Over the weekend, members of the US Action Working Group (USAWG) were alerted to the publication of the National Institutes of Health’s study protocol (as posted originally). The content of the published protocol caused a number of concerns across the community, chief among them that the Reeves criteria were apparently being used as the basis for selecting patients.
On Tuesday, NIH informed the community that the protocol that had been posted online was incomplete and prematurely published and that version of the protocol has been taken down. The NIH and the study’s Principal Investigator, Dr. Avi Nath, provided some encouraging clarifications: post-exertional malaise (PEM) would be required and study participants would meet multiple criteria, including the Canadian Consensus Criteria. Additionally, NIH said that Dr. Ian Lipkin is involved in study design and the study will include 40 patients, not including control groups.
There are, however, a number of open questions. Wednesday, the USAWG submitted a list of questions to the NIH regarding the study, engagement with the community on the protocol, the disease name, the study objectives, the subject selection criteria, symptom assessments, and study design.
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We invite everyone in this community to take a look at these questions and add your suggestions for additional questions or changes below. We plan to collate them and submit an additional list of questions.
35 thoughts on “USAWG submits questions to the NIH”
Why the age cutoff? I am 71, have no other medical conditions. I’ve had ME/CFS for over 45 years. My symptoms have never changed. Seems to me that I would be the perfect candidate for clinical trials given my long history.
i didn’t notice the age cutoff but think five year window is weird considering how hard it is for people to get diagnosed esp when health insurance in this country is so bad. i realize there’s an issue with comorbidities, but DUDE that’s leaving out a lot of people. my fear is that they will not get ME patients at all and data set will be useless.
Believe it or not, people are getting Dx’d a LOT faster and they are now on the lookout for these patients. The push is to get them Dx’s at 6 months and specialized clinicians will be Dxing for the study.
The 5 year window may have a purpose. They now know due to Hornig/Lipkin Cytokine studies the disease has 2 stages. This has nothing to do with severity as a patient can go severe overnight. It is the fact that in moderate to severe patients, the Cytokines are raging for 3 years and then collapse. This 5 year window is going to allow them to focus on that as well as prove out criteria until they have a diagnostic test.
I would ask for more on the rationale for choosing functional movement disorder as a comparison group. I think they’re patients like us with medically unexplained symptoms being given a wastebasket diagnosis (psych disguised with a fancy sounding name) which is impossible to prove. They could very well have underlying pathology which has yet to be discovered. FMD smells like somatoform rebranded and renamed and I think makes a terrible control group which could cause confusing results. They should study “FMD” patients independent of an ME/CFS study because I’ll bet something really is physically wrong with them, but pick a more appropriate comparison group for THIS study.
I’m worried about study participants experiencing debilitating PEM from the volume of tests being done in so short a time. Can the testing period be longer or be done in stages so as to not make subjects sicker as they are undergoing testing?
Please reconsider the use of the reeves consenus. It is way too broad and unspecific. Look at the sickest most bedbound people with this disease and it is painfully obvious that reeves criteria is lacking. The candadian is better, the international consensus is better still. There is a book out bt the International Associaiation for chroncfatigue syndrome/myalgic encephalomyelitis . It is called “Anew 2012 Primer for Clinical Practioners” Perhaps you could use this as a guide, but reeves ,no way…. I hope you will pick the sickest patients to study first as I believe you will find answers quicker there. This illness is real and very debilitating. You could damage this patient community very much by getting the diagnostic standards wrong.
i feel like reeves isn’t such a problem so much as the travel and stationary bike requirment. seems like researchers have never heard of severe ME!
Severe patients cannot be studied this way but they know they have the same biological expressions that can be measured using moderate patients that are not in relapse with bikes. There was a time I could have been in this study but not now. They want to “see” and “measure” PEM.
The OMF has the severe patients covered in their study. Yes, it is true the NIH did not fund them but the study is being funded privately.
Hi J L Marotta, this is Courtney Miller. I wanted to let you know that the Principal Investigator of the NIH study, Dr. Nath, and the Director of NINDS, Dr. Koroshetz, have told Robert Miller and me that patients will not be selected under the Reeves criteria. Patients will have to meet the Canadian Consensus Criteria, the new IOM criteria, have Post-Exertional Malaise, and have infectious onset. Post-infectious onset is the most defining characteristic of patient selection for this study, and will narrow the differences in patients who could be selected by these definitions. You can read additional details that we learned at this link, and NIH will make more thorough details public in the coming week or so. http://meaction.net/2016/02/09/positive-answers-to-initial-questions-re-nih-clinical-center-protocol/
Yes indeed, why not use the International Consensus? I beleive most sufferers would find this to best fit their experiences and symptoms and it allows for the empirical differences one observes within the ME population. It also dispenses with ‘malaise’ as too vague a term and replaces PEM with PENE (Post exertional neurological exhaustion). It also dispenses with ‘CFS’ and relegates ‘fatigue’ to where it belongs as a general phenomenon and neither a very useful diagnostic nor having a place in the name of a disease…stop ‘researchers’ looking in the wrong places as with the infamous PACE trial.
Personally I wouldn’t worry about participants getting a bad kickback from tests as a previous post suggests – they will have given informed consent, they will be allowed to withdraw at any time, they will be in control of what they do and don’t do and this will be in line with how they manage their own illness – there shouldn’t be any negative surprises for them. Many will already have worked out that they accept some kickback on a daily basis in order to have some semblance of a life and to try to achieve the positive benefits that activity brings us.
Regarding the Lyme patients, some patients classed as asymptomatic could have had symptoms (or did in another study), and it is not unexpected for some of these to go on to “[develop] a late manifestation of Lyme disease” ( http://cid.oxfordjournals.org/content/37/4/528.full ). Given that a number of different infections have been identified as being associated to onset of ME/CFS (http://www.ncbi.nlm.nih.gov/pubmed/19828908, http://www.ncbi.nlm.nih.gov/pubmed/16950834, http://www.ncbi.nlm.nih.gov/pubmed/16448567, http://www.ncbi.nlm.nih.gov/pubmed/11911112, http://www.ncbi.nlm.nih.gov/pubmed/24715153, http://www.ncbi.nlm.nih.gov/pubmed/19955554 ), it is not unreasonable to assume that Lyme could be an infection that could also be associated with the onset of ME/CFS. Although disparate CSF proteins have been found in Lyme patients as compared to ME/CFS patients (http://www.ncbi.nlm.nih.gov/pubmed/21383843 ), it was suggested to me that this could be related to a phenomenon proposed by Kerr, that the manifestation may vary slightly according to infection (reference above).
In summary, care should be taken that control patients truly belong in the expected group, rather than having the test illness or an illness rather like it.
i am very concerned about the comparison groups, that they are not clearly defined or simply poorly studied groups. I worry that the choice of compairson group is used to discredit a disease such as ME and added to that poor choice of cohort will muddy the waters even furhter.
So my question is why not choose MS as comparison group which has been done in the past year from the Griffith University team? Why not build on that. Also why not compare known brain inflammation disease to compare, replicate and build on the Watannabe study?
Secondly I worry a lot about the language of the study. This disease is not about fatigue. As long as researchers will use fatigue as the main research entity, we will be wasting time and money.
Here we have an opportunity for NIH to engage and open the discussion with patient community and our ME experts. So I am asking NIH to seriously engage with the community.
I agree, MS, Lupus, Parkinsons, any group.
Copying over two comments from @arainbowatnight from http://meaction.net/2016/02/09/positive-answers-to-initial-questions-re-nih-clinical-center-protocol/
I’m flabbergasted by their “comparison” group using “asymptomatic Lyme” patients…i.e. people assumed to be recovered just because they don’t have fatigue? I didn’t get fatigue from Lyme disease until a full year after the tick bite, many people go even longer.
I’ve read their clarification (posted here
) which further states:
“Asymptomatic Lyme was chosen to contrast post-infectious ME/CFS patients to patients who recovered from an infection.”
This is terrible for many reasons.
I’m very concerned that they do not understand how chronic Lyme disease works…hugely in part because, if they support the IDSA (infectious disease society of america) and CDC, they probably think it doesn’t even exist, choosing to ignore the multiple studies that have come out in recent years proving that Lyme disease can *and does* persist after antibiotic treatment, and that the standard 2-4 weeks of Doxycycline does not always cure it. A study published in 2011 actually showed (what Lyme Literate physicians have known for years) that all most antibiotics did, in fact, was (in vitro) cause the bacteria to change forms, until the coast was clear, at which point they emerged, *alive.* Do they understand this? The one-type-of-antibiotic approach actually CAUSED the bacteria to go into hiding, giving only the *illusion* of being asymptomatic! (
) This also happens in vivo in real people, but I don’t have a study to back it up (though one may exist–trying to save spoons by giving what I have available on-hand).
There ***absolutely, without a doubt*** needs to be a physician from the ILADS (international lyme and associated diseases society) on this team, or this study is doomed to fail, from ignorance of the facts at hand. It’s not their fault if they don’t already know, but if someone brings this to their attention–like us–and they do not listen, then it is their responsibility. I want to make it their responsibility, to use this information.
There’s also that they apparently don’t plan to test for Lyme disease, either in the “ME/CFS” group OR the Lyme comparison group?
It’s crucial to test the “ME/CFS” group, because misdiagnosis is rampant in our community. Plus, just because you have one disease doesn’t mean you can’t get another. Regardless of when/where it came from, there can’t be any Lyme disease in the ME/CFS group or the results will be biased. I think I’ve already pointed out that the “asymptomatic lyme” group may still actually be harboring the bacteria, also corrupting the validity of its control group.
And the testing? It can be and often is, terrible, so if they did actually choose to do it, it’d need to be with multiple methods.
The ELISA is awful. Here’s just ONE studied case of people who were immunocompromised (like me) who all tested negative in ELISA (like me) yet all tested positive via Western Blot (also like me):
This isn’t even mentioning the fact that after you get Lyme disease, it can suppress your immune system, causing negatives even in *immunocompetent* people! (Here’s a list of links to many studies, entitled “lyme disease leads to immunosuppression”
Meanwhile, the CDC literally states on its website (
“EIA [ELISA] tests are designed to be very ‘sensitive’, meaning that when they are used properly, almost everyone with Lyme disease will test positive.”
Yeah, that didn’t work out, did it. They also promote a “two tier” testing which says, you should *only* get a Western Blot *if your ELISA comes back positive*…which means people who fail the first one (like I did, like so many do) won’t even get the additional western blot, etc!
This study here, all the way back from 2005, found that the only way to diagnose it 100% was by using culture (which takes 3.5 weeks), skin PCR, AND serologic tests. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1248466/
Meanwhile the CDC recommends AGAINST using culture to detect Lyme disease…the same culture the researchers above found was one of the main components of confirming it.
Similarly, the ILADS frequently quotes the statistic “of patients with acute CULTURE-PROVEN Lyme disease, 20–30% remain seronegative on serial western blot sampling” (emphasis added). (
So not only do the subjects in both groups need to be tested to reflect a consistent, up-to-date level of accuracy, but they need to be tested in a way that have a high specificity…which most doctors know nothing about. If these NIH researchers actually do get someone to help them with Lyme testing, it cannot be someone who agrees with these CDC recommendations, which obviously don’t work. Hence the *pertinence* of recruiting an ILADS physician!
beth said what i was going to say: that the cdc et al exhibits selective blindness re: what they consider legit lyme symptoms. weird choices for comparison groups to be sure.
the disease process for both cfs and lyme seem extremely similar, ohioactionlyme for example submits that borrellia is yet another AIDS, and we have the same viral reactivation issues.
Comment #2 from @arainbowatnight:
Re: Lyme disease changing forms in vivo:
Feb 9, 2016
“Lyme borreliosis, caused by the spirochete Borrelia burgdorferi sensu lato, has grown into a major public health problem. We recently identified a novel morphological form of B. burgdorferi, called biofilm, a structure that is well known to be highly resistant to antibiotics. … Our morphological and histological analyses showed that significant amounts of Borrelia-positive spirochetes and aggregates exist in the BL tissues. Analyzing structures positive for Borrelia showed that aggregates, but not spirochetes, expressed biofilm markers such as protective layers of different mucopolysaccharides, especially alginate. Atomic force microscopy revealed additional hallmark biofilm features of the Borrelia/alginate-positive aggregates such as inside channels and surface protrusions. In summary, this is the first study that demonstrates the presence of Borrelia biofilm in human infected skin tissues.“
Totally agree w/ Beth And others. I know too many late stage Lyme patients who were diagnosed w/ ME years on end.
If they want an asymptomatic post infection group, why not choose clearcut post eppstein Barr disease patients who came out healthy again?
Second group: MS patients! Clearcut again. And many CNS similarities.
Engage for once in not using the F word!
Look for overlaps between already existing studies. Younger & Vanelzakker & zinn & Wanatabe: inflammation/ CNS / glia cells? / …
Build on those studies to examine FURTHER, instead of AGAIN.
Show the world You mean business this time. The real deal.
+1 for comments about comparison groups – Functional-Movement-Disorder, and Lyme-Infection-Without-Current-Symptoms.
if NINDS are confident they can prove beyond doubt, common shared pathology or disease mechanisms, it would be FABULOUS – but it’s a tiny trial that may find nothing – so a huge risk of losing credibility (and future research).
much less risk if they use known control groups – including Multiple Sclerosis, Rheumatoid Arthritis, etc.
My questions are regarding the viral discovery portion of phase I of the study.
First, the previously published protocol listed an exclusion for patients with active infection. As one of the hypothesis of the disease involves the presence of a persistent active enterovirus infection, how do you plan to address the possibility that you might exclude this important subgroup of patients?
Second, the protocol outlined by Dr. Nath during the CDC Ground Rounds mentioned viral discovery, specifically highlighting herpes serology. What other viruses will serological testing be done for? Will this include antibodies to enterovirus serotypes such as Coxsackie B and echovirus? What other viral discovery methods will be used, and how will you account for the possibility that viruses will not be found in body fluids and instead are present in tissues, as has been shown by various past studies on ME patients?
The Lead Investigator to the NIH Post Infectious CFS study is doomed with this “guy” Dr. Brian Walitt taking the lead. http://www.familypracticenews.com/specialty-focus/rheumatology/single-article-page/video-fibromyalgia-doesnt-fit-the-disease-model/e913134880916685f3005dac5459ab88.html
Did you think we wouldn’t uncover a self help guru lead investigator for the study? He has a psychiatric bent to Fibro and so we know what he is coming with for this study. We already want him thrown off the study, PERIOD!
Dr. Walitt must go. We want an infectious disease scientist and proven researcher taking the lead, PERIOD. Nancy Klimas, Mady Horning, Jose Montoya and the like. This is what this disease deserves!
GET WALITT OFF THE STUDY! NOTHING LESS THAN HIM BEING COMPLETELY FIRED!
Janet: I completely agree, Dr. Walitt should never be associated with ME/CFS studies! All I had to do is substitute ME/CFS each time he said Fibromyalgia in the video and found myself getting more and more enraged. “Problems in their lives”…”real to the people who have it”…”emotional overlay”…”we may create symptoms”,etc. etc.
We have come too far to let this arrogant character (I won’t even call him a doctor) take us back to days of Freud.
1. How can the control group with Functional Movement Disorder be considered well-defined, when they can merely present with symptoms atypical for known neurological diseases? It is impossible to ensure that such as a sample does not include biological illness, which could muddy the outcomes of ME/CFS patients compared to such a control group.
2. In detail, what is the purpose of the Lyme control group? If it’s used as a post-infectious control of people who have recovered, why not use people who have recovered from illnesses which have been shown to result in ME/CFS in prospective studies?
3. Why did the NIH select a Lead Clinical Investigator, Dr Brial Walitt, who has definitively stated that CFS is a somatoform illness, (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4750385/) and has consistently explained biomedical findings, such as genetic correlations and altered brain scans, in “controversial” illnesses in a purely psychosomatic context? How can it be trusted that his biases will not pollute the research or the reporting of that research?
4. Why are ME/CFS patients with active infections excluded from the research? It is contradictory when studying a post-infectious sample, and would also seem to exclude the rather normal experience of ME/CFS patients regarding chronic and reactivating infections. It also makes a premature assumption about what the cause cannot be, in a study which is looking for ongoing pathology.
5. Will this study have the statistical power to find significant results, when three controls groups are present? Wouldn’t the study be better served by removing the Lyme and FMD controls, and increasing the number of patients and healthy controls instead? How do those Lyme and FMD control groups strengthen the study, and do any such advantages outweigh the disadvantages of their introduction of uncertainty in the nature of those groups, and the unnecessarily dilution of statistical effects?
Very well put Valentijn!
6. Do the the investigators intend the two-day exercise to be in the form of maximal CPETs? If not, why not, since that is the form of exertion which has been shown to produce unique results in ME/CFS patients? If maximal CPETs are not used, will the authors refrain from speculating about ME/CFS patients not trying as hard? Will the patients consistently be encouraged to exert maximal effort? If the maximal CPET is not used, what is the investigators’ basis (from published research) for believing that submaximal exertion is relevant or will produce abnormal results in ME/CFS patients?
I have concerns about the use of the 2-day exercise test. I appreciate the value of an exercise challenge but would like to know if investigators have considered all the impliations of this particular test.
To me its inclusion seems risky, and premature, until more robust findings (including evaluatioin of safety).
1. We know it can take some patients a very long time to recover from these tests but there is no reliable data on safety: is it a good idea to use it, and will patients be warned of the dangers, as they would with any medical procedure?
2. Results from tests from different groups all find differences but don’t find the same differences (eg some find changes in VO2.max, some VO2.vt and some metabolic efficiency.) Doesn’t that limit it’s value as a diagnostic tool?
This blog reviews the published evidence, with quotes from Prof Betsy Keller:http://phoenixrising.me/archives/25762
and her 2014 paper
3. Perhaps most concerning of all, the preliminary protocol had willingness to undertake the exercise test as a condition of selection. Given this requires maximal exertion two days running, and given the danges of over-exertion in this illness, isn’t there are real danger this will select an unrepresentative subset of patients who tolerate exercise better than most?
Do the investigators have any data on how many patients are willing to undertake such a test/how representative they are of patients generally (even after excluding severe patients)?
An alternative might the use evaluation of gene expression after MODERATE exercise testing eg
A successful NIH-funded replication (N=140) was reported as completed by 2014, but as yet no results have been formally published:
Presumably the NIH could get details of results of this NIH-funded study from the investigators.
I don’t want to sound negative about a very intersting study, but I also want that study to be as good as possible – and not to put patients in harms way. I hope the investigators will think carefully about how best to assess the impact of exercise on patients.
Agree with Janet.
Wallit NOT OK for patient confidence in this study.
He shld be replaced.
researchers with proof of bias shldn’t be allowed. At all.
Brian Walitt and Fred Gill must be removed from the NIH study! This is of deep concern and importance!! They are stearing the study into a biopsychological study since that is their way of thinking about ME/CFS (and of Fibromyalgia). That is not what Collins promised us!
Why is it not more focus on mitochondrial dysfunction? The metabolism is mentioned as something to look into but it is not very specified. I would think it is quite obvious that mitochondrial dysfunction plays a big part in ME/CFS and it deserves much research.
It’s unclear why one would state: “Functional Movement Disorder was chosen to contrast post-infectious ME/CFS patients with a very well-studied group of patients with clear psychological illness with neurological presentation” and think that this would be helpful to the study somehow. It would seem this group is likely meant to control for the state of having symptoms yet be a negative control for biopathology. This would be based on assumptions based on negative findings (unless the FDA has approved a Medical Device to probe the psyche, of which I am unaware!) which are demonstrably unsound. For example, see “Psychogenic explanations of physical illness: Time to examine the evidence” [Wilshire C, Ward T, Victoria University of Wellington, Under Review].
*It is also unclear why it is thought that such an idea would play well with patients who in other years or other countries or with maleducated doctors and other HCPs and in society in general would themselves be classified as having “clear psychological illness with neurological presentation”. This is an objectionable idea through and through. We don’t appreciate it for ourselves, and we don’t appreciate seeing other people be patronized in this manner, either.*
Please note that fatigue as an exclusion is not sufficient to rule out possible ME/CFS cases. Don’t let the name fool you: Fatigue is not the sine qua non of ME/CFS. [Stein, 2005]
Also please note that there is such a thing as “fluctuating conditions”. [Steadman, Shreeve, Bevan. 2015] Many conditions change from time to time and the circumstances in which they do are not necessarily understood. The fact that something changes (under whatever condition, even one that is not understood) is not proof that it is psychogenic.
It is easy for doctors or anyone to believe something is faked because they do not understand what is going on and their training has unfortunately led them to believe they should generally understand things. This misunderstanding has happened with a great many diseases in the past, such as multiple sclerosis, asthma, Parkinson’s, and so many more it would make an awkwardly long list. Most likely it is past time to change the training so when doctors and researchers encounter something they do not immediately understand, that instead of falling into a maladaptive solution (like “functional disorder”, or its historical equivalents like “hysteria”) to solve their cognitive dissonance, they can instead seek a constructive solution that will actually support and help the patient, by asking good questions and furthering research, and learning to be comfortable with an unknown state (e.g., a diagnosis without a clear eitiology attached); meanwhile treating symptoms and comorbid conditions collaboratively with the patient, with the best science available.
Furthermore, it is my understanding that the NIMH considers that mental health may in some cases have non-biological risk factors, but if these gave rise to a disease, there would be biolocial sequalae, and it is the duty of the investigator to look for these biological sequalae. It may be inconsistent with the goal of the Institute that would be tasked with research about your FMD group’s condition to class them as “clearly” not having any biological factors. [NIH, n.d.]
It may be more useful to consider that a study of ME/CFS may help develop the tools to know which technologies to use to study the patients you would today class as having FMD, and develop new ones.
As I mentioned, not so long ago patients with multiple sclerosis might have been used as people having “clear psychological illness with neurological presentation”, but today MS and ME are compared and contrasted immunologically [e.g. Brenu 2016, Huth 2016, Dobryakova E 2015, White AT 2012], and MS may be used as a control group for ME/CFS or vice versa [Elfaitouri A 2013].
In summary, care should be taken that care should be taken that control patients truly belong in the expected group. Care should be taken that tests are not tared with a pathological result rather than with a healthy result.
Control groups should consist of both healthy patients, and patients whose biomedical characteristics are well-characterized. Patients whose biomedical characteristics are not well-characterized could be included in order to study their disease concurrently. However all the groups will need to be larger.
NIH got additional funding this year so funding cannot be an excuse for not being able to carry out good research. Besides which, ME/CFS has not gotten increases to keep up with inflation–which other diseases (that already have more than tenfold more funding per patient per annum, and diagnostic tests, and FDA-approved medications) have–and is overdue a simple inflationary increase even without “extra funding”.
Brenu EW and colleagues. 2016. J Immunol Res. A Preliminary Comparative Assessment of the Role of CD8+ T Cells in Chronic Fatigue Syndrome/Myalgic Encephalomyelitis and Multiple Sclerosis. https://www.ncbi.nlm.nih.gov/pubmed/26881265
Elfaitouri A and colleages. 2013. PLoS One. Epitopes of microbial and human heat shock protein 60 and their recognition in myalgic encephalomyelitis. https://www.ncbi.nlm.nih.gov/pubmed/24312270
Huth TK and colleagues. 2016. Scand J Ummunol. Pilot Study of Natural Killer Cells in Chronic Fatigue Syndrome/Myalgic Encephalomyelitis and Multiple Sclerosis. https://www.ncbi.nlm.nih.gov/pubmed/26381393
Dobryakova E and colleagues. 2015. Front Neurol. The Dopamine Imbalance Hypothesis of Fatigue in Multiple Sclerosis and Other Neurological Disorders. https://www.ncbi.nlm.nih.gov/pubmed/25814977 (Not my favorite hypothesis, though I didn’t read the full article.)
NIH, NIMH. n.d. Strategic Research Priorities, Objective 2. https://www.nimh.nih.gov/about/strategic-planning-reports/strategic-research-priorities/srp-objective-2/index.shtml
Steadman K, Shreeve V, Bevan S. 2015 Jan. Fluctuating Conditions, Fluctuating Support: Improving organizational resiliance to fluctuating conditions in the workforce. http://www.theworkfoundation.com/DownloadPublication/Report/378_FCFS_Final.pdf
Stein E. 2005. Assessment and Treatment of Patients with ME/CFS: Clinical Guidelines for Psychiatrists. http://www.mecfswa.org.au/UserDir/Documents/psychiatry_overview_me_cfs.pdf
White AT and colleagues. 2012. Psysosom Med. Differences in metabolite-detecting, adrenergic, and immune gene expression after moderate exercise in patients with chronic fatigue syndrome, patients with multiple sclerosis, and healthy controls. https://www.ncbi.nlm.nih.gov/pubmed/22210239
Wilshire C, Ward T. 2015 Nov. Psychogenic Explanations of Psysical illness: Time to examine the evidence. Victoria University of Wellington. Under Review. https://www.researchgate.net/publication/283476227_Psychogenic_explanations_of_physical_illness_Time_to_examine_the_evidence
very interesting and important post Janelle.
Brian Walitt and Fred Gill must be removed from the NIH study.
New controls must be chosen.
If any of these stand the study will most likely take us back not forward, I’m thinking Pace trial. Any of the goodwill patients and the NIH were starting to have will be lost.
Also the constant use of the word fatigue as the sole symptom in measuring illness is troubling, Ask any group of patients what their worst symptom is and you will get many answers, Major cognitive disfunction being one of the biggest. Also, the fatigue experienced in this disease is often very different from other fatiguing illnesses and varies from patient to patient. For example many have the Wired/tired/toxic affect. I personally miss being fatigued like a normal person might, I haven’t felt that way in 30 years.
Nath said one of the study aims is to understand the underlying physiology of fatigue.
Is he referring to PEM or fatigue?
What is his (and the other investigator’s) understanding of PEM, its triggers/impact/etc.?
How is PEM characterized for this study?
Will the data from this study be shared?
Given the many questions about the researchers conducting this study and worries about their potential interpretation of the study results, it is enormously important that precautions be taken so that this data can be made available to other researchers for further analysis after the study. It would be awful to see a repeat of the PACE issues here.
@viggster on Phoenix Rising pointed out
“NIH requires data to be shared, but there is an exception for small human studies so we need them to clarify whether they will make all data from this trial available to other scientists. NIH data sharing policy is here:
We have to insist on clarity about data sharing because of the small number of study participants !
Remember when you changed the SEP Panel because it was full of dentists who believed in psychosomatic pain in TMJ? A rheumatologist who believes in psychosomatic fibromyalgia is a similar problem. (No, ME/CFS is not a more fatiguing subtype of fibromyalgia.)
What are you going to do to show that you can learn and change, and remember input from one time to the next?
When are you going to make a dedicated full-time unit for ME which is fully committed to finding medical solutions to our medical problems?
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