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Harvard ME/CFS Collaboration Symposium June 8th 2019
- Thread starter Alvin
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Harvard Collaboration Research Presentations Now Available
Recordings of individual presentations from the OMF-funded Inaugural Harvard ME/CFS Collaboration Symposium "Finding Clarity" Community Day are now available. Please take the time to view the recordings here.
Symposium presentations included a clinician panel featuring Dr. Amel Karaa, Dr. Anthony Komaroff, and Dr. Donna Felsenstein and individual presentations by Dr. Michael VanElzakker, Dr. Ron Davis, Dr. Maureen Hanson, and Dr. Wenzhong Xiao. Introductory, overview and summary remarks were made by OMF Founder & CEO/President, Linda Tannenbaum and Dr. Ron Tompkins. View all recordings here.
For your reference, the symposium agenda and speaker bios are available here.
A comprehensive symposium summary, written by Dr. Chris Armstrong, is availablehere: The ME/CFS Harvard Collaboration building momentum.
Harvard Collaboration Research Presentations Now Available
Recordings of individual presentations from the OMF-funded Inaugural Harvard ME/CFS Collaboration Symposium "Finding Clarity" Community Day are now available. Please take the time to view the recordings here.
Symposium presentations included a clinician panel featuring Dr. Amel Karaa, Dr. Anthony Komaroff, and Dr. Donna Felsenstein and individual presentations by Dr. Michael VanElzakker, Dr. Ron Davis, Dr. Maureen Hanson, and Dr. Wenzhong Xiao. Introductory, overview and summary remarks were made by OMF Founder & CEO/President, Linda Tannenbaum and Dr. Ron Tompkins. View all recordings here.
For your reference, the symposium agenda and speaker bios are available here.
A comprehensive symposium summary, written by Dr. Chris Armstrong, is availablehere: The ME/CFS Harvard Collaboration building momentum.
rvallee
Senior Member (Voting Rights)
I don't know if they're limited recordings but I very much like the shortness of the presentations that are published.
I can handle 10-25 min, usually anyway. Multiple presentations that go for 1h each is just too much content to go through. This right here is a good model and the audio quality is excellent, always a plus.
I can handle 10-25 min, usually anyway. Multiple presentations that go for 1h each is just too much content to go through. This right here is a good model and the audio quality is excellent, always a plus.
Forbin
Senior Member (Voting Rights)
It was interesting to see Dr. Davis go over the "metabolic trap" again.
If I have this right...
IDO1 converts L-Tryptophan into L-Kynurenine in the cell. If there is too much L-Tryptophan in the cell, IDO1 gradually shuts down and the conversion ceases. If nothing intervenes, L-Tryptophan remains high and IDO1 would remain inhibited ("the trap"). L-Kynurenine would cease to be created.
However, in this situation IDO2 comes into play and takes over converting high levels of L-Tryptophan into L-Kynurenine. I assume this would keep up until the high levels of L-Tryptophan dropped back to where IDO1 could once again deal with them.
The scenario where IDO2 comes to the rescue is apparently very rare. So rare that evolution seems to be failing to "conserve" IDO2.
Apparently, IDO2 is damaged/non-functional in 75% of the population. This is obviously a high percentage, but Dr. Davis says IDO2 is damaged/non-functional in 100% of the 66 ME/CFS patients they've tested (20 of them severe).
So "broken" IDO2 may be a genetic predisposition for falling into a "metabolic trap," but only in the very rare circumstance where L-Tryptophan is higher than IDO1 can deal with.
To me, this begs the question, "What's conditions could be causing the high L-Tryptophan in the first place, and can they be associated with commonly ascribed ME/CFS triggers like severe infections?" In this scenario, a high level of L-Tryptophan seems to be the ultimate "trigger," but what are its precursors?
If I have this right...
IDO1 converts L-Tryptophan into L-Kynurenine in the cell. If there is too much L-Tryptophan in the cell, IDO1 gradually shuts down and the conversion ceases. If nothing intervenes, L-Tryptophan remains high and IDO1 would remain inhibited ("the trap"). L-Kynurenine would cease to be created.
However, in this situation IDO2 comes into play and takes over converting high levels of L-Tryptophan into L-Kynurenine. I assume this would keep up until the high levels of L-Tryptophan dropped back to where IDO1 could once again deal with them.
The scenario where IDO2 comes to the rescue is apparently very rare. So rare that evolution seems to be failing to "conserve" IDO2.
Apparently, IDO2 is damaged/non-functional in 75% of the population. This is obviously a high percentage, but Dr. Davis says IDO2 is damaged/non-functional in 100% of the 66 ME/CFS patients they've tested (20 of them severe).
So "broken" IDO2 may be a genetic predisposition for falling into a "metabolic trap," but only in the very rare circumstance where L-Tryptophan is higher than IDO1 can deal with.
To me, this begs the question, "What's conditions could be causing the high L-Tryptophan in the first place, and can they be associated with commonly ascribed ME/CFS triggers like severe infections?" In this scenario, a high level of L-Tryptophan seems to be the ultimate "trigger," but what are its precursors?
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