Has current research established cause of PEM

percyval577

Senior Member
Messages
404
Likes
440
Yes, and the OMF has come up with some findings in genes, there also has been findings by other researchers If I´m remembering right. Also here on the forum I think was some interesting poll or something like that, don´t know how reliable it would be. (Also an epigentic change from parents or grandparents would be thinkable, more difficult then to follow.)

A very interesting hint are the cfs outbreaks. Here 50% of people recover (as opposite to ten times less in endemic cases). Obviously there is some strength in outbreaks, therefore a lot of people got ill, but the genetic predisposition should be less imprortant. Also just therefore, probably, a lot of people recover.
So the urgent questions are:
-- which pathways could be disregulated by genetic predispositions? (this wont be an answere too easy, I guess)
-- which influences have helped 50% of epidemic cases to get out of the state?
This could be applied in a forced manner to some of the 95% of endemic cases and to some of the other 50% of epidemic cases, implicating:

The generel question is:
-- which pathway(s) would have gotten affected by the trigger? Maybe there are often two triggers (this also would be a good explanation for cfs outbreaks). In my case I know two triggers and the one pathway which has gotten altered, two times (with 25 years in between).

Then also:
-- why do we see outbreaks from enterovirus, but not from herpesvirus (if I believe what Hip recently said)?
-- why these triggers, so far known? What do they have in common? Herpesviruses will influences the arginine homeostasis to some extent (the levels in the blood during acute infection, I guess). What´s about enteroviruses? What´s about chemicals (the answeres get more difficult, I guess).


This must be looked at (next to the pem thing), what has become altered? What are the properties of the impact?
Then an influence by diet (maybe it is needed/helpful to produce extra mixtures) might well be a cure.
(I think this is in generel a new approach to some diseases, only one needed to know ...)

Sometimes I guess that the influence for reversing our infectional impact (and this probably will be the first influence needed) is to do something less to the body. It might be not conclusive:
-- An impact could take something out of the blood or tissue, resulting in counterrelease, with higher levels.
-- An impact could take something out of the blood or tissue, resulting in a deficiency for some time (only).
-- An impact could also add something to the blood or tissue for some time (only).

I think the question will not be if there is (in the chronic phase) too much or too less of something,
but if there will be needed a more or less unusual level of something
for reversing the impact.
 
Last edited:

Belbyr

Senior Member
Messages
364
Likes
765
Percy, could you post the OMF findings in the genetics of CFS or is this something yet to come out?
 

percyval577

Senior Member
Messages
404
Likes
440
@Belbyr, Ron Davis showed a list of geses they have found to be mutated in cfs when he presented four other findings in september 2018. It´s on youtube, here the thread leading to it:
https://forums.phoenixrising.me/threads/hear-ron-davis-iimec-13-presentation-video.61492/
It´s in the first third part somewhere.

Here a website by Simon McGrath about a mutation in a gene for collagen:
https://mecfsresearchreview.me/2018...emonstrates-an-inherited-component-to-me-cfs/
If I´m remembering right it was almost in 40% of sufferes found? Might be wrong, and can´t remember if this matches up with the finding Davis showed.
I am rather interested in it because making collagen should invovlve manganese, and I have a manganese (and arginine) issue.
 

percyval577

Senior Member
Messages
404
Likes
440
A third genrel key quesion should well be: Why hasn´t it been possible so far to establish an animal model for mecfs?
There are of course a lot of differnces, nevertheless a lot of human diseases have been made in animals.
One key difference might be the pyrmaidal system, though also monkeys have a great pyramidal system.
The key might be:

The human being is the onliest animal that sweats.

Dunstan et al 2017 Sex differences in amino acids lost via sweating ...
They also look at chronic fatique! and with success. So interesting will be:
Fluge et al 2016:
"Metabolic profiling indicates impaired pyruvate dehydr..." and then, it should be the other way round:
Tomas et al 2019:
"Mitochondrial complex activity in permeablilised cells of chronic ..." when there is no mt dysfunction.

There are four compounents in sweat:
electrolytes
amino acids
organic acids
urea

Here, a two hit theory of mecfs would suggest to look at such equations:

electrolyte x + amino acid y = signalling molecule (or whatever)


I have searched so far (there wont be too much known, I am afraid):
herpesviruses and coxiella burnetti are associated with arginine,
borrelia are associated with manganese
enterovirus 71 with some metals (electrolytes)

@hmnr asg I´ve read your post yesterday, maybe you are interested.
@Hip You are a mathmatician, a question could be: Why would a vaccination for hepatitisB comp. easliy trigger or even cause mecfs?
 
Last edited:

Wishful

Senior Member
Messages
1,222
Likes
1,712
Any vaccination triggers the immune system, and that seems to be enough to trigger ME if you're susceptible. I think it's quite possible that if a person who triggered on a vaccination had avoided the vaccination, they might instead have triggered on the next cold virus or bacteria to come along. I think that due to age, epigenetic changes or whatever, my body was simply ready to switch into the ME state, and the tetanus booster was just the first suitable trigger to occur.
 

Wishful

Senior Member
Messages
1,222
Likes
1,712
@Wishful I'm looking for articles that discuss how the immune system's response to an infection causes me/cfs. might you very kindly point me towards any? many thanks <3
Tough request. I can't recall any specific articles about that. I think it's mainly an observation that most people develop ME after some sort of immune activation event. There certainly is evidence that the immune system is involved in ME, and is also altered in ME. The immune system is also known to feed back on itself, so it seems quite reasonable for the immune system to somehow lock in to an abnormal state. I just don't recall any formal papers stating that hypothesis in proper medical terms, with specific cytokines or other biological pathways mentioned.

In my case, I'm pretty sure that t-cells were involved, since the first symptoms (soon after a tetanus booster) were a type-IV delayed food sensitivity, which involves t-cells. I did wonder why t-cells would be activated by a bacterial trigger, but I found: 'Tetanus toxoid (TT) is an antigen known to induce strong T cell specific immune responses in humans after vaccination.' So, it seems reasonable that the vaccination activated my t-cells, and my immune system got locked into an abnormal state. I had several temporary remissions in the first few months, so I think my immune system was borderline unstable, able to switch states due to external factors, but gradually got more biased against switching out of the abnormal state.

I'm pretty sure that other people have reported triggering on b-cell activation, so it seems that there are different ways for the immune system to trigger ME.