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Third Annual Community Symposium on the Molecular Basis of ME/CFS Sponsored by Open Medicine Foundation, sign up here! Sept 7th 2019


Senior Member
Unfortunately, I was unable watch it due to severe caregiving responsibilities, but are they cracking it? Have they cracked it? Are they close ?? How close? thanks to everyone for their hard work and painstaking efforts.

Ben H

OMF Volunteer Correspondent
Unfortunately, I was unable watch it due to severe caregiving responsibilities, but are they cracking it? Have they cracked it? Are they close ?? How close? thanks to everyone for their hard work and painstaking efforts.
I'll post my twitter summaries if it helps.

I've written a short summary/impression of the 2019 OMF Symposium. I hope it will be helpful for patients who were unable to watch.

Please be mindful that this summary is based on watching the livestream yesterday. So there could be some errors or missing parts. If you want to know something for sure or cite it, I recommend waiting for the individual talks to become available on youtube to rewatch.

Moreau finds something in the plasma

I think the most interesting finding came from the Canadian researcher Alain Moreau who said he put normal cells in ME/CFS plasma and found a strong rise in bio-impedance. He said: “There is something very specific in the plasma of the patients, exactly as doctor Davis has shown recently with similar technology.” There were subgroups with very some different responses. I think the findings are preliminary, but it seems that there’s yet another research team that has found ‘something in the blood’.

Negative findings for red blood cell deformability

Another important finding, but a rather disappointing one, came from Juan Santiago, professor of engineering at Stanford, who has been looking at red blood cell mechanics. After a long and impressive talk about the details of the testing device he has made, Santiago said: “what I’m going to show you may not be what you want to hear, but I want to say it honestly.” There was no significant difference between ME/CFS patients and controls in red blood cell deformability. He said that they’ve succeeded in making a new system that can measure red blood cell mechanical properties at high-throughput, which is corroborated by other, more standard measurements and is applicable to a variety of diseases. But given the data they have on ME/CFS, he said: “it is unlikely that this can be a marker in itself.” They did want to delve deeper into their results because there was a surprisingly large heterogeneity, not just in ME/CFS patients but also in the healthy controls. So figuring out what causes that heterogeneity might give some interesting insights or perhaps a way to clean up the data.

Revamping the ME/CFS centre at Stanford

There weren’t any other stunning findings revealed during the symposium, but there was some exciting news with regards to the ME/CFS research collaborative centres. The conference started off with some really good news. Ron Davis announced plans to revamp and renew the ME/CFS centre at Stanford with the support of Robert Harrington, Chair of Medicine at Stanford Univerity who recorded a video for the symposium. Ronald Tompkins talked about the new ME/CFS centre at Harvard affiliated hospitals, which now has an informational website (http://endmecfs.mgh.harvard.edu/). When Moreau joked that he has a new baby (by which he meant the new Canadian ME/CFS research collaborative), Tompkins retorted that his ‘baby’ is now 3 months old. Jonas Bergquist, who is leading the new ME/CFS research collaborative research centra in Uppsala, Sweden, said he had recently started a collaboration with the prestigious Karolinska institute to look at trace elements (copper, zink, etc.) and to do a PET microglia imaging study.

Lumper-splitter discussion

The keynote address by Maureen Hanson was quite interesting as she openly talked about her view on the illness. She said she is a ‘lumper’, meaning she thinks there is a main cause for most ME/CFS patients. She added an interesting analogy to explain what she meant: If you get hit by a car you can break your leg, your arm or have a concussion. That may look like different subgroups, but they all got hit by the car. During the conference, several researchers came forward with their view on this issue and openly declared whether they are a’ lumper’or ‘splitter’. While Robert Phair and Ronald Davis said they were like, Hanson lumpers, Mike Syder said he’s a splitter. He said that this has become the standard approach in complex diseases; whether it’s autism, diabetes, cancer or neurological diseases, all are now viewed as multifactorial. He said he himself was an example of the success of the splitting approach as a patient with type II diabetes who doesn’t respond to normal therapy but for whom another treatment does work. Ron Tompkins then weighed in, saying "my general view of this disease is compatible with both lumping and splitting." He explained that there may indeed be a common underlying cause but that it's important to look more closely at heterogeneity to come up with successful treatments.

Research findings

Onto the research findings. Hanson talked about abnormalities in CD4 and CD8 T-cells which she reported previously. She said there was no difference in the amount of extracellular vesicles between patients and controls but that the former did have more of the small ones. She said that the findings on cytokines are conflicting in ME/CFS but that it may not be their level count but their pattern of activity and communication that is abnormal in ME/CFS, something that she saw in the extracellular vesicles.

Moreau talked about his non-taxing stress test to induce PEM. When persons were used as their own control he saw a decrease in REM-sleep in the patients, but not the controls after the stress test. He’s also studying brain fog and found a large change in thrombospondin (TSP) in some ME/CFS subgroups, a molecule that is involved in vasoconstriction and could point to reduced brain flow to the brain. These are all preliminary findings though.

Fluge talked about the negative rituximab results and the Cyclo ME trial, which tested cyclosphosphamide, another chemotherapeutic drug that seemed to work in their cancer patients with comorbid ME/CFS. He said they have done a phase II trial of cyclophosphamide that looks promising, but because it’s not randomized and relies on subjective outcomes, it can’t say much about efficacy yet. He hoped to do a randomized controlled trial of cyclophosphamide with objective outcomes and emphasised that these trials have all sorts of useful spinoffs because a lot of data is collected on patients.

Tompkins said that he wanted to look at muscle biopsies, an area in which he has a lot of expertise from studying physical trauma. From Bergquist’s talk I remembered he said they are finding high titers of antibodies to muscarinic and (inaudible: cholinergic?) receptors in approximately 70% of their Swedish patient sample. Santiago reported the negative findings on red blood cell deformability.

Snyder’s talk wasn’t about ME/CFS but it gave some interesting insight into the potential of wearables. Snyder has been testing these devices for quite a while (during the talk he was wearing three watches and a ring, all collecting biological data). One of the things he discovered was that during airplane flights his oxygen saturation (spO2) dropped and that this correlated with fatigue. One time his spO2 dropped more than usual and that’s how he discovered he was sick and had Lyme disease. He also said there was a connection with increased heart rate and CRP (which indicates infection), suggesting that these relatively cheap devices might indicate when someone is getting sick. Snyder thought that these wearables could be used to collect big data on ME/CFS patients, even the most severe ones.

Robert Phair talked about his metabolic trap hypothesis. He explained that each of the four IDO2 mutations is not more common in the ME/CFS than in controls – there is not a statistically significant difference there. But according to the theory, each of these can increase susceptibility to ME/CFS. So what matters is what percentage of persons has none of these four IDO2 mutations. In healthy controls, this is around 10%, in ME/CFS patients 1,4%.

In his talk, Ron Davis highlighted two metabolites that were significantly different in severe ME/CFS patients compared to controls: very low indolepropionate (involved in neuroprotection, made by a clostridium in the gut) and high hydroxyproline (which could indicate collagen degradation). Davis also said they are identifying drugs that stop the abnormal impedance signal picked up by the nanoneedle. Examples are Capoxone (an MS-drug) and something called SS-31 (wich repairs mitochondria). Earlier during the day, Moreau said that he had also found a drug (thymoquinone) that normalizes the bioimpedance they are measuring. But he admitted that they have no idea yet what they are measuring, so it needs further study.

Closing remarks: "now we've got a scientific community"

During the closing panel discussion, Robert Phair said that the OMF, by holding these regular symposiums, has created a ME/CFS research community. He said, “that there's always been a patient community and now we've got a scientific community."

Earlier during the day, Maureen Hanson emphasized that this scientific community needs more funding to grow. She said that the NIH is only funding 14-16% of ME/CFS study proposals, meaning that some proposals get a good, very good or even excellent quality rating, but don’t get funded. According to Hanson people don’t realize the seriousness of ME/CFS and that they should start to worry about it. It’ not a rare illness and we don’t know how someone gets it. Few patients recover from it and there is no FDA-approved drug to treat it. Hanson noted that the recent NANDS report has some very good suggestions to build the field, but that it doesn’t have set-aside funding. “I would like to challenge this working group”, she said, “to come up with new initiatives involving set-aside funds for ME/CFS, next year when they report again.” Let’s hope they do.

Many thanks to the Open Medicine Foundation for sponsoring this symposium. On to next year!


Senior Member
Great Plains, US
Thank you so much for the summary, Michiel.

You forgot the part that was the most important, to me. Dr. Davis was listing the things his group was going to do in the future and he said that they are planning to look into mold! They are going to hire someone who knows about mold toxins. That was the best thing I've ever heard at a research conference!!!