Stephanie Taylor was on a flight home to California from New York in 2008 when she started to feel ill. When she stood up to disembark, she felt so dizzy that she would have fallen over if another passenger hadn’t caught her. She took to bed with aches, swollen limbs and joints, and a fever that spiked to 104. Over time, painful pustules formed on her fingers and in her nose and ears. Exertion would send her crashing into a state of near paralysis. Unable to eat solid food and too weak to stand in the shower, she had to be spoon-fed and washed by sponge. Her doctors suspected a viral infection but couldn’t identify a pathogen, and so she remained bedridden with extreme fatigue as her small video production business teetered on the edge of failure.
Emily Taylor, her 25-year-old daughter, gave up the lobbyist job she loved in Washington, D.C., and moved back west to take care of her mother, shuttling her from physician to physician. “I’m not exaggerating, we probably saw 30 different doctors,” she says. None could pinpoint what was wrong, and few were sympathetic to their plight. “The experiences ranged from ‘I’m sorry, I can’t help you’ to outright hostile.” Four years after Stephanie first fell sick, they found an endocrinologist who pored over mountains of medical records during a two-hour appointment and asked for more time to study her condition. “And three months later that doctor came back to us and said, ‘I think you have this illness called chronic fatigue syndrome,’” she says.
Officially known as myalgic encephalomyelitis/chronic fatigue syndrome, or ME/CFS, it is a condition that affects as many as 2.5 million people in the U.S. Sufferers complain of a diffuse range of symptoms that include fatigue, muscle pain, mental fuzziness, and sleep problems. While the cause is unknown, many patients become ill after a viral infection. Because the range of symptoms is wide and diffuse, and research has yielded no reliable biological marker with which to identify it, people like Taylor often search for years before receiving a diagnosis. Under her doctor’s supervision, she tried a variety of remedies and prescriptions — from over-the-counter medicine to diet and compression socks — and improved enough over the next few months to be able to take care of herself, even though she still spends most of her time in bed.
Emily was able to return to full-time work and dedicated herself to lobbying full time for her mother’s condition as vice-president at Solve ME/CFS Initiative. It hasn’t been easy. Research dollars tend to flow to attention-getting diseases with severe outcomes and a high prevalence, like Alzheimer’s or cancer; chronic fatigue had neither. Nor did it have a well-oiled network of supporters in the halls of power, so Emily began organizing a yearly advocacy day on Capitol Hill during which her team would visit lawmakers and ask unsuccessfully for several million dollars more in the CDC’s budget to study ME/CFS. Her fourth Advocacy Day was scheduled for April 21, 2020.
Early that year, Emily began reading reports that doctors in China had identified a new virus that was spreading there — a coronavirus. She recalled that there had been an outbreak of another coronavirus in China, SARS, in 2002. A subsequent study showed that some SARS patients later suffered long-lingering symptoms such as debilitating fatigue, muscle pain, disturbed sleep, and depression. It sounded a lot like ME/CFS to her. Indeed, given that chronic fatigue is known to manifest after a number of different viral infections, it might well have been. So when she read about the new outbreak, she foresaw a troubling possibility: The new coronavirus, like the old one, might not only spawn a wave of death but also leave in its wake a legacy of debilitating chronic illness.
By March, Advocacy Day — like everything else — looked certain to be canceled as the novel coronavirus spread across the globe. Still, there might be opportunity amid the crisis. Emily abandoned her push for research funding at the CDC and started sketching out a bill whose language tied ME/CFS to COVID and sought to fund research into both. She asked Columbia University physician-scientist Mady Hornig to write up a scientific paper describing how the pandemic might spawn a wave of chronic illness. Hornig readily agreed. “If history is a guide,” she wrote, “those infected with this novel coronavirus may be at risk for a profound, disabling disease … from which one never recovers.” Armed with the frightening report, Taylor went to Congress, which had just approved $2 trillion in pandemic relief, to ask for money for the pending emergency. After a virtual Advocacy Day, Maryland representative Jamie Raskin agreed to sponsor the legislation to put $60 million toward studying chronic fatigue syndrome as a possible aftereffect of COVID — the first time a bill specifically concerned with ME/CFS research had ever come before Congress. “We were unsuccessful in passing it,” Emily says, “but that opened the door.”
By then, over a million Americans had contracted COVID. Of those who recovered, the vast majority did so fully, while others who battled severe COVID were left with damage to their hearts, lungs, and other organs. A third category, including Hornig, fell somewhere in between. Six weeks after she got sick, “I began to have unusual sensory experiences,” she says. “It felt like all the nerves were swirling around.” All of a sudden, her heart would start racing. Her feet swelled and then her legs. And, above all, she felt crushing fatigue. “I felt as if I was a battery-powered piece of equipment where the adapter would just pull out and there’d be no energy whatsoever, so much so that I couldn’t move.” With the help of various medications, including beta blockers for hypertension, she began to feel better but never felt fully herself again.
Other COVID survivors took to Facebook and Twitter to report similarexperiences. A feminist wellness collective conducted an online survey and found that 90 percent of respondents had not yet recovered after an average 40 days. The most common symptoms were “fatigue (varying in severity), brain fog/concentration challenges, chills/sweats, trouble sleeping, and a loss of appetite.” The phenomenon was so new that there wasn’t yet a name for it. Some called it “COVID-19 long tail” or “long-haul COVID.” Elisa Perego, an archaeologist at University College London, used the term “Long Covid” for the first time in a tweet on May 20, 2020. It caught on and quickly became the default term for the mysterious syndrome. In the span of a few months, what had started as a hypothetical in Honig’s white paper had become terrifyingly real, gaining credibility in medicine, the media, and the government.
To the public, this new illness was something unfamiliar, a kind of after-plague. This characterization would be repeated over and over again, but there has been a dissenting opinion in medicine that is only now beginning to be heard publicly: that long COVID, in many cases, is not a new syndrome but represents the latest manifestation of ME/CFS, a medical phenomenon with a long history.
That history is also highly contentious. For decades, a disagreement simmered between patients and the medical Establishment over the fundamental nature of ME/CFS: Was it primarily a biological or psychological illness? The conventional wisdom eventually settled on the idea that it is biological, but adherents to the alternative view remained quietly steadfast, convinced that they had been defeated not by science but by advocacy. Now, with the world in the grip of a deadly pandemic, these opposing forces have found their disagreement transplanted to a new, larger battlefield.
In 1984, teachers at two high schools near Incline Village, Nevada, began complaining of mysterious flu-like symptoms. Within months, hundreds of local residents were reporting similar symptoms: debilitating fatigue as well as a range of problems like fuzzy cognition and muscle pain. The majority of patients were women, and the median age was 40. At first, investigators suspected the virus that causes mononucleosis and called the ailment “chronic Epstein-Barr virus syndrome.” But CDC investigators dispatched to the scene concluded that there was no causal link. Unable to find any other physical explanation for the suffering, they recommended that it be renamed “chronic fatigue syndrome.”
The Nevada doctors who’d first identified the syndrome were flooded with inquiries from anxious patients. It turned out that people all over the country had been experiencing similar symptoms that their doctors had been unable to find physical explanations for. Motivated by the surge in public interest, researchers intensified their efforts to find an underlying biological cause. They turned up some promising leads, including possible dysfunction of the temporal lobes and misregulation of a class of immune-system proteins called cytokines, but none panned out.
A similar syndrome had been recognized in the U.K. under the name myalgic encephalomyelitis, or ME. Some experts considered the two syndromes to be so similar as to be effectively the same and began using the term ME/CFS to embrace both. Medical history is full of phenomena like ME/CFS, conditions without clear biological markers, whose main symptoms are fatigue and pain that doctors have trouble diagnosing: In the 19th century, doctors used the terms nervous exhaustion, neurasthenia, hysteria, and DaCosta’s syndrome; in the 20th, effort syndrome, neurocirculatory asthenia, autonomic imbalance syndrome, chronic brucellosis, fibromyalgia, multiple chemical sensitivity, temporomandibular joint syndrome, and irritable bowel syndrome; in the 21st, chronic Lyme. Through the ages, patients “have tended to be middle-aged, middle-class women,” says Edward Shorter, a professor of the history of medicine at the University of Toronto. The same is true of ME/CFS; according to the CDC, most patients are women, most are white, and the most common age of onset is between 40 and 60. No reason for the long-standing gender disparity is known. All these mysterious conditions are known as “diagnoses of exclusion,” meaning that doctors arrived at the diagnosis after eliminating every possible biological explanation. Since the onset of these syndromes is often preceded by some kind of triggering medical event, like a viral infection, they are sometimes collectively called post-viral or post-infectious fatigue syndromes.
Within the medical profession, some researchers felt that chronic fatigue had to have an underlying physical cause and that this biological mechanism would inevitably be found. Others suspected that the disease had no such underpinning and was primarily psychological in nature. The brain’s stress response, they argued, can by itself produce just the kinds of symptoms seen in chronic fatigue. Under prolonged duress, human beings experience changes in the central nervous system that can manifest as sleep disorders, cognitive fuzziness, and physical sensations like shooting pains or intense sluggishness. These feelings arise in the brain, but to the sufferer it feels like they are out there, in their body.
In the decades after ME/CFS was first characterized, one of the most influential theories of its etiology was the cognitive behavioral model (CBM), which holds that some initial trauma, like infection or an emotional crisis, inflicts fatigue and pain on a patient who then tries to to avoid worsening their condition by minimizing physical activity. The more bed-bound a patient becomes, the more unpleasant exertion feels, the more they avoid it, and the more out-of-shape they become. “The result is a vicious circle of symptoms, avoidance, fatigue, demoralisation and depression — the clinical picture of CFS,” wrote Sir Simon Wessely, a professor of psychiatry at Kings College London, and his colleagues in the Journal of Neurology, Neurosurgery, and Psychiatry.
This is a crucial point: Even if this theory is correct and chronic fatigue is at least in part a psychological phenomenon, that is not to say that the illness is not real or “all in your head.” The suffering is real, and as Stephanie’s case shows, patients often do not receive sympathy or effective care. “In our society, there’s a sort of hierarchy of suffering, where if you have an MRI or you have a lab finding that says, ‘Here’s the problem,’ that gets validated more,” says Adam Gaffney, an ICU physician who is an assistant professor at Harvard Medical School. “Those that don’t have a clear corresponding mechanism or a lab test sometimes get devalued.”
The cognitive behavioral model of ME/CFS supports two methods for treatment. One, called cognitive behavioral therapy (CBT), involves helping patients to identify unhelpful thoughts about symptoms — such as “doing more will make me worse” — and then reject them if they are not true. The second is graded exercise therapy (GET), which helps to reverse the effects of inactivity through a gradual increase in physical exertion, perhaps by giving them a greater sense of efficacy and encouraging them to believe that they can get better. CBT has also been used against fatigue caused by other conditions, too, such as cancer, suggesting that even diseases with an obvious biological underpinning can generate psychiatric symptoms. Though it’s not clear why or how CBT works, from the perspective of its practitioners, it didn’t really matter. “The consensus was that this condition, whatever its nature, could be improved by interventions that were essentially behavioral and psychological,” says Michael Sharpe, a professor of psychological medicine at the University of Oxford.
There was just one problem: Many patients considered this viewpoint to be deeply offensive. To suggest that their suffering was psychological in origin was equivalent, in their view, to calling them crazy, and implied that they were responsible for their own suffering. “This institutionalized victim-blaming runs contrary to the science,” wrote one patient in a representative blog post, “and it has left the ME/CFS community of suffere
rs, advocates, and support organizations very, very angry.”
By the turn of the century, the internet allowed far-flung patients to find one another, and together with family members and activists, they began furiously pushing back against the medical Establishment’s framing of their disease. They argued that doctors were refusing to accept the reality of patients’ symptoms — or, worse, were gaslighting them. To them, it was yet another example of long-standing power imbalances in medicine: between those with authority and those without; between the well and the sick; between men (the doctors, mostly) and women (who made up the majority of patients). “To imply that it’s all in your head and that you can just pull up hard on your bootstraps to get better, that is not only demoralizing for the individual person, it’s ethically, scientifically, and medically, wrong,” says Hornig, the Columbia physician-scientist. “It’s really against the Hippocratic Oath. It is doing harm.”
A main target of their ire was graded exercise treatment (GET). They argued that pushing patients to exercise risked triggering an ME/CFS symptom called post-exertional malaise, in which a patient who expends too much mental or physical effort can become incapacitated for days. This in not just a torturous experience, they say, but risks causing permanent disability. “I’ve seen people relapse,” says Lucinda Bateman, a doctor who specializes in treating ME/CFS. “I’ve seen people develop chronic pain.” Instead, patient advocates promote an alternative approach called pacing, which is based on the idea that the ailment is incurable and encourages patients to carefully monitor their exertions in order to stay within their new limits.
To settle the questions of how best to treat these patients, in the mid-aughts the U.K. government funded the largest ME/CFS trial to date. Called PACE, it enrolled 641 patients into four different treatment protocols. All received specialist medical care, meaning that their doctors provided information and advice and medication for various symptoms. The first group received only that care; a second group also received GET; a third also received CBT; and the fourth also received pacing therapy. “Cognitive behaviour therapy and graded exercise therapy are moderately effective outpatient treatments for chronic fatigue syndrome when added to specialist medical care,” the authors concluded in their 2011 paper. “Adaptive pacing therapy added to specialist medical care is no more effective than specialist medical care alone.”
The response from patient advocates was swift and fierce. Forty-four letters of complaint were sent to the prestigious British medical journal The Lancet,and 8,000 people signed a declaration stating: “We the undersigned petition the Prime Minister to get the health service and medical profession to accept the World Health Organisation classification of ME/CFS as an organic neurological disorder and not as a psychosocial syndrome.” The editors of The Lancet were aghast, writing that “one cannot help but wonder whether the sheer anger and coordination of the response to this trial has been born … from an active campaign to discredit the research.”
One of the loudest voices decrying the PACE trial was that of a Berkeley academic named David Tuller, who in 2015 wrote a three-part, 15,000-word post that found fault with its protocol. His main criticism was that the trial’s investigators had a weak definition of recovered. Within the advocate community Tuller’s critique was viewed as “devastating.” But the study’s authors countered that their results were solid; while some patients had already improved with regard to some symptoms before the study began, none had fully recovered. (Since then, at least four other studies have reinforced the finding that GET and CBT are effective for treating chronic fatigue.)
Nevertheless, the advocates’ campaign was successful. The U.K. government retracted its endorsement of exercise treatment, advising physicians: “Do not offer people with ME/CFS … any programme that uses fixed incremental increases in physical activity or exercise, for example graded exercise therapy.” It continued to allow behavioral treatment, with the stipulation that it is not a cure and should only be offered to “improve [patients’] functioning and reduce the stress associated with having a chronic illness.” Some medical researchers watched these developments with dismay. “They’ve actually completely corrupted a British guideline process by perverting the evidence at all levels,” laments a U.K. scientist familiar with the process.
In the U.S., advocates focused their ire on Wiliam Reeves, an epidemiologist who served as the research chief at the CDC’s chronic viral diseases branch. Reeves had spent years looking for infectious agents that might cause ME/CFS, but after finding none, he concluded that patients were mostly suffering “maladaptive personality features and personality disorders.” Unsurprisingly, patients were enraged. “He had a bias that it was hysteria, that it was a mental-health thing,” says Bateman, the ME/CFS doctor. “The patient community just hated him so much.” In the wake of the criticism against him, Reeves was transferred out of his post in 2010. He died in his sleep two years later, but his passing did little to assuage the community’s enmity. “Gee, was he REALLY sick or was it just all in his head?” wrote one blog commenter after his death. “Bet he didn’t try hard enough to get over his mental illness. Sorry, but after the damage and deaths that man has caused so many millions of people I simply can not bring myself to have one ounce of any sympathy.”
Assailing the medical Establishment from the outside could only get ME/CFS patients and advocates so far, however. To effect real change, they worked to get on the expert panels that defined the disease’s symptoms and treatment. In 2014, the National Academy of Medicine convened a committee to reassess the diagnostic criteria for ME/CFS that included input from patients and caregivers. “It was the patient advocacy community who really forced the change,” says Bateman, who served on the committee. The 15-person panel was made up of the usual sort of academic experts but had three people who had direct experience with the disease themselves or as a caregiver for a family member. When the committee released its report in 2015, it rejected the previous mainstream view that the syndrome is psychological in origin and declared ME/CFS a “legitimate disease” burned by “unnecessary stigma” and “the misconception that it is a psychogenic illness or even a figment of the patient’s imagination.” In keeping with that determination, the CDC removed endorsements of CBT and GET from its website in 2017.
In the U.S. and the U.K., it was now a matter of public record that chronic fatigue is caused by as-yet-unidentified biological factors in the patient’s body. Few were left among the medical research community who were willing to publicly dissent. “You’re sort of taking the life in your hands if you come out in favor of psychogenesis today,” says Edward Shorter, the medical historian, “because all these highly militant groups will hop all over you.” Wessely, the Kings College London professor who helped pioneer the cognitive behavioral model, declined to comment citing “too many bad experiences in the past.”
Meanwhile, the search for a biological culprit continued.
Chronic fatigue’s new status was cemented just in time for its unexpected turn in the spotlight thanks to COVID. “We had just spent five years convincing everyone that this post-viral disease is real, and then as soon as we were finally able to convince everyone of that, the pandemic happened,” says Emily Taylor. “Lo and behold and we were up on the Hill, pounding on the doors of Congress saying there is going to be a post-viral disease syndrome with this virus.”
By summer 2020, long COVID went from an obscure phenomenon to a mainstream fear as countless people reported their sickness. Particularly impactful was a story by The Atlantic’s Ed Yong on June 4 entitled “COVID-19 Can Last For Several Months” that highlighted individual suffering. “Even reading a book is challenging and exhausting,” said one. “What small joys other people are experiencing in lockdown — yoga, bread baking — are beyond the realms of possibility for me.” The story was read over a million times, and more coverage followed elsewhere. The moral of these stories was that for all our fears of contracting COVID, the current pandemic was just a foretaste of what was coming: a tsunami of chronic illness whose dimensions could only be guessed at but which, based on the experience of patients with other post-infectious fatigue syndromes, could bring lifelong disability to millions of Americans. “Brace yourself,” wrote one advocate on the Health Rising website. “You might not end up being sick for a couple of months or a year or even five years. Think decades. Maybe even the rest of your life.”
The medical Establishment did not try to tamp down the sense of alarm but instead endorsed it. “Health professionals must listen to patients to understand their concerns, validate their experiences, and manage their symptoms,” wrote the editors of The Lancet, who a few years earlier had expressed skepticism about ME/CFS patient advocacy. Anthony Fauci asserted that patients who recover from COVID can develop “a post-viral syndrome that’s very strikingly similar to myalgic encephalomyelitis/chronic fatigue syndrome” — one of the first acknowledgments by a government health official that long COVID could, in part, be ME/CFS. The U.K.’s National Health Service announced that it would open 40 clinics to treat long COVID patients, and the U.S. did the same. By the fall, awareness of long COVID was so great that when Emily Taylor returned to Capitol Hill to lobby for $350 million in research, Congress authorized $1.15 billion, triple what she asked for.
In less than a year, a new illness had been established not by physicians or research scientists but by those suffering the disease and their advocates; they’d done an end run around medicine’s traditional mechanisms of accountability and made their case directly to the media and the government to take action. Even Establishment journalists found this disintermediation exciting. “There’s this very grassroots-driven way that medical knowledge is being acquired here that’s really quite different,” said New York Times reporter Pam Belluck on The Daily. “It’s not coming from the laboratory. It’s coming, in a lot of ways, from the patients themselves. And that may end up being a good thing for all kinds of patients. If doctors realize that they need to listen to patients more and take patient reports seriously, that could be something that helps transform medicine in a positive way.”
As a result of the bottom-up movement, long COVID had become famous and research into it well funded before it had been rigorously defined. It had a name, even if no one could say for certain what exactly it was.
In one effort to find answers, doctors at Mayo Clinic collected data on 108 patients who had come to them seeking care. In a study published this year, they found that in terms of symptoms, the patients fell into two main clusters. One group was mostly male and contained patients who had experienced severe acute COVID. These patients were still suffering the physical damage wreaked on their bodies; their most common symptom was difficulty breathing. The other segment, larger in number, was mostly female. These patients had experienced mild or no COVID symptoms when first infected and were suffering symptoms like fatigue, muscle pain, and sleep disorders weeks after they were infected. (When completed, the study was named “The Female-Predominant Persistent Immune Dysregulation of the Post-COVID Syndrome.”) This latter cluster of symptoms sounded like the ones that Emily Taylor had predicted and that Ed Yong had described in his article. But was their condition — is long COVID —the same thing as ME/CFS?
Part of the challenge in answering that question was that long COVID patients were reporting such a wide variety of symptoms — partly by design. Researchers didn’t want to risk excluding anyone who might be suffering from the underlying ailment. “It’s good to be inclusive and help everyone who may need it,” says Mayo Clinic physician Dacre Knight. The NIH has kept the definition deliberately vague: any symptoms that persisted past four weeks. That meant that anyone who’d come down with COVID and later experienced any of a long list of symptoms, including some very common ones like a headache or runny nose, met the definition of suffering from long COVID. Under this loose definition, as many as nearly half of everyone who comes down with COVID might be considered a long hauler.
To narrow the focus, the World Health Organization last fall proposed a more restrictive definition of long COVID: Symptoms must occur at least three months after initial onset of COVID, continue for at least two more months beyond that, and — most important — “cannot be explained by an alternative diagnosis.” This latter criteria essentially established long COVID as a diagnosis of exclusion, putting it much more in alignment with other post-infectious fatigue syndromes and indicated a subtle shift in mainstream thinking. “Many cases of long COVID are effectively ME/CFS by another name,” as Yong recently wrote for The Atlantic. The overlap between long COVID and ME/CFS also makes sense to some physicians who are skeptical that either has a biological underpinning. “There’s certainly some overlap in the common symptoms,” says Sharpe the Oxford professor. “So it is quite likely there is some commonality.”
For those who are convinced that the cause must be biological, a narrower definition of long COVID should improve their odds of finding it. Among the suspects receiving the most attention are minuscule blood clots, immune system dysfunction, and lingering residues of viral spike protein. The hope is that a breakthrough on one of these fronts will lead investigators to a “druggable target” — some receptor, hormone, or metabolic pathway whose key role in the disease can be derailed by the administration of a drug. The discovery of such a target wouldn’t just open the door to a cure. It would prove once and for all that long COVID really had been biological all along.
One of the first people to get COVID in the U.K. was a 64-year-old British professor of infectious diseases named Paul Garner. In 2020, he spent seven months trapped in a wrenching cycle of illness, exhaustion, and extreme emotion. “I started wondering whether I would be ill for the rest of my life,” he says. Garner published a personal essay in BMJ(formerly the British Medical Journal) describing his symptoms: sporadically aching muscles, an upset stomach, muddled thinking, dizziness. Sometimes he would feel better; then he’d relapse and feel “as though someone had hit me around the head with a cricket bat.” Looking for answers, he became active in online long-COVID groups and read up on advice for people with ME/CFS. To avoid triggering post-exertional malaise, he took the advice of patient advocates and carefully paced his activities. Despite his best efforts, a ten-minute bike ride sent him into a three-day relapse. Determined to pace himself more carefully, he paid careful and constant attention to his body. Yet for all his efforts his relapses only became more frequent.
Eventually, Garner decided to change course after talking to a psychologist in training who had had chronic fatigue syndrome herself. “She explained that when you get anything stressful, whether a virus or an emotional shock, it sets off a stress response in the reptilian part of the brain. A brand-new virus will certainly do that! Your nervous system is on high alert to shut your body down to conserve energy. And these deep, automatic responses to protect you can get dysfunctional after the virus has gone but the stress remains. So you’re left with this misadjusted set of regulatory functions, like an oversensitive smoke alarm.” She showed him that the way that he was thinking about his symptoms was affecting how he experienced them. By paying obsessive attention to his symptoms, he was increasing his stress levels and making them worse. Effectively, she was telling him how to use a cognitive behavioral technique.
Garner began to believe that recovery was possible. He stopped reading stories about chronic illness and practiced diverting attention from his bodily symptoms. He began exercising again. After several weeks, he was back nearly to his pre-COVID level of fitness. In January 2021, he wrote his final blog post for the BMJ. “I have recovered,” he wrote. “I did this by listening to people that have recovered … not people that are still unwell; and by understanding that our unconscious normal thoughts and feelings influence the symptoms we experience.” One might expect that his fellow long-COVID sufferers would have cheered on his recovery, but over a hundred people posted comments to his piece, the majority angry or dismayed. Others attacked him on Facebook and demanded he withdraw his recovery story. “I’ve had death threats,” he says.
Others have experienced similar pushback. This past March, a psychiatry resident at McMaster University in Ontario named Jeremy Devine wrote an opinion piece in The Wall Street Journal in which he argued that long-COVID symptoms are most likely psychological in origin and asserted that patients’ rejection of a psychiatric diagnosis was itself a common aspect of the syndrome. “Patients who struggle with chronic and vague symptoms often vehemently reject a physician’s diagnosis that suggests an underlying mental-health issue,” he wrote, “in part because of the stigma around mental illness and the false belief that psychologically generated symptoms aren’t ‘real.’”
The response was predictably heated. “On Twitter, it was a disaster,” Devine later told me. “Lots of DMs from people who were unhappy with me.” He got angry phone calls, and someone changed his outgoing voice-mail message to “something really unflattering.” A prominent patient-advocate blog ran a piece titled “Can McMaster University Medical School Psychiatrists Be Trusted to Treat ME/CFS Patients?” A woman called him to tell him that his article would cause people to commit suicide. “She was really upset with me,” Devine says. “I remember that being kind of hard to hear.”
The criticism has not changed his opinion on the syndrome or its treatment. “The evidence suggests a psychological or psychogenic explanation,” he says, “and we should be targeting that.” But he has stepped back from promoting that view.
While the psychiatric perspective on long COVID is largely absent from public discourse, it is alive and well in clinical practice. The U.S. government has not approved any therapies for long COVID per se, but patients with chronic fatigue who visit a long-COVID clinic will likely receive some form of CBT, exercise therapy, or both. “From our perspective, if you’re symptomatic, we’re going to try to address your symptoms,” says David Sousa, co-director of the Atlantic COVID Recovery Center in New Jersey. “If we can find a process that helps you with your symptoms, like getting you on a graded exercise program, it’s helpful.” This approach has been endorsed by researchers: Mayo Clinic physicians in April published a study that recommends treating chronic fatigue patients with “Cognitive Behavioral Therapy (CBT)… graded exercise, mindfulness, and sleep hygiene.”
Meanwhile, the biological theory of long COVID, like that for ME/CFS, still lacks compelling evidence. An NIH study published this May found that patients who’d tested positive for COVID and met the criteria for long COVID did not show any biomarkers for illness or any trace of residual virus. Nor did they show evidence of inflammation, immune system activation, or any organ damage. “We’ve not yet been able to identify a single, repeatable, reliable, objective marker,” Bateman, the ME/CFS doctor, acknowledges. How sick a person gets from acute COVID didn’t seem to have any bearing on whether they will later get long COVID, either. A study conducted this year found that getting vaccinated didn’t much affect a person’s chances of coming down with long COVID, as you’d expect if it was triggered by the virus.
Meanwhile, researchers have found at least one positive link between long COVID and psychological distress. A paper published this September in the journal JAMA Psychiatry found that patients suffering from “depression, anxiety, perceived stress, loneliness, and worry” experienced a 30 to 50 percent higher risk of long-COVID complications than those who didn’t. Given how stigmatized mental illness is in our society, it’s understandable that some patients might balk at the idea that long COVID is merely the latest manifestation of an endemic psychiatric condition that’s been around forever. But many on the advocacy side are loath to even discuss the idea that long COVID could be a psychiatric condition.
“I was coached a long time ago when it came to interviews about ME/CFS with the media, don’t even mention the negative stereotypes (i.e., don’t say ‘it’s not psychological’) because that implants the very idea and cements doubt,” Lucinda Bateman wrote me in an email. “At this point, it is ridiculous to discuss whether long COVID is ‘psychological’ or ‘physical, real, organic …’ We know long COVID has biological underpinnings because scientific research supports it, both now and historically with other post-viral syndromes.” To her and others, it’s only a matter of time until the underpinning is found. Constrained by the limits of acceptable discourse, science is effectively limited to looking for its keys only under the light of the lamppost. The NIH’s $1.15 billion long-COVID research project is specifically aimed at identifying “the underlying biological cause,” having apparently decided that there is one to begin with.
Emily, for her part, is entirely comfortable with how the discourse has been playing out. Through her efforts, and the efforts of numerous like-minded activists, the public has been roused not only to the dangers of the current crisis but to the lingering threat of an older one. Just before the pandemic, she says, she was talking to a congressional staffer about how many people were sick with ME/CFS. “They asked me: ‘Well, if so many people are sick, why are we not talking about it?’ And I said prophetic words: ‘If everybody got sick at the same time, it would be a much different story. But everyone gets sick piecemeal and we don’t really hear about it.’”
“And now here we are, unfortunately. Everybody got sick at the same time.”
This article originally ran on November 4, 2022 in New York magazine.