Stanford Community Symposium 2018: Phair, Metabolic traps, Tryptophan trap

https://s4me.info/threads/stanford-...traps-tryptophan-trap.6033/page-7#post-122456

To explain the 'inner' workings of the forum software a bit, where the forum produces a quote, either via the reply or the multiquote button, it produces a link to the original post and indicates it by a little up arrow

as can be seen in the example above. By using these a number of times I was able to arrive at the post I've linked to above.

 

I didnt read all those threads about possible metabolic problems but is it already sure that there are? For me it makes sense but i have no scientific background. It was already long time before these theories started to appear that i felt that i am not tired but that my body simply doesnt produce enough energie. So i think the metabolisme must to bé involved somehow.

 

I agree, faecal transplants, to me, are more topical and will wash away because whatever produces the microbiome composition in the intestines will just keep pumping out an altered composition and the walls will keep returning to the altered state.

We need to find out what is going on in the 'production system that manufactures the microbiome'. Something has been altered, blocked or is producing too much/too little of something in the manufacturing process.

I have a different area of microbiome change, not the gut, but wouldn't be surprised if the same thing that happened to me is affecting the gut in some PwME.

 

yes, me too. but im tired. much so. since all times.

im wondering, if babiturates like Thiopental could break that trap.

or perhaps less likely something like anti-benzo flumazenil
just cant imagine that there is no way out anymore.
shouldnt be possible such a thing...?

i dont understand this, but would just think, something that ousts the tryptophan in the cells, a more competetive substrate... perhaps a barbiturate or so

 

IN 2015
http://simmaronresearch.com/2015/03/
THE Pathway???
IFN-y also accelerates tryptophan degradation by activating the indoleamine-2,3 deoxygenase enzyme in the kynurenine pathway – Mady Hornig’s favorite pathway. That pathway produces neurotoxic substances that increase production of the excitatory neurotransmitter glutamate that some researchers believe is in play in both fibromyalgia and ME/CFS. Andrew Miller of Emory University has earmarked the kynurenine pathway in ME/CFS.

Mady was into it about trypofane,

Edit, kynurenine is transformed to kynurenine acid in the muscles, maybe poeple whit ME cant transforme the kynurenine to the harmless kynurenine acid??

 

i have access to two things:
1) an exercise incline track, lasting a couple of hours
2) leg muscles quickly shutting down to nonfunctional

next time, i will take a "gut abx" in between and see what will change.
i would think, it could help to reduce lactate issues.

could there be any other "self-tests" to narrow down on things regarding muscles ?

anything topical, anything to take... ?
breathing oxygen, breathing co2...
what ?

 

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6381042/

Published online 2019 Feb 13.
Suicide and Microglia: Recent Findings and Future Perspectives Based on Human Studies
Hisaomi Suzuki,1,† Masahiro Ohgidani,2,† Nobuki Kuwano,2 Fabrice Chrétien,3,4Geoffroy Lorin de la Grandmaison,5 Mitsumoto Onaya,1 Itaru Tominaga,1 Daiki Setoyama,6 Dongchon Kang,6Masaru Mimura,7 Shigenobu Kanba,2 and Takahiro A. Kato2,*

 

Talk by @RDP from the Emerge symposium titled "Metabolic Traps in ME/CFS", https://mecfsconference.org.au/videos/robert-phair/

 

Comment from Cort in one of his recent blogs on the updated thinking on the metabolic trap:

https://www.healthrising.org/blog/2019/05/07/threading-the-needle-nanoneedle-scores-big-in-first-me-cfs-test/

 

On PR Phair mentions that he has submitted a manuscript on the metabolic trap to a journal. If this is accepted, it might provide a starting point for pharma companies to begin some type of drug discovery.

On the more pessimistic side, I’m pretty sure Phair et al. don’t really have any idea how to unstick the trap.

 

Maybe it also depends on what triggers the trap in the first place. If the trap itself is a downstream effect of something else, and if that something else still still persists, then they might still be looking in the wrong place - at a knock-on effect rather than the root cause. But fingers crossed.

 

Really only stating the obvious here; I agree with your comment. I.e. the genetic data would need to be from people who tested positive using a biomedical diagnostic test e.g. the Raman spectroscopy test which measures (high) intracellular phenylalanine (Kara Morten, Cara Thomas and others) or nano-needle ---.


ME Action are lobbying for funding for the development of a diagnostic test and treatments https://www.meaction.net/…/announcing-millionsmissing-2019…/

 

Just wanted to drop in a note that I made from the recent IiME conference when Ron was talking about the metabolic trap.

 

@Andy what does that mean 'too high an error rate' if they haven't been able to disprove the theory. It seems contradictory. Is he still optimistic about trap?

 

That the data that they have that supports the trap theory is too imprecise for his liking, is my assumption. I'm just reporting what he said to us all as part of his presentation.

 

not shooting the messenger, but that's not what he said in this quick update last month

https://www.youtube.com/watch?v=0qYBQAiekPk

 

Well, like I said, that is my guess from what he said at IiME - I'm happy for my guess to be wrong but I can't explain why there may be a difference, if there is, between what he may have said in the video and at the conference.

 

That ties in with other presentations/posts by him and Robert Phair - culture material that everyone uses had a variable amount of tryptophan, Mass Spectometer not precise enough, PBMC's too variable - now narrowed testing to dentritic cells. However 66 out of 66 patients who have given blood samples having IDO2 damaging/loss of function mutations seems to be significant.
https://twitter.com/user/status/1137443236170141696

 

Speculation! I don't necessarily think this is a problem. Another way to maintain a stable disease state [i.e. where cells switch from using glucose, for energy production, to amino acids] would be to maintain the input signal - i.e. the exosome signalling. The fact that those with a defective IDO2 [or tyrosine] gene are worse is inherent in Ron's (wise) selection of very ill people.