Imbalanced Brain Neurochemicals in long COVID and ME/CFS: A Preliminary Study using MRI

[Florida Guy]

It seems to me that there are other ways to lower glutamate besides taking a drug to do it. Drugs always seem to have side effects, don't they? What I'm working on now is to lower glutamate in my diet, particularly the form MSG.

They sneak msg into food all the time. You will never never see it listed on the ingredients but they have about 100 names and ways to fool you. Any processed protein will have msg, I read where if you see the word protein, you might as well interpret it as msg because protein is not an ingredient, its part of food. So when they add isolated pea protein, for example, it includes msg. Modified starch is another name they use to hide it. My rule is if the ingredient list is two paragraphs of fine print, its no damn good.

This is why its best to eat unprocessed food as much as possible, among many other reasons

 

[bob800]

The crux of the issue is that none of these drugs address the vital aspects of glutamate's reuptake and metabolism by glial cells and potentially neurons, which are crucial for sustaining the Na+/K+ ATPase.

Thanks for the detailed reply. Is there a BBB-permeable drug that you think might address this, in a more direct manner than the other ones we discussed (like Riluzole)?

 

[Violeta]

@alcasa, thank you for this information about GLT-1.

I have just recently realized that neurotransmitter issue is probably the main cause of my problems, but I have a lot of catching up to do.

I started taking polygala tenuifolia, and it very quickly gave me amazing results, but I have to take a look at it from the GLT-1 perspective. I guess it works from a different angle, and maybe not the correct angle, so while it helps it might not be the best idea. Here's a summary of it's effect on glutamate:

"Polygala Tenuifolia acts as an MOA inhibitor which increases dopamine and norepinephrine in your brain. This ancient Chinese herb helps reduce cortisol, inhibits inflammation, and regulates glutamate AMPA receptors."

I just found this Japanese remedy, if you could take a quick look at the study and see if it's on the right path, I would appreciate it.

Yokukansan, a Traditional Japanese Medicine, Enhances the Glutamate Transporter GLT-1 Function in Cultured Rat Cortical Astrocytes​

https://www.hindawi.com/journals/ecam/2018/6804017/

In Chinese, the formula is called Yin Gan San, and here is a study related to the Chinese formula.

Chemical profile of the active fraction of Yi-Gan San by HPLC-DAD-Q-TOF-MS and its neuroprotective effect against glutamate-induced cytotoxicity​

https://pubmed.ncbi.nlm.nih.gov/25480519/

 

[Violeta]

@alcasa, thank you for this information about GLT-1.

I have just recently realized that neurotransmitter issue is probably the main cause of my problems, but I have a lot of catching up to do.

I started taking polygala tenuifolia, and it very quickly gave me amazing results, but I have to take a look at it from the GLT-1 perspective. I guess it works from a different angle, and maybe not the correct angle, so while it helps it might not be the best idea. Here's a summary of it's effect on glutamate:

"Polygala Tenuifolia acts as an MOA inhibitor which increases dopamine and norepinephrine in your brain. This ancient Chinese herb helps reduce cortisol, inhibits inflammation, and regulates glutamate AMPA receptors."

I just found this Japanese remedy, if you could take a quick look at the study and see if it's on the right path, I would appreciate it.

Yokukansan, a Traditional Japanese Medicine, Enhances the Glutamate Transporter GLT-1 Function in Cultured Rat Cortical Astrocytes​

https://www.hindawi.com/journals/ecam/2018/6804017/

In Chinese, the formula is called Yin Gan San, and here is a study related to the Chinese formula.

Chemical profile of the active fraction of Yi-Gan San by HPLC-DAD-Q-TOF-MS and its neuroprotective effect against glutamate-induced cytotoxicity​

https://pubmed.ncbi.nlm.nih.gov/25480519/

Glycyrrhiza may be the only herb from the Yokukansan formula needed for the Glt-1.

PS: The review is very complicated. And I just heard from someone on twitter that the formula didn't work for her. I don't know if I'll try it or not.

 

[Violeta]

My opinion is that for a lot of people with CFS there's been a loss in ATPasa Na/K+ for regulate the ion pump necessary to recycle glutamate, use it as energy and keep the pump up: so you are in a situation in which you have to much glutamate in synapses, too litle ATP to actually recycle it (glutamate pay its own price of ATP, if it is not reuptaken, the pump can't keep it up) and any kind of prolonged exertion leads heighten the problem

This mechanism explains PERFECTLY fenomena as Post Exertional Malaise. I will sometime in the future make a long post on it, I'm too unwell at the moment to further explain. But I think this could be all the disease for lot of people

Would thiamine deficiency cause the loss in ATPase Na/K+?

" In previous studies [13, 14, 23], we reported that YKS rectifies the following thiamine deficiency-induced abnormalities in the brain and cultured astrocytes of rats: astrocyte degeneration, increase in extracellular glutamate concentrations, decrease in GLAST-derived glutamate uptake, and reduced expression of GLAST proteins and mRNA."

In thiamine deficiency state, Na enters the cell and K leaves it.

This is not from the study, just a google search. Is this the "thiamine deficiency-induced abnormality in the brain that causes increase in extracellular glutamate concentrations?

"Since Na,K-ATPase is important for maintaining various cellular functions, its inhibition could result in diverse pathologic states. Inhibition of Na,K-ATPase causes high intracellular Na+ ion levels and subsequent increases in intracellular Ca2+ ion through the Na+/Ca2+ exchanger."

 

[linusbert]

@alcasa so you are saying glucose metabolism is yielding more atp because it brings more oxygen and oxygen is limiting factor, therefore while the burning of a fatty acid yields more atp in general than glucose, its doing so over a slower pace so in the same amount of time, glucose does yield more?

but its not new that the body uses mainly glucose in a oxygen-less or anaerobic situation like in exercising.
so if the body can meet its demands like in a aerobic situation there is no need to much burn the glucose and in fact make use of the more atp yielding fatty acids. ?

 

[Violeta]

Elliot Overton - Thiamine Deficiency Causes Intracellular Potassium Wasting

https://x.com/boretrol/status/1425608764728610819

Editing in: B2 helps with the use of B1, and also is valuable when one has the wired but tired feeling.

 

[Violeta]

Additionally, N-acetyl-aspartate levels were significantly higher in long COVID patients (p=0.012).

So is the high glutamate the aspartate's fault?

The afore body of data suggests that D-Asp is a central regulator molecule within glutamatergic system, that acts by activating this neurotransmission, on one hand directly by postsynaptic NMDAR activation while, on the other, evoking L-Glu efflux from cortical neurons.

New Evidence on the Role of D-Aspartate Metabolism in Regulating Brain and Endocrine System Physiology: From Preclinical Observations to Clinical Applications​

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7698810/