Article: Guilty!.... By Association? Taking Our Measure

You can view the page at http://forums.aboutmecfs.org/content.php?373-CFIDS-vernon-CFS-deckoff-jones-Guilty!-(By-Association)-Taking-Our-Measure-of-Our-Leaders

 

Thank you for your research and setting the record straight Cort

Let's use our collective power and energy to fight through government bureaucracies and to educate the masses, there is plenty of work to go around, so more power to whomever would like to take this on.

I dont care if the CAA, the WPI, the NIH or the Republic of China comes up with answers for us I just want to get well. And I will support anyone that is working towards that end.

 

Thank you, Cort. You are always the voice of reason and fairness. Your careful research is much appreciated!

 

Let's use our collective power and energy to fight through government bureaucracies and to educate the masses, there is plenty of work to go around, so more power to whomever would like to take this on.

I dont care if the CAA, the WPI, the NIH or the Republic of China comes up with answers for us I just want to get well. And I will support anyone that is working towards that end.

At heart we all want the same thing. If someone makes a mistake, I say forget about it and move on...We're only human. Let's give each of us a break -recommit to the main goal - healthy, happy, active lives Retro eek:) and move on...(to China if need be )

 

Sorry to be a Debbie Downer here, but I really didn't like the 2009 paper mentioned. It conflated chronic fatigue, prolonged fatigue and "CFS" by saying they were all one phenotype with slight differences. It said that the Reeves criteria should be used and said Fukuda didn't need to be revised (i guess as resistance to CCC). It said depression was an integral part of ME, not a secondary affect. Pretty bad paper.

I don't know enough about science to really look at her non-psyciatric papers.

I still think that her failure to come out strongly against the Reeves Criteria (on which she has her name) is a really huge problem that really overshadows her other contributions.


http://128.121.104.17/cfs-inform/CFS.case.def/hickie.etal08.pdf

Are chronic fatigue and chronic fatigue syndrome valid clinical entities across countries and health- care settings?
Ian Hickie, Tracey Davenport, Suzanne D. Vernon, Rosane Nisenbaum, William C. Reeves, Dusan Hadzi-Pavlovic, Andrew Lloyd, and the International Chronic Fatigue Syndrome Study Group$
Australian and New Zealand Journal of Psychiatry 2009; 43:2535
...
Discussion
Five domains of illness experience were derived empirically from multivariate analyses of large inter- national epidemiological and clinical datasets based on symptom reports of subjects with prolonged fatigue. These domains were robust across cultures and health-care settings and are consistent with the key criteria described in the 1994 international CFS case definition. They are best summarized as: pro- longed fatigue and musculoskeletal pain; impairedneurocognitive function; sleep disturbance; and symptoms suggestive of inflammation. From a psy- chiatric perspective, the only noteworthy variation is one of emphasis on the central role of mood disturbance. There has been a strong tendency in the medical and lay literature on CFS to suggest that depressive symptoms are simply an understandable psychological response to the severity or duration of
disability. These data argue that mood disturbance is a core component.
....
The present findings indicate that the core dimensions specified in the 1994 definition have construct validity and do not need to be revised. The International CFS Study Group also recommended that for research purposes, the diag- nosis of CFS should be made using validated instru- ments that allow standardized assessments of the major symptom domains of the illness. The present study supports that recommendation and suggests an empirical diagnostic algorithm similar to that used by the Centers for Disease Control and Prevention [51].
...
A great deal of research effort, particularly in mental health aspects of general medical care, continues to focus on whether such chronic fatigue states can be distinguished from other medical and psychiatric diagnoses and also from other similar medically unexplained syndromes (e.g. chronic pain, fibromyalgia, irritable bowel syndrome). We suggest that this international study supports the proposition that chronic fatigue states share a common and stereotyped set of symptom domains, and that these can be readily identified in the community and at all levels of health care. Consequently, it is likely that they share common risk factors, are underpinned by a common pathophysiology, and may respond to common treatment strategies. We also suggest that there is little to be gained by further reorganization of the diagnostic criteria, or the related diagnostic entities. It is time to consider whether chronic fatigue states should be included formally in future interna- tional classification systems both in psychiatry and in general medicine.
Conceptually, the present findings are consistent with the notion that the key symptom phenomena of chronic fatigue states are likely to share common central nervous system mechanisms, independent of any other precipitating illness (e.g. infection) or risk factors (e.g. prior mood disturbance).

 

That's fine Justin and I understand that. Again - my assertion is that you should look at a persons broad body of work...not a single paper and certainly not a single paper that was basically done by a large group ie the International Chronic Fatigue Syndrome Study Group - which she was a part of.

Let me give you some quotes from the abstracts of her other studies. They will probably quiet your mind a bit.

Demonstrating evidence for latent viral infection and possibly targeting parts of the immune system for therapy

A formal analysis of cytokine networks in chronic fatigue syndrome.
Broderick G, Fuite J, Kreitz A, Vernon SD, Klimas N, Fletcher MA.

Chronic Fatigue Syndrome (CFS) is a complex illness affecting 4 million Americans for which no characteristic lesion has been identified. Instead of searching for a deficiency in any single marker, we propose that CFS is associated with a profound imbalance in the regulation of immune function forcing a departure from standard pre-programmed responses...... These showed highly attenuated Th1 and Th17 immune responses in CFS. High Th2 marker expression but weak interaction patterns pointed to an established Th2 inflammatory milieu. Similarly, altered associations in CFS provided indirect evidence of diminished NK cell responsiveness to IL-12 and LT-α stimulus. These observations are consistent with several processes active in latent viral infection and would not have been uncovered by assessing marker expression alone. Furthermore this analysis identifies key sub-networks such as IL-2:IFN-γ:TNF-α that might be targeted in restoring normal immune function.

This study finds gene activity that could be causing the complement activation after exercise in CFS. With the spinal fluid study out recently this means we may evidence of complement activation in three areas; spinal fluid, genes and blood. Of course much more work has to be done.

Mol Med. 2009 Jan-Feb;15(1-2):34-42. Epub 2008 Nov 10.
Transcriptional control of complement activation in an exercise model of chronic fatigue syndrome.
Sorensen B, Jones JF, Vernon SD, Rajeevan MS.


Complement activation resulting in significant increases of C4a split product may be a marker of postexertional malaise in individuals with chronic fatigue syndrome (CFS). This study focused on identification of the transcriptional control that may contribute to the increased C4a in CFS subjects after exercise..... In conclusion, lectin pathway responded to exercise differentially in CFS than in control subjects. MASP2 down-regulation may act as an antiinflammatory acute-phase response in healthy subjects, whereas its elevated level may account for increased C4a and inflammation-mediated postexertional malaise in CFS subjects.

B-cell dysfunction (think EBV) and antibody mediated NK cell modulation of T-cells (antibodies are screwing up NK cells which are then screwing up T cells). CD 19 cells could be at the heart of CFS!

Behav Brain Funct. 2008 Sep 26;4:44.
Evidence of inflammatory immune signaling in chronic fatigue syndrome: A pilot study of gene expression in peripheral blood.Aspler AL, Bolshin C, Vernon SD, Broderick G.

BACKGROUND: Genomic profiling of peripheral blood reveals altered immunity in chronic fatigue syndrome (CFS) however interpretation remains challenging without immune demographic context.

CONCLUSION: Dissection of blood microarray profiles points to B cell dysfunction with coordinated immune activation supporting persistent inflammation and antibody-mediated NK cell modulation of T cell activity. This has clinical implications as the CD19+ genes identified could provide robust and biologically meaningful basis for the early detection and unambiguous phenotyping of CFS.

This study suggests that temporarily reducing cortisol levels sharply could snap the HPA axis back into proper functioning.

PLoS Comput Biol. 2009 Jan;5(1):e1000273. Epub 2009 Jan 23.
Model-based therapeutic correction of hypothalamic-pituitary-adrenal axis dysfunction.
Ben-Zvi A, Vernon SD, Broderick G.

The hypothalamic-pituitary-adrenal (HPA) axis is a major system maintaining body homeostasis by regulating the neuroendocrine and sympathetic nervous systems as well modulating immune function.

A candidate treatment that displays robust properties in the face of significant biological variability and measurement uncertainty requires that cortisol be further suppressed for a short period until adrenocorticotropic hormone levels exceed 30% of baseline. Treatment may then be discontinued, and the HPA axis will naturally progress to a stable attractor defined by normal hormone levels. Perhaps most importantly, a treatment course involving further reduction in cortisol, even transient, is quite counterintuitive and challenges the conventional strategy of supplementing cortisol levels, an approach based on steady-state reasoning.

You realize I could go on and on with this -give you 10 or fifteen studies to the one you pointed out. Some studies did not have positive results but they were almost all - except for the one you picked out and the ED - 'good ' subjects. Throw in the work that she's done with the CAA and you have a slam dunk in my opinion.

 

I don't really care about the papers she co-authored with Reeves when she was at the CDC. After all, she chose to leave the CDC and join the CFIDS association. That was then, this is now.

But it's "now" I have a problem with. In this week's WSJ article about the study finding unique proteins in the spinal fluid of ME/CFS patients, Suzanne Vernon is quoted as saying “It’s difficult to have a diagnostic test based on spinal fluid. You can’t just go poking everyone in the spine.” That bugged the heck out of me. I know that lumbar punctures aren't something to take lightly, but they are used as a diagnostic tool for serious neurological diseases, such as multiple sclerosis. Why not for ME/CFS? I would welcome a biomarker we could use for a diagnostic test, and I was disappointed that Suzanne Vernon seemed to wet-blanket the idea. I wish she'd spoken of the importance of biomarkers, or pointed out that the study shows CNS involvement, or that "authorities" can quit saying there's no medical evidence of disease. Or SOMETHING supportive.

 

That was an unfortunate way to end that article but if you look at her analysis of that paper you'll see that she suggests that you could start looking for the counterparts of those proteins (I guess?) in the blood samples at the Biobank. I don't know how you do that but did she did make that suggestion - so I suppose she is thinking about and maybe even working on an easier blood test (?)

 

Thanks again Cort for another reasoned analysis - then/now.

 

Cort, did you see what people wrote there about your statements on the good doctor's blog?

http://treatingxmrv.blogspot.com/2011/02/politics.html

I still want to know exactly how much money the CAA received from the government contracts and exactly what it was used for, including "administrative expenses".

Why hasn't Susan Vernon spoken out strongly and publicly about what has always been going on behind the scenes at the CDC including the prejudicial attitudes towards us, right from the beginning of her very well paid employment at the CAA?

Why hasn't she or anybody else at the CAA spoken out about what CBS wrote about in another thread -- that the government agencies are scared that XMRV will prove causative?

Why is the CAA so incredibly slow in issuing an RFA after more than two years without one, while sitting on millions of dollars in earmarked research money?

Why are so many vital questions continuously unanswered?

 

At heart we all want the same thing. If someone makes a mistake, I say forget about it and move on...We're only human. Let's give each of us a break -recommit to the main goal - healthy, happy, active lives Retro eek:) and move on...(to China if need be )

If Dr. Vernon now regards her endorsement of the "Empirical Definition" as a "mistake" she should say as much and push for an accurate case definition. We live with this "mistake". "Forget about it and move on"? To borrow a Utah Phillips line, "The past didn't go anywhere."

 

Are chronic fatigue and chronic fatigue syndrome valid clinical entities across countries and health-
care settings?
Ian Hickie, Tracey Davenport, Suzanne D. Vernon, Rosane Nisenbaum,
William C. Reeves , Dusan Hadzi-Pavlovic, Andrew Lloyd, and the
International Chronic Fatigue Syndrome Study Group

I would be sceptical of any ME/CFS paper that has Ian Hickie as an author, let alone the lead author. His views are not fundamentally different from Wessely, et al, and he is one of he most influential psychs in Australia, who has his name on some of the main papers in the MF/CFS world, including definition papers. But he has managed to keep a relatively low profile in the debate, though most longer term Australian patients will know of him. I strongly suspect he was the 'intellectual' driving force behind the appallingly biased first draft of the Australian Clinical Guidelines (1997?), which was basically a straight lift from the Wessely school, and which was seriously toned down and modified for the final and much more reasonable version (2003?) after loud and pointed objections.

In fairness to Hickie, he was a major force behind the national Beyond Blue project here for increasing the awareness of and support for depressive illnesses, which is a good thing, if handled properly.

 

But it's "now" I have a problem with. In this week's WSJ article about the study finding unique proteins in the spinal fluid of ME/CFS patients, Suzanne Vernon is quoted as saying “It’s difficult to have a diagnostic test based on spinal fluid. You can’t just go poking everyone in the spine.” That bugged the heck out of me. I know that lumbar punctures aren't something to take lightly, but they are used as a diagnostic tool for serious neurological diseases, such as multiple sclerosis. Why not for ME/CFS? I would welcome a biomarker we could use for a diagnostic test, and I was disappointed that Suzanne Vernon seemed to wet-blanket the idea. I wish she'd spoken of the importance of biomarkers, or pointed out that the study shows CNS involvement, or that "authorities" can quit saying there's no medical evidence of disease. Or SOMETHING supportive.

I'm not defending anyone here... I live in the UK, and so I don't have much of an insight into the CAA... But journalists often take a quote out of context, so it might be helpful to get a statement from Vernon on her opinion of the study. I'm only saying that because I know what the media are like, and often go out of their way to print something controversial, rather than representing the truth.

I think I read that the authors of the protein study have no intention of suggesting that everyone with ME should have a lumbar puncture, but they are going to use their initial findings of proteins in the spinal fluid to look for the same proteins in the blood of ME & Lupus patients. If any of those spinal fluid proteins are floating around in our blood, then they can use those as a very convenient biological marker. They say that's the next step of their research.

 

If Dr. Vernon now regards her endorsement of the "Empirical Definition" as a "mistake" she should say as much and push for an accurate case definition. We live with this "mistake". "Forget about it and move on"? To borrow a Utah Phillips line, "The past didn't go anywhere."

Actually it did. The CAA has repeatedly disavowed us of the ED.

http://www.cfids.org/cfidslink/2010/010607.asp#2a

What is the Associations position on the CFS research program at CDC? Do you support the CDCs empirical definition of CFS?

The Association has been very public in its criticism of the CFS Research Program at CDC. You can read a summary of our recent efforts. The Association does not support use of the CDCs empirical definition of CFS in federally funded research and has repeatedly urged that CDC discontinue selecting CFS cases for its studies using these guidelines. The Association has never funded any research based on the empiric definition, nor has any education supported by the Association been based on the empiric definition. Review the Associations applicant research guidelines for defining cases and its current eligibility criteria for the BioBank.

 

I'm not defending anyone here... I live in the UK, and so I don't have much of an insight into the CAA... But journalists often take a quote out of context, so it might be helpful to get a statement from Vernon on her opinion of the study. I'm only saying that because I know what the media are like, and often go out of their way to print something controversial, rather than representing the truth.

I think I read that the authors of the protein study have no intention of suggesting that everyone with ME should have a lumbar puncture, but they are going to use their initial findings of proteins in the spinal fluid to look for the same proteins in the blood of ME & Lupus patients. If any of those spinal fluid proteins are floating around in our blood, then they can use those as a very convenient biological marker. They say that's the next step of their research.

Dr. Vernon said as much.

The Associations scientific director, Suzanne D. Vernon, PhD, notes, I am particularly excited about this study and the new avenues it opens. Pairing this treasure trove list of proteins with the biological and clinical resources in the Associations SolveCFS BioBank will quicken the pace at which these biomarkers can be verified and validated, hopefully shortening the pipeline from benchside discovery to bedside application. The contributions made by this group to understanding the biology of CFS and nPTLS could
not have come at a more timely moment for the field and the patient community.

 

Cort, did you see what people wrote there about your statements on the good doctor's blog?

http://treatingxmrv.blogspot.com/2011/02/politics.html

I still want to know exactly how much money the CAA received from the government contracts and exactly what it was used for, including "administrative expenses".

Why hasn't Susan Vernon spoken out strongly and publicly about what has always been going on behind the scenes at the CDC including the prejudicial attitudes towards us, right from the beginning of her very well paid employment at the CAA?

Why hasn't she or anybody else at the CAA spoken out about what CBS wrote about in another thread -- that the government agencies are scared that XMRV will prove causative?

Why is the CAA so incredibly slow in issuing an RFA after more than two years without one, while sitting on millions of dollars in earmarked research money?

Why are so many vital questions continuously unanswered?

This particular article was supposed to answer any questions other than whether Dr. Vernon is being of service to the ME/CFS Community...

I can't answer for her but I think Dr. Vernon's work over the past few years speaks for itself. I'm more interested in the studies she's funding, the research she's doing. the researchers she's brought into this field and the Research Network and BioBank she's put together than in her making personal attacks on her colleagues - something that would probably viewed with dismay by many in the research community - thus undercutting her support.

Working in a professional manner that wins the trust of her peers in the research community is important. She been able to bring many new researchers to the field at the Banbury Conference (35% of whom had never studied CFS), in the studies the CAA is funding and in the grants she applied for ( seven institutions participated in the autoimmune grants). She's shown her ability to make connections outside the field.

This probably also shows up in the CAA's stellar list of candidates for the CFSAC community including Dr. Lipkin, Dr. Singh and Dr Holmberg and a few others.

Acting like that may not be as catchy or compelling to the CFS community but I think its what we need and its effective.

 

Acting like that may not be as catchy or compelling to the CFS community but I think its what we need and its effective.

I know you do, and that's fine. But this is not Corts Assiciation of America. It's a patients organization. And at this point the big majority of the patients is unsatisfied with the direction and leadership of the CAA.

 

I don't really care about the papers she co-authored with Reeves when she was at the CDC. After all, she chose to leave the CDC and join the CFIDS association. That was then, this is now.

But it's "now" I have a problem with. In this week's WSJ article about the study finding unique proteins in the spinal fluid of ME/CFS patients, Suzanne Vernon is quoted as saying “It’s difficult to have a diagnostic test based on spinal fluid. You can’t just go poking everyone in the spine.” That bugged the heck out of me. I know that lumbar punctures aren't something to take lightly, but they are used as a diagnostic tool for serious neurological diseases, such as multiple sclerosis. Why not for ME/CFS? I would welcome a biomarker we could use for a diagnostic test, and I was disappointed that Suzanne Vernon seemed to wet-blanket the idea. I wish she'd spoken of the importance of biomarkers, or pointed out that the study shows CNS involvement, or that "authorities" can quit saying there's no medical evidence of disease. Or SOMETHING supportive.

I also tend to take the "What have you done for me lately?" approach.

It's not Suzanne Vernon I have a big problem with. Her comment in the WSJ blog I thought came off sounding dopey - although I said at the time (and I'll say it again) I get what she was trying to say - that everyone would prefer a less-invasive test to be available for routine diagnostics, and hopefully we can get one. But the words in which it was expressed were kind of condescending. Her comments in other articles about the Schutzer study were better.

If it turns out we can't get a reliable blood test for ME/CFS in the near future, and we have to undergo lumbar puncture for confirmation of diagnosis for a while - or for all time - so be it. It's still about a billion times better than having no accepted diagnostic test.

It's Kim McCleary and her comments to the press about PACE that I consider beyond the pale, and to be in direct contravention to patients' interests.

 

This particular article was supposed to answer any questions other than whether Dr. Vernon is being of service to the ME/CFS Community...

I can't answer for her but I think Dr. Vernon's work over the past few years speaks for itself. I'm more interested in the studies she's funding, the research she's doing. the researchers she's brought into this field and the Research Network and BioBank she's put together than in her making personal attacks on her colleagues - something that would probably viewed with dismay by many in the research community - thus undercutting her support.

Working in a professional manner that wins the trust of her peers in the research community is important. She been able to bring many new researchers to the field at the Banbury Conference (35% of whom had never studied CFS), in the studies the CAA is funding and in the grants she applied for ( seven institutions participated in the autoimmune grants). She's shown her ability to make connections outside the field.

This probably also shows up in the CAA's stellar list of candidates for the CFSAC community including Dr. Lipkin, Dr. Singh and Dr Holmberg and a few others.

Acting like that may not be as catchy or compelling to the CFS community but I think its what we need and its effective.

Suzanne was absolutely instrumental in work such as the Light study and Broderick's systems modeling (which is now funding at $4.5 million by the NIH/DoD). Her contributions to the CFS field are extraordinary, not only in terms of the Association's research program but in serving as a resource to other researchers. We have asked her to be an ambassador to researchers one or two steps removed from CFS research, people who might be interested but have yet to get involved. She has shared her expertise with NIH, the XMRV task force, and a number of research groups. And she has always conducted herself with professionalism and drive. As far as the WSJ quote goes, that was one quote from a 30 minute interview and certainly Suzanne did not choose the quote that was used. This is common practice, as we all know.

It helps to remember to look at a person's body of work, instead of painting with broad brush strokes and making assumptions based on one or two pieces of evidence. Certainly Dr. Mikovits has given her share of interviews, and there have been numerous threads here where the majority have urged that readers not look at quotes out of context. This is only fair. Cort rightly points to the work of Drs. Jason, Klimas and Friedberg - and no one here should question their dedication to helping people with CFS, despite the stress-related aspects of some of their studies. It's easy to make a snap judgment in the moment. It is more difficult to look at the body of evidence, and not let preconceptions color our evalutions.

 

I also tend to take the "What have you done for me lately?" approach.

It's not Suzanne Vernon I have a big problem with. Her comment in the WSJ blog I thought came off sounding dopey - although I said at the time (and I'll say it again) I get what she was trying to say - that everyone would prefer a less-invasive test to be available for routine diagnostics, and hopefully we can get one. But the words in which it was expressed were kind of condescending. Her comments in other articles about the Schutzer study were better.

If it turns out we can't get a reliable blood test for ME/CFS in the near future, and we have to undergo lumbar puncture for confirmation of diagnosis for a while - or for all time - so be it. It's still about a billion times better than having no accepted diagnostic test.

It's Kim McCleary and her comments to the press about PACE that I consider beyond the pale, and to be in direct contravention to patients' interests.

I agree. I see this article as a diversion.

The issue is the CAA and how it has failed and is continuing to fail patients. No amount of PR or Spin will cover up that fact.