Sunday, September 30, 2018
For years I have stayed at the Cardinal Hotel in Palo Alto. This is an old-fashioned California hotel. It has a large, high-ceilinged, tile-floor lobby with fireplace and chandeliers. There is no air-conditioning. Cooling is via ceiling fans, the old fashioned way. Early on the morning of the conference, Saturday September 29, I walked across the fantastic landscape of Stanford’s campus, passing various sculptures by Rodin, Segal and Jack Zajac. The campus is littered with sculpture. It was a beautiful early morning walk, full of anticipation.
This is the second annual patients conference sponsored by Open Medicine Foundation. This conference was well-attended, for the second year in a row. Linda Tannenbaum, the driver of this organization, related to me that “this next year is going to be very important” in terms of advances in research. The conference day was preceded by three days of collaborative research conversations. Dr. Ron Davis said that this part of the conference was expanded - in terms of participants - by 50% this year. OMF seems to want to quickly and efficiently broaden their collaborative effort, which already is yielding results.
The conference was live-streamed so that some 3,000 patients and advocates world-wide could view the day’s proceedings. I write this brief report for those who might be too ill to follow the day-long presentations.
I was pleased to see Dr. Jose Montoya at this conference. He was missing at last year’s conference.
This was a very interesting day, this last Saturday in September. There was an anticipation of some good news on this research collaboration effort - and this conference delivered on this. From my perspective, there were several research areas to highlight. All are tied together.
1.Maureen Hanson gave a presentation on Metabolomics and ME. Maureen has worked in this field for some time and was noted as being a strong and independent researcher. Previously she has worked on the microbiome, but now seems to believe that the center of this illness more likely lies in the area of metabolomics. Various studies - including Dr. Naviaux’s - seem to line up in separating ME patient’s metabolic dysregulations from controls. There is hope that studies of dysfunctional key metabolic pathways can be further expanded or replicated and that soon some treatment interventions can be explored. As we already know, a central drug possibility is Suramin. Information on an upcoming Autism trial using Suramin can be found here. The hope is that ME will not be far behind. The search for other compatible drugs continues, researchers trying to match existing drugs or herbals to the metabolic disturbances. Dr. Ron Davis has a small chip that can be used to test existing drugs and herbals against ME patient’s blood. ME patients have blood that is noticeably different from controls, and the researchers look (with this chip) to see what drugs or herbs normalize ME patient’s blood.
2. The second important area of research was a lecture looking closely at clonal expansion in T-cells. This lecture, presenting research of Mark Davis’ lab, was delivered by Michael Sikora. This young researcher made an excellent presentation, perhaps the best of the day - in a day of terrific presentations - updating the research presented by Mark Davis at last year’s conference. There is clear evidence now that T cells in ME patients expand or replicate in the presence of “something. At the moment, the researchers are not sure why this clonal expansion takes place. The thought is that the T cells do this either in relation to a real pathogen, or as auto-immune reaction (the body attacking self). According to Mark Davis, a similar clonal expansion takes place in MS. It is a big deal to have proven and observed this clonal expansion, and it will be a big deal to find out why this happens. Again, the hope is that this discovery might lead to some specific treatments.
3. Closely related to this is the work of Dr. Jerad Younger, who studies inflammation in the brain of ME patients. His belief is that the ME brain is in an inflamed state. Dr. Younger showed scans demonstrating that ME patients have abnormal inflammation in the brain (compared to controls). He also is able to measure increased temperatures in parts of the brain that are abnormally inflamed. In listening to Dr. Younger, bells and whistles went off as he described the delicate situation of these patients with brain inflammation. It sounded like my daughter’s desperately precarious situation. Any stimulation - the mildest insult - makes the patient sick. The consequence is that the patient, like my daughter, can be subject to repeated daily episodes of feeling sick. Dr. Younger, who has done research regarding LDN in Fibromyalgia, says that LDN might be able to quell this inflammation somewhat. He emphasize that this is unproven in ME. He also postulated that trying to cool off the brain physically might be of benefit, but I was not sure what he actually meant.
4. The last important section was a presentation by Dr. Robert Phair. Dr. Phair is relatively new to this research group and has been pursuing his own hypothesis, what he calls, “a new way of looking at ME”. Dr. Phair started his presentation by citing Dr. David Bell’s 1994 book, “The Doctors Guide to Chronic Fatigue Syndrome”. He also cited Hillary Johnson’s seminal book "Osler’s Web", as being particularly instructive relative to characterizing the several well-known outbreaks of this illness. This outbreak history gave Dr. Phair a key. Dr. Phair’s first foray into examining his hypothesis of a "metabolic block" focused on one pathway involving energy (ATP) production, particularly the relationship of tryptophan to kynurenine. Dr. Phair proceeded to illustrate that this pathway is broken and that the block exists. Again, this effort offers a potential opening for treatments. More work needs to be done, including work on other pathways, but this result has arrived pretty quickly, after only eight months of work. Four new collaborations on this project have emerged from the scientific discussions.
Additional lectures were given by Wenzhong Xiao, Jonas Bergquist, Alain Moreau, Ron Tompkins. I would have liked to hear an update from Dr. Naviaux.
Professor Ron Davis spoke at several times, at one point presenting OMF’s work on developing a biomarker. He also gave insights into the unpredictable, yet positive, benefits of having a three-day working meeting with many willing collaborators. He gave examples of “what getting these people together means”.
Davis went on to describe the phenomenon of Trytophan being high and Kynurenine being low. Low Kynurenine is a problem. Kynurenine makes NAD, which controls many processes in the body. Kynurenine controls the immune system. Without kynurenine you cannot suppress auto-immunity. “Does that sound familiar?”
The lectures will be on YouTube soon, reflecting OMF’s model of sharing information. Viewing these videos, if possible, is worth the effort. Observing these lectures with their slides and question and answer sessions is a good way to "improve" this modest attempt to get some information out to those who might want it.
The bottom line is that much has happened since last year's conference. OMF is moving fast but they need more money to hire more researchers. Please consider supporting their work.