What possible cure/treatment/research excites you the most?

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hunter1899

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The trial doesn’t specifically mention fatigue as being hopefully fixed. Is that just semantics or is this really just focused on headaches and memory?

Otherwise it does sound interesting. Do we know when it’s supposed to be completed?
 
valentinelynx

valentinelynx

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The percent of ME/CFS patients turning up positive for CCI/AAI is truly astounding. The poll on this forum (see "Tracking CCI / AAI MRI & Treatment outcomes" under "Forums>Comorbid Conditions / Differential Diagnoses>Comorbid Conditions>Connective Tissue Disorders: EDS, CCI" now has 93 respondents, and continues to run 75% positive for "I have been tested for CCI / AAI / Chiari / Spinal Stenosis with specific scans and tested - Positive".

To me this suggests strongly that even for ME/CFS patients who don't find a clear spinal cause of their symptoms, something is probably going on in the brainstem. There a number of published articles on brainstem abnormalities in ME/CFS. See Brainstem-MEPedia for some references.
 
sometexan84

sometexan84

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godlovesatrier

godlovesatrier

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I guess all the main root cause analyses are interesting. CDR theory does interest me a lot, even if it sounds non specific and maybe a bit of a stretch. I find the sumarin treatment theory very interesting too.

Like some others I am not sure mito anti oxidant therapies will work as intended but they might for a subset.

Metabolic trap trial is very interesting too. I'm just hoping each one will get its biomarker test so that the relevant subset for each can be assigned the correct treatment protocol.
 
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hunter1899

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I’m still learning so a lot of this is Greek to me. Are these actually close to being real treatments or one of those breakthroughs that take decades to become something real and usable. I understand this stuff is extremely difficult, just trying to understand better.
 
sometexan84

sometexan84

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hunter1899 said:
I’m still learning so a lot of this is Greek to me. Are these actually close to being real treatments or one of those breakthroughs that take decades to become something real and usable.
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The Metabolic trap theory isn't that difficult to understand really. They found 100% of ME/CFS patients share a genetic mutation. A gene called IDO2.

You can get into the complexities by looking into the metabolic trap, what it is, and about IDO2. But, they say the mutation IDO2, causes low kynurenine. So, they're basically doing a trial to give patients kynurenine, to see if that fixes symptoms from this genetic mutation and CFS as a whole.

All I know is, there seems to be a massive push for CFS, research, studies, a lot more people are into it these last few years. Seems like ME/CFS research and awareness as a whole have grown exponentially over the past few years. So one might think we are going to be to a cure sooner rather than later.
 
Treeman

Treeman

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sometexan84 said:
The Metabolic trap theory isn't that difficult to understand really. They found 100% of ME/CFS patients share a genetic mutation. A gene called IDO2.
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Is it that people also have the mutation but don't have ME/CFS? This article is interesting, it say's "Accumulating evidence indicates that IDO2 acts as a pro-inflammatory mediator of autoimmunity" so it may be just down to the immune system not functioning correctly?

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5119657/
Abstract
Indoleamine 2,3-dioxygenase 2 (IDO2), a homolog of the better-studied tryptophan-catabolizing enzyme IDO1, is an immunomodulatory molecule with potential effects on various diseases including cancer and autoimmunity. Here, we review what is known about the direct connections between IDO2 and immune function, particularly in relationship to autoimmune inflammatory disorders such as rheumatoid arthritis and lupus. Accumulating evidence indicates that IDO2 acts as a pro-inflammatory mediator of autoimmunity, with a functional phenotype distinct from IDO1. IDO2 is expressed in antigen-presenting cells, including B cells and dendritic cells, but affects inflammatory responses in the autoimmune context specifically by acting in B cells to modulate T cell help in multiple model systems. Given that expression of IDO2 can lead to exacerbation of inflammatory responses, IDO2 should be considered a potential therapeutic target for autoimmune disorders.
 
sometexan84

sometexan84

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Treeman said:
But that was just the population in the study, "data of 20 severely ill patients". It maybe that they have no bearing on the rest of the ME/CFS community and/or just a proportion, a subset?
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That's true, 20 patients is a small number. They might have chosen severely ill patients for the study based on the idea that a severely ill patient could be more likely to produce abnormal results. Or rather, more obvious and apparent abnormal results.

It is definitely possible this will have no bearing on non-severe ME/CFS subsets. It's also possible that this theory will be debunked in the future and/or this treatment trial will fail. I guess we'll have to wait and see.
 
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