Dr Karl Morten - UK researcher based at Oxford University

Can someone tell me who is funding Karl's work so far? And is there any indication of when he will know if his recent application for funding has been awarded? I haven't been able to watch clip..

 

If you view it on youtube, under the video there are three dots. If you click on them, you're given the option to view the transcript. If you skip to the end of the video, it will show the entire transcript, and it's possible to copy it. When copying it into a text file, it inserts a linebreak after every timestap. I made a textfile where these linebreaks have been removed (with search and replace that uses a regex to distinguish between linebreaks that follow digits and those that follow lettes).

 

Thanks! I'll see if I can process it further.

 

Can you clarify a bit on this? Did the Myhill test look positive or not? Or was it another mito test that had the positive results?

 

I couldn't quite make sense of what Dr Morten was saying about this in the video.

 

I've read the transcript and it seems a blood test didn't work, but another mito test did. It's not entirely clear at that point.

 

I couldn't even make that much sense out of it. I wonder if he was pointing at the slide or doing something else that would have made it clear to the audience. I thought he was referring to two blood tests where one did something and the other didn't but I couldn't tell which was the Acumen test.

 

I watched some parts of this presentation twice. My understanding was that his team and the Newcastle team followed the Accumen test method and could not reproduce their results - no difference between patient and control.

He said that blood starts to change as soon as you draw it and 24 hours later it is different to what it was at the time of the draw. Patients send Accumen blood overnight, so there is a 24 hour delay between draw and processing. If you run the test on 24 hour blood vs fresh blood you get different results.

He then said that Newcastle ran the Seahorse mito test and found differences. So yes the mitochondial energy cycle is affected, but they could not determine that by following the Accumen procedure.

 

I was very impressed by Dr. Karl Morten. He has 30 years of Mitochondria research experience. He decided to enter the ME/CFS field as he wants to "make a difference for patients" in this next stage of his career. Despite being fairly new to the field he is already well connected and has set up collaborations with other researchers and doctors.

He seems to think out of the box. He did a plasma swap experiment with healthy muscle cells and showed oxygen consumption is different when mixed with patient plasma vs healthy plasma.

So refreshing to see another researcher enter the field and share results before publication.

I wonder what the unknown metabolite is at the 47min time point????? It was also mentioned in the August ME association PDF

 

Does any of this tie in with Ron Davis' teams work? (ie serum test/mystery molecule etc).

As much of the OMF stuff is not published I wonder if Dr Morten has watched any of the OMF presentations? (he didn't pronounce Fluge right which makes me wonder if he has only read papers, but I could be wrong of course).

Is Ron Davis aware of Dr Mortens work? @Ben H

(my only concerns with the presentation : starting with a Crawley paper [I remember a lot of criticism when Ron Davis used the same paper in one of his interviews], also although he acknowledges 'GET' is a dirty word he suggests at the end that there might be a group of pwME who might benefit, and other therapies eg cold, acupuncture are also cited as possible therapies. Somewhere he also mentions use of the Chalder FQ, although again he acknowledges that some people have a problem with it.)

 

Phew! Managed to publish ahead of the Christmas break. He did catch us by surprise with the Acumen-test research results and by publicly announcing the MRC application. But it made for an even more interesting presentation I think.

https://www.meassociation.org.uk/20...disease-pathology-in-me-cfs-21-december-2018/

 

OMF /Ron Davis announced the something in the serum a couple of years ago. I think it’s a very important finding and glad researchers are trying to investigate further

I’m really pleased Karl Morten is looking now for a larger grant. My fear regarding the MRC is that 1.5 years after Stephen Holgate started talking about trying to get more MRC funds ( after ten years of no pressure on them for consistent funding until the field could function alone) they are still not committing. Are they going to instead grant to KM and £1.6m over 4 years as their “we are doing something rather than nothing to hold up but not nearly enough” which they seem to prefer with CFS.

 

I am hoping there will be some additional positive news from the MRC and NIHR regarding biomedical research funding for ME/CFS in the New Year following CMRC efforts. I can't say more for now, but you may well have been following the 'Bioresource' developments in the CMRC summary minutes that are publicly available and heard about things from Prof. Holgate at the CMRC conference etc.

I hope very much the application, when finalised, from Dr Morten's team does meet with success from the MRC. But I have had some little experience of the application process - I was a member of the MEGA PAG - and it can seem very arbitrary. However, the MRC keeps mentioning its highlight notice on ME/CFS research, so - touch wood - this application makes it through the vetting process and the CMRC application does as well.

If both do then 2019 really could be THE year for funding ME/CFS in the UK.

 

Thanks. I did realise and was going to do what I used to do when more active on the forums - back in the PR days - and produce a blow-by-blow transcript. Just didn't have time.

 

As patients obviously we aren’t kept very informed or involved and just have to wait for drops of information, it sounds like insiders already have some knowledge. I’m not really understanding what the CMRC application you talk of is, i thought initially there was going to be a request for a step up on incentivising research via a funding call from the MRC like Norway did, rather than a grant application for the big data study as it seems ? . I’ve not been especially enthused by MEGA which seems to have been CMRC sole focus, as I think it’s a long and winding road approach when I need targeted urgent research, including on severe ME frankly but others here might think it’s very good .
There’s only a paragraph in the minutes on this, maybe MEA members are given more info. ....


I cannot view the CMRC as heroes on funding when the charities and Holgate were all Together since 2007.

 

I'm pretty sure Ron is aware of Dr Morten. If not I'll be forwarding the research to him.

I think it's really good line of enquiry, particularly being UK research. Hopefully they will get the funding.

On another note the point @wigglethemouse makes is a really good one-the method in which the blood is collected is extremely important, and the discrepancies that arise from that can be major. Time before analysis, how it has been stored, heparin, edta or other agents in the tube etc. Massive differences.

Hopefully they'll be able to replicate once all of these are matched. That would be good.


B

 

Has everybody seen that the MEA kindly provided a link to the slides from the talk?

https://www.meassociation.org.uk/wp...uckland-Karl-Morten-Presentation-12.12.18.pdf

 

A comment on his results as they concern GET

He mentioned elsewhere that half the patients doing GET drop out, which could be a reference to this study.

The patients that complete 6 months of GET are probably not the ones that are significantly harmed by it.

It's also possible that activity displacement is taking place (I believe one study found this, and other studies of CBT/GET found no increased levels of activity). So GET might appear to be harmless (in some or many cases) because the patients are not actually increasing their activity levels.

 

In the mitochondrion signaling, many, many proteins and ions are involved - anywhere on that path, something can go wrong. There is signaling between the ER and the mitochondrion (via the MAM = mitochondrion associated membrane), whereby both lie in close proximity so that Ca signals from the ER can enter the mitochondrion. For example, if the Ca signal is somehow disrupted, pyruvate dehydrogenase gets more inhibited which leads, e.g., to problems with ATP production . The mitochondrion itself is not dysfunctional, it doesn't get the correct signals or proteins etc.