By David Tuller, DrPH
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Time magazine recently published an opinion piece that calls for an end to biomedical research for long Covid—based, it seems, on what the authors view as the ME/CFS precedent. The title: “How to End the Futile Blame Game Over Failed Long COVID Research.” Although research still has “a vital role” to play, they argue, it needs to be “a different kind” that “no longer focuses on biomarkers and mechanisms” because such studies “are sure to provide ‘promising’ but false leads and divert resources.” (The piece was adapted from a recent article that was published by STAT.)
The authors are Steven Phillips, vice president for science and strategy at the COVID Collaborative, a TK, and a fellow of the American College of Epidemiology, and Michelle A. Williams, a professor of epidemiology at Harvard’s T.H. Chan School of Public Health. They are major players, and they should know better than this. In a prescient essay two years ago on the emerging health burden of long Covid two years in the New England Journal of Medicine, they called for “a formidable, well-funded domestic and international research agenda to identify causes, mechanisms, and ultimately means for prevention and treatment of long Covid.” Now they’ve apparently changed their minds, although the piece does not really explain or even mention this reversal.
Part of their current argument against biomedical research rides on the major deficiencies that have plagued the much-ballyhooed RECOVER initiative from the U.S. National Institutes of Health, as revealed in recent journalism investigations. From the authors’ perspective, the solution to these identified roadblocks is not to re-double efforts to get things right but to abandon the search for biomedical answers altogether.
I was struck that Phillips and Williams seem to be highlighting the parallels between long Covid and ME/CFS as if this were a major insight; they call it “a unifying hypothesis.” These connections have been discussed since the start of the pandemic, and were well-known when the authors wrote their 2021 piece. It is also not a secret that many long Covid patients qualify for and receive ME/CFS diagnoses. So it is unclear why they are touting this notion as if it might be revelatory news.
Beyond that, the parallels they draw between ME/CFS and long Covid research are the wrong ones. The main argument for their suggestion that biomedical research into long Covid should be dropped seems to be that decades of ME/CFS research has not yet managed to crack that puzzle. As they write: “The established track-record of ME/CFS research exploring cause and pathogenesis has been singularly unproductive. By analogy, the current research directed at finding diagnostic and mechanistic clues to Long COVID is a resource-intensive, lengthy uncharted process. In the ME/CFS paradigm it will produce further leads for more biomedical research, but with a low ultimate likelihood of helping patients.”
The authors do not point out that, for decades, federal agencies have devoted only paltry amounts to biomedical research for ME/CFS. They also fail to mention the disproportionate investment in research on psycho-behavioral interventions, like the discredited PACE trial and related studies, as well as the pathetic results from this body of research. Instead, they insist that biomedical research into long Covid is probably going to prove to be a useless endeavor. As they write: “Why is this research unlikely to be productive? Because either there is nothing to find, or currently available tools are insufficient to detect and validate mechanisms behind the myriad of symptoms.”
The authors provide no real evidence to support their assertion that there might be “nothing to find”—or at least, if there is something, that it cannot be identified with current technology. The latter sounds like this: “Gee, this is hard, let’s stop looking.” I have not previously heard this sort of defeatist view advanced as a reason to abandon biomedical research involving other complicated illnesses.
In basing their argument about long Covid on the experience of ME/CFS, the authors ignore a key difference. A major challenge with ME/CFS research has always been that patients are generally not diagnosed till years after the onset of illness—and years after any acute infection that might have triggered it. In the case of long Covid, the investigations start with a clear link between a specific virus and subsequent prolonged medical complaints. That offers an expanded range of possibilities to ascertain exactly what mechanisms might be driving the range of disabling symptoms—post-exertional malaise, brain fog, orthostatic intolerance, etc.
What remains unclear from this account is the authors’ theory of the case. Are they suggesting these are psychosomatic symptoms—what would previously have been lumped into the category of “medically unexplained symptoms” or what would now often be called “functional”? Do the authors believe these conditions are largely driven by depression, anxiety, and related mood states rather than pathophysiological sequelae of an acute coronavirus infection? Is that what they also believe about ME/CFS? If so, they should say so directly–or at least provide some insight into their thinking about the matter.
Instead of biomedical research, here’s what they’re calling for: “Focus should be on health services research and on measures that directly impact the welfare of Long COVID sufferers: prevention, improved prognosis, access to empathetic care and quality of life issues.” No one can reasonably disagree with the need for such investigations. But if you don’t find out what’s causing the symptoms, how do you improve prognosis or know what kind of care (empathetic or not) is appropriate? How do you “impact the welfare” of long Covid patients if you give up the search for what’s going wrong with them?