Prusty talks about his upcoming research on a podcast

[BrightCandle]

Ten people with ME/CFS in total or 10 severe, 10 mild, etc., do you recall ? 10 in total is an almost negiliable number.

About 10 of each of the 3 classifications, maybe only 5 health controls. That is assuming each dot in some of them is a person. Its not really a presentation of a study evaluating the value of Fibronectin, its more explatory research which came up with this surprising potential biomarker when they were trying to make sure the IgG and IgM results weren't actually implicating another protein that was captured in there causing the mitochondria fragmentation.

We can't view this as "Biomarker found and proven" research, its not what they were trying to determine.

 

[Consul]

Summary here

https://twitter.com/i/web/status/1656680666535194625

 

[Consul]

The thing i find odd about mitochondrial being the issue though is that the intramural study found no difference in energy metabolism in the metabolic chamber.

 

[Osaca]

About 10 of each of the 3 classifications, maybe only 5 health controls. That is assuming each dot in some of them is a person. Its not really a presentation of a study evaluating the value of Fibronectin, its more explatory research which came up with this surprising potential biomarker when they were trying to make sure the IgG and IgM results weren't actually implicating another protein that was captured in there causing the mitochondria fragmentation.

We can't view this as "Biomarker found and proven" research, its not what they were trying to determine.

I understand that. I was not trying to find out whether this was "Biomarker found and proven research", since that's in any case still a million miles off. I rather wanted to know if this was "throwing a dice and interpreting those results research", even though I do understand that unfortunately Prusty doesn't have access to much data (Hoping the German Biobank and especially more open source work will eventuall change that). Given this illness our data will a priori always be very problematic, throw into to that a lack of biobanks, of which the existing ones often use Fukunda or even psycholigal criterias for ME/CFS and you have a recipe for disaster.

 

[junkcrap50]

Do you think there should be a new thread that is about this presentation so that the info revealed in it is separate and new and not buried in page 9 or 10 of a thread?

 

[godlovesatrier]

"Fibronectin activates the CDR which causes microclots."

 

[BrightCandle]

A link to the presentation video, a random upload apparently a proper one coming at some point but this will get you the 22 minutes of presentation -

https://twitter.com/i/web/status/1656717544047214594

 

[Tsukareta]

How did other researcher miss the IgG / IgM pattern he describes ? they only measured IGG ? or technique was incorrect ?

 

[BrightCandle]

How did other researcher miss the IgG / IgM pattern he describes ? they only measured IGG ? or technique was incorrect ?

Or the patients. There has been a lot of dumb stuff around selection of patients and criteria. It was something another talk of the day got into by Jason Et el where getting severity and length of symptoms down is important to determining ME/CFS separately from Depression and other conditions with similar symptoms and my guess is a lot of groups are getting this wrong, often intentionally as the BPS cabal has often made the disease simply about fatigue.

 

[Osaca]

Regarding the Fibronection measurements:
HC vs. ME/CFS (AUC=0.665) = Poor discrimination
HC vs. severe ME/CFS (AUC=0.792) = Acceptable discrimination
Without a reasonable mechanism to describe this phenomenon, this seems insignificant (especially if you start accounting for Fibronection in other disease, i.e. larger HC cohorts) and like cherry-picking to obtain some favorable results in an environment with far too little data. Let's see what the paper entails, very much looking forward to that and further explanations in the upcoming talks.

 

[bthompsonjr1993]

I would caution anyone against allowing him to get your hopes up.

 

[Consul]

Well my understanding is that there are 3 proteins and together they might give good discrimination whereas 1 alone is a bit too weak. Also remember that in any mecfs patient cohort there is probably also a person or two that has parkinson or depression instead of mecfs so hard to get perfect discrimination i think. @Osaca

 

[Rufous McKinney]

moderate will improve

increasingly I feel my "moderate" state is by definition simply early severe.

I strongly suspect I am up in a chair FAR too much. That I should NOT be up as much as I am and it's just wearing me down further.

If I got anywhere at all, I simply want to fall over and collapse, and gravity can simply win.

 

[Tsukareta]

I don't think this is everything he has, didn't he say he wouldn't talk about the protein he thinks could be a biomarker in todays talk ? in general I don't feel that this is a case of the usual pet project that promises all the answers but leads nowhere, the whole thing seems like it could connect with what Ron Davis found about 'something in the blood' that was seemingly never followed up on fully for whatever reason.

 

[Osaca]

Well my understanding is that there are 3 proteins and together they might give good discrimination whereas 1 alone is a bit too weak. Also remember that in any mecfs patient cohort there is probably also a person or two that has parkinson or depression instead of me so hard to get perfect discrimination i think. @Osaca

Yes, we'll have to wait for the "missing protein" (I'm still keeping my hopes a bit up for this), the paper etc. before we draw any conclusions. However, from the data he presented today, 1 alone is not too weak, but even competely negligable at this point in time. You are absolutely right about what you are saying about the ME/CFS cohort (that's why longitudinal studies based on the Canadian consensus with subgroups are necessary), but the same also for the HC where undetected diseases can also be present. Furthermore if possible you need to include diseases in the HC as well. As an example you might otherwise just be detecting that some ME/CFS patients have diabetes or something else unrelated...

 

[Osaca]

I don't think this is everything he has, didn't he say he wouldn't talk about the protein he thinks could be a biomarker in todays talk ? in general I don't feel that this is a case of the usual pet project that promises all the answers but leads nowhere, the whole thing seems like it could connect with what Ron Davis found about 'something in the blood' that was seemingly never followed up on fully for whatever reason.

Unfortunately, Prusty's results of "he found something in the blood" which was the antiviral state and a significant finding even for other diseases, was also never followed up on. Were both of these results not reproducible?

 

[Consul]

Isnt the 2 other proteins Transferrin and alpha 2 macroglobulin or did i get that wrong.

 

[Osaca]

Isnt the 2 other proteins Transferrin and alpha 2 macroglobulin or did i get that wrong.

Those are the other 2 from the talk today. But from what he said he still found this missing biomarker protein which both of these aren't, nor is FN1 that, nor these 3 together.

 

[Consul]

Those are the other 2 from the talk today. But from what he said he still found this missing biomarker protein which both of these aren't, nor is FN1 that.

Okay. Im thinking that maybe low Transferrin could partly explain the low manganese in Ron Davis hair mineral samples. Quite a odd finding imo...

 

[Osaca]

Okay. Im thinking that maybe low Transferrin could partly explain the low manganese in Ron Davis hair mineral samples. Quite a odd finding imo...

Those results aren't (yet) published though are they? Why would low Transferrin only cause low manganese in the hair, but nowhere else? Furthermore a big chunk of Prusty's HC also have low Transferrin, do these also have low manganese in their hair? Without decent data or an explanation I'm unable to connect the two.