MEAction 2021 MECFS researchers video with R Davis,Prusty

https://www.youtube.com/watch?v=ul1haxH_7HI

 

I’d be thankful for anyone writing the salient points of this presentation

 

I've done a transcript of Dr. Bhupesh Prusty's interview, using the subtitles from Youtube.

Main take-aways for me were that he received two grants for these two projects:

1. A two-year project, funded by ME Research UK with ~270,000 GBP, with a focus on finding "autoantibodies that can target mitochondria for dysfunction"

2. A three-year project, funded by Amar Foundation (US) with 900,000 US$, with a focus on a "unique experimental approach" to "understand long-covid and the relationship of long-covid with ME/CFS"

According to Dr. Prusty, science is "on the right path" and he suspects some exciting developments in the next 3-5 years.

 

Thanks so much for the transcription, Lisa.

Prusty seems like a very nice, genuine guy and it's great that he is getting what appears to be sizable funding for his research.

It is also nice, I have to say, to see him give an estimation of progress without falling into the "right around the corner" trap. Like, I'm not happy to hear that he isn't on the verge of some imminent breakthrough, but at least I get the sense that he is giving his honest opinion.

 

And hoe long ago did Lipkin say pretty much the same thing?

The two things are not necessarily mutually exclusive. And perhaps this view makes the funders reluctant to give Ron any funding, if they can't be confident he will publish anything why give him him public money?

Exactly. If OMF's efforts and results remain outside of the usual way of distributing scientific information then that impedes the global effort to figure out ME.

ETA: deleted unnecessary word.

 

The important caveat that Lipkin included in his statement was that enough funding was provided. This still doesn't seem to be the case.

 

If nothing is published, most drugs cannot be prescribed off-label here in Canada. No publication, no evidence the drug works, drug is not covered.

if there is no publication, a particular test would not be covered, such as a diagnostic test.

re: doctor focusing on making patients better, there is an issue with liability in prescribing off-label. Then family doctors will usually not venture deep down into cell biology.

i worry that Dr Davis lacks understanding of how the health care systems work. Most patients do not have access to the privileges that they have from workplace, drs, connections, etc.

edit to add: no publication also means our disease remains underground, underfunded and left behind

 

Then, in my opinion, he should be making that clear, because otherwise people will understandably take it as OMF research policy, considering who he is.

 

I find this idea of not publishing your research - especially if you say you have significant-sounding findings - to be impractical and unscientific. It is self-sabotage, really. I am sure it's just a question of time priorities, but OMF needs to reconsider its strategy both in terms of the practical matter of advancing research understanding, and the kinds of comments made in public which can easily be used against the effort more broadly.

It's also no good creating an evidence base for treatment if you don't publish it. I mean...?

 

He's offering what he has, but making it appear that it’s more than what it is. I would rather hear that they're making progress in treating symptoms than getting people's hopes up and continue to say "cure". I feel it diminishes the seriousness of this illness.

 

From the vast amount of research I've read over the years (unable to read much now) it's pretty standard to say that the scientists expect significant results in 5 years, presumably because it ensures ongoing funding. Often the science is rubbish. This doesn't sound particularly rubbishy though.

 

He is not saying don't publish your research. He is saying the effort should be on finding cures not generating publications. Modern academia emphasizes publishing whether or not the article/research is important. If the researcher is overly concerned with generating publications for tenure and promotion (which is time-consuming), then the less time that they will spend on the actual research itself.

 

Maybe the results from 23andme tests could be useful. I just checked my test results from about 10 years ago, and there were several results from different IDO2 SNPs. At that time many of us had the test, so if we could get the actual
rs number-s, and they were analyzed in the test, we could have quite a few results in a short time. Just an idea.

 

Transcript of the second part of the video (Interview with Ron Davis & Janet Dafoe)

ETA the transcript of the last interview with Prof. Sarah Tyson

 

Quite right. "Publish or perish" is a common turn of phrase in academia. Gotta meet your quota of peer-reviewed published papers or risk losing your job! These pressures have trickle-down effects from research risk adversity (negative results are hard to get published) to pro forma studies designed just to generate a bunch of data that can be transformed into fast papers. The science suffers, and much time (and money) is squandered. It's how the system is set up, unfortunately.

 

I could not agree more, and I hope this is done as soon as possible. It does not seem that difficult compared to the other research and funding challenges. Something on this IDO2 mutation would be really interesting and as you say would spur interest from others. This approach seems to silo the research unnecessarily, potentially slowing things down whereas the goal is presumably to speed it up by not prioritising writing up research. Targeted papers - not pointless, but informative, transparent, and designed to catalyze the process - seem worth doing.

 

They seem vested in the IDO2 metabolic trap hypothesis, maybe a little too much in my view. I still haven't learned why they decided to pick that particular gene and mutation out of the tens of thousands of other genes. Even if they only consider genes that could create a bistable system and metabolic trap, Phair has already mentioned there are several other candidates.

The other question is how it ties into the Abilify improvements, which seems hard to understand. If they believe that the metabolic trap is the cause of the disease and that Abilify improves patients, then you'd think Abilify would affect kynurenine or tryptophan pathways in some way, but everything we hear is that it primarily affects dopamine.

I also think they should publish more. Actually, this paper from Moreau et al. who collaborate with OMF is in the 99th percentile of all articles of similar age according to metrics, so clearly such articles can have a big impact.