Channelopathy in CFS?

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Hi @Zebra
Yes, at least hereditary. My cytokines are dropping post orgasm below normal levels and bounce back 24h after O, some overshoot the upper normal limit. Cytokine release needs Intracellular calcium. So the latter may be decreasing upon that trigger. I suspect possible calcium channel issues. I asked the same question on the Dinet forum regarding POTS/dysautonomia but got no answers back what specific channels are involved for those syndromes/symptoms. My progesterone is elevated, I just scrolled through the discussions Pyrrhus posted and saw that it blocked TRPM3. And btw I'm not aware if there are men on this forum with elevated progesterone, maybe you guys know any causes. Triggery behaviour with regards to symptomatology is seen in MCAD and channelopathies. I had a Bell's palsy in the past as well. Also episodes of acute weakness but these are rare.

Edit: Here is a discussion about the sigma receptor which modulates calcium signaling via IP3.
https://forums.phoenixrising.me/threads/the-enigma-of-sigma-receptors.76484/
Already had that discussion on another forum. Progesterone blocks Sigma-1 and there is interaction with sodium channels: Antagonist action of progesterone at σ-receptors in the modulation of voltage-gated sodium channels
I have seen a paper in the past which mentioned this channel in POTS and IBS.
 
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sometexan84

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Are there channelopathies linked or associated with CFS?
At the very least associated, yes.

There's increased acetylcholine and adrenergic receptor antibodies in ME/CFS. Multiple studies can be found Googling this.

Aside from the muscarinic and adrenergic receptor antibodies (reported by many here), the following are others that have been reported by some in this forum: Voltage-Gated Calcium Channel, N-Type (VGCC), Endothelin-Receptor-A (ETAR), Angiotensin-II-Receptor-1 (AT1R), N-methyl-d-aspartate (NMDA) receptor, and GABABR (gamma-aminobutyric acid B receptor).

Aside from that, Enterovirus B infections are associated w/ ME/CFS, and some have cell tropism for natural killer cells (like Coxsackievirus B4). I suppose this means there's a chance that this could result in the calcium dysregulation via the decreased TRPM3 receptors on NK cells that Pyrrhus mentioned. The CVB's cleave proteins in infected cells that can mess w/ cell surface receptors and their functionality.

But that all sounds like a reach.