Correctives from Putrino & Iwasaki (and Others) to the Long-Covid-Is-Psychosomatic Claims

By David Tuller, DrPH

When the pandemic began, everyone involved in the ME, CFS, and ME/CFS domain assumed that there would be a wave of post-acute, prolonged complications, since every virus seems to leave in its wake a small but still significant number of people who report a range of non-specific symptoms. It was also widely predicted that many in the medical world would interpret these physical complaints as psychosomatic, psychogenic, or “functional,” to use the current buzzword in this complicated field.

That has all come to pass.

Luckily, the CBT/GET paradigm—as applied to ME/CFS, at least–was already in a state of collapse before the pandemic began. Not surprisingly, some of those who would be the biggest losers of this paradigm shift are among the most enthusiastic boosters of the notion that the long Covid phenomenon has been largely triggered not by any underlying pathophysiological processes but by pandemic-related anxiety, depression and other mood disorders arising from “psychosocial strain.”

So when it comes to long Covid, mainstream and scientific publications alike have lately published some pretty stupid crap–and that’s my professional assessment as both a journalist and public health academic. Two high-profile feature articles at the end of 2022—one in New York Magazine and the second in The New Republic—presented profoundly biased accounts of the history and science of post-viral illness. Both journalists flogged the idea that millions of people around the world whose health and daily lives have been ravaged by long Covid are most likely suffering from psychosomatic or functional conditions.

Right. Tell that to Pulitzer Prize-winner Jennifer Senior of The Atlantic, who just this week wrote about her own debilitating case of long Covid.

Then we’ve had the academic versions. I wrote a blog post about a poorly reasoned article in the Journal of Psychosomatic Research. In response to a similar piece in Lancet Respiratory Medicine called “A new paradigm is needed to explain long COVID,” a colleague and I sent a letter to the journal. (It was rejected, but it is posted here as a pre-print.)

The arguments seem to rely on some distorted logic: Mood disorders can impact health negatively and induce bodily sensations, therefore all health conditions and any bodily sensations we don’t fully understand must be caused by mood disorders. The first part is easy to agree with; the extrapolation in the second part is unwarranted and should be rejected.


And now some correctives

Now we’ve had some needed correctives. This week, Scientific American published a lengthy overview o called “Long COVID Now Looks like a Neurological Disease, Helping Doctors to Focus Treatments,” by Stefani Sutherland, a neuroscientist as well as a journalist. For Open Mind, an online magazine that explores scientific controversies and deceptions, journalist and author Ryan Prior has written a column called “Gaslighting Long Haulers” that puts the current situation in some historical context.

On the peer-reviewed front, Nature Reviews Microbiology last month published a review“Long COVID: major findings, mechanisms and recommendations” It was co-authored by two members of the formidable Patient-Led Research Collaborative, which has been a leader in pushing for investigations into long COVID. And earlier this week, Lancet Infectious Diseases published a robust rebuttal to the recent bullshit with a comment called “Why we need a deeper understanding of the pathophysiology of long COVID,” from Yale’s Akiko Iwasaki and Mt. Sinai’s David Putrino. (Here’s an interview with Dr Putrino from last year.)

The Iwasaki-Putrino essay pokes holes in the argument that the failure to have already unravelled all of long Covid’s pathophysiological mechanisms means that this outpouring of reported symptoms is largely the result of “psychosocial strain” and related constructs. Of course, the proof of a “functional” disorder is generally the lack of sufficient evidence to diagnose a biomedical or pathophysiological explanation for the reported symptoms. It is essentially a default position, with the determination often made based on normal or unremarkable findings on standard medical tests.

(That’s putting aside for a moment the sub-category specifically called functional neurological disorder, whose diagnostic criteria require the presence of what are said to be “positive” clinical signs of the condition.)

Iwasaki and Putrino address the issue directly in their analysis. Here’s a key paragraph:

“Despite the multifactorial pathogenesis, available data show that long COVID is an organic post-acute infection syndrome (PAIS) with clear physiological dysfunction that is often not consistently apparent using standard medical diagnostic tests. This discrepancy highlights the need for a new generation of more sensitive testing procedures for people with PAIS. Although it is not known whether pre-existing psychological diagnoses might influence the risk of long COVID (eg, by affecting the host endocrine and immune systems), it is neither productive nor clinically or scientifically valid to classify long COVID as a psychosomatic condition.”

A colleague pointed out an entertaining detail. Iwasaki and Putrino include a graphic of four colored gears, each representing one of the interlocking sets of risk factors that can lead to long Covid: blue for autoimmunity, red for viral reservoir, green for latent virus reactivation and yellow for tissue damage and dysfunction.

The graphic parallels a similar one in the Lancet Respiratory Medicine paper, in which the four gears bore a similar palette but instead represented triggers and risk factors related to psychological (e.g. illness perceptions, catastrophizing), social (e.g. lockdown, loss of roles), experiential (e.g. traumatic experience of illness, fear and grief), and biological (e.g. inflammation, deconditioning,  depression/anxiety) domains.

It made me chuckle to think of the Iwasaki-Putrino graphic and colors as a riposte—a subtle “idi na hui” to the Lancet Respiratory Medicine article. I hope the authors did it on purpose.