Sunday, April 17, 2011

What was missing from the NIH State of Knowledge Workshop?

In a word, clarity.

Whoever organized this conference has no coherent idea of what’s going on in this illness. Granted, there are many gaps in our knowledge, but there are also some pretty consistent themes that are well-recognized, at least by the patients and by some of the doctors that take care of them. Most people have post-exertional malaise. Most have sleep difficulties. Many, if not most, have one of the several manifestations of orthostatic intolerance or other autonomic nervous system dysfunction. Most have evidence of immunological dysfunction. Most have one or more viral infections. Some have other pathogens. Most have pain. Many have associated conditions such as irritable bowel syndrome, interstitial cystitis, fibromyalgia, multiple chemical sensitivity and pelvic pain syndrome. Most have neurocognitive problems, including memory loss, sensitivity to noise and light, word-finding difficulty, executive functions abnormalities. Many have muscle twitching or cramping. Many have low blood volume. And so on.

The Workshop was designed to confuse not to enlighten. This may have been deliberate, or it may be because the organizers (and who are they? Dennis Mangan? Suzanne Vernon?) simply don’t understand the disease well enough to organize it appropriately. They repeatedly said they were interested in reverse translational research, from the patient bedside to the lab bench, but they organized the conference according to medical specialties and research areas: infectious diseases, neurology, exercise physiology and energy metabolism were the medical specialties; systems biology and biomarkers were the research areas. They also included a treatment section, but no new treatments were discussed that can be put on the CDC website as effective treatments. No randomized controlled trials were reported. No acknowledgment that clinicians are having success treating with antivirals. Instead, supportive management was discussed. This traditional approach is what has impeded progress toward understanding ME/CFS for more than two decades. Everybody thinks their part of the elephant is the elephant.

They could, instead, have organized the conference around the prominent symptoms seen most commonly in people who have the disease. That is, organize it around what patients experience. What is happening in the bed. But they didn’t. Autonomic dysfunction is a prominent and measurable problem, but they didn’t have a session on autonomic dysfunction. There were three presentations on autonomic dysfunction-related topics, but they weren’t in the same session. Dr. Freeman talked about the autonomic nervous system in the Neurology session; Dr. Rowe talked about orthostatic intolerance in the Exercise Physiology and Energy Metabolism session (why?), and Dr. Biaggioni talked about Postural Tachycardia Syndromes in the Treatment session. Why weren’t these three presentations grouped, so that the audience would focus on this important symptom complex? Why was there no speculation about how various viruses might affect the autonomic nervous system and/or cardiovascular system? Dr. Biaggioni suggested that ME/CFS might be on a spectrum of dysautonomias. Why wasn’t this idea pursued? If the three presentations had occurred together this concept would undoubtedly have been discussed further. And, of course, why wasn’t there adequate time given to a discussion and formation of a future research plan, with dedicated funds, that would allow these three researchers to work together or separately to continue to study this important topic?

Here’s another example of this organizational problem: two researchers, Dr. Light and Dr. Snell, presented important data about post-exertional malaise, coming at the problem from very different angles. Dr. Snell’s presentation was in Exercise Physiology and Metabolism (there were, by the way, no other presentations on metabolism in this session, despite an abundance of research on oxidative stress in ME/CFS); Dr. Light’s presentation was in Neurology, for reasons that are unclear--adrenergic gene expression upregulation? Well, yes, but just as importantly inflammatory cytokine gene expression upregulation and acid-sensing ion channels gene expression upregulation. This presentation could as easily have been put in immunology or metabolism. But they both really belonged in a separate session called Biomarkers for Post-Exertional Malaise (or effort-induced exacerbation, a better name). This would help patients. Post-exertional malaise is considered by many to be the hallmark symptom of this disease. These two researchers say it can be reliably measured. That means it may be able to be understood and be treated. Or used to follow the response to treatment of other aspects of the disease. This is huge. Why was this not showcased in a separate session instead of being two separate pieces of information in a confusing mix of information? And if acid-sensing ion channels are up-regulated, as seen by Dr. Light, are they reacting to lactic acid produced as patients shift more quickly to anaerobic metabolism, as seen by Dr. Snell? What happens in the autonomic nervous system that upregulates the adrenergic receptors? Put the data right next to each other and scientists will begin to ask these questions. People who aren’t very familiar with this disease (the vast majority of NIH researchers) aren’t likely to make these connections when they’re not fully aware of which of the array of symptoms are most important. There’s a way to present this as confusing. And there’s a way to present it as an intriguing puzzle whose pieces are beginning to fall into place.

This is so important. If post-exertional malaise is the cardinal symptom of this disease then we need to know much, much more about it. It may be that it’s easier to find XMRV or other MLVs in the blood on the second day of a two-day exercise challenge. It may be that EBV re-activates on the second day. Or HHV-6. Or CMV, chlamydia, mycoplasma, etc. It may be that patients‘ orthostatic intolerance is worse after an exercise challenge. It may be that gut flora changes after an exercise challenge. Markers of oxidative stress may get worse. Symptoms of co-morbid conditions like IBS, IC and FM may be worse. Anecdotal evidence suggests that this is so. As someone suggested, it may be that some or all these things happen whenever the anaerobic threshold is exceeded, so it may not be necessary to subject patients to a maximal exercise challenge with the attendant risk of severe symptom exacerbation. Given the difficulty that patients have with coming into a lab and exercising two days in a row, studies should be designed looking at all of these issues (and others). This requires collaboration. And a research plan.

It also requires that people stop looking backwards. Many of the old studies of people with ME/CFS are flawed, because the research groups were not well defined or well described. Although the importance of this issue was fully explained by Dr. Jason at the beginning of the meeting, speakers such as Dr. Kent-Braun blithely reviewed studies that were ten and twenty years old without any mention of who comprised the data set. There also was no mention of a second exercise challenge in the studies she reviewed. She then came to the conclusion that there is no difference in several measures of exercise tolerance between patients and controls. No one questioned her about what criteria were used to define the patient groups in the many negative studies she cited or about the possibility that a single exercise challenge is not sufficient to distinguish patients from controls. No one commented on her own admission that she has been out of the field for years. Dr. Natelson presented data from more than 10 years ago that purported to show that patients with ME/CFS have no evidence of immune dysfunction. He neglected to mention how much the technology for finding immune markers has changed in the last ten years, as Dr. Klimas emphasized.

The somewhat testy interchange between Dr. Klimas and Dr. Natelson (she suggested he stick to his own specialty, neurology) illustrates another aspect of the questionable planning that went into this Workshop. While controversy and discussion is good, it was not necessary to schedule opposing points of view right after each other repeatedly. Dr. Klimas and Dr. Natelson. Dr. Coffin and Dr. Mikovits. Dr. Kent-Braun and Dr. Snell. Disagreement after disagreement. It gave the impression that there is no verifiable data in this disease. It fosters a sense of hopelessness, futility. Nothing to be found here. Keep on moving. If, instead, you put Dr. Snell and Dr. Light together you see consistency. Different ways of measuring it, but consistent abnormalities indicative of measurable post-exertional changes and the importance of repeat testing with an exercise challenge. If you put all the autonomic dysfunction data together you begin to form a picture. You stop. You look. You listen. You move forward, not away.

The session on biomarkers also gave the impression that there are none. (Of course, this is the stance the CDC takes on its website). Dr. Klimas presented some interesting data on potential immunologic biomarkers, which Dr. Vernon described as “overly optimistic”. Dr. Cook gave an interesting talk on the potential for functional neuroimaging to be a biomarker, but, as yet, this is only available as a research tool. Interestingly, he also found that it’s important to challenge the brain to see the differences between ME/CFS patients and controls. Dr. Dean talked theoretically about the as-yet-unrealized potential of genetic biomarkers. Significantly, he emphasized the importance of an accurate definition so it’s clear who has the disease and who doesn’t. He also emphasized the importance of looking at large numbers of patients, which requires adequate funding. Dr. Mikovits said her work on biomarkers was quite fruitful but she wasn’t given a chance to talk about it. Meanwhile, it looks like Dr. Snell and Dr. Light have found biomarkers that just need to be verified and operationalized. Why weren’t they in the biomarkers session? Why isn’t the NIH jumping on this and funding verification studies? Why isn’t Dr. Snell’s protocol on the CDC website? It may turn out that these particular biomarkers don’t identify all patients with ME/CFS, but they may, at the least, identify a very significant subgroup.

Another way this Workshop avoided rather than fostered clarity can be seen in the topics that weren’t even considered: mitochondrial dysfunction and associated oxidative stress (so much data not even mentioned), the other important associated infections, cardiac abnormalities, and, most importantly, the problems of the very sickest patients who have never been studied in any serious way. There was a wealth of knowledge in that room that was not even tapped. Dr. Lerner was in the audience and wasn’t allowed to speak, despite his success in treating patients with antivirals. Dr. Montoya, Dr. Brewer and many other clinicians with a lot of experience “at the bedside” weren’t there. Dr. Deckoff-Jones, with all of her expertise about retroviruses, also didn’t come. Rich van Konynenburg and Marian Lemle, both of whom have made major contributions to the understanding of possible metabolic abnormalities in ME/CFS, were in the audience and weren’t allowed to speak. The unscheduled patient statements were excellent, but each of them would probably have said something different if they’d had time to prepare. There were probably many other people in the audience who are experts on some aspect of this disease that weren’t allowed to speak. Instead, Kim McCleary was given ten minutes to blather about researchers acknowledging their funders (trolling for plugs for the CAA), “responsibly” bridging between scientific journals and popular media, and “helping” people affected by the research to understand the results and the next steps. Pull-eeze. It’s Kim as kindergarten teacher again, admonishing us to use our inside voices. And helping our little minds to understand what the big researchers are doing on our behalf. Oh, and there was the blatant plug for the CAA’s part in some of the research that was presented at the Workshop. Low on funds, Kim? Need some free advertising? Why was the CAA given such a prominent presence on the agenda? Many patients don’t feel the CAA represents their interests on any level. Isn’t this a conflict of interest on the part of the NIH? Annette Whittemore was there and wasn't invited to speak. What's up with that?

Meanwhile, there were some researchers who are new to the field and presented very interesting and promising data and ideas. But the question is: given all this confusion, the lack of funding, the unsolved definition problem, and the little lectures by McCleary about expressing their gratitude to their funding sources, will they come back?

Several of the newer researchers mentioned the importance of the definition. Despite the prominence given to this issue as the first topic of the Workshop, there was no action. There was no agreement that all taxpayer-funded research (CDC and NIH, both intramural and extramural) should be required to use the Canadian Consensus Criteria to define the patient sample. Or even Fukuda plus post-exertional malaise. Or at the very least repudiate the Reeves definition. Huge disappointment. Instead of re-summarizing the summaries, Suzanne Vernon could have exhibited leadership by insisting that at least this single task got done. Nothing. What’s the point of coming together to talk if you don’t even know what or who you’re talking about?

On to the research study design problems. Dr. Rowe pointed out that the heterogeneity of the patients makes it easy to disprove any given hypothesis or the utility of any given treatment. He showed great insight when he said that his own study had shown fluorinef was not statistically significantly helpful in ME/CFS, yet he uses it, and it’s very helpful in a subset of patients. He suggested that different study designs, including n of one studies where patients serve as their own controls, may be necessary.

And, of course, the funding. Several people made the point that ME/CFS is assigned to a part of the NIH (Office of Research in Women’s Health, or ORWH) that does not have money to fund research grants. As Dr. Baraniuk said, where is our home? Essentially, there is no head of an NIH Institute going to bat for us; no one is accountable to us. No one is making sure the correct definition is being used, that data is being collected to allow subsets and their unique responses to be identified, that the studies are large enough to identify subsets, and that they are FUNDED. The need for reverse translational research (patient bedside to lab bench, rather than vice versa) was discussed, but who is going to make this happen? Patients and their doctors have plenty of questions but who among the researchers are listening? Who is assigned to listen?

This isn’t a disease that is confined to women. Why are we consigned to an Office that has no money to disburse for research? It was announced that even the FDA has now assigned ME/CFS to a specific division, the Division of Pulmonology, Allergy and Rheumatology Products. One could certainly argue about that assignment (why not Infectious Diseases--don’t they have that at the FDA?), but at least you know who to call. And you know that person has some money.

Returning to what wasn’t there at this Workshop: again, they talked about reverse translational research from bedside to bench, but most of the doctors who are at the bedside having some success treating patients weren’t there. Instead, among the participants were the usual researchers espousing their usual tunnel vision theories. Some have had little or no success treating patients. Some haven't even tried.

Part of what was missing wasn't there because it hasn't been done, obvious things like longitudinal studies (even in Tuskegee they studied the patients despite deliberately not treating them, so at least someone else could benefit from a better understanding of the natural history of the disease), family studies, epidemiological studies of all the known outbreaks, a search for other outbreaks, in depth studies of the patients who are too sick to get to a clinic.

Another thing that wasn’t there was time for discussion. There were too many short talks, some of which were superfluous. Let me repeat: why wasn’t adequate time allotted for discussion and the formation of a future research plan, with dedicated funds, that would allow these researchers to work together or separately to continue to study this important, and possibly spreading, disease? It would have been gracious of Dr. Vernon to have ceded her time to foster such a discussion. It would have been prudent of Dr. Pinn to make sure that there was a plan for future research and funding mechanisms in place by the end of the meeting, or at least a plan to make a plan, rather than apologizing repeatedly for the lack of time as she ran out the clock.

What there was, of course, was a lot of talk about budget cuts. How ironic that the day ME/CFS finally gets NIH attention is the day the government is about to be shut down. It wasn’t shut down, of course, and, as far as we know, everybody at the NIH is still being paid. Dr. Collins didn’t look worried about where his next meal is coming from. As Dr. Baraniuk pointed out, millions of dollars are spent on giant studies of thousands of patients to prove that one cardiac drug is marginally better than another. We could learn so much from a few studies that looked at a number of measures before and after exercise. We could learn so much from a few studies of long-term antiviral and/or antiretroviral treatment. We could learn so much from a few longitudinal studies. We could learn so much from a few decent epidemiological studies of regional and family clusters. We could learn so much from a few appropriately designed studies of therapies for orthostatic intolerance. We could learn so much from the sickest patients. We could, unfortunately, learn so much from autopsies. We could learn so much even from a carefully designed Workshop that looked closely and dispassionately at what we do know about this disease. We have a lot of data, but it seems like no data because it’s not organized properly. Controversy is diverting (pun intended), but it doesn’t help the patients. This conference was designed to highlight the controversies. What patients and their caregivers need is clarity.

22 comments:

  1. Once again, Chris, you keep asking all the right questions.

    This workshop lacked one thing: An aim.

    It was a get-together of a few specialists, some people with a questionable raison d'être and a few others thrown in just to create controversy.

    And when they parted, nothing had changed. No plan, no follow-up, and again, NO MONEY. And for that, the CAA is thanking people in our names?

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  2. Brilliant article Chris. Can we not get you to organise the next event instead of having the usless CAA. Why do they get to be there anyway?

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  3. I sent an email to Dennis Mangan this morning, with not just the link, but the copied text, and a polite, brief note, suggesting that there are some very good insights in this article. I also suggested that he might consider sending it to the participants as part of the follow-up to the meeting.

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  4. Russian Gulag Prisoners would often write to Stalin begging for help.

    He would have a hearty laugh at them, as he was the one who put them there in the first place.

    Learning from Stalin's & Hitler's mistake of physically separating and murdering large groups together, modern mass murder is done in homes away from prying eyes. And in ways where there is no obvious physical traumas that anyone can clearly see, no matter how hard they try not to.

    You're writing to Stalin here, don't you know?

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  5. I found the workshop to be quite easy to follow, understand and appreciated what was presented.

    I found reading this long blog to be tiring and complicated and a waste of my energy. Everyone is a critic and it gets very, very tiresome.

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  6. Where were the epidemiologists indeed! 30 years and little or no epidemiology. We don't know the risk factors if you have the illness. We don't have studies if family members are catching ME. We have basic questions ignored.

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  7. Bravo! NIAID / NIH Ruscetti should have spoken. Infectious Disease
    Doctors should have been there . I should have been longer and yes no way should CAA be allowed to spill their crap all over and " contaminate" the minds of newly diagnosed patients and families . Men and children are sick where is their representation???

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  8. Thank you for this informative commentary. I am a CFS patient so it is hard for me to follow all of this. This conference could've accomplished so much more, but sadly it sounds like it didn't all while we CFS patients are left to wither away.

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  9. drat...i knew you should have been on the organizing committee. i sent mangan a note nominating you....apparently with hundreds of others who thought the same thing, drat!!

    i think there were some good presentations ( Mikovits, Broderick, Klimas, Dean, Theo) and many crappy ones (that lady w/studies from 20 years ago...what was the point!!!!);

    but your idea about structuring the meeting for complement rather than controversy is an excellent point.

    what most upset me was susan vernon and kim mccleary. in the past i have steered clear of the caa controversy....but seeing vernon in action made me believe that she is a damaging force in the patients quest to get well.

    kim...was a waste of time and space....basically she gave a presentation of everything the CAA has NOT done over the past twenty years.

    i still hold out hope for Dr. Mangan. I think he does want to help us..but is being steered wrongly by Vernon (who is an amazingly pushy, arrogant woman for someone who is so ineffective and highly disliked by her own patient community)

    i think a perfect contrast to what was wrong w/the NIH mtg can be seen in the slogan and theme of the InvestInMe...where they have goals and an obejective: treatment NOW!!!!!!!


    There was 1 treatment potential discussed at SOK Dr. Theo's Neuroprotek......otherwise it was like watching reruns from the early 90's....EBV treatment, Florinef, pacing, rest....hmm cant remember anything else.

    I actually cried while watching the SOK...it made me that depressed.

    Sorry for the novel. Thanks for your blog

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  10. Yes, clarity was certainly missing from this NIH Workshop co-organized by the CFIDS Assn of America. Clarity would have revealed that neither the NIH nor the CAA is doing anything to help people who suffer with this disease.

    The workshop was chaotic, disappointing, and depressing. We deserve better.

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  11. Excellent as usual Chris, well done for asking the questions we are long overdue answers for. This charade has been going on for long enough, we need proper research, funding and organisation. In the UK we have Wessely White and Sharpe and you guys have the CAA? Does anyone care about the patient anymore? The science is there people, for goodness sake use it. This illness needs to be redefined, get proper criteria and research - today. Not next year, not in 2020, today.

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  12. I love you, Chris. Thank you for this blog and for all you do.

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  13. As one of the sickest patients, thank you for helping us all.

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  14. Pls contact me, I am a PT who special. for yrs in finding innovative rx model to recognize and rx the 20% of persons who "failed," to respond to trad. treatment and interdisplinary rx programs. I've had this disease for over 10 years myself. I am among a handful of clinicians who pioneered the use of research grade surface electomyography to ID abnormal motor plans (especially slow twitch motor neuron fatigue failure) and rx the problems successfully. I want to do clinically based research to ID common findings, success/failure of specialized/contolled ex programs...then f/up research to prove efficacy of an rx model with semg eval/ms.re-ed/monitoring of response guiding the therapist's rx plan and simultaneously policing myofascial pain with MF release/Trigger Point release sessions. My email is kgr8day@msn.com. Thx for the feedback on the symposium and your ded. work and time! Other interested persons may contact me. I had a mission to bring this to mainstream PT as a viable treatment/evaluative tool and its use to prevent the devel of chronic injury and pain in general. My own CFIDS stopped me short. I have ideas on how I might cont. the fight. I invested 11 years to gain this knowledge and learned so much w/ my clients w/ whom I teamed up in helping them max.their progress. I feel like I am sitting on a secret weapon and don't want it to fade away due to my disability. Kate Keeling PT

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  15. Dr. Deckoff-Jones, though working for the WPI, is still a CFS/ME patient. She works part time, and every second of that time is focused on bringing a clinical service to the WPI. I am dead sure if she could have made it, she would have.

    This was a brilliant piece Chris. Just brilliant. Thank you so much for being there rerpresenting us all.

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  16. "Michael Sharpe:
    Chronic fatigue syndrome refers to a condition where people suffer from chronic—and we usually mean by that at least six months—fatigue, which has a very substantial effect on what they can do. So a condition which affects... people's ability to do day-to-day activities, although there are a lot of different definitions and that's the root of some of the controversy."
    -------------------------------------------
    It's absolutely mazing how dishonest people can create "controversy" just by repeating that something is controversial.
    There's nothing that stops anyone from going back to the original illness that caused CFS to be created. Find out exactly what it is. Nothing at all.
    So it's obvious on the face of it, that if they don't, it is because their goal is to keep CFS controversial.

    "What we-uhhve got he-ah, is a fayl-ur to
    in VEST e gate."

    And it's totally deliberate!

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  17. As I understand, Suzzane Vernon's husband has CFS. I do not know if this is correct, however, if it is, she probably has a pretty good understanding of CFS. That being said, I do not think the CFIDS association has accomplished enough for all the years they have had control. It is more than time for a change not including the CFIDS Association of America.

    Poor funding is not an excuse CAA. If you do your job correctly, funding should be less of a problem.

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  18. Interesting read, thank you PA.

    PA said....
    "Dr. Rowe pointed out that the heterogeneity of the patients makes it easy to disprove any given hypothesis or the utility of any given treatment. He showed great insight when he said that his own study had shown fluorinef was not statistically significantly helpful in ME/CFS, yet he uses it, and it’s very helpful in a subset of patients. He suggested that different study designs, including n of one studies where patients serve as their own controls, may be necessary."

    Within the last 12 months I heard discussion about ways to improve medical knowledge, one point that was raised is the need for use of more case reports.

    Knowing the outcome of a study conducted over a defined timeframe (which is usually quite brief) provides limited information. It should be relatively easy to follow up the subject/s of case report/s over years.

    We know that some people recover from ME/CFS. There are stories of recovery following decades of illness. These stories appear in the general media and many doctors claim to have treated patients who recovered. But we never seem to get the full story. A story of recovery such as the one described here, http://northern-district-times.whereilive.com.au/sport/story/diving-head-first-into-recovery/ contributes zilch to our collective knowledge base unless someone writes a verifiable case report. Reading between the lines, it seems that Ethan trained through the fatigue and gradually recovered his health. Or was there more to his recovery than that? Did he have ME/CFS, overtrained athletes syndrome or something else?

    An article in the newspaper ‘The Australian’ (Weekend section) on March 26-27 quotes Prof Andrew Lloyd who runs a clinic at the University of NSW, which “provides a 12-week individualised and mostly home-based [GET] program”. Lloyd said, "Our clinic has been oversubscribed, so it's clear that patients are benefiting from these treatments''. I hope he has better evidence than this for any claim of effectiveness. There are numerous clinics around my hometown that offer spurious cures for cancer, ME/CFS, autism, asthma, and on and on; they are oversubscribed too.

    Another article appeared in ‘The Australian’ in 2009:
    http://www.theaustralian.com.au/news/health-science/chronic-fatigue-syndrome-can-be-beaten/story-e6frg8y6-1225761725251
    The article refers to a fatigue rehabilitation program for adolescents run by the Austin Hospital in Melbourne. It is based on the British GET programs and claims to have achieved an 88% success rate since 1998. (Austin has sufficient funds to treat just 26 patients each year so I presume it carefully selects those most likely to benefit.) Apparently Austin has published its data, including a follow-up study. Bravo.

    A similar treatment program for adults is at the Royal Talbot Rehabilitation Centre in Melbourne. A 36 y/o construction manager entered the program with a degree of cynicism but afterwards credited it with his 75% recovery from an episode of CFS following a bout of glandular fever in 2006 – a case report that needs writing.

    On Monday Australia’s national broadcaster aired a one-sided piece on the UK PACE trial:
    http://www.abc.net.au/rn/healthreport/stories/2011/3192571.htm
    At the webpage a comment from Martha makes a good point; GET, in particular, is a very specific treatment, it’s not just any form of graded exercise. Martha suggests that most people, including healthcare professionals, don’t attend to detail, which means they foist a half-baked form of GET onto their patient. Martha wrote, 'It's what happens in the real world that matters not what happens in a tightly controlled research experiment.”
    Perhaps there should be mandatory reporting of adverse responses to therapies in the same way there is mandatory reporting of adverse responses to pharmaceuticals.

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  19. If Suzanne Vernon's husband has CFS--who knows? Anything is possible.

    But I wonder what it would have been like in that household when the Empirical Definition was published.

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  20. ditto all the comments re: brilliant blog. The key is that as far as I can tell no plans for funding and research came out of the meeting. Those are the only excuses for having such a meeting -- clear cut goals to be aimed at post this meeting and before the next one.

    It will have only been worth the effort if Mangin learns the right lessons and the next meeting is focused on specifics to be done.

    Otherwise, it all sounded like a variation of that stupid CFSAC meeting that has wasted all our time for years.

    It has nothing to do with whether it was an "interesting" meeting. I don't care if it was a fascinating meeting. What we don't need anymore (if ever) are meetings that do not move us forward.

    michael

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  21. Happy Mother's Day, PA!

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  22. Do you know what happened with the Singh study, Chris? Did the right-wing controlled Univ. of Utah force Singh, et. al. to slant their findings? If so, it makes you wonder about the integrity of the upcoming Lipkin study.

    The WPI continues to be where I put my faith and hope.

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