Bhupesh Prusty: "we are on a perfect path for identifying potential transferable factors in ME/CFS blood that can cause mito dysfunction..." GoFundMe

Rufous McKinney

Rufous McKinney

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xebex said:
like it! my vote is it's an undiscovered hormone. but i like the antibody idea too.
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Heh- maybe that is the BEST approach to fundraising. We create: the theories of ME...and we get Millions to VOTE and put in- say one dollar in their respective jars. If everybody put in one dollar- over the age of 18, we could acru- Millions.

Oh, but then we have to wait for: a winner to be revealed, via research (or Voodoo)
 
Rufous McKinney

Rufous McKinney

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xebex said:
:woot: that is genius! but yea your right, we have no idea when or if the answer will ever be drawn
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Since us ME victims so love: speculating on the theories...just seems like we could take advantage of this natural tendency for our egos to engage in the theories.

We would have- a mold jar, the EMF brigade....the its all the gut versus its all in your head! Or my vote- its all about collagen.
 
RYO

RYO

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ShepherdK said:
I think the transferrable factor ("something in the blood") is an antibody of some sort. I assumed this would have been closely studied, but it seems like novel antibodies are being discovered every couple of years. Antibodies would explain why some people recover (B-Cells vs long lived Plasma B-Cells), while others have the disease for years/indefinitely. There are also diseases that share many ME/CFS traits that are induced by mitochondrial auto-antibodies. If this is the case, then potentially the quickest way out would be rebooting the immune system entirely through an autologous stem cell transplant. Rituximab would only work in very early-stage patients, but identification is a challenge + Rituximab has serious side effects.

There are ways to control LPS introduced through the gut - I use NAC 500mg-1g daily during major probiotic and antibiotic regimens to handle the die-off response.
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I have often thought of autologous stem cell transplant as a potential treatment. I wonder if any of the Norwegian ME/CFS patients of Dr Fluge have undergone stem cell transplant.

In terms of connection to the gut, I was not thinking of LPS but instead MAIT cells as mentioned by Dr Unumatz.

However, I recall Dr Davis and others suggest exosomes as potential transferable factor. Hopefully more research in this area is forthcoming.
 
RYO

RYO

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@Rufous McKinney
I agree with both of your points.

It has yet to be elucidated how MAIT and TH17 cells are involved in immune perturbations in ME/CFS patients.

The question is how do you figure which cells are producing culprit exosomes and it’s contents.
 
Rufous McKinney

Rufous McKinney

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raghav said:
A drug exclusively for ME/CFS will take many years (see FDA approval).
However, as described in our text, Prusty and Naviaux think that there are
already drugs on the market that could help us. It is not yet possible to
say whether these drugs can cure.
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After reading about this potential senescent cell hypothesis which Dr. Prusty posted.....There is an excellent article on this topic in a recent Life Extention Publication and it includes discussion of plant-based Senolytics and has 19 references....

Life Extention Magazine Winter Edition 2019-2020...article page 8

https://www.lifeextension.com/magazine/2019/ss/combat-aging-by-removing-senescent-cells

I'd been hypothesizing that something about ME may relate to- too much cell death, apoptosis or something related to all that. So this is fascinating, as its somehow inter-related...inSTEAD of dying properly and being replaced, the cells are malingering...
 
Annikki

Annikki

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ShepherdK said:
CFSRemission is pretty legit - he just heavily subscribes to the "gut dysbiosis" theory of ME/CFS. I don't think he is wrong at all, however I don't believe he is correct either.

My theory on ME/CFS:
  1. Trigger Event (Viral, Bacterial, Fungal, etc)
    • EBV, CMV, VCV, HHV6, HHV7, Lymes, etc
    • Probably requires a severe or prolonged event to knock the body out of homeostasis.
  2. Negative Feedback Loop
    • Underlying genetic / environmental susceptibility
    • Immune metabolic changes leading to viral reactivations
    • Gut dysregulation / dysbiosis causing further inflammation and immune stress
    • Immune metabolic changes leading to hypersensitivity
    • Disrupting the negative feedback loop probably stops disease progression, however we don't know how to kick off a positive feedback loop in the other direction.
  3. Diseased Homeostasis
    • Body eventually reaches new homeostasis that represents a severe ME/CFS patient
    • Large effort to reset / reboot multiple systems to restore healthy homeostasis.
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I think there is good stuff on CFSRemission, it was just the idea in the article I dispute. I personally think gut dysbiosis isn't the cause of ME, since gut dysbiosis is a simple, isolated, problem and ME is a complex problem involving many systems in the body. I think gut dysbiosis is symptom as opposed a to cause of ME. Energy systems of the body malfunction in ME and gut bacteria don't play a role in these. Mitochondria, however, do indeed seem to be the logical culprits in ME symptoms. This gives me much faith in what Prusty et. al. are looking into.

I think it has to be a major problem causing ME; maybe viruses and or other equally devastating factors. I think the core problem in ME has side effects in other parts of the body, gut included. I've favored the idea a virus is involved (or bacterial like mycoplasma) because many CFS patients got CFS after getting sick with the flu or other illness. Something is likely hanging on the coat tails of a taxed immune system during the onset of CFS, something like virus or pathogen.

The cause of ME needs to be a pathogen to explain ME outbreaks in various towns and cities. As far as gut dysbiosis, any virus is likely to throw this out of whack. There are viruses which infect bacteria, too, though I'm not saying I at all think this is what happens in ME. I'm sharing this fact about viruses because I just saw this incredible documentary on viruses:
 
hmnr asg

hmnr asg

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Germany is one of the best places to get funded as a research scientist. Why has this person not been able to secure funds from the appropriate channels via his research lab (form the university that he is affiliated with)?

My first question to this person would be, did you apply for government research grants? if yes then why were you rejected? what is the response from their equivalent of NIH to his grant?

I would need to know these before I would give a penny to this person.

ps I donate money to OMF myself because of Ron Davis. Ron Davis is a world renowned scientist who has established his credibility a zillion times over. But who is this person?
 
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MonkeyMan

MonkeyMan

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Rufous McKinney said:
It seemed that patients wanted to help fund some immediate efforts, Dr. Prusty did not ask us to do it. At least thats the sense i got from the ...conversation. Maybe I'm wrong....
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That is my understanding as well. And in Robert Naviaux's latest newsletter, Dr Naviaux writes "Other exciting studies include a new collaboration with the brilliant virologist, Dr. Bhupesh Prusty at the University of Würzburg, Germany. Using a new, cell-based assay system, we are hot on the trail of both the identity and the biological control of the activity in ME/CFS blood that causes fatigue. This “fatigue factor” looks like it could be the same thing that coordinates the mitochondrial and metabolic features of the cell danger response (CDR) and inflammation 5 , changes impedance in the nanoneedle 10 , inhibits recovery from illness by blocking the healing cycle 9 , induces a dauer-like state 11 , and triggers collagen remodeling over time that can cause acquired forms of Ehlers Danlos-like syndromes. If successful, these studies will help fill in missing details in how suramin, copaxone, and elamipretide (SS31) might work to treat ME/CFS."

That is all the evidence I need that Dr Prusty is well worth our support.
 
P

perrier

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1,254
MonkeyMan said:
That is my understanding as well. And in Robert Naviaux's latest newsletter, Dr Naviaux writes "Other exciting studies include a new collaboration with the brilliant virologist, Dr. Bhupesh Prusty at the University of Würzburg, Germany. Using a new, cell-based assay system, we are hot on the trail of both the identity and the biological control of the activity in ME/CFS blood that causes fatigue. This “fatigue factor” looks like it could be the same thing that coordinates the mitochondrial and metabolic features of the cell danger response (CDR) and inflammation 5 , changes impedance in the nanoneedle 10 , inhibits recovery from illness by blocking the healing cycle 9 , induces a dauer-like state 11 , and triggers collagen remodeling over time that can cause acquired forms of Ehlers Danlos-like syndromes. If successful, these studies will help fill in missing details in how suramin, copaxone, and elamipretide (SS31) might work to treat ME/CFS."

That is all the evidence I need that Dr Prusty is well worth our support.
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Thanks Monkey Man. Is there any way you are able to post a link to Naviaux's newsletter, or how one might obtain it. Thanks.
 
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