Chris Armstrong - Melbourne ME/CFS researcher, research updates and general chat

MyalgicE

MyalgicE

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Dr Christopher Armstrong is an Australian scientist researching Myalgic Encephalomyelitis (ME). He moved to California late last year to take up a position at the Open Medicine Foundation.

Previously Dr Armstrong worked on biochemistry and molecular biology in the Bio21 Molecular Science and Biotechnology Institute at the University of Melbourne. He researched ME for eight years at the University of Melbourne, where he completed a PhD to pioneer the application of metabolomics.

We also talked about his community and political engagement:

“Patients have been patient for long enough.”

https://meaustralia.net/2019/02/20/meet-the-scientists-dr-christopher-armstrong/
 
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OMF Science Liaison Christopher Armstrong, PhD, is the guest speaker on the latest episode of Uninvisible Podcast with host and chronic disease patient advocate, Lauren Freedman. The Uninvisible Podcast focuses on invisible conditions and invisible chronic illness.

In this interview, Chris shared that OMFCA is focused on research to establish the biology of ME/CFS, to bring treatments to patients and educate the medical community. Chris emphasized that patients are at the forefront of researchers’ minds, focusing on getting treatments for patients as fast as possible while raising awareness to a broad audience. Chris also shared that the most significant change he sees in ME/CFS research in the last decade is the advances made by the Open Medicine Foundation.
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Listen to the full podcast here.

Uninvisible Podcast Episode #46 -Christopher Armstrong, PhD

https://www.omf.ngo/2019/10/31/christopher-armstrong-phd-speaks-out-on-uninvisible-podcast/
 
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Have listened to this now. Nothing really new, apart from Chris' background of which I was unaware, but a nice, thoughtful and wide-ranging discussion.
Tune in as Chris shares…

  • how he got involved in ME/CFS research
  • his main area of expertise: metabolomics
  • that ME/CFS outbreaks can be traced back as far as the mid-19thC, with symptoms commonly related to significant concerns with fatigue, sleep, pain, brain fog, and a 50% loss of general function
  • a description of PEM – post-exertional malaise – which is the main component of ME/CFS
  • that there are up to 50 symptoms associated with ME/CFS, but the main five are: PEM, fatigue, unrefreshing sleep, cognitive impairment, and pain
  • that ME/CFS is highly comorbid with fibromyalgia and other invisible illnesses
  • that ME/CFS was originally described as a flu- or polio-like illness; and was first properly explained by the Ramsay definition and given the moniker of “Myalgic Encephalomyelitis”
  • that patients need to have ME/CFS for 6+ months in order to receive a diagnosis
  • one of the major schools of thought with regard to ME/CFS: that it stems from a dysfunction of stress response in the body; it’s possible, however, that bacteria and other pathogens may also play a role in onset
  • that 1 in 200-300 people has ME/CFS
  • that ME/CFS is NOT categorized as a rare disease; but it’s treated by the medical community as such – creating stigma through lack of research and understanding
  • that ME/CFS has been commonly misdiagnosed as a form of hysteria – both in the past and in the present
  • that very few clinicians dig in deep enough with their patients in order to give them an ME/CFS diagnosis – but that burden is not just on doctors, as diagnostics and treatment guidelines need to be standardized in order to support their work
  • that the Open Medicine Foundation was built to provide effective treatments for ME/CFS patients
  • that meeting patients has inspired him in his work, even from the very beginning
  • the desperate need for funding for continued research into ME/CFS
  • the politics of funding medical research
  • that ME/CFS is often considered to be more a psychological than a physiological illness
  • that the National Institutes of Health (NIH) has been more receptive than some Aussie governing bodies when it comes to research into ME/CFS
  • the biggest bright spot in ME/CFS: the momentum of funding for research
  • OMF’s collaborative research initiatives with Harvard, Stanford, and others
  • that ME/CFS could be a collection of several diseases, and not one disease in and of itself
  • the importance of specifics in diagnostics
  • why medicine needs to be patient-centered
  • the importance of pacing in order to avoid a crash related to PEM
  • info on OMF’s current fundraising initiative, #TripleTuesday – and how to donate to ME/CFS research and have your donation tripled by partners!
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https://uninvisiblepod.com/2019/10/30/episode-46-chris-armstrong/
 
Jaybee00 said:
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That was an interesting presentation. Except that it didn't make clear which projects were just a plan and which were actually happening.

So I looked on the website (https://www.omf.ngo/omf-australia/) and it looks like the only study currently underway is the Ocular Motor study (confusingly with a wrong blurb on the intro page). Unless the website is not up to date, all the other OMF Australia studies seem to be still at various stages of planning.

The ocular study discussed in the video is progressing though:
Updates and Potential
  • IRB/clinical protocol completed and approved.

  • Preliminary trials on ME/CFS patients has already identified highly distinctive ocular motor changes in people with ME/CFS, which suggests disruption originating in the brainstem.

  • It appears that a fatigue phenotype will be able to be monitored using ocular motor testing.

  • A larger trial has begun this year with data collection ongoing and biofluid collection beginning.
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https://www.omf.ngo/ocular-motor-study/
 
Binkie4 said:
Hi Chris @MelbME. Thank you for taking the time to tell us more about the inspiration for the saline study. I also note you writing that it will tell you more about volume expansion which will also be interesting. It seems strange that these possible features of ME have had so little attention paid to them.

I was fortunate to be seeing an ME specialist privately when I was due to have heart testing which was then expected to lead to open heart surgery. He knew I was very concerned about losing functionality because of the testing and wrote me a detailed letter to pass to the heart surgeon recommending saline infusions, avoiding intense activity and spreading out the testing. Fortunately the heart hospital was willing to cooperate and I was able to follow the advice. I didn't go into PEM or lose functionality and felt well throughout the procedures.

We look forward to hearing how the research progresses.
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I think generally we see that 99% of studies are looking to compare ME/CFS and healthy patients to find a marker that is distinctly different in 90%+ ME/CFS patients as compared to the healthy controls. And this is a tempting route to go down. The idea is that this whole research field is held back without that pathology or biological anomaly that defines the disease. You find the biological difference and then build everything off that: characterisation studies, treatments to correct the pathology, diagnostics that are surrogate markers for the pathology or early markers of the pathology, etc.

Patients and researchers all get excited at the idea of looking at something completely different because it could be the marker we've been waiting for. There is a big push to just keep digging like this and I completely understand why that is. There is less excitement to go back and look at some of the pathology treatments present in 30-50% of patients to understand them and their contribution to the disease. The direct outcome of this research does help the 30-50% of patients with that pathology but there are indirect outcomes that get overlooked. The indirect outcome is that once you characterise a pathology nested in the disease, then you can start to build off that and extrapolate to mechanisms that may be universal without that exact pathology. I think this is a smarter investment of time but it's very much chipping away at the problem rather than looking for a magic bullet.
 
MelbME said:
I think generally we see that 99% of studies are looking to compare ME/CFS and healthy patients to find a marker that is distinctly different in 90%+ ME/CFS patients as compared to the healthy controls. And this is a tempting route to go down
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Arguably a biomarker would make it easier for family doctors to make a diagnosis and for patients to get a clear diagnosis without having to jump so many hoops. Legitimizing the disease in a hostile health care system is important.

Thank you for your work. Will take anything by now. It’s been 15+ years for me.
 
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Milo said:
Arguably a biomarker would make it easier for family doctors to make a diagnosis and for patients to get a clear diagnosis without having to jump so many hoops. Legitimizing the disease in a hostile health care system is important.

Thank you for your work. Will take anything by now. It’s been 15+ years for me.
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Yes exactly. This is why it's been such a dominant type of research in the field. We still do this type of research. Have explored a diagnostic in the past (am even doing it currently) and it's incredibly hard to get up but not impossible. If you don't know that the marker is tied to the disease mechanism then you have to prove its diagnostic ability against more than healthy, has to be able to distinguish MECFS from many other diseases to be diagnostic of MECFS.

Best bet might be a marker that enhances existing criteria to simplify it. The complexity of current diagnosis lies in the exclusion of other diseases.

The recent paper on Raman separating ME from MS was a good start in the right direction. That has potential worth watching. Also consider the diagnosis of pathologies in MECFS (POTS and preload) there's a lot of value to that too.
 
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Hello @MelbME

Welcome to this forum. I hope that OMF can focus on trialing serious treatments (i.e. NOT LDN) instead of funding basic/exploratory research.

Why? Because basic/exploratory research has not yielded any particularly significant/useful results over the past several decades. Therefore continuing to pursue basic research may not be fruitful.

So please let’s fund platform trials with cyclophosphamide (phase 3), daratumumab, alemtuzumab (campath), CAR T cell therapy, etc. I am optimistic that something will work.

Thank you for your consideration.
 
Jaybee00 said:
Because basic/exploratory research has not yielded any particularly significant/useful results over the past several decades. Therefore continuing to pursue basic research may not be fruitful.
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I don't think that's a good reason for stopping funding such research. There's so much more that could be sensibly explored, including replication of small promising studies that were too small to stand on their own.
 
Trish said:
I don't think that's a good reason for stopping funding such research. There's so much more that could be sensibly explored, including replication of small promising studies that were too small to stand on their own.
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If you have unlimited funding, then by all means pursue both. But you don’t. Personally I am much more interested in getting better than elucidating the exact mechanism by which the disease operates.
 
Jaybee00 said:
Hello @MelbME

Welcome to this forum. I hope that OMF can focus on trialing serious treatments (i.e. NOT LDN) instead of funding basic/exploratory research.

Why? Because basic/exploratory research has not yielded any particularly significant/useful results over the past several decades. Therefore continuing to pursue basic research may not be fruitful.

So please let’s fund platform trials with cyclophosphamide (phase 3), daratumumab, alemtuzumab (campath), CAR T cell therapy, etc. I am optimistic that something will work.

Thank you for your consideration.
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LIFT trial is a combination therapy of LDN+Mestinon that they want to assess long-term, they need to show each LDN and Mestinon alone as well to see if the combination therapy is better than both individually. It has a lot of support from clinicians based off their experience. Of course this isn't going to help everybody and I understand the frustration.

What is your interest in immune modulator treatments based on? Did they help you?
 
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MelbME said:
LIFT trial is a combination therapy of LDN+Mestinon that they want to assess long-term, they need to show each LDN and Mestinon alone as well to see if the combination therapy is better than both individually. It has a lot of support from clinicians based off their experience.
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Find it so interesting that clinicians talk up LDN and mestinon.. Have never spoken to a patient where either help primary ME symptoms, and most anecdotal online reports are negative.. Neither have helped me (Nor saline nor abilify). I think a lot of patients claim something helps them but are being overly optimistic. Inevitably I see then those same people still just as sick a few years later and not on the treatment they said was helping them.
 
Braganca said:
Find it so interesting that clinicians talk up LDN and mestinon.. Have never spoken to a patient where either help primary ME symptoms, and most anecdotal online reports are negative.. Neither have helped me (Nor saline nor abilify). I think a lot of patients claim something helps them but are being overly optimistic. Inevitably I see then those same people still just as sick a few years later and not on the treatment they said was helping them.
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I have found LDN helpful, and have taken it for a few years now. Of course it could be placebo, but I have tried plenty of drugs and its the only one I still take. Its also hard to know what treatments to test without a better understanding of what is causing the issues. Why try specific immunotherapies when these drugs have significant side-effects and we do not have any indication they would be helpful? I think it would be more problematic if these therapies were run and failed (which seems likely) as this could play into the BPS narrative. Wouldn't you think that if these drugs were the answer we would have found some evidence to justify their use by now?
 
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