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.