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Trial By Error: GET/CBT Ideologues Revive 1991 Oxford Criteria as Core Definition for Long Covid Research

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By David Tuller, DrPH

The Collaborative on Fatigue Following Infection, or COFFI, was formed in 2015 to promote the theories and treatment approaches embodied in the now-discredited and arguably fraudulent PACE trial and related research. In a nutshell, PACE and related research promoted the notion that the symptoms of patients with the clinical entity or entities variously called chronic fatigue syndrome, myalgic encephalomyelitis, ME/CFS, CFS/ME and other names could all be attributed to the effects of being physically deconditioned and of being afflicted with “unhelpful beliefs” about having an organic illness.

The recommended treatments were graded exercise therapy (GET) to get patients “reconditioned” and/or a specific form of cognitive behavior therapy (CBT) designed to alleviate them of their purportedly unhelpful beliefs. Since then, however, there has been a world-wide revulsion against PACE’s “unacceptable methodological lapses” (per 100+ international experts who signed Virology Blog’s 2018 letter to The Lancet), and both the US Centers for Disease Control and the UK’s National Center for Health and Care Excellence have flatly rejected its findings. These and related developments have dealt some serious blows to the credibility of the GET/CBT strategy.

COFFI has been pushing back. In a paper published last June called “A research agenda for post-COVID-19 fatigue” published in the Journal of Psychosomatic Research, members of the group referenced Professor Michael Sharpe’s 1991 case definition for chronic fatigue syndrome, which was abandoned long ago by most investigators in this field. That definition included a “sub-type” called “post-infectious fatigue syndrome.” Adopting that subtype (and using “infective” rather than “infectious”) the COFFI members have resurrected the Oxford criteria from the dead and essentially rebranded them. This appears to be a sly way of ignoring and seeking to maneuver around the fact that this approach has already been rejected in the ME/CFS domain.** [This paragraph has been corrected. See below.]

This effort isn’t all that surprising. For the GET/CBT ideological brigades, with the COFFI crew foremost among their ranks, the pandemic has served as an enormous opportunity to promote their hypotheses about psychogenic causation of the symptoms collectively being called long Covid. A key construct is pandemic-related “psychosocial strain”–a buzz phrase that has been highlighted by both Harvard physician Adam Gaffney and New Republic journalist Natalie Shure. The suggestion is that many among those counted as having long Covid most likely weren’t even infected with the coronavirus in the first place but are experiencing a form of post-traumatic stress disorder.

Of course, no one seriously disputes that psychosocial strain—whether experienced as anxiety, depression, stress, PTSD, or whatever–has physiological correlates that negatively impact health and can lead to somatic symptoms. No one seriously disputes that some people who never had covid-19 might also sometimes report troubling symptoms. No one seriously disputes that psychological counseling can be helpful for anyone going through a difficult and challenging period in life, and people living with chronic illnesses can have great difficulties and challenges.

But so what? The relevant question is whether most of the millions of formerly hard-working and productive individuals who now find themselves severely disabled but have no identified organ damage are mostly suffering from the effects of psychosocial strain or whether post-infectious pathophysiological processes are implicated. Whatever Professor Sharpe and others maintain, the evidence points to the latter. Something is really going on with people even though the results on standard tests tend to be normal; investigators continue to learn more all the time about the protean impact of coronavirus infection.

(Recent articles on the pathophysiology of long Covid can be read here, here, and here.)

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Reviving an ancient definition for current usage

The COFFI research agenda paper regurgitating and rebranding ancient ideas was published in the Journal of Psychosomatic Research (JPR). As the official journal of the European Association of Psychosomatic Medicine , the JPR has essentially served as an in-house promotional organ for investigators pushing the GET/CBT treatment paradigm for ME/CFS. (One of the lead PACE investigators, Professor Michael Sharpe, is currently president of the association.)

The journal has published some real whoppers, like Professor Peter White’s long-term follow-up to his trial of self-managed GET. The paper failed to mention in its highlights section that there were no—zero—differences between the intervention and comparison groups at long term follow-up. I brought this omission to the journal’s attention. The article was subsequently corrected.

To accomplish its goals of transforming an early but outdated CFS definition into the core long Covid construct, the COFFI research agenda paper offered this definition of post-infective fatigue syndrome: “Post-infective fatigue syndrome (PIFS) is defined as persistent, severe fatigue after an infection that cannot be explained by other medical or psychiatric conditions, which has been present for at least six months and significantly affects daily functioning.”

The reference for this definition is the 1991 paper in which Professor Sharpe–the Norma Desmond of this scientific domain (“I am big, it’s the pictures that got small”)–outlined the so-called “Oxford criteria” for chronic fatigue syndrome. The paper, which had several co-authors, was titled “A report–chronic fatigue syndrome: guidelines for research.”

This definition, which required no symptoms other than fatigue, has been rejected as inadequate by the international scientific community because it conflates the symptom of “chronic fatigue” with the clinical entity called “chronic fatigue syndrome.” In 2015, a review of the literature from the National Institutes of Health recommended that the Oxford criteria were “flawed” and should be “retired” from use because they could “cause harm.” The reasonable fear was that the  heterogeneity of study samples recruited with this definition would lead to meaningless results.

But that is not a concern of the COFFI crowd, which apparently believes this ancient definition focused solely on fatigue is perfect for our times—as the group’s name itself implies. As everyone knows by now, or should know, post-infectious conditions are not just about “fatigue” but involve a host of other symptoms—in particular the phenomenon of post-exertional malaise as well as cognitive dysfunctions, POTS or other conditions involving dysautonomia, sleep dysfunctions, and other non-specific medical complaints.

Fatigue is among the most common symptoms reported to doctors and is a sign of many conditions and diseases. Targeting this incredibly broad construct for intervention, while overlooking that in post-infectious illness it is generally accompanied by a cluster of other symptoms, is misguided and kind of stupid. In a 2015 report, the Institute of Medicine (now the National Academy of Medicine) found that “systemic intolerance”—an alternate name for post-exertional malaise—was the cardinal feature of the illness.

Some of the authors of this long Covid research agenda have demonstrated something of an integrity deficit in the past. That includes Australia’s Professor Andrew Lloyd, who seems eager to impose COFFI’s 1991 agenda on his compatriots. (I interviewed Professor Lloyd when I visited Australia five years ago, and wrote about it here and here.)

The senior author of the paper, Professor Hans Knoop from the Netherlands, co-wrote a Lancet commentary accompanying the PACE trial that claimed study participants had met a “strict criterion for recovery”—which was untrue, given that a significant minority of participants had already met a key outcome threshold at baseline. This bizarre and undisclosed feature of the study appears to meet common definitions of research misconduct from the US National Institutes of Health and the UK’s Medical Research Council.

The COFFI claims are grounded in flawed and bogus science. The relevant evidence in this field is based almost exclusively on findings from unblinded studies relying on subjective outcomes for claims of improvement—a recipe for generating an unknown amount of bias. Objective measures of function, such as the amount of physical movement as measured by actometers, a fitness step-test, employment status, and other indicators have almost always shown poor results in comparison with the subjective responses.

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A call to investigate “psychosocial predisposing and perpetuating factors”

In the US, the Centers for Disease Control and Prevention rejected the GET/CBT paradigm and switched gears in 2017, virtually “disappearing” references to the PACE trial from its pages. In 2021, the UK’s National Institute for Health and Care Excellence issued new ME/CFS recommendations that reversed the previous guidelines. Re-analyses of the trial data have documented that the treatments did not lead to recovery and that any improvements were marginal and well within what would be expected from the bias inherent in the study design.

The COFFI research agenda paper does address up front the importance of biomedical investigations. But since it would be hard for any major research proposal on long Covid to dismiss the need for biomedical investigations, the recommendation feels like throat-clearing. After this opening, the paper makes a special plea for the importance of investigating the role of “psychosocial predisposing and perpetuating factors that play a role in PIFS”:

“Previous research has shown that psychosocial factors, such as distressing life events, may predispose to developing PIFS, whereas symptoms of depression or anxiety, cognitive factors (i.e., illness beliefs) and behavioural factors (i.e., changes in activity patterns) may act as perpetuating factors. It is therefore unfortunate that there seems to be opposition to research into psychosocial predisposing and perpetuating factors that play a role in PIFS. At the moment little research is done into the role of psychosocial factors in post-COVID-19 fatigue.

The reason there is such “unfortunate” opposition to the proposed project is because the research documenting the purported “psychosocial predisposing and perpetuating factors” in post-viral conditions and ME/CFS in particular is mostly garbage. These studies often rely only on associations and correlations, which the authors then tend to interpret as causal relationships in their favored direction. The intellectual bankruptcy at the core of some of the research is distressing. As the CDC has stated bluntly, ME/CFS is not a psychological disorder.

The paper declared that “behavioural interventions were effective in reducing symptom severity and improving functional capacity for PIFS and for similar chronic fatigue states unrelated to infection.” Moreover, “exercise therapy was previously found to be effective in chronic fatigue syndrome, but its effectiveness has not yet been studied in PIFS.”

Interestingly, the authors did not cite PACE to support any of these claims, even though the authors themselves declared it was the “definitive” trial of GET and CBT for the illness. Perhaps that piece of crap has become too toxic for even these true believers to cite at face value. Instead, the authors cited two other papers on treatments for chronic fatigue syndrome, a study of cancer-related fatigue that is pretty irrelevant in this context, and a disputed Cochrane review on exercise therapy in which PACE was the largest trial included.

Unfortunately, the authors did not inform readers of the advisory that Cochrane itself slapped on the review, which essentially indicated that even its weak reported findings could not be taken at face value. In another problematic omission, the authors also do not inform readers that CDC, NICE and other major health organizations have rejected not just PACE itself but the entire treatment paradigm based on “predisposing and perpetuating factors.” Yet that rejected paradigm is what Professor Lloyd, Professor Knoop and their colleagues are proposing to impose on the long Covid patient community.

Please. When it comes to “post-infective fatigue syndrome,” the GET/CBT ideologues already had their big chance to prove their case. It was called the PACE trial, and it bombed. Enough already.

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**Correction: The initial version posted yesterday did not mention that the Oxford criteria included a “post-infectious” subtype. I had used the word “rechristened” to describe the authors’ decision to cite the 1991 paper, but that implied they had changed the name. (They did, from “infectious” to “infective,” but that change is obviously non-substantive.) Rather, they had just selected a subsidiary and largely ignored section of the paper to highlight. So “rebranded” is more accurate.

Trial By Error: An Interview with Meghan O’Rourke, Author of The Invisible Kingdom (Reprise)

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By David Tuller, DrPH

Last April, I interviewed poet, journalist and editor Meghan O’Rourke about The Invisible Kingdom, her insightful and affecting memoir of living with chronic illness. The book, a New York Times bestseller and a finalist for the National Book Award, has just been issued in paperback.  So I figured I’d re-post the interview.

As the book recounts, O’Rourke initially began experiencing perplexing physical signs and sensations not long after graduating from Yale in the late 1990s–“daily hives, dizziness, chronic pain, and drenching night sweats.” She struggled for years with a range of debilitating symptoms, and finally found some relief after being treated for chronic Lyme disease—itself a controversial diagnosis. In 2013, she wrote an extended piece on all this for The New Yorker.

The Invisible Kingdom was published at a timely moment, given our current global epidemic of post-viral illness, popularly known as long Covid but more formally called post-acute sequelae of SARS-CoV-2. The book helped generate greater awareness of some of the complex chronic conditions that lack widely accepted diagnostic tests. It is also filled with gorgeous and haunting sentences, like this one: “In the dark room where I listened to life happen around me when I was sick, I yielded a part of myself forever.”

In our conversation, we talked about O’Rourke’s own journey through this “invisible kingdom,” the challenges of finding appropriate medical care, the loneliness of being sick, the ravages of brain fog, the emergence of long Covid, and the struggle to find words to describe experiences and states of being that defy easy description.

H5N1 – It’s All About the Transmission

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by Gertrud U. Rey

Recent news headlines have been highlighting the global spread of H5N1, the strain of influenza virus that is typically associated with “bird flu.” This outbreak is the largest in recorded history, involving at least 50 million dead birds and countless non-human mammals, including sea lions, otters, mink, foxes, cats, dogs, and skunks. But what does this mean for us?

Although the virus has so far infected about 1,000 people worldwide, most of these infections have been in individuals who had direct contact with infected birds, and thus, the infections likely originated from those animals. There is currently no evidence to suggest that H5N1 can transmit efficiently from one person to another, a factor that is critical for triggering a human pandemic. As far as we know, there are several obstacles that prevent sustained human-to-human transmission of H5N1.

The first obstacle has to do with the host cell surface receptor that mediates viral entry for influenza virus infection in humans. To enter a cell, human influenza viruses bind receptors that consist of a sialic acid molecule linked to galactose via an alpha 2,6 glycosidic bond, and these receptors are located mostly on cells of the upper respiratory tract. In contrast, avian influenza viruses (including H5N1) preferentially bind sialic acids with an alpha 2,3 linkage (illustrated), which are abundant on cells of the avian digestive tract and cells of the human lower respiratory tract. Although H5N1 can infect and replicate in cells of the lower respiratory tract, its transmission to other humans from the lower respiratory tract is very inefficient, meaning that H5N1-infected people typically do not pass the virus on to others. In other words, because H5N1 cannot efficiently replicate in the upper respiratory tract, it doesn’t typically transmit among humans. In order for H5N1 to pass easily from one person to another, it would at the very least need to acquire an amino acid change that allows it to bind a sialic acid receptor with an alpha 2,6 galactose linkage.

sialic acid

A second obstacle that prevents sustained human-to human transmission of H5N1 influenza virus involves the H5N1 polymerase enzyme, which is responsible for replicating the viral genome. To function properly, this enzyme needs to be in an environment with a temperature of approximately 40℃ – the average temperature of the avian digestive tract. Because the human upper respiratory tract has a temperature range of 33-35℃, the H5N1 polymerase would need to adapt to function in this temperature range in order for H5N1 to replicate and transmit more effectively from this site.

A third obstacle relates to the pH inside the membrane vesicle that forms around a viral particle once it enters a host cell. This vesicle, called an “endosome,” transports the viral particle through the cytoplasm until the viral and endosomal membranes fuse to allow the viral RNA to enter the host cell cytoplasm. Human-adapted influenza viruses undergo this membrane fusion most efficiently in the low pH conditions of the endosomes of human cells. However, H5N1 viruses require a much higher pH for fusion, meaning that they could easily degrade in the low pH environment of the human endosome, and thus not produce an effective infection that could transmit virus to other humans.

The segmented structure of the influenza virus genome allows for frequent reassortment between segments, such that if a host cell is co-infected with two different strains of influenza virus, the segments can reassort to produce new virus strains. Pigs are susceptible to infection by both avian and human influenza viruses, making them likely mixing vessels for such reassortment events. Reassortment between the “right” influenza virus genes could lead to a new version of H5N1 that could infect and transmit from cells of the human upper respiratory tract, thus triggering efficient human-to-human transmission and a potential pandemic.  

Fortunately, many scientists are preparing for such a scenario by developing H5N1-specific diagnostic tools, antiviral drugs, and vaccines. For example, virologist Scott Hensley and colleagues have generated a highly promising monovalent mRNA vaccine that completely matches the currently circulating strain of H5N1. So far, the vaccine produces great antibody responses in mice, but it still needs to be tested in ferrets, and then obviously, humans. There are also many other research groups working on both H5N1-specific and multivalent influenza virus vaccines directed against all known influenza virus subtypes.

There is no way to predict if and when H5N1 will evolve so it can pass easily between humans, although the probability for such a phenomenon is as real as the recent emergence of SARS-CoV-2. Considering that the mortality rate from H5N1 infection in humans is estimated to be higher than 50%* (compared to less than 1% from SARS-CoV-2), the consequences of a potential H5N1 pandemic would be a lot worse than those of the present pandemic. The fact that H5N1 already appears to transmit fairly well between non-human mammals as evidenced by an outbreak on a Spanish mink farm is highly concerning. The current H5N1 outbreak warrants increased surveillance and preparedness, and it further highlights the importance of a comprehensive One Health approach for detecting and controlling pandemic threats.

*This estimate by the World Health Organization likely does not take into account the total number of infections, which is probably much higher than we think. A higher number of total infections would decrease the rate of mortality.

[A big thank you to Joanna Pulit-Penaloza for the useful discussions, which helped me clarify some of the concepts in this post.]

Trial By Error: After Maeve Boothby O’Neill’s Death, More Concerns About Severe ME Patients at NHS Hospitals

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By David Tuller, DrPH

I recently wrote an article for Codastory.com about Maeve Boothby O’Neill, who died from complications of severe ME in October, 2021, after three separate admissions to her local National Health Service hospital in Exeter, England. During her hospital stays, she and her family fought with the hospital over the need for tube-feeding or an alternate approach called total parenteral nutrition that bypasses the digestive system altogether.

Conflicts involving malnutrition are also at the crux of a dispute involving Alice Barrett, a current patient in the same facility, the Royal Devon and Exeter Hospital. The issue is the hospital’s tube-feeding policy, which requires patients to be able to sit up at an incline of at least 30% in order to minimize the risk of complications like aspiration pneumonia. This policy conforms to standard medical practice.

Addressing malnutrition in severe ME is a challenging domain of medical practice. At some point, it can become difficult or impossible for some patients to chew and swallow enough food to ingest sufficient nutrients and enough water to prevent dehydration. If that happens, it becomes necessary to find another way to keep patients alive—either tube-feeding or TPN, an intravenous approach that can be used when tube-feeding fails or is not possible.

But by the time ME patients deteriorate to that point, sitting up at even a 30% incline can be intolerable to them, because of postural orthostatic tachycardia syndrome (POTS), or other factors like post-exertional malaise (PEM).

“In severe cases a 30 degree raise of the upper body is enough to reduce brain blood flow causing light headedness, nausea, vertigo, sometimes even loss of consciousness,” said William Weir, an infectious disease physician who specializes in ME and has been involved as an outside consultant in both Maeve’s and Alice’s cases. Dr Weir said he has had severe ME patients who have been tube-fed at much lower angles and has advised the hospital that he believes it can be done safely.

My UC Berkeley friend and colleague John Swartzberg, an infectious disease physician, said that 30% “is a common target” for tube-feeding but should not be treated as absolute. “You have to weigh risks and benefits,” he said, noting that in this case, from what he could tell from the petition, the benefits certainly seemed to outweigh the risks.

Alice was diagnosed with ME in 2020 after graduating from Newcastle University with a history degree. By last spring, her health had deteriorated to the point where she was bedbound.

To raise awareness of the case and generate public pressure on the hospital, Barrett’s family last week started circulating a petition, which so far has received more than 10,000 signatures. “We need a suitable feeding option offered as soon as possible...Alice is running out of options and time,” declares the petition.

The family met with hospital staff today but so far no resolution to the impasse has been found, Debbie Barrett, Alice’s mother, told me.

“The frustrating thing is just a lack of understanding and ignoring our advice,” she wrote in an e-mail. “From the very beginning we said that 30 degrees incline would be problematic. Instead they pushed and pushed it without thinking of ME and POTS or the effects of PEM.”

Yesterday, The Times published a piece about the Barrett case and a second one elsewhere in England. The second case involves Sami Berry, 43, another severely ill ME patient suffering from nutrition issues and facing challenges at the Royal Berkshire Hospital, an NHS facility in Reading. The group #MEAction issued a press release about the case last week.

The Times article contained responses from both spokespeople for both hospitals:

“A spokesman for Royal Berkshire Hospital said: ‘Our clinical teams are in ongoing talks with Ms Berry and her family about her condition and most appropriate treatment. We cannot comment on the specifics to preserve patient confidentiality. However, as a trust, our highest priority is ‘always providing safe, appropriate and high-quality care to Ms Berry.‘

“Professor Adrian Harris, chief medical officer at Royal Devon University Healthcare NHS Foundation Trust, said: ‘ME is an incredibly complex and poorly understood disease. It is recognised that there is a global lack of evidence for the safe treatment and maintenance of people living with ME.’“

There is very little medical literature on the issue of addressing severe malnutrition in ME. One of the few, co-written by Dr Weir, is a 2021 report of five cases. Here’s the abstract:

“Very severe Myalgic Encephalomyelitis (ME), (also known as Chronic Fatigue Syndrome) can lead to problems with nutrition and hydration. The reasons can be an inability to swallow, severe gastrointestinal problems tolerating food or the patient being too debilitated to eat and drink. Some patients with very severe ME will require tube feeding, either enterally or parenterally. There can often be a significant delay in implementing this, due to professional opinion, allowing the patient to become severely malnourished. Healthcare professionals may fail to recognize that the problems are a direct consequence of very severe ME, preferring to postulate psychological theories rather than addressing the primary clinical need. We present five case reports in which delay in instigating tube feeding led to severe malnutrition of a life-threatening degree. This case study aims to alert healthcare professionals to these realities.”

Trial By Error: An Upcoming “Biopsychosocial” Long Covid Conference in Finland

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By David Tuller, DrPH

What is it with the health care establishments in northern Europe? Why are they so devoted to non-evidence-based approaches to treating serious medical conditions? Why do they trust arguably fraudulent research, like the PACE trial and Professor Esther Crawley’s pediatric Lightning Process study? Why are the authors of these studies respected and even esteemed among some high-level circles in these countries?

The mind boggles.

The latest on this front is an upcoming gathering in Finland that provides a platform to leading lights of the CBT/GET/’amygdala retraining” ideological brigades. Sponsored by Helsinki University Central Hospital (HUS) and scheduled for March 16th, it is called “Navigating the Unknown: Exploring Realities and Best Practices for Long Covid.”

Here are some of the questions the conference promises to explore: “What is the difference between long Covid and Post Intensive Care Syndrome? What are the relations of Long Covid and chronic fatigue syndrome (ME/CFS)? Are there some risk factors for developing symptoms of Long Covid?” Well, that all sounds reasonable enough.

Then there’s this: “This symposium will focus on the bio-psycho-social aspects of this disorder.” Uh, oh! More biopsychosocial propaganda.

Millions Missing Finland, an ME/CFS advocacy organization, has tweeted concerns about the gathering. In a thread that highlighted the problematic views of most of those presenting, the organization noted that “we find the speaker list peculiar and worrying.”

The list of speakers is indeed problematic but not surprising.

A prominent HUS physician, Helena Liira, is opining about “the Finnish experience from the Long Covid outpatient unit.” Dr Liira and I exchanged e-mails last year after I criticized a clinical trial for which she is the lead investigator. The trial, sponsored by HUS, is studying an intervention for people with “functional” disorders, including long Covid. The intervention is described as “amygdala and insula retraining”–even though the study includes no effort to measure anything related to anyone’s amygdala or insula.

Dr Liira is essentially running a trial of the Gupta Program—one of the multiple mind-body approaches currently being marketed to people with chronic illnesses, including long Covid. The eye-catching claim—that amygdalae and insulae are being retrained–is solely a marketing device derived from grand-sounding but largely meaningless speculations about the brain by the Gupta Program’s founder, Ashok Gupta. Whatever might be happening, there is no evidence that any amygdalae or insulae have undergone retraining.

Dr Liira and the ethical review committee that approved the study apparently see no problem with describing an intervention as purporting to involve something as complex as “amygdala and insula retraining”–even though this has zero to do with the study itself. They don’t think this sort of promotional hyperbole can possibly bias any of the study subjects. I disagree. Since the trial is already flawed for multiple reasons, as I discussed here, this nomenclature issue simply further undermines the credibility of any findings.

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Professor Sharpe is having a Norma Desmond moment

Also on the Helsinki conference schedule is Professor Michael Sharpe, one of the lead investigators of the PACE trial. Professor Sharpe frames legitimate criticism of his disastrous study not only as “harassment” but as an attack on Science itself. Whatever. The relevant point is that PACE and its GET/CBT approach have been rejected by the US Centers for Disease Control and Prevention, the UK’s National Institute for Health and Care Excellence, and other leading health agencies. The PACE trial has been used as a pedagogical tool in epidemiology graduate seminars at UC Berkeley–as a case study in awful, unethical research. And 100+ experts from around the world signed Virology Blog’s open letter to The Lancet about PACE’s “unacceptable methodological lapses”–as reported in The Times and BMJ.

Nonetheless, this Oxford don is having his Norma Desmond moment! (Watch this clip from the Hollywood classic Sunset Boulevard if you don’t know what I’m talking about.)

Besides his upcoming appearance in Helsinki, two major features in high-profile US publications—New York Magazine and The New Republic—recently included respectful interviews with Professor Sharpe. The articles presented long Covid as largely a “functional” or psychosomatic disorder and allowed Professor Sharpe to spout some of his standard self-serving slop. Apparently the journalists believe it is fine for a study to include participants who were already “recovered” on key outcomes at baseline–as was the case in the PACE trial. Apparently the organizers of the Helsinki conference agree. Enough said.

And then we have Professor Paul Garner discussing “how to recover from long covid.” It has been surprising to watch the entire BPS world, which claims to care about evidence-based medicine, accept one person’s illness narrative as proof that everyone should be able to cure themselves with strong manly thoughts—just like Professor Garner. I wrote about him here.

A psychologist from Bergen, Norway, Professor Gerd Kvale, is offering a talk on “concentrated treatment” for long Covid. Professor Kvale and colleagues have developed a three-day rehabilitation program, conducted in small groups, involving “a combination of teaching, individual conversations and physical activity and training.” And this: “Understanding and acceptance of the health challenges combined with techniques that aim to increase flexibility and activity are important. In particular, emphasis is placed on recognizing and getting help to break patterns that can contribute to maintaining the ailments.”

Hm. Sounds like a concentrated program of CBT/GET to me, perhaps with a little amygdala and insula retraining thrown in.

Avindra Nath, who is intramural clinical director of the National Institute of Neurological Disorders and Stroke at the US National Institutes of Health and a leading long Covid investigator, is giving a remote presentation called “What is long covid?” Dr Nath’s participation in the event has generated some comment and discussion on social media. Given the conference’s frank embrace of the biopsychosocial approach, his appearance could be seen as lending legitimacy to this overall orientation. To counter any criticism, the organizers could point to Dr Nath’s appearance, and maybe that’s why they invited him.

On the other hand, there’s value in injecting some scientific and biomedical realities into this slate of presentations. Perhaps Dr Nath’s talk will highlight enough hard facts to inoculate at least some audience members from buying into the psychosomatic framework that will otherwise dominate the proceedings. 

In any event, among those who care about serious science in this domain, the conference certainly risks damaging the medical center’s international credibility and reputation. Sad.

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TWiV 985: Bambi’s revenge

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TWiV reviews an outbreak of Marburg hemorrhagic fever in Equatorial Guinea, wild poliovirus type 3 shedding from a laboratory in the Netherlands, and white-tailed deer as a reservoir for previous SARS-CoV-2 variants of concern.

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