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Tag: gold standard

  • An Adorable Way to Study How Kids Get Each Other Sick

    An Adorable Way to Study How Kids Get Each Other Sick

    At the start of 2022, as the Omicron variant of the coronavirus blazed across the United States, Seema Lakdawala was in Pittsburgh, finalizing plans to open a brand-new day care. She had found the perfect facility and signed the stack of paperwork; she had assembled a hodgepodge of plushies, puzzles, and toys. It was the perfect setup, one that “I’ve been dreaming about for years,” Lakdawala, a virologist at Emory University, told me. She couldn’t help but swell with pride, later that spring, when she ushered in her establishments’ first attendees: five young ferrets—including one deliberately infected with the flu.

    Over the next several months, Lakdawala and her colleagues watched several cohorts of ferrets ping-pong flu viruses back and forth as they romped and wrestled and frolicked inside of a shared playpen. The researchers meticulously logged the ferrets’ movements; they took note of the surfaces and other animals that each one touched. Their early findings, now being prepared for publication in a scientific journal, could help researchers figure out how flu viruses most efficiently spread in group settings—not just among ferrets, but among human kids.

    Aerosols, droplets, face-to-face contact, contaminated surfaces—there are plenty of ways for flu viruses to spread. But the nitty-gritty of flu transmission remains “pretty much a black box,” says Aubree Gordon, an epidemiologist at the University of Michigan. Despite decades of research, “we really don’t know the relative importance of each potential route.” Now, though, ferrets in playpens could help researchers to tease out those dynamics—and even, someday, to design flu-blocking measures for bona fide day cares.

    Ferrets have long been the “gold standard for influenza infection and transmission,” says Nicole Rockey, an environmental engineer at Duke University who led the experiments with Lakdawala. The animals’ airway architecture is uncannily similar to ours, and unlike most lab mice, ferrets are vulnerable to catching and passing on flu viruses—even developing the same coughy, sniffly symptoms that so many humans do. But most flu-transmission experiments in ferrets remain limited to artificial circumstances: pairs of animals in tiny cages with dividers between them, where scientists ogle them inhaling each other’s air for days or even weeks. That’s not how animals catch one another’s infections in the wild, and it’s certainly not how human outbreaks unfold. “We don’t interact with each other for 48 hours straight through a perforated wall,” Rockey told me.

    A giant playpen outfitted with toys, air samplers, and video cameras isn’t exactly a natural habitat for a ferret. But the setup does tap into many of the animals’ impish instincts. Domesticated by humans over thousands of years, ferrets “are a very playful species, and they love to be social,” says Alice Dancer, an animal-welfare researcher at the University of London’s Royal Veterinary College. That makes them great models for not just flu transmission, but flu transmission among kids, who are thought to be major drivers of outbreaks. In their day care, the ferrets squabble over toys, clamber up play structures, and canoodle plush snakes; they chase one another around, and nap in big piles when they get tuckered out; they exchange affectionate nuzzles, bonks, and little play bites. Every interaction represents a potential transmission event; so, too, do the surfaces they touch, and the shared pockets of air from which they all breathe.

    Read: The flu may never be the same

    Already, the researchers have collected some results that, Lakdawala told me, are “changing the way I think about transmission a little bit.” In one early experiment, involving an infected animal cavorting with four uninfected ones, they were surprised to find that the ferret with the least direct contact with the flu “donor” was the only “recipient” in the room who got sick. It seemed counterintuitive, Lakdawala told me, until video footage revealed that the newly sickened recipient had been copying everything that the donor did—chewing the toys it chewed, rolling the balls it rolled, swiping the surfaces it swiped. It was as if the first ferret was leaving a trail of infectious breadcrumbs for the second one to snarf. If that finding holds up in other experiments, which the researchers are analyzing now, it could suggest that contaminated surfaces, or fomites, are playing a larger-than-expected role in passing the virus around, Rockey told me.

    Another of the team’s early findings points to a similar notion. When the researchers cranked up the ventilation in their ferret day cares, hoping to clear virus particles out of the air, they found that the same proportion of uninfected ferrets ended up catching the virus. This was disappointing, but not a total shock given how paws-on ferrets—and kids, for that matter—are with one another and their surroundings. It didn’t matter if the air in the room was being exchanged more than once every three minutes. Whenever the ferrets had their run of the room, the researchers would find virus particles smeared on the toys, the snack station, and the playpen walls.

    Ventilation wasn’t totally useless: More air exchanges, the team found, did seem to reduce the concentration of flu genetic material in the air, and the ferrets who got infected under those conditions were slower to start shedding the virus—a hint, Lakdawala thinks, that they might have taken in a lower infectious dose. Among humans, that might translate into less severe cases of disease, Gordon told me, though that would need to be confirmed.

    Whatever upshots Rockey and Lakdawala’s ferret findings might have for human day cares won’t necessarily apply to other venues. In offices, hospitals, and even schools for older kids, people are generally a lot less tactile with one another, and a lot better versed on hygiene. Plus, adult bodies just aren’t built like kids’, says Cécile Viboud, an epidemiologist at the Fogarty International Center at the National Institutes of Health. Their airways are bigger, stronger, and more developed—and some experiments suggest that, for at least some respiratory viruses, the older and larger people are, the more infectious aerosols they might expel. For adults, ventilation may matter all the more.

    Lakdawala and her colleagues are still mulling some other interventions that might work better for ferrets, and eventually kids: humidifiers, air purifiers, targeted cleaning, maybe even keeping individuals from crowding too closely into a portion of the playpen. (They don’t plan to experiment with handwashing or masking; imagine the difficulty of strapping an N95 to a ferret’s face.) Lakdawala is also mulling whether surfaces made of copper—which her team has shown can render flu viruses inactive within minutes—could play a protective role.

    But everything that happens in the ferrets’ playpens will still come with caveats. “It’s still an animal model, at the end of the day,” Viboud told me. For all the similarities between the ferret airway and ours, the way their little noses and snouts are shaped could affect how they cough and sneeze. And the researchers haven’t yet studied spread among ferrets with preexisting immunity to flu, which some day-care attendees will have. Ferrets are also more inclined to bite, wrestle, and defecate wherever they please than the average (potty-trained) kid.

    Still, for the most part, Lakdawala delights in how childlike the ferrets can be. They’re affectionate and mischievous; they seem to bubble with energy and glee. After discovering that the air-sampling robot stationed in the center of their day care was mobile, several of the ferrets began to take it for rides. In watching and sharing the footage at conferences, Lakdawala has received one piece of feedback, over and over again: Oh yeah, parents tell her. My kids do that too.

    Katherine J. Wu

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  • A Vaccine for Birth Control?

    A Vaccine for Birth Control?

    For half a century, Gursaran Pran Talwar has been developing what he hopes will be the next big thing in birth control. A nonagenarian who was once the director of India’s National Institute of Immunology, Talwar envisions bringing to market a new form of contraception that could block pregnancy without the usual trade-offs—an intervention that’s long-acting but reversible; cheap, discreet, and easy to administer; less invasive than an intrauterine device and more convenient than a daily pill. It would skip messy, sometimes dangerous side effects, such as weight gain, mood swings, and rare but risky blood clots and strokes. It would embody the sort of “set it and forget it” model that’s become a gold standard for health—and, in his words, be “accepted by the world over.”

    Talwar’s invention is now in early-stage clinical trials. If all goes well, it could become humanity’s first contraceptive vaccine—one that would prevent pregnancies in a way distinct from any birth control ever cleared for human use. Whether they’re packaged as pills, patches, implants, or shots, most common medical contraceptives work by flooding the body with hormones to put a pause on ovulation. Talwar’s vaccine would do something different: It leaves the menstrual cycle unaltered, instead leveraging the powers of the immune system to keep unwanted pregnancies at bay.

    But temporarily vaccinating against pregnancy is both brilliant in concept and devilishly difficult in execution, both scientifically and socially. Making a contraceptive vaccine effectively means “trying to immunize an animal against itself,” says Julie Levy, a feline-infectious-disease expert at the University of Florida who has worked on immunocontraceptives in animals. Which runs counter to the prime directive of immune systems, evolved over countless millennia to distinguish the foreign from the familiar and to leave the body’s most vital tissues alone. Solve that problem, and researchers will still be left with another: persuading people to take a fertility-hampering shot in an era of widespread vaccine hesitancy—while the specter of contraception’s problematic past still looms.

    For many decades, the most stubborn barriers in contraception have been not about science, but about access and acceptance. Talwar remembers those issues crystallizing sharply for him in the 1970s, he told me, when he encountered several groups of women in the holy city of Varanasi, who told him they were struggling to feed their large families.  Yet the women’s husbands weren’t eager to use condoms and they themselves weren’t satisfied with the pills and IUDs available at the time, which sometimes interfered with normal menstruation and ovulation, and triggered headaches and mood swings. “I wanted to make something free of all these problems,” Talwar told me.

    Read: The different stakes of male and female birth control

    Within a few years, he had cooked up a solution: a vaccine against hCG, a hormone exclusive to pregnancy that’s necessary for fertilized eggs to implant. Taught to neutralize hCG, Talwar reasoned, the immune system could stop a pregnancy from ever truly starting, without attacking other tissues. His hunch so far appears to have panned out. By the mid-1990s, his team had shown in small, early-stage clinical trials that most women receiving the shots could produce enough antibodies to prevent pregnancy for several months, in some cases more than a year. Of the 119 women in the trial whose antibody levels reached what Talwar deems a protective threshold, only one became pregnant over a period of almost two years. Several participants also went on to conceive after opting out of boosters, a sign that the shot’s effects were reversible.

    Almost immediately, though, drawbacks appeared. Immune responses are infamously variable across individuals—a major reason that the effectiveness of many shots designed against pathogens tops out around 60 to 80 percent. About a fifth of the women who received the hCG vaccine didn’t produce enough antibodies to meet the protective threshold. Those stats would still be enough to slow the transmission of, say, a deadly respiratory virus. But the expectations for a contraceptive “have to be different,” says Neel Shah, the chief medical officer of Maven Clinic, a virtual clinic for women’s and family health. The top IUDs on the market prevent more than 99 percent of pregnancies, require one appointment to insert, and last for up to a decade.

    For now, the hCG vaccine is more cumbersome than that. In its current iteration—a revamp of the successful ’90s recipe—it requires an initial series of at least three doses, spaced out over several weeks. It’s still unclear how people would figure out when, and how often, to boost without regular antibody tests. The answer will likely differ from person to person; that uncertainty alone could make these shots a tough sell, says Diana Blithe, a contraception expert at the National Institutes of Health. And although halting hormonal contraceptives can reset fertility back to baseline within days or weeks, some people with especially enthusiastic immune responses could end up waiting far longer for the hCG vaccine’s effects to wear off, says Aaron Hsueh, a reproductive biologist at Stanford. For that reason and more, Hsueh has said for years that he’s “not enthusiastic” about Talwar’s experimental shot.

    There is some reason to think these issues aren’t insurmountable. Immunocontraceptives have been used for decades by wildlife scientists to prevent pregnancies in all sorts of mammals—among them deer, horses, elephants, pigs, and seals—as a more humane alternative to culling. And in that context, at least, researchers have found a way to circumvent the need for frequent boosts. Certain animals can be dosed with nanoparticles that slowly release the vaccine’s ingredients over months and years, repeatedly tickling the immune system without any additional jabs, says Derek Rosenfield, a veterinarian and wildlife biologist at the University of São Paulo. Work in wild creatures, though, has also shown how hard it is to persuade the body to target its own hormones. To get their shots to work, veterinarians have needed to include powerful adjuvants, or vaccine ingredients meant to rile up the immune system—“some of the most potent ones ever developed,” Levy told me. Which exacts a tax for the shots’ potency: In some animals, such as cats, the vaccines can cause worrying side effects, including injection-site reactions.

    In humans, where safety standards must be stricter and effectiveness better, Talwar’s hCG vaccine has encountered some issues with tolerability, too. The shots so far do seem to be skirting the side effects of pills and IUDs. But some of the women in his team’s ongoing trials are developing painless but prominent nodules—a likely sign that the new recipe’s adjuvants are riling up the immune system a tad too much. To deliver on a discreet, low-maintenance contraceptive—something with, as Talwar puts it, “zero side effects”—they’ll need to tinker with dosing or ingredients.

    Gaps in the contraceptive market do need to be filled. Technology has come a long way since Talwar first spoke with the women in Varanasi, but “we need more options,” says Debanjana Choudhuri, the director of programs and partnerships at India’s Foundation for Reproductive Health Services. Nearly half the world’s pregnancies are unplanned, and access to existing contraception is inconsistent, inequitable, and still stymied by stigma and misinformation; even in places where availability isn’t an issue, some people hesitate over the trade-offs. A temporary contraception, packaged into a super-safe vaccine, could offer convenience and privacy, with potential appeal for young urbanites, who have already been enthusiastic about injectable contraceptives and might not mind getting boosts, Choudhuri told me. Most important, adding a vaccine to the repertoire gives people “another choice.”

    But for all its unique perks, a contraceptive vaccine could also come with social drawbacks. The history of contraception is riddled with abuses, often concentrated among poor populations, people struggling with mental-health issues, and communities of color. Vaccines’ primary purpose for centuries has been to fight infectious disease, and “pregnancy is not a disease,” Sanghamitra Singh, the policy-and-programs lead at the Population Foundation of India, told me. Implying—even unintentionally—that the condition is a problem to be eradicated could stigmatize the shot.

    Deploying the vaccine primarily in under-resourced populations could also raise the specter of the eradication of fertility in society’s most vulnerable subsects. Lisa Campo-Engelstein, a reproductive bioethicist at the University of Texas Medical Branch, worries that even the vaccine’s ease of administration—an ostensible benefit—could be viewed as a downside: Administering a shot without a patient’s full understanding or consent is easier than coercively inserting an IUD or forcing a daily pill. And in this pandemic era, a contraceptive vaccine will likely be met with pushback from people already disinclined toward shots—especially amid false accusations that other immunizations compromise fertility. On top of all that, a shot that goes after hCG can prevent only implantation, not fertilization, a guaranteed sticking point for people who believe that life begins at conception, and may argue that the vaccine triggers abortion.

    In part, the timing is just bad luck. Shortly after his original clinical trial results were published, in the ’90s, Talwar, already late into his 60s, was asked to retire from the National Institute of Immunology, he told me, and had to leave his vaccine behind. After he managed to revive his efforts with the help of independent funders, Indian regulators took nearly a decade to green-light a new recipe for clinical trials—just in time for the coronavirus pandemic to begin. Régine Sitruk-Ware, a reproductive endocrinologist at the Population Council’s Center for Biomedical Research, in New York, remembers the initial buzz around the human hCG vaccine when Talwar’s clinical-trial results were published. But in the absence of more progress, she and other researchers have moved on, she told me. Many now have their sights set on long-acting reversible male birth control, several new forms of which are now close to being publicly available, and could offer safe complements to female methods and make family planning more equitable.

    Read: Block that sperm!

    Still, Talwar, who will turn 97 in October, hasn’t lost hope; to him, the nodules represent one of the last major hurdles, and should be resolved soon. As his 100th birthday ticks closer, he’s even thinking of how he can expand his approach—repurposing the hCG shot, for instance, into immunotherapy against certain cancers that aberrantly produce the hormone. “I am healthy and hearty,” he told me. “I just hope and pray,” he said, that his invention might clear its final hurdles “before I call it a day.”

    Katherine J. Wu

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  • Somehow, the Science on Masks Still Isn’t Settled

    Somehow, the Science on Masks Still Isn’t Settled

    For many Americans, wearing a mask has become a relic. But fighting about masks, it seems, has not.

    Masking has widely been seen as one of the best COVID precautions that people can take. Still, it has sparked ceaseless arguments: over mandates, what types of masks we should wear, and even how to wear them. A new review and meta-analysis of masking studies suggests that the detractors may have a point. The paper—a rigorous assessment of 78 studies—was published by Cochrane, an independent policy institution that has become well known for its reviews. The review’s authors found “little to no” evidence that masking at the population level reduced COVID infections, concluding that there is “uncertainty about the effects of face masks.” That result held when the researchers compared surgical masks with N95 masks, and when they compared surgical masks with nothing.

    On Twitter, longtime critics of masking and mandates held this up as the proof they’d long waited for. The Washington Free Beacon, a conservative outlet, quoted a researcher who has called the analysis the “scientific nail in the coffin for mask mandates.” The vaccine skeptic Robert Malone used it to refute what he called “self-appointed ‘experts’” on masking. Some researchers weighed in with more nuanced interpretations, pointing out limitations in the review’s methods that made it difficult to draw firm conclusions. Even the CDC director, Rochelle Walensky, pushed back against the paper in a congressional testimony this week, citing its small sample size of COVID-specific studies. The argument is heated and technical, and probably won’t be resolved anytime soon. But the fact that the fight is ongoing makes clear that there still isn’t a firm answer to among the most crucial of pandemic questions: Just how effective are masks at stopping COVID?

    An important feature of Cochrane reviews is that they look only at “randomized controlled trials,” considered the gold standard for certain types of research because they compare the impact of one intervention with another while tightly controlling for biases and confounding variables. The trials considered in the review compared groups of people who masked with those who didn’t in an effort to estimate how effective masking is at blunting the spread of COVID in a general population. The population-level detail is important: It indicates uncertainty about whether requiring everyone to wear a mask makes a difference in viral spread. This is different from the impact of individual masking, which has been better researched. Doctors, after all, routinely mask when they’re around sick patients and do not seem to be infected more often than anyone else. “We have fairly decent evidence that masks can protect the wearer,” Jennifer Nuzzo, an epidemiologist at Brown University, told me. “Where I think it sort of falls apart is relating that to the population level.”

    The research on individual masking generally shows what we have come to expect: High-quality masks provide a physical barrier between the wearer and infectious particles, if worn correctly. For instance, in one study, N95 masks were shown to block 57 to 90 percent of particles, depending on how well they fit; cloth and surgical masks are less effective. The caveat is that much of that support came from laboratory research and observational studies, which don’t account for the messiness of real life.

    That the Cochrane review reasonably challenges the effectiveness of population-level masking doesn’t mean the findings of previous studies in support of masking are moot. A common theme among criticisms of the review is that it considered only a small number of studies by virtue of Cochrane’s standards; there just aren’t that many randomized controlled trials on COVID and masks. In fact, most of those included in the review are about the impact of masking on other respiratory illnesses, namely the flu. Although some similarities between the viruses are likely, Nuzzo explained on Twitter, COVID-specific trials would be ideal.

    The handful of trials in the review that focus on COVID don’t show strong support for masking. One, from Bangladesh, which looked at both cloth and surgical masks, found a 9 percent decrease in symptomatic cases in masked versus unmasked groups (and a reanalysis of that study found signs of bias in the way the data were collected and interpreted); another, from Denmark, suggested that surgical masks offered no statistically significant protection at all.

    Criticisms of the review posit that it might have come to a different conclusion if more and better-quality studies had been available. The paper’s authors acknowledge that the trials they considered were prone to bias and didn’t control for inconsistent adherence to the interventions. “The low to moderate certainty of evidence means our confidence in the effect estimate is limited, and that the true effect may be different from the observed estimate of the effect,” they concluded. If high-quality masks worn properly work well at an individual level, after all, then it stands to reason that  high-quality masks worn properly by many people in any situation should indeed provide some level of protection.

    Tom Jefferson, the review’s lead author, did not respond to a request for comment. But in a recent interview about the controversy, he stood by the practical implications of the new study. “There’s still no evidence that masks are effective during a pandemic,” he said.

    Squaring all of this uncertainty with the support for masking and mandates early in the pandemic is difficult. Evidence for it was scarce in the early days of the pandemic, Nuzzo acknowledged, but health officials had to act. Transmission was high, and the costs of masking were seen as low; it was not immediately clear how inconvenient and unmanageable masks could be, especially in settings such as schools. Mask mandates have largely expired in most places, but it doesn’t hurt most people to err on the side of caution. Nuzzo still wears a mask in high-risk environments. “Will that prevent me from ever getting COVID? No,” she said, but it reduces her risk—and that’s good enough.

    What is most frustrating about this masking uncertainty is that the pandemic has presented many opportunities for the U.S. to gather stronger data on the effects of population-level masking, but those studies have not happened. Masking policies were made on sound but limited data, and when decisions are made that way, “you need to continually assess whether those assumptions are correct,” Nuzzo said—much like how NASA collects huge amounts of data to prepare for all the things that could go wrong with a shuttle launch. Unfortunately, she said, “we don’t have Houston for the pandemic.”

    Obtaining stronger data is still possible, though it won’t be easy. A major challenge of studying the effect of population-level masking in the real world is that people aren’t good at wearing masks, which of course is a problem with the effectiveness of masks too. It would be straightforward enough if you could guarantee that participants wore their masks perfectly and consistently throughout the study period. But in the real world, masks fit poorly and slip off noses, and people are generally eager to take them off whenever possible.

    Ideally, the research needed to gather strong data—about masks, and other lingering pandemic questions—would be conducted through the government. The U.K., for example, has funded large randomized controlled trials of COVID drugs such as molnupiravir. So far, that doesn’t seem to have happened in the U.S.  None of the new studies on masking included in the Cochrane review were funded by the U.S. government. “The fact that we never as a country really set up studies to answer the most pressing questions is a failure,” said Nuzzo. What the CDC could do is organize and fund a research network to study COVID, much like the centers of excellence the agency has for fields such as food safety and tuberculosis.

    The window of opportunity hasn’t closed yet. The Cochrane review, for all of its controversy, is a reminder that more research on masking is needed, if only to address whether pro-mask policies warrant the rage they incite. You would think that the policy makers who encouraged masking would have made finding that support a priority. “If you’re going to burn your political capital, it’d be nice to have the evidence to say that it’s necessary,” Nuzzo said.

    At this point, even the strongest possible evidence is unlikely to change some people’s behavior, considering how politicized the mask debate has become. But as a country, the lack of conclusive evidence leaves us ill-prepared for the next viral outbreak—COVID or otherwise. The risk is still low, but bird flu is showing troubling signs that it could make the jump from animals to humans. If it does, should officials be telling everyone to mask up? That America has never amassed good evidence to show the effect of population-level masking for COVID, Nuzzo said, has been a missed opportunity. The best time to learn more about masking is before we are asked to do it again.

    Yasmin Tayag

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  • Trying to Stop Long COVID Before It Even Starts

    Trying to Stop Long COVID Before It Even Starts

    Three years into the global fight against SARS-CoV-2, the arsenal to combat long COVID remains depressingly bare. Being vaccinated seems to reduce people’s chances of developing the condition, but the only surefire option for avoiding long COVID is to avoid catching the coronavirus at all—a proposition that feels ever more improbable. For anyone who is newly infected, “we don’t have any interventions that are known to work,” says Akiko Iwasaki, an immunologist and long-COVID researcher at Yale.

    Some researchers are hopeful that the forecast might shift soon. A pair of recent preprint studies, both now under review for publication in scientific journals, hint that two long-COVID-preventing pills might already be on our pharmacy shelves: the antiviral Paxlovid and metformin, an affordable drug commonly used for treating type 2 diabetes. When taken early in infection, each seems to at least modestly trim the chance of developing long COVID—by 42 percent, in the case of metformin. Neither set of results is a slam dunk. The Paxlovid findings did not come out of a clinical trial, and were focused on patients at high risk of developing severe, acute COVID; the metformin data did come out of a clinical trial, but the study was small. When I called more than half a dozen infectious-disease experts to discuss them, all used hopeful, but guarded, language: The results are “promising,” “intriguing”; they “warrant further investigation.”

    At this point, though, any advance at all feels momentous. Long COVID remains the pandemic’s biggest unknown: Researchers still can’t even agree on its prevalence or the features that define it. What is clear is that millions of people in the United States alone, and countless more worldwide, have experienced some form of it, and more are expected to join them. “We’ve already seen early data, and we’ll continue to see data, that that will emphasize the impact that long COVID has on our society, on quality of life, on productivity, on our health system and medical expenditures,” says Susanna Naggie, an infectious-disease physician and COVID-drug researcher at Duke University. “This needs to be a high priority,” she told me. Researchers have to trim long COVID incidence as much as possible, as soon as possible, with whatever safe, effective options they can.

    By now, news of the inertia around preventive long-COVID therapies may not come as much of a shock. Interventions that stop disease from developing are, on the whole, a neglected group; big, blinded, placebo-controlled clinical trials—the industry gold standard—usually look to investigate potential treatments, rather than drugs that might keep future illness at bay. It’s a bias that makes research easier and faster; it’s a core part of the American medical culture’s reactive approach to health.

    Read: Long COVID has forced a reckoning for one of medicine’s most neglected diseases

    For long COVID, the terrain is even rougher. Researchers are best able to address prevention when they understand a disease’s triggers, the source of its symptoms, and who’s most at risk. That intel provides a road map, pointing them toward specific bodily systems and interventions. The potential causes of COVID, though, remain murky, says Adrian Hernandez, a cardiologist and clinical researcher at Duke. Years of research have shown that the condition is quite likely to comprise a cluster of diverse syndromes with different triggers and prognoses, more like a category (e.g., “cancer”) than a singular disease. If that’s the case, then a single preventive treatment shouldn’t be expected to cut its rates for everyone. Without a universal way to define and diagnose the condition, researchers can’t easily design trials, either. Endpoints such as hospitalization and death tend to be binary and countable. Long COVID operates in shades of gray.

    Still, some scientists might be making headway with vetted antiviral drugs, already known to slash the risk of developing severe COVID-19. A subset of long-COVID cases could be caused by bits of virus that linger in the body, prompting the immune system to wage an extended war; a drug that clears the microbe more quickly might lower the chances that any part of the invader sticks around. Paxlovid, which interferes with SARS-CoV-2’s ability to copy itself inside of our cells, fits that bill. “The idea here is really nipping it in the bud,” says Ziyad Al-Aly, a clinical epidemiologist and long-COVID researcher at Washington University in St. Louis, who led the recent Paxlovid work.

    Paxlovid has yet to hit the scientific jackpot: proof from a big clinical trial that shows it can prevent long COVID in newly infected people. But Al-Aly’s study, which pored over the electronic medical records of more than 56,000 high-risk patients, offers some early optimism. People who took the pills, he and his colleagues found, were 26 percent less likely to report lingering symptoms three months after their symptoms began than those who didn’t.

    Read: Inside the mind of an anti-Paxxer

    The pills’ main benefit remains the prevention of severe, acute disease. (In the recent study, Paxlovid-takers were also 30 percent less likely to be hospitalized and 48 percent less likely to die.) Al-Aly expects that the drug’s effectiveness at preventing long COVID—if it’s confirmed in other populations—will be “modest, not huge.” Though the two functions could yet be linked: Some long-COVID cases may result from severe infections that damage tissues so badly that the body struggles to recover. And should Paxlovid’s potential pan out, it could help build the case for testing other SARS-CoV-2 antivirals. Al-Aly and his colleagues are currently working on a similar study into molnupiravir. “The early results are encouraging,” he told me, though “not as robust as Paxlovid.” (Another study, run by other researchers, that followed hospitalized COVID patients found those who took remdesivir were less likely to get long COVID, but a later randomized clinical trial didn’t bear that out.)

    A clinical trial testing Paxlovid’s preventive potency against long COVID is still needed. Kit Longley, a spokesperson for Pfizer, told me in an email that the company doesn’t currently have one planned, though it is “continuing to monitor data from our clinical studies and real-world evidence.” (The company is collaborating with a research group at Stanford to study Paxlovid in new clinical contexts, but they’re looking at whether the pills  might treat long COVID that’s already developed. The RECOVER trial, a large NIH-funded study on long COVID, is also focusing its current studies on treatment.) But given the meager uptake rates for Paxlovid even among those in high-risk groups, Al-Aly thinks his new data could already serve a useful purpose: providing people with extra motivation to take the drug.

    The case for adding metformin to the anti-COVID tool kit might be a bit muddier. The drug isn’t the most intuitive medication to deploy against a respiratory virus, and despite its widespread use among diabetics, its exact effects on the body remain nebulous, says Stacey Schultz-Cherry, a virologist at St. Jude Children’s Research Hospital. But there are many reasons to believe it might be useful. Some research has shown that metformin can mess with the manufacture of viral proteins inside of human cells, Bramante told me, which may impede the ability of SARS-CoV-2 and other pathogens to reproduce. The drug also appears to rev up the disease-dueling powers of certain immune cells, and to stave off inflammation. Studies have shown that metformin can improve responses to certain vaccinations in humans and rodents, and researchers have found that people taking the drug seem less likely to get seriously sick from influenza. Even the diabetes-coronavirus connection may not be so tenuous: Metabolic disease is a risk factor for severe COVID; infection itself can put blood-sugar levels on the fritz. It’s certainly plausible that having a metabolically altered body, Schultz-Cherry told me, could make infections worse.

    Read: The promising treatment we’re not even trying for long COVID

    But the evidence that metformin helps prevent long COVID remains sparse. Carolyn Bramante, the scientist who led the metformin study, told me that when her team first set out in 2020 to investigate the drug’s effects on SARS-CoV-2 infections in a randomized, clinical trial, long COVID wasn’t really on their radar. Like many others in their field, they were hoping to repurpose established medicines to keep infected people out of the hospital; early studies of metformin—as well as the two other drugs in their trial, the antidepressant fluvoxamine and the antiparasitic ivermectin—hinted that they’d work. Ironically, two years later, their story flipped around. A large analysis, published last summer, showed that none of the three drugs were stellar at preventing severe COVID in the short term—a disappointing result (though Bramante contends that their data still indicate that metformin does some good). Then, when Bramante and her colleagues examined their data again, they found that study participants that had taken metformin for two weeks around the start of their illness were 42 percent less likely to have a long-COVID diagnosis from their doctor nearly a year down the road. David Boulware, an infectious-disease physician who helped lead the work, considers that degree of reduction pretty decent: “Is it 100 percent? No,” he told me. “But it’s better than zero.”

    Metformin may well prove to prevent long COVID but not acute, severe COVID (or vice versa). Plenty of people who never spend time in the hospital can still end up developing chronic symptoms. And Iwasaki points out that the demographics of long-haulers and people who get severe COVID don’t really overlap; the latter skew older and male. In the future, early-infection regimens may be multipronged: antivirals, partnered with metabolic drugs, in the hopes of keeping symptoms both mild and short-lived.

    But researchers are still a long way off from delivering that reality. It’s not yet clear, for instance, whether the drugs work additively when combined, Boulware told me. Nor is it a given that they’ll work across different demographics—age, vaccination status, risk factors, and more. Bramante and Boulware’s study cast a decently wide net: Although everyone enrolled in the trial was overweight or obese, many were young and healthy; a few were even pregnant. The study was not enormous, though—about 1,000 people. It also relied on patients’ individual doctors to deliver long-COVID diagnoses, likely leading to some inconsistencies, so other studies that follow up in the future could find different results. For now, this isn’t enough to “mean we should run out and use metformin,” Schultz-Cherry, who has been battling long COVID herself, told me.

    Other medications could still fill the long-COVID gaps. Hernandez, the Duke cardiologist, is hopeful that one of his ongoing clinical trials, ACTIV-6, might provide answers soon. He and his team are testing whether any of several drugs—including ivermectin, fluvoxamine, the steroid fluticasone, and, as a new addition, the anti-inflammatory montelukast—might cut down on severe, short-term COVID. But Hernandez and his colleagues, Naggie among them, appended a check-in at the 90-day mark, when they’ll be asking their patients whether they’re experiencing a dozen or so symptoms that could hint at a chronic syndrome.

    That check-in questionnaire won’t capture the full list of long-COVID symptoms, now more than 200 strong. Still, the three-month benchmark could give them a sense of where to keep looking, and for how long. Hernandez, Naggie, and their colleagues are considering whether to extend their follow-up period to six months, maybe farther. The need for long-COVID prevention, after all, will only grow as the total infection count does. “We’re not going to get rid of long COVID anytime soon,” Iwasaki told me. “The more we can prevent onset, the better off we are.”

    Katherine J. Wu

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  • The Masks We’ll Wear in the Next Pandemic

    The Masks We’ll Wear in the Next Pandemic

    On one level, the world’s response to the coronavirus pandemic over the past two and half years was a major triumph for modern medicine. We developed COVID vaccines faster than we’d developed any vaccine in history, and began administering them just a year after the virus first infected humans. The vaccines turned out to work better than top public-health officials had dared hope. In tandem with antiviral treatments, they’ve drastically reduced the virus’s toll of severe illness and death, and helped hundreds of millions of Americans resume something approximating pre-pandemic life.

    And yet on another level, the pandemic has demonstrated the inadequacy of such pharmaceutical interventions. In the time it took vaccines to arrive, more than 300,000 people died of COVID-19 in America alone. Even since, waning immunity and the semi-regular emergence of new variants have made for an uneasy détente. Another 700,000 Americans have died over that period, vaccines and antivirals notwithstanding.

    For some pandemic-prevention experts, the takeaway here is that pharmaceutical interventions alone simply won’t cut it. Though shots and drugs may be essential to softening a virus’s blow once it arrives, they are by nature reactive rather than preventive. To guard against future pandemics, what we should focus on, some experts say, is attacking viruses where they’re most vulnerable, before pharmaceutical interventions are even necessary. Specifically, they argue, we should be focusing on the air we breathe. “We’ve dealt with a lot of variants, we’ve dealt with a lot of strains, we’ve dealt with other respiratory pathogens in the past,” Abraar Karan, an infectious-disease physician and global-health expert at Stanford, told me. “The one thing that’s stayed consistent is the route of transmission.” The most fearsome pandemics are airborne.

    Read: The plan to stop every respiratory virus at once

    Numerous overlapping efforts are under way to stave off future outbreaks by improving air quality. Many scientists have long advocated for overhauling the way we ventilate indoor spaces, which has the potential to transform our air in much the same way that the advent of sewer systems transformed our water. Some researchers are similarly enthusiastic about the promise of germicidal lighting. Retrofitting a nation’s worth of buildings with superior ventilation systems or germicidal lighting is likely a long-term mission, though, requiring large-scale institutional buy-in and probably a considerable amount of government funding. Meanwhile, a more niche subgroup has zeroed in on what is, at least in theory, a somewhat simpler undertaking: designing the perfect mask.

    Two and a half years into this pandemic, it’s hard to believe that the masks widely available to us today are pretty much the same masks that were available to us in January 2020. N95s, the gold standard as far as the average person is concerned, are quite good: They filter out at least 95 percent of .3-micron particles—hence N95—and are generally the masks of preference in hospitals. And yet, anyone who has worn one over the past two and a half years will know that, lucky as we are to have them, they are not the most comfortable. At a certain point, they start to hurt your ears or your nose or your whole face. When you finally unmask after a lengthy flight, you’re liable to look like a raccoon. Most existing N95s are not reusable, and although each individual mask is pretty cheap, the costs can add up over time. They impede communication, preventing people from seeing the wearer’s facial expressions or reading their lips. And because they require fit-testing, the efficacy for the average wearer probably falls well short of the advertised 95 percent. In 2009, the federal government published a report with 28 recommendations to improve masks for health-care workers. Few seem to have been taken.

    These shortcomings are part of what has made efforts to get people to wear masks an uphill battle. What’s more,Over the course of the pandemic, several new companies have submitted new mask designs to NIOSH, the federal agency tasked with certifying and regulating masks,. Few, if any, have so far been certified. The agency appears to be overworked and underfunded. In addition, Joe and Kim Rosenberg, who in the early stages of the pandemic launched a mask company that applied unsuccessfully for NIOSH approval, told me the certification process is somewhat circular: A successful application requires huge amounts of capital, which in turn require huge amounts of investment, but investors generally like to see data showing that the masks work as advertised in, say, a hospital, and masks cannot be tested in a hospital without prior NIOSH approval. (NIOSH did not respond to a request for comment.)

    New products aside, there do already exist masks that outperform standard N95s in one way or another. Elastomeric respirators are reusable masks that you outfit with replaceable filters. Depending on the filter you use, the mask can be as effective as an N95 or even more so. When equipped with HEPA-quality filters, elastomerics filter out 99.97 percent of particles. And they come in both half-facepiece versions (which cover the nose and mouth) and full-facepiece versions (which also cover the eyes). Another option are PAPRs, or powered air-purifying respirators—hooded, battery-powered masks that cover the wearer’s entire head and constantly blow HEPA-filtered air for the wearer to breathe.

    Given the challenges of persuading many Americans to wear even flimsy surgical masks during the past couple of years, though, the issues with these superior masks—the current models, at least—are probably disqualifying as far as widespread adoption would go in future outbreaks. Elastomerics generally are bulky, expensive, limit range of motion, obscure the mouth, and require fit testing to ensure efficacy. PAPRs have a transparent facepiece and in many cases don’t require fit testing, but they’re also bulky, currently cost more than $1,000 each, and, because they’re battery-powered, can be quite noisy. Neither, let me assure you, is the sort of thing you’d want to wear to the movie theater.

    Read: Is it time to start masking again?

    The people who seem most fixated on improving masks are a hodgepodge of biologists, biosecurity experts, and others whose chief concern is not another COVID-like pandemic but something even more terrifying: a deliberate act of bioterrorism. In the apocalyptic scenarios that most worry them—which, to be clear, are speculative—bioterrorists release at least one highly transmissible pathogen with a lethality in the range of, say, 40 to 70 percent. (COVID’s is about 1 percent.) Because this would be a novel virus, we wouldn’t yet have vaccines or antivirals. The only way to avoid complete societal collapse would be to supply essential workers with PPE that they can be confident will provide infallible protection against infection—so-called perfect PPE. In such a scenario, N95s would be insufficient, Kevin Esvelt, an evolutionary biologist at MIT, told me: “70-percent-lethality virus, 95 percent protection—wouldn’t exactly fill me with confidence.”

    Existing masks that use HEPA filters may well be sufficiently protective in this worst-case scenario, but not even that is a given, Esvelt told me. Vaishnav Sunil, who runs the PPE project at Esvelt’s lab, thinks that PAPRs show the most promise, because they do not require fit testing. At the moment, the MIT team is surveying existing products to determine how to proceed. Their goal, ultimately, is to ensure that the country can distribute completely protective masks to every essential worker, which is firstly a problem of design and secondly a problem of logistics. The mask Esvelt’s team is looking for might already be out there, just selling for too high a price, in which case they’ll concentrate on bringing that price down. Or they might need to design something from scratch, in which case, at least initially, their work will mainly consist of new research. More likely, Sunil told me, they’ll identify the best available product and make modest adjustments to improve comfort, breathability, useability, and efficacy.

    Esvelt’s team is far from the only group exploring masking’s future. Last year, the federal government began soliciting submissions for a mask-design competition intended to spur technological development. The results were nothing if not creative: Among the 10 winning prototypes selected in the competition’s first phase were a semi-transparent mask, an origami mask, and a mask for babies with a pacifier on the inside.

    In the end, the questions of how much we should invest in improving masks and how we should actually improve them boil down to a deeper question about which possible future pandemic concerns you most. If your answer is a bioengineered attack, then naturally you’ll commit significant resources to perfecting efficacy and improving masks more generally, given that, in such a pandemic, masks may well be the only thing that can save us. If your answer is SARS-CoV-3, then you might worry less about efficacy and spend proportionally more on vaccines and antivirals. This is not a cheery choice to make. But it is an important one as we inch our way out of our current pandemic and toward whatever waits for us down the road.

    Read: The pandemic’s legacy is already clear

    For the elderly and immunocompromised, super-effective masks could be useful even outside a worst-case scenario. But more traditional public-health experts, who don’t put as much stock in the possibility of a highly lethal, deliberate pandemic, are less concerned about perfecting efficacy for the general public. The greater gains, they say, will come not from marginally improving the efficacy of existing highly effective masks but from getting more people to wear highly effective masks in the first place. “It’s important to make masks easier for people to use, more comfortable and more effective,” Linsey Marr, an environmental engineer at Virginia Tech, told me. It wouldn’t hurt to make them a little more fashionable either, she said. Also important is reusability, Jassi Pannu, a fellow at the Johns Hopkins Center for Health Security, told me, because in a pandemic stockpiles of single-use products will almost always run out.

    Stanford’s Karan envisions a world in which everyone in the country has their own elastomeric respirator—not, in most cases, for everyday use, but available when necessary. Rather than constantly replenishing your stock of reusable masks, you would simply swap out the filters in your elastomeric (or perhaps it will be a PAPR) every so often. The mask would be transparent, so that a friend could see your smile, and relatively comfortable, so that you could wear it all day without it cutting into your nose or pulling on your ears. When you came home at night, you would spend a few minutes disinfecting it.

    Karan’s vision might be a distant one. America’s tensions over masking throughout the pandemic give little reason to hope for any unified or universal uptake in future catastrophes. And even if that happened, everyone I spoke with agrees that masks alone are not a solution. They’re almost certainly the smallest part of the effort to ensure that the air we breathe is clean, to change the physical world to stop viral transmission before it happens. Even so, making and distributing millions of masks is almost certainly easier than installing superior ventilation systems or germicidal lighting in buildings across the country. Masks, if nothing else, are the low-hanging fruit. “We can deal with dirty water, and we can deal with cleaning surfaces,” Karan told me. “But when it comes to cleaning the air, we’re very, very far behind.”

    Jacob Stern

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  • The Other Abortion Pill

    The Other Abortion Pill

    In the months since the Supreme Court overturned Roe v. Wade, demand for medication abortion has soared. The method already accounted for more than half of all abortions in the United States before the Court’s decision; now reproductive-rights activists and sites such as Plan C, which shares information about medication abortion by mail, are fielding an explosion in interest in abortion pills. As authorized by the FDA, medication abortion consists of two drugs. The first one, mifepristone, blocks the hormone progesterone, which is necessary for a pregnancy to continue. The second, misoprostol, brings on contractions of the uterus that expel its contents. The combination is, according to studies conducted in the U.S., somewhere between 95 percent and 99 percent effective in ending a pregnancy and is extremely safe.

    The second drug, misoprostol, can also safely end a pregnancy on its own. That method has long been considered a significantly less effective alternative to the FDA-approved protocol. But a growing body of research has begun to challenge the conventional thinking. In situations where people use pills to end a pregnancy at home, studies have found far higher rates of success for misoprostol-only abortions than were found in clinical settings. One recent study in Nigeria and Argentina showed misoprostol-only abortion to be 99 percent effective.

    Even before new restrictions began to ripple across the U.S., mifepristone—often referred to as “the abortion pill”—was tightly controlled by the FDA, which requires that the drug be dispensed only by doctors certified to prescribe it and only to patients who’ve signed an agency-approved agreement. As efforts to ban that drug intensify, the relative availability of misoprostol, which can be obtained at pharmacies in every state and prescribed by any doctor, could make misoprostol alone a more common option for women seeking abortions, legally or clandestinely.

    Read: The future of abortion in a post-Roe America

    Already, the Austria-based nonprofit Aid Access, which helps women in the U.S. order pills through the mail, helped thousands of women procure misoprostol-only regimens in the first months of the coronavirus pandemic, when shipments of mifepristone were disrupted. At least one U.S. abortion provider, Carafem, has been offering its patients a misoprostol-only option for close to two years, and other reproductive-health groups are now considering offering the same regimen. This approach follows a path that has been well established in places around the world, where mifepristone has been scarce or unavailable, but in the U.S., it represents a real shift in abortion provision.

    If in the past mifepristone has garnered the bulk of attention from politicians and the public in the U.S., that focus may owe in part to an oft-told story about the origins of “the abortion pill” and its lone inventor, the renowned French researcher Dr. Étienne-Émile Baulieu. The reality is that of the two drugs, misoprostol has always mattered more.

    For his work on mifepristone, Baulieu won one of the most prestigious prizes in medicine, whose recipients tend to be discussed as candidates for a Nobel Prize, and received France’s Legion of Honor. A lengthy profile in The New York Times Magazine called him “a different kind of scientist.” And though the chemists George Teutsch and Alain Belanger actually synthesized the compound, Baulieu became, to American audiences, “the father of the abortion pill.”

    Yet mifepristone is not, by itself, a highly effective abortifacient. Taken alone, the drug ends a pregnancy only about two-thirds of the time, which is why it has always been administered in combination with a prostaglandin—a drug that mimics the function of hormones that promote menstrual cramping and inflammation.

    For years, doctors in Europe had been administering mifepristone with a prostaglandin called sulprostone. The combination was nearly 100 percent effective, but required multiple in-person visits to a clinic or hospital because sulprostone could only be given by injection. “Everyone had been looking for a prostaglandin that didn’t have to be either injected or kept frozen,” says Beverly Winikoff, the founder of Gynuity Health Projects, whose research on medication abortion helped win FDA approval in the United States.

    In Brazil, women had already found one. No individual, or individuals, have ever been widely credited for that discovery, the way Baulieu is credited for mifepristone. But scholars agree that the practice began in the country’s impoverished northeast soon after the drug went on the market in 1986.

    Manufactured by G.D. Searle & Company, misoprostol was developed to treat stomach ulcers. To women in Brazil, where abortion was and remains severely restricted, the warning on the label, to avoid taking the drug while pregnant, advertised its potential as an abortifacient. And when they found the drug safer and more effective than other clandestine methods, misoprostol’s popularity exploded. (To state the obvious, no one should interpret drug warnings for pregnant people as covert advertisements for effective abortion alternatives.)

    Soon, doctors in Brazil reported seeing fewer women with severe abortion-related complications, and Brazilian researchers began documenting the drug’s off-label use. The first such study appeared in a 1991 letter to the editor of The Lancet: Helena Coelho and her colleagues at the University of Ceara had found that knowledge of misoprostol’s capacity to induce abortion had “spread rapidly” among both women and pharmacy personnel. But it had also reached government officials, who limited sales to authorized pharmacies and, in one state, banned misoprostol entirely.

    Read: Women in the U.S. can now get safe abortions by mail

    That same year, Baulieu, the French researcher, announced that he had devised a simpler way to use mifepristone—by combining it with misoprostol, which, unlike sulprostone, could be taken by mouth. Writing in The New England Journal of Medicine, Baulieu did reference misoprostol’s use in Brazil, but only as an example of what not to do. Citing anecdotal reports of cranial malformations in infants exposed to misoprostol in utero, he and colleagues claimed that administering misoprostol alone would risk “embryonic abnormalities,” adding that G.D. Searle “strongly disapproved” of the practice.

    The reports of cranial anomalies were never confirmed. But Searle did take pains to prevent the use of misoprostol for abortion, at one point publicly warning doctors in the U.S. against administering the drug to pregnant women. Over time, researchers established other important uses for misoprostol, such as treating miscarriage and preventing postpartum hemorrhage. Yet during the lifetime of its patent, the company refused to research or register the drug for any reproductive-health indication.

    Meanwhile, Brazilian newspapers had seized on the dangers that Baulieu had cited, fueling fears that failed abortions would create “a generation of monsters.” That in turn provided Brazilian authorities with a public-health rationale for regulating misoprostol as a controlled substance, the “possession or supply” of which carries penalties even more punitive than those for drug trafficking. But through informal networks, feminist activists continued helping women access both misoprostol and information about how to safely use it at home. More than three decades later, experts now credit Brazil as the birthplace of self-managed medication abortion.

    In the past few years, researchers have more formally documented what these informal networks established. In clinical trials, medication abortion with misoprostol alone was effective in completing first-trimester abortion roughly 80 percent of the time. As a rule, “We think about clinical-trials data as the gold standard,” says Caitlin Gerdts, a vice president at Ibis Reproductive Health and a senior author on the study in Nigeria and Argentina. Yet when researchers have examined misoprostol’s use in nonclinical settings, they have found far higher rates of success, with 93 to 100 percent of participants reporting complete abortions using only misoprostol. Given the many studies showing high effectiveness in self-managed settings, Gerdts says, “I think it’s time to reconsider the idea of the clinical trials data as being paramount.”

    One reason for the greater effectiveness of misoprostol alone in studies of self-managed abortion may have to do with how the studies were designed. “The problem with clinical trials is that often when we ask somebody to follow up in a week or two weeks, the body hasn’t had enough time to expel all of the products of conception,” says Dr. Angel Foster, a health-science professor at the University of Ottawa, whose work on the Thailand-Myanmar border was the first to rigorously investigate the effectiveness of misoprostol alone for abortion outside a formal health system. “If there’s a smudge on an ultrasound, it’s not that there’s a continuing pregnancy—it’s just debris. But rather than let the uterus absorb it or expel it, we do an evacuation procedure and we count it as a failure.” In studies of self-managed abortion, she says, the follow-up period tends to be longer—three or four weeks—and surgical intervention may not always be an option.

    “I do think because of the way it’s been treated in clinical trials, misoprostol has been defined as much less effective than we now believe it to be,” Foster says. “We talk about mifepristone as ‘the abortion pill,’ but I think it’s more appropriate to think of it as a pretreatment or an adjunct therapy. Because it’s really the misoprostol that’s doing the lion’s share of the work.”

    Elizabeth Raymond, a senior medical associate at Gynuity and the lead author of a systematic review of clinical trials on the use of misoprostol alone for early abortion, acknowledges that the clinical studies may have been too quick to intervene. But she says the shorter follow-up period was not without reason. Using ultrasound and a blood test to measure the amount of hCG, or human chorionic gonadotropin, doctors can diagnose a complete abortion “quite quickly, certainly within one or two weeks,” she says, “and the researchers wanted to do the assessments as soon as reasonable. They saw no sense in delaying.” Raymond suspects that misoprostol alone isn’t quite as effective as reported in the study in Nigeria and Argentina, in part because that study relied on its subjects to self-report whether the abortion was complete. “I think it’s an intriguing study, and it’s true that misoprostol alone is more effective than we thought,” she says, “but I think the general feeling is, if you can get both drugs, you should do that. The combination is more effective, and it may cause less cramping and bleeding.”

    Those side effects aren’t a safety concern, says Dr. Julie Amaon, the medical director of Just the Pill, which delivers abortion medication to people in Wyoming, Montana, Colorado, and Minnesota. “But it’s something to keep in mind,” she says, adding that anyone self-managing an abortion at home should adhere to the WHO-recommended protocol and follow up with a doctor, whether in person, by phone, or by text, to ensure that the process is complete. In the U.S., the FDA has approved only the two-drug regimen; although the WHO’s recommendations also suggest a preference for medication abortion with both drugs, that agency does recommend misoprostol-only abortion “in settings where mifepristone is not available.”

    Read: The abortion pill can be used later than the FDA says

    Right now, lawmakers across the U.S. are working to put both drugs out of reach. Fourteen states now fully or partially ban both mifepristone and misoprostol. Of the two drugs, though, misoprostol is still more easily obtained, either by prescription in pharmacies or via nonprofit groups in the U.S. and overseas. The Biden administration has said that it intends to maintain access to medication abortion, but so far has not acted to ease the stricter regulations on mifepristone. As long as those restrictions remain in place, ending a pregnancy with misoprostol alone could become a more common choice for people with few options.

    According to the Guttmacher Institute, a reproductive-health-research group that supports abortion rights, though the rate is difficult to measure, in the past self-managed abortions probably haven’t occurred in the U.S. on a large scale. But as conditions in red states come to resemble those in Brazil, the practice could become more and more common. In this way, says Mariana Prandini Assis, a Brazilian social scientist who has written extensively on abortion, the fall of Roe may well lead to the normalization in America of self-managed abortion with pills—a choice once thought of as a last resort or an act of desperation. For that reason, she says, the Brazilian women who pioneered the use of misoprostol for abortion should be considered the “other inventors of ‘the abortion pill.’”

    Patrick Adams

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