NIH Intramural “ME/CFS” study finally published
NIH Intramural “ME/CFS” study finally published
Not a study about myalgic encephalomyelitis
The long awaited results from the NIH in-house "ME/CFS" study which began in 2016 have finally been published. Deep phenotyping of post-infectious myalgic encephalomyelitis/chronic fatigue syndrome, published on Feb 21, 2024 explains the study and findings.
I would normally not cover research that doesn't apply to myalgic encephalomyelitis (ME), but feel it is necessary to cover this one even though it didn’t use patients who have ME as defined by the International Consensus Criteria.
Many are not aware that chronic fatigue syndrome as defined by Fukuda (CFS-Fukuda) and ME as defined by the International Consensus Criteria (ME-ICC) are different patient groups, as well as that post-viral fatigue syndrome is not the same as ME. Because of this confusion, there will be an assumption that all the findings in this study will apply to ME even though they didn’t use the ME criteria for patient selection.
This article probably needs a trigger warning as it highlights issues that may negatively affect the future of people with ME.
NOTE: I am not a doctor and not a research scientist. I am approaching this as a lay person attempting to understand what has been published.
This article could have been several articles, but I wanted one place to refer back to as needed. Because this is such a long article, I have broken it into sections in case you want to skip some of it.
Initial thoughts
What is this study?
Who is in the study?
What is an ME study?
Findings in the study
Michael VanElzakker shares insights on the findings
Concerns from the start
Words matter
Effort Preference
Central Sensitization Syndrome by another name?
Deconditioning
Dueling descriptions
Input from others
Closing thoughts
Addendum: Media reports & Resources
1. Initial thoughts
My anger about the way the U.S. HHS, NIH and CDC have treated people with myalgic encephalomyelitis is hard to keep in check. This long awaited report didn't do anything to improve my opinion of these government agencies.
A main issue I have with this paper is some of the wording used can be interpreted in multiple ways. Because we have spent decades combating a narrative about ME that places the blame of the disease on a patient's behavior, I viewed this paper through a very critical lens. The distinct disease ME has been effectively buried under a vague narrative based on vague criteria and this paper continues that approach.
There may be some useful findings that more ME focused researchers can move forward with by using ME specific criteria. I still have hope we are making progress in the field of science. If you want to learn about researchers doing better science, check out some of my articles discussing good research found in the list HERE.
2. What is this study?
The U.S. National Institute of Health (NIH) began the process of doing an in-house study in 2016. They call this an “ME/CFS” study, but the parameters focus on sudden onset post-viral fatigue within less than 5 years.
Criteria used for patients are listed as meeting either ME/CFS-IOM (what is now on the CDC website), CFS-Fukuda or ME/CFS-Canadian Consensus Criteria. It is important to note that they indicated subjects could fit any of those three criteria. None were screened for ME as defined by the International Consensus Criteria (ME-ICC).
As stated in the paper’s introduction:
“Over 75 scientists and clinicians across 15 of the 27 institutes that comprise the NIH contributed to this multi-disciplinary work.”
“The participants underwent a multi-dimensional evaluation that included a wide range of physiological measures, physical and cognitive performance testing, and biochemical, microbiological, and immunological assays of blood, cerebrospinal fluid, muscle, and stool.”
“217 individuals underwent detailed case reviews entailing telephone interviews and medical record review…. Of these, 27 underwent in-person research evaluation and 17 were determined to have PI-ME/CFS by a panel of clinical experts with unanimous consensus. Twenty-one comparator healthy volunteers were recruited separately.”
3. Who is in the study?
While the NIH is calling this an "ME/CFS" study, we have known for years that the parameters were not chosen to select ME patients.
This is a post-viral fatigue study. While I am sure the patients in this study are sick, the screening focused on fatigue with an onset of less than five years. Subjects could not have had any indication of fatigue prior to onset. I know a person who applied as a participant who had fatigue in her medical records prior to her onset of illness. She was not accepted for the study despite explaining that the prior fatigue was caused by the kind of job she had and was nothing like the “fatigue” she felt after becoming ill with ME.
Fatigue is a common symptom seen in many conditions. There are many other known parameters for selecting patients who fit the criteria for ME. At the time of this study, the ME International Consensus Primer had been available for a few years. If they had utilized the International Consensus Criteria (ME-ICC), I would feel more confident this study applied to me.
The final number of participants was 17 and of those 17, four fully recovered after the study was done. It is exceedingly rare for there to be recovery once someone contracts ME. In my opinion, this is a strong indication that the patient selection was inadequate to be considered an ME study.
One of the 17 participants selected has publicly posted on Facebook about her health status. Her description indicates a severe level of illness. So while the parameters used may not have been sufficient to insure those participating have ME, it is possible there were some involved who have ME.
I don’t consider ME to be synonymous with ME/CFS. But most people lump CFS, ME/CFS, and ME under one umbrella. I discuss the problems with this approach in my article, ME/CFS is an Umbrella Term.
I was pleased to see the reporter for the New York Times, Pam Belluck, in her article Study of Patients With a Chronic Fatigue Condition May Offer Clues to Long Covid, also picked up on the fact that the patient selection was not a good representation of “ME/CFS”.
From the article:
“They selected rather healthy patients,” said Dr. Carmen Scheibenbogen, a professor of immunology at the Institute for Medical Immunology at Charité hospital in Berlin, who was not involved in the study. “I think there are a lot of interesting findings, it’s just disappointing because that was such a major approach and they selected patients which are not very representative.”
The article included something that I also thought exposed their flawed selection process:
“Beth Pollack, a research scientist at the Massachusetts Institute of Technology, noted that, in the years after participating, four of the 17 patients “spontaneously recovered” from the condition, which she said is “not typical of ME/CFS.””
This article focused on Jennifer Caldwell (a close friend of mine) and described her experience with contracting and living with ME well. I think Jennifer did a good job of explaining the reality of ME to the journalist.
I am also aware that Jennifer took part in most of the study but was not called back for all of it. As it turns out she is NOT one of the 17 whose data was used in the report. She was told the adjudicators saw she had some prior fatigue in her medical records which made her ineligible.
I wonder why they didn’t see that in the first place. What happened between her getting the first round of testing that led to her being removed from the study? Jennifer’s results from the NIH showed a number of abnormalities which helped her win her disability case with the government.
4. What is an ME study?
I have previously written about how ME/CFS is an umbrella term and how ME-ICC is not synonymous with CFS-Fukuda. In The meaning of CFS depends on who you ask I discuss the importance of differentiating between studies based on patients selected using the best research criteria and those studies that may only offer insight into symptoms seen in multiple patient groups.
To feel confident that a study applies to me (and ME), I look to see what criteria was used for patient selection. This study does not meet that bar.
I talk about the importance of patient selection for research HERE. From that article comes a quote from the International Consensus Primer:
“It is counterproductive to use inconsistent and overly inclusive criteria to glean insight into the pathophysiology of ME if up to 90% of the research patient sets may not meet its criteria (Jason 2009).”
Patients in an ME study should have confirmation of post-exertional neuroimmune exhaustion. This symptom is required for an ME diagnosis. But this study did not use the International Consensus Criteria to screen for participants. They used CFS-Fukuda (does not require PEM), Canadian Consensus Criteria or the IOM report criteria. Subjects could enter the study under any of those three criteria.
PEM is a problematic diagnostic unless patients are screened using the 2 day cardio-pulmonary exercise test (CPET) that offers objective evidence of post exertion symptom exacerbation on the second day of the test. This study did NOT include a 2 day test. PEM is seen in other diseases. For an ME study, researchers need to screen for post-exertional neuroimmune exhaustion (PENE). The article PEM is not equal to P.E.N.E. covers this topic.
5. Findings in the study
"National Institutes of Health have found differences in the brains and immune systems of people with post-infectious myalgic encephalomyelitis/chronic fatigue syndrome (PI-ME/CFS). They also found distinct differences between men and women with the disease."
I was very glad to see they found distinct differences between men and women. I think it is vital that researchers understand the importance of stratifying patient groups. I write about that in my article, U.S. NIH News.
There were findings of abnormal brain function, but they state:
“Standard clinical laboratory tests, brain imaging, measures of brain injury, and sleep architecture were unremarkable.”
Unremarkable brain imaging findings are inconsistent with what we know about ME. I was disappointed to see they didn’t do the SPECT scan testing recommended on page 4 of the ME IC Primer that explains how to see changes in the blood flow in the brain. I have had that test done. See article about that HERE about my experience getting a SPECT scan showing impaired blood flow to some areas of my brain. I think it is inappropriate to state that there are no changes to the brain itself without performing thorough testing.
In that statement, they indicate sleep structure was unremarkable as well.
Sleep Disorders and Sleep Deprivation: An Unmet Public Health Problem explains “sleep architecture as”:
“Sleep architecture refers to the basic structural organization of normal sleep. There are two types of sleep, non-rapid eye-movement (NREM) sleep and rapid eye-movement (REM) sleep. NREM sleep is divided into stages 1, 2, 3, and 4, representing a continuum of relative depth.”
I have yet to meet someone with ME who said they have normal sleep patterns. My own sleep study indicated there were issues with sleep architecture.
These findings cause me to question the kind of testing they did or the patients they studied.
6. Michael VanElzakker shares insight on the findings
In David Tuller’s video interview with Mike Van Elzakker they discuss this NIH study. The interview is included in David Tuller’s article Trial By Error: An Interview with Neuroscientist Michael VanElzakker about the Just-Published and Long-Awaited NIH Study. Michael VanElzakker makes several important points:
1 in 5 of those brought into the study had something other than ME/CFS. He pointed out how people are given this ME/CFS label without doctors doing a deep dive into what may be causing symptoms.
He talked about the importance of the paper’s hypothesis that “these changes are driven by antigen persistence of the infectious pathogen”. He thought these findings should be amplified. He talked about the importance of following up on that to find out what those antigens are for each patient and whether it is the same for all the patients. What is driving these immune system responses that are consistent with antigen persistence?
They discussed cutting edge technology that can look at T cell sequencing and look backward and figure out what the T cell is responding to. This is research to follow up on.
They discussed that this paper was written by a lot of people which showed in the varied perspectives presented in the paper.
Michael VanElzakker pointed out that it would have been beneficial if they had separated out actual results versus interpretations.
Michael discussed the interpretation of the results shown for the parietal junction. He said:
“I think if you were to get 100 neuroscientists together and ask them to name three brain regions involved in effort or movement or action they would be saying motor cortex, premotor, strium, basil ganglia, you know cerebellum…I don't think anybody would say temporal parietal junction.”
I think the missed diagnosis issue is an important take away. The screening tools in the ME IC Primer would go a long way to help overcome this issue.
[Edited on March 16, 2024 to add the following from Jama Network publication]
The article, NIH Study Provides Long-Awaited Insight Into Myalgic Encephalomyelitis/Chronic Fatigue Syndrome, by Quinn Eastman, PhD on March 15, 2024 stated the following quote from Nath.
“He added that several of the participants with ME/CFS who passed initial review, and then were excluded after an in-person evaluation, were diagnosed with serious conditions. Examples of diagnoses leading to exclusion at this stage included cancer, myositis, and the autoimmune liver disease primary biliary cholangitis. The physicians these individuals previously consulted had not identified these problems. Nath concluded that even if people who display ME/CFS-like symptoms don’t have ME/CFS, they may have another condition for which medical attention would be beneficial.”
I appreciate the discussion about needing deep phenotyping of every patient in order to really focus on health, treating every patient, and to make sure everyone is properly diagnosed. We need research being done that would lead to a panel of tests for a better diagnosis.
I realize I sound like a broken record, but the IC Primer testing on page 11 was created by experts who understood the biology of ME and they provided the kind of testing that could help rule in or rule out an ME diagnosis. That would be an excellent place to start to confirm patients are properly diagnosed.
It is well worth listening to the video to better understand why he cringed at some of the neurological interpretations! He gives another interpretation of why there may have been a deactivation of the temporal parietal junction. He also discusses some of the research he is doing. I recommend following Polybio Research Foundation. I talk about them in my article Viruses hiding in tissues. To learn more about Michael VanElzakker see his bio at Polybio Research Foundation.
7. Concerns from the start
MEadvocacy.org volunteers wrote articles expressing concerns about this study from the beginning. NIH Clinical Study: A Case of Continued Institutional Bias from Feb 2016 brought up initial concerns. From the article:
“The announcement of NIH’s recruitment request for the promised intramural study has come out. The heading for the study states ‘chronic fatigue syndrome’ but, to be accurate, they should have left the word “syndrome” out. It is basically a study of “unexplained fatigue”.
A follow-up article, Further Analysis of NIH Clinical CFS Study, discussed how the parameters were likely to exclude people with ME. Included in that article is the following which I think is very important.
“Then, to bias the study even further, one would logically select criteria and exclusions/inclusions for the CFS cohort that predominantly excludes those that have myalgic encephalomyelitis (ME). Such as... excluding anyone that has infections (infections are common in ME patients).”
I regularly have bacterial, viral or fungal infections due to my immune dysfunction and would not have been eligible to participate even if they had allowed those sick longer than 5 years.
Eileen Holderman, a long-time experienced advocate who was part of the CFS advisory committee, wrote about the study in the article, NIH Side Steps Critical Problems with the ME/CFS Study. This is an excellent article for anyone looking to see how this research study was developed. The following statement underscores that the publication of this paper may have lasting consequences which does not benefit people with ME.
“HHS needs to make concrete changes in order to affect real change in how ME is perceived and studied. Although NIH deems this study as only one piece of the puzzle, the Department has a record of turning that puzzle piece into a cornerstone of research dogma for decades to come.”
Other articles about this study from MEadvocacy.
Another long-time experienced advocate, Jeannette Burmeister, raised concerns as well in her “Thoughts About M.E.” blog from March 2016. Keep an Eye on Your Walitt: NIH Study Poses Dramatic Risk to Long-Term Disability Benefits discusses the risks to disability payments if ME/CFS is deemed a mental, nervous or emotional disease or disorder of any type.
“Many ME/CFS* sufferers are covered by employer-sponsored long-term disability (“LTD”) policies. These policies almost universally limit LTD benefits to 24 months for disability caused—or even just contributed to—by a mental/nervous disorder.”
8. Words matter
The following words or phrases used in this paper or the press release perpetuates the psychologizing language we have been dealing with for decades.
Feelings of discomfort
Feelings of fatigue
Mismatch between what someone thinks they can achieve and what their bodies perform
Decides how to exert effort
Effort preference
Central mediated disorder
The current reality is that there is a strong systemic bias against the ME patient community. I read through the press release, NIH study offers new clues into the causes of post-infectious ME/CFS with an eye for whether what they said would combat the gaslighting caused by the prevailing systemic bias.
The following is from the synopsis:
"...discovered how feelings of fatigue are processed in the brains of people with ME/CFS. Results from functional magnetic resonance imaging (fMRI) brain scans showed that people with ME/CFS had lower activity in a brain region called the temporal-parietal junction (TPJ), which may cause fatigue by disrupting the way the brain decides how to exert effort."
This description that uses words like "feelings of fatigue … may cause fatigue by disrupting the way the brain decides how to exert effort" are mischaracterizing the experience. I don’t “feel” fatigued - I am very sick. Using the word “decide” makes it sound like there is a choice about how to exert effort.
9. Effort Preference
The term “Effort Preference” is used over 25 times in the paper. Quotes from the paper:
“The Effort-Expenditure for Rewards Task (EEfRT)15 was used to assess effort, task-related fatigue, and reward sensitivity… Given equal levels and probabilities of reward, HVs chose more hard tasks than PI-ME/CFS participants…”
“Effort preference is how much effort a person subjectively wants to exert…. If there is developing fatigue, the effort will have to increase, and the effort:benefit ratio will increase, perhaps to the point where a person will prefer to lose a reward than to exert effort. Thus, as fatigue develops, failure can occur because of depletion of capacity or an unfavorable preference.”
David Tuller didn’t mince words when he wrote the following in his article, Trial By Error: An Interview with Neuroscientist Michael VanElzakker about the Just-Published and Long-Awaited NIH Study:
“Effort preference”—what the fuck? If you focus-grouped it, you couldn’t come up with a more demeaning and ridiculous name for the construct presumed to be driving the disabling symptoms that plague this particular group of patients. It is astoundingly tone-deaf–almost as bad as naming a devastating illness something as demeaning and ridiculous as “chronic fatigue syndrome.”
This does NOT take into account the experience of post-exertion exacerbation of symptoms. They seem to be interpreting that the choice to do a task is limited to just the experience of the task itself. It completely ignores the knowledge of activity leading to post-exertional exacerbation of symptoms experienced by people with ME.
I “can” go for a walk around the block. The enjoyment reward would be significant. But the knowledge that the aftermath of that walk would be symptoms that could land me in an emergency room is always part of my decision about doing a task.
While the task they were doing was not as physical as a walk, mental exertion (like writing this article) also takes a toll.
I also think we need to consider the situation of these patients. For someone who has ME, the trip to the NIH and the experience of being at the NIH would likely lead to post-exertional neuroimmune exhaustion.
I vehemently disagree with the following conclusion from the paper:
“Together these findings suggest that effort preference, not fatigue, is the defining motor behavior of this illness.”
In my opinion, “fatigue” nor “effort preference” is the defining motor behavior of this illness. Post-exertional neuroimmune exhaustion and all the other symptoms people with ME experience which are exacerbated by effort is what defines ME.
Conversations online brought up that the phrase “effort preference” is likely to be construed as that patients have a choice about this illness experience.
Murph on the Phoenix Rising Forum (Jason Murphy) took the time to dive into this “effort preference” part of the study. This is a bit of what he wrote… I recommend the entire post.
“Since we are all talking about the effort preference, I got the source data and plotted it in full granular detail.
“…I want to draw attention to the actual thing the construct "effort preference" is based on. It's not some all-encompassing insight that describes eternal truths about us. It's a very specific game involving deciding to push a button with your pinkie finger.”
“So my overall take is that learning is doing to dominate motivation after the first couple of tries, and so the trend over 50 trials is going to be driven be learning effects. I don't think it shows what they seem to imply it shows.”
When I asked Jason Murphy about sharing his post in my article he responded with:
“Yes, please do. I want people to know effort preference is not some great and terrible insight into our true essence but the output of a test on whether you'd like to push a button with your non dominant pinkie finger 98 times in 21 seconds!!”
Personally I would not have been able to do that test at all. I can’t do anything repetitive 98 times. I need many rest intervals. Muscle fatigability is a well documented symptom since the original Ramsay criteria.
“Generalised or localised muscle fatigue after minimal exertion with prolonged recovery time.”
My muscle fatigability has grown worse over the years. In the early years of having ME, I could hand write about a paragraph before my writing became illegible. The muscle fatigability that occurred immediately upon onset causes me to lose fine motor skills. At this point, I am lucky to legibly write an item on the grocery list before muscle fatigue affects my ability to hold a pencil. (Typing is also affected… but I rest my hands often to manage the limitations.)
10. Central Sensitization Syndrome by another name?
From the paper:
“Considering all the data together, PI-ME/CFS appears to be a centrally mediated disorder. We posit this hypothetical mechanism of how an infection can create a cascade of physiological alterations that lead to the PI-ME/CFS phenotype.
In conclusion, PI-ME/CFS is a distinct entity characterized by somatic and cognitive complaints that are centrally mediated. Fatigue is defined by effort preferences and central autonomic dysfunction.”
The phrase centrally mediated disorder is only used once in the paper which is odd since they are stating that PI-ME/CFS appears to be a “centrally mediated disorder”.
It was hard to find anything with this label that was directly related to the ME experience. Some of what I found online led to central sensitization syndrome. So I turned to ChatGPT (AI) to see what it said about what treatment options someone who has “centrally mediated disorder” could expect to have recommended.
The following is the reply for “How to treat a centrally mediated disorder”:
“Here are some general approaches:
Medications:
Analgesics: For pain management, medications like opioids, non-steroidal anti-inflammatory drugs (NSAIDs), or anti-seizure medications may be prescribed.
Neuromodulators: Medications like tricyclic antidepressants, selective serotonin and norepinephrine reuptake inhibitors (SSRIs/SNRIs), or antiepileptic drugs may be used to modulate neural activity.
Physical Therapy:
Physical therapists can help with exercises and interventions to improve muscle strength, flexibility, and coordination. This can be particularly useful for movement disorders or conditions affecting motor functions.
Occupational Therapy:
Occupational therapists focus on helping individuals regain and improve daily life skills, such as dressing, cooking, and other activities of daily living.
Cognitive Behavioral Therapy (CBT):
For disorders affecting mood, cognition, or behavior, CBT can be beneficial. It helps individuals develop coping strategies, manage stress, and change negative thought patterns.
Biofeedback:
Biofeedback techniques can assist individuals in gaining control over physiological processes, such as heart rate or muscle tension, which may be affected by centrally mediated disorders.
Interventional Procedures:
In some cases, procedures like nerve blocks, spinal cord stimulation, or other interventional approaches may be considered to modulate neural activity and alleviate symptoms.
Pharmacological Approaches:
Certain disorders may benefit from medications that specifically target neurotransmitter imbalances or other central nervous system abnormalities.
Lifestyle Modifications:
Adopting a healthy lifestyle, including regular exercise, a balanced diet, and stress management, can contribute to overall well-being and may positively impact centrally mediated disorders.
Supportive Therapies:
Support groups or counseling can be beneficial for individuals dealing with chronic conditions, providing emotional support and a platform to share experiences.”
The majority of these approaches are behavior modification and therapy which may lead doctors to minimize biological approaches.
11. Deconditioning
I was surprised to see the following statement about deconditioning. (I thought this myth had been dealt with.)
From Figure 10:
“…Both the autonomic and central motor dysfunction result in a reduction in physical activity. With time, the reduction in physical activity leads to muscular and cardiovascular deconditioning, and functional disability. All these features make up the PI-ME/CFS phenotype.”
I lost muscle function on the first day of illness. I did become deconditioned over time until my health stabilized (about the 4th year). I was able to slowly recondition my muscles but they will lose function when in bad post-exertional neuroimmune exhaustion. The reconditioning of my muscles has had no impact on the underlying muscle fatigability, neuro, immune or cardiac issues connected to ME.
12. Dueling descriptions
We have had dueling descriptions over the years. In my opinion, the ME IC Primer offers one of the best descriptions out of all the criteria created over the years. I think this new description can be weaponized against patients.
The description from this paper:
“Considering all the data together, PI-ME/CFS appears to be a centrally mediated disorder.”
Description currently given on the CDC website for ME/CFS
“Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a disabling and complex illness.”
Description from the International Consensus Criteria
“..is a complex disease involving profound dysregulation of the central nervous system (CNS) and immune system, dysfunction of cellular energy metabolism and ion transport and cardiovascular abnormalities.”
If we are going to overcome the systemic bias experienced for decades, I think we all need to use the more descriptive description.
13. Input from others
Since this NIH paper was published, many long-time advocates have been speaking out about the way the findings were presented.
Hillary Johnson, author of Osler’s Web and The Why: The historic ME/CFS Call to Arms, raised more issues. Her Feb 21, 2024 tweets include:
“These findings, FOR THE FIRST TIME, suggest a link between specific abnormalities in the brain and ME.” From NIH press release. Full out lie, a farce. Brain abnormalities in ME have been published for decades. Predictable NIH blather. Who in science will call them out on this?”
“NIH: no difference in cognitive performance on neuropsych tests; no difference in NK cells; no difference in 40 minute (!) tilt table testing. R U kidding me? And NIH claiming their work is best ME study ever?”
“NIH: four of 17 patients experienced spontaneous remission? This paper should have come with an apology. NIH is still hung up on figuring out: is ME real? Effort should have been isolating cause instead. Gov needs to fund but stay out of MD research.”
On March 1, 2024 David Putrino (of Putrino Labs) gave a presentation at the Neurological aspects of ME/CFS Webinar that included comments about this study. His slide referencing this study was titled “First: Do no harm - avoiding the integration of WEAK science into clinical practice”. The slide included the following points:
Low n - far too low to be taken seriously
Careless clinical characterizations of people in the ME/CFS cohort (“effort preference”, etc)
Overconfident conclusions made about weak/inconclusive immunological and neurophysiological findings
Details about this conference can be found HERE.
I appreciate Dr. Blitshteyn’s post on X from Feb 21 which states:
“Their conclusion: 👇
👀 "PI-ME/CFS is a distinct entity characterized by somatic and cognitive complaints that are centrally mediated. Fatigue is defined by effort preferences and central autonomic dysfunction."
✔️ My conclusion, based on their comprehensive data:👇
"PI-ME/CFS is a central nervous system (CNS) disorder. Fatigue is defined by autonomic dysfunction unrelated to psychological or psychiatric causes."
‼️Important to remember:‼️
👉 You didn't cause your disease.
👉 Your disease is not based on your effort or your effort preferences.
👉 I have not met one person with #MECFS, #LongCovid, #Dysautonomia, etc. who wanted to be sick and/or didn't want to get better.
👉 Therapies should concentrate on modulating immunologic, autoimmune, autonomic, metabolic and mitochondrial dysfunction ➡️➡️ improved CNS 🧠disorder.”
Jeannette Burmeister on X brought up an important point about the ramifications of the paper’s conclusions.
“You know what's suddenly become even more dangerous? An ICD code for PEM. Because PEM is what's being psychologized by NIH through the false and reverse-engineered claim that PEM is an aberrant experience of "fatigue" caused by faulty brain wiring.”
I agree with this concern. To learn more about the proposal to add a post-exertional malaise (PEM) code to the U.S. ICD, see my article, PEM symptom code proposal - a dog's breakfast.
14. Closing thoughts
I am concerned that this paper does not significantly change the dangerous status quo. It certainly does not provide any recognition or support for the Severe ME patients. It did generate a great deal of news coverage which included input from patients who provided good insight into ME. (Thank you Jennifer Caldwell and others!)
Because most people don’t understand that ME is a distinct disease which has been lumped in with people who have been given an ME/CFS or CFS label, it is likely that most will view this study as being about ME.
For those doctors who have been psychologizing patients, I don’t think what the NIH wrote will change that attitude.
For those doctors who already understand that ME is a multi-system, severely debilitating disease that devastates patients' lives, I don’t think this paper offers much useful information to help patients get better care.
I hope the various news reports will help family and friends have more compassion leading to better support.
They showed neurological abnormalities. Unfortunately, they state that these abnormalities are functional and not structural so I doubt this will help us stop the gaslighting from neurologists.
I hope the immune dysfunction findings will open the door for more funding to that line of research.
Colleen
Media reports
News reports varied in the way they presented the information.
Some of the early reports exposed the reality about patients highlighting biological findings.and seemed sympathetic to the plight of patients. Others picked up on the “effort preference” narrative and other behavior modification aspects that may perpetuate the psychologizing of patients. The following is a list of some of the articles published about this paper.
Expert reaction to study of deep phenotyping of patients with post-infectious ME/CFS - Science Media Centre
People with Myalgic Encephalomyelitis/Chronic Fatigue Syndrome May Have an “Exhausted” Immune System - Scientific American
Clues to a better understanding of chronic fatigue syndrome emerge from a major study - WUNC Public Radio
Scientists find link between brain imbalance and chronic fatigue syndrome - The Guardian
Study of Patients With a Chronic Fatigue Condition May Offer Clues to Long Covid - The New York Times
ME/CFS Experts Express 'Dismay' at Aspects of NIH Study - Medscape
Is chronic fatigue syndrome all in your brain? - Harvard Health Publishing
Sweeping chronic fatigue study brings clues but not clarity to mysterious syndrome “Megaworkup” revealed brain and immune differences in a small patient group
Advocacy blogs
Hillary Johnson
Jeannette Burmeister
Jeannette has written extensively about this NIH study since it was first conceived. She has followed up with this blog that covers the history of those involved (including “Team Tired”). From this latest blog:
“I take no pleasure in the fact that some of us accurately predicted the outcome of this study to be a delivery vehicle for the introduction of a new psych label for ME—which turned out to be the concept of effort preference—re-branding post-exertional malaise (PEM) and pacing as psychological.”
Resources
Walitt, B., Singh, K., LaMunion, S.R. et al. Deep phenotyping of post-infectious myalgic encephalomyelitis/chronic fatigue syndrome. Nat Commun 15, 907 (2024). https://doi.org/10.1038/s41467-024-45107-3
The National Library of Canada Cataloguing-in-Publication Data: Myalgic Encephalomyelitis – Adult & Paediatric: International Consensus Primer for Medical Practitioners. ISBN 978-0-9739335-3-6 https://drive.google.com/file/d/1A0Bvtl4xRUkP3fEJSGMujdPaqQ1-QCIE/view
Institute of Medicine (US) Committee on Sleep Medicine and Research; Colten HR, Altevogt BM, editors. Sleep Disorders and Sleep Deprivation: An Unmet Public Health Problem. Washington (DC): National Academies Press (US); 2006. 2, Sleep Physiology. Available from: https://www.ncbi.nlm.nih.gov/books/NBK19956/
Information provided here or in comments is not to be considered medical advice
Beautifully written. Thank you for taking the time and energy to break this down.
I appreciate the trigger warning - I am not up to reading all the bad news these days, but will share without reading because I completely trust you and your writings and analyses. Thank-you so much Colleen for covering this crucial implications of this "study" and the "definition" that we all protested back in the time leading up to 2016..