The good news: cause of muscle weakness ME/CFS discovered

C

Consul

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wabi-sabi said:
Proper sodium levels are maintained by the Na/K ATPase pump. Without that pump working, the nerve can't send signals. This pump powers quite a lot in cells.

aculty.washington.edu/chudler/ap.html#:~:text=Action%20potentials%20are%20caused%20when,ions%20rush%20into%20the%20neuron.
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The high sodium levels was found in the muscles though, the nerves could be a different story.
 
wabi-sabi

wabi-sabi

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Rufous McKinney said:
given every thing the body does requires ATP energy, it just seems like there are so many opportunities for damage to mitochondria/ and energy production and every chemical reaction the body does.
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Exactly!

This increased sodium result is helpful in that it shows in detail how everything breaks when there's no ATP. What it's not helpful for is showing "the cause" of muscle weakness. It's one part of a very complex picture.

It's like when the power goes out in your house, the pipes freeze and burst and food rots in the fridge, etc. etc. You need to know all of those details to fix things, but you shouldn't think that the melted ice cream is the whole story.
 
Rufous McKinney

Rufous McKinney

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wabi-sabi said:
What it's not helpful for is showing "the cause" of muscle weakness. It's one part of a very complex picture.
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I. think its fine to generate diverse hypotheses, but label them clearly as such.

We "run out of something rapidly". What is it?

Why we "ran out of something" may not be because of "something ATP" instead it could be: the big SWITCH on the wall is stuck ON. The next thing that happens is we run out of something.
 
SWAlexander

SWAlexander

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Just a short emphasis. I´m not well, Have the nasty flu.

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Original publication:
Muscle sodium content in patients with Myalgic Encephalomyelitis/Chronic Fatigue Syndrome

https://translational-medicine.biomedcentral.com/articles/10.1186/s12967-022-03616-z#Sec12

Pathophysiology of skeletal muscle disturbances in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS)
https://translational-medicine.biomedcentral.com/articles/10.1186/s12967-021-02833-2
 
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Gingergrrl

Gingergrrl

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wabi-sabi said:
Dr. Scheibenbogen has been looking at autoantibodies on ME/CFS, but they are autoantibodies to a different part of the nervous system than in LEMS. The ME/CFS autoantibodies would mess up the way the blood vessels work, meaning cells don't get enough oxygen, meaning the can't make ATP.

If this is correct, then muscles are weak in ME/CFS because the have no fuel to power contraction. In LEMS, muscles are weak because the signal to contract isn't getting sent properly. Dr. S's hypothesis would fit with excess sodium in muscle cells, because the pump that is supposed to get rid of the sodium can't run, because it doesn't have any fuel either.
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Thank you for explaining that @wabi-sabi and I apologize for my delayed response! When you referred to Dr. Scheibenbogen's autoantibodies, did you mean the anti-muscarinic Abs, or the alpha & beta-adrenergic Abs, or both kinds? (meaning both muscarinic and adrenergic)

I tested positive (in 2016 to 2018) for nine of the Cell Trend autoantibodies and I also test positive consistently for the LEMS autoantibodies that attack the calcium channel. I (sort of) understand the calcium channel Abs & LEMS but I still struggle to understand the Cell Trend Abs and this new discovery with the sodium pump.

Thankfully, the extreme muscle weakness that affected my ability to breathe, walk, use my arms, etc, completely resolved with IVIG & Rituximab and has never returned. I still hope to fully understand it better some day but I never quite am able to retain the science :headslap:! I have other medical issues that are intermittent, and I still take 6-7 meds per day, but my muscle weakness & shortness of breath has never returned for which I am forever grateful.
 
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wabi-sabi

wabi-sabi

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Gingergrrl said:
When you referred to Dr. Scheibenbogen's autoantibodies, did you mean the anti-muscarinic Abs, or the alpha & beta-adrenergic Abs, or both kinds? (meaning both muscarinic and adrenergic)
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Both. I think she is talking about these receptors here: https://doctorlib.info/physiology/medical/77.html

Based on a quick google, in LEMS the broken calcium channels mean the nerve endings can't release acetylcholine. Acetylcholine is supposed to be the signal from the nerve to the muscle to contract.

Dr. S hypothesizes (with all those receptors you mentioned) that the breakdown is in the nervous system itself. Part of that, with the muscarinic receptor breakdown, is the inability to received an acetylcholine signal In LEMS, it's the interface between the nervous system and muscular system that breaks. So it's the place the breakdown happens that's different, as well as the signal that's getting sent (or not).

Does this make sense? I'm a bit tired right now.
 
J

Jjnz

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I didn't have much muscle weakness outside if the normal deconditioning, I have muscle endurance issues and elongated recovery. Curious if excess sodium might allow one to sweat more , I certainly do that
 
Gingergrrl

Gingergrrl

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wabi-sabi said:
Dr. S hypothesizes (with all those receptors you mentioned) that the breakdown is in the nervous system itself. Part of that, with the muscarinic receptor breakdown, is the inability to received an acetylcholine signal In LEMS, it's the interface between the nervous system and muscular system that breaks. So it's the place the breakdown happens that's different, as well as the signal that's getting sent (or not).
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Do you think my muscle weakness & lung weakness was so severe b/c I had both the anti muscarinic autoantibodies and the LEMS autoantibodies (and others)?

The last few weeks I’ve actually been able to climb stairs and lift/carry heavier things (but I don’t want to get too excited about this new development in case it is temporary and doesn’t last)!
 
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