Ed Yong | The Atlantic

Fatigue Can Shatter a Person

2023-07-27T07:00:00-04:00

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Alexis Misko’s health has improved enough that, once a month, she can leave her house for a few hours. First, she needs to build up her energy by lying in a dark room for the better part of two days, doing little more than listening to audiobooks. Then she needs a driver, a quiet destination where she can lie down, and days of rest to recover afterward. The brief outdoor joy “never quite feels like enough,” she told me, but it’s so much more than what she managed in her first year of long COVID, when she couldn’t sit upright for more than an hour or stand for more than 10 minutes. Now, at least, she can watch TV on the same day she takes a shower.

In her previous life, she pulled all-nighters in graduate school and rough shifts at her hospital as an occupational therapist; she went for long runs and sagged after long flights. None of that compares with what she has endured since getting COVID-19 almost three years ago. The fatigue she now feels is “like a complete depletion of the essence of who you are, of your life force,” she told me in an email.

Fatigue is among the most common and most disabling of long COVID’s symptoms, and a signature of similar chronic illnesses such as myalgic encephalomyelitis (also known as chronic fatigue syndrome or ME/CFS). But in these diseases, fatigue is so distinct from everyday weariness that most of the people I have talked with were unprepared for how severe, multifaceted, and persistent it can be.

For a start, this fatigue isn’t really a single symptom; it has many faces. It can weigh the body down: Lisa Geiszler likens it to “wearing a lead exoskeleton on a planet with extremely high gravity, while being riddled with severe arthritis.” It can rev the body up: Many fatigued people feel “wired and tired,” paradoxically in fight-or-flight mode despite being utterly depleted. It can be cognitive: Thoughts become sluggish, incoherent, and sometimes painful—like “there’s steel wool stuck in my frontal lobe,” Gwynn Dujardin, a literary historian with ME, told me.

Fatigue turns the most mundane of tasks into an “agonizing cost-benefit analysis,” Misko said. If you do laundry, how long will you need to rest to later make a meal? If you drink water, will you be able to reach the toilet? Only a quarter of long-haulers have symptoms that severely limit their daily activities, but even those with “moderate” cases are profoundly limited. Julia Moore Vogel, a program director at Scripps Research, still works, but washing her hair, she told me, leaves her as exhausted as the long-distance runs she used to do.

And though normal fatigue is temporary and amenable to agency—even after a marathon, you can will yourself into a shower, and you’ll feel better after sleeping—rest often fails to cure the fatigue of long COVID or ME/CFS. “I wake up fatigued,” Letícia Soares, who has long COVID, told me.

Between long COVID, ME/CFS, and other energy-limiting chronic illnesses, millions of people in the U.S. alone experience debilitating fatigue. But American society tends to equate inactivity with immorality, and productivity with worth. Faced with a condition that simply doesn’t allow people to move—even one whose deficits can be measured and explained—many doctors and loved ones default to disbelief. When Soares tells others about her illness, they usually say, “Oh, yeah, I’m tired too.” When she was bedbound for days, people told her, “I need a weekend like that.” Soares’s problems are very real, and although researchers have started to figure out why so many people like her are suffering, they don’t yet know how to stop it.

Fatigue creates a background hum of disability, but it can be punctuated by worse percussive episodes that strip long-haulers of even the small amounts of energy they normally have.

Daria Oller is a physiotherapist and athletic trainer, so when she got COVID in March 2020, she naturally tried exercising her way to better health. And she couldn’t understand why, after just short runs, her fatigue, brain fog, chest pain, and other symptoms would flare up dramatically—to the point where she could barely move or speak. These crashes contradicted everything she had learned during her training. Only after talking with physiotherapists with ME/CFS did she realize that this phenomenon has a name: post-exertional malaise.

Post-exertional malaise, or PEM, is the defining trait of ME/CFS and a common feature of long COVID. It is often portrayed as an extreme form of fatigue, but it is more correctly understood as a physiological state in which all existing symptoms burn more fiercely and new ones ignite. Beyond fatigue, people who get PEM might also feel intense radiant pain, an inflammatory burning feeling, or gastrointestinal and cognitive problems: “You feel poisoned, flu-ish, concussed,” Misko said. And where fatigue usually sets in right after exertion, PEM might strike hours or days later, and with disproportionate ferocity. Even gentle physical or mental effort might lay people out for days, weeks, months. Visiting a doctor can precipitate a crash, and so can filling out applications for disability benefits—or sensing bright lights and loud sounds, regulating body temperature on hot days, or coping with stress. And if in fatigue your batteries feel drained, in PEM they’re missing entirely. It’s the annihilation of possibility: Most people experience the desperation of being unable to move only in nightmares, Dujardin told me. “PEM is like that, but much more painful.”

Medical professionals generally don’t learn about PEM during their training. Many people doubt its existence because it is so unlike anything that healthy people endure. Mary Dimmock told me that she understood what it meant only when she saw her son, Matthew, who has ME/CFS, crash in front of her eyes. “He just melted,” Dimmock said. But most people never see such damage because PEM hides those in the midst of it from public view. And because it usually occurs after a delay, people who experience PEM might appear well to friends and colleagues who then don’t witness the exorbitant price they later pay.

That price is both real and measurable. In cardiopulmonary exercise tests, or CPETs, patients use treadmills or exercise bikes while doctors record their oxygen consumption, blood pressure, and heart rate. Betsy Keller, an exercise physiologist at Ithaca College, told me that most people can repeat their performance if retested one day later, even if they have heart disease or are deconditioned by inactivity. People who get PEM cannot. Their results are so different the second time around that when Keller first tested someone with ME/CFS in 2003, “I told my colleagues that our equipment was out of calibration,” she said. But she and others have seen the same pattern in hundreds of ME/CFS and long-COVID patients—“objective findings that can’t be explained by anything psychological,” David Systrom, a pulmonologist at Brigham and Women’s Hospital, told me. “Many patients are told it’s all in their head, but this belies that in spades.” Still, many insurers refuse to pay for a second test, and many patients cannot do two CPETs (or even one) without seriously risking their health. And “20 years later, I still have physicians who refute and ignore the objective data,” Keller said. (Some long-COVID studies have ignored PEM entirely or bundled it together with fatigue.)

Oller thinks this dismissal arises because PEM inverts the dogma that exercise is good for you—an adage that, for most other illnesses, is correct. “It’s not easy to change what you’ve been doing your whole career, even when I tell someone that they might be harming their patients,” she said. Indeed, many long-haulers get worse because they don’t get enough rest in their first weeks of illness, or try to exercise through their symptoms on doctors’ orders.

People with PEM are also frequently misdiagnosed. They’re told that they’re deconditioned from being too sedentary, when their inactivity is the result of frequent crashes, not the cause. They’re told that they’re depressed and unmotivated, when they are usually desperate to move and either physically incapable of doing so or using restraint to avoid crashing. Oller is part of a support group of 1,500 endurance athletes with long COVID who are well used to running, swimming, and biking through pain and tiredness. “Why would we all just stop?” she asked.

Some patients with energy-limiting illnesses argue that the names of their diseases and symptoms make them easier to discredit. Fatigue invites people to minimize severe depletion as everyday tiredness. Chronic fatigue syndrome collapses a wide-ranging disabling condition into a single symptom that is easy to trivialize. These complaints are valid, but the problem runs deeper than any name.

Dujardin, the English professor who is (very slowly) writing a cultural history of fatigue, thinks that our concept of it has been impoverished by centuries of reductionism. As the study of medicine slowly fractured into anatomical specialties, it lost an overarching sense of the systems that contribute to human energy, or its absence. The concept of energy was (and still is) central to animistic philosophies, and though once core to the Western world too, it is now culturally associated with quackery and pseudoscience. “There are vials of ‘energy boosters’ by every cash register in the U.S.,” Dujardin said, but when the NIH convened a conference on the biology of fatigue in 2021, “specialists kept observing that no standard definition exists for fatigue, and everyone was working from different ideas of human energy.” These terms have become so unhelpfully unspecific that our concept of “fatigue” can encompass a wide array of states including PEM and idleness, and can be heavily influenced by social forces—in particular the desire to exploit the energy of others.

As the historian Emily K. Abel notes in Sick and Tired: An Intimate History of Fatigue, many studies of everyday fatigue at the turn of the 20th century focused on the weariness of manual laborers, and were done to find ways to make those workers more productive. During this period, fatigue was recast from a physiological limit that employers must work around into a psychological failure that individuals must work against. “Present-day society stigmatizes those who don’t Push through; keep at it; show grit,” Dujardin said, and for the sin of subverting those norms, long-haulers “are not just disbelieved but treated openly with contempt.” Fatigue is “profoundly anti-capitalistic,” Jaime Seltzer, the director of scientific and medical outreach at the advocacy group MEAction, told me.

Energy-limiting illnesses also disproportionately affect women, who have long been portrayed as prone to idleness. Dujardin notes that in Western epics, women such as Circe and Dido were perceived harshly for averting questing heroes such as Odysseus and Aeneas with the temptation of rest. Later, the onset of industrialization turned women instead into emblems of homebound idleness while men labored in public. As shirking work became a moral failure, it also remained a feminine one.

These attitudes were evident in the ways in which two successive U.S. presidents dealt with COVID. Donald Trump, who always evinced a caricature of masculine strength and chastised rivals for being “low energy,” framed his recovery from the coronavirus as an act of domination. Joe Biden was less bombastic, but he still conspicuously assured the public that he was working through his COVID infection while his administration prioritized policies that got people back to work. Neither man spoke of the possibility of disabling fatigue or the need for rest.

Medicine, too, absorbs society’s stigmas around fatigue, even in selecting those who get to join its ranks. Its famously grueling training programs exclude (among others) most people with energy-limiting illnesses, while valorizing the ability to function when severely depleted. This, together with the tendency to psychologize women’s pain, helps to explain why so many long-haulers—even those with medical qualifications, like Misko and Oller—are treated so badly by the professionals they see for care. When Dujardin first sought medical help for her ME/CFS symptoms, the same doctor who had treated her well for a decade suddenly became stiff and suspicious, she told me, reduced all of her detailed descriptions to “tiredness,” and left the room without offering diagnosis or treatment. There is so much cultural pressure to never stop that many people can’t accept that their patients or peers might be biologically forced to do so.

No grand unified theory explains everything about long COVID and ME/CFS, but neither are these diseases total mysteries. In fact, plenty of evidence exists for at least two pathways that explain why people with these conditions could be so limited in energy.

First, most people with energy-limiting chronic illnesses have problems with their autonomic nervous system, which governs heartbeat, breathing, sleep, hormone release, and other bodily functions that we don’t consciously control. When this system is disrupted—a condition called “dysautonomia”—hormones such as adrenaline might be released at inappropriate moments, leading to the wired-but-tired feeling. People might suddenly feel sleepy, as if they’re shutting down. Blood vessels might not expand in moments of need, depriving active muscles and organs of oxygen and fuel; those organs might include the brain, leading to cognitive dysfunction such as brain fog.

Second, many people with long COVID and ME/CFS have problems generating energy. When viruses invade the body, the immune system counterattacks, triggering a state of inflammation. Both infection and inflammation can damage the mitochondria—the bean-shaped batteries that power our cells. Malfunctioning mitochondria produce violent chemicals called “reactive oxygen species” (ROS) that inflict even more cellular damage. Inflammation also triggers a metabolic switch toward fast but inefficient ways of making energy, depleting cells of fuel and riddling them with lactic acid. These changes collectively explain the pervasive, dead-battery flavor of fatigue, as “the body struggles to generate energy,” Bindu Paul, a pharmacologist and neuroscientist at Johns Hopkins, told me. They might also explain the burning, poisoned feelings that patients experience as their cells fill with lactic acid and ROS.

These two pathways—autonomic and metabolic—might also account for PEM. Normally, the autonomic nervous system smoothly dials up to an intense fight-and-flight mode and down to a calmer rest-and-digest one. But “in dysautonomia, the dial becomes a switch,” David Putrino, a neuroscientist and rehabilitation specialist at Mount Sinai, told me. “You go from sitting to standing, and your body thinks, Oh, are we going hunting? You stop, and your body shuts down.” The exhaustion of these dramatic, unstable flip-flops is made worse by the ongoing metabolic maelstrom. Damaged mitochondria, destructive ROS, inefficient metabolism, and chronic inflammation all compound one another in a vicious cycle that, if it becomes sufficiently intense, could manifest as a PEM crash. “No one is absolutely certain about what causes PEM,” Seltzer told me, but it makes sense that “you have this big metabolic shift and your nervous system can’t get back on an even keel.” And if people push through, deepening the metabolic demands on a body that already can’t meet them, the cycle can spin even faster, “leading to progressive disability,” Putrino said.

Other factors might also be at play. Compared with healthy people, those with long COVID and ME/CFS have differences in the size, structure, or function of brain regions including the thalamus, which relays motor signals and regulates consciousness, and the basal ganglia, which controls movement and has been implicated in fatigue. Long-haulers also have problems with blood vessels, red blood cells, and clotting, all of which might further stanch their flows of blood, oxygen, and nutrients. “I’ve tested so many of these people over the years, and we see over and over again that when the systems start to fail, they all fail in the same way,” Keller said. Together, these woes explain why long COVID and ME/CFS have such bewilderingly varied symptoms. That diversity fuels disbelief—how could one disease cause all of this?—but it’s exactly what you’d expect if things as fundamental as metabolism go awry.

Long-haulers might not know the biochemical specifics of their symptoms, but they are uncannily good at capturing those underpinnings through metaphor. People experiencing autonomic blood-flow problems might complain about feeling “drained,” and that’s literally happening: In POTS, a form of dysautonomia, blood pools in the lower body when people stand. People experiencing metabolic problems often use dead-battery analogies, and indeed, their cellular batteries—the mitochondria—are being damaged: “It really feels like something is going wrong at the cellular level,” Oller told me. Attentive doctors can find important clues about the basis of their patients’ illness hiding amid descriptions that are often billed as “exaggerated or melodramatic,” Dujardin said.

Some COVID long-haulers do recover. But several studies have found that, so far, most don’t fully return to their previous baseline, and many who become severely ill stay that way. This pool of persistently sick people is now mired in the same neglect that has long plagued those who suffer from illnesses such as ME/CFS. Research into such conditions is grossly underfunded, so no cures exist. Very few doctors in the U.S. know how to treat these conditions, and many are nearing retirement, so patients struggle to find care. Long-COVID clinics exist but vary in quality: Some know nothing about other energy-limiting illnesses, and still prescribe potentially harmful and officially discouraged treatments such as exercise. Clinicians who better understand these illnesses know that caution is crucial. When Putrino works with long-haulers to recondition their autonomic nervous system, he always starts as gently as possible to avoid triggering PEM. Such work “isn’t easy and isn’t fast,” he said, and it usually means stabilizing people instead of curing them.

Stability can be life-changing, especially when it involves changes that patients can keep up at home. Over-the-counter supplements such as coenzyme Q10, which is used by mitochondria to generate energy and is depleted in ME/CFS patients, can reduce fatigue. Anti-inflammatory medications such as low-dose naltrexone may have some promise. Sleep hygiene may not cure fatigue, but it certainly makes it less debilitating. Dietary changes can help, but the right ones might be counterintuitive: High-fiber foods take more energy to digest, and some long-haulers get PEM episodes after eating meals that seem healthy. And the most important part of this portfolio is “pacing”—a strategy for carefully keeping your activity levels beneath the threshold that causes debilitating crashes.

Pacing is more challenging than it sounds. Practitioners can’t rely on fixed routines; instead, they must learn to gauge their fluctuating energy levels in real time while becoming acutely aware of their PEM triggers. Some turn to wearable technology such as heart-rate monitors, and more than 30,000 are testing a patient-designed app called Visible to help spot patterns in their illness. Such data are useful, but the difference between rest and PEM might be just 10 or 20 extra heartbeats a minute—a narrow crevice into which long-haulers must squeeze their life. Doing so can be frustrating, because pacing isn’t a recovery tactic; it’s mostly a way of not getting worse, which makes its value harder to appreciate. Its physical benefits come at mental costs: Walks, workouts, socializing, and “all the things I’d do for mental health before were huge energy sinks,” Vogel told me. And without financial stability or social support, many long-haulers must work, parent, and care for themselves even knowing that they’ll suffer later. “It’s impossible not to overdo it, because life is life,” Vogel said.

“Our society is not set up for pacing,” Oller added. Long-haulers must resist the enormous cultural pressure to prove their worth by pushing as hard as they can. They must tolerate being chastised for trying to avert a crash, and being disbelieved if they fail. “One of the most insulting things people can say is ‘Fight your illness,’” Misko said. That would be much easier for her: “It takes so much self-control and strength to do less, to be less, to shrink your life down to one or two small things from which you try to extract joy in order to survive.” For her and many others, rest has become both a medical necessity and a radical act of defiance—one that, in itself, is exhausting.

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Who’s the Cutest Little Dolphin? Is It You?

2023-06-26T15:00:00-04:00

Across human cultures and languages, adults talk to babies in a very particular way. They raise their pitch and broaden its range, while also shortening and repeating their utterances; the latter features occur even in sign language. Mothers use this exaggerated and musical style of speech (which is sometimes called “motherese”), but so do fathers, older children, and other caregivers. Infants prefer listening to it, which might help them bond with adults and learn language faster.

But to truly understand what baby talk is for, and how it evolved, we need to know which other animals use it, if any. The great apes don’t seem to vocally, but might use a gestural equivalent. Squirrel monkeys and rhesus macaques use special calls when talking to youngsters, but they’re very different from human baby talk, which is a modified version of normal speech. Zebra finches are closer to us: When singing in front of juveniles, adults add longer pauses between musical phrases and repeat introductory notes. Greater sac-winged bat mothers also change their pitch and timbre when signaling to pups, but again, it’s hard to tell if they’re using a distinct call or doing something analogous to baby talk. To make an inarguable case for the latter, you’d need to study a species that talks with both infants and older peers using the same standardized, identifiable call. In other words, you’d need a dolphin.

Every bottlenose dolphin produces its own unique signature whistle, which is the closest thing any animal has to a human name. Dolphins can recognize individuals through these whistles and will sometimes copy one another’s, perhaps as a form of address. They use their whistles frequently, to announce their position when separated from their pod, or as an introduction when meeting up with new groups. Calves develop their own signature whistles based on those they hear around them, and once learned, the whistles can go unchanged for at least 12 years.

Laela Sayigh, a zoologist at the Woods Hole Oceanographic Institution, has been studying the signature whistles of bottlenoses in Sarasota Bay, Florida, since 1986 as part of the world’s longest-running study of wild dolphins. She and her colleagues regularly catch these animals, check their health, and record their calls before releasing them. Sometimes, they catch mothers and calves together, and the animals exchange signature whistles throughout the process. By analyzing 19 such moments, recorded over 34 years, Sayigh’s student Nicole El Haddad showed that mothers raised and widened the pitch of their signature whistles when calling to their calves, just as humans do when talking to their babies.

“We were just blown away by how consistent the effect was,” Sayigh told me. Between their intelligence and strong personality, dolphins behave unpredictably enough that scientists who study them are used to gleaning faint patterns amid messy data. But in this study, every mom changed its signature whistle around its calf in the same way. “The data are extraordinary and impressive,” Sabine Stoll, who studies language evolution at the University of Zurich, told me.

Dolphin baby talk isn’t exactly the same as ours—dolphin whistles don’t get more repetitive—but it’s certainly “the most convincing case of child-directed communication found in nonhuman animals to date,” Mirjam Knörnschild from the Museum of Natural History in Berlin, who led the study on sac-winged bats, told me. And its existence in a species separated from us by more than 90 million years of history is likely a “stunning” example of convergent evolution, Stoll said.

If both species evolved baby talk independently, perhaps they did so for similar reasons. Human parents can better grab their infants’ attention through high-pitched baby talk than through normal speech, and dolphin mothers might do the same. Keeping her signature whistle but raising its pitch “would be a pretty foolproof way for the mom to say ‘This whistle is meant for you’ to the calf, and for the calf to know My mom is talking to me right now and no one else,” Sayigh said. That specificity would allow both of them to keep close contact in a raucous ocean where many dolphins might be sounding off at once.

Human baby talk is also thought to strengthen a baby’s bond with its caregivers, and to help it learn language by exaggerating important features of the spoken word. The same could well apply to dolphins, which also stay with their mother for a long time, and learn calls by listening to their peers. But testing these ideas would be incredibly hard without separating mothers and their calves—an experiment that Sayigh said would cross an ethical line. She showed that dolphin baby talk exists; its exact role “is just one of those things that might have to go unanswered,” she said.

The Cancer-Drug Shortage Is Different

2023-06-26T07:00:00-04:00

Last November, FDA inspectors found almost farcical conditions when they inspected an Indian manufacturing plant that supplies medical drugs to the United States. The plant, owned by Intas Pharmaceuticals, had hardly any working systems for ensuring the purity or sterility of its products. And its employees were trying to conceal evidence of these problems by shredding and hiding documents or, as one quality-control officer admitted, dousing them in acid.

Intas provided America with a lot of frontline chemotherapy drugs—half of the country’s supply in some cases—that are used to treat more than a dozen types of cancer. When the disastrous inspection led the company to halt production, other manufacturers couldn’t make up the difference. Hospitals are now reeling: In a recent survey, 93 percent of U.S. cancer centers said they were experiencing a shortage of the drug carboplatin, while 70 percent were low on another, cisplatin.

Even short delays in cancer treatment can increase a patient’s odds of death, and substitute medications may be less effective or more toxic, if they exist at all. Chemo drugs often run dry—“I can’t think of a year in the past 10 or 12 where we didn’t face some kind of shortage,” Yoram Unguru, a pediatric oncologist at the Herman & Walter Samuelson Children’s Hospital at Sinai, told me—but the current crisis is unprecedented in scale, for reasons that go beyond Intas’s woes. Fourteen cancer drugs are currently scarce, jeopardizing the care of hundreds of thousands of Americans. “I’ve been doing this forever, and this is absolute lunacy,” Patrick Timmins III, a gynecologic oncologist at Women’s Cancer Care Associates, told me.

By delivering drugs at lower doses or over longer intervals, most oncologists are still managing to treat most of their patients—but barely. “Patients often say to us, I just need a plan,” Eleonora Teplinsky, an oncologist at Valley Health System, told me, and the shortages riddle every plan with question marks. Some institutes have already been forced to ration care. Timmins no longer has enough cisplatin and carboplatin to treat patients with recurrent tumors, even though those drugs can improve one’s quality of life or offer decent odds of another remission. “A lot of people are going to be hurt,” he told me. “Lives will be shortened.” Such tragedies are especially galling because the drugs in shortage aren’t expensive, state-of-the-art treatments that patients might struggle to access anyway, but cheap ones that have existed for decades. “It’s just unfathomable that a patient wouldn’t be able to receive them,” Amanda Fader, a gynecologic oncologist at Johns Hopkins, told me.

Intas screwed up, but how could one manufacturer’s downfall trigger such widespread problems? The coronavirus pandemic made plain how reliant the U.S. is on brittle international supply chains, but this much-discussed fragility doesn’t explain the current shortages: Cancer drugs are not scarce for the same reasons that yeast, toilet paper, or couches were. They’re scarce because the market for some of our most important medicines—the ones that should be most accessible—is utterly dysfunctional, in a way that is both very hard to fix but also entirely fixable.

Many recent supply-chain problems were caused by an external force—a pandemic, a hurricane, a stuck ship—that throttled a product’s availability, leading to surging demand and dwindling stocks. But most cancer-drug shortages are caused by internally generated problems, created within the market because of its structure. In other words, “they’re self-inflicted wounds,” Marta Wosińska, a health-care economist at the Brookings Institution, told me.

Generic drugs such as cisplatin are sold at extremely low prices, which overall have fallen by more than 50 percent since 2016. These ever-tightening margins have forced many manufacturers to tap out of the market; for example, the U.S. gets all its vincristine, an anti-leukemia drug, from just one company.

Such drugs are also hard to make. Because they’re injected into the bloodstream, often of severely ill people, they must be manufactured to the highest possible standards, free of microbes and other contaminants. But quality costs money, and generic drugs are so unprofitable that manufacturers can rarely afford to upgrade machinery or train employees. If anything, they’re compelled to cut corners, which makes them vulnerable to spontaneous manufacturing problems or disastrous inspections. And because they usually run at full capacity, any disruption to production has severe consequences. The affected manufacturer might fail to financially recover and leave the market too. Its competitors might struggle to ramp up production without triggering their own cascading shortages. And the drugs, which were never profitable enough to manufacture in surplus, quickly run out.

These principles apply not only to cancer drugs but to generics as a whole, dozens or hundreds of which have been in shortage at any given time for the past decade. The markets that produce them are frail and shrinking. And even when a drug is manufactured by many companies, they might all rely on the same few suppliers for their active pharmaceutical ingredients (APIs)—the chemicals at the core of their medicines. Mariana Socal, a pharmaceutical-market expert at Johns Hopkins, has shown that a third of the APIs in America’s generic-drug supply are made in just two or three (mostly overseas) facilities, and another third are made in just one.

The supply chains that link these chemicals to finished drugs are also frustratingly opaque. Consider fludarabine, one of the cancer drugs that’s currently in shortage. The FDA has approved 12 companies to make it, but just five actually market it; only because of a Senate-committee inquiry is it publicly known that of those five, only one makes the drug itself; two others get theirs from Europe, and one of those used to supply the final two. Meanwhile, six facilities are registered to make fludarabine’s API, but it’s again unclear which ones really do, or which manufacturers they supply, or even, for one of them, which country it is in. The fludarabine market is clearly weaker than it first appears, but how weak is hard to gauge. The same goes for cisplatin and carboplatin, Socal told me: She and other experts thought their markets looked resilient, until the Intas shutdown dispelled the illusion.

This opacity masks not only the market’s weaknesses but also its strengths. Erin Fox, a drug-shortage expert at the University of Utah Health, oversees a drug budget of more than $500 million, and would love to spend it on manufacturers that make the most reliable medicines, even if their products cost a little more. But “we just don’t know which products are higher-quality than others,” she told me. The FDA has an internal scoring system that it uses to decide which facilities to inspect, Fox said, but because those data aren’t publicly available, manufacturers can distinguish themselves only through price. “We get a race to the bottom where companies undercut each other to get the lowest price, and then quit either because their manufacturing is so poor, or they can’t afford to make medicines anymore,” Fox said. As Wosińska and Janet Woodcock of the FDA identified in 2013, “The fundamental problem … is the inability of the market to observe and reward quality.”

The average generic-drug shortage lasts for about a year and a half. Many people I spoke with hoped that the current wave could abate more quickly if other manufacturers slowly ramp up. The FDA is also looking to import scarce drugs from international suppliers, and has temporarily allowed a Chinese company to sell its cisplatin in the U.S. But ultimately, “it’s very hard to solve a shortage after it started,” Allan Coukell, of the nonprofit Civica Rx, told me. They need to be prevented from happening at all.

Some commonly suggested preventive measures might not work very well, because they misdiagnose the problem. Politicians often focus on bolstering domestic manufacturing, but Wosińska, Fox, and others told me that many drug shortages have been caused by manufacturing problems in American facilities. Because American drugmakers are subject to the same flawed markets as foreign ones, moving the problem inshore doesn’t actually solve it. Nor does stockpiling generic drugs, though a worthwhile idea. These strategies work well against an external shock like a pandemic, Wosińska said: When faced with unpredictable external forces, it pays to build a large buffer. But because the shocks that cause drug shortages arise from predictable forces inherent to the market, the best bet is to reimagine the market itself—a “very difficult problem but a solvable one,” Stephen Colvill, the executive director and a co-founder of the nonprofit RISCS, told me.

A few new initiatives show how this could be done. Civica Rx, which was launched in 2018, sources generic drugs from manufacturers that it vets for quality; it then builds up rolling six-month inventories of those drugs, which it supplies to hospitals through long-term contracts. (Civica is also building its own generics-manufacturing facility in Virginia.) RISCS, founded in 2019, uses confidential data from manufacturers to rate generic-drug products according to the robustness of their supply chains. The FDA has also been developing its own rating system—the “quality management maturity” (QMM) program—that assesses a manufacturer’s quality-control practices; the program successfully completed two pilots but is still being developed and has no firm launch date, an FDA spokesperson said.

In theory, these initiatives should allow hospitals to make better purchasing decisions, and shift the market toward drug companies that are least likely to be responsible for shortages. In practice, Wosińska thinks that hospitals need to be pulled into such a culture shift. For example, she and her colleague Richard G. Frank argue that Medicare could reward hospitals for proactively choosing reliable vendors or participating in programs like Civica. The FDA could support such a scheme by finally launching its QMM program. Congress could require manufacturers to disclose more details about their products and suppliers, so that supply chains can be fully mapped. HHS could offer loans to generic-drug manufacturers for upgrading or expanding their facilities. The point, Wosińska told me, is to do all of this at once, and shift the market into a new stable state. The solution, she said, needs to be comprehensive.

It also needs to be coordinated. The drug-shortage problem lingers partly because “it’s not obvious who’s responsible for solving it,” Joshua Sharfstein, a health-policy expert at Johns Hopkins, told me. The FDA is a candidate, but economic matters sit outside its wheelhouse. Instead, Sharfstein and others suggest that the drug-shortage problem could be owned by the Administration for Strategic Preparedness and Response. It already works to shore up medical supplies in the event of emergencies such as pandemics or natural disasters, and ongoing shortages of generic drugs are effectively a perpetual state of emergency that we’re trapped in.

Meanwhile, the exact consequences of the shortages are hard to measure. Some of today’s cancer patients will suffer, or even die, because they couldn’t get treated in time, or were given lower doses, or were given more toxic drugs as substitutes. But it’s almost impossible to know if any individual person would have fared better in a world where shortages never happened: If they died, was it because of a few weeks’ delay or because their tumor was always going to be hard to treat? The impact of the shortages can only really be assessed at a population level, and that evidence takes a long time to collect. “I don’t think we’ll see the full downside for many years,” Yoram Unguru told me.

The measures needed to prevent such shortages will also take years to implement—if they ever are. The coronavirus pandemic revealed just how frail our supply chains and health-care system are, but it also showed how quickly attention and resources can disappear once a problem is thought to abate. But the drug problem isn’t abating, and is actually compounding the problems the pandemic created. When health-care workers can’t help their patients, whether because their hospitals are inundated by COVID or because their drugs have run out, the resulting moral distress can be unbearable. Such conditions during the pandemic drove so many health-care workers to quit that “you can feel the system shaking,” Patrick Timmins III said. He worries that this exodus followed by the current drug shortages are “a one-two punch” that will be visible to outsiders only when they have neither the drugs to cure them nor the health-care workers to treat them.

These Animals Shouldn’t Be Alive, Much Less Sprinting

2023-05-31T08:00:00-04:00

Updated at 11:22 p.m. on June 8, 2023

In October 2016, while hiking through a treacherous mountain pass, John Tuthill saw something move. He was almost 8,000 feet above sea level in Washington’s Alpine Lakes Wilderness, braving high winds and temperatures well below freezing. Although he and his hiking companion initially thought that they had the trail to themselves, they soon noticed small, brown specks zipping over the virgin snow. When Tuthill looked closely at them, he was astonished to see that they were insects, existing in an environment where insects shouldn’t be alive, let alone active.

As a neuroscientist who works with flies, Tuthill knew that insect nervous systems shut down when the creatures get too cold, so even species that can tolerate subzero temperatures tend to do so by entering a dormant state. And yet here were insects, running about in apparent defiance of both biology and physics. “It immediately blew my mind,” Tuthill told me. That’s how he came to study snow flies.

Snow flies are a group of insects so obscure that very few scientists in history have ever studied them. They don’t have wings, and so get about by sprinting in a spiderlike way. And they do so in conditions so cold that most insects would struggle to move at all. Tuthill, who is a neuroscientist at the University of Washington, tells me that he often anesthetizes fruit flies by chilling them to 2 degrees Celsius (36 degrees Fahrenheit), which paralyzes them. But snow flies can keep running even when their bodies hit –7 degrees Celsius (19 degrees Fahrenheit). They actually prefer temperatures close to freezing: Hold them in your hand, and they’ll become agitated, but put them in a fridge, and they’re … well … chill.

[Read: Is the insect apocalypse really upon us? ]

Very little is known about snow flies, in part because even collecting them requires being a good skier or mountaineer. In 2019, Tuthill tried encouraging members of the public to capture and send him snow flies, but few people tried, and most of those who did sent spiders by mistake. He and his colleagues had to collect most of the individuals they studied—a task he didn’t mind one bit. “They coincidentally have the same idea of what a good day is as a backcountry skier,” and are most active when the sun is shining on a few feet of fresh powder, Tuthill told me. “People in my lab have tried to raise them, but I personally don’t want that to work, because every time there’s a perfect day, I cancel my meetings and go out collecting snow flies.”

By studying the captured insects, Tuthill’s colleague Dominic Golding discovered how they cope with one of the biggest threats of subzero living—ice. Once ice starts to form in an insect’s bodily fluids, the spreading crystals will quickly kill them. But snow flies can sense when that fatal process begins, and stop it through self-amputation. Using thermal cameras, Golding filmed many moments in which a wave of ice would race up a snow fly’s leg only for that leg to detach from the body within seconds.

Their close relatives—spindly, slow-flying crane flies—use a similar trick if their legs are caught by predators, which they sense using neurons that detect pulls and tugs. Tuthill thinks that snow flies have placed the same defensive reflex under the control of neurons that sense temperature instead. These detect the small bursts of heat that occur when ice first forms, and trigger a muscular contraction that jettisons the freezing limb. This strategy is unorthodox, to say the least. Katie Marshall, a zoologist at the University of British Columbia, told me that cold-adapted animals cope with ice by either loading their blood with antifreeze that stops crystals from forming, or letting crystals form and withstanding them. Snow flies do neither; their unique solution—self-amputation—might be dramatic, but it is successful. In the wild, Tuthill has seen many three-legged snow flies, still moving at a pretty good clip, he said.

And their speed is all the more impressive given that their nervous systems shouldn’t work at all. To fire, neurons must pump electrically charged molecules out through their membranes and then allow those molecules to reenter by opening small gates. But as the temperature drops, the pumps slow down, the gates stop opening, and neurons stop firing. The snow flies must have adaptations that allow their neurons to defy these thermal constraints, but Tuthill doesn’t yet know what they are. Compared with other insects, he says, snow flies aren’t actually that cold-tolerant. Their superpower is the ability to stay active right until the moment they freeze.

[Read: A pivotal mosquito experiment could not have gone better]

Adult snow flies don’t eat, so when they skitter over snow fields, they’re specifically searching for mates. When two find each other, they have sex immediately and audaciously: Despite being completely exposed to predators, and highly visible against a white backdrop, they’ll spend 30 minutes or more “in full view on the surface of the snow,” Tuthill writes. But hardly any predators are around to see them, which may be why they adapted to run over glaciers at all. And although animals that live in extreme environments are often treated as champions that endure barely bearable conditions, Tuthill wonders if snow flies actually have it pretty good. “If you go through metamorphosis on the right day, and it’s bluebird with two feet of powder, and you meet your lover … it’s a good life if it works out,” he told me.

Or while it lasts. Within the next two decades, Washington is set to end the winter with about half as much snow as it did last century. By the 2080s, it will have 70 percent less. Snow flies will likely be pushed to higher altitudes, but “at some point, they’ll run out of mountain,” Marshall told me. Most people won’t notice their absence; hardly anyone noticed they were there to begin with. But losing snow flies would still mean losing an incredible example of life’s tenacity—its ability to persist in the unlikeliest of environments using adaptations we barely understand, running against the odds until they eventually run out of time.

The Fight Over Animal Names Has Reached a New Extreme

2023-05-25T08:00:00-04:00

Updated at 6:36 p.m. on May 26, 2023

Stephen Hampton has been watching birds for more than 50 years, and for almost all of that time, he thought nothing of names like Townsend’s warbler or Anna’s hummingbird: “They were just the names in the bird book that you grow up with,” he told me. Then, a few years ago, Hampton realized how Scott’s oriole—a beautiful black-and-yellow bird—got its name.

Darius Couch, a U.S. Army officer and amateur naturalist, named the oriole in 1854 after his commander, General Winfield Scott. Sixteen years earlier, Scott dutifully began a government campaign of ethnic cleansing to remove the Cherokee people from their homelands in the Southeastern United States. His soldiers rounded up Cherokee, separated their families, looted their homes, and crammed them into stockades and barges, where many of them died. Thousands of Cherokee, including Hampton’s great-great-grandfather and dozens more of his ancestors, were forced to move west along the Trail of Tears. Scott’s oriole is a monument to a man who oversaw the dispossession of Hampton’s family, and saying its name now “hits me in the gut, takes my breath away,” Hampton, who is a citizen of the Cherokee Nation, wrote in 2021.

The common names of almost 150 North American birds are eponyms—that is, they derive from people. A disproportionate number of these names were assigned in the early 19th century by the soldier-scientists who traveled westward across the U.S. Bestowing eponyms to honor commanders, benefactors, family members, and one another, they turned the continent’s avifauna into tributes to “conquest and colonization,” as Hampton wrote. Many birders are now pushing to remove these eponyms, arguing that too many of them tie nature’s beauty and the pure joy of seeing a new species to humanity’s worst grotesqueries. “I didn’t ask for any of this information; I was just trying to bird,” Tykee James, the president of D.C. Audubon Society, told me. But now “we should do better because we know better—that’s the scientific process.”

Similar sentiments have spread in other countries and animal groups. Many animals whose names had included ethnic and racial slurs now have new names, including a moth in North America and several birds in Sweden and South Africa. In the U.S., at least one bird with an eponym has been renamed, and the American Ornithological Society is developing a process for renaming more.

These discussions have pushed many biologists and wildlife enthusiasts to reconsider the very act of naming—the people who get to do it, and the responsibilities they ought to shoulder. Whether common ones such as giraffe or scientific ones such as Giraffa camelopardalis, names act first as labels, allowing people to identify and classify living things. But names are also value-laden, reflecting the worldviews of the people who choose them. And some have come to believe that honoring any person, no matter their sins or virtues, reflects the wrong values. In this view, the practice of affixing an entire life-form with the name of a single individual must end entirely.

When the ornithologist Robert Driver petitioned the American Ornithological Society in 2018 to rebrand McCown’s longspur, his proposal was rejected. This species was named after an Army officer who accidentally shot one of the birds, and who also waged campaigns against Indigenous tribes before joining the Confederacy; members of an AOS committee, which maintains an official list of common names for North American birds, variously said that “judging historical figures by current moral standards is problematic,” and that they were “concerned about where we would draw the line.”

But the tide of opinion turned in May 2020. On the same day that a police officer murdered George Floyd, a white woman in New York City’s Central Park falsely told the cops that she was being threatened by Christian Cooper, a Black birder who had asked that she leash her dog. A video of that incident went viral, drawing the birding world into the debates over race and justice that were sweeping America. As Confederate statues and monuments fell nationwide, many birders argued that problematic eponyms also needed to be toppled. In June that year, Jordan Rutter and Gabriel Foley founded Bird Names for Birds, a campaign to rename all American birds that have eponyms. In July, the AOS reconsidered Driver’s proposal because of “heightened awareness of racial issues,” and the following month announced that the newly christened thick-billed longspur would be McCown’s no longer.

Many other eponyms present similar cases for change, although none have been altered yet. John Kirk Townsend, whose name still graces two birds and almost a dozen mammals, dug up the graves of Native Americans and sent their skulls to the physician Samuel George Morton, who wanted to prove that Caucasians had bigger brains than other people; those remains are still undergoing a lengthy process toward burial or repatriation. John Bachman was a practitioner and defender of slavery, reasoning that Black people, whom he compared to domesticated animals, were so intellectually inferior to Caucasians as to be “incapable of self-government”; Bachman’s sparrow was named by his friend, John James Audubon. And Audubon, the most renowned—and, more recently, notorious—figure in American ornithology and the namesake of an oriole, a warbler, and a shearwater, also robbed Native American graves for Morton’s skull studies, while casually buying and selling slaves. “People have been singing his praises for 150 years, but in the last 15 years, he has turned out to be quite a monster,” says Matthew Halley, an ornithologist and historian, who has also found evidence that Audubon committed scientific fraud by fabricating a fake species of eagle that helped launch his career. In light of Audubon’s actions, several local chapters of the National Audubon Society have renamed themselves, as has the society’s union. In March, though, the national society’s board of directors voted to keep the name, on the grounds that it would allow the organization to “direct key resources and focus towards enacting the organization’s mission.”

The drive to change these eponyms has faced the same now-familiar criticisms as the push to remove Confederate monuments. Proponents have been charged with erasing history but counter that they are clarifying it: People tend to assume that an eponym represents the individual who actually described the species, when it’s usually an honorific, sometimes exalting people with no connection to birds at all. (Anna’s hummingbird, for instance, was named after Anna Masséna, a French courtier and naturalist’s wife.) Halley also rejects the AOS’s original argument that modern birders are inappropriately judging the past using today’s standards. Townsend, for example, who came from a Quaker family and had an abolitionist for a sister, “was going against the moral teachings of his own community,” Halley told me. Meanwhile, Black people have always rejected slavery, just as Natives have always opposed ethnic cleansing, Hampton said. What’s changed is their presence in communities that typically decide what animals are called.

Critics have also argued that names are meant to be stable, and changing them sows confusion. But there’s precedent in the bird world for updating them: In 1957, the AOS revised 188 common bird names to achieve better transatlantic consistency, and it has changed dozens more since 1998. Names change all the time, for scientific and cultural reasons, and given a choice between stability and respect for people whose ancestors were harmed by early ornithologists, “I come down on the side of respect,” David Allen Sibley, a renowned author and illustrator of bird field guides, said in 2021.

For some scientists, the eponym problem is about more than the egregious misdeeds of a few individuals. As Europeans spread to other continents, they brought not only invasive species that displaced native ones but also invasive nomenclature that ousted long-standing native terms for plants and animals. In Africa, the scientific names of a quarter of local birds, reptiles, amphibians, and mammals are eponyms, mostly from Europe. On the biodiverse Pacific island of New Caledonia, more than 60 percent of plant eponyms honor French citizens. Countless species around the world have been named after European scientists whose travels were made possible by imperial ventures aimed at expanding territories or extracting natural resources. “We have romantic ideas of these explorers going around the world, seeing beautiful things, and naming them, and we forgot how they got there to begin with,” Natalia Piland, an ecologist at Florida International University, told me.

Such naming patterns still continue. Piland and her colleagues found that since 1950, 183 newly identified birds have been given eponyms, and although 96 percent of these species live in the global South, 68 percent of their names honor people from the global North. In 2018, the Rainforest Trust, an American conservation nonprofit, auctioned off the rights to name 12 newly discovered South American species, leading to a frog named after Greta Thunberg and a caecilian named after Donald Trump. (A similar auction in 2005 landed a Bolivian monkey with the name of the internet casino GoldenPalace.com.) The beloved British naturalist David Attenborough has more than 50 species named after him, most of which live in Africa, Asia, Australia, and South America. That is not to begrudge Attenborough, Thunberg, or Trump; having a species named after you is widely considered a great honor, but globally, such honorees are still disproportionately people of European descent—a perpetuation of colonialism through taxonomy.

Some scientists have proposed reinstating Indigenous names for animals wherever possible. But many species live across the territories of different Indigenous groups, or migrate across national or continental divides, making it hard to know whose names to prioritize. And if native names are applied without native consultation, the result can smack of cultural appropriation. Emma Carroll from the University of Auckland took on both challenges in naming a recently identified species of beaked whale. Carroll spent a year consulting Indigenous groups in countries where the new whale’s specimens had been found. In South Africa, the Khoisan Council suggested using the word //eu//’eu, which means “big fish” and is now immortalized in the scientific name Mesoplodon eueu. For the common name, Carroll asked a Māori cultural expert in New Zealand to draw up a shortlist, which she then ran past a local council. She eventually named the creature “Ramari’s beaked whale” after Ramari Stewart—a Māori whale expert whose work was pivotal in identifying the new species, and who has been “working to bridge Western science and mātauranga [Maori knowledge] for decades,” Carroll told me. Fittingly, ramari also means “a rare event” in the Māori language, and beaked whales are famously elusive.

Inspired by Carroll’s example, Eric Archer of the NOAA used a similar approach when describing a new species of bottlenose dolphin. He initially wanted to name it after Jim Mead—a respected scientist to whom Archer owes his career. But after feeling that this pattern of honoring close colleagues was too insular, he consulted the Nanticoke Lenni-Lenape Tribal Nation, whose ancestors lived in the lands where the first specimen of the dolphin was found. Eventually, he named it Tamanend’s bottlenose dolphin after an iconic 17th-century chief.

But these names, too, sit uneasily with Steve Hampton, the birder and Cherokee Nation citizen, who told me that many Indigenous communities would see them as recapitulating “colonizer practices.” If the intent is to symbolize a connection between the animals and the people who share its land, “then take the apostrophe-s off,” Hampton said. Those two characters invoke ownership, as if an individual could lay claim to an entire species—a fundamentally colonial way of thinking, no matter whether the honoree is an Indigenous woman or a European man. By that logic, the issue with eponyms isn’t that some of them honor people who did vile things. It’s that animals shouldn’t be named after people at all.

Doing away with all eponyms avoids, if nothing else, the problem of judging who, exactly, is objectionable enough to have their name stripped away from a species. Kevin Thiele, a botanist and director of Taxonomy Australia, argues, for instance, that the scientific community can easily expunge eponyms that honor “history’s monsters” without jettisoning the practice altogether; he told me that “a good cutoff might be if a person had influence, and thus has an eponym, as a result of egregious acts.” For example, the Australian flowers that he studies—Hibbertia—are named after George Hibbert, an 18th-century Englishman and amateur botanist whose fortunes and status derived almost entirely from the transatlantic slave trade. By contrast, hundreds of species are named after Charles Darwin, who certainly had racist views and benefited from colonialism, but who is honored because he profoundly shaped our understanding of nature. (Darwin also staunchly opposed slavery.) Hibbertia should go, but Darwin’s eponyms can stay, Thiele says.

But Halley, the historian, suspects that people “who want to go in with a scalpel don’t know the full extent of the improprieties in the historical records,” he told me, and a clean slate would be preferable. Carlos Daniel Cadena, a Colombian ornithologist, agrees. “There’s a lot of potential to make these discussions ugly if we start going name by name and trying to decide which person was good or bad,” he told me. “And in 200 years, will we all be despicable because we trashed the planet or ate meat?”

Others argue that, more importantly, the act of honoring a person through an organism’s name dishonors the organism itself. It treats animals and plants as inanimate objects like buildings or streets, constructed and owned by humans, instead of beings with their own lives and histories. “It doesn’t sit well with me to think of an individual human becoming the signifier of an entire species,” Piland said. A more descriptive name, meanwhile, is a chance to tell a creature’s story. Joseph Pitawanakwat, an Anishinaabe educator, notes that many of his people’s bird names are layered with meaning—onomatopoeias that mimic calls, and descriptions of habitat and behavior, all embedded in a single word that could have been coined only through a deep understanding of the animals. English names could be similarly descriptive: Thick-billed longspur tells you something about the bird that might help you recognize it in a way that McCown’s longspur does not.

These arguments are gaining traction. This March, Patrícia Guedes from the University of Porto and an international group of 10 colleagues published a commentary saying that “naming a biological species after a human was and is never right—regardless of good intentions.” But even if the scientific community as a whole agreed with this principle, the logistics of changing or banning eponyms are not simple. Many people who have animals named after them are still alive; changing those names would effectively strip them of an honor. And Cadena said that many Latin American researchers bristle when they’re told that they shouldn’t name animals after their colleagues. “North Americans and Europeans have named things after themselves for centuries, and now we cannot do it?” Cadena told me.

Changing the scientific names of animals is especially tricky because such names are formally governed by the International Commission for Zoological Nomenclature (ICZN)—a group of 26 scientists who volunteer time outside their main jobs. They simply lack the person-power to oversee changes to even a fraction of the tens of thousands of scientific eponyms, Thomas Pape, the ICZN president, told me—and it’s not in their remit to change even one. Consider Anophthalmus hitleri, a rare Slovenian beetle that was named after Adolf Hitler in 1933 and is now threatened by enthusiastic Nazi-memorabilia hunters. The ICZN still won’t change its name, because “we stand absolutely firm on not regulating based on ethics,” Pape told me. “It’s not our mandate.”

But, though he argues that set names are important for allowing scientists to unambiguously communicate about the organisms they study, Pape also admits that “it’s strange that we keep talking about stability when we keep changing names.” Scientific names change frequently, when a species is reclassified or split into several new ones. They can also change because scientists uncover an alternative name that was assigned first and then forgotten, or because they violate Latin grammar. There are also routes for changing scientific names through societal force of will. Pape cites the case of Raymond Hoser, an Australian amateur herpetologist who has assigned hundreds of new names to questionably defined species and genera of reptiles—often on shaky scientific grounds, usually in his own self-published journal, and in many cases honoring his family members and pets. Other taxonomists are simply refusing to use his names; if that continues, “it might be possible for the ICZN to rule that those names should not be used,” Pape told me.

Common names are even easier to shift, because there’s typically no formal process for doing so. In 1993, a zoologist decided to name a predatory marine worm with scissorlike jaws the “Bobbit worm,” referencing the incident in which Lorena Gallo (then Bobbitt) cut off her husband’s penis. Other biologists, who noted that the name mocks a woman who survived repeated domestic and sexual abuse, have just started calling the worm “sand striker” instead. In this vein, common names that are deemed offensive enough could change organically as people stop using them, Eric Archer, the NOAA biologist, told me. “I don’t think it’s necessarily something that should be done by fiat,” he said.

For North American birds, there is a standardized list of common names, maintained by the AOS. It has no legal standing but is widely followed by birders, conservationists, and, notably, the federal government. Name changes would carry far more clout if the AOS ratified them. It has traditionally been unwilling to, but after the events of 2020, it formed a committee to develop a process for identifying and changing “harmful or exclusionary English bird names.” Hampton and James are part of that 11-person committee, which Cadena co-chairs. They wouldn’t reveal specifics of their recommendations, which they’re set to present on June 15 to the governing body of the AOS, but at least some of them have come around to the idea that all eponyms should go. And they stressed that they wanted to unite the birding world rather than divide it.

Any changes, they imagine, would mean that rookie and veteran birders alike would have something new to learn, while the entire community could be involved in concocting new monikers—a practice that could generate more excitement about birds at a time when many species desperately need to be protected. Hampton acknowledged that community involvement can be risky—“we have talked about ‘Birdy McBirdface’ many times,” he said, referencing the crowdsourced boat-naming campaign from 2016 that yielded Boaty McBoatface—but he and other committee members think it’d be worth it to open up the right to name nature to a much broader swath of society than the one that has long held it. Wildlife doesn’t belong to it, or to anyone, and shouldn’t be named as if it does.

That’s the view of every birder under 40 whom Hampton talks to, and every person of color—demographics that will have a growing say over our custodianship of the natural world. “Everyone in our committee knows that 20 or 30 years from now, the next generation will be changing all of these names if we don’t,” Hampton said. To him, it feels inevitable. Perhaps future generations will also look upon this moment and see our own historical foibles embedded in the names we now choose. Or perhaps they’ll see a turning point when people stopped seeing animals as vessels for human legacies but as entities with their own worth and stories, reflected in their very names.

This story was updated to clarify that the AOS’s bird-names committee will initially present its findings internally.

One of Evolution’s Biggest Moments Was Re-created in a Year

2023-05-12T10:32:27-04:00

All the living things that we can see evolved from those that we can’t. Every human, bird, tree, and flower can trace its ancestry across a few billion years back to microscopic, single-celled organisms such as bacteria. That change from micro to macro, from one cell to many, was one of the most pivotal evolutionary journeys in Earth’s history. It is also among the hardest to imagine. Multicellular creatures, with their large size, complex body, and specialized tissues and organs, are so much more complicated than single-celled ones that it seems impossibly hard for the latter to turn into the former. But in fact, the process might have been “relatively simple,” William Ratcliff, an evolutionary biologist at Georgia Tech, told me. He and his team managed to replicate it in his laboratory in a matter of years.

In 2010, Ratcliff started working with brewer’s yeast, the single-celled fungus we use to make bread and beer. He repeatedly grew the yeast in liquid-filled tubes, shook them, and then used the cells that sank fastest to start new cultures. By favoring cells that stick together and settle faster, this simple procedure radically changed the yeast within just 60 days. Now whenever a cell divided in two, the new cells didn’t drift apart as they normally would; instead, they remained attached, creating beautiful, branching snowflakes that comprised dozens of cells. The yeast had evolved multicellularity in just two months.

But they then seemed stuck. Ratcliff had hoped that the snowflakes would continue getting bigger and more complex, but the annoyingly fragile entities never grew beyond a few hundred cells. Their branched shape was the problem: If any break can sever a large chunk off the main flake, that means “the strength of the group, no matter how big, is the strength of a single cell-cell connection,” Ratcliff told me. And once the snowflakes hit a certain size, “you look at them the wrong way, and they break.”

G. Ozan Bozdag, a member of Ratcliff’s team, solved the problem by depriving the snowflakes of oxygen. Scientists usually assume that oxygen is good for multicellularity, but because smaller organisms can use it more efficiently than larger ones, Bozdag reasoned that the latter might gain an advantage in the gas’s absence. He tested this idea with a new version of the shake-settle-and-seed experiment, which he started in 2018. For months, the oxygen-deprived snowflakes remained microscopic, but after a year or so, Bozdag could see the clusters with his own eyes. After 600 days of evolution, the snowflakes had become 20,000 times bigger, each containing half a million cells instead of just a few hundred. They now appeared as visible blobs, the largest of which were a millimeter wide—the size of fruit flies.

Together with physicist Peter Yunker, Ratcliff showed that the snowflakes busted through the size ceiling by lengthening each individual cell and strengthening the connections among cells. But more important, they evolved an entirely new structure, which the team saw using a powerful microscope. The branches had started wrapping around one another—less a radiating snowflake than a densely knotted mass of vines. This structure stops sections from easily breaking off and bestows incredible resilience: Yeast snowflakes are normally 100 times weaker than gelatin, but once entangled, they have the strength and toughness of wood. From what Ratcliff calls “dumb clumps of cells,” they had evolved what might reasonably be called a body.

“This is the most exciting study I’ve seen in a long time,” Leslie Babonis, an evolutionary biologist at Cornell University who was not involved in the study, told me. To her, it shows that the real challenge of multicellularity isn’t just keeping cells connected to their neighbors but keeping them strongly connected. Merely having a body is not enough; only when organisms have tough bodies that don’t readily fall apart can they evolve more complex traits such as specialized tissues and organs.

That’s what Ratcliff and his team have started to see. In the microscopic snowflakes, every cell behaves in much the same way, but in larger clusters, cells might perform one of at least three different roles: Some grow fast, others add sturdiness, and yet others self-destruct. (The latter might give the clusters a way of reproducing, by shedding small fragments into the environment.) The yeast have even evolved a way of moving fluid through their body, bringing nutrients to the cells deep inside them, and getting rid of waste.

A basic circulation, a life cycle, division of labor—these are all emergent traits that arise only once the yeast evolve strong bodies, and which cannot be predicted by studying any one constituent cell. They show that the snowflakes really are existing and evolving as multicellular organisms, as wholes that are more than the sum of their parts.

Throughout the history of life, multicellularity evolved on at least 25 independent occasions. Fungi may have done it much as Ratcliff’s yeast did, with small groups of cells that gained strength through entanglement. Animals, which had very different single-celled ancestors, probably became multicellular in a different way. But despite these differences, “every multicellularity story is going to be a version of the same basic process,” Ratcliff said. Single cells became groups, which could then become tough, which could then become big and complicated. “Look back through history, and you can’t imagine how animals evolved from a single-celled ancestor, because it’s such a big change,” Ratcliff said. “But that’s the beauty of this experiment: Every single change makes sense and looks straightforward.”

He doesn’t know what further changes are in store for the snowflake yeast, but he hopes to find out. Bozdag is still continuing the experiment; even during the early years of the coronavirus pandemic, he visited the team’s mostly shuttered lab every day to set up new generations. Ratcliff’s plan is to keep it going for decades, or “until we’re too old to keep doing it.”

The Sea-Urchin Murderer Has Finally Been Apprehended

2023-04-24T08:00:00-04:00

When Mya Breitbart heard that something was killing off sea urchins en masse, she thought: Oh no, not again.

The long-spined sea urchin—a fist-size ball of black defensive spines—is a crucial and common part of the Caribbean’s coral reefs. In 1983, a strange affliction all but wiped them out. The urchins began behaving aberrantly, moving into dangerous open water instead of sheltering in crevices. Their spines, which they normally point at threats, became unresponsive and eventually fell off, making them easy targets for fish. Even if they weren’t attacked, they died within days of their first symptoms, as if they’d been eaten from the inside out. By 1984, up to 98 percent of them were dead—with disastrous consequences. By eating algae, which compete with corals for space, sea urchins allow reefs to flourish and expand. When they died, the algae gained the upper hand, and the corals receded. The urchin population was so badly hit that, despite active restoration efforts, they recovered by only 12 percent in the intervening 40 years. And no one ever worked out what originally killed them.

Then, in January 2022, urchins at St. Thomas island began dying again in the same gruesome way. By March, the affliction had spread to nine other islands. When reports reached Breitbart, who is a microbiologist at the University of South Florida, she feared that history would repeat itself. “It’s not that one dead sea urchin strikes fear in the heart of scientists, but corals are being assaulted and diseased on so many fronts that losing the urchins felt like another big blow to the reefs,” Breitbart told me. “I thought, We can’t let this one go.”

Breitbart quickly assembled a team of 48 scientists from 12 countries, including Ian Hewson, who had studied a similar degenerative disease in starfish, and Christina Kellogg, an expert on corals and their microbes. “Everyone dropped everything” to work on the case, Breitbart said, because they knew how quickly corals can suffer when urchins disappear. But they also knew that such mysteries usually take years or decades to get solved—if they ever are. At first, it looked like this case would be similarly frustrating: When the team collected tissue samples from urchins across the Caribbean and did a thorough genetic analysis to search for disease-causing microbes, they couldn’t find any of the usual suspects. No viruses or bacteria were responsible for the urchins’ plight. The only organism whose genes were present in the sick urchins and not the healthy ones was something unexpected—a previously unknown species of ciliate.

Ciliates are microscopic, single-celled creatures that swim using a coat of beating hairs, or cilia—picture a furry, turbo-charged amoeba. They’re found almost anywhere there is water, including in the bodies of marine animals such as urchins. Ciliates are usually harmless, but there are a few documented cases of them acting as parasites, causing diseases in corals and even sharks. And one of those miscreant species is a close relative of the new one that Breitbart’s team found in the dying Caribbean urchins.

Still, a ciliate seemed like such an unlikely mass murderer that Breitbart wasn’t fully convinced. Fortunately, while the geneticists were working, team members Yasu Kiryu and Thierry Work were independently examining the urchin tissues under microscopes. Both investigations culminated at a single meeting, and when Team Gene announced that they had found the telltale sequence of a ciliate, Team Microscope pulled up their slides to reveal clear images of ciliates infesting the spines and bodies of the urchins. Both groups had independently identified the same unexpected suspect—and to seal the case, they grew the new ciliate in the laboratory and showed that it could kill healthy urchins within a week.

That the researchers not only found the urchin killer, but did so in just three months, is an unprecedented feat. Stony corals in Florida and the Caribbean have been plagued by disease since 2014, and the perpetrator is still unknown. The same goes for sea stars in the Pacific Northwest, which have been hit by a degenerative illness for roughly the same amount of time. Breitbart credits her team, experienced members such as Hewson who had learned how to efficiently study these kinds of die-offs, and a “not insignificant amount of luck.” “I had a brand new graduate student working with me,” she said, “and I kept saying, ‘This isn’t the way it usually goes.’”

Many questions still remain. If the same killer ciliate was responsible for the 1983 die-off, why did it stay dormant for almost 40 years before striking again? If it’s a newcomer, where did it come from, and how does it spread? And perhaps most important, what can be done to stop it? Kellogg has also been looking for possible treatments that would kill the ciliate but spare the urchins, and she has some promising candidates.

Hewson thinks the team’s success bodes well: Every time they investigate a die-off of this kind, they get a little better at it—and they’ll need to be. Mass-mortality events among wildlife are becoming more common. Climate change is forcing animals to move to new ranges, allowing species that never previously coexisted to trade pathogens. Meanwhile, climatic upheavals and environmental degradation are also subjecting animals to more stress, weakening their immune system. “Things that maybe weren’t related to mass mortality in the past will start to cause new diseases,” Hewson said. The urchin die-off may not have started in exactly this way, but it’s still a harbinger of events to come. “I’d fully expect us to see more of this kind of thing in the future,” he said.

But 40-plus scientists can’t drop everything to investigate every new epidemic; there simply isn’t enough funding, expertise, or person-power to go around. In this case, doing so was clearly worth it, because the long-spined sea urchin is a keystone species—ones that play a disproportionately influential role in holding their ecosystem together. In this age of epidemics, such creatures may get triaged while others are neglected. “It’s going to be a matter of prioritizing, which is very hard,” Breitbart said.

Long COVID Is Being Erased—Again

2023-04-19T15:05:58-04:00

Updated at 6:29 p.m. ET on April 21, 2023

Charlie McCone has been struggling with the symptoms of long COVID since he was first infected, in March 2020. Most of the time, he is stuck on his couch or in his bed, unable to stand for more than 10 minutes without fatigue, shortness of breath, and other symptoms flaring up. But when I spoke with him on the phone, he seemed cogent and lively. “I can appear completely fine for two hours a day,” he said. No one sees him in the other 22. He can leave the house to go to medical appointments, but normally struggles to walk around the block. He can work at his computer for an hour a day. “It’s hell, but I have no choice,” he said. Like many long-haulers, McCone is duct-taping himself together to live a life—and few see the tape.

McCone knows 12 people in his pre-pandemic circles who now also have long COVID, most of whom confided in him only because “I’ve posted about this for three years, multiple times a week, on Instagram, and they’ve seen me as a resource,” he said. Some are unwilling to go public, because they fear the stigma and disbelief that have dogged long COVID. “People see very little benefit in talking about this condition publicly,” he told me. “They’ll try to hide it for as long as possible.”

I’ve heard similar sentiments from many of the dozens of long-haulers I’ve talked with, and the hundreds more I’ve heard from, since first reporting on long COVID in June 2020. Almost every aspect of long COVID serves to mask its reality from public view. Its bewilderingly diverse symptoms are hard to see and measure. At its worst, it can leave people bed- or housebound, disconnected from the world. And although milder cases allow patients to appear normal on some days, they extract their price later, in private. For these reasons, many people don’t realize just how sick millions of Americans are—and the invisibility created by long COVID’s symptoms is being quickly compounded by our attitude toward them.

Most Americans simply aren’t thinking about COVID with the same acuity they once did; the White House long ago zeroed in on hospitalizations and deaths as the measures to worry most about. And what was once outright denial of long COVID’s existence has morphed into something subtler: a creeping conviction, seeded by academics and journalists and now common on social media, that long COVID is less common and severe than it has been portrayed—a tragedy for a small group of very sick people, but not a cause for societal concern. This line of thinking points to the absence of disability claims, the inconsistency of biochemical signatures, and the relatively small proportion of severe cases as evidence that long COVID has been overblown. “There’s a shift from ‘Is it real?’ to ‘It is real, but …,’” Lekshmi Santhosh, the medical director of a long-COVID clinic at UC San Francisco, told me.

Yet long COVID is a substantial and ongoing crisis—one that affects millions of people. However inconvenient that fact might be to the current “mission accomplished” rhetoric, the accumulated evidence, alongside the experience of long haulers, makes it clear that the coronavirus is still exacting a heavy societal toll.

As it stands, 11 percent of adults who’ve had COVID are currently experiencing symptoms that have lasted for at least three months, according to data collected by the Census Bureau and the CDC through the national Household Pulse Survey. That equates to more than 15 million long-haulers, or 6 percent of the U.S. adult population. And yet, “I run into people daily who say, ‘I don’t know anyone with long COVID,’” says Priya Duggal, an epidemiologist and a co-lead of the Johns Hopkins COVID Long Study. The implication is that the large survey numbers cannot be correct; given how many people have had COVID, we’d surely know if one in 10 of our contacts was persistently unwell.

But many factors make that unlikely. Information about COVID’s acute symptoms was plastered across our public spaces, but there was never an equivalent emphasis that even mild infections can lead to lasting and mercurial symptoms; as such, some people who have long COVID don’t even know what they have. This may be especially true for the low-income, rural, and minority groups that have borne the greatest risks of infection. Lisa McCorkell, a long-hauler who is part of the Patient-Led Research Collaborative, recently attended a virtual meeting of Bay Area community leaders, and “when I described what it is, some people in the chat said, ‘I just realized I might have it.’”

Admitting that you could have a life-altering and long-lasting condition, even to yourself, involves a seismic shift in identity, which some people are understandably loath to make. “Everyone I know got Omicron and got over it, so I really didn’t want to concede that I didn’t survive this successfully,” Jennifer Senior, a friend and fellow staff writer at The Atlantic, who has written about her experience with long COVID, told me. Duggal mentioned an acquaintance who, after a COVID reinfection, can no longer walk the quarter mile to pick her kids up from school, or cook them dinner. But she has turned down Duggal’s offer of an appointment; instead, she is moving across the country for a fresh start. “That is common: I won’t call it ‘long COVID’; I’ll just change everything in my life,” Duggal told me. People who accept the condition privately may still be silent about it publicly. “Disability is often a secret we keep,” Laura Mauldin, a sociologist who studies disability, told me. One in four Americans has a disability; one in 10 has diabetes; two in five have at least two chronic diseases. In a society where health issues are treated with intense privacy, these prevalence statistics, like the one-in-10 figure for long COVID, might also intuitively feel like overestimates.

Some long-haulers are scared to disclose their condition. They might feel ashamed for still being sick, or wary about hearing from yet another loved one or medical professional that there’s nothing wrong with them. Many long-haulers worry that they’ll be perceived as weak or needy, that their friends will stop seeing them, or that employers will treat them unfairly. Such fears are well founded: A British survey of almost 1,000 long-haulers found that 63 percent experienced overt discrimination because of their illness at least “sometimes,” and 34 percent sometimes regretted telling people that they have long COVID. “So many people in my life have reached out and said, ‘I’m experiencing this,’ but they’re not telling the rest of our friends,” McCorkell said.

Imagine that you interact with 50 people on a regular basis, all of whom got COVID. If 10 percent are long-haulers, that’s five people who are persistently sick. Some might not know what long COVID is or might be unwilling to confront it. The others might have every reason to hide their story. “Numbers like 10 percent are not going to naturally present themselves in front of you,” McCone told me. Instead, “you’ll hear from 45 people that they are completely fine.”

Illustration by Paul Spella / The Atlantic; Getty

The same factors that stop people from being public about their condition—ignorance, denial, or concerns about stigma—also make them less likely to file for disability benefits. And that process is, to put it mildly, not easy. Applicants need thorough medical documentation; many long-haulers struggle to find doctors who believe their symptoms are real. Even with the right documents, applicants must hack their way through bureaucratic overgrowth, likely while fighting fatigue or brain fog. For these reasons, attempting to measure long COVID through disability claims is a profoundly flawed exercise. Even if people manage to apply, they face an average wait time of seven months and a two-in-three denial rate. McCone took six weeks to put an application together, and, despite having a lawyer and extensive medical documentation, was denied after one day. McCorkell knows many first-wavers—people who’ve had long COVID since March 2020—“who are just getting their approvals now.”

An alternative source of data comes from the Census Bureau’s Current Population Survey, which simply asks working-age Americans if they have any of six forms of disability. Using that data, Richard Deitz, an economics-research adviser at the Federal Reserve Bank of New York, calculated that about 1.7 million more people now say they do than in mid-2020, reversing a years-long decline. These numbers are lower than expected if one in 10 people who gets COVID really does become a long-hauler, but the survey doesn’t directly capture many of the condition’s most common symptoms, such as fatigue, neurological problems beyond brain fog, and post-exertional malaise, where a patient’s symptoms get dramatically worse after physical or mental exertion. About 900,000 of the newly disabled people are also still working. David Putrino, who leads a long-COVID rehabilitation clinic at Mount Sinai, told me that many of his patients are refused the accommodations required under the Americans With Disabilities Act. Their employers won’t allow them to work remotely or reduce their hours, because, he said, “you look at them and don’t see an obvious disability.”

Long COVID can also seem bafflingly invisible when people look at it with the wrong tools. For example, a 2022 study by National Institutes of Health researchers compared 104 long-haulers with 85 short-term COVID patients and 120 healthy people and found no differences in measures of heart or lung capacities, cognitive tests, or levels of common biomarkers—bloodstream chemicals that might indicate health problems. This study has been repeatedly used as evidence that long COVID might be fictitious or psychosomatic, but in an accompanying editorial, Aluko Hope, the medical director of Oregon Health and Science University’s long-COVID program, noted that the study exactly mirrors what long-haulers commonly experience: They undergo extensive testing that turns up little and are told, “Everything is normal and nothing is wrong.”

The better explanation, Putrino told me, is that “cookie-cutter testing” doesn’t work—a problem that long COVID shares with other neglected complex illnesses, such as myalgic encephalomyelitis/chronic-fatigue syndrome and dysautonomia. For example, the NIH study didn’t consider post-exertional malaise, a cardinal symptom of both ME/CFS and long COVID; measuring it requires performing cardiopulmonary tests on two successive days. Most long-haulers also show spiking heart rates when asked to simply stand against a wall for 10 minutes—a sign of problems with their autonomic nervous system. “These things are there if you know where to look,” Putrino told me. “You need to listen to your patients, hear where the virus is affecting them, and test accordingly.”

Contrary to popular belief, researchers have learned a huge amount about the biochemical basis of long COVID, and have identified several potential biomarkers for the disease. But because long COVID is likely a cluster of overlapping conditions, there might never be a singular blood test that “will tell you if you have long COVID 100 percent of the time,” Putrino said. The best way to grasp the scale of the condition, then, is still to ask people about their symptoms.

Large attempts to do this have been relatively consistent in their findings: The U.S. Household Pulse Survey estimates that one in 10 people who’ve had COVID currently have long COVID; a large Dutch study put that figure at one in eight. The former study also estimated that 6 percent of American adults are long-haulers; a similar British survey by the Office for National Statistics estimated that 3 percent of the general population is. These cases vary widely in severity, and about one in five long-haulers is barely affected by their symptoms—but the remaining majority very much is. Another one in four long-haulers (or 4 million Americans) has symptoms that severely limit their daily activities. The others might, at best, wake every day feeling as if they haven’t had any rest, or feel trapped in an endless hangover. They might work or socialize when their tidal symptoms ebb, but only by making big compromises: “If I work a full day, I can’t also then make dinner or parent without significant suffering,” JD Davids, who has both long COVID and ME/CFS, told me.

Some people do recover. A widely cited Israeli study of 1.9 million people used electronic medical records to show that most lingering COVID symptoms “are resolved within a year from diagnosis,” but such data fail to capture the many long-haulers who give up on the medical system precisely because they aren’t getting better or are done with being disbelieved. Other studies that track groups of long-haulers over time have found less rosy results. A French one found that 85 percent of people who had symptoms two months after their infection were still symptomatic after a year. A Scottish team found that 42 percent of its patients had only partially recovered at 18 months, and 6 percent had not recovered at all. The United Kingdom’s national survey shows that 69 percent of people with long COVID have been dealing with symptoms for at least a year, and 41 percent for at least two.

The most recent data from the U.S. and the U.K. show that the total number of long-haulers has decreased over the past six months, which certainly suggests that people recover in appreciable numbers. But there’s a catch: In the U.K., the number of people who have been sick for more than a year, or who are severely limited by their illness, has gone up. A persistent pool of people is still being pummeled by symptoms—and new long-haulers are still joining the pool. This influx should be slower than ever, because Omicron variants seem to carry a lower risk of triggering long COVID, while vaccines and the drug Paxlovid can lower that risk even further. But though the odds against getting long COVID are now better, more people are taking a gamble, because preventive precautions have been all but abandoned.

Even if prevalence estimates were a tenth as big, that would still mean more than 1 million Americans are dealing with a chronic illness that they didn’t have three years ago. “When long COVID first came on the scene, everyone told us that once we have the prevalence numbers, we can do something about it,” McCorkell told me. “We got those numbers. Now people say, ‘Well, we don’t believe them. Try again.’”

To a degree, I sympathize with some of the skepticism regarding long COVID, because the condition challenges our typical sense of what counts as solid evidence. Blood tests, electronic medical records, and disability claims all feel like rigorous lines of objective data. Their limitations become obvious only when you consider what the average long-hauler goes through—and those details are often cast aside because they are “anecdotal” and, by implication, unreliable. This attitude is backwards: The patients’ stories are the ground truth against which all other data must be understood. Gaps between the data and the stories don’t immediately invalidate the latter; they just as likely show the holes in the former.

Laura Mauldin, the disability sociologist, argues that the U.S. is primed to discount those experiences because the country’s values—exceptionalism, strength, self-reliance—have created what she calls the myth of the able-bodied public. “We cannot accept that our bodies are fallible, or that disability is utterly ordinary and expected,” she told me. “We go to great pains to pretend as though that is not the case.” If we believe that a disabling illness like long COVID is rare or mild, “we protect ourselves from having to look at it.” And looking away is that much easier because chronic illnesses like long COVID are more likely to affect women—“who are more likely to have their symptoms attributed to psychological problems,” Mauldin said—and because the American emphasis on work ethic devalues people who can’t work as much or as hard as their peers.

Other aspects of long COVID make it hard to grasp. Like other similar, neglected chronic illnesses, it defies a simplistic model of infectious disease in which a pathogen causes a predictable set of easily defined symptoms that alleviate when the bug is destroyed. It challenges our belief in our institutions, because truly contending with what long-haulers go through means acknowledging how poorly the health-care system treats chronically ill patients, how inaccessible social support is to them, and how many callous indignities they suffer at the hands of even those closest to them. Long COVID is a mirror on our society, and the image it reflects is deeply unflattering.

Most of all, long COVID is a huge impediment to the normalization of COVID. It’s an insistent indicator that the pandemic is not actually over; that policies allowing the coronavirus to spread freely still carry a cost; that improvements such as better indoor ventilation are still wanting; that the public emergency may have been lifted but an emergency still exists; and that millions cannot return to pre-pandemic life. “Everyone wants to say goodbye to COVID,” Duggal told me, “and if long COVID keeps existing and people keep talking about it, COVID doesn’t go away.” The people who still live with COVID are being ignored so that everyone else can live with ignoring it.

This article originally misstated the name of the bank where Richard Deitz works.

The Pandemic’s Legacy Is Already Clear

2022-09-30T07:00:00-04:00

Recently, after a week in which 2,789 Americans died of COVID-19, President Joe Biden proclaimed that “the pandemic is over.” Anthony Fauci described the controversy around the proclamation as a matter of “semantics,” but the facts we are living with can speak for themselves. COVID still kills roughly as many Americans every week as died on 9/11. It is on track to kill at least 100,000 a year—triple the typical toll of the flu. Despite gross undercounting, more than 50,000 infections are being recorded every day. The CDC estimates that 19 million adults have long COVID. Things have undoubtedly improved since the peak of the crisis, but calling the pandemic “over” is like calling a fight “finished” because your opponent is punching you in the ribs instead of the face.

American leaders and pundits have been trying to call an end to the pandemic since its beginning, only to be faced with new surges or variants. This mindset not only compromises the nation’s ability to manage COVID, but also leaves it vulnerable to other outbreaks. Future pandemics aren’t hypothetical; they’re inevitable and imminent. New infectious diseases have regularly emerged throughout recent decades, and climate change is quickening the pace of such events. As rising temperatures force animals to relocate, species that have never coexisted will meet, allowing the viruses within them to find new hosts—humans included. Dealing with all of this again is a matter of when, not if.

In 2018, I wrote an article in The Atlantic warning that the U.S. was not prepared for a pandemic. That diagnosis remains unchanged; if anything, I was too optimistic. America was ranked as the world’s most prepared country in 2019—and, bafflingly, again in 2021—but accounts for 16 percent of global COVID deaths despite having just 4 percent of the global population. It spends more on medical care than any other wealthy country, but its hospitals were nonetheless overwhelmed. It helped create vaccines in record time, but is 67th in the world in full vaccinations. (This trend cannot solely be attributed to political division; even the most heavily vaccinated blue state—Rhode Island—still lags behind 21 nations.) America experienced the largest life-expectancy decline of any wealthy country in 2020 and, unlike its peers, continued declining in 2021. If it had fared as well as just the average peer nation, 1.1 million people who died last year—a third of all American deaths—would still be alive.

America’s superlatively poor performance cannot solely be blamed on either the Trump or Biden administrations, although both have made egregious errors. Rather, the new coronavirus exploited the country’s many failing systems: its overstuffed prisons and understaffed nursing homes; its chronically underfunded public-health system; its reliance on convoluted supply chains and a just-in-time economy; its for-profit health-care system, whose workers were already burned out; its decades-long project of unweaving social safety nets; and its legacy of racism and segregation that had already left Black and Indigenous communities and other communities of color disproportionately burdened with health problems. Even in the pre-COVID years, the U.S. was still losing about 626,000 people more than expected for a nation of its size and resources. COVID simply toppled an edifice whose foundations were already rotten.

In furiously racing to rebuild on this same foundation, America sets itself up to collapse once more. Experience is reputedly the best teacher, and yet the U.S. repeated mistakes from the early pandemic when faced with the Delta and Omicron variants. It got early global access to vaccines, and nonetheless lost almost half a million people after all adults became eligible for the shots. It has struggled to control monkeypox—a slower-spreading virus for which there is already a vaccine. Its right-wing legislators have passed laws and rulings that curtail the possibility of important public-health measures like quarantines and vaccine mandates. It has made none of the broad changes that would protect its population against future pathogens, such as better ventilation or universal paid sick leave. Its choices virtually guarantee that everything that’s happened in the past three years will happen again.

The U.S. will continue to struggle against infectious diseases in part because some of its most deeply held values are antithetical to the task of besting a virus. Since its founding, the country has prized a strain of rugged individualism that prioritizes individual freedom and valorizes self-reliance. According to this ethos, people are responsible for their own well-being, physical and moral strength are equated, social vulnerability results from personal weakness rather than policy failure, and handouts or advice from the government are unwelcome. Such ideals are disastrous when handling a pandemic, for two major reasons.

First, diseases spread. Each person’s choices inextricably affect their community, and the threat to the collective always exceeds that to the individual. The original Omicron variant, for example, posed slightly less risk to each infected person than the variants that preceded it, but spread so quickly that it inundated hospitals, greatly magnifying COVID’s societal costs. To handle such threats, collective action is necessary. Governments need policies, such as vaccine requirements or, yes, mask mandates, that protect the health of entire populations, while individuals have to consider their contribution to everyone else’s risk alongside their own personal stakes. And yet, since the spring of 2021, pundits have mocked people who continue to think this way for being irrational and overcautious, and government officials have consistently framed COVID as a matter of personal responsibility.

Second, a person’s circumstances always constrain their choices. Low-income and minority groups find it harder to avoid infections or isolate when sick because they’re more likely to live in crowded homes and hold hourly-wage jobs without paid leave or the option to work remotely. Places such as prisons and nursing homes, whose residents have little autonomy, became hot spots for the worst outbreaks. Treating a pandemic as an individualist free-for-all ignores how difficult it is for many Americans to protect themselves. It also leaves people with vulnerabilities that last across successive pathogens: The groups that suffered most during the H1N1 influenza pandemic of 2009 were the same ones that took the brunt of COVID, a decade later.

America’s individualist bent has also shaped its entire health-care system, which ties health to wealth and employment. That system is organized around treating sick people at great and wasteful expense, instead of preventing communities from falling sick in the first place. The latter is the remit of public health rather than medicine, and has long been underfunded and undervalued. Even the CDC—the nation’s top public-health agency—changed its guidelines in February to prioritize hospitalizations over cases, implicitly tolerating infections as long as hospitals are stable. But such a strategy practically ensures that emergency rooms will be overwhelmed by a fast-spreading virus; that, consequently, health-care workers will quit; and that waves of chronically ill long-haulers who are disabled by their infections will seek care and receive nothing. All of that has happened and will happen again. America’s pandemic individualism means that it’s your job to protect yourself from infection; if you get sick, your treatment may be unaffordable, and if you don’t get better, you will struggle to find help, or even anyone who believes you.

In the late 19th century, many scholars realized that epidemics were social problems, whose spread and toll are influenced by poverty, inequality, overcrowding, hazardous working conditions, poor sanitation, and political negligence. But after the advent of germ theory, this social model was displaced by a biomedical and militaristic one, in which diseases were simple battles between hosts and pathogens, playing out within individual bodies. This paradigm conveniently allowed people to ignore the social context of disease. Instead of tackling intractable social problems, scientists focused on fighting microscopic enemies with drugs, vaccines, and other products of scientific research—an approach that sat easily with America’s abiding fixation on technology as a panacea.

The allure of biomedical panaceas is still strong. For more than a year, the Biden administration and its advisers have reassured Americans that, with vaccines and antivirals, “we have the tools” to control the pandemic. These tools are indeed effective, but their efficacy is limited if people can’t access them or don’t want to, and if the government doesn’t create policies that shift that dynamic. A profoundly unequal society was always going to struggle with access: People with low incomes, food insecurity, eviction risk, and no health insurance struggled to make or attend vaccine appointments, even after shots were widely available. A profoundly mistrustful society was always going to struggle with hesitancy, made worse by political polarization and rampantly spreading misinformation. The result is that just 72 percent of Americans have completed their initial course of shots and just half have gotten the first of the boosters necessary to protect against current variants. At the same time, almost all other protections have been stripped away, and COVID funding is evaporating. And yet the White House’s recent pandemic-preparedness strategy still focuses heavily on biomedical magic bullets, paying scant attention to the social conditions that could turn those bullets into duds.

Technological solutions also tend to rise into society’s penthouses, while epidemics seep into its cracks. Cures, vaccines, and diagnostics first go to people with power, wealth, and education, who then move on, leaving the communities most affected by diseases to continue shouldering their burden. This dynamic explains why the same health inequities linger across the decades even as pathogens come and go, and why the U.S. has now normalized an appalling level of COVID death and disability. Such suffering is concentrated among elderly, immunocompromised, working-class, and minority communities—groups that are underrepresented among political decision makers and the media, who get to declare the pandemic over. Even when inequities are highlighted, knowledge seems to suppress action: In one study, white Americans felt less empathy for vulnerable communities and were less supportive of safety precautions after learning about COVID’s racial disparities. This attitude is self-destructive and limits the advantage that even the most privileged Americans enjoy. Measures that would flatten social inequities, such as universal health care and better ventilation, would benefit everyone—and their absence harms everyone, too. In 2021, young white Americans died at lower rates than Black and Indigenous Americans, but still at three times the rate of their counterparts in other wealthy countries.

By failing to address its social weaknesses, the U.S. accumulates more of them. An estimated 9 million Americans have lost close loved ones to COVID; about 10 percent will likely experience prolonged grief, which the country’s meager mental-health services will struggle to address. Because of brain fog, fatigue, and other debilitating symptoms, long COVID is keeping the equivalent of 2 million to 4 million Americans out of work; between lost earnings and increased medical costs, it could cost the economy $2.6 trillion a year. The exodus of health-care workers, especially experienced veterans, has left hospitals with a shortfall of staff and know-how. Levels of trust—one of the most important predictors of a country’s success at controlling COVID—have fallen, making pandemic interventions harder to deploy, while creating fertile ground in which misinformation can germinate. This is the cost of accepting the unacceptable: an even weaker foundation that the next disease will assail.

In the spring of 2020, I wrote that the pandemic would last for years, and that the U.S. would need long-term strategies to control it. But America’s leaders consistently acted as if they were fighting a skirmish rather than a siege, lifting protective measures too early, and then reenacting them too slowly. They have skirted the responsibility of articulating what it would actually look like for the pandemic to be over, which has meant that whenever citizens managed to flatten the curve, the time they bought was wasted. Endemicity was equated with inaction rather than active management. This attitude removed any incentive or will to make the sort of long-term changes that would curtail the current disaster and prevent future ones. And so America has little chance of effectively countering the inevitable pandemics of the future; it cannot even focus on the one that’s ongoing.

If change happens, it will likely occur slowly and from the ground up. In the vein of ACT UP—the extraordinarily successful activist group that changed the world’s approach to AIDS—grassroots organizations of long-haulers, grievers, immunocompromised people, and others disproportionately harmed by the pandemic have formed, creating the kind of vocal constituency that public health has long lacked.

More pandemics will happen, and the U.S. has spectacularly failed to contain the current one. But it cannot afford the luxury of nihilism. It still has time to address its bedrocks of individualism and inequality, to create a health system that effectively prevents sickness instead of merely struggling to treat it, and to enact policies that rightfully prioritize the needs of disabled and vulnerable communities. Such changes seem unrealistic given the relentless disappointments of the past three years, but substantial social progress always seems unfeasible until it is actually achieved. Normal led to this. It is not too late to fashion a better normal.

Long COVID Has Forced a Reckoning for One of Medicine’s Most Neglected Diseases

2022-09-26T08:00:00-04:00

Kira Stoops lives in Bozeman, Montana—a beautiful mountain town where it sometimes feels like everyone regularly goes on 50-mile runs. Stoops, however, can’t walk around her own block on most days. To stand for more than a few minutes, she needs a wheeled walker. She reacts so badly to most foods that her diet consists of just 12 ingredients. Her “brain fog” usually lifts for a mere two hours in the morning, during which she can sometimes work or, more rarely, see friends. Stoops has myalgic encephalomyelitis, or chronic fatigue syndrome (ME/CFS). “I’m considered a moderate patient on the mild side,” she told me.

ME/CFS involves a panoply of debilitating symptoms that affect many organ systems and that get worse with exertion. The Institute of Medicine estimates that it affects 836,000 to 2.5 million people in the U.S. alone, but is so misunderstood and stigmatized that about 90 percent of people who have it have never been diagnosed. At best, most medical professionals know nothing about ME/CFS; at worst, they tell patients that their symptoms are psychosomatic, anxiety-induced, or simply signs of laziness. While ME/CFS patients, their caregivers, and the few doctors who treat them have spent years fighting for medical legitimacy, the coronavirus pandemic has now forced the issue.

A wide variety of infections can cause ME/CFS, and SARS-CoV-2, the coronavirus that causes COVID-19, is no different: Many cases of long COVID are effectively ME/CFS by another name. The exact number is hard to define, but past studies have shown that 5 to 27 percent of people infected by various pathogens, including Epstein-Barr virus and the original SARS, develop ME/CFS. Even if that proportion is 10 times lower for SARS-CoV-2, the number of Americans with ME/CFS would still have doubled in the past three years. “We’re adding an immense volume of patients to an already dysfunctional and overburdened system,” Beth Pollack, a scientist at MIT who studies complex chronic illnesses, told me.

The U.S. has so few doctors who truly understand the disease and know how to treat it that when they convened in 2018 to create a formal coalition, there were only about a dozen, and the youngest was 60. Currently, the coalition’s website lists just 21 names, of whom at least three have retired and one is dead, Linda Tannenbaum, the CEO and president of the Open Medicine Foundation, told me. These specialists are concentrated on the coasts; none work in the Midwest. American ME/CFS patients may outnumber the population of 15 individual states, but ME/CFS specialists couldn’t fill a Major League Baseball roster. Stoops, who is 39, was formally diagnosed with ME/CFS only four years ago, and began receiving proper care from two of those specialists—Lucinda Bateman of the Bateman Horne Center and David Kaufman from the Center for Complex Diseases. Bateman told me that even before the pandemic, she could see fewer than 10 percent of the patients who asked for a consultation. “When I got into those practices, it was like I got into Harvard,” Stoops told me.

ME/CFS specialists, already overwhelmed with demand for their services, now have to decide how to best use and spread their knowledge, at a time when more patients and doctors than ever could benefit from it. Kaufman recently discharged many of the more stable ME/CFS patients in his care—Stoops among them—so that he could start seeing COVID long-haulers who “were just making the circuit of doctors and getting nowhere,” he told me. “I can’t clone myself, and this was the only other way to” make room for new patients.

Bateman, meanwhile, is feverishly focused on educating other clinicians. The hallmark symptom of ME/CFS—post-exertional malaise, or PEM—means even light physical or mental exertion can trigger major crashes that exacerbate every other symptom. Doctors who are unfamiliar with PEM, including many now running long-COVID clinics, can unwittingly hurt their patients by encouraging them to exercise. Bateman is racing to spread that message, and better ways of treating patients, but that means she’ll have to reduce her clinic hours.

These agonizing decisions mean that many existing ME/CFS patients are losing access to the best care they had found so far—what for Stoops meant “the difference between being stuck at home, miserable and in pain, and actually going out once or twice a day, seeing other humans, and breathing fresh air,” she told me. But painful trade-offs might be necessary to finally drag American medicine to a place where it can treat these kinds of complex, oft-neglected conditions. Kaufman is 75 and Bateman is 64. Although both of them told me they’re not retiring anytime soon, they also won’t be practicing forever. To make full use of their expertise and create more doctors like them, the medical profession must face up to decades spent dismissing illnesses such as ME/CFS—an overdue reckoning incited by long COVID. “It’s a disaster possibly wrapped up in a blessing,” Stoops told me. “The system is cracking and needs to crack.”

Many ME/CFS specialists have a deep knowledge of the disease because they’ve experienced it firsthand. Jennifer Curtin, one of the youngest doctors in the field, has two family members with the disease, and had it herself for nine years. She improved enough to make it through medical school and residency training, which showed her that ME/CFS “just isn’t taught,” she told me. Most curricula don’t include it; most textbooks don’t mention it.

Even if doctors learn about ME/CFS, America’s health-care system makes it almost impossible for them to actually help patients. The insurance model pushes physicians toward shorter visits; 15 minutes might feel luxurious. “My average visit length is an hour, which doesn’t include the time I spend going over the patient’s 500 to 1,700 pages of records beforehand,” Curtin said. “It’s not a very scalable kind of care.” (She works with Kaufman at the Center for Complex Diseases, which bills patients directly.) This also explains why the cohort of ME/CFS clinicians is aging out, with little young blood to refresh them. “Hospital systems want physicians to see lots of patients and they want them to follow the rules,” Kaufman said. “There’s less motivation for moving into areas of medicine that are more unknown and challenging.”

ME/CFS is certainly challenging, not least because it’s just “one face of a many-sided problem,” Jaime Seltzer, the director of scientific and medical outreach at the advocacy group MEAction, told me. The condition’s root causes can also lead to several distinct but interlocking illnesses, including mast cell activation syndrome, Ehlers-Danlos syndrome, fibromyalgia, dysautonomia (usually manifesting as POTS), and several autoimmune and gastrointestinal disorders. “I’m still amazed at how often patients come in with Complaint No. 1, and then I find five to seven of the other things,” Kaufman said. These syndromes collectively afflict many organ systems, which can baffle doctors who’ve specialized in just one. Many of them disproportionately affect women, and are subject to medicine’s long-standing tendency to minimize or psychologize women’s pain, Pollack told me: An average woman with Ehlers-Danlos syndrome typically spends 16 years getting a diagnosis, while a man needs only four.

People with long COVID might have many of these conditions and not know about any—because their doctors don’t either. Like ME/CFS, they rarely feature in medical training, and it’s hard to “teach someone about all of them when they’ve never heard of any of them,” Seltzer said. Specialists like Bateman and Kaufman matter because they understand not just ME/CFS but also the connected puzzle pieces. They can look at a patient’s full array of symptoms and prioritize the ones that are most urgent or foundational. They know how to test for conditions that can be invisible to standard medical techniques: “None of my tests came back abnormal until I saw an ME/CFS doctor, and then all my tests came back abnormal,” said Hannah Davis of the Patient-Led Research Collaborative, who has had long COVID since March 2020.

ME/CFS specialists also know how to help, in ways that are directly applicable to cases of long COVID with overlapping symptoms. ME/CFS has no cure but can be managed, often through “simple, inexpensive interventions that can be done through primary care,” Bateman told me. Over-the-counter antihistamines can help patients with inflammatory problems such as mast cell activation syndrome. Low doses of naltrexone, commonly used for addiction disorders, can help those with intense pain. A simple but rarely administered test can show if patients have orthostatic intolerance—a blood-flow problem that worsens other symptoms when people stand or sit upright. Most important, teaching patients about pacing—carefully sensing and managing your energy levels—can prevent debilitating crashes. “We don’t go to an ME/CFS clinic and walk out in remission,” Stoops told me. “You go to become stabilized. The ship has 1,000 holes, and doctors can patch one before the next explodes, keeping the whole thing afloat.”

That’s why the prospect of losing specialists is so galling. Stoops understands why her doctors might choose to focus on education or newly diagnosed COVID long-haulers, but ME/CFS patients are “just so lost already, and to lose what little we have is a really big deal,” she said. Kaufman has offered to refer her to generalist physicians or talk to primary-care doctors on her behalf. But it won’t be the same: “Having one appointment with him is like six to eight appointments with other practitioners,” she said. He educates her about ME/CFS; with other doctors, it’s often the other way round. “I’m going to have to work much harder to receive a similar level of care.”

At least, she will for now. The ME/CFS specialists who are shifting their focus are hoping that they can use this moment of crisis to create more resources for everyone with these diseases. In a few years, Bateman hopes, “there will be 100 times more clinicians who are prepared to manage patients, and many more people with ME/CFS who have access to care.”

For someone who is diagnosed with ME/CFS today, the landscape already looks very different than it did just a decade ago. In 2015, the Institute of Medicine published a landmark report redefining the diagnostic criteria for the disease. In 2017, the CDC stopped recommending exercise therapy as a treatment. In 2021, Bateman and 20 other clinicians published a comprehensive guide to the condition in the journal of the Mayo Clinic. For any mainstream disease, such events—a report, a guideline revision, a review article—would be mundane. For ME/CFS, they felt momentous. And yet, “the current state of things is simply intolerable,” Julie Rehmeyer, a journalist with ME/CFS, told me. Solving the gargantuan challenge posed by complex chronic diseases demands seismic shifts in research funding, medical training, and public attitudes. “Achieving shifts like that takes something big,” Rehmeyer said. “Long COVID is big.”

COVID long-haulers have proved beyond any reasonable doubt that acute viral infections can leave people chronically ill. Many health-care workers, political-decision makers, and influencers either know someone with long COVID or have it themselves. Even if they still don’t know about ME/CFS, their heightened awareness of post-viral illnesses is already making a difference. Mary Dimmock’s son developed ME/CFS in 2011, and before the pandemic, one doctor in 10 might take him seriously. “Now it’s the flip: Only one doctor out of 10 will be a real jerk,” Dimmock told me. “I attribute that to long COVID.”

But being believed is the very least that ME/CFS patients deserve. They need therapeutics that target the root causes of the disease, which will require a clear understanding of those causes, which will require coordinated, well-funded research—three things ME/CFS has historically lacked. But here, too, “long COVID is going to be a catalyst,” Amy Proal, the president of the Polybio Research Foundation, told me. She is leading the Long Covid Research Initiative—a group of scientists, including ME/CFS researchers, that will use state-of-the-art techniques to see exactly how the new coronavirus causes long COVID, and rapidly push potential treatments through clinical trials. The National Institutes of Health has also committed $1.15 billion to long-COVID research, and while some advocates are concerned about how that money will be spent, Rehmeyer notes that the amount is still almost 80 times greater than the paltry $15 million spent on ME/CFS every year—less than any other disease in the NIH’s portfolio, relative to its societal burden. “Even if 90 percent is wasted, we’d be doing a lot better,” she said.

While they wait for better treatments, patients also need the medical community to heed the lessons that they and their clinicians have learned. For example, the American Academy for Family Physicians website still wrongly recommends exercise therapy and links ME/CFS to childhood abuse. “That group of doctors is very important to these patients,” Dimmock said, “so what does that say to them about what this disease is all about?”

Despite all evidence to the contrary, many clinicians and researchers still don’t see ME/CFS as a legitimate illness and are quick to dismiss any connection between it and long COVID. To ensure that both groups of patients get the best possible treatments, instead of advice that might harm them, ME/CFS specialists are working to disseminate their hard-won knowledge. Bateman and her colleagues have been creating educational resources for clinicians and patients, continuing-medical-education courses, and an online lecture series. Jennifer Curtin has spent two years mapping all the decisions she makes when seeing a new patient, and is converting those into a tool that other clinicians can use. As part of her new start-up, called RTHM, she’s also trying to develop better ways of testing for ME/CFS and its related syndromes, of visualizing the hefty electronic health records that chronically ill patients accumulate, and of tracking the treatments they try and their effects. “There are a lot of things that need to be fixed for this kind of care to be scalable,” Curtin told me.

Had such shifts already occurred, the medical profession might have had more to offer COVID long-haulers beyond bewilderment and dismissal. But if the profession starts listening to the ME/CFS community now, it will stand the best chance of helping people being disabled by COVID, and of steeling itself against future epidemics. Pathogens have been chronically disabling people for the longest time, and more pandemics are inevitable. The current one could and should be the last whose long-haulers are greeted with disbelief.

New centers that cater to ME/CFS patients are already emerging. RTHM is currently focused on COVID long-haulers but will take on some of David Kaufman’s former patients in November, and will open its waiting list to the broader ME/CFS community in December. (It is currently licensed to practice in just five states but expects to expand soon.) David Putrino, who leads a long-COVID rehabilitation clinic in Mount Sinai, is trying to raise funds for a new clinic that will treat both long COVID and ME/CFS. He credits ME/CFS patients with opening his eyes to the connection between long COVID and their condition.

Every ME/CFS patient I’ve talked with predicted long COVID’s arrival well before most doctors or even epidemiologists started catching up. They know more about complex chronic illnesses than many of the people now treating long COVID do. Despite having a condition that saps their energy, many have spent the past few years helping long-haulers navigate what for them was well-trodden terrain: “I did barely anything but work in 2020,” Seltzer told me. Against the odds, they’ve survived. But the pandemic has created a catalytic opportunity for the odds to finally be tilted in their favor, “so that neither patients nor doctors of any complex chronic illness have to be heroes anymore,” Rehmeyer said.

One of Long COVID’s Worst Symptoms Is Also Its Most Misunderstood

2022-09-12T07:00:00-04:00

On March 25, 2020, Hannah Davis was texting with two friends when she realized that she couldn’t understand one of their messages. In hindsight, that was the first sign that she had COVID-19. It was also her first experience with the phenomenon known as “brain fog,” and the moment when her old life contracted into her current one. She once worked in artificial intelligence and analyzed complex systems without hesitation, but now “runs into a mental wall” when faced with tasks as simple as filling out forms. Her memory, once vivid, feels frayed and fleeting. Former mundanities—buying food, making meals, cleaning up—can be agonizingly difficult. Her inner world—what she calls “the extras of thinking, like daydreaming, making plans, imagining”—is gone. The fog “is so encompassing,” she told me, “it affects every area of my life.” For more than 900 days, while other long-COVID symptoms have waxed and waned, her brain fog has never really lifted.

Of long COVID’s many possible symptoms, brain fog “is by far one of the most disabling and destructive,” Emma Ladds, a primary-care specialist from the University of Oxford, told me. It’s also among the most misunderstood. It wasn’t even included in the list of possible COVID symptoms when the coronavirus pandemic first began. But 20 to 30 percent of patients report brain fog three months after their initial infection, as do 65 to 85 percent of the long-haulers who stay sick for much longer. It can afflict people who were never ill enough to need a ventilator—or any hospital care. And it can affect young people in the prime of their mental lives.

Long-haulers with brain fog say that it’s like none of the things that people—including many medical professionals—jeeringly compare it to. It is more profound than the clouded thinking that accompanies hangovers, stress, or fatigue. For Davis, it has been distinct from and worse than her experience with ADHD. It is not psychosomatic, and involves real changes to the structure and chemistry of the brain. It is not a mood disorder: “If anyone is saying that this is due to depression and anxiety, they have no basis for that, and data suggest it might be the other direction,” Joanna Hellmuth, a neurologist at UC San Francisco, told me.

And despite its nebulous name, brain fog is not an umbrella term for every possible mental problem. At its core, Hellmuth said, it is almost always a disorder of “executive function”—the set of mental abilities that includes focusing attention, holding information in mind, and blocking out distractions. These skills are so foundational that when they crumble, much of a person’s cognitive edifice collapses. Anything involving concentration, multitasking, and planning—that is, almost everything important—becomes absurdly arduous. “It raises what are unconscious processes for healthy people to the level of conscious decision making,” Fiona Robertson, a writer based in Aberdeen, Scotland, told me.

For example, Robertson’s brain often loses focus mid-sentence, leading to what she jokingly calls “so-yeah syndrome”: “I forget what I’m saying, tail off, and go, ‘So, yeah …’” she said. Brain fog stopped Kristen Tjaden from driving, because she’d forget her destination en route. For more than a year, she couldn’t read, either, because making sense of a series of words had become too difficult. Angela Meriquez Vázquez told me it once took her two hours to schedule a meeting over email: She’d check her calendar, but the information would slip in the second it took to bring up her inbox. At her worst, she couldn’t unload a dishwasher, because identifying an object, remembering where it should go, and putting it there was too complicated.

Memory suffers, too, but in a different way from degenerative conditions like Alzheimer’s. The memories are there, but with executive function malfunctioning, the brain neither chooses the important things to store nor retrieves that information efficiently. Davis, who is part of the Patient-Led Research Collaborative, can remember facts from scientific papers, but not events. When she thinks of her loved ones, or her old life, they feel distant. “Moments that affected me don’t feel like they’re part of me anymore,” she said. “It feels like I am a void and I’m living in a void.”

Most people with brain fog are not so severely affected, and gradually improve with time. But even when people recover enough to work, they can struggle with minds that are less nimble than before. “We’re used to driving a sports car, and now we are left with a jalopy,” Vázquez said. In some professions, a jalopy won’t cut it. “I’ve had surgeons who can’t go back to surgery, because they need their executive function,” Monica Verduzco-Gutierrez, a rehabilitation specialist at UT Health San Antonio, told me.

Robertson, meanwhile, was studying theoretical physics in college when she first got sick, and her fog occluded a career path that was once brightly lit. “I used to sparkle, like I could pull these things together and start to see how the universe works,” she told me. “I’ve never been able to access that sensation again, and I miss it, every day, like an ache.” That loss of identity was as disruptive as the physical aspects of the disease, which “I always thought I could deal with … if I could just think properly,” Robertson said. “This is the thing that’s destabilized me most.”

Robertson predicted that the pandemic would trigger a wave of cognitive impairment in March 2020. Her brain fog began two decades earlier, likely with a different viral illness, but she developed the same executive-function impairments that long-haulers experience, which then worsened when she got COVID last year. That specific constellation of problems also befalls many people living with HIV, epileptics after seizures, cancer patients experiencing so-called chemo brain, and people with several complex chronic illnesses such as fibromyalgia. It’s part of the diagnostic criteria for myalgic encephalomyelitis, also known as chronic fatigue syndrome, or ME/CFS—a condition that Davis and many other long-haulers now have. Brain fog existed well before COVID, affecting many people whose conditions were stigmatized, dismissed, or neglected. “For all of those years, people just treated it like it’s not worth researching,” Robertson told me. “So many of us were told, Oh, it’s just a bit of a depression.”

Several clinicians I spoke with argued that the term brain fog makes the condition sound like a temporary inconvenience and deprives patients of the legitimacy that more medicalized language like cognitive impairment would bestow. But Aparna Nair, a historian of disability at the University of Oklahoma, noted that disability communities have used the term for decades, and there are many other reasons behind brain fog’s dismissal beyond terminology. (A surfeit of syllables didn’t stop fibromyalgia and myalgic encephalomyelitis from being trivialized.)

For example, Hellmuth noted that in her field of cognitive neurology, “virtually all the infrastructure and teaching” centers on degenerative diseases like Alzheimer’s, in which rogue proteins afflict elderly brains. Few researchers know that viruses can cause cognitive disorders in younger people, so few study their effects. “As a result, no one learns about it in medical school,” Hellmuth said. And because “there’s not a lot of humility in medicine, people end up blaming patients instead of looking for answers,” she said.

People with brain fog also excel at hiding it: None of the long-haulers I’ve interviewed sounded cognitively impaired. But at times when her speech is obviously sluggish, “nobody except my husband and mother see me,” Robertson said. The stigma that long-haulers experience also motivates them to present as normal in social situations or doctor appointments, which compounds the mistaken sense that they’re less impaired than they claim—and can be debilitatingly draining. “They’ll do what is asked of them when you’re testing them, and your results will say they were normal,” David Putrino, who leads a long-COVID rehabilitation clinic at Mount Sinai, told me. “It’s only if you check in on them two days later that you’ll see you’ve wrecked them for a week.”

“We also don’t have the right tools for measuring brain fog,” Putrino said. Doctors often use the Montreal Cognitive Assessment, which was designed to uncover extreme mental problems in elderly people with dementia, and “isn’t validated for anyone under age 55,” Hellmuth told me. Even a person with severe brain fog can ace it. More sophisticated tests exist, but they still compare people with the population average rather than their previous baseline. “A high-functioning person with a decline in their abilities who falls within the normal range is told they don’t have a problem,” Hellmuth said.

This pattern exists for many long-COVID symptoms: Doctors order inappropriate or overly simplistic tests, whose negative results are used to discredit patients’ genuine symptoms. It doesn’t help that brain fog (and long COVID more generally) disproportionately affects women, who have a long history of being labeled as emotional or hysterical by the medical establishment. But every patient with brain fog “tells me the exact same story of executive-function symptoms,” Hellmuth said. “If people were making this up, the clinical narrative wouldn’t be the same.”

Earlier this year, a team of British researchers rendered the invisible nature of brain fog in the stark black-and-white imagery of MRI scans. Gwenaëlle Douaud at the University of Oxford and her colleagues analyzed data from the UK Biobank study, which had regularly scanned the brains of hundreds of volunteers for years prior to the pandemic. When some of those volunteers caught COVID, the team could compare their after scans to the before ones. They found that even mild infections can slightly shrink the brain and reduce the thickness of its neuron-rich gray matter. At their worst, these changes were comparable to a decade of aging. They were especially pronounced in areas such as the parahippocampal gyrus, which is important for encoding and retrieving memories, and the orbitofrontal cortex, which is important for executive function. They were still apparent in people who hadn’t been hospitalized. And they were accompanied by cognitive problems.

Although SARS-CoV-2, the coronavirus that causes COVID, can enter and infect the central nervous system, it doesn’t do so efficiently, persistently, or frequently, Michelle Monje, a neuro-oncologist at Stanford, told me. Instead, she thinks that in most cases the virus harms the brain without directly infecting it. She and her colleagues recently showed that when mice experience mild bouts of COVID, inflammatory chemicals can travel from the lungs to the brain, where they disrupt cells called microglia. Normally, microglia act as groundskeepers, supporting neurons by pruning unnecessary connections and cleaning unwanted debris. When inflamed, their efforts become overenthusiastic and destructive. In their presence, the hippocampus—a region crucial for memory—produces fewer fresh neurons, while many existing neurons lose their insulating coats, so electric signals now course along these cells more slowly. These are the same changes that Monje sees in cancer patients with “chemo fog.” And although she and her team did their COVID experiments in mice, they found high levels of the same inflammatory chemicals in long-haulers with brain fog.

Monje suspects that neuro-inflammation is “probably the most common way” that COVID results in brain fog, but that there are likely many such routes. COVID could possibly trigger autoimmune problems in which the immune system mistakenly attacks the nervous system, or reactivate dormant viruses such as Epstein-Barr virus, which has been linked to conditions including ME/CFS and multiple sclerosis. By damaging blood vessels and filling them with small clots, COVID also throttles the brain’s blood supply, depriving this most energetically demanding of organs of oxygen and fuel. This oxygen shortfall isn’t stark enough to kill neurons or send people to an ICU, but “the brain isn’t getting what it needs to fire on all cylinders,” Putrino told me. (The severe oxygen deprivation that forces some people with COVID into critical care causes different cognitive problems than what most long-haulers experience.)

None of these explanations is set in stone, but they can collectively make sense of brain fog’s features. A lack of oxygen would affect sophisticated and energy-dependent cognitive tasks first, which explains why executive function and language “are the first ones to go,” Putrino said. Without insulating coats, neurons work more slowly, which explains why many long-haulers feel that their processing speed is shot: “You’re losing the thing that facilitates fast neural connection between brain regions,” Monje said. These problems can be exacerbated or mitigated by factors such as sleep and rest, which explains why many people with brain fog have good days and bad days. And although other respiratory viruses can wreak inflammatory havoc on the brain, SARS-CoV-2 does so more potently than, say, influenza, which explains both why people such as Robertson developed brain fog long before the current pandemic and why the symptom is especially prominent among COVID long-haulers.

Perhaps the most important implication of this emerging science is that brain fog is “potentially reversible,” Monje said. If the symptom was the work of a persistent brain infection, or the mass death of neurons following severe oxygen starvation, it would be hard to undo. But neuroinflammation isn’t destiny. Cancer researchers, for example, have developed drugs that can calm berserk microglia in mice and restore their cognitive abilities; some are being tested in early clinical trials. “I’m hopeful that we’ll find the same to be true in COVID,” she said.

Biomedical advances might take years to arrive, but long-haulers need help with brain fog now. Absent cures, most approaches to treatment are about helping people manage their symptoms. Sounder sleep, healthy eating, and other generic lifestyle changes can make the condition more tolerable. Breathing and relaxation techniques can help people through bad flare-ups; speech therapy can help those with problems finding words. Some over-the-counter medications such as antihistamines can ease inflammatory symptoms, while stimulants can boost lagging concentration.

“Some people spontaneously recover back to baseline,” Hellmuth told me, “but two and a half years on, a lot of patients I see are no better.” And between these extremes lies perhaps the largest group of long-haulers—those whose brain fog has improved but not vanished, and who can “maintain a relatively normal life, but only after making serious accommodations,” Putrino said. Long recovery periods and a slew of lifehacks make regular living possible, but more slowly and at higher cost.

Kristen Tjaden can read again, albeit for short bursts followed by long rests, but hasn’t returned to work. Angela Meriquez Vázquez can work but can’t multitask or process meetings in real time. Julia Moore Vogel, who helps lead a large biomedical research program, can muster enough executive function for her job, but “almost everything else in my life I’ve cut out to make room for that,” she told me. “I only leave the house or socialize once a week.” And she rarely talks about these problems openly because “in my field, your brain is your currency,” she said. “I know my value in many people’s eyes will be diminished by knowing that I have these cognitive challenges.”

Patients struggle to make peace with how much they’ve changed and the stigma associated with it, regardless of where they end up. Their desperation to return to normal can be dangerous, especially when combined with cultural norms around pressing on through challenges and post-exertional malaise—severe crashes in which all symptoms worsen after even minor physical or mental exertion. Many long-haulers try to push themselves back to work and instead “push themselves into a crash,” Robertson told me. When she tried to force her way to normalcy, she became mostly housebound for a year, needing full-time care. Even now, if she tries to concentrate in the middle of a bad day, “I end up with a physical reaction of exhaustion and pain, like I’ve run a marathon,” she said.

Post-exertional malaise is so common among long-haulers that “exercise as a treatment is inappropriate for people with long COVID,” Putrino said. Even brain-training games—which have questionable value but are often mentioned as potential treatments for brain fog—must be very carefully rationed because mental exertion is physical exertion. People with ME/CFS learned this lesson the hard way, and fought hard to get exercise therapy, once commonly prescribed for the condition, to be removed from official guidance in the U.S. and U.K. They’ve also learned the value of pacing—carefully sensing and managing their energy levels to avoid crashes.

Vogel does this with a wearable that tracks her heart rate, sleep, activity, and stress as a proxy for her energy levels; if they feel low, she forces herself to rest—cognitively as well as physically. Checking social media or responding to emails do not count. In those moments, “you have to accept that you have this medical crisis and the best thing you can do is literally nothing,” she said. When stuck in a fog, sometimes the only option is to stand still.

A New Test for an Old Theory About Dreams

2022-08-25T14:00:00-04:00

When Massimo Scanziani’s daughter was young, he’d often see her eyes twitching beneath her eyelids while she was sleeping. These rapid eye movements (or REMs) are so obvious, Scanziani told me, that he can hardly believe that they were described just seven decades ago. In 1953, Eugene Aserinsky and Nathaniel Kleitman identified a special phase of sleep when neurons were abuzz and eyes were shut but flitting about. During this phase, now called “REM sleep,” people tended to have vivid dreams. Maybe, Kleitman suggested, the eye movements reflected “where and at what the dreamer was looking” in their virtual world.

Several researchers tested this “scanning hypothesis” in the ’50s and ’60s by waking sleeping volunteers when their eyes twitched and asking them what they had just dreamed. Perhaps unsurprisingly, these crude methods failed to produce consistent results. But despite alternative explanations—maybe the movements lubricate the closed eye or arise from random brain activity—the scanning hypothesis remains popular. And through a clever experiment involving mice, Scanziani and his colleague Yuta Senzai, who are both neuroscientists at UC San Francisco, think they’ve finally shown that eye twitches are a direct line into an inner dream world.

As a mouse moves, a group of neurons in its brain tracks the direction of its head, acting like an internal compass. Some of these neurons fire when the mouse turns left; others buzz when it turns right. By analyzing a mouse’s activity, a scientist can tell you where it is facing without ever looking at the rodent itself. And during REM sleep, even though a mouse’s head isn’t moving, its head-direction cells still fire as if it were exploring.

Scanziani and Senzai reasoned that, by recording the activity of these neurons with implanted electrodes, they could work out where sleeping mice are looking in their dream worlds. They then showed that the signals from this internal compass matched the movements of the rodents’ eyes (which they could track because mice often sleep with their eyes slightly open). When a mouse seems to move its head around in its dream, its eyes flick in the same direction, to the same degree, and at the same moment. “The rodent is certainly exploring the environment in its dream,” Scanziani told me. “By looking at its moving eyes, we have a window into its dreaming brain.”

These results suggest that “in their dreams, mice are attending to the events unfolding before them and interacting with them actively, intentionally, and dynamically,” says David Peña-Guzmán, a philosopher at San Francisco State University and the author of When Animals Dream. Many philosophers would regard that as “a clear indicator of consciousness,” he told me.

But other sleep researchers are not convinced that Scanziani and Senzai showed what they think they showed. Sara Aton, a neuroscientist at the University of Michigan, told me that head and eye movements are so tightly coupled when mice (and humans) are awake that you wouldn’t expect them to suddenly disconnect during sleep. That they remain linked doesn’t tell us whether mice are perceiving a dream world, let alone gazing about it. “We simply can’t read that out from the brain,” Aton said. Mark Blumberg, a neuroscientist at the University of Iowa, agrees. “The link to dreams is gratuitous,” he told me. Scanziani and Senzai “assert that they’re peering into the virtual world of dreams, but they haven’t done so—nor can they.”

At first glance, this might seem like a semantic argument: “I can say that we’re looking at coordinated activity of distinct parts of the brain occurring during REM sleep that strongly resembles the activity that the brain has when it’s awake, or I can call it a dream,” Scanziani said. But those things aren’t necessarily identical, and Blumberg argues that equating them could distract us from understanding the role of REM sleep.

He notes that when eyes move during this phase, other body parts twitch too, including limbs and whiskers. These movements look like more evidence of dreams spilling into reality—sleeping dogs chasing imagined rabbits—but they might represent something simpler. Blumberg argues that the brain uses REM sleep to test-drive the body. The brain pings the neurons that control muscles, creating twitches; it then collects sensory information from those moving limbs. By testing those connections during times of stillness, it can refine and recalibrate the network to work more efficiently during times of wakeful chaos. According to this view, REM-phase movements aren’t about dreams at all. They’re the work of a brain that’s learning how to more effectively pilot a body.

This explanation better accounts for aspects of REM sleep that don’t easily fit with the scanning hypothesis. For example, people who are born blind still move their eyes during sleep, even though they don’t dream visually and clearly aren’t looking around. Also, the REM phase of sleep is longest in newborn humans, mice, and other mammals whose infants are relatively helpless at birth. These are exactly the individuals whose brain would need the most time to get to grips with their body. By contrast, if the twitches are linked to dreams, “why would newborns twitch so much when they have so little to dream about?” Blumberg said.

Since its discovery, REM sleep has been associated with dreaming (even though we dream in non-REM sleep too). And because dreams are so fascinating, they became the focus of our attempts to understand REM—the sun that other hypotheses orbit around. But what if they aren’t central? Scanziani told me that dreams might arise because the brain replays memories after “a long day of experiences” to better organize what it has learned, or “generates and explores possibilities to help us make better predictions when we’re awake.” This is essentially what the test-drive hypothesis argues, except here, the brain is just testing the connections within itself, rather than those with the rest of the body. It’s intuitive to see the dreams and twitches of REM sleep as connected phenomena. But perhaps they’re two independent reflections of a brain that’s relentlessly recalibrating.

The Creature That Gave Up Parasitism for … Wait, What?

2022-07-26T08:00:00-04:00

In the late 19th century, when scientists first discovered the single-celled creature called Nephromyces, they thought it was a parasitic fungus. They were wrong. Instead, it’s … well … how to even describe it? It’s a reformed parasite. It’s a creature of extremes, surviving in a world of acids and dining on, of all things, kidney stones. And perhaps strangest of all, it’s an organism that cannot survive as an individual. A single ant will do badly away from its colony; a single Nephromyces wouldn’t even get that far.

Nephromyces can be found all along the eastern coast of the U.S., living inside the bodies of translucent, blobby animals called sea squirts. Some sea squirts look like beautiful glass vases; those that house Nephromyces, known as sea grapes, look more like cysts that have grown bunny ears.

Inside each sea grape is a large organ called a renal sac, so named because scientists originally thought it was a kidney. But as the biologist Mary Beth Saffo once told The New York Times, “If it was a kidney, it was a pretty odd one.” For a start, it has no opening. It accumulates the chemicals you’d expect in a kidney—uric and oxalic acids, crystallized into what are essentially kidney stones—but instead of excreting these as a normal kidney would, it stores them for the sea grape’s entire life. As a result, the sac is extremely acidic. Despite that, it’s teeming with life. Cut into one, and “cells just pour out,” Saffo told me.

Scientists first noticed these cells in the 1870s. They came in a variety of shapes—blobs and threads, barrels and baskets. Researchers deduced that these were all different life stages of the same organism, which was named Nephromyces after the Greek for “kidney fungus.” But as Saffo showed in 2010, after sequencing its DNA, Nephromyces isn’t a fungus at all. It’s part of a group of nefarious single-celled organisms called the “apicomplexans,” whose members cause diseases such as malaria and toxoplasmosis. There are about 6,000 species of apicomplexans, and they’re almost all parasites.

Almost all. If Nephromyces is a parasite, it’s a pretty odd one. It doesn’t seem to harm its sea-grape host in any way. And though sea grapes aren’t born with Nephromyces, they always acquire these cells from the surrounding seawater. Every adult sea grape that’s ever been examined harbors hordes of Nephromyces in its renal sac—a 100 percent infection rate that actual parasites almost never achieve, because their hosts tend to fight back. The sea grape doesn’t, which suggests that Nephromyces’s presence is benign, if not beneficial. It just sits there in the renal sac, minding its own business, eating kidney stones. It’s a black sheep in a family of vampires—a creature that has abandoned its relatives’ penchant for exploitation. Such transitions are incredibly rare. Parasites usually become so dependent on their hosts that they lose genes, traits, and body parts that they need for a free-living life. That’s why many organisms take up parasitism but very few ever give it up. How did Nephromyces manage?

One possibility: It has help. In 1990, Saffo showed that Nephromyces is chronically infected with bacteria—microbes that live inside it, just as it lives inside the sea grape. Many creatures are home to internal bacteria, which might provide them with nutrients that are missing from their diet, or help them to digest food they otherwise could not. Perhaps, then, the bacteria in Nephromyces perform similar services. Do they help it to digest the kidney stones around it? Do they provide it with nutrients that its parasitic ancestors lost the ability to make?

Like others before him, Chris Lane, from the University of Rhode Island, assumed that sea grapes contain just one species of Nephromyces, which contains just one species of bacteria, perhaps a pretty odd one. But when he looked closer, he found that they’re pretty odd ones. By sequencing the DNA inside the renal sacs, his students found evidence of a much larger community—many kinds of bacteria, and dozens of Nephromyces species.

The team showed that the bacteria in the community belong to three major groups, which Lane thinks of as “flavors.” Each species of Nephromyces contains one and only one of these flavors (perhaps because there simply isn’t space for more). The bacteria are crucial; they help Nephromyces produce essential vitamins and amino acids that it otherwise couldn’t get. But here’s the catch: No single flavor of bacteria can provide all of the nutrients that Nephromyces requires. It needs all three flavors together—but no species can ever have more than one. For that reason, no Nephromyces species can thrive on its own. They must exist as a community—a multispecies swarm that survives by trading the nutrients that their respective bacteria provide. Lane describes it as a “hippie commune.” In the wild, he showed, sea grapes tend to harbor somewhere between three and eight Nephromyces species.

Is this what it takes for a parasite to give up parasitism? Because, to be honest, “it’s a bit of a mess,” Lane told me. Remember that each sea grape picks up Nephromyces from the surrounding seawater. And Nephromyces does well only if different species with the right bacterial flavors somehow manage to co-infect a single sea grape. “This is just a dumb situation,” Lane said. “It seems like it shouldn’t exist, but here we are.”

“The first time you see something like this, you say to yourself: Go home, evolution, you’re drunk,” John McCutcheon, an evolutionary biologist at Arizona State University, told me. “But evolution doesn’t go out looking for simple solutions to things: It cobbles together solutions from what’s there.” The results can be bafflingly complicated. McCutcheon and his colleagues have studied an insect with bacteria living inside its cells and bacteria living inside those—bugs in bugs in bugs. They found an entire dynasty of bacteria that are splitting into new species inside the bodies of cicadas. “Now we all know to look for crazy combinations,” he said.

With Nephromyces, many mysteries still remain. Are the blobs, barrels, and other shapes actually different life stages, as scientists once thought, or different species, as Lane now suspects? How do the different Nephromyces species ensure that enough of them get inside the same sea grape? How did the different species even evolve? (Many organisms diversify into a variety of species when each gets to exploit a different corner of the environment—but where are the niches in a sea grape’s renal sac?) Are there Nephromyces species that cheat—that contain no bacteria of their own and instead mooch off the nutrients produced by the rest of the commune? (“We think so,” Lane told me.) Also, how does the sea grape benefit from the community inside its body, if at all? Lab-raised sea grapes that lack Nephromyces “do just fine,” Lane said. And though many animals depend on internal microbes for nutrients, sea grapes “live in almost laughably nutrient-rich ocean waters,” Saffo told me.

“We’re not even close to getting to the bottom of this,” she said. “The details get filled in and get even more confusing.”

America Was in an Early-Death Crisis Long Before COVID

2022-07-21T08:30:09-04:00

Jacob Bor has been thinking about a parallel universe. He envisions a world in which America has health on par with that of other wealthy nations, and is not an embarrassing outlier that, despite spending more on health care than any other country, has shorter life spans, higher rates of chronic disease and maternal mortality, and fewer doctors per capita than its peers. Bor, an epidemiologist at Boston University School of Public Health, imagines the people who are still alive in that other world but who died in ours. He calls such people “missing Americans.” And he calculates that in 2021 alone, there were 1.1 million of them.

Bor and his colleagues arrived at that number by using data from an international mortality database and the CDC. For every year from 1933 to 2021, they compared America’s mortality rates with the average of Canada, Japan, and 16 Western European nations (adjusting for age and population). They showed that from the 1980s onward, the U.S. started falling behind its peers. By 2019, the number of missing Americans had grown to 626,000. After COVID arrived, that statistic ballooned even further—to 992,000 in 2020, and to 1.1 million in 2021. Were the U.S. “just average compared to other wealthy countries, not even the best performer, fully a third of all deaths last year would have been prevented,” Bor told me. That includes half of all deaths among working-age adults. “Think of two people you might know under 65 who died last year: One of them might still be alive,” he said. “It raises the hairs on the back of my neck.”

These counterfactuals puncture two common myths about America’s pandemic experience: that the U.S. was just one unremarkable victim of a crisis that spared no nation and that COVID disrupted a status quo that was strong and worth restoring wholesale. In fact, as one expert predicted in March 2020, the U.S. had the worst outbreak in the industrialized world—not just because of what the Trump and Biden administrations did, but also because of the country’s rotten rootstock. COVID simply did more of what life in America has excelled at for decades: killing Americans in unusually large numbers, and at unusually young ages. “I don’t think people in the United States actually have any awareness of just how poorly we do as a country at letting people live to old age,” Elizabeth Wrigley-Field, a sociologist at the University of Minnesota, told me.

Although Bor’s study has yet to be formally reviewed, Wrigley-Field and five other independent researchers vouched for its quality to me. “The paper is extremely important, and the researchers who produced this know what they’re doing,” Steven Woolf, a population-health expert at Virginia Commonwealth University, told me. “It builds on, and considerably expands, what we’ve already known.”

Several studies, for example, have shown that America’s life expectancy has tailed behind other comparable countries since the 1970s. By 2010, that gap was already 1.9 years. By the end of 2021, it had grown to 5.3. And although many countries took a longevity hit because of COVID, America was once again exceptional: Among its peers, it experienced the largest life-expectancy decline in 2020 and, unlike its peers, continued declining in 2021. But Bor says that people often misinterpret life-expectancy declines, as if they simply represent a few years shaved off the end of a life. Someone might reasonably ask: What’s the big deal if I die at 76 versus 78? But in fact, life expectancy is falling behind other wealthy nations in large part because a lot of Americans are dying very young—in their 40s and 50s, rather than their 70s and 80s. The country is experiencing what Bor and his colleagues call “a crisis of early death”—a long-simmering tragedy that COVID took to a furious boil.

In every country, the coronavirus wrought greater damage upon the bodies of the elderly than the young. But this well-known trend hides a less obvious one: During the pandemic, half of the U.S.’s excess deaths—the missing Americans—were under 65 years old. Even though working-age Americans were less likely to die of COVID than older Americans, they fared considerably worse than similarly aged people in other countries. From 2019 to 2021, the number of working-age Americans who died increased by 233,000—and nine in 10 of those deaths wouldn’t have happened if the U.S. had mortality rates on par with its peers. “This is a damning finding,” Oni Blackstock, the founder and executive director of Health Justice, told me.

[Read: How did this many deaths become normal?]

The crisis of early death was evident well before COVID. As many studies and reports have shown, since the turn of the 21st century, “midlife ages are where health and survival in the U.S. really go off the rails,” Wrigley-Field told me. “The U.S. actually does well at keeping people alive once they’re really old,” she said, but it struggles to get its citizens to that point. They might die because of gun violence, car accidents, or heart disease and other metabolic disorders, or drug overdoses, suicides, and other deaths of despair. In all of these, the U.S. does worse than most equivalent countries, both by failing to address these problems directly and by leaving people more vulnerable to them to begin with.

Consider how many years the missing Americans would have collectively enjoyed had they survived—all the birthdays and anniversaries that never happened. In other rich countries, the total “years of life lost” have flatlined for the past five decades. In the U.S., they have soared: In 2021 alone, the 1.1 million missing Americans lost 25 million years of life among them. That number doesn’t account for the events that preceded many of these deaths—the “years of disability, illness, and loss of human potential, creativity, and dignity,” Laudan Aron, a health-policy researcher at the Urban Institute, told me. And, especially in the case of middle-aged deaths, they left behind young dependents, whose own health might suffer as a result. The sheer number of missing Americans, and the “profound ripple effects” of their absence, are “really hard to wrap one’s head around,” Aron said.

[Read: The final pandemic betrayal]

These staggering numbers also help contextualize COVID’s toll. The coronavirus caused the largest single-year rise in mortality since World War II, becoming the third leading cause of death in the U.S., after only heart disease and cancer. But this enormous tragedy unfolded against an already tragic backdrop: The number of missing Americans from 2019 is larger than the number of people who were killed by COVID in 2020 or 2021. This isn’t to minimize COVID’s impact; it simply shows that in the Before Times, America had “very successfully normalized to an extremely high level of death on the scale of what we experienced in the pandemic,” Justin Feldman, a social epidemiologist at Harvard, told me. And when COVID drove those levels skyward, America proved that “we’ll accept even more deaths compared to our already poor historical norms,” Feldman said.

Such deaths, though obvious on a graph, are hidden from Americans with social privilege. In the summer of 2020, Bor remembers having an outdoor barbecue with a friend who grew up in a low-income housing project. “At that point, six months in, he knew six people in his close circle who had been killed by COVID,” Bor told me. “I still don’t.” The fact that half of the working-age Americans who died last year should still be alive “isn’t visceral if you haven’t lost anyone,” he said.

The current mortality crisis was long in the making. In terms of mortality, America’s peer countries—many of which had been hammered by World War II and its aftermath—began catching up with it in the mid-1970s before overtaking in the early 1980s. That was a pivotal era, when globalization, automation, and a growing service industry led to huge losses in mining, manufacturing, and other blue-collar sectors. The U.S. profoundly failed to protect its citizens from these changes. Its social safety net—state assistance for parents, or people facing job, food, or housing insecurity—was meager; its public-health system was languishing after decades of underinvestment; and unlike every other wealthy country, it lacked universal health care. These factors “privatized risk,” Bor and his colleagues wrote in their paper, “tying health more closely to personal wealth and employment.” As labor unions declined and minimum wages stagnated, more Americans had fewer resources to lean on if their health declined. Poorer Americans already lived, on average, shorter lives than rich ones, and that gulf started to widen.

Other particularly American choices exacerbated the stresses on the health of the country’s citizens, again weighing more heavily on less wealthy people. A growing mass-incarceration industry punished them. A deregulatory agenda that began with Ronald Reagan’s administration left them vulnerable to unhealthy foods, workplace hazards, environmental pollutants, guns, and opioids. “America basically says: If you’re poor, you don’t have access to safe choices,” Bor told me.

Factors like social inequalities and frayed social safety nets are the fundamental weaknesses of American society, which more specific problems like opioids, metabolic disorders, and COVID exploit. During the pandemic, for example, poor and minority groups were more likely to be infected because they lived in crowded housing, distrusted medical leaders, and couldn’t work from home or take time off when sick. And instead of addressing these foundational problems, policy makers instead focused on personal responsibility.

America’s drastic underperformance in health also stems from its history of segregation and discrimination. Racist policies have obviously harmed the health of minorities. But as the policy expert Heather McGhee and the physician Jonathan Metzl have independently argued, elites have long marshaled the racial resentment of poor white Americans to undermine support for public goods that would benefit everyone, such as universal health care. Per Frederick Douglass and other Black leaders, “They divided both to conquer each.”

[Read: How public health took part in its own downfall]

COVID, for example, disproportionately killed Black, Latino, and Indigenous Americans—a trend that, when highlighted to white people, reduces their concern about the pandemic and their support for safety measures. But in 2021, young white Americans still died at three times the rate of the average resident of other peer nations, while young Black and Indigenous Americans died at rates five- and eightfold higher, respectively. “There are thousands of racial-disparity studies that compare Black people to white people—but white Americans are a terrible counterfactual,” Bor told me. They’re frogs in the same pot, boiling more slowly but boiling nonetheless. By using them as a baseline, we ignore how “everyone is harmed by the status quo in the U.S.,” Blackstock told me, while also underestimating how dire things really are for people of color. (The same problem applies to income inequality: White Americans living in the richest 1 percent of counties still have higher rates of maternal and infant mortality than the average residents of wealthy countries.)

So, “what happens now?” Bor asked me. “Are we going to have 1 million missing Americans a year, every year, going forward? Or more?” His study doesn’t suggest a reason for optimism, but it does provide a defense against nihilism. The entire concept of missing Americans is rooted in a comparison with other countries, which shows that these early deaths aren’t inevitable. The U.S. could at least start moving in the direction of its peers by adopting policies that work elsewhere, such as universal health care, minimum-wage increases, federally required paid sick leave, and better unemployment insurance.

But “the inability of our politics to generate policies that manage health threats is grim,” Bor said. None of the weaknesses that COVID exposed have been addressed; some, like the chasm-sized health gaps between rich and poor or white and Black, have been widened. Vaccines significantly reduce the risk of dying from COVID, but their power is blunted by low uptake, new variants, the lifting of almost all infection-thwarting protections, and the looming loss of COVID funding. Reactionary laws that hamstring what public-health departments can do in emergencies will make the U.S. vulnerable to the new viruses that will inevitably assault it in future years. America’s already underperforming health-care system has been badly battered by the pandemic, and weakened by waves of health-care-worker resignations. In recent months, the Supreme Court has constrained both gun and carbon-emission regulations, while clearing the road for states to restrict or ban abortions—a move that could easily boost America’s already sky-high maternal mortality rates. The climate is still changing rapidly, exposing people who have no choice but to work outside to the ravages of heat.

As much of the country returns to normal, Bor’s study makes plain what normal actually meant—and, as I wrote in 2020, that normal led to this. “A lot of Americans may be under the impression that we had a bad go of it during COVID, and once the pandemic is over, they can go back to having the best health in the world,” Woolf told me. “That is a gross misconception.”

How to Successfully Smash Your Face Against a Tree

2022-07-14T11:00:00-04:00

In my third year of reporting on the coronavirus pandemic, I find woodpeckers, which can ram their heads against hard surfaces about 20 times a second, to be incredibly relatable. But the birds’ extraordinary behavior raises an obvious question: Why, as one team of scientists wrote in 1976, is the countryside “not littered with dazed and dying woodpeckers”?

The just-as-obvious answer is that woodpecker skulls have adaptations, such as spongy bone in the front of their skulls, that absorb or dissipate the shocks from their pecks, protecting their squishy brains. This explanation features in books, news articles, zoo displays, and scientific papers. “You can’t avoid it,” Sam Van Wassenbergh, a biologist at the University of Antwerp, told me. It’s so accepted that some scientists have tried to work out exactly which parts of the skull absorb shocks, while others have designed helmets and other protective technology inspired by the birds. There’s just one problem: As Van Wassenbergh and his colleagues have now shown, woodpecker heads don’t absorb shocks at all.

Although the shock-absorption idea seems superficially sound, “the more you think about it, the less sense it makes,” Van Wassenbergh said. Woodpeckers peck trees to send messages, dig out hidden insects, and excavate nesting holes; many of their body parts—strong beaks, grasping feet, and stiff, strut-like tails—have evolved to maximize the kinetic energy they deliver with each blow. If their skulls absorbed that energy, they’d just need to pound harder, which would negate any benefits from the absorption. If what you need is a hammer, why strap a cushion onto its head?

To check his suspicions, Van Wassenbergh and his colleagues filmed three woodpecker species as they hammered into wood, using high-speed cameras that could capture 4,000 frames every second. The team then analyzed every frame to see how parts of the birds’ head move relative to one another. If the skull really was absorbing shocks, then upon each peck, the brain should decelerate far less than the beak—just as when a car hits a bump, its body jerks less than its wheels do. But the videos revealed that, in fact, when a woodpecker pecks wood, its entire head, including the brain, comes to a stop at the same rate. (The team used the position of the eye as a proxy for the front of the brain, because the two are jammed closely together in woodpeckers, with little room for movement.) “That really lays to rest the idea that some part of the head is acting as a shock absorber,” Margaret Rubega, an ornithologist at the University of Connecticut who wasn’t involved in the study, told me.

[From the July/August 2022 issue: How animals perceive the world]

Even if woodpeckers did absorb shocks, it wouldn’t help them. Using simulations of a black woodpecker’s head, Van Wassenbergh showed that a shock-absorbing skull would force the bird to spend more energy on pecking for no benefit. As Rubega said, “You don’t use a spring to hammer a nail with.” Instead, you use … well … a hammer, which is what the woodpecker’s head essentially is—a rigid structure that has evolved not to absorb shocks but to preserve them. “This makes intuitive sense,” says Lorna Gibson, an engineer at MIT who has studied woodpeckers and was always skeptical of the shock-absorption idea. “I’m not sure why [it] was accepted.”

The zoological literature is full of similarly false ideas that persisted for years or decades before being corrected: that hummingbirds drink by using their tongues as straws; that cheetahs overheat when hunting; that mantis shrimps have kaleidoscopic rainbow vision; that honey badgers follow birds to honey; or that Komodo dragons kill with bacteria-laden bites. Some of these factoids began as assumptions that somehow calcified into received wisdom without anyone checking them. Others were outright fabrications, or arose from preliminary studies that were exaggerated or overgeneralized. Many are still repeated today.

[Read: Mantis shrimp eyes are totally overrated]

In the case of woodpeckers, few previous studies ever filmed and analyzed live birds, relying solely on digital simulations or observations of their skulls. This is typical of humans’ knowledge of birds: We make a lot of assumptions but do little actual testing. “We have no idea how the stress of pecking, or biting, or anything really, is accommodated by the skull, nor how this varies between species with different skull and beak shapes, diets, and behaviors,” Jen Bright at the University of Hull, in the U.K., told me.

But Van Wassenbergh also suspects that many researchers have been misled by a simple form of anthropomorphism. “It’s logical to think that, if I was this bird, I’d like to have a helmet or an airbag,” he said. But although we use such tools to protect us from unwanted impacts, a woodpecker is trying to smash its face against a tree. Its needs are completely different from ours, which means that features in its skull are probably not analogous to safety equipment. The spongy mass of bone at the front of the skull looks like it could be an airbag—but clearly doesn’t act like one. The long tongue, which, when retracted, wraps around the back of the skull and into the bird’s forehead, looks like a possible seat belt—but, again, clearly isn’t one. Engineers who are looking to woodpecker skulls for inspiration might think twice, Van Wassenbergh told me: “This bird has gone through millions of years of trying to minimize shock absorption … which isn’t what you want in a helmet.”

But if woodpeckers lack some built-in helmet, then how do they peck wood without sustaining traumatic brain injuries? A human who headbutted a tree at woodpecker speed would absolutely be concussed. But we have extremely large brains—a fact that, ironically, we seem to forget. Woodpeckers have smaller and lighter brains than ours, which greatly reduces the pressure that they experience upon each peck. According to Van Wassenbergh’s calculations, a woodpecker would have to hit a tree at twice its normal speed, or peck something four times stiffer than the average tree, to get a concussion. “If by accident they hit a piece of metal, I can still imagine that they’d suffer a concussion, but for their natural behavior, what they do is relatively safe,” he said.

[Read: Hummingbirds are where intuition goes to die]

Van Wassenbergh hasn’t yet checked if woodpeckers have evolved especially small brains for birds of their size, or differently shaped ones: A more spherical brain, he noted, would be better at resisting shocks than an elongated one. The birds may also have adaptations that help them cope with the damage that even subconcussive impacts can create; perhaps their brains have little fluid so that they can’t slosh around too much. Whatever the case, the secret to the woodpecker’s percussive powers appears to be deceptively simple: They just have small brains. Maybe I should try that the next time I’m tempted to smash my face into the nearest solid object.

Is BA.5 the ‘Reinfection Wave’?

2022-07-11T15:36:08-04:00

Updated at 1:17 p.m. ET on July 12, 2022

Well, here we go again. Once more, the ever-changing coronavirus behind COVID-19 is assaulting the United States in a new guise—BA.5, an offshoot of the Omicron variant that devastated the most recent winter. The new variant is spreading quickly, likely because it snakes past some of the immune defenses acquired by vaccinated people, or those infected by earlier variants. Those who have managed to avoid the virus for close to three years will find it a little harder to continue that streak, and some who recently caught COVID are getting it again. “People shouldn’t be surprised if they get infected, and they shouldn’t be surprised if it’s pretty unpleasant,” Stephen Goldstein, a virologist at the University of Utah, told me.

That doesn’t mean we’re about to have a surge on the scale of what we saw last winter, or that BA.5 (and its close cousin BA.4) will set us back to immunological square one. Goldstein told me that he takes “some level of comfort” in the knowledge that, based on how other countries have fared against BA.5, vaccines are still keeping a lot of people out of hospitals, intensive-care units, and morgues. The new variant is not an apocalyptic menace.

But it can’t be ignored, either. Infections (and reinfections) still matter, and by increasing both, BA.5 is extending and deepening the pandemic’s ongoing burden. “We will not prevent all transmission—that is not the goal—but we have to reduce the spread,” Maria Van Kerkhove, an infectious-disease epidemiologist at the World Health Organization, told me. “It’s not over, and we are playing with fire by letting this virus circulate at such intense levels.”

The age of Omicron began shortly after Thanksgiving, as the new variant swept through the U.S., ousting its predecessor, Delta. That initial version of Omicron, now known as BA.1, was just the first of a mini-dynasty of related variants that have since competed against one another in a grim game of succession. BA.2 took over from BA.1, and caused a surge in the spring. BA.4 and BA.5 are spreading even more quickly: First detected in South Africa in January and February, they have since displaced BA.2 all over the world, leading to surges in both cases and hospitalizations. In the U.S., BA.5 now accounts for about 54 percent of all COVID infections, and BA.4, about another 17 percent. (Most of this article will deal with BA.5 alone because it already seems to be outcompeting its cousin.) Hospitalizations have risen to their highest level since March.

You might assume that a new variant gains dominance by being inherently more transmissible than its forerunners. Using that logic, buttressed by some back-of-the-envelope calculations, some commentators have claimed that BA.5 is as transmissible as measles, making it among the most contagious viral diseases in history. But those calculations are “fully wrong,” Trevor Bedford, a virologist at the Fred Hutchinson Cancer Research Center, told me. Variants can spread rapidly without being any better at finding new hosts, as long as they’re better at slipping past those hosts’ immune defenses. That property—immune evasion—likely enabled BA.1 to oust Delta last winter. It might also explain why BA.5 is rising now.

When people are vaccinated or infected, they develop antibodies that can neutralize the coronavirus by sticking to its spike proteins—the studs on its surface that the pathogen uses to recognize and infect our cells. But BA.4 and BA.5 have several mutations that change the shape of their spikes, which, like swords that no longer fit their sheaths, are now unrecognizable to many antibodies that would have disarmed older variants. That’s why, as many studies have now consistently shown, antibodies from triple-vaccinated people, or people who had breakthrough infections with earlier variants, are three to four times less potent at neutralizing BA.4 or BA.5 than BA.1 or BA.2. This means that most people are now less protected against infection than they were two months ago—and that some people who got COVID very recently are getting reinfected now. “I hear from a lot of people who just had COVID in February, March, or April and now have it again,” Anne Hahn, a virologist and immunologist at Yale, told me.

As my colleague Katherine J. Wu has reported, the consequences of reinfections are still unclear. It’s unlikely that each subsequent bout of COVID is worse for an individual than the previous one; this idea has proliferated because of a recent preprint, which really only showed that getting reinfected is worse than not being reinfected. Nor should people worry that, as one viral news article recently suggested, “it is now possible to be reinfected with one of Omicron’s variants every two to three weeks.” BA.5 is different from its forebears but not from itself; although someone could catch the new variant despite having recently had COVID, they’d be very unlikely to get infected again in the near future.

[Read: You are going to get COVID again … and again … and again]

Though previous immunity has been dialed down a few notches, since BA.5 showed up, it hasn’t disappeared entirely. “We’re seeing that new infections are disproportionately people who haven’t been infected before,” Meaghan Kall, an epidemiologist at the U.K. Health Security Agency, told me. About half of those in England who have been infected in the current wave are first-timers, even though they account for just 15 percent of the country’s population. This clearly shows that although reinfections are a serious problem, the population still has some protection against catching even BA.5.

The degree to which the new variant escapes immunity is also a shadow of what we saw last winter, when Omicron first arrived. For comparison, antibodies in vaccinated people were 20 to 40 times worse at neutralizing BA.1 than the original coronavirus. BA.5 reduces their efficiency threefold again—a small gain of sneakiness on top of its predecessor’s dramatic flair for infiltration. “BA.5 is doing what Omicron does but with a marginally more effective immune evasion,” Kall told me. “I don’t believe that it represents a massive paradigm shift.”

Why, then, does it feel like we’re in a reinfection wave right now, with anecdotal reports being prominent in a way they weren’t seven months ago? It’s because Omicron completely changed our baseline. Before its arrival, only a third of Americans had ever experienced COVID. By the end of February, almost 60 percent had. We’re hearing more about reinfections now in part because the number of people who could possibly be reinfected has doubled.

BA.5’s impact on society will differ greatly around the world. Both South Africa and the U.K. have experienced only small rises in hospitalizations and deaths despite surging BA.5 cases, showing that “protection from vaccines against severe disease and death is still really strong,” Kall said. Portugal hasn’t been so lucky, with deaths climbing to levels that approach those of the first Omicron surge. These differences should be expected. On top of their demographic differences, countries are now complicated patchworks of immunity; citizens vary in how many times they’ve been infected or vaccinated, which vaccines they’ve gotten, and which variants they’ve encountered.

Still, it’s possible to predict what might happen as BA.5 ascends in the U.S. by looking at its effective reproduction number, or Rt—the average number of people whom each infected person then infects. The original version of Omicron, BA.1, “came in really hot,” Trevor Bedford told me. With an initial Rt of between 3 and 3.5, he estimates that it infected almost half the country in a few months, including 3 million to 4 million people a day at its peak. (These numbers are higher than the official counts, which have always been underestimates.) BA.2 was less ferocious: With an initial Rt of 1.6, it infected about one in 10 Americans in the spring, and peaked at roughly 500,000 daily infections. BA.4 and BA.5 have a slightly higher Rt but should “mostly mirror the BA.2 epidemic,” Bedford told me. It might not look that way on recent charts of new cases, where the close overlap between BA.4/BA.5’s rise and BA.2’s decline creates “the illusion of a plateau,” Bedford said, but the U.S. is nonetheless experiencing its third Omicron surge. He expects BA.5 to infect 10 to 15 percent of Americans over the next few months.

Of course, it doesn’t have to. The Biden administration, other political leaders, and many media figures have promoted laxer COVID policies, on the grounds that vaccines are still reducing the risk of death and hospitalization. But this stance is foolish for several reasons.

Even if the infection-fatality ratio for COVID—the risk that an infected person will die—falls to the level of seasonal flu, rare events stack up when the virus is allowed to spread unchecked. Bedford estimates that in such a scenario, COVID could still plausibly kill 100,000 Americans every year, “which is a lot!” he said. “It’s not like in the peak of the pandemic, but it’s a major health burden.” That burden is still mainly borne by the elderly; low-income workers; Black, Latino, and Indigenous Americans; and immunocompromised people. The entire Omicron dynasty may well have arisen from chronic infections in immunocompromised patients, in whose bodies the virus can evolve more rapidly, which suggests a self-interested case for preventing infections in this group, along with the more obvious moral rationale.

Death isn’t the only outcome that matters, either. Even without sending people to the hospital, infections can lead to the persistent and in many cases disabling symptoms of long COVID—a risk that vaccines seem to lower but not fully avert. “I’m not worried about dying from COVID, but I’m personally cautious because of worries about long COVID,” Bedford told me. “I’m not a hermit, but I’m taking mitigation measures to try not to get sick.” And even “mild” infections can still be awful. Dan Barouch, an infectious-disease specialist at Harvard Medical School, told me that friends and colleagues have “felt pretty terrible at home, sometimes for weeks, but weren’t sick enough to go to the ICU and get intubated. There’s a lot of time missed from school and work.” Waves of sick employees are still disrupting sectors that were already reeling from the Great Resignation—including the health-care system. An exodus of experienced colleagues and untenable levels of burnout have trapped health-care workers in a chronic state of crisis, which persists even when hospitalization numbers are low, and deepens whenever the numbers climb.

Preventing infections still matters, and vaccines are still a crucial means of doing so. After a frustrating delay, Omicron-specific boosters are on the way, and the FDA has recommended that these include components of BA.4 and BA.5. The updated shots won’t be ready until October at the earliest, by which time new variants could have arisen. But “even if we don’t nail the match exactly,” Goldstein said, these boosters should expand people’s antibody repertoire, leaving them better defended against not just the Omicron dynasty but also other variants that could follow. Still, “it’s important not to overpromise the efficacy of Omicron-specific boosters,” Barouch said. In terms of preventing infections, clinical data suggest that they’ll be modestly better than current vaccines, but not substantially so. And even if we get the long-desired shots that protect against all coronaviruses, it may be difficult to persuade Americans to get them.

Vaccines were never going to end the pandemic on their own. They needed to be complemented by other protective measures such as masks, better ventilation, rapid tests, and social support like paid sick leave, which were either insufficiently deployed or rolled back. And with stalled COVID funding jeopardizing supplies of tests, treatments, and vaccines, the U.S. will continue its long streak of being underprepared for new variants.

Consider BA.2.75, another member of the Omicron family, which has many spike mutations not seen in its cousins. In India, where that subvariant was first identified, it seems to be spreading at a rate double that of BA.5 and comparable to that of BA.1, Bedford told me. This worrying picture is based on a small number of samples, and BA.2.75’s actual pace may be slower. It may also struggle to spread in places like the U.S., where BA.5 already rules. But no matter what happens, this round of variants won’t be the last we contend with.

The belief that viruses inevitably evolve into milder versions is a myth: Such futures are possible but in no way guaranteed. The coronavirus could yet evolve into more severe variants, although vaccines would still be expected to blunt their sting. It could become even more contagious, although the traits that would give it a speed boost, such as higher viral loads or tighter attachments to human cells, can’t ratchet up forever. “It’s already super-transmissible, and there’s not much to gain there,” Anne Hahn told me.

Immune evasion is another matter. The virus is likely now locked with the human immune system in a perpetual evolutionary arms race. A variant emerges to circumvent our existing immunity, then vaccines and infections gradually rebuild our defenses … until another variant emerges. This is exactly what happens with flu, but the coronavirus seems to be changing even more quickly. The big uncertainty is whether the next variants will erode immunity to the small degrees that scientists expect (as BA.5 is doing) or whether they’ll do something dramatic and unexpected (as BA.1 did). This is what “living with COVID” means—a continual cat-and-mouse game that we can choose to play seriously or repeatedly forfeit.

The stakes of that game depend on a very simple question: Should we still care about preventing infections? If the answer is “not so much,” which is the implicit and sometimes explicit posture that America’s leaders have adopted, then BA.5 changes little. But if the answer is “yes,” as I and most of the experts I talk to still believe, then BA.5 is a problem.

This article originally misstated the proportion of people with COVID in England who are first-timers.

America Is Sliding Into the Long Pandemic Defeat

2022-06-27T07:00:00-04:00

In 2018, while reporting on pandemic preparedness in the Democratic Republic of Congo, I heard many people joking about the fictional 15th article of the country’s constitution: Débrouillez-vous, or “Figure it out yourself.” It was a droll and weary acknowledgment that the government won’t save you, and you must make do with the resources you’ve got. The United States is now firmly in the débrouillez-vous era of the COVID-19 pandemic.

Across the country, almost all government efforts to curtail the coronavirus have evaporated. Mask mandates have been lifted on public transit. Conservative lawmakers have hamstrung what public-health departments can do in emergencies. COVID funding remains stalled in Congress, jeopardizing supplies of tests, treatments, and vaccines. The White House and the CDC have framed COVID as a problem for individuals to act upon—but action is hard when cases and hospitalizations are underestimated, many testing sites have closed, and rose-tinted CDC guidelines downplay the coronavirus’s unchecked spread. Many policy makers have moved on: “We’re heading into the midterms, and I think there’s a real desire to show confidence that they’ve solved this,” Céline Gounder, an infectious-disease specialist and the editor at large for public health at Kaiser Health News, told me.

But COVID is far from solved. The coronavirus is still mutating. Even at one of the lowest death rates of the pandemic, it still claims the lives of hundreds of Americans daily, killing more than twice as many people as die, on average, in car accidents. Its costs are still disproportionately borne by millions of long-haulers; immunocompromised people; workers who still face unsafe working conditions; and Black, Latino, and Indigenous Americans, who are still dying at higher rates than white Americans. When Kirsten Bibbins-Domingo, an epidemiologist and physician at UC San Francisco, works with low-income, Black, and Latino communities in the Bay Area, their concerns are less about returning to normal and more about “how to keep themselves safe,” she told me. “Take it from a tuberculosis activist that you can lose political will, public attention, and scientific momentum and still have a disease that kills over a million people each year,” Mike Frick of the Treatment Action Group told me. “We’re seeing the TB-ification of COVID start.”

For any disease, there is a moral case against neglecting those who are most vulnerable; for COVID, there’s also still a self-interested case for even the privileged and powerful to resist the pull of neglect. For more than a year, the U.S. has focused on using vaccines and drugs to avert severe disease and death, while deprioritizing other means of preventing infections, such as masks and ventilation. To a degree, this strategy is working: Cases and hospitalizations recently spiked again, while ICU admissions rose gently and deaths have remained stable. And yet, infections still matter, and are affecting all of American society, including the vaxxed-and-done. The coronavirus periodically takes waves of educators and health-care workers out of action; the entire health-care system is now perpetually overburdened and unable to provide its former standard of care. People are still being disabled by long COVID, often without ever landing in the hospital. And uncontrolled infections are a gift to the virus, which keeps birthing new variants that could prolong the current level of crisis or send it spiraling back into a greater level of disruption.

Many sensible policies—say, mask mandates that toggle on in grocery stores, public transport, and other essential spaces when community transmission is high—seem unlikely in this political climate. What, then, is still on the table? Right now, “I feel like I’m screaming into the wind,” Matifadza Hlatshwayo Davis, the health director for St. Louis, told me. But while others get to simply say “We’re screwed” and move on, she said, “I have to drive into work and figure it out.” Débrouillez-vous, indeed.

I have interviewed dozens of other local officials, community organizers, and grassroots groups who are also swimming furiously against the tide of governmental apathy to push some pandemic response forward, even if incrementally. This is an endeavor that all of American society would benefit from; it is currently concentrated among a network of exhausted individuals who are trying to figure out this pandemic, while living up to public health’s central tenet: Protect the health of all people, and the most vulnerable especially. The late Paul Farmer, who devoted his life to providing health care to the world’s poorest people, understood that when doing such work, victories would be hard-won, if ever won at all. Referencing a line from The Lord of the Rings, he once said, “I have fought the long defeat.” In the third year of the COVID pandemic, that fight will determine how America fares against the variants and viruses still to come.

In a study of 177 countries, people’s level of trust—in the government and especially in one another—predicted COVID infection rates and vaccine uptake. In America, trust is in short supply, and accordingly, the country has underperformed throughout the pandemic despite its considerable resources. This problem is getting worse: A poll from January found that only 44 percent of respondents trusted the CDC’s statements on COVID, down from 55 percent in 2020—a decline that spanned the political spectrum.

As the pandemic has revealed, even powerful biomedical tools such as vaccines sputter in practice if disadvantaged people can’t access them, or if distrusting people refuse to use them. America’s recurring mistake is to create such technofixes at warp speed, while neglecting the systems that actually deploy those tools. Those systems—the country’s social infrastructure—are so porous that a multitude of smaller projects are necessary to patch each and every hole. Once lost, trust is hard to regain at scale. But it can slowly be rebuilt.

America actually has an entire workforce that specializes in earning trust: community health workers. They’re hired for their empathy, their strong local ties, and their personal experience with hardship. Breanna Burke, a community health worker in Bristol, Tennessee, where she has lived since she was 3, told me that her job is to “get to the root cause of ongoing health issues,” with the understanding that a person’s circumstances constrain their choices. For example, she helped one of her diabetic clients plan a budget to keep their power on so they could keep their insulin cold; another time, she figured out that a patient whose pain wouldn’t stop had been sleeping on a hardwood floor for nine months, and contacted a local women’s club to raise money for a mattress.

When COVID hit, Burke provided people with emergency food supplies so they could weather quarantine in safety, and talked others through their hesitancy over getting vaccinated. She can do that because her nonjudgmental approach and shared life experience make her trustworthy—the secret to community health workers’ extraordinary effectiveness. In three randomized trials involving people living in poor parts of Philadelphia, Shreya Kangovi, a physician at the University of Pennsylvania, showed that people who see community health workers spend 66 percent fewer days in the hospital than those who receive usual care. In her research, Kangovi also found that every dollar invested in said workers returns $2.47 to the average Medicaid payer. If their work on COVID prevention fulfills even part of that promise, it could be a crucial lifeline for the badly stretched health-care system.

Such efforts are part of a long-standing tradition. In the early 20th century, public health was a broader enterprise than it is now. It included not just physicians and scientists, but also labor-union leaders, housing reformers, and social activists, who attempted to right big societal problems such as unsafe workplaces and dilapidated neighborhoods. Even as the field professionalized, pockets of people with no official qualifications repeatedly stepped up to protect their communities’ health. Alongside their more radical activities, the Black Panther Party and the Young Lords provided vital health services for Black and Puerto Rican communities in the 1970s. In the ’80s and ’90s, ACT UP—the AIDS Coalition to Unleash Power—fought for the creation of HIV treatments, and changed the legal definition of AIDS and the way the FDA approved new drugs.

More recently, Stephen B. Thomas, a health-policy professor at the University of Maryland who has turned Black barbers and stylists into health-care advocates, worked with those shops and salons to provide COVID vaccines. And in early 2021, the sociologist Elizabeth Wrigley-Field and a small group of volunteers began setting up their own vaccination events at local mosques, for the many East African refugee and immigrant families in their neighborhood of Seward, Minnesota. The community had been heavily targeted with vaccine misinformation for more than a decade, but the group, the Seward Vaccine Equity Project, included trusted local figures—Inari Mohammed, an Oromo epidemiology student and long-standing member of a neighborhood mosque; Saida Mohamed, a gregarious Somali pharmacy owner whose store doubles as a social hub; and Ramla Bile, an experienced Somali civil-rights organizer. They identified local leaders, including a soccer coach and a local union staffer, and recruited attendees through conversations at Section 8 house towers and immigrant-owned small businesses. Ultimately, they delivered more than 500 vaccine doses. That might seem insignificant when 73 million Americans remain unvaccinated, but several hundred Seward residents are now substantially safer, which Wrigley-Field counts as a win.

The impact of community work can feel small in the face of a pandemic’s scale, as if people are merely mopping up the stragglers left behind by national initiatives. In fact, such work is foundational. It creates a bedrock of trust and solidarity, without which public health cannot operate. The problem isn’t that community work is trivial; it’s that there hasn’t been enough of it. And for many of the people I spoke with, such work acts as a vaccine against nihilism. The pandemic has fostered beliefs that people are inherently selfish or permanently polarized. Neither is true, Wrigley-Field told me: Despite the persistent myth that unvaccinated people today are all unreachable holdouts, “every time we organize an event, people come,” she said. She and her team were still giving people their first doses this January. Her goal is now simple: “Do something that helps, even when it’s very small,” she said. “I believe that doing the small stuff now is setting us up for bigger things.”

Going bigger means ultimately compelling state or federal governments to commit to some kind of sustained COVID response. Over the past two years, tranches of concerned Americans have begun to coalesce into new interest groups, for whom public health is a top priority, to push for better pandemic protections. Public-health professionals often lament that the field has been consistently underfunded because it lacks a vocal constituency. But as the historian Amy Fairchild of Ohio State University and her colleagues have noted, public health had more political power in the early 20th century, partly because it allied itself with a broader coalition of organizations. It now has a rare chance to rebuild those alliances.

After Kristin Urquiza’s father died of COVID in June 2020, she founded the nonprofit Marked by COVID—a group of activists united in their grief and their desire to permanently memorialize America’s 1-million-plus COVID deaths. The group now has about 100,000 members, Urquiza told me. In 2017, when the longtime activist Paul Davis helped coordinate a nationwide campaign to save the Affordable Care Act, he thought his database of 7,000 people was “huge,” he told me. Now he is the policy director of Right to Health Action, an advocacy group that formed in the spring of 2020, and his database of COVID activists “is about 150,000,” he said. Other groups represent the millions of long-haulers who have been wrestling with the debilitating symptoms of long COVID, or communities that have been disproportionately harmed by the pandemic. A mixed team of public-health practitioners, health-care workers, educators, and others created the People’s CDC to “push back on harmful narratives that we don’t need COVID protections,” such as testing and masks, Lucky Tran, an activist and a science communicator, told me.

Though disparate, these groups share many qualities. Many feel abandoned by their government. Many feel that they cannot return to “normal,” and that a better normal can be fashioned instead. Many aren’t interested in shaming people over individual choices, but want structural changes that will make society safer for everyone. And most, to be blunt, are really pissed. In this, they could be successors to ACT UP, which was immensely effective despite staying relatively small: “A few thousand people were able to win lifesaving AIDS treatments for millions,” Davis, who is an ACT UP alumnus, told me. The pandemic activists he now works with dwarf that old community in numbers, and to his mind are just as motivated. Long-haulers have already won important victories, including pressing institutions such as the World Health Organization and the CDC to formally recognize long COVID, and so securing substantial research dollars for long-COVID research from the National Institutes of Health and private philanthropists. Their symptoms often keep them depleted physically and mentally, but although this work only adds to their strain, they feel they have no choice but to do it. “Our pain, grief, and disability isn’t going away,” Lisa McCorkell, a long-COVID advocate and co-founder of the Patient-Led Research Collaborative, told me.

Groups of impassioned but inexperienced activists can often struggle to do little beyond merely existing. Achieving power in the U.S. requires more than angry individuals, Jane McAlevey, an organizer and the author of A Collective Bargain, told me; it needs “a well-built organization that can actually channel people’s rage effectively,” she said. ACT UP did that by drawing wisdom from its predecessors, and becoming “involved with basically every community that was vulnerable at the time,” as the historian Sarah Schulman once said. Similarly, several of the newly formed pandemic groups have already started working with one another, veterans of ACT UP, organizations advocating for chronic illnesses like myalgic encephalomyelitis, and health-care workers’, teachers’, and labor unions.

These groups vary considerably in their goals, which include permanent COVID memorials, better funding for long COVID, global vaccine equity, and more. These goals aren’t mutually exclusive, but the protoplasmic coalition still “needs a skeleton, an organizing principle to tie it together,” Gregg Gonsalves, a Yale epidemiologist and ACT UP alumnus, told me. That could be as simple as a push for a robust public-health system that centers the needs of the most vulnerable people. ACT UP achieved its many concrete victories without insisting that its members conform to specific messages, uniting instead around the idea that HIV deserved more public attention.

Building a stronger public-health system demands an unfettering of the moral imagination: Americans need to believe that their government should invest in systems that keep everyone safer from disease—and to trust that such systems are even possible. But throughout his decades-long career, Gonsalves has witnessed social safety nets being repeatedly shredded, leading to “a collapse of any faith in the state to do good,” he told me. That faith eroded further when public institutions buckled during the pandemic, and when two successive administrations failed to control the coronavirus. The resulting “pandemic fatigue” is not just a craving for the status quo, but a deep cynicism over the possibility of something better. In one study, most Americans preferred a better, fairer post-pandemic future, but mistakenly thought a “back-to-normal” one was more popular—and so more likely. “People can imagine a world with crypto-banking and the metaverse, so why is it so hard to imagine a world with less disease and death?” Céline Gounder of Kaiser Health News said.

Even in the débrouillez-vous era, the nascent COVID constituency can still push for big policies that would prevent disadvantaged groups from suffering a disproportionate burden of disease and death. In December 2021, as Omicron swept the U.S., then–White House Press Secretary Jen Psaki replied sarcastically when a reporter asked why rapid tests weren’t widely available. “Should we just send one to every American?” Psaki said. But after two weeks of public outcry, the administration announced plans to do just that. To date, every household has been able to order up to 16 free tests—still insufficient, months too late, but invaluable nonetheless for families that can’t afford these expensive products. Several people I talked with mentioned the rapid-test turnaround as a rare and recent example of a positive, nationwide pandemic policy—and a sign that such policies are still achievable.

Similarly, the government could still promote the use of masks even if it won’t mandate them when the risk of transmission is high. In the 2000s, as HIV faded from public concern, health departments responded by making condoms as accessible as possible; New York City alone distributes tens of millions every year to bars and nightclubs. As Jay Varma, a physician at Weill Cornell Medicine who advised the New York City mayor’s office during the pandemic’s first year, has suggested, states and cities could follow the same playbook now, flooding public indoor spaces with free, high-quality masks, such as KF94s, KN95s, or N95s. Doron Dorfman, a disability-law expert at Syracuse University College of Law, is also leveraging the court system in favor of masking. He argues that requiring people to wear masks around immunocompromised students or employees—who may still have higher risks of infection and illness despite being vaccinated—counts as a reasonable accommodation under the Americans With Disabilities Act; the Eighth Circuit Court of Appeals accepted this argument, as did a federal district court in Virginia.

“Even if you get crumbs from the federal government, the scale is such that even crumbs save a lot of lives,” Matthew Cortland, a disabled policy analyst and lawyer at Data for Progress, told me. Cortland and others see the greatest potential in improving the air we breathe. The coronavirus spreads primarily through shared air, making indoor spaces riskier than outdoor ones. After misguidedly focusing on surface-cleaning hygiene theater, both the government and industry leaders are now starting to grasp the importance of ventilation and filtration. The White House has launched a Clean Air in Buildings Challenge (but falls short of actually mandating businesses to take action or providing dedicated funding). Varma and Cortland have both pitched officials the idea of assigning public buildings letter grades for air quality, just as there are grades for food safety in restaurants; that would tell immunocompromised people which essential spaces are safer in the absence of mask mandates. “People really like being able to breathe! Across the political spectrum!” Cortland told me, dryly. What’s missing, Cortland said, are detailed checklists of the kind that tell businesses how to make physical spaces accessible to disabled people; nothing similar exists for indoor air. “Businesses are telling me they need granular guidance, and it’s not there,” Cortland said. “But it could be.”

Cities and counties can also act in the face of sluggish national policy. The antiviral Paxlovid is effective only when taken shortly after symptoms first appear, so New York City created a free, same-day home-delivery system for the drug, and the city’s hotline also works for people who don’t have a regular doctor. Manhattan Borough President Mark Levine has been working on COVID safety bags—tests, high-quality masks, and Paxlovid information—that can be sent to every home or distributed via community groups. Alameda County, in California, recently reinstated an indoor mask mandate because of growing hospitalizations, and other left-leaning areas could follow suit: Polling by Data for Progress found that 80 percent of Democratic voters support mask mandates on public transportation, for instance. “Maybe that’s a place where local public-health activism can make an impact,” Cortland told me.

Activist groups can also push for grander upgrades to the U.S. public-health system, and longer-term funding to safeguard them. During the pandemic, the U.S. plastered over the wounds of its bleeding institutions with “taped-together systems of volunteers” and temporary scale-ups of important services such as testing and contact tracing, Amy Kapczynski, a global-health expert at Yale Law School, told me. When these Band-Aids fall off, the wounds beneath them reopen. What the U.S. needs, instead, is to rebuild its “infrastructure of care,” Kapczynski said, so that its epidemic responses aren’t subject to boom-and-bust cycles of emergency funding, and so that vulnerable populations aren’t left in the lurch whenever attention and resources wane.

It could, for example, massively expand its corps of community health workers, who are often overlooked because they “tend to be rural people, people of color, and women, without a lot of letters behind their name,” Kangovi, the UPenn physician, told me. In the U.S. there are just 61,000 of them, in contrast to roughly 1 million physicians—a ratio indicative of a health-care system that “waits for people to get sick and feeds them to us to make a livelihood off of,” Kangovi said. For years, doctors and nurses have been called frontline workers, and therein lies the problem: If emergency rooms are the front lines of a nation’s pandemic response, that response has already failed. The real front lines are in people’s homes—the places where community health workers operate.

The Biden administration has committed $226.5 million to training another 13,000 community health workers, which still feels insufficient for a country that spent $4.1 trillion on health care in 2020. Had a bigger system been in place before COVID arrived, “it would have made a real difference,” Kapczynski said, echoing many others I interviewed. Several of America’s biggest pandemic problems—plateauing vaccination rates, the mental-health toll, the erosion of trust—are exactly the problems that community health workers are good at solving. Scaling up their numbers could effectively be an Operation Warp Speed for trust—a way of making face-to-face solutions work at a national scale.

The débrouillez-vous phase of the pandemic will be as patchwork as those that preceded it. And there are limits to what local officials can do in the absence of “anything even remotely resembling a national coordinated response,” Lindsay Wiley, a health law expert at UCLA, told me. Philadelphia, for example, reinstated an indoor mask mandate in April as local case numbers rose, only to rescind it four days later. There used to be “a clear understanding that locals would implement the CDC’s guidance in a way that worked best in their community,” Theresa Chapple, a local public-health official in the Chicagoland area, told me. “Now, if you’re doing anything different, it’s seen as going against the CDC.” Matifadza Davis, the St. Louis health director, told me the city has the authority to reinstate a mask mandate, but that it’s hard to use that power when surrounding counties won’t—or risk being sued by the state’s attorney general if they try. “Getting sued like that is exhausting, and we have a country full of health officials who’ve spent years dealing with lawyers and judges,” Wiley said. “There’s a chilling effect.”

States also can’t spend at a deficit; only the federal government can. Only federal leaders have the power and pockets to approve new vaccines and buy them at scale; to distribute vaccines to poorer countries that still desperately need them; to force a systematic improvement in indoor air; to push for universal paid sick leave and other measures that would allow vulnerable workers to protect their health without risking their income; and to truly create what the U.S. so sorely needs—a sustainable infrastructure that can keep more people from getting COVID, regardless of their social circumstances.

Such a world is always possible. The 1960s and ’70s saw a bloom of bold public-health initiatives—the passage of the Clean Air Act, the Clean Water Act, Medicare, and Medicaid, and the creation of the Environmental Protection Agency, the Occupational Health and Safety Administration, and what are now called federally qualified health centers. Upcoming decades could still witness a similar blooming.

“What’s standing in the way? It’s our political will—the way we think about our society and ourselves,” Beatrice Adler-Bolton, who co-hosts Death Panel, a podcast about the political economy of health, told me. “As we’ve gone through the pandemic, and our hope for policies has been ratcheted down, there still needs to be room for big ideas.” As a disabled person who studies disability, she has had to repeatedly renew her own sense of worth in the face of social structures that dismiss her value. That has made her practiced at hoping and calling for transformative policies. She echoes the organizer and abolitionist Mariame Kaba in saying “hope is a discipline”—not a fuzzy emotion, but the product of effortful work. And “in the process of imagining what could be better, I find hope,” Adler-Bolton said.

Will These Be the Last Polar Bears on Earth?

2022-06-16T14:00:00-04:00

The last surviving member of a species—the individual whose death brings extinction—is called an endling. Those individuals can sometimes be identified, even named. Many more of them live and die unseen. For example, archaeological evidence shows that the woolly mammoth endling lived about 4,000 years ago on Wrangel Island, 87 miles off the coast of Siberia. Mammoths survived there for millennia after the rest of their kind were wiped out by changing climate and human hunters. But eventually, through some combination of factors, including extreme weather events and harmful mutations acquired through heavy inbreeding, they also perished. I thought about them as I listened to Kristin Laidre talking about polar bears.

Laidre, who is an ecologist at the University of Washington, has identified a unique group of polar bears that lives in Greenland’s southeastern tip. Genetically isolated from other populations, the bears’ habits make them less dependent on sea ice—the floating, frozen platforms on which most polar bears hunt, travel, and raise their young. As sea ice disappears, so do the polar bears’ odds of survival. Those in Southeast Greenland seem better suited to a warming world, and could persist while the rest of the Arctic becomes uninhabitable.

“Does this mean polar bears are saved?” Laidre told me. “It doesn’t.” Like the Wrangel mammoths, they might outlast others of their kind, but they won’t hold out forever. Perhaps Southeast Greenland is simply the place where the polar-bear endling will live out its species’ final days.

[Read: The last of its kind]

About 26,000 polar bears are left in the wild, divided into 19 subpopulations that live in different corners of the Arctic. One of these subpopulations lives along 2,000 miles of mostly uninhabited coastline in East Greenland, and had never been properly studied. In 2011, Laidre and her colleagues began a decade-long effort to count these bears so the Greenland government could set conservation goals and subsistence-hunting quotas. Following talks with local subsistence hunters, the team began systematically working its way along the coast.

The researchers hit Southeast Greenland in 2015, mostly to be thorough. A very fast current rips down Greenland’s eastern flank, filling the southeast with small and sparsely packed ice floes—“a difficult landscape for a polar bear to use,” Laidre told me. She and her colleagues guessed that some bears might live in the region’s fjords, but “I remember flying into one and expecting not to see very much,” Laidre said. “Within 10 minutes, we saw six bears all within a few kilometers of each other.” On a normal bear-spotting flight, she’d expect to see one every hour or so. What were so many polar bears doing in a place that should be mostly bear-free?

That first trip was short-lived, but Laidre knew she had to go back, even though Southeast Greenland has volatile weather, a harsh coastline, almost no human settlements, and no spots for fuel or food. To work there, the researchers buried barrels of fuel along the snowy coastline, creating makeshift depots that a helicopter could hopscotch between. When they found polar bears, they’d tranquilize them from the moving helicopter, collect physical measurements and tissue samples, and (if the bear was an adult female) fit a tracking collar.

[Read: What scientists learned from strapping a camera to a polar bear]

Usually, the team commuted from a base two hours away. But one evening, the scientists decided to sleep in an abandoned mining camp, with the aim of starting the next day nearer the animals. They got their wish: That night, Laidre heard the sound of large paws treading on squeaky snow, and woke to find … a polar bear running off with her bag of polar-bear-tissue samples. She exited the camp, pursuing the bear while banging a metal spoon against a frying pan. It dropped the precious bag and fled. “Then we realized it also had taken a few bites of our helicopter,” she told me.

From the hard-won data, the team realized that “these are seriously local bears,” Laidre said. Although polar bears usually roam over large distances, those in Southeast Greenland stay in the same fjord for years. Even when they accidentally got caught in the rapid eastern current and were swept off to the south, they’d just swim to shore and trundle back to the same fjord they started from. Their homebody instincts are so strong that they never interact with bears that live further up the coast. It’s as if an invisible wall at 64 degrees north separates the southeast bears from their northeast cousins.

The bears’ DNA told the same story. “Polar bears are remarkably genetically similar to each other,” Beth Shapiro, an evolutionary biologist at UC Santa Cruz, told me. But the Southeast Greenland bears are so distinct from the 19 known subpopulations that when Shapiro’s team first analyzed the samples that Laidre had collected, “we thought we’d done something wrong,” she said. These are the most genetically isolated polar bears in the world—a 20th subpopulation that’s been mostly self-contained in a corner of Greenland for a few hundred years, and possibly longer.

Like all other polar bears, those in Southeast Greenland use sea ice as platforms from which they hunt seals. That ice is available for only about 100 days of the year, which isn’t enough. But at other times, the bears can survive because of the unusual landscape they inhabit: In lieu of sea ice, they use freshwater icebergs that are funneled into the fjord by a glacier. This “glacial mélange” is the secret of their survival, at least for now. In other parts of the Arctic, polar bears might enjoy almost twice as many ice-covered days in a year, but they’re still faring poorly “because once that ice is gone, they don’t have access to an alternative,” Laidre said.

[Photos: A visit to Churchill, Manitoba, during polar-bear season]

The Southeast Greenland polar bears are “bears of the future,” Laidre added. As the Arctic warms, the number of ice-free days will increase, and more polar bears will experience the same conditions that their Southeast Greenland counterparts currently face. Most won’t have a glacial backup, and will die. If carbon emissions continue along their current course, nearly all of the subpopulations will likely be wiped out by the end of this century. The Southeast Greenland subpopulation is “an example of what may happen in a warming Arctic, as the bears persist in smaller groups in smaller areas at the fringes of their range, and become progressively more isolated, with increasing inbreeding over time,” Andrew Derocher, a polar-bear researcher at the University of Alberta, told me.

“This shouldn’t be spun as ‘Somehow, glaciers will save polar bears,’” Laidre said. Most populations don’t have access to glacier fronts, and besides, glaciers “are in retreat essentially everywhere in Greenland,” John Whiteman, the chief research scientist at Polar Bears International, told me. That’s one reason “it’s highly unlikely,” Derocher said, that even the Southeast Greenland bears will “persist far into the future with the warming that is predicted.” There also aren’t enough of them to sustain a thriving population, and their birth rates are already worryingly low. Inbreeding might eventually riddle them with genetic problems.

“I don’t think it’s totally hopeless for polar bears, but we need strong action to limit human-caused climate change if we want to save them,” Laidre said. Otherwise, the Southeast Greenland population could be the modern equivalent of the Wrangel Island mammoths—the last survivors of a world that no longer has a place for them.

How Animals Perceive the World

2022-06-13T06:00:00-04:00

Photographs by Shayan Asgharnia

This article was featured in One Story to Read Today, a newsletter in which our editors recommend a single must-read from The Atlantic, Monday through Friday. Sign up for it here.

Within the 310,000 acres of Wyoming’s Grand Teton National Park, one of the largest parking lots is in the village of Colter Bay. Beyond the lot’s far edge, nestled among some trees, is a foul-smelling sewage-pumping station that Jesse Barber, a sensory ecologist at Boise State University, calls the Shiterator. On this particular night, sitting quietly within a crevice beneath the building’s metal awning and illuminated by Barber’s flashlight, is a little brown bat. A white device the size of a rice grain is attached to the bat’s back. “That’s the radio tag,” Barber tells me. He’d previously affixed it to the bat so that he could track its movements, and tonight he has returned to tag a few more.

From inside the Shiterator, I can hear the chirps of other roosting bats. As the sun sets, they start to emerge. A few become entangled in the large net Barber has strung between two trees. He frees a bat, and Hunter Cole, one of his students, carefully examines it to check that it’s healthy and heavy enough to carry a tag. Once satisfied, Cole daubs a spot of surgical cement between its shoulder blades and attaches the tiny device. “It’s a little bit of an art project, the tagging of a bat,” Barber tells me. After a few minutes, Cole places the bat on the trunk of the nearest tree. It crawls upward and takes off, carrying $175 worth of radio equipment into the woods.

I watch as the team examines another bat, which opens its mouth and exposes its surprisingly long teeth. This isn’t an aggressive display; it only looks like one. The bat is unleashing a stream of short, ultrasonic pulses from its mouth, which are too high-pitched for me to hear. Bats, however, can hear ultrasound, and by listening for the returning echoes, they can detect and locate objects around them.

Echolocation is the primary means through which most bats navigate and hunt. Only two animal groups are known to have perfected the ability: toothed whales (such as dolphins, orcas, and sperm whales) and bats. Echolocation differs from human senses because it involves putting energy into the environment. Eyes scan, noses sniff, and fingers press, but these sense organs are always picking up stimuli that already exist in the wider world. By contrast, an echolocating bat creates the stimulus that it later detects. Echolocation is a way of tricking your surroundings into revealing themselves. A bat says “Marco,” and its surroundings can’t help but say “Polo.”

[Join us: Ed Yong and Clint Smith in conversation at Sixth and I]

The basic process seems straightforward, but its details are extraordinary. High-pitched sounds quickly lose energy in air, so bats must scream to make calls that are strong enough to return audible echoes. To avoid deafening themselves, bats contract the muscles in their ears in time with their calls, desensitizing their hearing with every shout and restoring it in time for the echo. Each echo provides a snapshot in time, so bats must update their calls quickly to track fast-moving insects; fortunately, their vocal muscles are the fastest known muscles in any mammal, releasing up to 200 pulses a second. A bat’s nervous system is so sensitive that it can detect differences in echo delay of just one- or two-millionths of a second, which translates to a physical distance of less than a millimeter. A bat thus gauges the distance to an insect with far more precision than humans can.

Echolocation’s main weakness is its short range: Some bats can detect small moths from about six to nine yards away. But they can do so in darkness so total that vision simply doesn’t work. Even in pitch-blackness, bats can skirt around branches and pluck minuscule insects from the sky. Of course, bats are not the only animals that hunt nocturnally. In the Tetons, as I watch Barber tagging bats, mosquitoes bite me through my shirt, attracted by the smell of the carbon dioxide on my breath. While I itch, an owl flies overhead, tracking its prey using a radar dish of stiff facial feathers that funnel sound toward its ears. These creatures have all evolved senses that allow them to thrive in the dark. But the dark is disappearing.

A big brown bat’s ability to echolocate allows it to thrive in the dark. (Shayan Asgharnia for The Atlantic)

Barber is one of a growing number of sensory biologists who fear that humans are polluting the world with too much light, to the detriment of other species. Even here, in the middle of a national park, light from human technology intrudes upon the darkness. It spews forth from the headlights of passing vehicles, from the fluorescent bulbs of the visitor center, and from the lampposts encircling the parked cars. “The parking lot is lit up like a Walmart because no one thought about the implications for wildlife,” Barber says.

Many flying insects are fatally attracted to streetlights, mistaking them for celestial lights and hovering below them until they succumb to exhaustion. Some bats exploit their confusion, feasting on the disoriented swarms. Other, slower-moving species, including the little brown bats that Barber tagged, stay clear of the light, perhaps because it makes them easier prey for owls. Lights reshape animal communities, drawing some in and pushing others away, with consequences that are hard to predict.

To determine the effect of light on the bats of Grand Teton, Barber persuaded the National Park Service to let him try an unusual experiment. In 2019, he refitted all 32 streetlights in the Colter Bay parking lot with special bulbs that can change color. They can produce either white light, which strongly affects the behavior of insects and bats, or red light, which doesn’t seem to. Every few days during my visit, Barber’s team flips their color. Funnel-shaped traps hanging below the lamps collect the gathering insects, while radio transponders pick up the signals from the tagged bats. These data should reveal how normal white lights affect the local animals, and whether red lights can help rewild the night sky.

Cole gives me a little demonstration by flipping the lights to red. At first, the parking lot looks disquietingly infernal, as if we have stepped into a horror movie. But as my eyes adjust, the red hues feel less dramatic and become almost pleasant. It is amazing how much we can still see. The cars and the surrounding foliage are all visible. I look up and notice that fewer insects seem to be gathered beneath the lamps. I look up even farther and see the stripe of the Milky Way cutting across the sky. It’s an achingly beautiful sight, one I have never seen before in the Northern Hemisphere.

Every animal is enclosed within its own sensory bubble, perceiving but a tiny sliver of an immense world. There is a wonderful word for this sensory bubble—Umwelt. It was defined and popularized by the Baltic German zoologist Jakob von Uexküll in 1909. Umwelt comes from the German word for “environment,” but Uexküll didn’t use it to refer to an animal’s surroundings. Instead, an Umwelt is specifically the part of those surroundings that an animal can sense and experience—its perceptual world. A tick, questing for mammalian blood, cares about body heat, the touch of hair, and the odor of butyric acid that emanates from skin. It doesn’t care about other stimuli, and probably doesn’t know that they exist. Every Umwelt is limited; it just doesn’t feel that way. Each one feels all-encompassing to those who experience it. Our Umwelt is all we know, and so we easily mistake it for all there is to know. This is an illusion that every creature shares.

[Read: An ingenious injection can create infrared vision]

Humans, however, possess the unique capacity to appreciate the Umwelten of other species, and through centuries of effort, we have learned much about those sensory worlds. But in the time it took us to accumulate that knowledge, we have radically remolded those worlds. Much of the devastation that we have wrought is by now familiar. We have changed the climate and acidified the oceans. We have shuffled wildlife across continents, replacing indigenous species with invasive ones. We have instigated what some scientists have called an era of “biological annihilation,” comparable to the five great mass-extinction events of prehistory. But we have also filled the silence with noise and the night with light. This often ignored phenomenon is called sensory pollution—human-made stimuli that interfere with the senses of other species. By barraging different animals with stimuli of our own making, we have forced them to live in our Umwelt. We have distracted them from what they actually need to sense, drowned out the cues they depend upon, and lured them into sensory traps. All of this is capable of doing catastrophic damage.

A sea turtle’s hatchlings can be diverted away from the sea by artificial lights. For mice, human-made noise
can mask the sounds of predators. (Shayan Asgharnia for The Atlantic)

In 2001, the astronomer Pierantonio Cinzano and his colleagues created the first global atlas of light pollution. They calculated that two-thirds of the world’s population lived in light-polluted areas, where the nights were at least 10 percent brighter than natural darkness. About 40 percent of humankind is permanently bathed in the equivalent of perpetual moonlight, and about 25 percent constantly experiences an artificial twilight that exceeds the illumination of a full moon. “‘Night’ never really comes for them,” the researchers wrote. In 2016, when the team updated the atlas, it found that the problem had become even worse. By then, about 83 percent of people—including more than 99 percent of Americans and Europeans—were under light-polluted skies. More than a third of humanity, and almost 80 percent of North Americans, can no longer see the Milky Way. “The thought of light traveling billions of years from distant galaxies only to be washed out in the last billionth of a second by the glow from the nearest strip mall depresses me to no end,” the visual ecologist Sönke Johnsen once wrote.

At Colter Bay, Cole flips the lights from red back to white and I wince. The extra illumination feels harsh and unpleasant. The stars seem fainter now. Sensory pollution is the pollution of disconnection. It detaches us from the cosmos. It drowns out the stimuli that link animals to their surroundings and to one another. In making the planet brighter and louder, we have endangered sensory environments for countless species in ways that are less viscerally galling than clear-cut rain forests and bleached coral reefs but no less tragic. That must now change. We can still save the quiet and preserve the dark.

Every year on September 11, the sky above New York City is pierced by two columns of intense blue light. This annual art installation, known as Tribute in Light, commemorates the terrorist attacks of 2001, with the ascending beams standing in for the fallen Twin Towers. Each is produced by 44 xenon bulbs with 7,000-watt intensities. Their light can be seen from 60 miles away. From closer up, onlookers often notice small flecks, dancing amid the beams like gentle flurries of snow. Those flecks are birds. Thousands of them.

This annual ritual unfortunately occurs during the autumn migratory season, when billions of small songbirds undertake long flights through North American skies. Navigating under cover of darkness, they fly in such large numbers that they show up on radar. By analyzing meteorological radar images, Benjamin Van Doren showed that Tribute in Light, across seven nights of operation, waylaid about 1.1 million birds. The beams reach so high that even at altitudes of several miles, passing birds are drawn into them. Warblers and other small species congregate within the light at up to 150 times their normal density levels. They circle slowly, as if trapped in an incorporeal cage. They call frequently and intensely. They occasionally crash into nearby buildings.

Migrations are grueling affairs that push small birds to their physiological limit. Even a night-long detour can sap their energy reserves to fatal effect. So whenever 1,000 or more birds are caught within Tribute in Light, the bulbs are turned off for 20 minutes to let the birds regain their bearing. But that’s just one source of light among many, and though intense and vertical, it shines only once a year. At other times, light pours out of sports stadiums and tourist attractions, oil rigs and office buildings. It pushes back the dark and pulls in migrating birds.

In 1886, shortly after Thomas Edison commercialized the electric light bulb, about 1,000 birds died after colliding with illuminated towers in Decatur, Illinois. More than a century later, the environmental scientist Travis Longcore and his colleagues calculated that almost 7 million birds die each year in the United States and Canada after flying into communication towers. The lights of those towers are meant to warn aircraft pilots, but they also disrupt the orientation of nocturnal avian fliers, which then veer into wires or each other. Many of these deaths could be avoided simply by replacing steady lights with blinking ones.

“We too quickly forget that we don’t perceive the world in the same way as other species, and consequently, we ignore impacts that we shouldn’t,” Longcore tells me in his Los Angeles office. Our eyes are among the sharpest in the animal kingdom, but their high resolution comes with the cost of low sensitivity. Unlike most other mammals, our vision fails us at night, so we crave more nocturnal illumination, not less.

[Read: The dark side of light]

The idea of light as a pollutant is jarring to us, but it becomes one when it creeps into places where it doesn’t belong. Widespread light at night is a uniquely anthropogenic force. The daily and seasonal rhythms of bright and dark remained largely inviolate throughout all of evolutionary time—a 4-billion-year streak that began to falter in the 19th century.

When sea-turtle hatchlings emerge from their nests, they crawl away from the dark shapes of dune vegetation toward the brighter oceanic horizon. But lit roads and beach resorts can steer them in the wrong direction, where they are easily picked off by predators or squashed by vehicles. In Florida alone, artificial lights kill baby turtles in the thousands every year. They’ve wandered into a baseball game and, more horrifying, abandoned beach fires. The caretaker of one property in Melbourne Beach found hundreds of dead hatchlings piled beneath a single mercury-vapor lamp.

Female crickets struggle to find the best mates when noise pollution masks the males’ songs. (Shayan Asgharnia for The Atlantic)

Artificial lights can also fatally attract insects, contributing to their alarming global declines. A single streetlamp can lure moths from 25 yards away, and a well-lit road might as well be a prison. Many of the insects that gather around streetlamps will likely be eaten or dead from exhaustion by sunrise. Those that zoom toward vehicle headlights will probably be gone even sooner. The consequences of these losses can ripple across ecosystems. In 2014, as part of an experiment, the ecologist Eva Knop installed streetlamps in seven Swiss meadows. After sunset, she prowled these fields with night-vision goggles, peering into flowers to search for moths and other pollinators. By comparing these sites to others that had been kept dark, Knop showed that the illuminated flowers received 62 percent fewer visits from pollinating insects. One plant produced 13 percent less fruit even though it was visited by a day shift of bees and butterflies.

The presence of light isn’t the only factor that matters; so does its nature. Insects with aquatic larvae, such as mayflies and dragonflies, will fruitlessly lay their eggs on wet roads, windows, and car roofs, because these reflect horizontally polarized light in the same way bodies of water do. Rapidly flickering light bulbs can cause headaches and other neurological problems in humans, even though our eyes are usually too slow to detect these changes; what, then, do they do to animals with faster vision, like insects and small birds?

Colors matter, too. Red is better for bats and insects but can waylay migrating birds. Yellow doesn’t bother turtles or most insects but can disrupt salamanders. No wavelength is perfect, Longcore says, but blue and white are worst of all. Blue light interferes with body clocks and strongly attracts insects. It is also easily scattered, increasing the spread of light pollution. It is, however, cheap and efficient to produce. The new generation of energy-efficient white LEDs contain a lot of blue light, and the world might switch to them from traditional yellow-orange sodium lights. In energy terms, that would be an environmental win. But it would also increase the amount of global light pollution by two or three times.

[From the April 2020 issue: Ed Yong on how we can save giraffes from extinction ]

After talking with Longcore, I head home to Washington, D.C., on a red-eye flight. As the plane takes off, I peer out the window at Los Angeles. The twinkling grid of lights stirs the same primordial awe that comes from watching a starry sky or a moonlit sea. But as the illuminated city recedes beneath my window, that amazement is tinged with unease. Light pollution is no longer just an urban problem. Light travels, encroaching even into places that are otherwise untouched by human influence. The light from Los Angeles reaches Death Valley, one of the largest national parks in the United States, more than 150 miles away. True darkness is hard to find.

So is true silence.

It’s a sunny April morning in Boulder, Colorado, and I’ve hiked up to a rocky hillside, about 6,000 feet above sea level. The world feels wider here, not just because of the panoramic view over conifer forests but also because it is blissfully quiet. Away from urban ruckus, quieter sounds become audible over greater distances. On the hillside, a chipmunk is rustling. Grasshoppers snap their wings together as they fly. A woodpecker pounds its beak against a nearby trunk. Wind rushes past. The longer I sit, the more I seem to hear.

Two men puncture the tranquility. I can’t see them, but they’re somewhere on the trail below, intent on broadcasting their opinions to all of Colorado. Then I realize I can also hear faraway vehicles zooming along a highway beyond the trees. Denver hums in the distance, an ambient backdrop that I had all but blocked out. I notice the roaring engines of a plane flying overhead. After my hike, I meet up with Kurt Fristrup, who says he’s been backpacking since the mid-1960s. In that time, aircraft emissions have increased nearly sevenfold. “One of my favorite parlor tricks when friends visit is to ask, at the end of the hike, if they heard any aircraft,” he tells me. “People will say they remember one or two. And I’ll say there were 23 jets and two helicopters.”

Before he retired, Fristrup was a scientist at the National Park Service’s Natural Sounds and Night Skies Division, a group that works to safeguard (among other things) the United States’ natural soundscapes. To protect them, the team first had to map them, and sound, unlike light, can’t be detected by satellites. Fristrup and his colleagues spent years lugging recording equipment to almost 500 sites around the country, capturing nearly 1.5 million audio samples. They found that human activity doubles the background-noise levels in 63 percent of protected spaces like national parks, and increases them tenfold in 21 percent. In the latter places, “if you could have heard something 100 feet away, now you can only hear it 10 feet away,” Rachel Buxton, a former National Park Service research fellow, told me. Aircraft and roads are the main culprits, but so are industries like oil and gas extraction, mining, and forestry, which fill the air with drilling, explosions, engine noises, and the thud of heavy tires. Even the most heavily protected areas are under acoustic siege.

Busy roads may drown out the alarm calls of songbirds like the tufted titmouse. (Shayan Asgharnia for The Atlantic)

In towns and cities, the problem is worse, and not just in the United States. In 2005, two-thirds of Europeans were immersed in ambient noise equivalent to perpetual rainfall. Such conditions are difficult for the many animals that communicate through calls and songs. Scientists have found that noisy neighborhoods in Leiden, in the Netherlands, compel great tits to sing at higher frequencies so that their notes don’t get masked by the city’s low-pitched hubbub. Nightingales in Berlin are forced to belt out their tunes more loudly to be heard over the surrounding din. Urban and industrial noise can also change the timing of birds’ songs, suppress the complexity of their calls, and prevent them from finding mates. Noise pollution masks not only the sounds that animals deliberately make but also the “web of unintended sounds that ties communities together,” Fristrup says. He means the gentle rustles that tell owls where their prey is, or the faint flaps that warn mice about impending doom.

In 2012, Jesse Barber and his colleagues Heidi Ware Carlisle and Christopher McClure built a phantom road. On a ridge in Idaho that acts as a stopover for migrating birds, the team set up a half-mile corridor of speakers that played looped recordings of passing cars. A third of the usual birds stayed away. Many of those that didn’t paid a price for persisting. With tires and horns drowning out the sounds of predators, the birds spent more time looking for danger and less time looking for food. They put on less weight and were weaker during their arduous migrations. The phantom-road experiment was pivotal in showing that wildlife could be deterred by noise and noise alone, detached from the sight of vehicles or the stench of exhaust. Hundreds of studies have come to similar conclusions. In noisy conditions, prairie dogs spend more time underground. Owls flub their attacks. Parasitic Ormia flies struggle to find their cricket hosts.

Sounds can travel over long distances, at all times of day, and through solid obstacles. These qualities make them excellent stimuli for animals but also pollutants par excellence. Noise can degrade habitats that look idyllic and make otherwise livable places unlivable. And where will animals go? In 2003, 83 percent of the contiguous United States lay within about a kilometer of a road.

Even the seas can’t offer silence. Although Jacques Cousteau once described the ocean as a silent world, it is anything but. It teems with the sounds of breaking waves and blowing winds, bubbling hydrothermal vents and calving icebergs, all of which carry farther and travel faster underwater than in air. Marine animals are noisy, too. Whales sing, toadfish hum, cod grunt, and bearded seals trill. Thousands of snapping shrimp, which stun passing fish with the shock waves produced by their large claws, fill coral reefs with sounds similar to sizzling bacon or Rice Krispies popping in milk. Some of this soundscape has been muted as humans have netted, hooked, and harpooned the oceans’ residents. Other natural noises have been drowned out by the ones we added: the scrapes of nets that trawl the seafloor; the staccato beats of seismic charges used to scout for oil and gas; the pings of military sonar; and, as a ubiquitous backing track for all this commotion, the sounds of ships.

[Read: These animals are feasting on the ruins of an extinct world]

“Think about where your shoes come from,” the marine-mammal expert John Hildebrand tells me. I look; unsurprisingly, the answer is China. Some tanker carried my shoes across the Pacific, leaving behind a wake of sound that radiated for miles. From 1945 to 2008, the global shipping fleet more than tripled, and began moving 10 times more cargo at higher speeds. And in the past 50 years, shipping vessels have multiplied the levels of low-frequency noise in the oceans 32-fold—a 15-decibel increase over levels that Hildebrand suspects were already 10 to 15 decibels louder than in pre-propeller seas. Because giant whales can live for a century or more, there are likely whales alive today that have personally experienced this growing underwater racket and now can hear only a small fraction of their former range. As ships pass in the night, humpback whales stop singing, orcas stop foraging, and right whales become stressed. Crabs stop feeding, cuttlefish change colors, damselfish are more easily caught. “If I said that I’m going to increase the noise level in your office by 30 decibels, OSHA would come in and say you’d need to wear earplugs,” Hildebrand tells me. “We’re conducting an experiment on marine animals by exposing them to these high levels of noise, and it’s not an experiment we’d allow to be conducted on ourselves.”

Because of the way we have upended the worlds of other animals, senses that have served their owners well for millions of years are now liabilities. Smooth vertical surfaces, which don’t exist in nature, return echoes that sound like open air; perhaps that’s why bats so often crash into windows. Dimethyl sulfide, the seaweedy-smelling chemical that once reliably guided seabirds to food, now also guides them to the millions of tons of plastic waste that humans have dumped into the oceans; perhaps that’s one reason an estimated 90 percent of seabirds eventually swallow plastic. Manatees can detect the currents produced by objects moving in the water with whiskerlike hairs found all over their body, but not with enough notice to avoid a loud, fast-moving speedboat; boat collisions are responsible for at least a fifth of deaths among Florida’s manatees. Odorants in river water can guide salmon back to their stream of birth, but not if pesticides in that same water blunt their sense of smell. Weak electric fields at the bottom of the sea can guide sharks to buried prey, but also to high-voltage cables.

Manatee whiskers can detect currents in the water, but not quickly enough to dodge loud, fast boats. (Shayan Asgharnia for The Atlantic)

Some animals have come to tolerate the sights and sounds of modernity. Others even flourish among them. Some urban moths have evolved to become less attracted to light. Some urban spiders have gone in the opposite direction, spinning webs beneath streetlights and feasting on the attracted insects. In some Panama towns, nighttime lights drive frog-eating bats away, allowing male túngara frogs to load their songs with sexy flourishes that would normally attract predators as well as mates. Animals can adapt, by changing their behavior over an individual lifetime and by evolving new behaviors over many generations.

[Read: Why some moths are evolving to avoid artificial light]

But adaptation is not always possible. Species that mature and breed slowly can’t evolve quickly enough to keep pace with levels of light and noise pollution that double every few decades. Creatures that have already been confined to narrow corners of shrinking habitats can’t just up and leave. Those that rely on specialized senses can’t just retune their entire Umwelt.

Our influence is not inherently destructive, but it is often homogenizing. In pushing out species that cannot abide our sensory onslaughts, we leave behind smaller and less diverse communities. And beyond polluting the world with unwanted sensory stimuli, we’re also removing natural stimuli that animals have come to depend on, flattening the undulating sensescapes that have generated the wondrous variety of animal Umwelten.

Consider Lake Victoria, in East Africa. It is home to more than 500 species of cichlid fish that are found nowhere else. That extraordinary diversity arose partly because of light. In deeper parts of the lake, light tends to be yellow or orange, while blue is more plentiful in shallower waters. These differences affected the eyes of the local cichlids and, in turn, their mating choices. The evolutionary biologist Ole Seehausen found that female cichlids from deeper waters prefer redder males, while those in the shallows are drawn to bluer ones. These diverging penchants acted like physical barriers, splitting the cichlids into differently colored forms. Diversity in light helped create diversity in vision, in color, and in species. But over the past century, runoff from farms, mines, and sewage filled the lake with nutrients that spurred the growth of clouding, choking algae. The old light gradients flattened in some places, the cichlids’ colors and visual proclivities no longer mattered, and the number of species collapsed. By turning off the light in the lake, humans also switched off the sensory engine of diversity, contributing to what Seehausen has called “the fastest large-scale extinction event ever observed.”

As those species go extinct, so too do their Umwelten. With every creature that vanishes, we lose a way of interpreting the world. Our sensory bubbles shield us from the knowledge of those losses. But they don’t protect us from the consequences. In the woodlands of New Mexico, the ecologists Clinton Francis and Catherine Ortega found that the Woodhouse’s scrub-jay avoids the noise of compressors used in extracting natural gas. The scrub-jay spreads the seeds of piñon pine trees, and a single bird can bury thousands of pine seeds a year. They are so important to the forests that, in quiet areas where they still thrive, pine seedlings are four times more common than in noisy areas they have abandoned, Francis and colleagues found in a later study.

Left: As babies, clown fish use sounds to find their way to the safety of a coral reef. Right: To avoid excessive noise, prairie dogs spend more time underground. (Shayan Asgharnia for The Atlantic)

Piñon pines are the foundation of the ecosystem around them—a single species that provides food and shelter for hundreds of others, including Indigenous Americans. To lose three-quarters of them would be disastrous. And because they grow slowly, “noise might have hundred-plus-year consequences for the entire ecosystem,” Francis tells me.

A better understanding of other creatures’ senses can show us how we’re defiling the natural world—and can also point to ways of saving it. In 2016, the marine biologist Tim Lamont (formerly Tim Gordon) traveled to Australia’s Great Barrier Reef to begin work for his doctorate. Lamont should have spent months swimming amid the corals’ vivid splendor. Instead, a heat wave had forced the corals to expel the symbiotic algae that give them nutrients and colors. Without these partners, the corals starved and whitened in the worst bleaching event on record, and the first of several to come. Snorkeling through the rubble, Lamont found that the reefs had been not only bleached but also silenced. Snapping shrimp no longer snapped. Parrotfish no longer crunched. Those sounds normally help guide baby fish back to the reef after their first vulnerable months out at sea. Soundless reefs were much less attractive.

Lamont feared that if fish avoided the degraded reefs, the seaweed they normally eat would run amok, overgrowing the bleached corals and preventing them from rebounding. He and his colleagues set up loudspeakers that continuously played recordings of healthy reefs over patches of coral rubble. The team would dive every few days to survey the local animals. After 40 days, he ran the numbers and saw that the acoustically enriched reefs had twice as many young fish as silent ones and 50 percent more species. They had not only been attracted by the sounds but stayed and formed a community. “It was a lovely experiment to do,” Lamont says. It showed what conservationists can accomplish by “seeing the world through the perceptions of the animals you’re trying to protect.”

[From the July 2019 issue: The last of its kind]

Lamont’s experiment was possible only because the team managed to record the sounds of the healthy reefs before they were bleached. Natural sensescapes still exist. There is still time to preserve and restore them before the last echo of the last reef fades into memory. And in most cases, the work ahead of us is considerably simpler. Instead of adding stimuli that we have removed, we can simply remove those that we added. Radioactive waste can take millennia to degrade. Persistent chemicals like the pesticide DDT can thread through the bodies of animals long after they are banned. Plastics will continue to despoil the oceans even if all plastic production halts tomorrow. But light pollution ceases as soon as lights are turned off. Noise pollution abates once engines and propellers wind down. Sensory pollution is an ecological gimme—a rare example of a planetary problem that can be immediately and effectively addressed. And in the spring of 2020, the world did unknowingly address it.

The body clock of the barred tiger salamander is disrupted by artificial light at night. (Shayan Asgharnia for The Atlantic)

As the coronavirus spread, public spaces closed. Flights were grounded. Cars stayed parked. Cruise ships stayed docked. About 4.5 billion people—almost three-fifths of the world’s population—were told or encouraged to stay home. As a result, many places became substantially darker and quieter. With fewer planes and cars on the move, the night skies around Berlin were half as bright as normal. Alaska’s Glacier Bay, a sanctuary for humpback whales, was half as loud as the previous year, as were cities and rural areas throughout California, New York, Florida, and Texas. Sounds that would normally be muffled became clearer. City dwellers around the world suddenly noticed singing birds.

[Read: Artificial lights tell the story of the pandemic]

In a multitude of ways, the pandemic showed that sensory pollution can be reduced if people are sufficiently motivated—and such reductions are possible without the debilitating consequences of a global lockdown. In the summer of 2007, Kurt Fristrup and his National Park Service colleagues did a simple experiment at Muir Woods National Monument, in California. On a random schedule, they stuck up signs that declared one of the most popular parts of the park a quiet zone and encouraged visitors to silence their phones and lower their voices. These simple steps, with no accompanying enforcement, reduced the noise levels in the park by three decibels, equivalent to 1,200 fewer visitors.

To truly make a dent in sensory pollution, bigger steps are needed. Lights can be dimmed or switched off when buildings and streets are not in use. They can be shielded so that they stop shining above the horizon. LEDs can be changed from blue or white to red. Quiet pavements with porous surfaces can absorb the noise from passing vehicles. Sound-absorbing barriers, including berms on land and air-bubble curtains in the water, can soften the din of traffic and industry. Vehicles can be diverted from important areas of wilderness, or they can be forced to slow down: In 2007, when commercial ships in the Mediterranean began slowing down by just 12 percent, which saves fuel and reduces emissions, they produced half as much noise. Such vessels can also be fitted with quieter hulls and propellers, which are already used to muffle military ships (and would make commercial ones more fuel-efficient).

We could regulate industries causing sensory pollution, but there’s not enough societal will. “Plastic pollution in the sea looks hideous and everyone is worried, but noise pollution in the sea is something we don’t experience so directly, so no one’s up in arms about it,” Lamont says. And as we desecrate sensory environments, we grow accustomed to the results. Our blinding, blaring world becomes normal, and pristine wilderness feels more distant.

But the majesty of nature is not restricted to canyons and mountains. It can be found in the wilds of perception—the sensory spaces that lie outside our Umwelt and within those of other animals. To perceive the world through others’ senses is to find splendor in familiarity, and the sacred in the mundane. Wonders exist in a backyard garden, where bees take the measure of a flower’s electric fields, leafhoppers send vibrational melodies through the stems of plants, and birds behold the hidden palettes of ultraviolet colors on their flock-mates’ feathers. Wilderness is not distant. We are continually immersed in it. It is there for us to imagine, to savor, and to protect.

Barn owls track prey using stiff facial feathers that funnel sound toward their ears. (Shayan Asgharnia for The Atlantic)

In 1934, after considering the senses of ticks, dogs, jackdaws, and wasps, Jakob von Uexküll wrote about the Umwelt of the astronomer. “Through gigantic optical aids,” he wrote, this unique creature has eyes that “are capable of penetrating outer space as far as the most distant stars. In its Umwelt, suns and planets circle at a solemn pace.” The tools of astronomy can capture stimuli that no animal can naturally sense—X-rays, radio waves, gravitational waves from colliding black holes. They extend the human Umwelt across the universe and back to its very beginning. The tools of biologists are more modest in scale, but they, too, offer a glimpse into the infinite. Scientists have used night-vision goggles to show that nocturnal bees can see in extreme darkness, clip-on microphones to eavesdrop on the vibrational songs of leafhoppers, and electrodes to listen in on the pulses of electric fish. With microscopes, cameras, speakers, satellites, and recorders, people have explored other sensory worlds. We have used technology to make the invisible visible and the inaudible audible.

No creature could possibly sense everything, and no creature needs to. Evolving according to their owner’s needs, the senses sort through an infinity of stimuli, allowing through only what is relevant. To learn about the rest is a choice. The ability to dip into other Umwelten is our greatest sensory skill. A moth will never know what a zebra finch hears in its song, a zebra finch will never feel the electric buzz of a black ghost knifefish, a knifefish will never see through the eyes of a mantis shrimp, a mantis shrimp will never smell the way a dog can, and a dog will never understand what it is like to be a bat. We will never fully do any of these things either, but we are the only animal that can try. Through patient observation, through the technologies at our disposal, through the scientific method, and, above all else, through our curiosity and imagination, we can try to step into perspectives outside our own. This is a profound gift, which comes with a heavy responsibility. As the only species that can come close to understanding other Umwelten, but also the species most responsible for destroying those sensory realms, it falls on us to marshal all of our empathy and ingenuity to protect other creatures, and their unique ways of experiencing our shared world.

This article has been adapted from Ed Yong’s latest book, An Immense World: How Animal Senses Reveal the Hidden Realms Around Us. It appears in the July/August 2022 print edition with the headline “Our Blinding, Blaring World.”

Rats Learned to Hide and Seek. Scientists Learned Way More.

2022-05-26T09:42:57-04:00

Before they could do anything else, the neuroscientists had to teach the rats how to play hide-and-seek.

Michael Brecht at the Humboldt University of Berlin concocted the idea. His student Annika Reinhold trained six of their lab rodents to scurry around a room filled with obstacles and cardboard boxes, and either locate the hidden human or find a hiding spot themselves. As I reported in 2019, the rats picked up the game in mere weeks. They clearly understood the rules and played strategically, starting their searches in past hiding locations or keeping quiet while hiding. And they had fun. Once found, they’d sometimes prolong the game by running away and hiding again. When they eventually reunited with Reinhold, they’d jump in place excitedly—a behavior known as Freudensprung, or “joy jumps.” And they didn’t need to be conditioned to play with edible treats; tickles were enough of a reward.

The researchers enjoyed themselves too. But they were also working toward one of neuroscience’s most elusive goals: studying the brains of free-moving and naturally behaving animals. Traditionally, experimenters have been limited to highly artificial settings. They train mice and rats to do basic tasks—pressing a lever, say, in response to simple stimuli such as light or sounds—then measure their brain activity and average those measurements over hundreds or thousands of repetitions. This approach produces results that are less likely to be statistical flukes, but it’s also rather reductive. It collapses the complexity of animal lives into the simplest of actions. And it just can’t be used to study some of the most interesting behaviors of all, including play. Play is about freewheeling spontaneity; brain research usually involves control and conditioning. How could the latter ever be used to investigate the former?

[From the March 2019 issue: A journey into the animal mind]

Unexpectedly, hide-and-seek offered a way. Juan Sanguinetti-Scheck and his colleagues implanted wireless electrodes into four of the playful rodents—specifically in the prefrontal cortex (PFC), a brain region involved in social interactions and decision making. As the animals hid and sought, the electrodes continuously recorded the activity of about 30 individual neurons in their PFCs. Sanguinetti-Scheck collected those data before the coronavirus pandemic started; then his colleague Bence Bagi did something unusual with them.

Typically, researchers look at how animals’ neural activity changes when they do something specific, like scurrying into a hiding place. Bagi did the opposite. He started with the raw data from the electrodes, and trained an algorithm to identify moments when the PFC neurons fired in distinctive ways. He then cross-referenced these “brain states” against videos of the hide-and-seek games to see what the rats were doing at the time.

One brain state appeared whenever a rat was “running in a determined fashion,” Sanguinetti-Scheck, who is now at Harvard, told me. Another occurred when the rats, which were kept inside a box at the very start of each game, first poked their heads out. Yet another showed up whenever the rats approached or interacted directly with the scientists. Even though every game of hide-and-seek was different, and the rats were free to do what they liked, their PFCs still buzzed in consistent ways during specific events. That’s a “potential milestone in neuroscience,” Sergio Pellis, a neuroscientist at the University of Lethbridge who studies rat play and wasn’t involved in the study, told me. It means that neuroscientists can look inside the chaotic brain of a freely playing rat and find genuine signals amid the noise—all “in a rigorous way,” Emily Dennis, a neuroscientist at Princeton who was also not involved in the study, told me. “I find it incredibly exciting.”

[Read: So what’s the point of playtime?]

This approach also allows scientists to look past their human biases. The usual neuroscientific paradigm—start with behavior, then look at the brain—relies on people correctly interpreting a very different species’ actions. But Sanguinetti-Scheck and Bagi’s reversed process let the rats’ own brains reveal what the rodents were doing, without researchers and their preconceptions getting in the way. “We can discover things that are more than just the things we set out to discover,” Sanguinetti-Scheck said. For example, two distinctive brain states occurred whenever the rats were walking along or exploring a wall—behaviors that the researchers hadn’t thought to pay attention to. But it makes sense that walls matter to rats; they navigate the world with touch-sensitive whiskers.

So far, the team can correlate patterns of brain activity with what the rats are doing. But the scientists don’t know what those states actually represent. Does the shift from one state to another mark a moment when the rat decides to undertake a new course of action, or when the rat’s understanding of the game is changing? These are still open questions, and the hide-and-seek experiments get the team closer to answering them. So will other new techniques such as DeepLabCut, an AI-based tool that can track animal movements, which allows neuroscientists to analyze a creature’s behavior with the same sophistication that they can now bring to neural recordings. Sanguinetti-Scheck imagines a future where researchers can study the brains of not just free-moving animals but free-living ones too.

[Read: In defense of play]

“Neuroscience is experiencing a paradigm shift toward the study of more natural behaviors, and [this study] raises the bar substantially,” Shreya Saxena from the University of Florida, who was not involved in the study, told me. She hopes it’ll inspire younger neuroscientists to embrace “joie de vivre” in their work. For centuries, researchers have investigated the inner workings of the brain by studying confined animals doing simple and specific things that they’ve been trained to do thousands of times over. Scientists will uncover much more when they can truly watch brains doing what brains evolved to do—driving animal bodies as agents of agency, possibility, and flexibility. And perhaps, as the hide-and-seekers did, they’ll have more fun in the process.

So, Have You Heard About Monkeypox?

2022-05-19T14:31:00-04:00

Updated at 9:51 a.m. on May 20, 2022

Yesterday afternoon, I called the UCLA epidemiologist Anne Rimoin to ask about the European outbreak of monkeypox—a rare but potentially severe viral illness with dozens of confirmed or suspected cases in the United Kingdom, Spain, and Portugal. “If we see those clusters, given the amount of travel between the United States and Europe, I wouldn’t be surprised to see cases here,” Rimoin, who studies the disease, told me. Ten minutes later, she stopped mid-sentence to say that a colleague had just texted her a press release: “Massachusetts Public Health Officials Confirm Case of Monkeypox.”

The virus behind monkeypox is a close relative of the one that caused smallpox but is less deadly and less transmissible, causing symptoms that include fever and a rash. Endemic to western and central Africa, it was first discovered in laboratory monkeys in 1958—hence the name—but the wild animals that harbor the virus are probably rodents. The virus occasionally spills over into humans, and such infections have become more common in recent decades. Rarely, monkeypox makes it to other continents, and when it does, outbreaks “are so small, they’re measured in single digits,” Thomas Inglesby, the director of the Johns Hopkins Center for Health Security, told me. The only significant American outbreak occurred in 2003, when a shipment of Ghanaian rodents spread the virus to prairie dogs in Illinois, which were sold as pets and infected up to 47 people, none fatally. Just last year, two travelers independently carried the virus to the U.S. from Nigeria but infected no one else.

The current outbreaks in Europe and the U.S. are different and very concerning. The first case, which was identified in the United Kingdom on May 7, fit the traditional pattern: The individual had recently traveled to Nigeria. But several others hadn’t recently been to endemic countries, and some had had no obvious contact with people known to be infected. This suggests that the monkeypox virus may be surreptitiously spreading from person to person, with some number of undetected cases. (The incubation period between infection and symptoms is long, ranging from five to 21 days.) “It’s uncommon to see this number of cases in four countries at the same time,” Inglesby said. (The count is now 11: Since we spoke on Wednesday, monkeypox has also been confirmed in Sweden, Italy, Germany, Belgium, France, Canada, and Australia.)

These monkeypox outbreaks are also unique because … well … they’re occurring in the third year of a pandemic, “when the public is primed to be more acutely aware of outbreaks,” Boghuma Kabisen Titanji, a physician at Emory University, told me. “I don’t think that’s necessarily a good thing.” When it comes to epidemics, people tend to fight the last war. During the West African Ebola outbreak of 2014, American experts had to quell waves of undue paranoia, which likely contributed to the initial downplaying of the coronavirus. Now, because the U.S. catastrophically underestimated COVID, many Americans are panicking about monkeypox and reflexively distrusting any reassuring official statements. “I don’t think people should be freaking out at this stage,” Carl Bergstrom of the University of Washington told me, “but I don’t trust my own gut feelings anymore, because I’m so sick of all this shit that I tend to be optimistic.”

Monkeypox, then, is a test of the lessons that the world has (or hasn’t) learned from COVID. Can we better thread the needle between panic and laxity, or will we once again eschew uncertainty in a frantic quest for answers that later prove to be wrong?

To be clear, monkeypox isn’t COVID—they’re different diseases caused by different viruses with markedly different properties. COVID was completely unfamiliar when it first appeared, but monkeypox is a known quantity, and experts on the virus actually exist. One of them, Andrea McCollum of the CDC, told me that based on existing studies, monkeypox doesn’t spread easily, and not over long distances through the air. It transmits via contaminated surfaces or prolonged proximity with other people, which is why most outbreaks have been small, and why people have mostly transmitted the disease to either household members or health-care workers. “This isn’t a virus that, as far as we’re aware, would really take off in a population like COVID,” she said. “It really requires close contact for human-to-human transmission.”

Of course, we have heard that before. In early 2020, many experts claimed that COVID spread only via contaminated surfaces or close-splashing droplets—hence the six-feet rules and hygiene theater. Now it is widely accepted that the disease spreads through smaller and farther-reaching aerosol particles—hence the importance of ventilation and masks. But that doesn’t mean history is repeating with monkeypox. A 2012 study suggested that the virus can persist in aerosols for several days—but that was under artificial laboratory conditions, and persistence is just one small part of the infection process. Chad Roy, an aerobiologist at Tulane University School of Medicine who led that study, told me that compared to the SARS-CoV-2 coronavirus, monkeypox is "an altogether different virus and the risk of natural transmission by aerosol far less likely.” And the fact remains that past monkeypox outbreaks have been inconsistent with a virus that travels as easily as the coronavirus. “Monkeypox does not scream ‘airborne’ at me; COVID-19 did,” Linsey Marr, an aerosol expert at Virginia Tech, told me.

Then again, Marr is less certain about monkeypox than she was about COVID. And Titanji notes that our knowledge of monkeypox is based on just 1,500 or so recorded cases, as of 2018. “I’ve seen a lot of people writing as if everything we know about monkeypox is definitive and finalized, but the reality is that it is still a rare zoonotic infection,” she said. For that reason, “I’m in Team Cautious,” she said. “We can’t use what happened with previous monkeypox outbreaks to make sweeping statements. If we’ve learned anything from COVID, it’s to have humility.”

For decades, a few scientists have voiced concerns that the monkeypox virus could have become better at infecting people—ironically because we eradicated its relative, smallpox, in the late 1970s. The smallpox vaccine incidentally protected against monkeypox. And when new generations were born into a world without either smallpox or smallpox-vaccination campaigns, they grew up vulnerable to monkeypox. In the Democratic Republic of Congo, this dwindling immunity meant that monkeypox infections increased 20-fold in the three decades after smallpox vanished, as Rimoin showed in 2010. That gives the virus more chances to evolve into a more transmissible pathogen in humans. To date, its R0—the average number of people who catch the disease from one infected person—has been less than 1, which means that outbreaks naturally peter out. But it could eventually evolve above that threshold, and cause more protracted epidemics, as Bergstrom simulated in 2003. “We saw monkeypox as a ticking time bomb,” he told me.

This possibility casts a cloud of uncertainty over the current unusual outbreaks, which everyone I spoke with is concerned about. Are they the work of a new and more transmissible strain of monkeypox? Or are they simply the result of people traveling more after global COVID restrictions were lifted? Or could they be due to something else entirely? So far, the cases are more numerous than a normal monkeypox outbreak, but not so numerous as to suggest a radically different virus, Inglesby told me. But he also doesn’t have a clear explanation for the outbreak’s unusual patterns—nor does anyone else.

Answers should come quickly, though. Within days, scientists should have sequenced the viruses from the current outbreaks, which will show whether they harbor mutations that might have changed their properties. Within weeks, European epidemiologists should have a clearer idea of how the existing cases began, and whether there are connections between them. As for the U.S., McCollum told me that she is standing by for more cases. The day after we spoke, another suspected case was announced—a patient being cared for at Bellevue Hospital in New York City.

The U.S. is, of course, in a better position with monkeypox than with COVID. Although the nation hadn’t planned for a coronavirus pandemic, it has spent decades thinking about how to handle smallpox bioterrorism. The two cases of monkeypox in 2021 provided handy test runs for those plans, which are now unfolding smoothly. For example, the case in Massachusetts was identified when the patient’s physician, having reviewed reports from the U.K., called the state’s public-health department on Tuesday. Within 12 hours, the department had collected and tested the patient’s samples. The next day, more samples arrived at the CDC, which confirmed monkeypox. “All of that worked really well,” McCollum said. “We’re a fairly well-oiled machine.”

Also, there’s already a vaccine. One smallpox vaccine is 85 percent effective at preventing monkeypox and has already been licensed for use against the virus. And as another bioterrorism precaution, stockpiles of three smallpox vaccines are large enough “to vaccinate basically everyone in the U.S.” Inglesby said. And though monkeypox patients usually get just supportive care, a possible treatment does exist and has also been stockpiled: Tecovirimat, or TPOXX, was developed to treat smallpox but would likely work for monkeypox too.

Monkeypox may also be less deadly than is frequently claimed. The oft-cited fatality rate of about 10 percent applies to a strain that infected people in the Congo Basin. The West African strain, which several of the current cases have been linked to, has a fatality rate closer to 1 percent—and that’s in poor, rural populations. “We haven’t seen fatalities in people who’ve had monkeypox in high-resource settings,” Rimoin said.

Still, as COVID has shown, even when a disease doesn’t kill you, it can hardly count as “mild.” Monkeypox might not take off in the way that COVID did, but for those who get it, it remains a “substantial illness,” McCollum said. “If individuals are sick, they’re often sick for two to four weeks. It’s urgent to identify people early, get them treatment, and identify contacts.” It helps that one common symptom is an obvious rash, which looks like an extreme version of chickenpox. But unlike chickenpox, the monkeypox rash is usually preceded by a fever, the lesions are initially more painful than itchy, and the lymph nodes are often inflamed. “The constructive thing to do is to make sure that the public is aware of what monkeypox looks like,” Titanji said.

For that reason, she added, it’s important to avoid stigmatizing infected people. Many of the current cases are in men who identify as gay, bisexual, or men who have sex with men—an unusual pattern not seen in previous monkeypox outbreaks. That has raised questions about a new route of transmission, but sex obviously involves prolonged close contact, which is how the virus normally spreads. As COVID showed, early narratives about a disease can rapidly and prematurely harden into accepted lore. And if those narratives turn into stigma, they could stop people from coming forward with symptoms.

Communication might prove to be one of monkeypox’s hardest challenges, as it has been with COVID. “We need leaders who are saying, ‘Here’s what we know; here’s what we don’t know; we’ll find out; and we’ll be back tomorrow,’” Inglesby said. But some leaders have lost credibility during the recent pandemic, while others are being drowned out by armchair experts who have amassed large followings. “All of a sudden, everyone’s an expert in monkeypox,” Titanji said.

What COVID Hospitalization Numbers Are Missing

2022-05-18T08:00:00-04:00

For weeks now, as COVID-19 cases have ticked upward in the Northeast and mid-Atlantic, pundits and political leaders have offered a supposedly reassuring refrain: Cases might be climbing, but hospitalizations aren’t yet following suit. In some places, that has been true. Several health-care workers around the country told me they’re seeing the lowest caseloads since last summer. A few aren’t having to treat COVID patients at all. Others are only seeing mildly sick people who need little more than IV fluids. “I don’t think there’s a huge amount of anxiety over what the next month might bring,” Debra Poutsiaka, an infectious-disease specialist at Tufts Medical Center, told me. “I could be wrong. I hope not.”

The Biden administration shares those hopes: Having apparently given up on curtailing the coronavirus, it is counting on vaccines and treatments decoupling infection from severe illness enough to prevent the health-care system from becoming inundated again. The CDC’s current guidelines effectively say that Americans can act as if COVID is not a crisis—until hospitalizations reach a high enough threshold.

The country still may be heading to that point. Hospitalizations are climbing in 43 states, especially in the Northeast. In Vermont, the rate of new admissions has already neared the peak of the recent Omicron surge. Earlier this month, “three different emergency-room docs said this is by far the worst that COVID has been at any point,” Tim Plante, an internist at the University of Vermont, told me. “They’re bewildered that it’s happening again.” Meanwhile, people in most of New York City are now advised to mask indoors again, after rising hospitalizations triggered the CDC’s “high” alert level.

But even in calmer spots, Biden’s strategy overlooks a crucial truth: The health-care system is still in crisis mode. The ordeals of the past two years have tipped the system—and its people—into a chronic, cumulative state of overload that does not fully abate in the moments of respite between COVID waves.

Some of the problems I’ve written about before: Even in quieter periods, health-care workers are scrambling to catch up with backlogs of work that went unaddressed during COVID surges, or patients who sat on health problems and are now much sicker. Those patients are more antagonistic; verbal and physical assaults are commonplace. Health-care workers can also still catch COVID, keeping them from their jobs, while surges elsewhere in the world create supply-chain issues that keep hospitals from running smoothly. All this, on top of two years of devastating COVID surges, means that health-care workers are so exhausted and burned out that those words have become euphemisms. In trying to describe his colleagues’ mental state, Plante brought up Migrant Mother—the famous photo from the journalist Dorothea Lange, which captured unimaginable hardships in a single haunting expression. “That look in her eyes is what I see in folks who’ve been on the front lines,” Plante told me.

Enough health-care workers—nurses, in particular—have quit their jobs that even when hospitals aren’t deluged, the remaining workforce must care for an unreasonable number of patients over longer hours and more shifts. In a survey of nearly 12,000 nurses, conducted by the American Nurses Foundation this January, 89 percent said that their workplace was short-staffed, and half said the problem was serious. Worse, almost a quarter said that they were planning on leaving their jobs within the next six months, and another 30 percent said they might. Even if just a small fraction of them follow through on their intentions, their departure would heap more pressure upon a workforce that is already shouldering too much. “There’s a palpable concern that this can’t be our new normal,” Beth Wathen, president of the American Association of Critical-Care Nurses, told me.

The problems are substantial and numerous enough that “if this moment was occurring without the horror of the moments that preceded it, we’d be shocked,” Lindsay Ryan, a physician at UC San Francisco, told me. “The calamity of the last years has numbed us to the calamity of the present moment.”

America’s current pandemic strategy is predicated on the assumption that people can move on from COVID, trusting that the health-care system will be ready to hold the line. But that assumption is a fiction. Much of the system is still intolerably stressed, even in moments of apparent reprieve. And the CDC’s community guidelines are set such that by the time preventive actions are triggered, high levels of sickness and death will be locked in for the near future. For many health-care workers, their mental health and even their commitment to medicine are balanced on a precipice; any further surges will tip more of them over. “I feel like I’m holding on by a thread,” Marina Del Rios, an emergency physician at the University of Iowa, told me. “Every time I hear a new subvariant is coming along, I think: Okay, here we go.”

During the Omicron surge, Kelley Cabrera, a nurse based in New York, watched three patients die in a single shift. While zipping another in a body bag, “something in me broke,” she told me. “I told my friend, 'I cannot do another shift like this again.’” She couldn’t sleep; when she did, she had nightmares about work. Once the surge abated, she quit her job, and now does short-term travel contracts. “When we’re in the middle of a trauma, our brain has this incredible capacity to go into survival mode," Mona Masood, a psychiatrist who founded a support line for physicians, told me. "It’s only afterward, when we let go of that, that there’s this surge of grief, sorrow, anxiety, and fear.” In those moments of calm, many health-care workers decide they’ve had enough.

The resulting staff shortages are especially acute in rural areas. Kelly McGrath, a chief medical officer in Idaho, told me that the two hospitals where he works will have lost eight of their 20 physicians by the end of the summer—and despite intense efforts, he has struggled to replace any of them. Meanwhile, one of the hospitals normally has a full staff of 13 registered nurses and has turned over 21 since the pandemic began. And the hospitals still have to care for about 28,000 people spread across an area the size of Massachusetts. “Workforce was always a challenge in rural health care, but we’ve gone from a challenge to a crisis,” McGrath told me. “I’ve never seen anything like it.”

COVID itself depletes the depleted workforce further by periodically taking out waves of health-care workers. Being vaccinated, those workers mostly incur mild or moderate symptoms, but must nonetheless stay away from medically vulnerable patients. (Mild infections can still put them at risk of long COVID, too.) This means that COVID can still hammer the health-care system even without sending a single person to the hospital. “The choice to lift all restrictions means that anyone who lives in the community will get COVID more—and that includes the workforce that takes care of patients,” Kathleen McFadden, a chief resident at Massachusetts General Hospital, told me. She had just recovered from a bout of COVID, during which already stressed colleagues had to fill in for her.

Scott Olson / Getty

Even when missing people can be replaced, missing knowledge cannot. The pandemic pushed many veteran health-care workers into early retirement, lowering the average experience level in American hospitals. “I don’t think the public really understands how great the loss of this generational knowledge is,” Cabrera told me. In her current job, she had just four days of orientation, which she describes as “shockingly short,” from some people who had been in the ER for less than a year. When inexperienced recruits are trained by inexperienced staff, the knowledge deficit deepens, and not just in terms of medical procedures. The system has also lost indispensable social savvy—how to question an inappropriate decision, or recognize when you’re out of your depth—that acts as a safeguard against medical mistakes. And with established teams now ruptured by resignations, many health-care workers no longer know—or trust—the people at their side. “In an industry where our communication has to be spot-on and effective, that’s a setup for unsafe conditions,” Lisa Zegan, a patient safety officer based in Maryland, told me.

The health-care workers who’ve stayed in their jobs also face several long-term problems that the pandemic exacerbated. Hospitals still depend on a just-in-time economy, and brittle international supply chains that regularly snap in the COVID era. The Shanghai lockdown precipitated a global shortage of contrast fluids, which are used in medical imaging like CT scans and MRIs; hospitals are postponing scans and the surgeries that depend on them. “We get shortage emails popping up all the time, and I never used to get these,” Lindsay Ryan told me. Hours before we spoke, she got an email warning of a crucial shortage of concentrated saline—essentially super-salt, which is used to treat severe electrolyte abnormalities. “When you need it, you need it,” Ryan said.

These staffing and supply problems are all happening at a time when “our hospital capacity is running high due to folks catching up on care and other needs,” Nathan Chomilo, a pediatrician and health-care leader based in Minnesota, told me. And now, in some places, flu and other respiratory viruses that had been almost completely suppressed by widespread masking are back in force. People who were infected with COVID in past surges are returning with heart failure, diabetes, respiratory problems, and lingering symptoms of long COVID.

Absurdly, it’s often hard to get people out of the hospital, Sara Wolfson, a geriatrician at Nebraska Medicine, told me. Many elderly patients still need care after they’ve stabilized, but it’s hard to discharge them, because long-term care facilities and home-health agencies are also incredibly short-staffed and unable to accommodate new patients. Some people in Wolfson’s care have ended up staying in the hospital for 40 to 45 days longer than they needed to. These logjams take up beds that are needed for elective surgeries, which hurts a hospital’s bottom line. And such deficits will become more consequential as emergency COVID funding dries up. “Some people may look at the funds as welfare for hospitals, but that money was key to keeping our staff whole while we took big losses,” McGrath told me.

Health-care workers are still providing the best care they can possibly give. But the limits of their best have been severely constrained by a medical system that was stretched thin well before COVID arrived and has been diminished with every surge since. This compounds exhaustion with moral injury—the distress that comes from knowing what good care looks like and being unable to provide it. And when things go wrong, “the hospital isn’t coming in to apologize to patients,” Cabrera said. “We apologize. We face the brunt of everything.” At the same time they are struggling to provide care, they must also handle, for example, people who are annoyed to find hospitals still enforcing visitation rules to protect vulnerable patients. “We’re dealing with very angry people: I don’t understand, the pandemic’s over, I don’t have to wear a mask,” Wolfson told me. “It piles onto the exhaustion. You get tired of explaining.”

Each fresh challenge layers upon the cumulative bedrock of two traumatic years. Every time McFadden passes a particular room in her hospital, she is yanked back to the spring of 2021. She remembers a patient saying “I’m really, really scared, Kathleen” before having every possible bad complication of COVID and lapsing into a coma from which she has still not awoken. Those words feel like they’re still echoing in the walls of McFadden’s workplace. “That’s one of maybe 50 stories I could tell you,” she said. “I walk past those rooms and relive those memories. The rest of the world has moved on, but you can’t simply move on from your profession turning into trauma day after day.”

These problems are not obvious when looking at bed-occupancy charts or hospitalization curves. The entire health-care system has effectively developed a chronic illness. Its debilitating symptoms are persisting long after its initial acute sickness and affecting every part of its body. And because they are invisible to the outside, they are easy to dismiss. They aren’t accounted for in the calculations that are supposed to keep the country from hurtling back into another, unmanageable bout with COVID.

Health-care workers sometimes feel as if they are living in a different world from those around them. Through the pandemic, they have wrestled with the gulf between the horrors they saw in their workplaces and the casual attitudes they beheld outside. For many, that cognitive dissonance is greater than ever. The relentless surges locked them in a two-year dystopian stasis, from which they are emerging to find that their old lives are unrecognizable. Many callers to Mona Masood’s physician support line have talked about lost friendships and imminent divorces. “We were holding back this wall, and it gave everyone a chance to keep going and get through,” Masood said. But that created a chasm between health-care workers and the rest of society—a pattern that Masood also hears among veterans returning from war. “I feel distanced from my outside-of-hospital friendships,” Marina Del Rios told me.

Alejandra Villa Loarca / Newsday RM / Getty

Some health-care workers have turned toward one another, finding solace in the camaraderie that comes from facing trauma together. “For those that remain, there’s that band-of-brothers-and-sisters feeling,” McGrath told me. Others doubled down on the idealistic sense of mission that first got them into medicine. McFadden feels less burned out on days when she spends more time at patients’ bedsides, rather than staring at electronic medical records. “Making other people feel human in the hospital reminds me of the humanity still deep inside me,” she recently tweeted.

But for a third group, the only way out is to pull away—by quitting, moving to less stressful roles, or shifting to temporary work. “I was putting so many other people’s needs ahead of my own, which is what nurses tend to do,” Cabrera told me. But eventually, “there was this realization: I don’t have to be this miserable.” Worryingly, this group includes much of health care’s next generation. In the American Nurses Foundation’s recent survey, nurses under 35 were twice as likely to report burnout as those over 55, and more likely to be planning on quitting.

Many hospitals are now facing an unenviable bind. Without chances to recover from the past two years, more people will leave, and the staffing crisis will deepen. But for many people, recovery means doing less—at a time when institutions need their workers to do more. “For health-care workers, that’s not our problem; that’s the system’s problem,” Masood told me. “When you say burnout, you’re blaming people for feeling a very normal outcome of being put in a situation that’s depleting us of our energy and humanity. When a house catches fire, we don’t say it was burned out. We say it was burned down, and then we look for the source.” For too long, the U.S. has relied on the “individual grit” of its health-care workers, Jennifer Sullivan, an emergency physician who runs strategic operations for the South’s Atrium Health system told me. Its challenge, now, is to create a health-care system that’s as resilient as the people in it have been forced to be.

We Created the ‘Pandemicene’

2022-04-28T05:00:00-04:00

For the world’s viruses, this is a time of unprecedented opportunity. An estimated 40,000 viruses lurk in the bodies of mammals, of which a quarter could conceivably infect humans. Most do not, because they have few chances to leap into our bodies. But those chances are growing. Earth’s changing climate is forcing animals to relocate to new habitats, in a bid to track their preferred environmental conditions. Species that have never coexisted will become neighbors, creating thousands of infectious meet-cutes in which viruses can spill over into unfamiliar hosts—and, eventually, into us. Many scientists have argued that climate change will make pandemics more likely, but a groundbreaking new analysis shows that this worrying future is already here, and will be difficult to address. The planetary network of viruses and wildlife “is rewiring itself right now,” Colin Carlson, a global-change biologist at Georgetown University, told me. And “while we thought we understood the rules of the game, again and again, reality sat us down and taught us: That’s not how biology works.”

In 2019, Carlson and his colleague Greg Albery began creating a massive simulation that maps the past, present, and future ranges of 3,100 mammal species, and predicts the likelihood of viral spillovers if those ranges overlap. The simulation strained a lot of computing power; “every time we turn it on, an angel dies,” Carlson told me. And the results, which have finally been published today, are disturbing. Even under the most optimistic climate scenarios, the coming decades will see roughly 300,000 first encounters between species that normally don’t interact, leading to about 15,000 spillovers wherein viruses enter naive hosts.

“It’s a little harrowing,” says Vineet Menachery, a virologist at the University of Texas Medical Branch. The study suggests that the alarming pace at which new or reemergent viruses have caused outbreaks in recent decades “is not some abnormal situation,” Menachery told me, “but what we should be expecting, maybe even with an acceleration.”

Carlson and Albery drolly nicknamed their study “Iceberg,” denoting a huge and mostly hidden threat that we unwittingly collide with. Indeed, their simulation revealed that mammalian viruses have already been dramatically reshuffled, to a degree that likely can’t be undone even if all carbon emissions cease tomorrow. The Anthropocene, an era defined by humanity’s power over Earth, is also an era defined by viruses’ power over us—a Pandemicene. “The moment to stop climate change from increasing viral transmission was 15 years ago,” Carlson said. “We’re in a world that’s 1.2 degrees warmer [than preindustrial levels], and there is no backpedaling. We have to prepare for more pandemics because of it.”

The Iceberg study suggests that new spillovers will follow surprising rules. For example, the team assumed that these events would be concentrated in the Arctic because warming temperatures nudge animals toward higher, cooler latitudes. But if two species move northward in parallel, nothing changes. The real drama occurs, for instance, when animals seek higher, cooler altitudes, and when those living on opposite sides of a mountain meet in the middle. This means that spillovers will be concentrated not in the poles, but in the mountainous and species-rich parts of tropical Africa and southeast Asia.

Southeast Asia will also be especially spillover-prone because it’s home to a wide range of bats. Flight gives bats flexibility, allowing them to react to changing climates more quickly than other mammals, and to carry their viruses farther. And bats in Southeast Asia are highly diverse, and tend to have small ranges that don’t overlap. “You shake that like a snowglobe and you get a lot of first encounters,” Carlson said.

Such events will also be problematic elsewhere in the world. In Africa, bats are probably the natural reservoirs for Ebola. Thirteen species could potentially carry the virus, and as global warming forces them to disperse, they’ll encounter almost 3,700 new mammal species, leading to almost 100 spillovers. So far, the biggest Ebola outbreaks have occurred in West Africa, but Carlson said that within decades, the disease could easily become a bigger problem for the continent’s eastern side too. “And that’s emblematic of everything,” he told me: Every animal-borne disease will likely change in similarly dramatic ways.

These reshufflings are bad news for bats and other animals, which will have to cope with unfamiliar infections on top of the hardships of climate change. Even one newly introduced disease can reshape an ecosystem, and many such wildlife epidemics have occurred in recent decades. “For species in poor health, showing up in new habitats and being bombarded by disease is probably not good for their conservation,” Carlson said. And spillovers that initially occur between other mammals could someday affect us: The original SARS virus hopped from bats to humans via civets, and HIV reached us from monkeys via chimpanzees and gorillas. For an animal virus to jump into humans, geography, biological compatibility, and other factors must line up in just the right way. Each event is unlikely: Imagine playing Russian roulette using a gun with a million chambers. But as the climate changes, we’re loading more of those chambers with bullets, and pulling the trigger more frequently. Carlson can’t say whether climate-induced viral reshuffling directly led to the current pandemic, but they certainly make such events more likely.

The Iceberg simulation also showed that such events will be disproportionately common in areas that are likely to be settled by humans or used as cropland. “Species are going to move to spaces that are a little uphill and environmentally stable—and that’s where we have built cities,” Carlson told me. This unhappy coincidence means that the places where their viruses will explore new hosts “just happen to be our backyards.”

Several case studies suggest that the Iceberg’s predictions are just the tip of the … well, you know. For example, melting sea ice recently allowed a virus that normally infects North Atlantic seals to jump into the Pacific Northwest’s sea otters. But Iceberg, ironically, didn’t consider either melting ice or marine mammals. It didn’t consider birds, which harbor their own coterie of viruses, including several dangerous influenza strains. It didn’t consider potential pathogens other than viruses, such as fungi or bacteria. “I don’t think they’re overstating the problem,” Raina Plowright, a spillover expert at Montana State University, told me. The effects of climate change are compounded by habitat loss and other destructive forces in unpredictable ways, she said, which could force species to move and mingle even more radically than Iceberg simulated.

This is already happening. At first, Carlson and Albery assumed that the changes they simulated would occur in the later half of this century. But instead, their simulation suggested that we could be living through the peak era of spillovers right now. The problem will worsen as the world warms, but it’s plenty warm already—so most of the predicted viral reshufflings are either happening or about to. And to Carlson’s surprise and dismay, that remains true even if we successfully curb greenhouse-gas emissions henceforth. There are many good reasons to slow the pace of climate change, but the Pandemicene, having been unleashed, cannot be rebottled.

The revelations are “so large and heavy to behold that even as we were writing them, we didn’t want to,” Carlson said. But despite every attempt that he and Albery made to naysay their own work, the simulation kept spitting out the same results. They confirm that three of our greatest existential threats—climate change, pandemics, and the sixth mass extinction of wildlife—are really intertwined parts of the same mega-problem. To tackle it, “we need atmospheric scientists talking to ecologists talking to microbiologists talking to demographers,” Rachel Baker, whose research at Princeton focuses on climate and disease, told me.

The study “is not uplifting,” but being informed is useful, Sadie Ryan, a medical geographer at the University of Florida, told me. Efforts to surveil wild animals for worrying viruses can now be targeted to hot spots where those creatures will be, instead of simply their current whereabouts, Ryan said. Artificial intelligence makes identifying the most concerning pathogens easier. Vaccines can be prepared ahead of time, and more quickly than before.

But pandemics are inherently unpredictable, and no amount of prevention will fully negate their risk. The world must be ready to meet the viruses that slip through the net. That means fortifying public health and health-care systems, strengthening social safety nets, and addressing all the weaknesses of the pre-COVID normal that made the world so vulnerable to the current pandemic and will leave it susceptible to the next. The world, in its desire to move past COVID, is already forgetting the lessons of the recent past, and perhaps assuming that a generation-defining crisis will occur only once a generation. “But no, all of this could happen again tomorrow,” Carlson said. And “if this many viruses are undergoing host jumps this much,” multiple pandemics could strike together.

Carlson sounded rattled when I spoke with him, his anxiety about his findings cloaked by gallows humor. He told me that the Iceberg study was both the hardest and the most meaningful thing he’s ever done. He and Albery worked on the project from the small apartment they shared during the early pandemic. They kept the bar napkin on which they first drafted the title of their eventual paper on their fridge. The study’s grim results have been a huge burden to bear, but they and their team bore it together. Today, their paper has been published, the world will know, and Carlson will testify before Congress about the need to prepare for spillovers. “And then,” he told me, “we’ll start the project of fixing it.”

The Final Pandemic Betrayal

2022-04-13T09:06:07-04:00

Photo Illustrations by Aaron Turner

Lucy Esparza-Casarez thinks she caught the coronavirus while working the polls during California’s 2020 primary election, before bringing it home to her husband, David, her sister-in-law Yolanda, and her mother-in-law, Balvina. Though Lucy herself developed what she calls “the worst flu times 100,” David fared worse. Lucy took him to the hospital on March 20, the last time she saw him in the flesh. He died on April 3, nine days before their wedding anniversary, at the age of 69. Lucy said goodbye over Skype. During that time, Yolanda fell ill too; after two months in the hospital, she died on June 1. Balvina, meanwhile, recovered from her bout with COVID-19, but, distraught after losing two children in as many months, she died on June 16. Lucy found herself alone in her home for the first time in 23 years. Because the hospital never returned David’s belongings, she didn’t even have his wedding ring.

Lucy had coped with the losses of her father, sister, and mother in the two decades before the pandemic. But she told me that what she feels now is fundamentally different. She never got to comfort David before he died, never got to mourn him in the company of friends, and never escaped the constant reminders of the disease that killed him. Every news story twisted the knife. Every surge salted the wound. Two years later, she is still inundated by her grief. “And now people are saying we can get back to normal,” she told me. “What’s normal?”

The number of people who have died of COVID-19 in the United States has always been undercounted because such counts rely on often-inaccurate death certificates. But the total, as the CDC and other official sources suggest, will soon surpass 1 million. That number—the sum of a million individual tragedies—is almost too large to grasp, and only a few professions have borne visceral witness to the pandemic’s immense scale. Alanna Badgley has been an EMT since 2010, “and the number of people I’ve pronounced dead in the last two years has eclipsed that of the first 10,” she told me. Hari Close, a funeral director in Baltimore, told me that he cared for families who “were burying three or four people weeks apart.” Maureen O’Donnell, an obituary writer at the Chicago Sun-Times, told me that she usually writes “about people who had a beautiful arc to their life,” but during the pandemic, she has found herself writing about lives that were “cut short, like trees being cut down.” On average, each person who has died of COVID has done so roughly a decade before their time.

In just two years, COVID has become the third most common cause of death in the U.S., which means that it is also the third leading cause of grief in the U.S. Each American who has died of COVID has left an average of nine close relatives bereaved, creating a community of grievers larger than the population of all but 11 states. Under normal circumstances, 10 percent of bereaved people would be expected to develop prolonged grief, which is unusually intense, incapacitating, and persistent. But for COVID grievers, that proportion may be even higher, because the pandemic has ticked off many risk factors.

Deaths from COVID have been unexpected, untimely, particularly painful, and, in many cases, preventable. The pandemic has replaced community with isolation, empathy with judgment, and opportunities for healing with relentless triggers. Some of these features accompany other causes of death, but COVID has woven them together and inflicted them at scale. In 1 million instants, the disease has torn wounds in 9 million worlds, while creating the perfect conditions for those wounds to fester. It has opened up private grief to public scrutiny, all while depriving grievers of the collective support they need to recover. The U.S. seems intent on brushing aside its losses in its desire to move past the crisis. But the grief of millions of people is not going away. “There’s no end to the grief,” Lucy Esparza-Casarez told me. “It changes. It morphs into something different. But it’s ongoing.”

By upending the entire world, COVID could have created a shared experience that countered the loneliness of grief. But most of the people I’ve been speaking with feel profoundly lonely—detached from society, from their support network, and especially from their loved ones at the moment of their death.

Sabila Khan’s dad, Shafqat, had an aggressive form of Parkinson’s disease, and she knew their time together was limited. “But every time I imagined him dying, I imagined us being with him,” she told me. In her mind, the family would encircle his bed, filling his final moments with tributes of love and gratitude. Instead, none of them saw him for a full month before his death. The rehab facility where he was temporarily staying closed its doors to visitors in March 2020. The family kept in touch with him through daily calls, but after COVID hit the facility and took Shafqat’s voice, he stopped answering. On April 6, he was rushed to a hospital just three blocks away from the family’s house, but when he died 8 days later, “he might as well have been on a different planet,” Sabila told me.

Donovan James Jones loved WWE and church. “He made his own decision to be baptized,” his mother, Teresita Horne, said. “He was so proud.”

Most of the grievers I interviewed had similar experiences, especially during the early pandemic. From the last time they saw their loved one in person to the moment they said goodbye on a grainy screen, their separation was absolute. They weren’t allowed to visit. Communication was impossible once ventilators became necessary. Updates were scarce because hospitals were overwhelmed. There was just the waiting. Some waited while fighting for their own life. Teresita Horne had spent more than a week on a breathing machine when her 13-year-old son, Donovan, died in a different hospital; she watched him die on her phone. “I remember screaming,” she told me. “When your kids are sick, they need you, but I couldn’t be there to comfort him. I couldn’t hold his hand one last time.”

These experiences share qualities with other devastating crises. Sarah Wagner, an anthropologist at George Washington University who researches death and mourning, sees similarities between the experiences of COVID grievers and people whose loved ones went missing during wars. “Families didn’t know what happened and are left to imagine those horrible last moments” in a way that “still troubles their grief years later,” she told me. Sabila Khan, for example, knows little about her father’s final days, except that he likely spent them “in a warzone of an ER,” she told me. “What was he thinking? How do I even come to terms with that?” Many grievers know that dying from COVID is long and grueling. Sherry Congrave Wilson was tearful but unflinching when she told me that Felicia Ledon Crow, her best friend of 30 years, died suffering and alone. “I just hope and pray that she had a loving nurse, someone around who was kind to her,” Congrave Wilson said.

The aftermath of a COVID death is lonely too. Social rituals can help people cope with guilt and uncertainty, but during much of the pandemic, funerals, wakes, and shivas haven’t happened. Kristin Urquiza, a co-founder of the nonprofit Marked by COVID, lost her father in June 2020; aside from a bizarre virtual funeral where the connection kept glitching, she still hasn’t been able to mourn and celebrate him with the hundreds of people who loved him. And without outlets for collective expression, grief can stew. Hari Close, the funeral director, told me that some people felt they had failed their loved ones twice over, first by not being with them at the end and again by not being able to celebrate their life.

After death, routine and social connection can help mourners cope. But grievers have been deprived of both because of America’s continued failure to control the pandemic. “In addition to mourning my dad, there was that extra layer of mourning my life,” Sabila said. Several people told me that friends or family members who once would have been supportive pillars became distant or unhelpful, either because they began to swallow pandemic misinformation or because they were simply exhausted. When Rekha, a family friend of mine who lives in Seattle, lost her dad in 2013, “everyone I knew showed up and took care of me,” she told me. That didn’t happen when her mother died of COVID this January because “everyone’s depleted,” she said. (The Atlantic is identifying Rekha by only her first name to protect her extended family’s desire for privacy.)

Shafqat Khan loved activism, sports, and books—American, British, South Asian classics and serials, and, “when he was especially desperate,” his daughter Sabila’s young-adult novels, she said.

While support has vanished, reminders of loss have proliferated. Many people have found themselves isolating in now-emptier homes. The phones on which they watched their loved ones die sit in their hands every day. The disease that has caused them so much pain has been perpetually on the news and on people’s lips—a miasma of triggers that has kept their grief raw. “To have to confront on an almost hourly basis everyone’s feelings about this situation that we’re in made it so much worse,” Kristin Urquiza told me.

Many of the people I interviewed felt that their loved ones immediately became statistics—that their individual tragedy was subsumed by the pandemic’s enormity, and that people were constantly discussing every aspect of the crisis except for grief. “In American culture, grief is already a very isolating experience, but it has been even more isolating this time around—which is weird because we’re all supposed to be in this collective experience together,” Rekha said. The pandemic’s circumstances have left her and millions of others in an almost paradoxical state of mass isolation. They’ve all shared in the same tragedy but feel so very alone.

When COVID grievers tell others about their loss, they tend to get the same responses. Do you know how they were exposed? Did they have a preexisting condition? Were they vaccinated? Every griever I interviewed has faced these questions, from online trolls and close friends alike, and with shocking immediacy. People regularly ask Rekha if her dead mother was vaccinated before they offer condolences or sympathies. “It’s not just one time; it’s all the time,” she said. “It’s all the time,” Kristin Urquiza echoed. “Pretty much from every person,” says Christina Faria, who lost her mother, Viola, late last year.

In 1989, the grief expert Kenneth Doka coined the term disenfranchised grief to describe situations where people struggle to cope with losses that aren’t “socially sanctioned, openly acknowledged, or publicly mourned.” That’s exactly what many Americans who have lost someone to COVID are experiencing. The words we normally use to console grievers honor the relationships that death disrupts: I’m sorry for your loss. But the questions that COVID grievers get “reduce the person to the disease,” Rebecca Morse, who studies death and loss at Divine Mercy University and is a former president of the Association for Death Education and Counseling, told me. And they cast judgment upon the circumstances around their infection, “which makes these deaths stigmatized and shameful,” Morse said. If the deceased was unvaccinated, went to a bar, or had preexisting health problems, their life becomes devalued, and their death becomes less tragic. When hearing about Viola’s death, “everyone is like, ‘Oh, she was 76’ or ‘She had heart surgery’ or ‘She was overweight. What did you expect? Of course she was going to be the one to die,’” Christina told me. Especially after vaccines became available, COVID became lumped with causes of death such as lung cancer, liver disease, and AIDS, which society classifies as self-inflicted and therefore worthy of blame rather than sympathy. Instead of getting support, many COVID grievers have been forced to defend their loved ones and justify their grief.

“Everyone is having a fear response,” Rekha told me. They’re grasping for signs that their choices, or their lack of preexisting conditions, make them safe. But that instinct easily turns data into stigma. If someone’s death fits with population-wide trends—if they were older, chronically ill, or unvaccinated—their loss is explicable, and therefore dismissible. The compulsion to explain away a death is so strong that although Rekha’s mother was thriving, beyond having high blood pressure, even people who knew her were quick to retrofit poor health onto their memories. They’ll claim she was frail, as if “COVID was the last little bit of her dying anyway,” Rekha told me. “And, like, You were around her, and she was fine!”

At the other extreme, people whose deaths don’t fit with population-wide trends are also dismissed as statistical outliers who inconveniently complicate accepted notions of safety. Teresita Horne keeps hearing that kids aren’t at risk from COVID, even though she knows many parents who have lost children of Donovan’s age. “You don’t hear about them,” she told me. The odds that a child will die of COVID are incredibly low, but if your child is part of the numerator, it doesn’t matter how large the denominator is. Similarly, vaccines are extremely effective at preventing COVID deaths—but some vaccinated people still die, Christina’s mother among them. “Everyone assumes she wasn’t vaccinated,” she told me. “They want to believe that people didn’t do all the things they needed to do to be safe—and that’s not true for a lot of people.” When Cleavon Gilman, an ER doctor, honors such folks on Twitter, he gets accused of undermining confidence in vaccines, or even being an anti-vaxxer. “It’s gotten to the point where if someone was vaccinated and died from COVID, people think you shouldn’t talk about it,” he told me.

Grievers must also deal with lies and mocking. On the day that Esparza-Casarez’s husband died in April 2020, she watched a press conference in which Donald Trump stated that the virus “is going away.” Zach, an artist who lives in St. Louis, saw a clip of Ted Cruz mocking masks at the Conservative Political Action Conference while his father lay dying in a hospital. (The Atlantic has agreed to identify him by only his first name to avoid heightening tensions in his family that have already been exacerbated by the pandemic.) “It was just a punch in the gut … the mania, the cheering, the applause,” he told me. “Imagine if you lost someone to cancer and half the country was making fun of cancer all the time,” he said. “Imagine that it’s just everywhere, every day, and it doesn’t go away.”

Mark Urquiza loved karaoke, the Dallas Cowboys, hunting, NASCAR, and people; he was the life of the party and “never met a stranger,” his daughter, Kristin, said.

These dynamics have silenced many grievers, deepening their already intense isolation. Martha Greenwald, a writer in Kentucky, runs a site called Who We Lost where people can post stories of their loved ones; many do so because the site doesn’t allow comments, making it a rare space where they can share their grief without risking judgment.

Sympathy is even scarcer for people whose loved ones bought into COVID disinformation. Kristin Urquiza’s father, Mark, took COVID seriously at first but let his guard down in May 2020. Trump had said it was time to reopen society, Arizona Governor Doug Ducey lifted restrictions, and Mark, a lifelong Republican, said, “Why would they say it’s safe if it’s not safe?” Kristin recalled. “That’s when I lost the battle with my dad.” Later, after he caught COVID, most likely at a bar, and before he went into the hospital for the last time, she asked him if he felt betrayed. “My dad never, ever hesitated with his words, but there was just this long pause, and he quietly said yes,” she told me. People have told her that Mark deserved what he got. But Kristin sees him as yet another victim of the disinformation that ran rampant among his social circles, his media universe, and the elected leaders he trusted. “That shouldn’t result in a death sentence,” she said.

For more than two years, COVID has tested America’s institutions—its political apparatus, its information networks, its public-health system, its hospitals—and found them all wanting. Several grievers told me stories in which many failing systems crashed down upon their loved ones. A refugee with a family to feed isn’t eligible for financial assistance and so carries on working at an oil change station throughout a COVID surge, and gets infected. Local hospitals are overwhelmed, so a mother moves in with her daughter elsewhere in the country and catches COVID from her grandkids. An immunosuppressed organ-transplant recipient dies of COVID after their child brings it home from school. The employees at a doctor’s office don’t learn that they’re COVID-positive for days, because the holidays have created a backlog of tests, so a mother who turns up for an appointment in the intervening time gets COVID from them.

These complicated chains of events mean that “if you lost someone to COVID, you don’t even know where to begin to find accountability,” Alex Goldstein, who runs a memorial Twitter account called @FacesofCovid, told me. Do you blame Trump or Joe Biden? Your governor or your mayor? The person who infected your loved one or the person who infected that person? Those who sow misinformation or those who buy into it? The entire world? “Blame has been placed all over, and responsibility is so diffuse,” Wagner, the anthropologist at George Washington University, told me. “It’s harder to create clear narratives,” which makes the tragedy feel that much more senseless.

Many grievers end up blaming themselves. Should I have pulled them out of that nursing home? Should I have pushed them harder to get vaccinated? And worst of all: Did I give them COVID? “There are so many little pivot points where things could have gone a different way,” Rebecca Morse, the death-and-loss expert, told me. “Imagining what could or should have been done can increase both your anger and your guilt.” Rekha told me that her anger comes in waves, “and I don’t even know what to be angry at,” she said. “I feel like we’re all culpable to different degrees.”

Many grievers are finding the current phase of the pandemic especially hard. For the families of the first 100,000 Americans to die of COVID, “there was at least a sense that the world had stopped,” Sabila Khan told me. Now, grieving families are told that we must learn to live with the virus that only just tore a hole in their lives. Jeannina Smith, a doctor at the University of Wisconsin at Madison, cares for organ-transplant recipients, who are on immunosuppressive drugs and are therefore particularly vulnerable to disease; she told me that she lost more patients in the Omicron surge than at any previous point in the pandemic. “They did everything right—they got vaccinated and boosted and were so careful,” Smith said, and their loved ones must now mourn them “while society is saying that COVID is over.”

Felicia Ledon Crow loved orchids, tulips, DIY, reggae, and walks. She and her friend Sherry Congrave Wilson talked about “getting old together” and being “these crazy hip old ladies,” Congrave Wilson told me.

After Christina Faria’s mother died on December 29, 2021, her friends said it was a harsh reminder that the pandemic wasn’t over. “But here we are, not even three months later, and no one talks about her anymore,” Christina told me in March. She has several disabilities that make her vulnerable to respiratory infections, and Viola was her primary caregiver; she’s now struggling to pay her bills, keep her home, and protect her health. And yet, she told me, her friends are getting annoyed that she still wants to wear a mask when she isn’t required to.

Many grievers are starved for sympathy and patience because our popular understanding of grief is wrong. An influential but misleading model suggests that it progresses through five stages—denial, anger, bargaining, depression, and acceptance. But in fact, it doesn’t involve discrete stages, doesn’t proceed along a predictable linear path, and might not end in acceptance. “Closure” is a simplistic myth. Grief, as it actually unfolds, is erratic, and in many cases slow. Rekha remembers feeling pressured to move past her dad’s death in 2013; she now feels an extreme version of the same compulsion, as if society is insisting that this is the moment for everyone to move past their pandemic grief together. In mid-March, after an especially tough week, she told her husband that she didn’t know why she was having a bad flare-up of grief. He reminded her that her mother died a month ago. “I had internalized this feeling that it’s time to be done with it,” she said, “and I have to remind myself that it just happened.”

Even people who lost their loved ones at the start of the pandemic are still hurting. “Time itself heals nothing,” Morse told me. Time simply gives people chances to learn ways of coping. But those chances have been stripped away by two years of social isolation and upended daily routines. And “without grappling with the daily reality of the loss, the mind doesn’t fully process what happened,” Natalia Skritskaya, an expert in prolonged grief at Columbia University, told me.

Instead, many people “created a time capsule,” Morse said, locking their grief away without ever learning how to live with it. When society reopens, the capsule does too, and the grievers reemerge, still raging and sorrowful while everyone else has moved on. “You’re repeating the same parts of grief all over again and not able to get past it,” Keyerra Snype, a health-care worker, told me. She lost her grandmother Shirley during the first COVID surge, and more than two years later, “it’s difficult all over again,” she said.

David Casarez loved sci-fi, golf, California’s Moonstone Beach, and gardening. “I called him the ‘orchid whisperer,’” his wife, Lucy, said.

Others are trapped in a pandemic time capsule, too, including those whom we rely on to witness death, prevent it, or deal with its aftermath. Hari Close, the funeral director, told me that “even though people think we are used to death, it’s been overwhelming trying to comfort families in their loss,” especially while losing family members and colleagues himself. Cleavon Gilman, the ER doctor, told me that many health-care workers are traumatized after two years of repeatedly telling families that their loved one has died, “hearing that shrill cry on the phone over and over, and then going outside to see a world that’s acting like we’re lying about the numbers.” (Gilman also lost three colleagues to the pandemic: two nurses who died of COVID and a mentor who died of suicide after witnessing the first surge.) Alanna Badgley, the EMT, felt like something broke after Omicron arrived. In February, “at one point, I just started crying and couldn’t stop,” she told me. “I’m just so sad, and I don’t know how to feel better. It’s not like depression. It feels like grief.”

Some of the grievers I talked with feel kinship with COVID long-haulers, whose lives have been flattened by months or years of relentless symptoms and who similarly feel dismissed, ignored, and isolated. They didn’t die of COVID, but many nonetheless lost much of their former life. After getting infected in October 2020, Alexis Misko can no longer muster enough energy to stand for more than 10 minutes or sit upright for more than an hour. She was once an occupational therapist and an avid hiker, and “I grieve constantly for that person,” she wrote in 2021. Nick Güthe told me that after getting long COVID, his wife, Heidi Ferrer, went from being “one of the healthiest people I knew” to living with extreme fatigue and excruciating pain. “In the last weeks of her life, she couldn’t walk, eat most foods she enjoyed, or read a book,” Nick said. “It felt like bees were stinging her ankles all day long.” Heidi died of suicide last May. The doctor who treated her at the hospital and confirmed her death to Nick had never heard of long COVID.

In her book The Myth of Closure, Pauline Boss, a therapist and pioneer in the study of ambiguous loss, offers some advice for pandemic grievers: “It is not closure you need but certainty that your loved one is gone, that they understood why you could not be there to comfort them, that they loved you and forgave you in their last moments of life,” she wrote. Instead of waiting for a clean but mythical endpoint to one’s loss, it is better to search for “meaning and purpose in our lives after this horrific time in history,” she said.

Nick Güthe now pours his energy into raising awareness of long COVID, in part to honor one of Heidi’s last requests to him. “I’ve had to talk a lot of people with long COVID off the same ledge that my wife was on, and it’s been hard to turn away from that,” he said. “I’ve saved quite a few people at this point.” Alex Goldstein also feels compelled to continue posting tributes to the deceased on his @FacesofCOVID account, because it’s all the recognition that some grievers get. “A lot of folks tell me that when it’s late at night and they’re thinking about their loved one, they’ll go to the tweet and look at replies from strangers around the world,” he told me. Four days after her dad died, Sabila Khan started a Facebook group for COVID grievers, which now has 14,000 members. Shafqat was an activist who spent years advocating for Pakistani immigrants, and “this has become a way for me to keep his memory and good work alive,” Sabila told me. “It gives me purpose in my grief.”

In contrast to these grassroots efforts, national moments of mourning and remembrance have been rare and fleeting. A few art projects have powerfully commemorated the losses, but briefly. After collective tragedies, “the rites and rituals of mourning are meant to bring groups back together,” Wagner, the anthropologist, told me. “We’re seeing a process that’s almost antithetical to that, because mourning has been so fragmented and suspended.” Sabila told me that even as a Muslim, she felt more solidarity among fellow Americans after 9/11 than over the past two years. “We didn’t have that rallying moment with COVID,” she told me.

Shirley Snype loved butterflies, the Investigation Discovery channel, the color purple, and “her kitten, Cici,” her granddaughter Keyerra said.

Some of the people I interviewed felt relieved when Biden presided over a lighting ceremony in February 2021, when the COVID death toll was just half what it currently is. But Kristin Urquiza told me that such gestures are “insignificant in comparison to the massive amount of death and suffering that we’ve had.” The nonprofit that she co-founded, Marked by COVID, is pushing the U.S. toward actions more fitting in scale. It wants the first Monday of March to be marked as a national COVID Memorial Day, and for permanent memorials to be erected around the country. “Putting my grief into a physical thing would take off some of the emotional heaviness,” Keyerra Snype told me. And having a solid, lasting memorial would go some way to assuring grievers that their loss is real, and that their loved ones mattered. Urquiza said that she’s striving for the country not just to remember her dad but to remember everything that cost him his life. “We can’t just put this in a memory hole, or we’ll forget,” she said. “I don’t want anyone to ever feel what I’ve had to feel.”

Wagner has seen similar dynamics after past atrocities, in which bereaved family members found themselves having to fight for recognition and reconciliation. “Why on earth should someone who lost multiple members of their family not be allowed to be with their grief, instead of bearing the responsibility for repairing society?” she said. “When it isn’t politically expedient for those in positions of power to commemorate the deaths and extend forms of reparation, it falls on the families.”

If there’s one thing Teresita Horne wants the world to know about Donovan, it’s that “he was one of the kindest souls anyone would have met,” she told me. Kindness is also the thing she most wants from everyone else, no matter their politics or their positions on the pandemic’s numerous controversies. One million people died in just over two years. It should be incontestable that they are gone, that they mattered, and that the millions more who loved them should get the grace and space to grieve and mourn.

All portraits featured here are courtesy of family and friends of the people pictured.

What Can One Disease Do to a Landscape?

2022-04-07T11:20:53-04:00

The past two years have shown just how badly a disease that originated in wildlife can upend the human world. But epidemics can also move in the opposite direction, with equally dramatic results. Argentina’s San Guillermo National Park, for example, was once dominated by the puma—a top predator that, by controlling grazing animals, determined the patterns of plants across the landscape. But the puma was ousted from its role as the park’s chief terra-former by a disease, which radically reshaped the entire ecosystem in a few short years.

Julia Monk of Yale and Justine Smith of UC Davis were well placed to watch the outbreak unfold. For years, they had been studying the park’s wildlife, including its vicuñas—smaller relatives of llamas. San Guillermo was home to 5,000 to 10,000 vicuñas, before their numbers began to crash in 2017. In 2019, Monk saw just 80 of them. “We went from driving around and seeing them everywhere to going for days without seeing any,” she told me.

The vicuñas had been decimated by a disease called sarcoptic mange, which is caused by a microscopic mite that burrows into an animal’s skin. In domestic dogs, the mites cause itching and hair loss; in vicuñas, the consequences are more severe. These animals have some of the finest wool on the planet, which allows them to survive on cold and windy mountains. By robbing them of their hair, mange deprives them of warmth. In advanced cases, the disease also locks their joints, paralyzing them. Smith remembers seeing mange-ridden vicuñas in a snowstorm, exposed to the elements and unable to walk to shelter.

Local vets and farmers had never seen mange afflicting San Guillermo’s vicuñas in any of the past five decades. So where did the disease come from? A team led by Marcela Uhart of UC Davis found an important clue: The mites that had infected the dead vicuñas were all almost genetically identical, which suggested that they had all come from a single source. Around the world, livestock and pets are known to pass mange mites to wild species; in San Guillermo, the most likely culprits were domestic llamas, which had been introduced into the surrounding area in 2009 and would wander in and out of the national park. Some had been diagnosed with mange.

[Read: The cascading consequences of the worst disease ever]

The vicuñas’ absence rippled through the rest of the park’s wildlife. They used to be the major prey of San Guillermo’s pumas, which then left behind carcasses that fed Andean condors—huge vultures that, with 11-foot-long wingspans, are the world’s largest flying birds. Vicuña carcasses made up almost 90 percent of the condors’ diet, and as the mange outbreak spread, the condors flew elsewhere in search of food. “In earlier years, you’d see condors flying overhead every day, no question,” Monk said. “In 2019, we saw condors once or twice in three and a half months.” If the exiled condors try to scavenge livestock carcasses from the closest farmlands, they risk being poisoned, either by pesticides in the meat or by poisons that farmers deliberately add to keep the birds away.

The park’s vegetation has also changed. In the past, the vicuñas used to avoid the park’s canyons in favor of its open plains, where they could more easily spot approaching pumas. As a result, the canyons were grass-covered but the plains were barren, as “the plants had been eaten down to almost nothing by these vicuñas,” Smith told me. But mange erased the difference between the canyons and the plains, increasing grass cover in the latter by up to nine times. The plains went from “completely barren ground, nothing but gravel, to this highly productive grassland,” Smith said.

The forces that shape the land are now different. Pumas used to dominate, patterning the park’s plants by concentrating the vicuñas in the plains. By killing the vicuñas, mange nullified the pumas’ influence. (Monk said she isn’t sure whether the number of pumas has declined; their scats suggest that they’re weathering the loss of their major prey by shifting to smaller targets.)

Having brought mange to San Guillermo, humans could conceivably do something about it. The disease can be treated with—ahem—ivermectin, and “especially when the population is close to nothing, it wouldn’t be too hard,” Smith said. But it’s unclear whether vicuñas would then rebound. The grasses that have sprouted in the plains are feeding invasive European hares, which seem to have at least doubled in numbers since the mange outbreak began. If the pumas start eating hares, they might sustain themselves at a level that prevents the decimated vicuñas from eventually bouncing back.

[Read: A starfish epidemic is decimating the oceans]

For decades, scientists have shown that the presence or absence of predators can trigger dramatic food-chain chain reactions—or “trophic cascades,” in the lingo of ecologists. Parasites and diseases should have similar effects, but to prove that they do, scientists need to collect data about an ecosystem before and after an outbreak occurs. And since “we rarely know when and where that will be, we tend to lack ‘before’ data,” Julia Buck, an ecologist at the University of North Carolina at Wilmington, told me. By good fortune, Monk and Smith had arrived in San Guillermo before mange did, and they knew what the park’s baseline was in the pre-epidemic years.

Wildlife epidemics are becoming more common. In 2015, a bacterial infection wiped out two-thirds of the world’s saiga, a big-nosed Asian antelope. An unknown epidemic killed songbirds across the eastern and midwestern United States last year. The fungus that causes white-nose syndrome is hammering North American bats. Contagious cancers are killing Tasmanian devils. In a few cases, the ripple effects of these diseases are clear. In 2013, a mystery illness disintegrated the starfish of America’s Western Seaboard: These unlikely predators are the coastal equivalent of pumas, and in their absence, their sea-urchin prey were free to devour offshore kelp forests. A deadly fungus that humans inadvertently carried around the world has ravaged the planet’s amphibians, wiping out 90 species and leaving more than 100 others close to extinction; the snakes that eat those amphibians have also dwindled.

“My guess is that this happens more often than we have evidence for,” Smith said. As humans and our livestock expand into the ranges of wild species, we create more opportunities for diseases to spill over in both directions. And as San Guillermo’s mange outbreak shows, the growing threat of wildlife epidemics can’t be managed by simply segregating animals in protected spaces. The park is six hours away from the nearest town. It sees almost no tourists. “It’s really remote and it was still exposed to this disease that was probably anthropogenic,” Smith said. If mange can reshape San Guillermo, “what places are really safe?”