CFS Central: At the NIH conference, you talked about the need for someone to lead the interdisciplinary research. Do you want the CAA [CFIDS Association of America] to do this?
Dr. Suzanne Vernon: The Association is transforming to leverage and lead the kind of collaborative research that can be fostered by talent and technology from diverse disciplines. But the federal agencies, particularly the NIH and the Centers for Disease Control & Prevention, must engage more deeply in supporting this kind of research and directing their resources – human and financial – to the expanded study of nature of CFS at the molecular, cellular and clinical levels. It was clear to many of us who attended the State of the Knowledge Workshop that collaboration and leadership are required in equal measure to advance diagnostics, treatments and patient care. This is the Association’s core strategy to make CFS widely understood, diagnosable, curable and preventable.
CFS Central: Is the NIH helping to fund the CAA’s biobank?
Vernon: No, the Association launched the SolveCFS BioBank with the help of gifts from individuals, all of whom are affected directly by CFS. We’re grateful for their support to build this important repository of clinical information and samples voluntarily provided by well-characterized CFS patients and healthy controls who share our commitment to advancing the understanding of CFS.
CFS Central: In your view, what are some of the more important findings raised in the conference?
Vernon: Having worked on CFS for 13 years, it feels to me like there is tremendous synergy around the need to be more collaborative across institutions, disciplines and settings (basic research, applied research and clinical research) to develop a shared set of tools that will accelerate the pace of discovery. The involvement of so many top people from the NIH at the meeting (especially under the circumstances of a near government shut-down) and Dr. Wanda Jones’ leadership at the Department of Health and Human Services make this a very hopeful and promising time.
CFS Central: Why did you ask Dr. John Coffin what’s next for XMRV but didn’t ask Dr. Judy Mikovits?
Vernon: As I recall, we were already behind schedule and the moderators were moving on to the next topic in a very tightly packed agenda. It is also well established from Dr. Mikovits’ presentation at this meeting and in other recent presentations that the WPI will pursue its XMRV-focused studies and continue participating in the blood safety study and the multi-center study being coordinated by Ian Lipkin of Columbia University.
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Can you please fill us in on what Suzanne Vernon's and Kim McCleary's roles were at SOK and how they obtained those positions? There are rumors going around about how they are working closely with Dr. Mangan. Their involvement makes me very uncomfortable, and I know that I'm not the only one.
ReplyDeleteWow, she's so clueless and incompetent, she basically admits to the set up question.
ReplyDeleteSad Sad Sad.
ReplyDeleteAm I the only one who finds Vernon's answers wooden and unconvincing? She sounds like a management consultant rather than a scientist or advocate. Love her use of the words "Synergy" & "Leverage" btw. Not!
ReplyDeleteWhat a complete load of flannel from Dr. Vernon.
ReplyDeleteThe woman made no real contribution to the SoK. She hasn't got a clue about research priorities and evidently can't see the wood for the trees.
A case of the blind leading the blind ?
She manages to say very little with so many words.
ReplyDeleteThe CAA does not speak for us! It is a rogue organization with it's own agenda that is orthogonal to that of the patients it claims to represent.
ReplyDeleteThanks, Mindy. The CAA does not speak for us, it speaks for itself.
ReplyDeleteSign the petition!
http://www.change.org/petitions/petition-to-disassociate-from-cfids-association-of-america-as-our-advocacy-representative#comments
I think Suzanne helped with the first template agenda. After that Mary and I developed our own agenda and presented it. Most of what we wanted was there, although it was packed. Good sign in that we have a good deal of science to discuss. Bad sign in that researchers had no time to discuss gaps.
ReplyDeleteSuzanne is pleasant and not pushy which is to say that personally dealing with her was fine. FROM an organizational standpoint the CAA is now a research org, defines themselves as such and there were a number of researchers who stated they got some funds from the CAA. ALl that is good.
WHat is really sad though, it that many CAA supporters, patients in general and people on Capitol hill, saw the CAA as advocating for patients on all levels. Now it behoves the CAA to support research funding for reasons of self interest Can they subsist on donations Maybe they can. WPI will have to subsist on donations, won't they?
SO with a 180 direction change that has transpired over the last 5 years, we have to come up with as many efforts as we can to form a community. THAT does not mean we have to agree. We never will.
One more comment. Dr. Coffin cut himself out when he said to leave XMRV behind. Maybe that was an wish..like..ONLY IF I HAD NO BECOME involved cause it is making my life hell. I know there was a time crunch at this meeting. THIS was NOT one of the times. People were eager to hear what Judy and Coffin had to say. OF course Judy will continue with her work. If she did not it would show that she has doubts about the stability of the SCIENCE collaborators scientific methods. Clearly, she does not. More later.
Lastly, someone suggested to me that the CFS researchers themselves have no platform, no community. Huh. Think about it. ALl humans who get things done belong to groups with similar common goals. Our folks need to find ways to meet, talk, yell, create and strategize.....
Those with ME are trying to have it recognized. What we really need is to actively challenge and dissociate from Pandora/MCWPA and those groups trying to brand and mass market the bogus ME/CFS construct and to create another broad open ended category which will keep CFS in play no matter what.
ReplyDeleteThe key word, I believe, in her answers is "preventable." If you're looking at the "cellular, molecular, and clinical" basis of "CFS" you are not looking for an infectious cause. It's only when one finds the pathogen that causes CFS that one can "prevent" it from spreading. So, taking her at her word, she wants to spend more years researching the HPA access stuff, and all the diddling little stuff that gets us no closer to treatments. Yes, the cellular and molecular (I'm not sure what she means by clinical) stuff is important, but it can come later, as with AIDS -- lots of research happened after the HIV virus was identified, and some of it led to better and better drugs to treat AIDS, but the key to it all was indentifying the HIV virus.
ReplyDeletemichael
"...the Association’s core strategy to make CFS widely understood, diagnosable, curable and preventable."
ReplyDeleteTHE most beneficial step that anyone studying ME/CFS could take RIGHT NOW (MUST take) to move the science forward is to stop polluting the scientific literature with poorly defined cohorts.
Past studies using cohorts that are not clearly ME (Canadian Consensus, Fukuda with PEM, ???) ought to be viewed for what they are - NOISE - distracting, detrimental, worse that useless noise.
Noise (and the simple act of giving noise a place at the table) does nothing to help make ME "...widely understood, diagnosable, curable and preventable."
The NIH (or any other funding source) ought not fund ANY studies with poorly defined cohorts and this needs to be made explicit.
As for the CAA, if they are serious about research, they ought to be leading this charge.
The importance of clean cohorts, standardization and data that was interpretable was emphasized repeatedly at the SoK conference.
Throwing out all studies with poorly defined cohorts would dramatically reduce the pool of "CFS data" upon which future studies could be based. Fantastic! Most of it is junk that's getting in the way and obscuring the essential mechanisms in ME.
I'm watching to see if ANYONE has the guts to address this critical issue directly and explicitly. I know that doing so would piss off a lot of "scientists," specifically "scientists" that ought to piss off ME patients because they care more about their vitaes than they care about ME patients and moving the research forward.
Well said Pat!
ReplyDeleteNow if the CAA is a research org, not an advocacy org, we need to make it clear that there are others in the patient community that are advocates. I don't like the fact that they seemed to take over that role at the SoK. I'm hoping the Coalition can perform the advocacy function. As far as research, does the CAA plan on funding the WPI? Wouldn't that be nice.
Karen Ravitz
Thank you for taking the time to do this interview. The most telling response in my opinion is her answer regarding the "most important findings" from the workshop. She did not answer the question - how is it possible that she had no response to this most interesting and most important question?
ReplyDeleteI’ve read Dr. Vernon’s answers several times and still don’t have any idea what she said. Somebody tell me what I’m missing. Why does she sound like a politician?
ReplyDeleteAssuming the CAA was once a patient advocacy group, does its charter permit it to reinvent itself as a research organization? Have CFS patients been involved in this transition?
ReplyDeleteBravada
I am not understanding something about the biomarkers. It is my understanding she wants to put research money into finding biomarkers for CFS to be used in diagnosis. Shouldn't we first be putting research money into finding the cause of CFS so we can get the proper treatment? Are these biomarkers going to help us to find that cause?
ReplyDeleteI also do not understand why people with CFS keep on donating money to the CFIDS Association of America when they have made so little progress and have participated in the psychological studies. I am suprised that doesn't piss more people off.
Biomarkers are critical to allow for proper cohorts. A true Me/CFS cohort must be defined by its biomarkers and not by clinical (mainly self reported) criteria. we are actually closer to a set of biomarkers than most think. Once we can use them the process of nailing down the pathogen(s) involved will be much clearer and faster.
ReplyDeleteTo IanH:
ReplyDeleteCould you expand on your comment that "we are actually closer to a set of biomarkers than most think"? On which biomarkers is there consensus now? To which are we close? Anything else?
Thanks,
Bravada
Bravada,
ReplyDeleteThere is no consensus generally because the subjects/patients that make up the studies are so mixed and attempts to identify biomarkers are confounded by this mix. The case definition ie. the diagnostics even as espoused by Leonard Jason will not be reliable enough to separate the groups to allow for effective biochemical markers.
For example we know that RNase-L fragmentation is a marker for ME (as well as other illnesses). However when some studies examine this among their subjects it is not consistent. The reason it is not consistent is that the cohort is not consistent. Similarly when looking at a cytokine profile such as suggested by Nancy Klimas, the fit is not reliable.
The process that will move ahead better is to take the known set of markers (they do not have to be exclusive to ME) as a cluster and remove all other patients who do not fit that cluster because CFS symptoms is not a disease, it is a set of symptoms. (The same applies to Fibromyalgia - it is not a disease).
Just looking at the immunological literature you see the biomarkers. Don't look at the neurological literature, it is very confusing and not exclusive enough.
The main markers are:
RNase-L fragmentation - range maybe a factor
Cytokine profile
NKcell(bright) levels
NKcell(dim) levels
NKcell(dim) function level
There are others which need a little clarifying.
Take this group and work with it. Investigate:
XMRV,HHV6, HHV7, CMV, enteroviruses, etc. Gut bacterial responses to stress, pesticide residue levels, etc.
Sorry everybody who does not fit will have to wait.
"Biomarkers are critical to allow for proper cohorts. A true Me/CFS cohort must be defined by its biomarkers and not by clinical (mainly self reported) criteria. we are actually closer to a set of biomarkers than most think. Once we can use them the process of nailing down the pathogen(s) involved will be much clearer and faster."
ReplyDeleteThank you very much for explaining that Ian!
Thanks, Ian, for the synopsis.
ReplyDeleteAs a donor to the CAA who has earmarked my funds for only research and has decreased my donations contingent on what the CAA does next, I was disappointed by Dr. Vernon's response to Nancy Klimas suggestion that researchers share blood samples they already have in their freezers to work out subtypes, etc. Dr. Vernon said that that was a cause of the confusion and suggested that we needed to have start anew -- e.g. I saw this as her way of promoting the Biobank, which is fine.
ReplyDeleteBUT Dr. Vernon, starting anew takes time, resources, money -- patients have been waiting for decades to get answers! The best years of my life are passing me by. You talk about collaboration? Walk the talk! Use the samples and resources we have already AND get new blood samples. You didn't need to shut down Dr. Klimas' well-placed comment.
I do think shared blood samples is necessary for efficient and complete analyses.Professor Klimas' suggestion was valuable. Particularly International samples as most countries are doing their best to muffle this illness. I remember Paul Cheney mentioning that New Zealand was one of the countries not supplying blood for their research. Shame on New zealand.
ReplyDeleteHowever Nancy also mentioned the importance of longitudinal sampling. This is important in ME/CFS because the symptoms are cyclical or undulating and so is the biochemistry. Hence the need for new blood samples taken in line with symptom severity.