#MECFS #pwME
1/13
Some of the responses here, conspiracy claims, personal attacks, insinuations, and insults, have been far below any reasonable standard of civil discourse. I am not posting this for that audience, but for people who are suffering.
2/13
Disclaimer: this is not medical advice and not a treatment recommendation. It is only a report of what seems to help me personally and should be discussed with a physician.
3/13
This is not evidence. At most, it is an n=1 case report based on repeated stop-and-go observations and changes in function and symptom perception.
4/13
My working hypothesis: excessive glutamatergic and noradrenergic signaling may keep the body in a state of persistent physiological overactivation. That may be metabolically costly and worsen exhaustion.
5/13
A parallel hypothesis is that IL-1β-related signaling, microglial activation, and chronic low-grade inflammation may contribute to the “sickness behavior” component: flu-like, poisoned, or hungover symptoms.
6/13
The pharmacological backbone for me is pregabalin. It binds the α2δ subunit of presynaptic voltage-gated calcium channels, reducing calcium influx and lowering release of excitatory neurotransmitters such as glutamate and norepinephrine.
7/13
Functionally, pregabalin may reduce neuronal hyperexcitability, sensory amplification, and autonomic overactivation. In my case, it seems to reduce excitatory load rather than merely sedate.
8/13
Lorazepam (Ativan) may complement this. It is a positive allosteric modulator of the GABA-A receptor, enhancing inhibitory signaling. In simple terms: less excitatory output, more inhibitory tone.
9/13
I also considered synergistic agents:
Lamotrigine may reduce pathological firing via voltage-gated sodium channel blockade and may also reduce glutamate release.
10/13
Memantine is an uncompetitive NMDA receptor antagonist and may dampen pathological tonic glutamatergic activity without fully suppressing physiological neurotransmission.
11/13
Regarding IL-1β, anakinra would be a more direct mechanistic option as an IL-1 receptor antagonist, but it is not financially realistic for me.
12/13
Colchicine is a more tentative option, potentially relevant upstream of IL-1β, but it carries substantial risks, including myopathy/neuromyopathy.
13/13
Any such approach requires strict patient selection, careful risk-benefit assessment, and close monitoring, especially of renal and hepatic function. This is not advice for self-experimentation.
@sibylle_berlin
Appendix:
To objectify all of it regarding bodily functions and physiological outcome
(Last 12 months)
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