By David Tuller, DrPH
For the second time in a few weeks, a major US news organization has provided Professor Michael Sharpe, lead PACE investigator and one-time Virology Blog commenter, with a high-profile platform to disseminate his typical blather and nonsense. Both articles—the first in New York Magazine, the second in The New Republic–-have presented the long Covid phenomenon as largely psychosomatic.
I wrote an extended twitter thread and a blog post about the pretty awful New York Magazine piece, which highlighted my 15,000-word investigation of the PACE trial but misrepresented my criticisms. I won’t bother more about that article for now. As for The New Republic‘s iteration by Natalie Shure, an experienced science and health journalist, poet Meghan O’Rourke, author of The Invisible Kingdom, has written an excellent thread about it.
Let me stipulate first that “long Covid” might be a useful phrase for popular talk but can be too loose and imprecise for scientific discourse. As commonly deployed, it obviously covers an extremely heterogeneous group. And there is general agreement that some subsets of patients under the long Covid umbrella suffer from identifiable coronavirus-related organ damage and/or recognizable clinical entities like post-ICU syndrome.
It should also should be possible to agree that people with symptoms for a couple of months after acute infection should not be casually lumped in with patients continuing to report symptoms for two years—even though some of the published research involves just this sort of lumping. Natural post-viral recovery can take many months, even longer. The traditional requirement in ME and CFS case definitions that symptoms must have continued for six months has been a crude but not fool-proof way to distinguish people experiencing a slow but steady post-viral recovery from those who continue to remain impaired.
The main controversies around long Covid seem to involve the subset of patients with prolonged, non-specific symptoms that overlap with those in ME and CFS case definitions: post-exertional malaise or post-exertional symptom exacerbation, prolonged exhaustion, cognitive impairment, sleep disorders, and orthostatic intolerance, among others. When I refer in this post and more generally to long Covid, I am largely focused on this subset.
“A dramatic illustration of suffering driven by psychosocial distress”
Shure acknowledges the overlaps between long Covid and ME/CFS but seems to have taken the wrong lessons from them—just like Professor Sharpe and her other main sources. She briskly presents the case for considering long Covid to be a serious pathophysiological disease, then swats it down and promotes the counter-notion that the phenomenon is, in fact, “a dramatic illustration of suffering driven by psychosocial distress.”
She further writes: “A chronic illness that appeared to be triggered by viral infection could just as easily have been triggered by the trauma of the pandemic itself. That long Covid, ME/CFS, and related diagnoses disproportionately target women perhaps stems from the fact that, in a patriarchal world, women face more adversity and have less control over their lives.”
(Note to Shure: Auto-immune disorders also disproportionately target women. Does that perhaps stem from the fact that, in a patriarchal world, women face more adversity and have less control over their lives? Asking for a friend with an auto-immune disorder who lives in a patriarchal world and faces adversity.)
The article’s lengthy opening section recounts the story of a woman who believed she suffered from progressive dementia but was later diagnosed, to her relief, with functional neurological disorder. The author also interviewed Professor Sharpe; two of his former students, neurologists Professor Alan Carson and Professor Jon Stone; Dr Mark Hallett, an FND expert at the US National Institutes of Health; Zachary Grin, a physical therapist who treats FND patients; and Professor Paul Garner. (The less said about Garner the better–except to note that he seems to have had a somewhat lengthy but normal post-viral recovery.)
To point out the obvious, this is not a robust range of views on which to ground the broad suggestion that long Covid as well as ME/CFS and related disorders are likely varieties or manifestations of psychosocial distress and FND. Shure critiques studies investigating biomedical aspects of long Covid but does not give the investigators a voice beyond her second-hand accounts of their work. If she has interviewed any actual long Covid or ME/CFS patients or any clinicians who have treated them besides Professor Carson and Dr Hallett, it is not apparent from the article.
And then Shure writes this: “Meanwhile, there is evidence hinting that some symptoms chalked up to long Covid may well be functional.”
The only hint of evidence presented here is that Professor Carson and Dr Hallett say they have seen long Covid patients whose symptoms, by their account, did not arise as pathophysiological responses to coronavirus infection. For example, Shure reports, Professor Carson “determined that one long Covid patient who was unable to walk had functional paralysis that was likely triggered by his traumatic hospitalization early in the pandemic.”
Right. That’s pretty much the extent of Shure’s “evidence.”
After discussing this patient with “functional paralysis,” Shure adds this: “For Carson, the idea that the etiology of this man’s symptoms would render him less worthy of care or sympathy than someone whose symptoms are caused by physical tissue damage is troubling.”
But here’s the neat thing: Neither Alan Carson nor Natalie Shure needs to be “troubled” over this idea! I have not seen any advocates arguing that patients with psychological trauma are “less worthy of care or sympathy” than those with tissue damage. This framing is part of a straw-person argument that Professor Sharpe and his ideological comrades have hyped for a long time—that anyone who rejects their anti-scientific assertions is denigrating people with mental illness or minimizing the impacts of psychological disorders.
It should be possible to disagree with the stupidities espoused by Professor Sharpe and his colleagues without being accused of denigrating or insulting people with mental health challenges. Many ME/CFS and long Covid patients understandably object to sweeping and unproven claims that their symptoms should be attributed to anxiety, depression and other mood and emotional disorders. This is not a dismissal of the suffering of people with mental illness and it should not be portrayed as such.
The PACE findings were “mundane” so no big deal, writes Shure
When it comes to PACE, Shure’s account is way off. She refers to the PACE findings on GET and CBT as so “mundane” that “the tenacity of the response is suprising.” It is only surprising to people who do not understand the impact the trial has had on clinical practice in the UK and around the world and the deceptive way in which it was promoted and marketed–not to mention that it is arguably a fraudulent piece of research.
Shure writes that “an extended court battle forced Sharpe and his co-researchers to hand over their data, which detractors reanalyzed and claimed undermined the PACE conclusions.” In fact, this was more than a “claim.” The re-analyses did indeed undermine the PACE findings, as everyone but Professor Sharpe and those ignorant or gullible enough to listen to him understand. (I was a co-author of the most comprehensive re-analysis paper.)
Shure further writes that “advocates have successfully gotten GET and CBT withdrawn from official ME/CFS treatment guidelines in the United States and the U.K.” This is disingenuous. Of course advocates pressed agencies to drop their recommendations for GET and CBT, given the poor quality of evidence pushed by Professor Sharpe and his cronies. Why shouldn’t they?
But the US Centers for Disease Control and Prevention and UK’s National Institute for Health and Care Excellence did not change their policies because big scary ME/CFS advocates made them do it. They revised their recommendations because they could no longer stand behind the PACE trial and other subpar studies. Patients should be applauded for bringing research flaws to light, not criticized based on Professor Sharpe’s testimony. He’s an unreliable narrator–no matter how many times American journalists regurgitate his mutterings.
8 thoughts on “Trial By Error: Is the Long Covid Phenomenon an Expression of “Psychosocial Distress”?”
The problem with the concept of “functional illness” and FND is that it is pseudo-scientific. Nothing is actually explained scientifically – no brain pathology is demonstrated that explains the illness.
A pleasant, accurate and readable piece of journalism and science. Thanks David
@Snow Leopard – FND-Portal (whoever he is) might disagree with you since I’ve heard him chatting about part of the brain being implicated in FNDs although I can’t remember which part.
On a third reading of Ms Shure’s article, I have a few observations (there are many more but I need to go and buy food and get back to work).
First: She has omitted to cite Kanaan et al on ‘the function of ‘functional’ a mixed methods review http://dx.doi.org/10.1136/jnnp-2011-300992 which makes it clear that ‘hysteria’ hasn’t gone away, it’s just hidden behind a term which has remained vibrant because of it’s ambiguity and can be used to infer one thing to patients and another to their caring doctors. This mitigates against the Patients as Partners era of medicine so doesn’t feel healthy to me.
Second: Although there was mention of how patients with a FND dx have been treated in the past (in the sense of being treated with ‘appalling contempt’, not in the sense of what medical treatment they received) there wasn’t enough critical appraisal of why this happened (and still does) or the impact of this on the doctors who did/do it. It can’t be good for their psyches and they may need an intervention since the ‘clinician heal thyself’ deal doesn’t appear to be working.
Third: We know from Alex Berry’s paper about revising a FND dx that patients who want to change their functional diagnosis to a structural one face ‘psychological resistance’ from their neurologists but we don’t know why these neurologists feel the need to put up resistance. As we move forwards with Long Covid, this needs to be addressed and Ms Shure doesn’t seem to be aware of this, as far as I can tell from her article. I am aware that there wasn’t space for her to discuss all the questions patients may have about the approaches – including resistance – in neurology but I hope she will dive into this in any future articles and look into the FND Society’s approach to patient engagement which is suboptimal at best and mimics ‘appalling contempt’ at worst.
Finally, we know the term ‘functional’ is used because it aids diagnostic acceptance because it doesn’t overtly point to a mental health diagnosis, yet FND is in DSM. So a wider discussion about medical gaslighting could have been proposed in Ms Shure’s article.
There’s a paragraph in Shure’s article, that includes a quote by Mark Hallett, that altogether seems, to me at least, to imply that 30% of neurology cases in general have a functional cause. I believe that, on more than one occasion, Hallett has reported that he found a 30% or ‘third’ rate for functional cases as a proportion of clinic cases of movement disorders e.g. in this podcast -https://soundcloud.com/user-820167999/a-neurological-journey?utm_source=mobi&utm_campaign=social_sharing&utm_terms=mobi_display_ads_experiment_v3.control and in this article -https://movementdisorders.onlinelibrary.wiley.com/doi/abs/10.1002/mds.27713 – but I don’t think I’ve ever come across him reporting a similar or identical rate for functional cases amongst neurological cases in general. Perhaps I missed something and there is evidence for such a rate but, if so, it would be nice to see it. Maybe Shure could share it with us? A 30% rate across general neurology would be at odds with the 16% figure obtained by Sharpe, Stone, Carson and colleagues in their much-referenced Scottish Neurological Symptoms Study. Their 16% rate also included cases of ‘psychological symptoms’ (that presumably differ to an extent from ‘functional’ ones). Getting to the bottom of the 30% rate kind of matters, I think. If a mistake’s been made then I imagine that Hallett, given his credentials, would probably want to flag it up and put things straight. If there’s no error, (and I’ve interpreted the paragraph correctly), then I’d like to see the evidence behind this 30% rate so I can try to figure out why it differs so much from that found in Scotland.
Good points. The percentage rate apparent discrepancy merits further elaboration.
Thanks Dredd. If explanation or elaboration aren’t forthcoming then I think the next stop should be the NIH to ask what they think the prevalence of functional disorders and positively identified FND are. I’d hope that they’d have a clear idea that’s backed up by solid evidence.
Have these eminent scientists considered that just maybe the reason women are more affected by auto-immune disorders is because the female immune system is way more complicated than in men. This is for the very simple reason that women need to be able to cope with pregnancy without their immune system turning on the foetus, which by definition is not fully their DNA.
Thanks for all your work this year, David.
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