Kitty
Senior Member (Voting Rights)
How about the mysterious 'something in the blood'?
Hopefully Audrey and Charlie will have some results to report next year.

How about the mysterious 'something in the blood'?
I think that if deep relaxation produced immediate remission, we'd know about it - lots of PwME have tried deep relaxation. Even sleep, which ought to be deeply relaxing, doesn't produce remission every morning (in fact, quite the opposite). I suspect lots of us feel better after deep rest during the daytime but without thinking that we're temporarily cured - just that we've got a few more spoons for a short while.
I think the experience with anaesthetic must point to something else, and it's interesting that you've seen several reports of post-anaesthetic remission. I wonder what that thing could be?
But you would have to find proof 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.
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.The problem is why the immune signal is jammed on?
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.I think the experience with anaesthetic must point to something else, and it's interesting that you've seen several reports of post-anaesthetic remission. I wonder what that thing could be?
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.
Is that related to the Julie Rehmeyer mould avoidance thing? https://www.healthrising.org/forums/threads/julie-rehmeyers-mold-avoidance-recovery-story.3429/attributed to a long walk in the desert
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.I had very good function during my remissions, but sometimes I'd still get the distinct pattern of symptoms I now know is PEM.
How about the mysterious 'something in the blood'?
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.I suspect lots of us feel better after deep rest during the daytime but without thinking that we're temporarily cured - just that we've got a few more spoons for a short while.
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.especially since problems can be induced in healthy muscle tissue by incubating it with ME blood serum for two days.
Is that related to the Julie Rehmeyer mould avoidance thing? https://www.healthrising.org/forums/threads/julie-rehmeyers-mold-avoidance-recovery-story.3429/
In relation to the thread I think that 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.
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.
In relation to the thread I think that 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.
My friend was also a subgroup who benefitted from high dose B12. I did not, it made me feel worse.
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.
There is some suggestion that more people with ME than in the normal population experience B12 deficiency