Article: Not One Alone: CFIDS Association Board of Directors Take a Stand For the Power Of 'We'

Article: Not One Alone: CFID Association Board of Directors Take a Stand For the Powe

You can view the page at http://forums.aboutmecfs.org/content.php?276-Not-One-Alone-CFID-Association-Board-of-Directors-Take-a-Stand-For

 

First of all, Thank you Parvo for using your precious energy to share your thoughts on this. That was the most nuanced yet inspiring piece on the CAA I've read in quite in some time.

I'm re-posting the following from my facebook page http://www.facebook.com/profile.php?id=100001592712409. I may have borrowed bits and pieces from here, so I hope you guys don't mind:

I have spoken with many patients & physicians that share my sentiments toward the CAA. The question we all end up asking is "Ok now what?" It seems there are few options:

1) Patients all have the right to stop donating if they disagree with what the CAA is doing.

2) Start a new organization. It seems that many attempts have been had and always flame out, because patients either don't have the energy to execute them on the level that they originally envisioned or because the political bickering and dealing with what is by nature a very sensitive constituency (and for good reason) soon overwhelms. I think there should be a single organization that deals solely with advocacy (reaching out to media, political leaders, maybe even lobbying). Perhaps the MCWPA can consolidate these efforts.

3) Try to effect change from within. This would require either the CAA deciding to, at the very least, utilizing the voices of its constituency & donor base. Infiltrating the board of directors with new blood in the form of patients that have a clear vision of reform & will bring the voices of the patient community into the boardroom.

We can tear down the CAA all we want, but riot without a backup plan will leave us in rubbles.


I think the increasingly polarized opinions on the CAA have been rooted in

1) Management that is seemingly out of touch with the wants and needs of the patient community. There is sparse online collaboration and dialogue between the CAA and its constituency (us), despite thriving interconnectivity between patients in the last few years on online forums & facebook. Jennifer Spotila (board member), Wilhelmina Jenkins (ex-board member), and a few I might be forgetting, have been gracious enough to come out and answer questions with grace when conversations reach boiling points, but they give boilerplate disclosures and leave an impression of damage control when what patients are looking for is an eagerness on the CAA's part to listen to us, digest, and regurgitate at internal meetings and management decisions.

2) Spreading themselves too thin. As Cort has mentioned multiple times, this is a small organization. Contrary to what many may think, private donations have average out to little over a million a year. Without a large staff and moderate resources, the CAA has aimed at trying to educate the public and convert CFS into a mainstream illness. As Cort has also mentioned, they have funded considerable research, including viral, given their resources, including a grant to Dr. Broderick that has snowballed into over $4 million in gov't grants for CFS research. They have a leading role in the BWG, started a biobank project that has beaten expectations with over 1000 patients (with a focus on Canadian Consensus Criteria) signed up.

From an outsider's perspective, this efficiency may look like the makings of a successful organization, but as part of the constituency, I'm more concerned about outcomes than efficiency. As Marc mentioned, there needs to a way to measure performance in areas that the constituency cares about. Do patients want the CAA to spend precious dollars on the "Faces of CFS" campaign and other "education & awareness" campaigns? What if the majority of donors want the CAA to focus on research? Should management in that scenario continue to take a "Well we have the experience to know better" attitude?

I don't think an organization with 8 people on staff and ~$1 million in private donations a year can effect a seismic shift if it divides those resources between advocacy and research. I think it needs to pick one focus & see it through. Government grants have largely exceeded private donations to the CAA in the last few years, but the CAA is first and foremost a patient advocacy organization and should be beholden to us, and not a middleman between patients and the government and beholden to both. If that means rejecting grants that oppose with the CAA's mission statement (To stimulate research aimed at the
early detection, objective diagnosis and effective treatment of CFS through expanded public, private and commercial investment) then so be it.

3) And of course, there is XMRV. Many patients are seething because the CAA had 20+ years to fund retroviral research, and the WPI took the cake on that within 2-3 years. Of course, Marc himself decided to pull the plug on Elaine DeFreitas because of the mauling she had received from the gov't, but we can wax on all we want about the past: it's not going to change what happened.

Now that XMRV has been discovered, the CAA seems to be taking a staunch position of caution, deferring any commitment to the retrovirus with Suzanne Vernon saying it might be a "passenger virus." Their leadership in the BWG does imply that they are very interested in finding out though.

I understand that the CAA may be taking a conservative position in case XMRV turns out to be yet another failed "cause" and CFS falls back to being multifactorial, multi-subset disease. It's always safer to commitment to the common denominator right? But again, this comes back to the question: what do patients want? Do they want innovation in retroviral research & full-speed-ahead at the possible expense of getting mauled by federal and media criticism? I believe that most patients would say Yes, if it means we get to the bottom of whether a retrovirus plays a role in causation of our illness. Even if it means we have to start from scratch in the aftermath.

 

I think you make some really good points mJoey and I appreciate your nuanced take on all this.

I want to point out that with regards to this

Do patients want the CAA to spend precious dollars on the "Faces of CFS" campaign and other "education & awareness" campaigns?

That it's my understanding that that money came from the CDC )and did not come out of their research budget) or from the CAA's coffer's.

What if the majority of donors want the CAA to focus on research? Should management in that scenario continue to take a "Well we have the experience to know better" attitude?

My understanding is that the CAA is focusing mostly on research now and that is where most of its money is going.

Many patients are seething because the CAA had 20+ years to fund retroviral research, and the WPI took the cake on that within 2-3 years. Of course, Marc himself decided to pull the plug on Elaine DeFreitas because of the mauling she had received from the gov't,

Research discoveries can be as much a case of serendipity as well as hard work. Its not to the WPI's discredit that the discovery came about because Dr. Silverman asked them to look into it but to say the WPI was better or suggest they had more gifted researchers working for them than the researchers the CAA used in its grants is just not fair... Both groups have done excellent research and have utilized excellent researchers. Why use one as a bludgeon to beat up on the other? We have too few researchers interested in this disorder to do that. Its not like we have researchers clamoring to study people with CFS - quite the opposite.

I do want to point out what was left out of "Osler's Web" - the last study, funded by the CAA, in which Dr. DeFreitas was unable to distinguish people with CFS from healthy controls using patients from Dr. Bell, just as she did in her first study. Why anyone would have continued on after that point is kind of unclear to me given that no one else had been able to duplicate her results. Her similar results in multiple sclerosis also failed the test of time! This is a difficult field that has tripped up even the best of researchers at times.

Thanks for your balanced post!

 

A leadership role in the BWG????

Is the CAA taking a leadership role in the BWG?

What does that mean, exactly? Yes, they are a member, albeit one that cannot offer a level of expertise, lab space or any other bloody thing that is critical to the work being conducted. So, what is the CAA DOING (ya know, a verb) there? They are not chairing the meeting and related activities, those roles are spoken for. They're not reporting anything to patients, even so much as "phase 2 is more complicated than expected, please be patient we haven't forgotten you."

So seriously, how do patients benefit in the bargain? Whatever that bargain may be.

 

I agree entirely.

Waiting for exact and definitive information about the cause of illness for the entire CFS population, before we can be treated with appropriate respect like other sick people, is precisely the problem. In our case it is even worse, and research cannot be funded properly until a cause has been found. It's a Catch-22.

I am only really posting now, though, to clarify that ME does not in my assessment carry special prejudicial baggage in the UK - or at least, no more so than any of the alternatives. There are probably people still around who think "ME=psychological", but in general they dare not say so in public any more. At best, they may cautiously suggest that it may be, but in my very limited exploration of the opinion of people I've spoken to in the last year, the situation is this:

They haven't heard of "ME/CFS". They generally haven't heard of "CFS" - unless they know someone who has it. They have almost all heard of ME. And they think it was long ago established that ME is real and physical, and are startled to hear that this is still in any dispute, and shocked to hear that research is not taking place. In fact, they tend not to believe that government-funded medical research is not taking place. That argument was supposedly settled a decade ago...they don't realise that nothing has changed.

That's why "CFS" was coined, of course: because they had lost the argument and needed to re-define. I increasingly try to get into the habit of just calling it ME.

You are quite right that illnesses should not need a full understanding of the pathophysiology to justify a medical name. Most illnesses, actually, are inaccurately described, up until the point where they are fully understood - at which point, they hopefully cease to exist. Myalgic encephalomyelitis is as good an approximation as any, and it's a really big sign of progress that ME has finally been incorporated into the name in the US. Small though that step at CFSAC may appear, it's hugely significant, as evidenced by the rapid and immediate responses that turned "ME/CFS" as stated at CFSAC into "CFS/ME" when it hit the press.

I think one can look at the history of how these names were coined and analyse it like this. "ME" means "real". "CFS" means "imaginary". "ME/CFS" means "real, or maybe imaginary". "CFS/ME" means "imaginary, maybe real".

So the right name for our illness is ME, and we use "ME/CFS" only in order to remain in contact with those who know that label.

Let's condemn our slave name to the dustbin of history. Have you ever met a patient who liked the name "CFS"? I very much doubt it...so in the absence of a good alternative, ME will do for me.

(Only downside being, of course, the PR domain name! Would not be a simple process to ditch that...but hey, we can still feel proud, as a US-based site, that we got the 'ME' in there ahead of the game...)

Thanks so much for that info. I didn't know what the state of affairs was since the days of the "ME's All in The Mind" headlines that Jason quotes in "Politics Science and the Emergence of a New Disease" (which kind of ignores the body of knowledge about ME, but Jason's team stands up for us so I don't bother about that; I just add an article by Dowsett if I need to make that point). That's good to know. I will keep advocating for the use of ME immediately and do it with a clear conscience unless some other UK people pipe up to tell me differently.

 

Cort you made a couple of statements in your posts and I'm wondering if they have another deeper meaning? Do you know something? They are:

“How did that idea come to pass? Was it their cautionary stance on XMRV? I understand that it was upsetting (and a mistake in some ways) but it doesn't look it was such a bad way to go right now.”

“That is the big puzzle isn't it? How was a small lab able to do what all these other labs have not been able to do? I think we'll find out soon”

 

one thing missing

If anybody from the CAA is watching and/or from the CFSAC. I have a simple suggestion that would help lend credibility to the efforts your organzations in the minds of the patient community.

Please list on you websites goals, activities, and results(with expected completion dates) related to:

1) the efforts involved in finding treatments for CFS/ME

2) Efforts for diagnosing CFS/ME

3) efforts for defining if XMRV is found in CFS/ME patients. (Dr illa singh had some ood ideas on this one)

4) other productive activities

A comments section below the website list would allow the CFS/ME community to monitor and comment on the progress.

Without an effective (and transparent) way of tracking activities and results there is no way to know if anybody is doing any good.

 

Originally Posted by Cort

I don't disagree that we would be better off if we had acted more aggressively. I simply question how aggressive we are willing to be. AIDS and Civil Rights movements were a piece of cake compared to CFS; both groups already lived in communities - they were right next to each other; they already had strong social ties through churches and other organizations - they were already physical communities..

The Civil Rights movement and the ACT UP people did not have the internet, the community online, that we now have. They did have healthy members helping them, and after all the mixing up of definitions to the point where a depressed patient can be considered, by the Oxford and Reeves (Empirical) definitions as having ME/CFS, they also had far more clarity.

I think this is what the CAA and Phoenix Rising need. Clarity. Focussed anger. An end to apologist texts trying to be all things to all people. We all have to stop pulling our punches, and tell it straight, all the time. If that creates enemies, so be it. Being effective will always upset some.

• Use the Canadian Consensus Criteria - Fukuda was the first knife in the back. Where is post exertional malaise (or meltdown, as I prefer to call it) in Fukuda? Why does Fukuka exclude tests to confirm an ME/CFS diagnosis?
  
• Never use the nigger name, always preface with ME eg ME/CFS until such a time as the physical cause of this disease is universally recognized.
  
• Support and fund the WP1
  
• Give no credence to somatoform models of ME/CFS

PS I just want to thank Parvo and second every word she wrote. Respect. Rest up, now. We need you.

 

Lots of questions, more than I can answer, but I will offer a few answers.

Jennifer Spotila (board member), Wilhelmina Jenkins (ex-board member), and a few I might be forgetting, have been gracious enough to come out and answer questions with grace when conversations reach boiling points, but they give boilerplate disclosures and leave an impression of damage control when what patients are looking for is an eagerness on the CAA's part to listen to us, digest, and regurgitate at internal meetings and management decisions.

I am sorry to hear that you think I am offering "boilerplate disclosures" or doing damage control. I have answered as many individual questions as possible, frequently disclosing new information here or more details about topics. I do my best to respond to private messages and emails as well. Some questions I simply can't answer because of confidentiality restrictions. But I do listen, digest, learn, and carry what I learn back to the Board meetings. And Board members listen to what I (and others) have to say about the patient community or parts of the patient community. But what is said in online forums is not the only source of relevant information for the Board, nor are these topics the only relevant topics. The Board strives to make decisions considering as many angles to an issue as possible.

Do patients want the CAA to spend precious dollars on the "Faces of CFS" campaign and other "education & awareness" campaigns? What if the majority of donors want the CAA to focus on research?

The Board made the decision in 2008 to adopt the new strategy: To stimulate research aimed at the early detection, objective diagnosis and effective treatment of CFS through expanded public, private and commercial investment. We made the decision at that time to stop conducting general public awareness and education activities (we still conduct patient education activities like the webinars). We believe, and our donors and others in the patient community told us, that research is the key. Research will provide the evidence that is needed for more effective public awareness and education campaigns.

Many patients are seething because the CAA had 20+ years to fund retroviral research

It's been discussed repeatedly on PR and other forums that the Association has funded millions of dollars in viral and retroviral research. The decision to stop funding DeFrietas was made on the recommendation of a research committee (made up of researchers). The Association's current grant-making model is extramural - we ask for applications from outside researchers and conduct review for strategic and scientific merit. I can't comment on applications that were not funded, but I can say that the Association has always striven to find pilot projects that needed seed money in order to secure funding from larger sources (just as Dr. Broderick has done). This means looking for new or even risky ideas, and I think our research record speaks to the breadth of topics the Association has funded.

Is the CAA taking a leadership role in the BWG?

Dr. Vernon is a member of the Blood Working Group, and Ms. McCleary is a member of the AABB's XMRV Task Force. Neither of these are "leadership" roles in the sense of running the committees. However, through participation in these committees, Vernon and McCleary have been able to educate members about CFS, represent the needs and perspectives of the patients, and report information back to the community when able. I hope everyone understands that there are strict confidentiality requirements on both committees, and the Association has never violated those restrictions. But we have provided extensive reports when information is made public, and drawn on our contacts with the committees to create resources such as the extensive Q&A document in September. The educational information distributed at blood banks was created with the Association's input. And we have been able to arrange events like Dr. Louis Katz's webinar on XMRV and blood safety, and the just announced webinar on the Blood Working Group Phase II results (that thread is here).

I'm paraphrasing Cort with this one, but he wondered why all our Board members are not on the forums?

There are a variety of reasons. One, to be frank, is the way both my statements and the Association's communications are picked over with a magnifying glass and fine-toothed comb. It takes time to be as specific and clear as we can be so that when statements are read, they are understood as much as possible. Readers have every right to analyze, question and criticize statements made by organizations, and it forces organizations to be very very clear. Multiplying that effort by 15 Board members does not make much sense, especially if one or two can do the same. I seek clarification and information when needed, and do my best to be clear.

Board members have many responsibilities - raise money, oversee the organization, set strategy, etc. And our Board members can be described by one or more of the following: housebound by illness, caretaker of a patient, extensive travel for work, job requiring 60+ hours per week, parent of young children. I have dedicated much time and effort to participation on Phoenix Rising and Facebook, but not every Board member has that time. And we need our Board members to focus on their primary responsibilities to the organization. As I said above, I do my best to report back what I learn online to the Board.

 

Hey Jennifer,

I appreciate you taking the time to respond to some of my points.

Please don't get me wrong: I do believe you are earnest in your responses. I believe you try to tell us what you can, but due to confidentiality agreements or because you don't want to jeopardize the decision-making abilities of the board, your responses end up sometimes (no not always) leaving an impression of quelling a fire instead of addressing the kindling. Not knowing what sort of direction the CAA took on XMRV research was such an example a few months ago, but now I see that the association is earnestly trying to corroborate (or refute) the link with further evidence. And of course, I understand you are just one board member which funnels a disproportionate amount of public opinion onto you. Basically what I'm saying is: this isn't personal. I think the source of my complaints are structural in nature: the lack of engagement in general between the whole board and the public, not only online (although that probably be the best bang for you guys' energy and money) but via market research. Perhaps you have done such polling, and I'm just not aware of it, in which case please correct me.

Every time these threads pop up, hotbutton key phrases gets brought up to skew opinions of the Association's current work: Peter White, CBT/GET, Elaine DeFreitas (widely considered our Joan of Arc whether or not that reputation is warranted). Personally I understand that there has been a bunch of turnover in the Association and we need to focus on the present. No this doesn't mean that I think that mistakes should be ignored, but I want to see whether lessons have been learned and not harp on the past for the sake of harping. Cort informed me that the "faces of CFS" campaign and other education & awareness campaigns were all funded with government grants. I know the "faces" campaign was, but I wasn't aware the other education & awareness campaigns were exclusively tied to grants. Can you please shed some light on this? (I would comb through the financial statements again, but that is really beyond my energy allotment right now--my last foray when I posted comments under pen name "Joseph Chang", created because of surveillance during a disability lawsuit not to mislead anyone, crashed me pretty hard).

I know a lot of people take issue with the CAA's approach to advocacy. I do too, but I also believe that no organization with 8 people and under $1 million in donations last year can fund substantial research, run a full-fledged website, send out a monthly chronicle, rent out an office, and be our greatest hope for ACT-OUT advocacy. Adam Smith had it right: we need to stick to our competitive advantages and put our full weight behind them: specialize specialize specialize. I would love nothing more than to see the MCWPA or another organization become our ACT-OUT representation.

I appreciate that you changed your mission statement in 2008 to stimulate more research, and I would love nothing more than to see that renewed mission be cast in stone this time.

Thank you for clarifying on the role of Dr. Vernon.

And this is off-the-cuff: I really hope to see the WPI and CAA collaborate. When I look at the two orgs, I see unique competitive advantages and rife potential for synergy. Obviously I'm not privy to a lot that goes on behind the scenes, but I also know that power players can get caught up in what goes behind the scenes and lose sight of the big picture all too easily. I truly don't believe most patients want to see the CAA go away; no quite the opposite: I think they want to see them lend their considerable political and financial weight behind the movement and at least see it through. And it's not just about XMRV: if that doesn't pan out, I look at WPI and I see a focus on immunology that works seamlessly with the research that the CAA has funded. Of course, you might be shaking your head at my naivete and directing my whimsical wonderings to a parallel collaborative universe. In which case, I would still love to know why.

I'm trying to filter through the pathos to get at the hard facts, and threads like this are very helpful to this end when people come out of the woodworks to respond.

 

THERE ARE NO SUBSETS IN CFS.....Virtually every researcher I know of would love to find subsets...because then you would have discrete types of patients that they can study without the 'other types' of patients confounding their results....
...
It all comes down to research. Until you can prove subsets with research studies everything else is just talk! You'll never get someone to study a 'subset' until they can prove it exists. Because no one has done that... there is no science showing verifiable subsets and until there is its all just going to be 'CFS'.

Actually, there have been a couple of methods of determining subsets proposed. Nobody has bothered to try to replicate them so we don't know if they're verifiable, but there are indeed possibilities. There's no reason under the sun why we shouldn't be campaigning to replicate some of these studies:

Kerr et al. have written three articles on their genomics approach

Kerr JR, Burke B, Petty R, Gough J, Fear D, Mattey DL, Axford JS, Dalgleish AG, Nutt DJ. "Seven genomic subtypes of chronic fatigue syndrome/myalgic encephalomyelitis: a detailed analysis of gene networks and clinical phenotypes." J Clin Pathol. 2008 Jun;61(6):730-9. Epub 2007 Dec 5. PMID: 18057078

Kerr JR. "Gene profiling of patients with chronic fatigue syndrome/myalgic encephalomyelitis." Curr Rheumatol Rep. 2008 Dec;10(6):482-91. PMID: 19007540

Abstract: Chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME) is a multisystem disease, the pathogenesis of which remains undetermined. Following two microarray studies, we reported the differential expression of 88 human genes in patients with CFS; 85 of these genes were upregulated and 3 were downregulated. The top functional categories of these 88 genes were hematologic disease and function, immunologic disease and function, cancer, cell death, immune response, and infection. Clustering of quantitative polymerase chain reaction data from CFS/ME patients revealed seven subtypes with distinct differences in Short Form (SF)-36 scores, clinical phenotypes, and severity. Gene signatures in each subtype implicate five human genes as possible targets for specific therapy. Development of a diagnostic test for subtype status is now a priority. The possibility that these subtypes represent individual host responses to particular microbial infections is being investigated and may provide another route to specific therapies for CFS patients.

Zhang L, Gough J, Christmas D, Mattey DL, Richards SC, Main J, Enlander D, Honeybourne D, Ayres JG, Nutt DJ, Kerr JR. "Microbial infections in eight genomic subtypes of chronic fatigue syndrome/myalgic encephalomyelitis." J Clin Pathol. 2010 Feb;63(2):156-64. Epub 2009 Dec 2. PMID: 19955554

BACKGROUND: The authors have previously reported genomic subtypes of chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME) based on expression of 88 human genes.

AIM: To attempt to reproduce these findings, determine the specificity of this signature to CFS/ME, and test for associations between CFS/ME subtype and infection.

METHODS: Expression levels of 88 human genes were determined in blood of 62 new patients with idiopathic CFS/ME (according to Fukuda criteria), six patients with Q-fever-associated CFS/ME from the Birmingham Q-fever outbreak (according to Fukuda criteria), 14 patients with endogenous depression (according to DSM-IV criteria) and 29 normal blood donors.

RESULTS: In patients with CFS/ME, differential expression was confirmed for all 88 genes. Q-CFS/ME had similar patterns of gene expression to idiopathic CFS/ME. Gene expression in patients with endogenous depression was similar to that in the normal controls, except for upregulation of five genes (APP, CREBBP, GNAS, PDCD2 and PDCD6). Clustering of combined gene data in CFS/ME patients for this and the authors' previous study (117 CFS/ME patients) revealed genomic subtypes with distinct differences in SF36 scores, clinical phenotypes, severity and geographical distribution. Antibody testing for Epstein-Barr virus, enterovirus, Coxiella burnetii and parvovirus B19 revealed evidence of subtype-specific relationships for Epstein-Barr virus and enterovirus, the two most common infectious triggers of CFS/ME.

CONCLUSIONS: This study confirms the involvement of these genes in CFS/ME.

This does go along with Dowsett's assertion that only enteroviral infection counts as true ME and other kinds of infections leading to similar symptoms are different diseases. I don't have a huge issue with whether we say different diseases or different subtypes (although different subtypes seems more convenient to me among the community of those of us with long-lasting disease and PEM) as long as we make some progress towards understanding and treating our disease(s).

Then you have, of course, Natleson et al.'s symptom-based analysis (and Kerr et al. are saying their findings correlate with symptoms so we may be looking at some of the same sets actually).

Janal MN, Ciccone DS, Natelson BH. "Sub-typing CFS patients on the basis of 'minor' symptoms." Biol Psychol. 2006 Aug;73(2):124-31. Epub 2006 Feb 10. PMID: 16473456

Fatigue Research Center and Department of Psychiatry, New Jersey Medical School, University of Medicine and Dentistry of New Jersey, Newark, NJ 07101, USA.

Abstract

The diagnosis of chronic fatigue syndrome (CFS), an illness characterized by medically unexplained fatigue, depends on a clinical case definition representing one or more pathophysiological mechanisms. To prepare for studies of these mechanisms, this study sought to identify subtypes of CFS. In 161 women meeting 1994 criteria for CFS, principal components analysis of the 10 'minor' symptoms of CFS produced three factors interpreted to indicate musculoskeletal, infectious and neurological subtypes. Extreme scores on one or more of these factors characterized about 2/3 of the sample. Those characterized by the neurological factor were at increased risk of reduced scores on cognitive tests requiring attention, working memory, long-term memory or rapid performance. In addition, the neurological subtype was associated with reduced levels of function. Those characterized by the musculoskeletal factor were at increased risk for the diagnosis of fibromyalgia (chronic widespread pain and mechanical allodynia) and reduced physical function. Those characterized by the infectious factor were less likely to evidence co-occurring fibromyalgia, and showed lesser risk of functional impairment. The prevalence of disability was increased in those with the highest scores on any of the subtypes, as well as in those with high scores on multiple factors. Depression and anxiety, while frequently present, were not more prevalent in any particular subtype, and did not increase with the severity of specific symptom reports. Results suggest that subtypes of CFS may be identified from reports of the minor diagnostic symptoms, and that these subtypes demonstrate construct validity.

Then, of course, you have this little matter of the Fukuda mandate:

http://myalgic-encephalomyelitis.com/Fukuda_Criteria2.html

In formal studies, cases of the chronic fatigue syndrome and idiopathic chronic fatigue should be subgrouped before analysis or stratified during analysis by the presence or absence of essential variables, which should be routinely established in all studies. Further subgrouping by optional variables can be done according to specific research interests.

Essential Subgrouping Variables

1. Any clinically important coexisting medical or neuropsychiatric condition that does not explain the chronic fatigue. The presence or absence, classification, and timing of onset of neuropsychiatric conditions should be established using published or freely available instruments, such as the Composite International Diagnostic Instrument (34), the National Institute of Mental Health Diagnostic Interview Schedule (35), and the Structured Clinical Interview for DSM-III(R) (36)

2. Current level of fatigue, including subjective or performance aspects. These levels should be measured using published or widely available instruments. Examples include instruments by Schwartz and colJeagues (37), Piper and colleagues (38), rupp and colleagues (39), Chalder and colleagues (40), and Vercoulen and colleagues (41).

3. Total duration of fatigue.

4. Current level of overall functional performance as measured by published or widely available instruments, such as the Medical Outcomes Study Short Form 36 (42) and the Sickness Impact Profile (43).

Optional Subgrouping Variables

Examples of optional variables include:

1. Epidemiologic or laboratory features of specific interest to researchers. Examples include laboratory documentation or self- reported history of an infectious illness at the onset of fatiguing illness, a history of rapid onset of illness, or the presence or level of a pal1icular immunologic marker.

2. Measurements of physical function quantified by means such as treadmill testing or motion-sensing devices.

Please notice that presence/absence of psychiatric and medical conditions is mandatory, as is level and length of fatigue and level of functionality.

Having followed the MANDATE of Fukuda would have saved us a lot of grief.

Why is no one insisting on this at least?

Jennifer, please bring this up with the CAA board ASAP (stratification mandate of Fukuda, and the subset possibilities that exist and require replication studies).

That the CDC would not follow their official definition (and not be asking/reminding outside research community to do this as well, and including it prominently as part of the definition) is outrageous and unconscionable. This goes for use of Reeves inclusion crieteria, too. The best definition approach is to switch to something which more properly defines ME/CFS, but the CDC should AT LEAST follow their own official definition!!!!!

Of course, we can try to inform this stratification info with later research (such as that the Chalder scale is inappropriate for severe lengthy disease, and maybe with other items needed to add to the mandatory list, etc.) In fact, Fukuda did say later research should be informative:

These research tools will evolve as new knowledge is gained. Second, none of the provisions in these guidelines, especially the definition of idiopathic chronic fatigue and subgroups of the chronic fatigue syndrome, establish new clinical entities. Rather, these definitions were designed to facilitate comparative studies. Finally, general reference to these guidelines should not be substituted for clear and detailed methodologic descriptions when reporting studies. The lack of detailed information about the sources, selection, and evaluation of study participants (including controls), case definitions, and measurement techniques in reports of chronic fatigue syndrome research has contributed substantially to our current difficulties in interpreting research findings.

Yet the CDC's website recommends the exact same set of tools as Fukuda did. There has seriously been no progress that they have noticed since 1994? No progress at all in 18 years? Not even these?

Whistler T, Jones JF, Unger ER, Vernon SD. "Exercise responsive genes measured in peripheral blood of women with chronic fatigue syndrome and matched control subjects." BMC Physiol. 2005 Mar 24;5(1):5. PMID: 1579042
Viral Exanthems and Herpesvirus Branch, Centers for Disease Control and Prevention, Atlanta, GA 30333

Exercise-responsive genes differed between CFS patients and controls. These were in genes classified in chromatin and nucleosome assembly, cytoplasmic vesicles, membrane transport, and G protein-coupled receptor ontologies. Differences in ion transport and ion channel activity were evident at baseline and were exaggerated after exercise, as evidenced by greater numbers of differentially expressed genes in these molecular functions.

CONCLUSION: These results highlight the potential use of an exercise challenge combined with microarray gene expression analysis in identifying gene ontologies associated with CFS.

Cameron B, Galbraith S, Zhang Y, Davenport T, Vollmer-Conna U, Wakefield D, Hickie I, Dunsmuir W, Whistler T, Vernon S, Reeves WC, Lloyd AR; Dubbo Infection Outcomes Study. "Gene expression correlates of postinfective fatigue syndrome after infectious mononucleosis." J Infect Dis. 2007 Jul 1;196(1):56-66. Epub 2007 May 24. PMID: 17538884
School of Medical Sciences, University of New South Wales, Sydney, Australia.

RESULTS: Differential expression of 733 genes was identified when samples collected early during the illness and at the late (recovered) time point were compared. Of these genes, 234 were found to be significantly correlated with the reported severity of the fatigue symptom factor, and 180 were found to be correlated with the musculoskeletal pain symptom factor. Validation by analysis of the longitudinal expression pattern revealed 35 genes for which changes in expression were consistent with the illness course. These genes included several that are involved in signal transduction pathways, metal ion binding, and ion channel activity.

CONCLUSIONS: Gene expression correlates of the cardinal symptoms of PIFS after IM have been identified. Further studies of these gene products may help to elucidate the pathogenesis of PIFS.

Sorensen B, Jones JF, Vernon SD, Rajeevan MS. "Transcriptional control of complement activation in an exercise model of chronic fatigue syndrome." Mol Med. 2009 Jan-Feb;15(1-2):34-42. Epub 2008 Nov 10. PMID: 19015737
Division of Viral and Rickettsial Diseases, National Center for Zoonotic, Vector-Borne, and Enteric Diseases, Centers for Disease Control and Prevention, Atlanta, Georgia 30333, United States of America.

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.

And we must insist upon replication of existing proposed subgroups and further development of subgroups as well. This is the only way we are going to get proper treatment for individuals.

 

Is the CAA taking a leadership role in the BWG?

What does that mean, exactly? Yes, they are a member, albeit one that cannot offer a level of expertise, lab space or any other bloody thing that is critical to the work being conducted. So, what is the CAA DOING (ya know, a verb) there? They are not chairing the meeting and related activities, those roles are spoken for. They're not reporting anything to patients, even so much as "phase 2 is more complicated than expected, please be patient we haven't forgotten you."

So seriously, how do patients benefit in the bargain? Whatever that bargain may be.

I didn't mean to imply that they are taking a leadership role - they are there - they are connected in there. That's all.

 

Cort you made a couple of statements in your posts and I'm wondering if they have another deeper meaning? Do you know something? They are:

No I don't know anything!

How did that idea come to pass? Was it their cautionary stance on XMRV? I understand that it was upsetting (and a mistake in some ways) but it doesn't look it was such a bad way to go right now.

After a year with XMRV still up in the air unfortunately - we still have no conclusions - that's all I'm referring to. You know, its harder than it looked at the time.

That is the big puzzle isn't it? How was a small lab able to do what all these other labs have not been able to do? I think we'll find out soon

By that I just mean that I think we'll have the answers soon. I found Dr. Mikovits statement today that they culture for what, 3 weeks, while the others have cultured for half that time interesting..that could settle things right there.

 

Originally Posted by Cort


The Civil Rights movement and the ACT UP people did not have the internet, the community online, that we now have. They did have healthy members helping them, and after all the mixing up of definitions to the point where a depressed patient can be considered, by the Oxford and Reeves (Empirical) definitions as having ME/CFS, they also had far more clarity.

I think this is what the CAA and Phoenix Rising need. Clarity. Focussed anger. An end to apologist texts trying to be all things to all people. We all have to stop pulling our punches, and tell it straight, all the time. If that creates enemies, so be it. Being effective will always upset some.

• Use the Canadian Consensus Criteria - Fukuda was the first knife in the back. Where is post exertional malaise (or meltdown, as I prefer to call it) in Fukuda? Why does Fukuka exclude tests to confirm an ME/CFS diagnosis?
  
• Never use the nigger name, always preface with ME eg ME/CFS until such a time as the physical cause of this disease is universally recognized.
  
• Support and fund the WP1
  
• Give no credence to somatoform models of ME/CFS

What can I say, Jace - I agree.

 

jspotila said: CAA plans to

craft CFS-specific legislation to define a comprehensive federal response (a tactic used by other disease-groups such as Parkinson's and autism).

sounds like a very good idea.

Otis said:

First, it's lives we're talking about. Our lives, our friends, spouses and our kid's lives, etc. The stakes don't get higher and an overt sense of urgency is paramount. I don't get that *at all* from the CAA's public face.

What's in a minute? That's not much is it? HELL YES. Multiply that minute times the number of those suffering.

Secondly this is a very unique moment in history. One that may not roll around again any time soon and it needs to be pounced upon. ALL IN. NOTHING LESS.

This is it for me in a nutshell. Anything less than "all in" is imprudent and inappropriate imo.

Marty said:

Contrary to the CAA statement, I think that one good advocacy organization would make a huge difference. We could turn the world upside down if we had a good leader with paid staff. After the CAA brought in Kim, I stopped supporting them because I saw our money going to what I thought was ineffective government campaigns before we had good science. Now we have 20 years of proof that medical, and therefore public, support is not only still missing, but ME/CFS is still a joke. Magazines and TV and doctors and the public are still calling it "chronic fatigue". I wouldn't think of telling anyone I have this disease.

I have to agree with Roy, but let me first say that I have always found Kim to be a very nice and capable person. In fact I agreed with her "cooperative" approach. I thought that our whole problem was information based. If we could just distribute information packages documenting the great science that we had even 20 years ago, the government and the people would be amazed and be educated. It was best to treat everyone respectfully and use our "inner voices" and little by little, being right would win. It didn't work for AIDS and it didn't work for ME/CFS.

I'm older now, and the evidence says that I was wrong. It is not a problem of information; do you know how many hundreds of thousands of letters and information packages have been sent? And millions of patient-hours putting them together? Kim said that she has sat at every ME/CFSAC meeting for 20 years, and what has been accomplished? I watched the last two ME/CFSAC meetings; I pulled my hair out and wanted to throw rocks at my TV screen. I heard the CDC rep, Beth, try to explain to the committee how ME/CFS has psychological underpinnings. For heavens sake, WE HAVE GOTTEN NOWHERE. The smart thing to do is to change tactics, CAA.

I think this piece by Marty is very insightful. 5,000 (according to Komoroff) articles in peer reviewed med journals showing frank biological pathology has served to only somewhat improve public perception of us and has done nothing to change NIH and CDC's mistreatment of us (i would attribute the ostensible change in attitude emanating very recently from NIH to the efforts of WPI and individual patients). To me, this clearly shows that CAAs mission of focusing on research is misguided. I think we've got to put the majority of our resources into raising hell. We ideally should be holding our members of congress more accountable. HHS will never help us unless forced to do so from above (congress). i'd welcome any suggestions as to how to do this from Marty or others. Perhaps organizing letter writing to the house and senate committees responsible for CDC and NIH; other suggestions?

I agree strongly with parvofighter too on the hotbutton issues. CAA should be funding studies on mortality in ME and how about the extremely strong connection between ME and very rare lymphomas?- there has never been a real study on these topics!! What about looking at "CAV", the defreitas retrovirus, again with hopefully advanced tools we have now? what about funding Lipkin or someone like him to do the type of research the NYTimes said he does isolating common virus dna and rna from sufferers. NY Times claimed his lab can do this in a few days. I think CAA funds some great studies, but i think i has to be even more focused on studies that will have high-impact on our advocacy efforts (and finding a cure).