HHS officials have made confusing statements about the goals of the P2P Workshop, but I have obtained documents through FOIA that give us insight into the structure of the meeting. Two versions of the Workshop draft agenda strongly suggest that the meeting will be focused on the broad category of unexplained fatigue, and the most effective treatments for that symptom.
The Agenda Documents
I obtained these two agenda documents from NIH through a FOIA request. The first is titled “DRAFT Agenda” (previously obtained by another advocate, as well) and the second is titled “Agenda Example.” Neither document is dated, but circumstantial evidence suggests that both were drafted after the January 2014 Working Group meeting.
The Draft includes a list of possible speakers, including several advocates to address the “Patient Perspective.” My name is on that list, but I have not been contacted by anyone at NIH at any time about serving in that capacity. I don’t even know who put my name forward. Whether an invitation will be extended to me remains to be seen.
The Key Questions as presented in the Draft and Example documents are likely out of date, now that the systematic review protocol has been published. The Questions from the evidence review will structure the meeting, but the agendas are important indicators of NIH’s perspective and overall approach to the meeting.
Framing With Fatigue
Both of the documents include the same description of the overview that will begin the meeting:
Dr. Maier will detail the topic and why it is of public health importance:
Overwhelming fatigue or malaise as a public health problem
Controversies that exist
Treating ME/CFS with drug and non-drug therapies
Just to be sure you didn’t miss it, here’s is the framing for this meeting on ME/CFS: Overwhelming fatigue or malaise as a public health problem. Not ME/CFS as a public health problem. Not post-exertional malaise as a public health problem. Not cognitive dysfunction and disability as a public health problem. To NIH, “overwhelming fatigue” is the public health problem.
This is so wrong. It ignores what we’ve been saying about our experiences for years. It ignores the science on PEM and cognitive dysfunction. It ignores the fundamental question of what disease or diseases are being included in the CFS bucket. In fact, it steps back in time to the Oxford definition: overwhelming fatigue alone.
The real public health problem is that since 1988, CFS has been a wastebasket and dumping ground for people with unexplained chronic fatigue. Some of those people have depression, anxiety, MS, and other illnesses. Some of those people have medically unexplained fatigue. Some of those people have a disease characterized by PEM and cognitive dysfunction.
To lump all of that together as a public health problem of “overwhelming fatigue” completely and utterly misses the point. It perpetuates the hand waving and blurred lines in the government’s approach to my disease, and there’s just no excuse for it at this point.
Treatment Barges In
At the May 2013 CFSAC meeting, Dr. Maier said that treatment research was part of the evidence review, but she portrayed it as relating back to the case definition question:
The goal of the evidence-based methodology workshop is to understand and identify how the evidence shows up for case definitions, for outcomes, for interventions, and for treatments. If it turns out that some interventions have more impact or a more positive outcome for post-exertional malaise, then we’re going to know that post- exertional malaise in a case definition is probably going to be a good thing to do. Dr. Maier, May 23, 2013 CFSAC Minutes, p. 11. (emphasis added)
But now we know that the evidence review will ask about treatment harms and benefits, and the characteristics of subgroups, responders and non-responders. The agenda documents reveal what this treatment focus will look like.
The Draft Agenda focuses on tools to measure outcomes, rather than comparative effectiveness of treatments. The Agenda Example document is very different. Here are the treatment presentations from that document (each topic allocated 20 minutes):
Cognitive Behavioral Therapy
Graded Exercise Programs
Symptom-based Medication Management
Harms
Patient-Centered Outcomes
Quality of Life
So we have an evidence review that lumps all the case definitions together, including Oxford. And we have an agenda that gives more time to CBT and GET than it does to symptom-based medication. And there is nothing here on disease-modifying treatment, like rituximab, Ampligen, or antivirals.
The topic selection and allocation of time among these treatment topics sends a subtle but powerful message to the Panel of non-ME/CFS experts, especially in light of the failure to distinguish among the case definitions at the outset. Previous evidence reviews, including AHRQ’s review from 2001 and the Brurberg, et al review published in February found no significant differences among case definitions or treatment outcomes, but those reviews were not set up to critically examine those differences. And as I’ve already pointed out, this current review assumes that differences among definitions represent subtypes and not separate diseases.
Design Flaws
The agenda documents show that the P2P Workshop is fundamentally flawed. The meeting is framed with the public health problem of “overwhelming fatigue.” The evidence review will include studies on adults with fatigue, and exclude those with unspecified underlying diagnoses. All the case definitions are lumped together for the purposes of assessing the reliability of those definitions and the effectiveness of treatments.
The evidence review and meeting agenda should begin with the proper scientific question: are ME and CFS the same disease, separate diseases, or points along a spectrum of fatiguing illnesses? That was the original starting question in the AHRQ evidence review contract, by the way. But it’s gone. The decision was made (not sure by whom) to assume the answer: that it is all one disease, separated only by subgroups. That assumption is the fatal flaw in this entire enterprise.
Remember that the P2P outcome will be decided by a panel of non-ME/CFS experts. We don’t know how they will be screened for bias. We won’t know who they are until shortly before the meeting. We will have no input into their selection.
This is not good science. This is sloppy, not precise. To revisit Dr. Maier’s jury analogy: this process will ask the allegedly impartial jury (selected by only one side) to reach conclusions based on evidence that has been marred by bias and assumptions. Maybe they will reach the right conclusions, or maybe the deck is stacked against us.
We have to find ways to speak out about this. I’m working on something right now, and there will be ways for you to express your own concerns. I hope you will join me.
Thank you for this, Jennie. Great review.
In addition to asking if ME and CFS are the same disease, I think that HHS has to also ask whether the concept of CFS, as defined by Oxford, Fukuda and EMpirical, is even a valid clinical entity to begin with. The idea of taking all the conditions that cause chronic fatigue for which we do not yet have a medical explanation and stuffing them into the same bucket without any scientific proof that they are biologically related is unscientific.
As you say, the public health crisis – I’d say the public health menace – is that the disease characterized by the 2003 Canadian Consensus Criteria and the 2011 ME ICC has been ignored and denied through such bad science.
Great reporting! Is it any wonder why I have been living with this overwhelming sense of impending doom for the past three months? I hope they get it right soon, there is no reason for all this governmental mediocracy.
I agree with Mary. The Fukuda was a response to the ME that is in US. They did not think it was ME, but it was. As has been shown, the Strauss goal, for which he believed Fukuda criteria promoted, was to do away with a distinct disease entity and just identify fatigue as the problem. Seems his influence at NIH is still there. Fukuda has been useful in studying ME, as the many biological abnormalities found in Fukuda CFS patients show (gene expression, anaerobic threshold, etc.) But, it is imperfect and needs to be replaced.
But Oxford doesn’t even come close to ME. It doesn’t identify any disease.
Simply put, we have idiopathic chronic fatigue, we have chronic fatigue and then we have ME, which is also known as CFS.
As I read Jennie’s blog, I am again reminded that alllllllll of this is because of the name “chronic fatigue syndrome.” It amazes me that the name itself has made everyone think the disease is fatigue. If the name of diabetes had been “pee a lot syndrome” then they would do a study on everyone who reports peeing a lot and declare it revealing of diabetes. It’s all in the terminology. The diseases / conditions don’t change, but the name and definition confuses EVERYONE, even people who should know better.
I think I should write an article on this.
I meant, we have idiopathic chronic fatigue, then we have chronic fatigue from other illnesses, and then we have ME, which is also known as CFS.
“If it turns out that some interventions have more impact or a more positive outcome for post-exertional malaise, then we’re going to know that post-exertional malaise in a case definition is probably going to be a good thing to do.”
There’s a flaw in that logic. What if it turns out that those interventions have a more negative outcome for post-exertional malaise? Does that then imply that it should NOT be used in a case definition?
YES! I was turning this over in my mind, too. Treatment outcomes can give us clues about pathophysiology, a bedside to bench approach. But it does NOT make sense for case definition.
“Quality of life”
That’s a death and dying statement…..
That should be on a different systematic review such as one for hospice care, not a case definition for an illness. Non medical people will wonder if they should be giving us the shovels
to dig our graves with that one.
Yes, I sound sarcastic, but not really because non medical people who do not know illness, that will be the first thing they think. And, the one or the few that are wise enough, will see something isn’t right with this process.
This is useful. It helps to be able to better understand and to be able to document the government’s behavior. But, unfortunately, the relative value of this sort of information, given our limited capacity to produce it, is continuously outweighed by the government’s ability to brush us off like flies.
At what point do we stop fleshing out the narrative of determined obfuscation, arrogance, and ignorance on the part of the government (a, literally, never-ending process) and begin to find ways to convey our story to the only agent that truly matters — the public?
I agree there are problems but I don’t see any way to answer the question below scientifically.
“The evidence review and meeting agenda should begin with the proper scientific question: are ME and CFS the same disease, separate diseases, or points along a spectrum of fatiguing illnesses?”
With ME you have symptoms and clinical descriptions – which vary, by the way, quite a bit between the outbreaks. After that there are NO ME studies that determine immune or endocrine or metabolic or any other kind of dysfunction that is present in it.
I don’t see how you can determine if ME is different from CFS if you have no biological data to differentiate it from CFS? It’s possible they looked at the evidence on ME and concluded that that question was impossible to answer in a scientific manner (i.e. with data). We don’t even really have data on Oxford vs Fukuda because no one explicitly compared the two (ie Fukuda patients have X problems and Oxford patients have y problems.)
While I agree that the statement regarding fatigue and malaise is rather vague it may be that it was not intended to be very precise. We’ll see what happens, but is being PEM is excluded by not being specifically included?. I hope not. If it is this whole thing went down the tubes – Maier should know better.Is there any way we can see the documents?
The agenda sounds disasterous but then again it’s hard to know how it would be any different once they narrowed their focus to treatment studies which are dominated by CBT…That’s really bad and it’s not going to say anything new anyway.
So basically the IOM process has thus far been everything patients’ hoped for and the P2P has thus far been everything patients have feared? Excellent.
I also don’t see how there’s any getting around the CBT/GET issue. Psychobabblers in the UK have historically been the most successful in getting funding for their crap CBT/GET studies, psychobabbler CBT/GET proponents inhabit an area of ‘medicine’ that has little to no scientific accountability which means they can make any sort of pronouncements they want no matter what the evidence really says, and biomedical ME/CFS researchers continue to be stymied in their attempts to do legitimate research because it has been much more convenient for governments to listen to the psychobabblers and ignore the issue than it is to actually do something competent so that progress is made.
I’m not sure, but I think we can only hope that someone on the P2P acknowledges the fact that 1) the only benefits shown thus far for CBT/GET involve ‘moderate’ improvements on a handful of questionnaires, 2) that these results are not correlated in any way with any sort of improvement on any of numerous objective measures of outcomes, and 3) the authors of the CBT/GET studies themselves state that the ‘treatments’ they provide are not just similar to, but actually consist of, ‘the essence of the placebo response’. This is reinforced by the fact that all of these psychological ‘therapies’ have similar ‘response rates’ of around an additional 15%, which is basically what would be expected from a placebo effect. Furthermore, not only have CBT/GET studies not shown any improvements in objective measures of outcomes, but in fact actually the reverse is true- CBT/GET studies have repeatedly shown that there are no improvements in objective measures of outcomes.
I guess we should just make clear at the next CFSAC meeting that if the federal govt. wants decades of more antagonism from ME/CFS patients then they can continue to do what they’re currently doing with the P2P, but if they do continue to do what they’re doing then patients are just going to s*** all over their sloppy bs garbage and it’s just going to be more of the same.
I have no problem with them discussing CBT and GET, but the context you described is absolutely essential. As is examining harms and drop out rates – Tom Kindlon has done great work on that. We will have to rely very heavily on whoever is chosen to present on these topics to provide that proper context. My fear is that the evidence review will not examine these issues with sufficient detail, which means the report will not present them, which means the Panel won’t have them, and it will come down to whoever NIH selects to present on the topic to fill in those gaps.
@cort
Cort wrote: I agree there are problems but I don’t see any way to answer the question below scientifically.
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“The evidence review and meeting agenda should begin with the proper scientific question: are ME and CFS the same disease, separate diseases, or points along a spectrum of fatiguing illnesses?”
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I agree with Jennie, the posing of a definitional question at the very start of the meeting is essential. Although Though I’m not sure it would be helpful to require a choice between, on the one hand, ME and CFS as being exclusive of one another, and on the other, as their being part of a single continuum.
There are both semantic and statistical uncertainties in an ME versus CFS polarity such that the terms and their associated diagnostic criteria could involve a large range of complex overlaps. If we use a simple Venn diagram model everything from a small ME circle sitting in the exact middle of an all encompassing CFS circle, to a small CFS circle laying tangentially to a larger ME circle could be possible. I would give the definitional question a more nuanced range of rhetorical answers by allowing multiple overlaps and multiple spectra within which a range of continua may be evident. This would demonstrate the level of uncertainty that the current state of (lack of) knowledge provides – and highlight the sheer scale of the ‘gaps’ that the P2P is apparently so concerned with. The gaps are far greater than the ‘knowns’; I would use the image of islands in the Southern Pacific Ocean – way more unknown sea than islands of certainty.
It’s not necessary for the definitional question to be answerable – it is not needed as the basis for a single working hypothesis, but that doesn’t stop it from having scientific validity. One doesn’t need a single falsifiable hypothesis for the creation of the Moon to be able undertake Lunar Exploration, it is enough to start by saying what do we know ? and from that “what else would be really useful to know”.
Thank you, Jennie (and all). Please do post suggestions for how to (try to) most effectively speak out against this “stratagem.”
Regarding post 10, I wanted to add that (to my understanding – and also to help me get the main points down) even when CBT/GET is alleged to have shown a slight, subjective improvement, this “improvement” does not last, and CBT/GET can additionally, even permanently, worsen some people’s condition. Plus, these outcomes – pitiful as they are – are associated with those who were the least sick to begin with. And we don’t even know what condition/illness they actually had.
If CBT/GET could be encapsulated, no one would buy it. No one. A: “Here, take this pill.” B: “Why? What does it do?” A: “Absolutely nothing. Or you could become permanently bedridden.” B: :/
@John – Do you (or anyone) have references handy for info regarding 1) CBT/GET and the placebo effect and 2) CBT/GET fail to create objective improvement? Thank you.
Where’s Ess? Ess, I miss your spirited voice. : )
Ohhh, Ren, thank you. I’ve been sitting back on this one . . . as many are aware, ’tis no surprise whatsoever that this is what is happening with the culmination of the P2P arm of the IOM contract — the disastrous runaway train wreck HHS saga of redefining ME/CFS in their predetermined outcome–ready set to bury us for another 30 + years — and so I’ve had nothing more to offer; it’s been said time and time again.
However, as you have sought me out, and thank you, Ren 🙂 please see my comments re CBT and GET #1 at ME/CFS Forums regarding Deborah Waroff’s interview with Dr. Anthony Komaroff; link below.
http://www.mecfsforums.com/index.php/topic,20280.msg162265.html#msg162265
Onward we go!
Thank you, Jennie for explaining this. I am in a wiped-out state, so the explanations are helpful.
If the IOM and HHS and NIH are only looking at fatigue, that’s absurd. Fatigue comes with all sorts of ailments, and overwork of all types. It’s how my friends feel if they burn the candle at both ends, stay up late doing things. Then they sleep late for a few days and they are fine.
Whereas we end up collapsing for days if we overexert ourselves or even just exert ourselves. And what kind of exercise? On good days, I can do 12 leg lifts on my bed and 5 modified knee bends (after resting). On bad days when I’ve done something outside the day before, I can barely do 2 leg lifts. It takes 3 days before I can do 12 again and I can’t do more than that.
So, we’re back to just fatigue. How disheartening. To quote a blogger with ME/CFS, she doesn’t have fatigue. She has muscle pain, neurological problems, exhaustion and cognitive difficulties.
If P2P is only concerned with questions of research, then there is a challenge for patients to articulate the problem that CFS and ME may not be the same thing. Taking the extreme epidemiological views –( Reeves versus Jason ?), one can conclude (as many patients do) that even where the CFS of Reeves and ME of Jason coincide, the latter is only a small and discrete cohort within the former. Unfortunately this neat picture can’t be easily maintained when the perspective is moved from a population level to the individual sufferer.
To take just three disease elements which patients who are familiar with ME research would likely agree upon as having a potential role in their illness – a) a genetic predisposition (evidenced by the gender differential), b) an environmental aspect (pathogen, toxin, allergen) and c) autoimmunity (as per Fluge & Mella) one can quickly see that a wide range of possible disease processes can be suggested. At least nine variants appear to be possible depending upon how many elements are accepted as being necessary to meet a test for ME or CFS or ME/CFS
1.Single element – environment : pathogen i.e chronic infection, or chronic toxic exposure
2.Single element – non gene mediated endemic autoimmunity
Multiple Elements (#s)
3.Non gene mediated autoimmunity stimulated by environment (pathogen) (x 2 )
4.Non gene mediated autoimmunity stimulated by environment (allergen) (x 2)
5.Genetic predisposition producing endemic autoimmunity (x 2)
6.Genetic predisposition stimulated by environment (pathogen) producing autoimmunity (x 3)
7.Genetic predisposition stimulated by environment (allergen) producing autoimmunity (x 3)
8.Non gene mediated autoimmunity stimulated by environment (pathogen + allergen) (x 3)
9.Genetic predisposition stimulated by environment (pathogen + allergen) producing autoimmunity (x4)
Note – the above involves a mangling of different classes so not a meaningful analysis in itself, it’s just to show how, even within the patient view, there is no one definable illness that could be ME that is definitely not CFS or vice versa. Any of the above could be part of the Reeves population and in the absence of definitive biomarkers there is no means to exclude those from Reeves to arrive at a Jason population. This might seem like a crazy way of looking a things but it does set in relief the mismatch between what patients believe they ‘know’ and the kind of critical process that P2P seems supposed to be.
What patients know is that their illness is no longer “medically unexplained.” This alone takes it out of the “CFS” characterization by the very definition of “CFS.” Emerging research is uncovering the many neurological and immunological abnormalities along with energy production problems present in this illness. These abnormalities account for the symptoms experienced and reported by the patients. No, we don’t have the complete picture of this illness or its cause, but that should not put it into the “medically unexplained CFS” category. There are many, many illnesses for which we do not know the cause or the complete pathophysiology. What is unexplained is why there is such a great effort on the part of governments and some in the research and medical arena to downplay and obfuscate the nature of this illness by burying it in “fatigue.” It is time to do away with the whole ill-conceived concept of “chronic fatigue syndrome” and to recognize this illness for the serious, debilitating muti-systemic neurological, immunological, energy deficient disease it truly is. Further research will only continue to substantiate this.
AGREED!
@Sandra
Well said, Sandra!!
Ditto to what Sandra said and comments in response to her words.
How can the government, researchers and some doctors and science writers continue to label this as “fatigue” when more and more objective tests are finding abnormalities of many types?