Dr Karl Morten - UK researcher based at Oxford University

Dr Morten currently doesn't have the time to engage fully on the forum but he has kindly given me permission to reproduce the following.

Dear Andy

I have had a look at the comments and questions on the site. Most of which we are asking as well and plan to address in our new project. The MRC application is crucial for our ME/CFS research. Due to be submitted Jan 16th, it will be a busy time when we get back to the UK.

Our funding from the MEA only runs until the end of Jan 2019. I hope to obtain interim funding to keep my team together until we find out about the grant July 2019.

The Welcome trust and crowd funding are other options. The £1.6Million will give us an excellent base from which to develop and expand our research in Oxford and with collaborators throughout the world. I feel it is a strong application for the UK which has been developing over the last 2 years. Getting the Oxford clinical sections together have been the difficult parts and in my view is the major challenge we face in ME/CFS research in the UK probably more so than the funding. Without well diagnosed patients we will get no where fast. NHS support in this area does not give the clinicians involved time to do research and we need to bring in new Clinician Scientists to drive this forwards. I touched on this in my talk. Problems with the PACE trial should not be ignored but we need to draw a line under everything at some point to attract people into the field. We have an excellent Psychiatrist Beata Godlewska running a 7T imaging study in Oxford on the Brains of ME/CFS patients. The data is very much around the biology of the brain with plans to run follow up metabolomics on Plasma in Jan 2019. Beata is Polish which is is probably telling us something.

The NIH study will yield some interesting results when it is completed as they have really dug deep into the disease and the causes of the symptoms.

I probably wont have the time to engage with S4Me in the short term as will be too pre-occupied with grants and papers. If we get proper funding to work in the area I will be definitely look to be more involved. We have good local connections with the local OMEGA group who I regularly give up dates to.

Best wishes
Karl​
 
strategist said:
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.
Click to expand...

All comes back to the question, what evidence is there that many of these GET patients are actually increasing their activity levels? A change in questionnaire answering behaviour is not the same as an increase in activity or activity intensity.
 
strategist said:
My thoughts keep coming back to this because it's so encouraging. Karl Morten comes across as informed and motivated to get good research going.



The grant application by Morten is to the MRC. @Jonathan Edwards do you think the hyping of the Pariante study is because Morten is seen as dangerous competitor that could take funding away from biopsychosocial approaches?
Click to expand...

In short I agree with you strategist - I've just used more words!

Morten highlights Fluge and Mella's 2016 publication which as he (Morten) says demonstrates a blockage in the pyruvate dehydrogenase bridge (PDH). He states that the gene expression of PDH is about half of what you would expect; the effect is that glucose (normal cellular fuel) cannot be utilised to make energy (ATP). He then demonstrates the effect of ME plasma on cultured muscle cells (increased oxygen consumption - cellular energy production "problem") compared to control (plasma from healthy people).

He does deal with psychological approach by saying something about improvement; however, I didn't personally feel he was saying something objectionable. I assume that CBT is appropriately used, e.g. in the case of a biological illness, where it is not presented as a cure but as a means of dealing (psychologically) with the consequences.

He touches fascinatingly on the role of mitochondria in immunity, and the change in shape of mitochondria (he was speaking before Prusty's NIH presentation last month), in response to a question. Also, note that he is one of the authors of a paper on phenylalanine as a potential diagnostic test. It's a test which (from memory) can be scaled up; plus we can now compare the results to the change in shape of the mitochondria.

To me this guy is a well intention-ed eminent scientist who wants to do something to benefit people rather than academia. I.e. put his knowledge to better use. I'm a relative lay person; this guy strikes me as the real deal - I'm glad he's working on this.

ME Action are lobbying for the validation/development of a diagnostic test for ME https://www.meaction.net/…/announcing-millionsmissing-2019…/

@obeat
 
wigglethemouse said:
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.
Click to expand...
What does the difference in results after 24 hrs mean. If there is a clear difference to healthy controls after 24 hours would even that not imply something awry?
 
wigglethemouse said:
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
Click to expand...

Can anyone explain why this cannot be developed ointo a diagnostic test i.e. "He did a plasma swap experiment with healthy muscle cells and showed oxygen consumption is different when mixed with patient plasma vs healthy plasma"?

@Andy
@JaimeS
 
FMMM1 said:
Can anyone explain why this cannot be developed ointo a diagnostic test i.e. "He did a plasma swap experiment with healthy muscle cells and showed oxygen consumption is different when mixed with patient plasma vs healthy plasma"?

@Andy
@JaimeS
Click to expand...
I believe that Karl will have something to say on this subject in our Q&A with him, but feel free to post this or any other question on this thread, https://www.s4me.info/threads/question-collection-thread-for-s4me-q-a-with-dr-karl-morten-university-of-oxford-sept-2019.10827/
 
Merged thread

Karl Morten's crowdfunding campaign, "Understanding the causes of ME/CFS"

Myalgic Encephalomyelitis/Chronic Fatigue Syndrome is a condition affecting 20 million people worldwide, but it remains a puzzle to both the medical profession and patients. Complex symptoms make it difficult to diagnose and only 5% of patients make a full recovery.

Research into the causes has been limited due to lack of funding, but the recent identification of high levels of L-form bacteria in the blood of ME/CFS patients suggests a compromised immune system could be a biological cause of the illness.

Dr Karl Morten at the University of Oxford proposes to lead a major research project to investigate this possible cause in detail. It will be the largest project of its kind in Europe, involving three ME/CFS research centres over 4-5 years. With your support, we hope it will be a game-changer for this debilitating condition.
Click to expand...
Donate via link at https://www.development.ox.ac.uk/mecfs

Exciting new research initiative in ME/CFS

In collaboration with researchers in Poland, Spain and Oxford we are launching a £1.6 million campaign to support clinical research infrastructure in the three countries and to explore the exciting new research area linking the presence of L-form bacteria and fungi as a key disease driver in ME/CFS.

Our industrial collaborator SoftCell Biologicals have already committed $750,000 to the project to support whole genome sequencing bacteria in the blood of patients and controls.

The project will run over 5 years and allow us to build towards competitive funding applications to larger UK funders.
Click to expand...
From https://www.wrh.ox.ac.uk/team/karl-morten

Edit reason: formatting and minor text.
 
Last edited by a moderator:
Karl is aware that people, and in particular our members, will be interested in more detail about the project, so more comprehensive details will be released soon(-ish). We are likely to have the chance of another Q&A with him as well.
 
Andy said:
Out of hand how? If you don't support the work, don't donate.
Click to expand...

We are being asked to donate left right and centre - and that's before taking into account traditional donations to the charities or support groups.

Our community has limited resources. I just don't feel this is a sustainable way of doing business.

We have a duty to explore and understand why these projects aren't / can't get funded through grants. I know it's hard - I worked in academia - but it's worth understanding.
 
InitialConditions said:
We are being asked to donate left right and centre - and that's before taking into account traditional donations to the charities or support groups.

Our community has limited resources. I just don't feel this is a sustainable way of doing business.

We have a duty to explore and understand why these projects aren't / can't get funded through grants. I know it's hard - I worked in academia - but it's worth understanding.
Click to expand...

KM seemingly pointed out at the CMRC that both applications they’d made were refused. I know they made a big one to the MRC which was turned down. Did they try again? . I agree with your point and although I’ve actually asked my pareNts (who hav gift aid as tax payers ) to donate for me to this As it looks really good, I have a limited amount and it’s just taking away what I’d be giving elsewhere where we are being asked to fund everything too

on the website KM essentially blames funding and That’s what frustrates me about MRC CFS position. Immensely. We are crying out for research, they talk endlessly about need to encourage it and then they turn down the good stuff available to fund....

however in the U.K. charities are falling way short of the £10 m / year we could reasonably raise if we didn’t have a multitude of factors seemingly Preventing that which means whilst the involved feel burdened, tens of thousands with the illness and their families aren’t donating anything. MS society is raising 27m / year. ME charities around £2m. I’d like a discussion as to why this vast difference because it’s a crucial deficit in the system which means state funders can’t rely on charities to get the seed stufff done and we clearly aren’t able to rely on state funders to step in to fill in the gap ( I would argue they should) . The loosers In that is the long suffering patient.
 
Last edited:
Research into the causes has been limited due to lack of funding, but the recent identification of high levels of L-form bacteria in the blood of ME/CFS patients suggests a compromised immune system could be a biological cause of the illness.
Click to expand...
I am puzzled by this. I thought Ron Davis's team had not found any higher levels than in healthy people of bacteria or viruses in the blood of ME patients.

Edit: I respect Karl Morton, but I am also concerned about crowdfunding for this size of budget. It seems totally unrealistic to me. When LSHTM did an appeal a couple of years ago, I think they got about £15,000, and even the combined fundraising of the MEA and AfME for research is probably in tens of thousands per year.
 
Trish said:
I am puzzled by this. I thought Ron Davis's team had not found any higher levels than in healthy people of bacteria or viruses in the blood of ME patients.
Click to expand...

This is precisely the thing I am getting at with my comments. I am pretty well-versed in M.E. science and potential leads...but I've never heard of L-form bacteria.

It would be good if we could put some questions to Karl.
 
Cinders66 said:
KM seemingly pointed out at the CMRC that both applications they’d made were refused. I know they made a big one to the MRC which was turned down. Did they try again? . I agree with your point and although I’ve actually asked my pareNts (who hav gift aid as tax payers ) to donate for me to this As it looks really good, I have a limited amount and it’s just taking away what I’d be giving elsewhere where we are being asked to fund everything too

on the website KM essentially blames funding and That’s what frustrates me about MRC CFS position. Immensely. We are crying out for research, they talk endlessly about need to encourage it and then they turn down the good stuff available to fund....

however in the U.K. charities are falling way short of the £10 m / year we could reasonably raise if we didn’t have a multitude of factors seemingly Preventing that. MS society is raising 27m / year. ME charities around £2m. I’d like a discussion as to why this vast difference because it’s a crucial deficit in the system which means state funders can’t rely on charities to get the seed stufff done and we clearly aren’t able to rely on state funders to step in to fill in the gap. The loosers In that is the long suffering patient.
Click to expand...

Yes, the pot is self-limiting. It must be divided up - with winners and losers.

One issue with our illness compared with M.S is the rate of patients who are in work and earning a salary that can allow them to donate.
 
as posted on the CMRC thread

Click to expand...

RE: point three on this slide

see
Michiel Tack said:
It seems that the sole ME/CFS research team in Poland is prescribing GET based on the deconditioning theory to all ME/CFS patients that come to their centre. And they do not seem to make an effort to obtain reliable data out of this.
Click to expand...
https://www.s4me.info/threads/the-i...-2019-zalewski-et-al.12896/page-2#post-226470

and this is the team in Poland for the new research proposal.
 
Last edited:
You must log in or register to reply here.
Back
Top Bottom