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

[Judee]

It's hard because I don't have one medical or scientific person's theory I can name. I just think it is infectious in nature, though the type of infection (viral, bacterial, parasitic, or even yeast/mold or several of these together) can vary for each person.

Sorry. I don't know how to be more specific than that.

 

[Art Vandelay]

It's hard because I don't have one medical or scientific person's theory I can name. I just think it is infectious in nature, though the type of infection (viral, bacterial, parasitic, or even yeast/mold or several of these together) can vary for each person.

I agree. My view is that it's due to chronic infection(s).

I think VanElzakker is on the right track but the reality is more complicated than his hypothesis.

 

[Imse]

I voted none, because I have a feeling that all of the mentioned hypothesises are more a result of the real cause, whatever that is.

I've lived with ME for more than 25 years and I have seen hypothesises and cures come and go, but I do believe one day the cause will be found and everything will bring sense.

 

[BrightCandle]

Given how most of these have things we can do something towards treating and yet no treatment has shown any universality so far I think they are probably all wrong and arent root causes.

 

[sometexan84]

I voted none, because I have a feeling that all of the mentioned hypothesises are more a result of the real cause, whatever that is.

Given how most of these have things we can do something towards treating and yet no treatment has shown any universality so far I think they are probably all wrong and arent root causes.

Those are solid observations. I think many of these hypotheses are being explored in an effort to treat ME/CFS.

Infection(s) + ?????? = ME/CFS (where the ?????? might be treatable)

And the infections play a role in every single one of these I believe....
If one pans out, there could be treatment that doesn't involve anti-virals

IDO Metabolic Trap
EBV can inhibit IDO induction/production through increased production of (TNF-α) and (IL-6).

B2 adrenergic receptor dysfunction
This has links w/ POTS. POTS, often linked to viral trigger and ensuing autoimmunity.

Cell Danger Response
The whole idea here surrounds viruses, bacteria, fungi, and parasites

Ken Lassesen's "gut" model
This guy suggests gut dysbiosis leads to CFS symptoms. What causes that? Bacterial and viral infections.

Mackay-Tate hypothalamus hypothesis
Dysfunction of paraventricular nucleus, in the hypothalamus. Possible cause? Epstein–Barr virus

Methylation cycle
This one suggest it's the CAUSE of viral and intracellular bacterial reactivation (EBV, CMV, HHV-6, etc)

Nitric oxide hypothesis (NO/ONOO cycle)
Says as much in the description I'd posted...
Viral or bacterial infection induces one or more cytokines that lead to increased nitric oxide levels, which react with superoxide radicals to generate the potent oxidant peroxynitrite

Nitrogen metabolism
hmm... this one's tricky. But this would involve the increase in oxidative (and nitrosative) stress, typical in CFS. Bacterial and viral infection are linked to this. Or maybe the infections lead to increased cytokines that lead to altered nitrogen metabolism.

Omega 3 fatty acid
Caused by "low grade viral infection"

RCCX Theory
Suggests the gene mutations can lead to immune dysregulation, leading to chronic viral infections.

Vagus Nerve Hypothesis
Again, it's in the description....
In some individuals, the symptoms of chronic fatigue syndrome (CFS) are caused by an infection in or around the vagus nerve

Viral Cardiomyopathy
Again, in description...
CFS is a persistent nonpermissive herpes virus infection of the heart

 

[sometexan84]

Ken Lassesen's "gut" model (Ken Lassesen)
Ken's website CFS Remission
CFS is caused by a stable dysfunction of the gut microbiome

https://soundcloud.com/user-306234208%2Fep-49-interview-ken-lassesen-using-ai-to-improve-the-gut-microbiome

 

[xebex]

@sometexan84 great summary!

because there are so many theories and so many trials that show so many “seperate” disfunctions I truly believe that genetic susceptibility with viral trigger creates one or more of these downstream effects/theories. The reason it’s so hard to treat is because most people have more than one thing going on.

 

[sometexan84]

BTW, regarding Ken Lassesen's "gut" model...

I've stumbled on his website here and there - https://cfsremission.com/. But I recommend checking it out. I spent more time on his site today, and he has some good info.

He's had CFS 4 times, and every time put it into remission w/ microbiome alterations.

If nothing else, skim through this post: So which theory of ME/CFS? He says that his microbiome model can explain all the various ME/CFS conditions and symptoms.

I'm not saying it's the #1 hypothesis, but I do suggest checking it out.

 

[Abrin]

I guess it can be overwhelming to see a large list of ME/CFS hypotheses all at once. For patients who have had ME/CFS for 10 or 20 years or longer, these hypotheses would have appeared one by one, when they were first published. At the time they are first proposed, you get lot of discussion about them on Phoenix Rising, and they become the interesting topic of the moment, so you learn about them via the discussion.

This whole post has definitely been a strange walk down memory lane for me. (Well, at least for the parts of my memory that are still working! ) How strange it is now to look back to see how much has changed over the decades when it comes to ME/CFS and yet how much has still stayed the same.

 

[Krokus]

I was given a fluoroquinolone. At that time I had no more an infection. From that day on I developed ME/CFS connected with many food and chemical sensitivities. Because I spent a long time in the quinolone scene, I noticed I was not the only one developing it after taking that kind of medication. Because through its own mechanism of inhibiting the GABA receptors and activating the NMDA receptor it fits into the NO ONOO cycle (Pall).
In addition I have several autoantibodies (cell trend)
I assume there are many different starting points but farther down there are likely only a few routs like the inflammation cascades.
And there may be subgroups in our ME/CFS community.
I hope that further research will find out

 

[Wishful]

to generate the potent oxidant peroxynitrite

I consider that hypothesis very likely wrong, since peroxynitrite scavengers make my ME symptoms much worse.

 

[bertiedog]

I am currently impressed by the ongoing work on Covid and do wonder if something similar has caused ME/CFS in a subset of people.

The hypothesis is that the original virus changes many aspects of our body's essential functions so that even when it has gone patients are left with many symptoms affecting different parts of their body. The symptoms are varied and individual and devastating to many younger people who were extremely fit prior to Covid.

What particularly interested me was that I have heard many of the Long Covid patients report they have developed what sounds like POTS let alone extreme fatigue. Many of them feel as if they are getting better and then have massive relapses and this is how I was at the beginning of my ME journey 20 years ago even though the original 2 weeks of flu took place in 1979 and changed my nervous system never to really recover "normal" function. I did recover a degree of energy but the severe vertigo attacks and migraines still plague me now. Actually thankfully I don't get vertigo anymore, occasional dizziness has replaced that but I do get severe almost daily migraines/headaches.

Of course it is extremely frustrating to watch videos of so many scientists with explanations of their research which always to my non scientific brain sound reasonable but inevitable these all seem to fall by the wayside when their research isn't confirmed by fellow scientists in further trials.

I am very hopeful that the work of so many scientists throughout the world will shed light on what could be going on in ME/CFS through their work on Long Covid. It's just that time is rather running out for me personally as I will be 73 next March but it would be wonderful for a real breakthrough to happen soon for all the younger people whose lives are so horribly changed when they develop ME.

Pam

 

[Rufous McKinney]

it would be wonderful for a real breakthrough to happen soon for all the younger people whose lives are so horribly changed when they develop ME.

yeah...understood...I'm 67 and this has been the saga of a lifetime.

o that even when it has gone patients are left with many symptoms affecting different parts of their body. T

I think we don' t yet know: the virus is all gone. Its potentially parked in some tissue someplace. I think they found it in autopsied brains...

This need for biopsied tissue is a huge deal with the studies.

 

[Krokus]

@ Wishful
with which ONOO scavanger did you had problems?

 

[Wishful]

with which ONOO scavanger did you had problems?

Cinnamon, resveratrol, rosemary, and a couple of other herbs or spices that I can't remember offhand. They all seemed to trigger the same increase in symptoms in a dose-dependent manner. Why should reducing ONOO- make my symptoms worse? One hypothesis is that my symptoms are mostly from kynurenines, and ONOO- is what turns IDO off, so reducing that should increase TRP -> KYN catalysis.

 

[sometexan84]

One hypothesis is that my symptoms are mostly from kynurenines, and ONOO- is what turns IDO off, so reducing that should increase TRP -> KYN catalysis.

Actually, I believe it's the other way around. That the symptoms come from Tryptophan being too high, and Kynurenine being too low. Due to the IDO impairments. That's why the trial is based on additional Kynurenine supplementation.

The OMF research center in Montreal is looking into increased thrombospondin-1 (TSP-1) levels, which might also be a result of the IDO2 metabolic trap.

 

[Davsey27]

What if elements of combinations of those theories are going on at once.Seems to make things trickier.Would be nice if a chunk of funding that went to space programs went to me/cfs as well as other health conditions that may be difficult to treat

 

[Rufous McKinney]

That's why the trial is based on additional Kynurenine supplementation.

Yes- and so Where is Some Kynurinine? Can it be obtained?

 

[sometexan84]

Yes- and so Where is Some Kynurinine? Can it be obtained?

hahaha
Well, I mean, the trial isn't over as far as I know. And they did warn against people going out and using this as a treatment before they've tested it out.

 

[Judee]

That the symptoms come from Tryptophan being too high, and Kynurenine being too low. Due to the IDO impairments.

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