Too many ME/CFS hypotheses! Where do you lean? (POLL)

[RobeAnJa]

I saw an interesting recovery story in a Facebook group. Man with ME for 10+ years. Homebound since 2016 reported full recovery/remission (working full time, no symptoms) with treatment: Valcyte, Ritonavir and Otezla/Apremilast. What theory could his doctor have had for this treatment?

 

[roller]

changed my vote
with covid some things happened (again) i didnt have in years plus some other odd things
...when looking up ACE+bradykinin (the covid culprits) which impressingly might explain that... i found, they are what scheibenbogen actually proposes for mecfs...
(hope i dont totally misunderstand this document
https://www.sciencedirect.com/science/article/pii/S1568997220300823 )

im wondering, if covid now proves that scheibenbogen/wirth were right?

 

[Wishful]

Actually, I believe it's the other way around. That the symptoms come from Tryptophan being too high, and Kynurenine being too low.

That's one hypothesis, and I consider it a very narrow view type of hypothesis; it makes some logical sense when looking at a single cell, but isn't based on whole-body observations. It doesn't match my observations of my ME. My symptoms definitely increase when TRP increases in my brain, and also when IFN-g increases, which should increase IDO.

I presently seem to be suffering from some sort of immune activation event, and 20 minutes after ingesting quickly-digested carbs, my symptoms flare up, which I consider to be due to insulin response increasing TRP transport into my brain. I'm considering taking part of a tryptophan tablet to see what happens, but those tablets are around 15 years old, so I'm not sure if it's still TRP (or maybe some toxic breakdown product). I think it's the TRP content in meat that's been bothering me lately.

 

[sometexan84]

Have you seen @kurt's series of posts on high tryptophan:
https://forums.phoenixrising.me/blo...complex-fungal-intolerance-introduction.2668/

I had not. I went though it now though, thanks. It's definitely interesting, and well-documented (like all his stuff).

EDIT - my "like all his stuff" comment above might sound confusing. I thought this was "Cort" (Johnson), but instead it's "Kurt" and I don't know who that is.

While I can't say I buy into the fungal intolerance theory (mostly because it doesn't match up well with my tests/symptoms/conditions), I DO believe that fungal and bacterial infections have been downplayed. I actually just got my microbiome test kit from Thryve and I'm excited to get my results back.

At any rate, I hope he's not right, cause that would be a major curveball in my treatment approach.

 

[sometexan84]

changed my vote
with covid some things happened (again) i didnt have in years plus some other odd things
...when looking up ACE+bradykinin (the covid culprits) which impressingly might explain that... i found, they are what scheibenbogen actually proposes for mecfs...
(hope i dont totally misunderstand this document
https://www.sciencedirect.com/science/article/pii/S1568997220300823 )

im wondering, if covid now proves that scheibenbogen/wirth were right?

It appears to be a solid idea and w/ proven treatment. Too bad it costs $20,000

 

[roller]

haha... how many thousands of euros did i pay for some idiot blood test with same even more idiot 60 minute blahblah around?
if $20.000 had kept me in life and somewhere near a "workforce" i would have happily paid.

 

[Wishful]

@sometexan84 , I skimmed the bradykinin paper, and didn't get the feeling that it applied to my ME. I noticed that they kept saying "a subset of ME", which to me suggests a downstream effect of ME. Various other bits of it caught my attention for not fitting my ME. I got the feeling that they'd found an abnormal measurement on a cellular level, and put effort into creating a theory which they then fit whatever ME symptoms could possibly be explained by it, which isn't all that difficult, since ME has so many different symptoms and patterns of responses.

 

[phillybadboy]

I have the only correct explanation , this is my own guess , I would call it aerobic glycolysis energy production in chronic fatigue , muscle in cfs patients have higher levels of oxidative stress , they have an upregulated antioxidant system , they have a diversion of glucose into the pentose phosphate pathway . they have a higher than normal expression of PKM2 and lower activity of p53 . lowers levels of p53 activity leads to less atp production from oxidative phosphorylation . so when there is time for a need in atp (during physical activity ) they use aerobic glycolysis to get their atp, leading to higher than normal lactate levels

 

[sometexan84]

haha... how many thousands of euros did i pay for some idiot blood test with same even more idiot 60 minute blahblah around?
if $20.000 had kept me in life and somewhere near a "workforce" i would have happily paid.

You should get tested for elevated ß2 adrenergic receptor (ß2AdR) autoantibodies.

Some have had symptom relief lasting 6-12 months after Immunoadsorption (IA). They appear to still be tinkering w/ their IA treatment to make it last longer....

Immunoadsorption to remove ß2 adrenergic receptor antibodies in Chronic Fatigue Syndrome CFS/ME

Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: Efficacy of Repeat Immunoadsorption