Five ways to reduce your ME/CFS "wired but tired" hyperaroused brain state

[alcasa]

I also have generalized anxiety with an edge on social anxiety that come with my PTSD package. Things do get very tricky but over the past few years and recently I've been able to really dissect what is going on because wired and tired PEM and purely mentally stemming symptoms go hand in hand which will make each other worse. IF my brain signalling is under control even if I encounter a trigger I will get a little jolt with noticeable tension in the usual areas of my body but it won't spiral into that signature PEM "I'm going to lose my mind" feeling when I an't escape a stressful situation. It's as if my brain doesn't have any break system on it and when a strong enough signal erupts with excitation everything can go haywire with intense generalized anxiety and increased trigger reactivity very quickly. If it gets too bad I will get complete social dysfunction with vocal/communication difficulties, and need to sit alone in quiet environment for a long while to reset myself. This depending on how severe that over excitation was can take many hours, sometimes I won't get a good break till the next day. This will even happen with good feelings of excitation, it's not limited to just being triggered in another way.

It will also trigger immune reactions and flu like symptoms when it gets that high. I'm not sure what is really going on under the surface though. It FEELS like the over excitation is continuously reactivating a virus or some kind of infection. I have had mental windows of feeling "normal" before socially and mentally but these are extremely rare. The last time this happened was I kid you not when I ate some bad scallops and got food poisoning. I didn't feel good overall but my social communication got massive improvements including my vocal problems, my anxiety levels dropped to almost nothing save for what my triggers did at a baseline which was manageable with some manual self reasoning, my sensory issues just disappeared, and work was a breeze because of how low the PEM level got. When I got home I just started wondering what to do next and how productive I was going to be, everything was suddenly so much brighter. Unfortunately the next day and forward as I recovered it all creeped back in indistinguishable from before.

My friend…

When my disease started 6 years ago I had EXACLY the same symptoms you have now and, I should say… I’m now pretty sure it’s a glutamate thing

 

[Dysfunkion]

My friend…

When my disease started 6 years ago I had EXACLY the same symptoms you have now and, I should say… I’m now pretty sure it’s a glutamate thing

I'm sure it plays a a big role but say for example if I consume a lot of it in food it doesn't specifically trigger much but making me feel more wired and anxious in a background fashion though. I think if it is a major culprit anyways then I think it's being released in the brain in such high quantities somehow that no amount of food consumed can match that release and the body has a hard time disposing of it creating a bunch of downstream problems. I also have an idea that ammonia and lactic acid also play a role in the mess that in some way the if it is a major component to what is happening just adds more fuel to the glutamate fire.

 

[CristianSerious]

Which supplements did you find helped the most the racing thoughts ?

 

[Blazer95]

NAG depletes IL-17. For those with excess it might be great but mine is too low and i respond very badly to NAG.

Racing thoughs and hyper arousal can also be downregulated by some SSRI Like Citalopram f.e. its believed to regulate some 5-HT receptors that are involved in the Central nervous system.

I'm a big fan because Citalopram SSRI has improved me from mod-severe to moderate and the effects still holds on since months now.

Also Lots of people on my Facebook Report good benefits from pregabalin as it downregulated the cns aswell.

 

[alcasa]

NAG helps through brain excitation. Everything for a lot of us is a question or calcium channels, glutamate, excitation recycling, ATP, dopamine and noradrenaline

I just take too long to write about it… but Goldstein an Marco got so close to the answer it’s unreal they are not more quoted

 

[Violeta]

NAG helps through brain excitation. Everything for a lot of us is a question or calcium channels, glutamate, excitation recycling, ATP, dopamine and noradrenaline

I just take too long to write about it… but Goldstein an Marco got so close to the answer it’s unreal they are not more quoted

Do you have any thoughts on hypoxia possibly being a cause?

I am looking up calcium channels and I see there are different types. Do you know which ones are involved in the glutamate issue?

What is your address on Twitter, I would like to follow you.

 

[Violeta]

Do you have any thoughts on hypoxia possibly being a cause?

I am looking up calcium channels and I see there are different types. Do you know which ones are involved in the glutamate issue?

What is your address on Twitter, I would like to follow you.

@alcasa, I just looked up hippocampus, glutamate, calcium channels, and I am seeing TLR4 and LPS.

LPS is something Ray Peat always talked about. I have been thinking about it for a different reason, but am wondering how much of a part it plays in the cause of ME/CFS. I'll keep reading.

 

[Violeta]

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Presynaptic L-Type Ca2+ Channels Increase Glutamate Release Probability and Excitatory Strength in the Hippocampus during Chronic Neuroinflammation​

https://pubmed.ncbi.nlm.nih.gov/32747440/

This study is with respect to epilepsy, but the information seems as if it could be extrapolated to other neurological conditions.

Neuroinflammation is thought to have a pathogenetic role in epilepsy, a disorder characterized by an imbalance between excitation/inhibition. Fine adjustment of network excitability and regulation of synaptic strength are both implicated in the homeostatic maintenance of physiological levels of neuronal activity. Here, we focused on the effects of chronic neuroinflammation induced by lipopolysaccharides on hippocampal glutamatergic and GABAergic synaptic transmission. Our results show that, on chronic stimulation with lipopolysaccharides, glutamatergic, but not GABAergic, neurons exhibit an enhanced synaptic strength and changes in short-term plasticity because of an increased glutamate release that results from an anomalous contribution of L-type Ca2+ channels to neurotransmitter release