alcasa
Glutamate +ATP pantheist
- Messages
- 31
Hi!
I’ve reached partial remissions after trying interventions that:
NAG, mentioned by Hip, also calms me via glutamate, but I suspect it works by reducing receptors. It leaves me mildly sedated and doesn’t fully prevent PEM.
Given that many here have tried NAC, aspirin, and progesterone without much success, I’d say glutamate uptake deficit is just one CFS subtype. My case is unusual in its symptoms:
I doubt most here have this form of CFS, but I’m convinced Jay Goldstein was describing this in particular. He noted a syndrome involving channelopathies responsive to nimodipine/nifedipine, and highlighted two neurotransmitters whose modulation strongly affected patients: norepinephrine and glutamate. He also observed hypoperfusion, paradoxically he got his patients improving with noradrenaline with further increased the hypoperfusion, with ketamine offering further benefit.
This fits me perfectly. Before keto, I had low NA signalling but was highly sensitive to it via CaV1.2, so NA drugs like amphetamines improved symptoms for some time after taking them but they worsened my depersonalziation. For my first year, I was “tired but wired,” which I can only attribute to a glutamate uptake deficit. Over time, wiredness faded as I lost function, likely from receptor downregulation secondary to impaired reuptake.
Everything aligns: read Goldstein’s work through the lens of glutamate uptake deficits and CaV1.2 or CaV2.1/2.2 hypersensitivity, and the interplay with NA signalling and “tired but wired” PEM becomes obvious. In my case, glutamate uptake with CaV 1.2 being probably one of the main glutamate contributors explain everything.
The only barrier now is persistent dysautonomia from keto. Until I reduce it, I can’t test progesterone, aspirin, or other GLT-1-targeting drugs without sharply cutting glutamatergic exocytosis. I'm trying it by lying in bed all day and trying to get down my allostatic point of sympathetic activation but I'm not being very successful at it.
Bests
I’ve reached partial remissions after trying interventions that:
- Reduce excitation via CaV1.2 – vitamin K2, nimodipine.
- Increase glutamate uptake – NAC, aspirin, progesterone (with more to test).
NAG, mentioned by Hip, also calms me via glutamate, but I suspect it works by reducing receptors. It leaves me mildly sedated and doesn’t fully prevent PEM.
Given that many here have tried NAC, aspirin, and progesterone without much success, I’d say glutamate uptake deficit is just one CFS subtype. My case is unusual in its symptoms:
- No PEM from physical exertion, only from mental work or study.
- My CFS was triggered by PROLONGED MENTAL EFFORT without any disease or virus.
- I've had problems with exerting myself mentally and with social anxiety all my life. I always was a different kid.
- Anything raising adrenaline/noradrenaline worsens PEM – fasting, exercise or keto make it worse.
- CaV1.2 is key for me, as NA/adrenaline increase its phosphorylation, boosting glutamate release.
- High-dose NAC completely prevents PEM and lowers anxiety/social phobia.
- Depersonalisation occurs late at night when glutamate activity is downregulated, or after heavy mental work or NA/adrenaline surges.
- CaV1.2 blockers ease symptoms but are weaker than NAC in doing so. Progesterone and aspirin may help energy by boosting GLT-1, though this remains theoretical.
- Also NAC rebound is the worst thing I experienced in my life while using NAC I'm almost normal, without crashes or anxiety.
- Residual high adrenaline from two years of keto means I can’t yet tolerate progesterone without panic attacks, though this is improving.
I doubt most here have this form of CFS, but I’m convinced Jay Goldstein was describing this in particular. He noted a syndrome involving channelopathies responsive to nimodipine/nifedipine, and highlighted two neurotransmitters whose modulation strongly affected patients: norepinephrine and glutamate. He also observed hypoperfusion, paradoxically he got his patients improving with noradrenaline with further increased the hypoperfusion, with ketamine offering further benefit.
This fits me perfectly. Before keto, I had low NA signalling but was highly sensitive to it via CaV1.2, so NA drugs like amphetamines improved symptoms for some time after taking them but they worsened my depersonalziation. For my first year, I was “tired but wired,” which I can only attribute to a glutamate uptake deficit. Over time, wiredness faded as I lost function, likely from receptor downregulation secondary to impaired reuptake.
Everything aligns: read Goldstein’s work through the lens of glutamate uptake deficits and CaV1.2 or CaV2.1/2.2 hypersensitivity, and the interplay with NA signalling and “tired but wired” PEM becomes obvious. In my case, glutamate uptake with CaV 1.2 being probably one of the main glutamate contributors explain everything.
The only barrier now is persistent dysautonomia from keto. Until I reduce it, I can’t test progesterone, aspirin, or other GLT-1-targeting drugs without sharply cutting glutamatergic exocytosis. I'm trying it by lying in bed all day and trying to get down my allostatic point of sympathetic activation but I'm not being very successful at it.
Bests
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