Prusty talks about his upcoming research on a podcast

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Osaca

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Sizzle said:
Searched but haven't found anything that made sense
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Going by some of the other comments of the user it seems possible that it's a troll. The answer of Prusty regarding the role of Drp1 of course stays extremely relevant.
 
Rufous McKinney

Rufous McKinney

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13,489
Osaca said:
Finally, it was also part of a treatment that was partially successful https://sci-hub.se/https://doi.org/10.1016/j.mehy.2018.08.014 even though this treatment is not really confirmed and could be b.s. It was Frank Comhaire’s treatment with sodium dichloroacetate (DCA) to increase pyruvate dehydrogenase (PDH) which allegedly works well for some, but not for others.
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in Jan of 2020, I read a research paper from Japanese researchers regarding COVID (the new pandemic) and DCA was recommended as part of protocol. (remember, this is when we were starting to horde the toilet paper?) (and no masks existed?)

I bought three jars of DCA and it sits in my cabinet unopened.

If it turns out that the Cure..........and I never tried it cause it sort of SCARES me I seem to not be very good at experimenting.
 
Forummember9922

Forummember9922

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Osaca said:
  1. Prusty’s 2020 paper mentioned the down regulation of this protein.
  2. It has often / previously appeared in the ME/CFS literature (https://pubmed.ncbi.nlm.nih.gov/28018972/). Pyruvate dehydrogenase deficiency causes many problems including lactic acidosis, progressive neurological and neuromuscular degeneration and if it’s induced by a genetic mutation (not a reactivated virus) death during childhood https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4003492/. As such it is something that has been found before, but maybe only he was able to connect the dots as he mentioned in his interview?
  3. Furthermore, it’s stimulation reverses the induction of itaconate https://jlb.onlinelibrary.wiley.com/doi/full/10.1002/JLB.3MR0322-692RR.
  4. Finally, it was also part of a treatment that was partially successful https://sci-hub.se/https://doi.org/10.1016/j.mehy.2018.08.014 even though this treatment is not really confirmed and could be b.s. It was Frank Comhaire’s treatment with sodium dichloroacetate (DCA) to increase pyruvate dehydrogenase (PDH) which allegedly works well for some, but not for others.
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Seems worth a try and thank you for all this info I will try some DCA myself but for the sake of argument doesn't Prusty's magical mystery molecule require bone marrow involvement eh? I believe other therapeutic implications RE PDH would be ALA and Carnitine ? I hope we are not derailing too far :) Cool stuff
 
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Tsukareta

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The original 'CFS' epidemics or at least Lake Tahoe was partly caused by toxic mold behaving in an unusual way, corrupt doctors came in and tried to pin the blame solely on viruses when not every patient in the epidemic had elevated EBV, this was probably part of a wider agenda to put the worlds attention onto viruses for unknown reason. It is possible however that what most people with ME/CFS suffer is caused by virus with no involvement of mold, but if so I believe its likely a different disease that the original 'CFS' from Lake Tahoe, this is all explained by Erik Johnson. Its also possible that the onset of this process supposedly discovered by Prusty requires toxic mold exposure to create the precursor state required. One of the 'poster childs' of ME/CFS Jenn Brea actually turned out to have toxic mold as the root cause of their illness, which then lead to CCI and therefore MECFS symptoms. I think we should be cautious about going tunnel vision about viruses, as I initially had the standard presentation but 3 years into the illness I noticed strong reactions to a wooden building in the garden that had rapidly become a bit moldy due to water damage. 5 years + into the illness the mold specific symptoms started to appear and I got much worse, i'm notwdoing total mold avoiidnce and living in a tent and my more recent neurological symptoms have greatly improved, but still have many of the limitations I developed in recent months, though stabilized or slightly improved. Bear in mind what he says, this treatment is complex... whereas considering if mold is a factor is easier to do and test.
 
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annaloecher

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Forummember9922 said:
Maybe the ideas are outdated so forgive me if I am going back in time. C1Q is shown to be higher in CFS patients so that would not be the missing protein. I bring it up for thought because methods used to address c1q issues can be stem cells or bone marrow transplants and he mentioned bone marrow is a key factor. Some discussion on c1q was had on phoenixrising already when these findings came out.
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he doesn’t say C1q is high in MECFS patients. he has found high levels of anti-C1q autoantibodies which target C1q. therefore C1q is low in MECFS patients. he also mentions there is published research that exercise decreases C1q which could explain PEM.

honestly i think you‘re right and C1q is what he‘s talking about. it sure makes a lot of sense to me because C1q is somehow connected to bone marrow/stem cells and monocytes. i also read a study saying C1q deficiency in SLE is linked to interferon and JAK STAT activation which would form a connection to phair‘s hypothesis.
 
O

Osaca

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344
Forummember9922 said:
Seems worth a try and thank you for all this info I will try some DCA myself but for the sake of argument doesn't Prusty's magical mystery molecule require bone marrow involvement eh? I believe other therapeutic implications RE PDH would be ALA and Carnitine ? I hope we are not derailing too far :) Cool stuff
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To be honest I, myself, don't think it's PDH, C1q or any of the other things that have been mentioned here. But I think having the discussion is interesting and after all that is what Prusty wanted.
 
V

Vlad83

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55
Murph said:
He didn't give much away, but he does say this:
"the bone marrow is the key because the source of the cells is the bone marrow"
idk, maybe this is about a protein deficiency in platelets, or b-cells, or monocytes?
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He was saying that his HHV reactivation / mitochondrial breakdown model can explain all pathologies found in ME/CFS because this can occur in any cell. I think his mention of the bone marrow is simply speculation on the possible mechanism of how this may cause immune dysfunction. If HHV6 is reactivated in the bone marrow then immune cells that are produced there will be dysfunctional or there will not be enough of them produced.
 
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Tsukareta

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From what he said it sounds like it could be a protein thats produced by cells which originate in the bone marrow, but perhaps this protein could circulate and affect the whole body, or other parts of the immune system ? its going to feel like a long wait to find out what his paper says.
 
Belbyr

Belbyr

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Tsukareta said:
From what he said it sounds like it could be a protein thats produced by cells which originate in the bone marrow, but perhaps this protein could circulate and affect the whole body, or other parts of the immune system ? its going to feel like a long wait to find out what his paper says.
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I think he mentioned he would have a paper by the time he speaks on it in 2-3 weeks, or I could have been hearing things...
 
O

Oliver3

Senior Member
Messages
931
Tsukareta said:
The original 'CFS' epidemics or at least Lake Tahoe was partly caused by toxic mold behaving in an unusual way, corrupt doctors came in and tried to pin the blame solely on viruses when not every patient in the epidemic had elevated EBV, this was probably part of a wider agenda to put the worlds attention onto viruses for unknown reason. It is possible however that what most people with ME/CFS suffer is caused by virus with no involvement of mold, but if so I believe its likely a different disease that the original 'CFS' from Lake Tahoe, this is all explained by Erik Johnson. Its also possible that the onset of this process supposedly discovered by Prusty requires toxic mold exposure to create the precursor state required. One of the 'poster childs' of ME/CFS Jenn Brea actually turned out to have toxic mold as the root cause of their illness, which then lead to CCI and therefore MECFS symptoms. I think we should be cautious about going tunnel vision about viruses, as I initially had the standard presentation but 3 years into the illness I noticed strong reactions to a wooden building in the garden that had rapidly become a bit moldy due to water damage. 5 years + into the illness the mold specific symptoms started to appear and I got much worse, i'm notwdoing total mold avoiidnce and living in a tent and my more recent neurological symptoms have greatly improved, but still have many of the limitations I developed in recent months, though stabilized or slightly improved. Bear in mind what he says, this treatment is complex... whereas considering if mold is a factor is easier to do and test.
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How would you square up the similarities between long covid and mold?
 
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Oliver3

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931
Rufous McKinney said:
perhaps nobody has yet analyzed mold exposure in long covid victims.
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I'm not disputing it. Just asking the question. I'm sure mould plays a part for some. But is it the main cause
We've seen a novel virus go through the population and now there's an illness very similar to m.e. if not m.e.
I'm just genuinely curious as to thinking what would the connection be in this example
 
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Tsukareta

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150
I already considered that and its definitely a counterpoint to the idea that many CFS cases are caused by unrecognised possibly historic mold exposures, because the symptoms of LC seem to be different enough. Viruses are implicated in some of these mold associated illnesses though, I had new issues in 2020 and 2021 but I didn't start to get the really impactful new symptoms like degraded wrist joints until shortly after I had a bad virus in december of 2021 which gave me a 40c fever and I actually ended up going to hospital over it because I couldn't eat or drink initially which made me think maybe I had pancreatitis, it happened the day after drinking lots of alcohol and having a big campfire in the middle of winter ( my functioning level was relatively good for CFS person at that point ). In the Lake Tahoe incident there was a mystery 'chinese flu' which was blamed for causing the epidemic, then it changed to EBV re-activation because there was a new test which could detect it. The overarching theory is that exposure to some types of mold particularly stachybotrys weakens or disables the immune system which means that when you then have a virus it causes chronic disease, which doesn't seem too far out of line with what Prusty is sort of talking about. This is opposed to people who say that levels of mycotoxins in their body make them ill, or chronic inflammation caused by a sensitivity to the spores ( CIRS ). I can't test if I have CIRS because the very specific tests for it are not really available to the average person in the UK and I can't afford some private doctor.
 
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Osaca

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Sizzle

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