the time attended his lecture and told me that there was no way in hell he was prescribing Klonopin to his ME patients when I asked for a prescription.

 

Rings a bell. Same basic concept behind amitriptyline which I was prescribed in 1996. It did help a bit but also exacerbated heart arrhythmia. I would rather let things tick along as nature evolved.

Trying to shut down the CNS is a risky business. Could end up addicted or like Matthew Perry or Michael Jackson, dead for seeking peace. Personally I feel it would be best if we knew what we were dealing with before venturing down that route.

 

I recently read that the gut cells send signals to t-cells identifying which food molecules they should ignore. My ME started with a type IV reaction to one food, then pretty much all foods (unless I avoided a food family for 5 days). 2.5 years later, food poisoning switched the type IV reaction off. That might indicate a global switch for t-cells or a signal specific to those gut cells, and that switch can be turned on and off. Neurons might also be involved in this signalling, so it's possible that ME alters just one or a few neurons involved in this process. I can accept the existence of this sort of switch in the immune system.

 

I've written here about my experience of remission after an anaesthetic. It happened only once and I've had a number of anaesthetics of various kinds. I've always assumed it was due to the specific drugs used.

 

That is interesting but hard to know on an n=1 basis what happened. Was that just an ME fluctuation event or dosimetry related or specific to the type of anaesthetic?

I would comment that even if there is one type of anaesthetic which is more effective in causing temporary remission we still need to ask why. Neither of the competing hypotheses are ruled out and the question we need to ask is whether it is because it shuts down brain activity better causing better restfulness or whether it has a direct effect on a putative neuroimmune interface or "switch" which causes a systemic change in the brain leading to temporary remission from ME's cognitive symptoms.

This is all very speculative, just following the rabbit hole. I have a lot of respect for the late Dr Paul Cheney's clinical experience and observations even if some of the therapies he discussed and tried were doctor-patient hybrids born of the desperation of PWME in the land of the free willing to try anything to recover. He certainly tried ampligen and people have discussed differences in antibiotics etc in relation to circumstances surrounding remissions but to date no reliable therapy has emerged. Heavens I remember one exPWME describing a remission attributed to a long walk in the desert.

But attribution based on coincidence is not a reliable scientific method. Reflecting on that maybe it is not the anaesthetic but the procedure, cutting through the skin and its pain receptors and roughing up the autonomic nervous system, which might temporarily change things for some PWME by releasing endorphins and adrenalin as though responding to injury, which technically surgery is? Hence the anaesthetic.

 

Is that related to the Julie Rehmeyer mould avoidance thing? https://www.healthrising.org/forums/threads/julie-rehmeyers-mold-avoidance-recovery-story.3429/

 

I have had complete remission of all symptoms for some days, though usually about six hours. I have also had restoration of energy but with other symptoms remaining. Spontaneous remission of symptoms is not random in my opinion, just hard to pin down as to cause. My experience fits entirely with the idea that some signal is suppressed, but its likely to be a complex signal, not one single factor. However I suspect that something is orchestrating the signal as well, some kind of feedback loop.

In my best case I went from slow shuffling across a room to a five hour brisk walk in just days, and I only stopped at five hours because I had run out of time, I needed to get ready for the next day at a medical conference. After a week or so I started getting brutal headaches. I am guessing as to why.

The worst example was a substance I shall not name, which completely restored energy but did not fix fatigue or other symptoms, for which I had to double the dose every three days. I gave up when the dose became ridiculous. Then I crashed because it was propping up my energy - and this is why I do not name it. I regard it as potentially dangerous.

On two other occasions I had sudden remission of symptoms, there were more instances but I forget the detail. In one I started running, and ran over a mile, despite being unfit, all the way home. In the other I went from struggling to even understand physical chemistry problems at university, to easily solving them in my head. Its a daunting experience to see these gains disappear about six hours later. On one very good day a remission was just before one of my biochemistry exams. The exam was a breeze, and I finished more than an hour early.

 

This needs a serious follow-up, especially since problems can be induced in healthy muscle tissue by incubating it with ME blood serum for two days. A signal is in our blood, and I have seen speculation that it might be due to our large numbers of vesicles containing a large number of substances.

Edited to change "the signal" to "a signal". There might be additional neurological or non-blood signals this research does not elucidate.

 

My suspicion is that we can restore our short term muscle energy store. This means we have enough muscle energy to function, but its gone very fast.

 

From about 6 years ago
https://www.s4me.info/threads/suddenly-feel-completely-well.7170/#post-129547

 

Karl Morten has talked about trying to replicate this work. Initially on a few samples he thought he had. But when he tried to scale up with biobank samples the results did not hold up. He thought it was related to blood collection and processing/freezing and wanted to retry with fresh samples. But for that he said he ideally needs a local clinic that can refer patients, and a phlebotomist on call so that blood can be processed immediately.

In the recent Action for ME webinar a presentation was made about replicating the muscle incubation work. But to me it seemed to again be using frozen blood, but hopefully the sample collection and processing was well controlled and that will make the difference.

 

Ah ! That could be it. It is quite thought provoking given the prominence of Jen Brea's mould avoidance quest in "Unrest". It would seem, regrettably, not to have helped her though it helped Julie. How does one account for that?

I have no reason not to believe the story and reported conclusions from Julie's self experimentation but was trying to state the case for reserving judgement based on cautious systematic scepticism rather than leaping to conclusions about associations. On further consideration I can believe that an immune response to mould could trigger ME/CFS because as stated before, I think it is likely that ME is due to a chronically activated immunological response.

IMHO it is possible it may have been a very specific trigger for Julie if we take accounts of recovery due to mould avoidance at face value as a fairly rare phenomenon even among ME/CFS patients. Though I believe its real enough as we know that in some people it can cause life threatening severe respiratory conditions, as in the case of poor little Awaab Ishak. https://en.wikipedia.org/wiki/Death_of_Awaab_Ishak

In relation to the thread I think the ME/CFS immune response could be considered the "switch" and every which way it can be triggered chronically would account for the many subtypes of ME/CFS which I suspect exist. So mould activated immune reaction is one subtype and may cause ME/CFS but not all ME/CFS is mould activated immune reaction. With that way of looking at ME/CFS, it makes sense that just because mould avoidance worked for Julie doesn't mean it will work for everyone with ME/CFS.

 

I communicated with a pwME that I met in person for several years who did not develop ME from a known trigger/viral infection. Her onset was gradual over several years. Mould and MCS was a huge issue for her and mould avoidance did improve her symptoms. We both saw the same ME specialist but he did not give her a diagnosis of ME. We also saw the same Virologist and her immune phenotyping profile was worse than mine. The Virologist gave her a diagnosis of ME and helped her apply for disability benefits which were approved.

 

In order to achieve mould avoidance it is likely you have to change a lot of things (home, work, climate zone, etc), so it is not clear on the basis of anecdote alone if mould is necessarily the only or even a significant factor. I understand a significant number of people are certain that their ME is mould triggered, which may very well be correct, but we need more data.

 

My friend was also a subgroup who benefitted from high dose B12. I did not, it made me feel worse.

 

It would be great to have a much better natural history of ME. There are so many basics we just don’t know.

I benefit from B12 when I am in B12 deficit, but only until my B12 levels are corrected when further B12 has no impact, though I do need a maintenance dose to avoid returning into deficit. There is some suggestion that more people with ME than in the normal population experience B12 deficiency, though we lack data on what percentage are involved. In consequence we have no idea if the anecdotal evidence of B12 helping some of us reflects a genuine effect on some people’s underlying ME or if this is just an artefact of picking up on unrecognised B12 deficiency that is either unrelated to the ME or a down stream consequence of ME for some of us.

If B12 deficiency is a downstream effect of ME, we still don’t know if this results from a direct physiological process or an indirect consequence such as poorer diet.

[edited to add - Similarly I experience a correlation between my ME severity and a broad idea of how good my diet is, though I don’t know if good diet improves my ME status or if I simply have more energy to ensure a better diet when my ME is milder.]

 

Agree. If a pwME has food sensitivities and intolerances, as my friend did, then it would make sense that B12 deficiencies would be a factor.

I became depleted in magnesium after I developed delayed PEM from exercising again.

 

The onset of my B12 deficiency could have coincided with the development of two food intolerances, although it didn't make itself known until several years later.

It was my doctor who suggested this. He said it can be years before symptoms appear in people who develop malabsorption, because they began with adequate B12 stores in their liver. There's an efficient recirculation loop and they may still be absorbing some vitamin, so depletion is slow.

If food intolerances are the result of some kind of change in the gut, maybe it's not implausible it could also impair the cells that absorb B12? (Only wondering aloud, I've no idea really. )