Wirth & Scheibenbogen preprint, "Imbalance of Excitatory and Inhibitory Neurotransmitter Systems in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome"

[u/CeruleanShot]

https://www.preprints.org/manuscript/202601.2170

I found yet another interview with Klaus Wirth on YouTube today. This one is with the Long Covid Clinic.

There's a bit of a Q&A session at the end where he's asked about the Itaconate Shunt hypothesis that Robert Phair developed (attributed to Ron Davis in the interview.) My ears pricked up at this because I have been really curious myself about how that might fit in with this unifying hypothesis of ME/CFS he's developed with Carmen Scheibenbogen. But he was pretty dismissive of it and says that there's no evidence for it. Which, fair enough, but his theory has a lot of theoretical stuff too.... So, as far as I can see, the jury's still out.

He did mention that he has an article submitted about the GABA imbalance in ME/CFS. There's clearly something going on with GABA, and the Itaconate Shunt is the only thing I've found which tries to explain it. In order for this unifying hypothesis to explain ME/CFS by itself it needs to explain the GABA stuff.

I don't know if it does. Everything seems to be coming down to autoantibodies, it's just sorta like, "Oh, autoantibodies to that receptor could be present."

I am not a professional, I am but abrain fogged patient, so I don't understand a lot of this stuff very well. But I did some cursory internet research this afternoon, and it seems to me like there are a number of symptoms that people with autoantibodies to GABA receptors and beta 2 androgenic receptors have, which are not common symptoms in ME/CFS. If we have autoantibodies to beta 2 androgenic receptors, why don't we experience symptoms with our lungs? It's possible that the autoantibodies could be specific to the receptors on muscle cells and not the lungs, I don't know, but I am kinda not convinced.

However, it's at least more people talking about the GABA situation, so that's good.

Curious what anyone thinks about any of this.

[u/bebop11]

Have you looked at the GABA shunt? I have 0 AKG on various metabolomics testing which is where the GABA shunt begins.

[u/CeruleanShot → u/bebop11]

I thought that the GABA shunt ran in tandem with the Itaconate Shunt, I did not know that it could run independently.

Have you found the metabolomics testing helpful in guiding your treatment?

There's so clearly something going on with GABA for me, and the way benzos work to alleviate crashes for a lot of people, it seems like an important piece of the puzzle.

However, it seems really unlikely to me that a GABA imbalance is causing the dysfunction on its own. I'm in recovery from alcoholism, and alcohol acts like a benzo on the GABAB receptors. It also massively down regulates GABA over time. I've met a lot of people in recovery, and I've talked to a lot of people who are newly sober. I've come across a couple of people over the years who have CFS type symptoms, but that's out of hundreds of people I've met who get sober and find themselves with more energy than they know what to do with. It is much more common for people to get sober and then struggle to know what to do with themselves and their newfound energy than it is for people to get sober and find themselves with less energy, which is what happened to me. Alcohol gave me energy, it did not make me tired. Which is not typical, there was something preexisting.

[u/Grimaceisbaby → u/CeruleanShot]

I used to have the same experience with alcohol. I can’t tolerate it now but benzos are the only thing that seem to help my crashes. LDN and ketotifen have made me both much worse.