These days, strolling through downtown New York City, where I live, is like picking your way through the aftermath of a party. In many ways, it is exactly that: The limp string lights, trash-strewn puddles, and splintering plywood are all relics of the raucous celebration known as outdoor dining. These wooden “streeteries” and the makeshift tables lining sidewalks first popped up during the depths of the coronavirus pandemic in 2020, when restaurants needed to get diners back in their seats. It was novel, creative, spontaneous—and fun during a time when there wasn’t much fun to be had. For a while, outdoor dining really seemed as though it could outlast the pandemic. Just last October, New York Magazine wrote that it would stick around, “probably permanently.” But now someone has switched on the lights and cut the music. Across the country, something about outdoor dining has changed in recent months. With fears about COVID subsiding, people are losing their appetite for eating among the elements. This winter, many streeteries are empty, save for the few COVID-cautious holdouts willing to put up with the cold. Hannah Cutting-Jones, the director of food studies at the University of Oregon, told me that, in Eugene, where she lives, outdoor dining is “absolutely not happening” right now. In recent weeks, cities such as New York and Philadelphia have started tearing down unused streeteries. Outdoor dining’s sheen of novelty has faded; what once evoked the grands boulevards of Paris has turned out to be a janky table next to a parked car. Even a pandemic, it turns out, couldn’t overcome the reasons Americans never liked eating outdoors in the first place. For a while, the allure of outdoor dining was clear. COVID safety aside, it kept struggling restaurants afloat, boosted some low-income communities, and cultivated joie de vivre in bleak times. At one point, more than 12,700 New York restaurants had taken to the streets, and the city—along with others, including Boston, Los Angeles, Chicago, and Philadelphia—proposed making dining sheds permanent. But so far, few cities have actually adopted any official rules. At this point, whether they ever will is unclear. Without official sanctions, mounting pressure from outdoor-dining opponents will likely lead to the destruction of existing sheds; already, they keep tweeting disapproving photos at sanitation departments. Part of the issue is that as most Americans’ COVID concerns retreat, the potential downsides have gotten harder to overlook: less parking, more trash, tacky aesthetics, and, oh God, the rats. Many top New York restaurants have voluntarily gotten rid of their sheds this winter. The economics of outdoor dining may no longer make sense for restaurants, too. Although it was lauded as a boon to struggling restaurants during the height of the pandemic, the practice may make less sense now that indoor dining is back. For one thing, dining sheds tend to take up parking spaces needed to attract customers, Cutting-Jones said. The fact that most restaurants are chains doesn’t help: “If whatever conglomerate owns Longhorn Steakhouse doesn’t want to invest in outdoor dining, it will not become the norm,” Rebecca Spang, a food historian at Indiana University Bloomington, told me. Besides, she added, many restaurants are already short-staffed, even without the extra seats. In a sense, outdoor dining was doomed to fail. It always ran counter to the physical makeup of most of the country, as anyone who ate outside during the pandemic inevitably noticed. The most obvious constraint is the weather, which is sometimes pleasant but is more often not. “Who wants to eat on the sidewalk in Phoenix in July?” Spang said. The other is the uncomfortable proximity to vehicles. Dining sheds spilled into the streets like patrons after too many drinks. The problem was that U.S. roads were built for cars, not people. This tends not to be true in places renowned for outdoor dining, such as Europe, the Middle East, and Southeast Asia, which urbanized before cars, Megan Elias, a historian and the director of the gastronomy program at Boston University, told me. At best, this means that outdoor meals in America are typically enjoyed with a side of traffic. At worst, they end in dangerous collisions. Cars and bad weather were easier to put up with when eating indoors seemed like a more serious health hazard than breathing in fumes and trembling with cold. It had a certain romance—camaraderie born of discomfort. You have to admit, there was a time when cozying up under a heat lamp with a hot drink was downright charming. But now outdoor dining has gone back to what it always was: something that most Americans would like to avoid in all but the most ideal of conditions. This sort of relapse could lead to fewer opportunities to eat outdoors even when the weather does cooperate. But outdoor dining is also affected by more existential issues that have surmounted nearly three years of COVID life. Eating at restaurants is expensive, and Americans like to get their money’s worth. When safety isn’t a concern, shelling out for a streetside meal may simply not seem worthwhile for most diners. “There’s got to be a point to being outdoors, either because the climate is so beautiful or there’s a view,” Paul Freedman, a Yale history professor specializing in cuisine, told me. For some diners, outdoor seating may feel too casual: Historically, Americans associated eating at restaurants with special occasions, like celebrating a milestone at Delmonico’s, the legendary fine-dining establishment that opened in the 1800s, Cutting-Jones said. Eating outdoors, in contrast, was linked to more casual experiences, like having a hot dog at Coney Island. “We have high expectations for what dining out should be like,” she said, noting that American diners are especially fussy about comfort. Even the most opulent COVID cabin may be unable to override these associations. “If the restaurant is going to be fancy and charge $200 a person,” said Freedman, most people can’t escape the feeling of having spent that much for “a picnic on the street.” Outdoor dining isn’t disappearing entirely. In the coming years there’s a good chance that more Americans will have the opportunity to eat outside in the nicer months than they did before the pandemic—even if it’s not the widespread practice many had anticipated earlier in the pandemic. Where it continues, it will almost certainly be different: more buttoned-up, less lawless—probably less exciting. Santa Barbara, for example, made dining sheds permanent last year but specified that they must be painted an approved “iron color.” It may also be less popular among restaurant owners: If outdoor-dining regulations are too far-reaching or costly, cautioned Hayrettin Günç, an architect with Global Designing Cities Initiative, that will “create barriers for businesses.” For now, outdoor dining is yet another COVID-related convention that hasn’t quite stuck—like avoiding handshakes and universal remote work. As the pandemic subsides, the tendency is to default to the ways things used to be. Doing so is easier, certainly, than coming up with policies to accommodate new habits. In the case of outdoor dining, it’s most comfortable, too. If this continues to be the case, then outdoor dining in the U.S. may return to what it was before the pandemic: dining “al fresco” along the streetlamp-lined terraces of the Venetian Las Vegas, and beneath the verdant canopy of the Rainforest Cafe. from https://ift.tt/pFmqlwO Check out http://natthash.tumblr.com
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Airplane bathrooms are not most people’s idea of a good time. They’re barely big enough to turn around in. Their doors stick, like they’re trying to trap you in place. That’s to say nothing of the smell. But to the CDC, those same bathrooms might be a data gold mine. This month, the agency has been speaking with Concentric, the public-health and biosecurity arm of the biotech company Ginkgo Bioworks, about screening airplane wastewater for COVID-19 at airports around the country. Although plane-wastewater testing had been in the works already (a pilot program at John F. Kennedy International Airport, in New York City, concluded last summer), concerns about a new variant arising in China after the end of its “zero COVID” policies acted as a “catalyst” for the project, Matt McKnight, Ginkgo’s general manager for biosecurity, told me. According to Ginkgo, even airport administrators are getting excited. “There have been a couple of airports who have actually reached out to the CDC to ask to be part of the program,” Laura Bronner, Ginkgo’s vice president of commercial strategies, told me. Airplane-wastewater testing is poised to revolutionize how we track the coronavirus’s continued mutations around the world, along with other common viruses such as flu and RSV—and public-health threats that scientists don’t even know about yet. Unlike sewer-wide surveillance, which shows us how diseases are spreading among large communities, airplane surveillance is precisely targeted to catch new variants entering the country from abroad. And unlike with PCR testing, passengers don’t have to individually opt in. (The results remain anonymous either way.) McKnight compares the technique to radar: Instead of responding to an attack after it’s unfolded, America can get advance warning about new threats before they cause problems. As we enter an era in which most people don’t center their lives on avoiding COVID-19, our best contribution to public health might be using a toilet at 30,000 feet. Fundamentally, wastewater testing on airplanes is a smaller-scale version of the surveillance that has been taking place at municipal water networks since early 2020: Researchers perform genetic testing on sewage samples to determine how much coronavirus is present, and which variants are included. But adapting the methodology to planes will require researchers to get creative. For one thing, airplane wastewater has a higher solid-to-liquid ratio. Municipal sewage draws from bathing, cooking, washing clothes, and other activities, whereas airplane sewage is “mainly coming from the toilet,” says Kata Farkas, a microbiologist at Bangor University. For a recent study tracking COVID-19 at U.K. airports, Farkas and her colleagues had to adjust their analytical methods, tweaking the chemicals and lab techniques used to isolate the coronavirus from plane sewage. Researchers also need to select flights carefully to make sure the data they gather are worth the effort of collecting them. To put it bluntly, not everyone poops on the plane—and if the total number of sampled passengers is very small, the analysis isn’t likely to return much useful data. “The number of conversations we’ve had about how to inconspicuously know how many people on a flight have gone into a lavatory is hysterical,” says Casandra Philipson, who leads the Concentric bioinformatics program. (Concentric later clarified that they do not have plans to actually monitor passengers’ bathroom use.) Researchers ended up settling on an easier metric: Longer flights tend to have more bathroom use and should therefore be the focus of wastewater testing. (Philipson and her colleagues also work with the CDC to test flights from countries where the government is particularly interested in identifying new variants.) [Read: Are our immune systems stuck in 2020?] Beyond those technical challenges, scientists face the daunting task of collaborating with airports and airlines—large companies that aren’t used to participating in public-health surveillance. “It is a tricky environment to work in,” says Jordan Schmidt, the director of product applications at LuminUltra, a Canadian biotech company that tests wastewater at Toronto Pearson Airport. Strict security and complex bureaucracies in air travel can make collecting samples from individual planes difficult, he told me. Instead, LuminUltra samples from airport terminals and from trucks that pull sewage out of multiple planes, so the company doesn’t need to get buy-in from airlines. Airplane surveillance seeks to track new variants, not individual passengers: Researchers are not contact-tracing exactly which person brought a particular virus strain into the country. For that reason, companies such as Concentric aren’t planning to alert passengers that COVID-19 was found on their flight, much as some of us might appreciate that warning. Testing airplane sewage can identify variants from around the world, but it won’t necessarily tell us about new surges in the city where those planes land. Airplane-wastewater testing offers several advantages for epidemiologists. In general, testing sewage is “dramatically cheaper” and “dramatically less invasive” than nose-swab testing each individual person in a town or on a plane, says Rob Knight, a medical engineering professor at UC San Diego who leads the university’s wastewater-surveillance program. Earlier this month, a landmark report from the National Academies of Sciences, Engineering, and Medicine (which Knight co-authored) highlighted international airports as ideal places to seek out new coronavirus variants and other pathogens. “You’re going to capture people who are traveling from other parts of the world where they might be bringing new variants,” Knight told me. And catching those new variants early is key to updating our vaccines and treatments to ensure that they continue to work well against COVID-19. Collecting more data from people traveling within the country could be useful too, Knight said, since variants can evolve at home as easily as abroad. (XBB.1.5, the latest variant dominating COVID-19 spread in the U.S., is thought to have originated in the American Northeast.) To this end, he told me, the CDC should consider monitoring large train stations or seaports too. [Read: The COVID data that are actually useful now] When wastewater testing first took off during the pandemic, the focus was mostly on municipal facilities, because they could provide data for an entire city or county at once. But scientists have since realized that a more specific view of our waste can be helpful, especially in settings that are crucial for informing public-health actions. For example, at NYC Health + Hospitals, the city’s public health-care system, wastewater data help administrators “see 10 to 14 days in advance if there are any upticks” in coronavirus, flu, or mpox, Leopolda Silvera, Health + Hospitals’ global-health deputy, told me. Administrators use the data in decisions about safety measures and where to send resources, Silvera said: If one hospital’s sewage indicates an upcoming spike in COVID-19 cases, additional staff can be added to its emergency department. Schools are another obvious target for small-scale wastewater testing. In San Diego, Rebecca Fielding-Miller directed a two-year surveillance program for elementary schools. It specifically focused on underserved communities, including refugees and low-income workers who were hesitant to seek out PCR testing. Regular wastewater testing picked up asymptomatic cases with high accuracy, providing school staff and parents with “up to the minute” information about COVID-19 spread in their buildings, Fielding-Miller told me. This school year, however, funding for the program ran out. Even neighborhood-level surveillance, while not as granular as sampling at a plane, hospital, or school, can provide more useful data than city-wide testing. In Boston, “we really wanted hyperlocal surveillance” to inform placements of the city’s vaccine clinics, testing sites, and other public-health services, says Kathryn Hall, the deputy commissioner at the city’s public-health agency. She and her colleagues identified 11 manhole covers that provide “good coverage” of specific neighborhoods and could be tested without too much disruption to traffic. When a testing site lights up with high COVID-19 numbers, Hall’s colleagues reach out to community organizations such as health centers and senior-living facilities. “We make sure they have access to boosters, they have access to PPE, they understand what’s going on,” Hall told me. In the nearby city of Revere, a similar program run by the company CIC Health showed an uptick in RSV in neighborhood wastewater before the virus started making headlines. CIC shared the news with day-care centers and helped them respond to the surge with educational information and PPE. [Read: Whatever happened to toilet plumes?] According to wastewater experts, hyperlocal programs can’t usher in a future of disease omnipotence all by themselves. Colleen Naughton, an environmental-engineering professor at UC Merced who runs the COVIDPoops19 dashboard, told me she would like to see communities with no wastewater surveillance get resources to set it up before more funding goes into testing individual buildings or manhole covers. The recent National Academies report presents a future of wastewater surveillance that includes both broad monitoring across the country and testing targeted to places where new health threats might emerge or where certain communities need local information to stay safe. This future will require sustained federal funding beyond the current COVID-19 emergency, which is set to expire if the Biden administration does not renew it in April. The United States needs “better and more technology, with a funding model that supports its development,” in order for wastewater’s true potential to be realized, Knight said. Airplane toilets may very well be the best first step toward that comprehensive sewage-surveillance future. from https://ift.tt/rNzX80b Check out http://natthash.tumblr.com Of the dozens of hormones found in the human body, oxytocin might just be the most overrated. Linked to the pleasures of romance, orgasms, philanthropy, and more, the chemical has been endlessly billed as the “hug hormone,” the “moral molecule,” even “the source of love and prosperity.” It has inspired popular books and TED Talks. Scientists and writers have insisted that spritzing it up human nostrils can instill compassion and generosity; online sellers have marketed snake-oil oxytocin concoctions as “Liquid Trust.” But as my colleague Ed Yong and others have repeatedly written, most of what’s said about the hormone is, at best, hyperbole. Sniffing the chemical doesn’t reliably make people more collaborative or trusting; trials testing it as a treatment for children with autism spectrum disorder have delivered lackluster results. And although decades of great research have shown that the versatile molecule can at times spark warm fuzzies in all sorts of species—cooperation in meerkats, monogamy in prairie voles, parental care in marmosets and sheep—under other circumstances, oxytocin can turn creatures from rodents to humans aggressive, fearful, even prejudiced. Now researchers are finding that oxytocin may be not only insufficient for forging strong bonds, but also unnecessary. A new genetic study hints that prairie voles—fluffy, fist-size rodents that have long been poster children for oxytocin’s snuggly effects—can permanently partner up without it. The revelation could shake the foundations of an entire neuroscience subfield, and prompt scientists to reconsider some of the oldest evidence that once seemed to show that oxytocin was the be-all and end-all for animal affection. Cuddles, it turns out, can probably happen without the classic cuddle hormone—even in the most classically cuddly creatures of all. [Read: The weak science behind the wrongly named moral molecule] Oxytocin isn’t necessarily obsolete. “This shouldn’t be taken as, ‘Oh, oxytocin doesn’t do anything,’” says Lindsay Sailer, a neuroscientist at Cornell University. But researchers have good reason to be a bit gobsmacked. For all the messy, inconsistent, even shady data that have been gathered from human studies of the hormone, the evidence from prairie voles has always been considered rock-solid. The little rodents, native to the midwestern United States, are famous for being one of the few mammal species that monogamously mate for life and co-parent their young. Over many decades and across geographies, researchers have documented how the rodents nuzzle each other in their nests and console each other when stressed, how they aggressively rebuff the advances of other voles that attempt to homewreck. And every time they checked, “there was oxytocin, sitting in the middle of the story, over and over again,” says Sue Carter, a behavioral neurobiologist who pioneered some of the first studies on prairie-vole bonds. The molecular pathways driving the behaviors seemed just as clear-cut: When triggered by a social behavior, such as snuggling or sex, a region of the brain called the hypothalamus pumped out oxytocin; the hormone then latched on to its receptor, sparking a slew of lovey-dovey effects. Years of follow-up studies continued to bear that thinking out. When scientists gave prairie voles drugs that kept oxytocin from linking up with its receptor, the rodents started snubbing their partners after any tryst. Meanwhile, simply stimulating the oxytocin receptor was enough to coax voles into settling down with strangers that they’d never mated with. The connection between oxytocin and pair bonding was so strong, so repeatable, so unquestionable that it became dogma. Zoe Donaldson, a neuroscientist at the University of Colorado at Boulder who studies the hormone, recalls once receiving dismissive feedback on a grant because, in the words of the reviewer, “We already know everything that there is to know about prairie voles and oxytocin.” So more than a decade ago, when Nirao Shah, a neurogeneticist and psychiatrist at Stanford, and his colleagues set out to cleave the oxytocin receptor from prairie voles using a genetic technique called CRISPR, they figured that their experiments would be a slam dunk. Part of the goal was, Shah told me, proof of principle: Researchers have yet to perfect genetic tools for voles the way they have in more common laboratory animals, such as mice. If the team’s manipulations worked, Shah reasoned, they’d beget a lineage of rodents that was immune to oxytocin’s influence, leaving them unfaithful to their mates and indifferent to their young—thereby proving that the CRISPR machinery had done its job. That’s not what happened. The rodents continued to snuggle up with their families, as if nothing had changed. The find was baffling. At first, the team wondered if the experiment had simply failed. “I distinctly remember sitting there and just being like, Wait a sec; how is there not a difference?” Kristen Berendzen, a neurobiologist and psychiatrist at UC San Francisco who led the study, told me. But when three separate teams of researchers repeated the manipulations, the same thing happened again. It was as if they had successfully removed a car’s gas tank and still witnessed the engine roaring to life after an infusion of fuel. Something might have gone wrong in the experiments. That seems unlikely, though, says Larry Young, a neuroscientist at Emory University who wasn’t involved in the new study: Young’s team, he told me, has produced nearly identical results in his lab. The explanations for how decades of oxytocin research could be upended are still being sussed out. Maybe oxytocin can attach to more than one hormone receptor—something that studies have hinted at over the years, Carter told me. But some researchers, Young among them, suspect a more radical possibility. Maybe, in the absence of its usual receptor, oxytocin no longer does anything at all—forcing the brain to blaze an alternative path toward affection. “I think other things pick up the slack,” Young told me. That idea isn’t a total repudiation of the old research. Other prairie-vole experiments that used drugs to futz with oxytocin receptors were performed in adult animals who grew up with the hormone, says Devanand Manoli, a psychiatrist and neuroscientist at UCSF who helped lead the new study. Wired to respond to oxytocin all through development, those rodent brains couldn’t compensate for its sudden loss late in life. But the Stanford-UCSF team bred animals that lacked the oxytocin receptor from birth, which could have prompted some other molecule, capable of binding to another receptor, to step in. Maybe the car never needed gas to run: Stripped of its tank from the get-go, it went all electric instead. It would be easy to view this study as yet another blow to the oxytocin propaganda machine. But the researchers I spoke with think the results are more revealing than that. “What this shows us is how important pair bonding is,” Carter told me—to prairie voles, but also potentially to us. For social mammals, partnering up isn’t just sentimental. It’s an essential piece of how we construct communities, survive past childhood, and ensure that future generations can do the same. “These are some of the most important relationships that any mammal can have,” says Bianca Jones Marlin, a neuroscientist at Columbia University. When oxytocin’s around, it’s probably providing the oomph behind that intimacy. And if it’s not? “Evolution is not going to have a single point of failure for something that’s absolutely critical,” Manoli told me. Knocking oxytocin off its pedestal may feel like a letdown. But it’s almost comforting to consider that the drive to bond is just that unbreakable. from https://ift.tt/DAsJYNM Check out http://natthash.tumblr.com For all the legwork that public-health experts have done over the past few years to quash comparisons between COVID-19 and the flu, there sure seems to be a lot of effort nowadays to equate the two. In an advisory meeting convened earlier today, the FDA signaled its intention to start doling out COVID vaccines just like flu shots: once a year in autumn, for just about everyone, ad infinitum. Whatever the brand, primary-series shots and boosters (which might no longer be called “boosters”) will guard against the same variants, making them interchangeable. Doses will no longer be counted numerically. “This will be a fundamental transition,” says Jason Schwartz, a vaccine policy expert at Yale—the biggest change to the COVID-vaccination regimen since it debuted. Hints of the annual approach have been dropping, not so subtly, for years. Even in the spring of 2021, Pfizer’s CEO was floating the idea of yearly shots; Peter Marks, the director of the FDA’s Center for Biologics Evaluation and Research, teased it throughout 2022. This past September, Joe Biden officially endorsed it as “a new phase in our COVID-19 response,” and Ashish Jha, the White House’s COVID czar, memorably highlighted the convenience of combining a flu shot and a COVID shot into a single appointment: “I really believe this is why God gave us two arms.” Still, in today’s meeting, FDA officials were pushier than ever in their advocacy for the flu-ification of COVID vaccines. “We think that simplification of the vaccination regimen would contribute to easier vaccine deployment, better communication, and improved vaccine coverage,” Jerry Weir, the FDA’s director of the division of viral products, said at the meeting. The timing is important: After renewing the U.S.’s pandemic-emergency declaration earlier this month, the Biden administration seems set to allow its expiration this coming April. That makes the present moment awfully convenient for repackaging a chaotic, crisis-caliber vaccination paradigm as a scheduled, seasonal, normal-seeming one. A once-a-year strategy, modeled on a routine recommendation, suggests that “we’re no longer in emergency mode,” says Maria Sundaram, a vaccine researcher at the Marshfield Clinic Research Institute. Or at least, that’s the message that the public is likely to hear. But federal regulators may be trying to fit a COVID-shaped peg into a flu-shaped hole. The experts I spoke with largely agreed: Eventually, someday, annual autumn shots for COVID “will probably be sufficient,” says Gregory Poland, a vaccinologist at Mayo Clinic. “Are we ready for that yet? I’m not sure that’s the case at all.” Even in the short term, COVID-vaccination tactics need a revamp. “It’s clear above all that the current approach isn’t working,” Schwartz told me. Despite abundant supply, demand for COVID boosters in the U.S. has been abysmal—and interest seems to be declining with each additional dose. Last fall’s bivalent shot has reached the arms of only 15 percent of Americans; even among adults over 65—a majority of whom sign up for flu shots each fall—the vaccination rate hasn’t yet reached 40 percent. For most of the time that COVID shots have been around, figuring out when to get them has been a hassle, with different guidelines and requirements that depend on age, sex, risk factors, vaccination history, and more. Pharmacies have had to stock an absurd number of vials and syringes to accommodate the various combinations of brands and dose sizes; record-keeping on flimsy paper cards has been a total joke. “I do this for a living, and I can barely keep track,” Schwartz said. Recommendations on the proper timing and number of doses have also changed so many times that many Americans have simply checked out. After the bivalent recipe debuted, polls found that an alarming proportion of people didn’t even know the shot was available to them. Streamlining COVID-vaccine recommendations will remove a lot of that headache, Sundaram told me. Most people would need to keep only one mantra in mind—one dose, each fall—and could top off their flu and COVID immunity at the same time. Burdens on pharmacies and clinics would be lower, and communication would be far easier—a change that could make an especially big difference for those with children, among whom COVID-vaccine uptake has been the lowest. “It’ll be more scheduled, more systematic,” says Charlotte Hobbs, a pediatric infectious-disease specialist at the University of Mississippi Medical Center. COVID shots could simply be offered at annual well-child visits, she told me. “It’s something we already know works well.” The advantages of a flu-ified COVID shot aren’t just about convenience. If we have to shoehorn COVID vaccines into an existing paradigm, Sundaram told me, influenza’s is the best candidate. SARS-CoV-2, like the flu, is excellent at altering itself to dodge our defenses; it spreads readily in winter; and our immunity to infection tends to fade rather quickly. All of that adds up to a need for regularly updated shots. Such a system has been in place for decades for the flu: At the end of each winter, a panel of experts convenes to select the strains that should be targeted by the next formulation; manufacturers spend the next several months whipping up big batches in time for an autumn-ish rollout. The pipeline depends on a global surveillance system for flu viruses, as well as regular surveys of antibody levels in the community to suss out which strains people are still protected against. The premise has been so well vetted by now that researchers can skip the chore of running large-scale clinical trials to determine the efficacy and safety of each new, updated recipe. But a seasonal strategy works best for a seasonal virus—and SARS-CoV-2 just isn’t there yet, says Hana El Sahly, an infectious-disease physician at Baylor College of Medicine. Though flu viruses tend to hop between the globe’s hemispheres, alternately troubling the north and the south during their respective cold months, this new coronavirus has yet to confine its spread to one part of the calendar. (Marks, of the FDA, tried to address this concern at today’s meeting, asserting that “we’re starting to see some seasonality” and that fall was indeed the very sensible for an annual rollout.) SARS-CoV-2 has also been spitting out concerning variants and subvariants at a faster rate than the flu (and flu shots already have a hard time keeping up with evolution). The FDA’s new proposal suggests picking SARS-CoV-2 variants in June to have a vaccine ready by September, a shorter timeline than is used for flu. That still might not be fast enough: “By the time we detect a variant, it will have ripped through the global population and, in a few more weeks, died down,” El Sahly told me. The world got a preview of this problem with last year’s bivalent shot, which overlapped with the dominance of its target subvariants for only a couple of months. A flu model for COVID would make more sense “if we had stable, predictable dynamics,” says Avnika Amin, a vaccine epidemiologist at Emory University. “I don’t think we’re at that point.” Murkiness around vaccine effectiveness makes this transition complicated too. Experts told me that it’s gotten much more difficult to tell how well our COVID vaccines are working, and for how long, fueling debates over how often they should be given and how often their composition should change. Many people have now been infected by the virus multiple times, which can muddy calculations of vaccine effectiveness; better treatments also alter risk profiles. And many researchers told me they’re concerned that the data shortcuts we use for flu—measures of antibodies as a proxy for immune protection—just won’t fly for COVID shots. “We need better clinical data,” El Sahly told me. In their absence, the hasty adoption of a flu framework could lead to our updating and distributing COVID shots too often, or not often enough. A flu-ish approach also wouldn’t fix all of the COVID vaccines’ problems. Today’s discussion suggested that, even if a new COVID-shot strategy change goes through, officials will still need to recommend several different dose sizes for several different age groups—a more complex regimen than flu’s—and may advise additional injections for those at highest risk. At the same time, COVID shots would continue to be more of a target for misinformation campaigns than many other vaccines and, at least in the case of mRNA-based injections, more likely to cause annoying side effects. These issues and others have driven down interest—and simply pivoting to the flu paradigm “is not going to solve the uptake problem,” says Angela Shen, a vaccine-policy expert at Children’s Hospital of Philadelphia. Perhaps the greatest risk of making COVID vaccines more like flu shots is that it could lead to more complacency. In making the influenza paradigm a model, we also threaten to make it a ceiling. Although flu shots are an essential, lifesaving public-health tool, they are by no means the best-performing vaccines in our roster. Their timeline is slow and inefficient; as a result, the formulations don’t always match circulating strains. Already, with COVID, the world has struggled to chase variants with vaccines that simply cannot keep up. If we move too quickly to the fine-but-flawed framework for flu, experts told me, it could disincentivize research into more durable, more variant-proof, less side-effect-causing COVID shots. Uptake of flu vaccines has never been stellar, either: Just half of Americans sign up for the shots each year—and despite years of valiant efforts, “we still haven’t figured out how to consistently improve that,” Amin told me. Whenever the COVID-emergency declaration expires, vaccination will almost certainly have to change. Access to shots may be imperiled for tens of millions of uninsured Americans; local public-health departments may end up with even fewer resources for vaccine outreach. A flu model might offer some improvements over the status quo. But if the downsides outweigh the pluses, Poland told me, that could add to the erosion of public trust. Either way, it might warp attitudes toward this coronavirus in ways that can’t be reversed. At multiple points during today’s meeting, FDA officials emphasized that COVID is not the flu. They're right: COVID is not the flu and never will be. But vaccines can sometimes become a lens through which we view the dangers they fight. By equating our frontline responses to these viruses, the U.S. risks sending the wrong message—that they carry equal threat. from https://ift.tt/i2L19qF Check out http://natthash.tumblr.com In the dark early days of the pandemic, when we knew almost nothing and feared almost everything, there was a moment when people became very, very worried about toilets. More specifically, they were worried about the possibility that the cloud of particles toilets spew into the air when flushed—known in the scientific literature as “toilet plume”—might be a significant vector of COVID transmission. Because the coronavirus can be found in human excrement, “flushing the toilet may fling coronavirus aerosols all over,” The New York Times warned in June 2020. Every so often in the years since, the occasional PSA from a scientist or public-health expert has renewed the scatological panic. In retrospect, so much of what we thought we knew in those early days was wrong. Lysoling our groceries turned out to not be helpful. Masking turned out to be very helpful. Hand-washing, though still important, was not all it was cracked up to be, and herd immunity, in the end, was a mirage. As the country shifts into post-pandemic life and takes stock of the past three years, it’s worth asking: What really was the deal with toilet plume? The short answer is that our fears have not been substantiated, but they weren’t entirely overblown either. Scientists have been studying toilet plume for decades. They’ve found that plumes vary in magnitude depending on the type of toilet and flush mechanism. Flush energy plays a role too: The greater it is, the larger the plume. Closing the lid (if the toilet has one) helps a great deal, though even that cannot completely eliminate toilet plume—particles can still escape through the gap between the seat and the lid. Whatever the specifics, the main conclusion from years of research preceding the pandemic has been consistent and disgusting: “Flush toilets produce substantial quantities of toilet plume aerosol capable of entraining microorganisms at least as large as bacteria … These bioaerosols may remain viable in the air for extended periods and travel with air currents,” scientists at the CDC and the University of Oklahoma College of Public Health wrote in a 2013 review paper titled “Lifting the Lid on Toilet Plume Aerosol.” In other words, when you flush a toilet, an unsettling amount of the contents go up rather than down. Knowing this is one thing; seeing it is another. Traditionally, scientists have measured toilet plume with either a particle counter or, in at least one case, “a computational model of an idealized toilet.” But in a new study published last month, researchers at the University of Colorado at Boulder took things a step further, using bright-green lasers to render visible what usually, blessedly, is not. John Crimaldi, an engineering professor and a co-author of the study, who has spent 25 years using lasers to illuminate invisible phenomena, told me that he and his colleagues went into the experiment fully expecting to see something. Even so, they were “completely caught off guard” by the results. The plume was bigger, faster, and more energetic than they’d anticipated—“like an eruption,” Crimaldi said, or, as he and his colleagues put it in their paper, a “strong chaotic jet.” Within eight seconds, the resulting cloud of aerosols shoots nearly five feet above the toilet bowl—that is, more than six feet above the ground. That is: straight into your face. After the initial burst, the plume continues to rise until it hits the ceiling, and then it wafts outward. It meets a wall and runs along it. Before long, it fills the room. Once that happens, it hangs around for a while. “You can sort of extrapolate in your own mind to walking into a public restroom in an airport that has 20 toilet stalls, all of them flushing every couple minutes,” Crimaldi said. Not a pleasant thought. The question, then, is not so much whether toilet plume happens—like it or not, it clearly does—as whether it presents a legitimate transmission risk of COVID or anything else. This part is not so clear. The 2013 review paper identified studies of the original SARS virus as “among the most compelling indicators of the potential for toilet plume to cause airborne disease transmission.” (The authors also noted, in a dry aside, that although SARS was “not presently a common disease, it has demonstrated its potential for explosive spread and high mortality.”) The one such study the authors discuss explicitly is a report on the 2003 outbreak in Hong Kong’s Amoy Gardens apartment complex. That study, though, is far from conclusive, Mark Sobsey, an environmental microbiologist at the University of North Carolina at Chapel Hill, told me. The researchers didn’t rule out other modes of transmission, nor did they attempt to culture live virus from the fecal matter—a far more reliable indicator of infectiousness than mere detection. Beyond that, Sobsey said, there is little evidence that toilet plumes spread SARS or COVID-19. In his own review, published in December 2021, Sobsey found “no documented evidence” of viral transmission via fecal matter. This, at least, seems to track with the three years of pandemic experience we’ve all now endured. Although we can’t easily prove that bathrooms don’t play a significant role in spreading COVID-19, we haven’t seen any glaring indications that they do. And anyway, the coronavirus has found plenty of other awful ways to spread. Just because toilet plume doesn’t seem to be a vector of COVID transmission, though, doesn’t mean you can forget about it. Gastrointestinal viruses such as norovirus, Sobsey told me, present a more serious risk of transmission via toilet plume, because they are known to spread via fecal matter. The only real solutions are structural. Improved ventilation would keep aerosolized waste from building up in the air, and germicidal lighting, though the technology is still being developed, could potentially disinfect what remains. Neither, however, would stop the plume in the first place. To do that, you would need to change the toilet itself: In order to create a smoother and thus better-contained flush, you could change the geometry of the bowl, the way the water enters and exits, or any number of other variables. Toilet manufacturers could also, you know, stop producing lidless toilets. But none of that will save you the next time you find yourself staring into a toilet’s blank maw. Crimaldi suggests wearing a mask in public bathrooms to protect against not just the plume created when you flush but also the plumes left by the person who used the bathroom before you, the person who used it before them, and so on. You don’t need to have any great affection for masking as a public-health intervention to consider donning one for a few minutes to avoid literally breathing in shit. Sobsey offered another bit of unconventional bathroom-hygiene advice, which he acknowledged can only do so much to protect you: If you find yourself in a public restroom with a lidless toilet, he said, consider washing your hands before you flush. Then “hold your breath, flush the toilet, and leave.” from https://ift.tt/ZXMYufq Check out http://natthash.tumblr.com If you haven’t been pregnant, you’d be forgiven for thinking the language of pregnancy is all baby bumps, bundles of joy, and comparisons to variously sized fruits. But in the doctor’s office, it’s a different story. The medical lexicon for moms-to-be can be downright harsh. Case in point: the phrase geriatric pregnancy, which, until recently, was used to refer to anyone pregnant after their 35th birthday. This unfortunate term is thought to stem from a concept that dates back to the 1970s, when amniocentesis, a procedure to screen for genetic abnormalities, was becoming routine. That year, the National Institutes of Health identified 35 as the age at which the risk that the test would harm the fetus was roughly equal to the chance of a fetus being born with Down’s syndrome. In the four-plus decades since, advancements in screening technology have made that calculation essentially obsolete—and the idea that your 35th birthday is some sort of cliff-of-no-return absurd. Moms, for their part, always hated the phrase: When Jamila Larson, a 49-year-old mother of two in Hyattsville, Maryland, was called “geriatric” by a midwife in 2011, “it felt like a gut punch,” she told me. Though you’ll still hear it occasionally, this term has (thankfully) been on its way out for a while. One reason is changing demographics. As more and more women give birth after turning 35—in 2020, about one in five babies in the United States was born to a mom who had passed that birthday—labeling them as particularly “old” no longer makes sense. Last August, the American College of Obstetricians and Gynecologists (ACOG) announced that its preferred terminology is now “pregnancy at age 35 years or older”—or, even better, that doctors and researchers should simply indicate patients’ age in five-year increments starting from the age of 35. This is how progress works: When a medical term outlasts its usefulness, we thank it for its service and move on. So it may surprise you to learn that a litany of dubiously appropriate and medically inaccurate words are still used to describe pregnancy and childbirth. Over the past decade, the field of medicine has acknowledged that language has the power to perpetuate bias among doctors, and worked to scrub its vocabulary of such terms, including schizophrenic (which reduces a person to a stigmatized disease), drug abuser (which reduces a person to their addiction), and sickler (a derogatory term for someone with sickle-cell disease). And yet, doctors continue to describe women’s bodies using charged terms such as hostile uterus, incompetent cervix, and habitual aborter—words that arguably sound worse than the now-shunned geriatric pregnancy. Why do some words evolve, while others insist on haunting moms’ medical charts like ghosts of medicine past? [Read: The culture war over ‘pregnant people’] Geriatric pregnancy got a spurt of publicity in 2021, when the makers of the fertility and motherhood app Peanut turned their attention to the minefield of pregnancy language. After a video of a distraught woman whose doctor told her she would be “geriatric” if she were to get pregnant garnered attention on the app, Peanut launched a campaign to come up with more neutral-sounding alternatives to existing medical language. That April, they released a glossary of proposed replacements. Still, more attention from the public doesn’t always translate into institutional action: Although 20,000 people have downloaded Peanut’s glossary, there hasn’t been any official movement within medicine to do away with the original terms. Across the U.S., doctors are still doling out diagnoses that sound not only archaic, but downright weird. Many of these terms are enshrined in the global catalog of diseases that doctors use to report procedures to insurance companies, known as the ICD-11. The latest version of that glossary, released in 2022, still includes the phrase elderly primigravida, which is basically a synonym for geriatric pregnancy. In 2016, during her second pregnancy, Larson’s notes read “elderly multigravida”—meaning she was both over 35 and had been pregnant before. Or consider incompetent cervix, a term that is in both the ACOG dictionary and the ICD-11. Really, it means a pregnant person’s cervix has dilated before the pregnancy is complete, which can lead to premature birth or miscarriage. Meena Khandelwal, an ob-gyn and the director of research for obstetrics and gynecology at Cooper University Health Care in Camden, New Jersey, told me she avoids using the phrase in front of patients (she sometimes uses weak cervix instead, though she isn’t sure that it’s much better). But because incompetent cervix is entrenched in insurance codes and her hospital’s record-keeping system, the phrase is likely to show up in patients’ notes anyway. [Read: She got pregnant. His body changed too.] To be sure, communicating that the cervix has opened early is crucial; it prompts doctors to monitor the situation using ultrasound, to temporarily sew the cervix closed, or to try another treatment. Providers need to be able to inform one another about patients quickly and clearly; one could argue that is a much more important function of medical jargon than protecting patients’ feelings. The point of language evolution is not to make words so gentle that they become meaningless. But in many cases, the existing language is less clear and precise than gentler alternatives. For example, failure to progress—a general term meaning that labor has lasted longer than expected--says nothing about the reason the labor is slow. And calling a patient “geriatric” offers less information than simply stating whether she is in her 30s, 40s, or 50s. The outdated words even have the potential to worsen patient outcomes: a 2018 study on physician bias found that when doctors read stigmatizing language in a patient’s charts, they tended to have more negative attitudes toward the patient and treat their pain less aggressively. Besides, “incompetent” is a strange way to describe whether a cervix is open or closed. It makes it sound like this organ should be worried about its next annual review. This odd quality unites many pregnancy-related terms: They make it sound as if the pregnant person, or their body part, could have chosen a different path. When you are told your uterus is being “hostile” or are accused of “failure to progress,” it’s hard not to feel like you’ve somehow failed the assignment. “It sends a message of ‘You could be normal, but you’re not. You’re not working with us here,’” says Kristen Syrett, an associate professor of linguistics at Rutgers University. Even geriatric pregnancy, which doesn’t explicitly apply blame, seems to suggest that a mom-to-be has knowingly brought more risk upon her unborn child by choosing pregnancy “later” in life. [Janice Wolly: My first pregnancy] Many moms told Peanut that the most devastating label they encountered was habitual aborter. That term usually refers to someone who experiences multiple miscarriages before 20 weeks of pregnancy, a condition that affects 1 to 2 percent of women. (Its cousin is spontaneous abortion, which means such a miscarriage has happened once). From a purely medical perspective, abortion refers to any procedure that terminates a pregnancy, and includes procedures to empty the womb after a miscarriage. But in layman’s terms, it has come to mean a chosen termination of a pregnancy. That, plus the implication that aborting is a bad habit you can’t seem to break, made the term feel particularly inappropriate. “It’s really horrific if you think about it,” says Somi Javaid, an ob-gyn and the founder of the health-care company HerMD, who consulted on the Peanut project. This sense of blame becomes more acute when you consider that for many people, reproductive organs are intimately tied to a sense of identity and self-worth—at least compared with, say, the kidneys. In the context of wanting a child, it’s difficult to hear that your uterus is “hostile” or your cervix is “incompetent” without thinking that those terms apply to your whole self. Even physicians can be taken aback: When Javaid was in her 20s, her own doctor deemed her “infertile” in her notes on account of her “old” uterus—meaning that its lining had thinned, a side effect from a fertility medication she was taking. “It felt like being slapped in the face,” she told me. “The impact of the word was not muted by my knowledge at all.” Medical terms can, and do, change. But usually the field is responding to larger shifts in the culture, rather than leading the charge. That’s what happened with the phrase pregnant women, which organizations including the ACLU and the CDC have been incrementally phasing out in favor of pregnant people, a term that has sparked vigorous debate about inclusive language and feminism. Last February, ACOG followed suit, announcing that it would “move beyond the exclusive use of gendered language” to better encompass the fact that people of all genders can become pregnant. [Helen Lewis: Why I’ll keep saying ‘pregnant women’] With geriatric pregnancy, the change was likely more bottom-up, starting with doctors themselves. After all, for many, it was personal: The length and intensity of medical training increases the odds that doctors will have children later than other women—that they will be, in their own language, geriatric moms, says Monica Lypson, a vice dean at Columbia University's medical school who researches equity and inclusion. Lypson was deemed “geriatric” when she was pregnant at age 36—a choice of words she found “jarring” as a patient. Perhaps because incompetent cervix, habitual aborter, and the like refer to conditions that aren’t so common, many providers don’t realize just how hurtful they can be. Ariel Lefkowitz, an internal-medicine physician who cares for patients with pregnancy complications in Toronto, told me that he used to think of failure to progress the same way as he thought of kidney failure or heart failure. He didn’t notice the negative connotations until his wife, Sarah Friedlander, started training to be a birth educator and pointed them out. Now he sees that “it’s a lot more loaded, it’s a lot more personal,” he said. That realization pushed him to think harder about the bias embedded in medical language in other fields, such as failure to cope. “We’re so medicalized and supposedly neutral and in this clinical environment,” said Lefkowitz, who in 2021 co-wrote an editorial in the journal Obstetric Medicine on the importance of inclusive language in obstetrics. “It’s very easy to become numb to the ridiculous ways in which we speak.” The outdated terms that are currently stuck in the ICD-11, doctors’ offices, and the pages of medical journals may yet change. More doctors are recognizing that how patients perceive their words can have real impacts on health outcomes, says Julia Raney, a primary-care provider for adolescents who has created workshops on using mindful language in clinical settings. Accordingly, medicine is moving toward more person-centered care, including a focus on concrete risks rather than on blame and stereotypes. For instance, in her work with teens, Raney will note that they have a BMI in the 95th percentile rather than refer to them as simply “obese.” The goal is not to shield the patient from reality, but to better define their medical needs. Like ACOG’s move to designate moms as “35–39” or “40–44” rather than “of advanced maternal age,” this has the double benefit of being both less judgmental and more medically precise. [Anya E. R. Prince: I tried to keep my pregnancy secret] Doctors also have new reasons to be careful with their language. Since April 2021, an “open notes” law has given patients the right to freely and electronically access just about everything their doctors write about them. While the rule is still largely unknown to patients, open notes can make doctors more conscious (and, sometimes, anxious) about how what they write could affect their patients. “I think we’re all aware of that when we write anything,” Steve Lapinsky, an editor in chief of the journal Obstetric Medicine, told me. This increased transparency, he said, might just be the kick medicine needs to accelerate the pace of language change and do away with terms like incompetent cervix once and for all. from https://ift.tt/DKWBH2N Check out http://natthash.tumblr.com For months, the winter forecast in the United States seemed to be nothing but viral storm clouds. A gale of RSV swept in at the start of autumn, sickening infants and children in droves and flooding ICUs. After a multiyear hiatus, flu, too, returned in force, before many Americans received their annual shot. And a new set of fast-spreading SARS-CoV-2 subvariants had begun its creep around the world. Experts braced for impact: “My biggest concern was hospital capacity,” says Katelyn Jetelina, who writes the popular public-health-focused Substack Your Local Epidemiologist. “If flu, RSV, and COVID were all surging at the same time—given how burned out, how understaffed our hospital systems are right now—how would that pan out?” But the season’s worst-case scenario—what some called a “tripledemic,” bad enough to make health-care systems crumble—has not yet come to pass. Unlike last year, and the year before, a hurricane of COVID hospitalizations and deaths did not slam the country during the first month of winter; flu and RSV now appear to be in sustained retreat. Even pediatric hospitals, fresh off what many described as their most harrowing respiratory season in memory, finally have some respite, says Mary Beth Miotto, a pediatrician and the president of the Massachusetts chapter of the American Academy of Pediatrics. After a horrific stint, “we are, right now, doing okay.” With two months to go until spring, there is plenty of time for another crisis to emerge: Certain types of influenza, in particular, can be prone to delivering late-season second peaks. “We need to be careful and recognize we’re still in the middle,” Jetelina told me. But so far, this winter “has not been as bad as I expected it to be.” No matter what’s ahead, this respiratory season certainly won’t go down in history as a good one. Children across the country have fallen sick in overwhelming numbers, many of them with multiple respiratory viruses at once, amid a nationwide shortage of pediatric meds. SARS-CoV-2 remains a top cause of mortality, with its daily death count still in the hundreds, and long COVID continues to be difficult to prevent or treat. And enthusiasm for new vaccines and virus-blocking mitigations seems to be at an all-time low. Any sense of relief people might be feeling at this juncture must be tempered by what’s in the rearview: three years of an ongoing pandemic that has left more than 1 million people dead in the U.S. alone, and countless others sick, many chronically so. The winter may be going better than it could have. But that shouldn’t hold us back from tackling what’s ahead this season, and in others yet to come. Not all of this past autumn’s gloomy predictions were off base. RSV and flu each rushed in on the early side of the season and led to a steep rise in cases. But both viruses made rather hasty exits: RSV hit an apparent apex in mid-November, and flu bent into its own decline the following month. The staggered peaks “helped us quite a bit, in terms of hospitals being stressed,” says Sam Scarpino, the director of AI and life sciences at the Institute for Experiential AI at Northeastern University. In recent days, coronavirus cases and hospitalizations have been tilting downward, too—and severe-disease rates seem to be holding at a relative low. Just under 5 percent of hospital beds are currently occupied by COVID patients, compared with more than four times that fraction this time last year. And weekly COVID deaths are down by almost 75 percent from January 2022. (Death, though, has always been a lagging indicator, and the mortality numbers could still shift upward soon.) Despite some dire predictions to the contrary, the fast-spreading XBB.1.5 subvariant didn’t spark “some giant Omicron-type wave and crush everything,” says Justin Lessler, an infectious-disease modeler at the University of North Carolina at Chapel Hill. “In that sense, I feel good.” [Read: How worried should we be about XBB.1.5?] No one can say for sure why we dodged winter’s deadliest bullets, but the population-level immunity that Americans have built up over the past three years clearly played a major role. “That’s a testament to how vaccination has made the disease less dangerous for most people,” says Cedric Dark, an emergency physician at Baylor College of Medicine. Widespread immunization, combined with the fact that most Americans have now been infected, and many of them reinfected, has caused severe-disease rates to plunge, and the virus to move less quickly than it otherwise would have. Antiviral drugs, too, have been slashing hospitalization rates, at least for the meager fraction of recently infected people who use them. The gargantuan asterisk of long COVID still applies to new infections, but the short-term effects of the disease are now more on par with those of other respiratory illnesses, reducing the number of resources that health-care workers must marshal for each case. The virus, too, was more merciful than it could have been. XBB.1.5, despite its high transmissibility and penchant for dodging antibodies, doesn’t so far seem more capable of causing severe disease. And the fall’s bivalent shots, though not a perfect match for the newcomer, still improve the body’s response to viruses in the Omicron clan. Competition among respiratory viruses may have also helped soften COVID’s recent blows. In the days and weeks after one infection, bodies can become more resilient to another—a phenomenon known as viral interference that can reduce the risk of simultaneous or back-to-back infections. On population scales, interference can push down surges’ peaks, or at the very least, separate them, potentially keeping hospitals from being hit by a medley of microbes all at once. It’s hard to say for sure: “Many things go into when an epidemic wave happens—human behavior, temperature, humidity, the biology of the virus, the biology of the host,” says Ellen Foxman, an immunologist at Yale. That said, “I do think viral interference probably does play a role that has not been appreciated.” None of the experts I spoke with was ready to issue a blanket phew. Overlapping waves of respiratory illness have already led to nonstop sickness, especially among children, draining resources at every point in the pediatric caregiving chain. Kids were kept out of school, and parents stayed home from work; after a glut of COVID-related closures in New Mexico, schools and day cares running low on teachers had to call in the National Guard. Inundated with illnesses, pediatric emergency rooms overflowed; adult-care units had to be repurposed for children, and some hospitals pitched tents on their front lawns to accommodate overflow. Local stopgaps weren’t always enough: At one point, a colleague of Miotto’s in Boston told her that the closest available pediatric ICU bed was in Washington, D.C. [Read: The worst pediatric-care crisis in decades] By any metric, for the pediatric community, “it’s been a horrible season, the worst,” says Yvonne Maldonado, a pediatrician at Stanford. “The hospitals were bursting, bursting at the seams.” The flow of fevers has ebbed somewhat in recent weeks, but remains more flood than trickle. “It’s not over: We still don’t have amoxicillin in general, and we still struggle to get fever medication for people,” Miotto said. A parent recently told her that they’d gone to almost 10 pharmacies to try to fill an antibiotic prescription for their child. And pediatric providers across the country are steeling themselves for what the coming weeks could bring. “I think we could still see another surge,” says Joelle Simpson, the division chief of emergency medicine at Children’s National Hospital. “In prior years, February has been one of the worst months.” The season’s ongoing woes have been compounded by preexisting health-care shortages. Amid a dearth of funds, some hospitals have reduced their number of pediatric beds; a mass exodus of workers has also limited the resources that can be doled out, even as SARS-CoV-2 testing and isolation protocols continue to stretch the admission and discharge timeline. “Hospitals are in a weaker position than they were before the pandemic,” says Joseph Kanter, Louisiana’s state health officer and medical director. “If that’s the environment in which we are experiencing this year’s respiratory-virus season, it makes everything feel more acute.” Those issues are not limited to pediatrics: Now that COVID is a regular part of the disease roster, workloads have increased for a contingent of beleaguered clinicians that, across the board, seems likely to continue to shrink. In many hospitals, patients are getting stuck in emergency departments for several hours, even multiple days—sometimes never making it to a bed before being sent home. “It seems like hospitals everywhere are full,” Dark told me, not just because of COVID, but because of everything. “The vast majority of the work I do, and that I bet you what most of my colleagues are doing, is taking place in waiting rooms.” The U.S. has come a long way in the past three years. But still, “the cumulative toll of these winter surges has been higher than it needs to be,” says Julia Raifman, a health-policy researcher at Boston University. Had more people gone into winter up to date on their COVID vaccines, the virus’s mortality rate could have been driven down further; had more antiviral drugs and other protections been prioritized for the elderly and immunocompromised, fewer people might have been imperiled at all. If relief is percolating across the country right now, that says more about a shift in standards than anything else. “Our threshold for what ‘bad’ looks like has just gotten so out of whack,” Simpson told me. This winter could have been as grim as recent ones, Scarpino told me, with body-filled freezer trucks in parking lots and hospitals on the brink of collapse. But an improvement from those horrific lows isn’t much to brag about. And this winter—three years into combatting a coronavirus for which we have shots, drugs, masks, and more—has been nowhere close to the best one imaginable. The concern now, experts told me, is that the U.S. might accept a winter like this one as simply good enough. Regular vaccine uptake could dwindle even further; another wild-card SARS-CoV-2 variant could ignite another conflagration of cases. If that did happen, some researchers worry that we’d be slow to notice: Genomic surveillance is down, and many tests are being taken, unreported, at home. And with so many different immune histories now scattered across the globe, it’s getting tougher for modelers like Lessler to predict where and how quickly new variants might take over. The country does have a few factors working in its favor. By next winter, at least one RSV vaccine will almost certainly be available to protect the population’s youngest, eldest, or both. mRNA-based flu vaccines, which are expected to be far faster to develop than currently available shots, are also in the works, and will likely make it easier to match doses to circulating strains. And if, as Foxman hopes, SARS-CoV-2 eventually settles into a more predictable, seasonal pattern, infections will be less of a concern for most of the year and season-specific immunizations could be easier to design. [Read: Should everyone be masking again?] But no vaccine will do much unless enough people are willing and able to take it—and the public-health infrastructure that’s led many outreach efforts remains underfunded and understaffed. Kanter worries that the nation may not be terribly willing to invest. “We’ve fallen into this complacency trap where we just accept a given amount of mortality every year as unavoidable,” he told me. It doesn’t have to be that way, as the past few years have shown: Treatments, vaccines, clean indoor air, and other measures can lower a respiratory virus’s toll. By the middle of spring, the U.S. will be in a position to let the public-health-emergency declaration on COVID lapse—a decision that could roll back protections for the uninsured, and ratchet up price points on shots and antivirals. This winter’s retrospective is likely to influence that decision, Scarpino told me. But relief can breed complacency, and complacency further slows a sluggish public-health response. The fate of next winter—and of every winter after that—will depend on whether the U.S. decides to view this season as a success, or to recognize it as a shaky template for well-being that can and should be improved. from https://ift.tt/MPEQBTl Check out http://natthash.tumblr.com Over the past week, my breakfast routine has been scrambled. I have had overnight oats, beans on sourdough, corned-beef hash and fried rice, and, on a particularly weird morning, leftover cream-of-broccoli soup. Under normal circumstances, I would be eating eggs. But right now, I’m in hoarding mode, jealously guarding the four that remain from a carton purchased indignantly for six dollars. For that price—50 damn cents each!—my daily sunny-side-up eggs will have to wait. The perfect moment beckons: Maybe a toasted slab of brioche will call for a luxurious soft scramble, or maybe I will cave to a powerful craving for an egg-salad sandwich. Eggs, that quintessential cheap food, have gotten very, very expensive in the United States. In December, the average price for a dozen eggs in U.S. cities hit an all-time high of $4.25, up from $1.78 a year earlier. Though the worst now seems to be behind us, there’s still a way to go before consumer prices hit reasonable levels, and now Americans are starting to crack. Online, the shortage has recently hatched endless memes: In some posts, people pretend to portion out eggs in plastic baggies, like drug dealers (Pablo Eggscobar, anyone?); another recurring bit suggests painting potatoes to hunt at Easter. The high prices have even led to egg smuggling, and raised the profile of “rent-a-chicken” services where customers can borrow hens, chicken feed, and a coop for a couple hundred bucks. Surging egg prices are partly a familiar story of pandemic-era inflation. Producing eggs costs more because fuel, transportation, feed, and packaging are more expensive now, Jada Thompson, an agricultural economist at the University of Arkansas, told me. And it doesn’t help that there are no great substitutes for eggs. But a big reason that prices are so high right now is because of the avian flu—a virus that infects many types of birds and is deadly for some. Right now, we’re facing the worst-ever wave in the U.S., which has decimated chicken flocks and dented America’s egg inventory. Just over the past year, more than 57 million birds have died from the flu. Some much-needed relief from sky-high egg prices is likely coming, but don’t break out the soufflé pans yet. All signs suggest that avian flu is here to stay. If such rampant spread of the virus continues, “these costs are not going to come down to pre-2022 levels,” Thompson told me. Cheap eggs may soon become a thing of the past. This isn’t the first time American egg producers have encountered the avian flu, but dealing with it is still a challenge. For one thing, the virus keeps changing. It has long infected but not killed waterfowl and shorebirds, such as ducks and geese, but by 1996, it had mutated into the “highly pathogenic” H5N1, a poultry-killing strain that is named for the nasty versions of its “H” and “N” proteins. (They form spikes on the virus’s surface—sound familiar?) In 2014 and 2015, H5N1 ignited a terrible outbreak of avian flu, which gave U.S. poultry farmers their first taste of just how bad egg shortages could get. But this outbreak is like nothing we’ve seen before. The strain of avian flu that’s behind this wave is indeed new, and in the U.S. the virus has been circulating for a full year now—far longer than during the last big outbreak. The virus has become “host-adapted,” meaning that it can infect its natural hosts without killing them, so wild waterfowl are ruthlessly efficient at spreading the virus to chickens, Richard Webby, the director of the World Health Organization Collaborating Center for Studies on the Ecology of Influenza in Animals and Birds, told me. Many of these wild birds are migratory, and during their long journeys between Canada and South America, they descend on waterways and poop virus from the sky over poultry farms. Chickens stand no chance: The fleshy flaps on their heads may turn blue, their eyes and neck may swell, and, in rare instances, paralysis occurs. An entire poultry flock can be wiped out in 48 hours. Death is swift and vicious. Everything about this current wave has aligned to put a serious dent in our egg supply. Most eggs in the United States are hatched in jam-packed industrial egg farms, where transmission is next to impossible to stop, so the go-to move when the flu is detected is to “depopulate,” the preferred industry term for killing all of the birds. Without such a brutal tactic, Bryan Richards, the emerging-disease coordinator at the U.S. Geological Survey, told me, the current wave would be much worse. But this strategy also means fewer eggs, at least until new chicks grow into hens. That takes about six months, so there just haven’t been enough hens lately—especially for all the holiday baking people wanted to do, Thompson said. By the end of 2022, U.S. egg inventory was 29 percent lower than it had been at the beginning of the year. The chicken supply, in contrast, is robust because avian flu tends to affect older birds, like egg layers, Thompson said; at six to eight weeks old, the birds we eat, known as broilers, are not as susceptible. Also, she added, wild-bird migration pathways are not as concentrated in the Southeast, where most broiler production happens. Egg eaters should be able to return to their normal breakfast routines soon enough. New hens are now replenishing the U.S. egg supply—while waterfowl are wintering in the warmer climes of South America rather than lingering in the U.S. Since the holidays, “the price paid to the farmers for eggs has been decreasing rapidly, and usually, in time, the consumer price follows,” Maro Ibarburu, a business analyst at Iowa State University’s Egg Industry Center, told me. Still, going forward, it may be worth rethinking our relationship with eggs. There’s no guarantee that eggs will go back to being one the cheapest and most nutritious foods. When the weather warms, the birds will return, and “it’s highly likely that upon spring migration, we could see yet another wave,” said Richards. Europe, which experienced the H5N1 wave about six months before the Americas did, offers a glimpse of the future. “They went from being in a situation where the virus would come and go to a position where essentially it came and stayed,” Webby told me. If we're lucky, though, birds will develop natural immunity to the virus, making it harder to spread, or the U.S. could start vaccinating poultry against the flu, which the country has so far been reluctant to do. Omelets aside, curbing the spread of avian flu is in our best interest, not just to help prevent $6 egg cartons, but also to avoid a much scarier possibility—the virus spilling over and infecting people. All viruses from the influenza-A family have an avian origin, noted Webby; a chilling example is the H1N1 strain behind the 1918 flu pandemic. Fortunately, though some people have been infected with H5N1, very few cases of human-to-human spread have been documented. But continued transmission, over a long enough period, could change that. The fact that the virus has recently jumped from birds into mammals, such as seals and bears, and has spread among mink, is troubling because that means that it is evolving to infect species that are more closely related to us. “The risk of this particular virus [spreading among humans] as it is now is low, but the consequences are potentially high,” said Webby. “If there is a flu virus that I don’t want to catch, this one would be it.” More than anything, the egg shortage is a reminder that the availability of food is not something we can take for granted going forward. Shortages of staple goods seem to be striking with more regularity, not only due to pandemic-related broken supply chains and inflation but also to animal and plant disease. In 2019, swine fever decimated China’s pork supply; the ongoing lettuce shortage, which rapper Cardi B bemoaned earlier this month, is due to both a plant virus and a soil disease. Last September, California citrus growers detected a virus known to reduce crop yields. By creating cozier conditions for some diseases, climate change is expected to raise risk of infection for both animals and plants. And as COVID has illustrated, any situation in which different species are forced into abnormally close quarters with one another is likely to encourage the spread of disease. Getting used to intermittent shortages of staple foods such as eggs and lettuce will in all likelihood become a normal part of meal planning, barring some sort of huge shift away from industrial farming and its propensity for fostering disease. These farms are a major reason that these foods are so inexpensive and widely available in the first place; if cheap eggs seemed too good to be true, it’s because they were. Besides, there are always alternatives: May I suggest cream-of-broccoli soup? from https://ift.tt/ZMju7rP Check out http://natthash.tumblr.com It shouldn’t be hard to persuade people to take a sip of yerba mate. It’s completely natural. It makes you feel simultaneously energized and relaxed. You can drink it all day without feeling like your stomach acid is burning through your esophagus. It’s the preferred caffeine source of Lionel Messi, Zoe Saldaña, and the Pope. I’m drinking yerba mate with my Argentinian mother-in-law as I write this, and I’ll probably be drinking it with her or my husband when you read it. And yet, my track record for tempting friends into tasting it is abysmal. The average Argentinian or Uruguayan drinks more than 26 gallons of the green infusion each year, but as far as I can tell, the average North American has never even tried South America’s most consumed beverage—at least not in its traditional form. After more than 100 years, plenty of added sugar, and growing consumer desire for “clean caffeine,” something companies are calling yerba mate is finally on shelves near you. But in this land of individualism and germophobia, the real thing will simply never catch on. The plant has been seen as a moneymaking commodity since Europeans first arrived in the Americas. Long before North Americans rejected yerba mate, European colonizers were falling head over heels for the stuff. Within a few decades of their arrival in what is now Paraguay in the early 16th century, the Spanish were already drinking the local infusion they’d picked up from the indigenous Guaraní. The Guaraní people had used yerba mate—which they called ka’a—as a stimulant and for its medicinal effects since time immemorial. They collected leaves from a particular species of holly, dried them, and then either chewed the ka’a or placed it in an orange-size gourd to be steeped in water and passed among friends. The Spanish liked the energy yerba mate gave them and began selling the leaves. But according to Christine Folch, the author of the upcoming book Yerba Mate: A Stimulating Cultural History, Jesuit missionaries in Paraguay were the ones who transformed yerba mate into a true cash crop, by developing techniques for cultivating it on a large scale—methods that relied on the forced labor of indigenous people. Yerba-mate use exploded. By the 1700s, it was consumed all over South America:from what is now Paraguay across Peru, Bolivia, southern Brazil, Uruguay, Argentina, and Chile. In the United States, the first major push to popularize and cultivate yerba mate didn’t happen until 1899, when representatives from Brazil and Paraguay boasted about its benefits at the International Commercial Congress in Philadelphia. Soon after, the first U.S.-based firm, the Yerba Maté Tea Company, was founded. The company’s marketing slogan was straightforward and catchy: “Drink Yerba Maté Tea and be happy.” “Here, then, we have an ideal drink,” a 1900 Yerba Maté Tea Company pamphlet proclaimed, “one that promotes digestion, gives immediate strength of the body and brain and acts soothingly upon the nervous system.” Plus, it added, “the ladies will be especially interested to know that it exercises absolutely no bad effects upon the complexion.” The promotion frothed up interest: Curious individuals wrote to their local newspaper asking where to buy yerba mate, and farmers searched for information on how to grow it. Newspaper articles from the time prophesied a future when yerba mate might displace tea and coffee. Entrepreneurs formed new companies hawking yerba mate; some saw Prohibition as a perfect opening for the buzzy nonalcoholic drink. It was peddled hot and cold. In the 1930s, the United States Army even considered distributing daily rations of the beverage to soldiers. And yet, by the end of the 1930s, demand remained low. Marketers were perplexed, writing, “When can we expect an increase in consumption? The United States and France have proven themselves impervious to all temptation.” Americans just didn’t seem to have a taste for yerba mate; one 1921 review in the New York Herald read, “The flavor and taste were of a peculiar rank and insipid nature. If our South American friends can relish this beverage they are very welcome to all of it that grows.” [Read: The quest to make the best worst cup of coffee] True, yerba mate is bitter and tastes like freshly cut grass. But coffee tastes like burnt rubber the first time you try it, and Americans can’t get enough. Something deeper is going on here. Ximena Díaz Alarcón, an Argentinian marketing and consumer-trends researcher, says it makes sense that Americans never put down their mugs of coffee or tea to pick up a gourd filled with yerba mate. “There’s no cultural fit,” she told me from her home in Buenos Aires. Traditionally, yerba mate is consumed from a shared gourd through a shared straw called a bombilla. “Here in Argentina,” Alarcón said, “mate is a cultural habit, it is a tradition, and it is about sharing with others.” But sitting down for an hour or two and sharing a beverage, especially from the same straw, is not something Americans are accustomed to. Still, even when entrepreneurs of the past stripped away the communal aspect of yerba mate and sold it to North Americans in individual tea bags, coffee and tea definitively won out. That makes sense: A huge part of the appeal of mate is the ritual and community of it, not just the compounds it contains. Bagged mate simply doesn’t have as much going for it. In order to persuade Americans who have no connection to the tradition of yerba mate to incorporate it into their lives, the drink has to be both convenient and superior to coffee or tea—in the process, losing the very things that make it so beloved in South America. [From the April 2020 issue: Capitalism’s favorite drug] Over the past decade, Americans’ burgeoning thirst for healthy, plant-based caffeinated drinks has helped bring yerba mate into food fashion—at least superficially. Today, you can find it at the corner store and at major grocery chains such as Whole Foods and Walmart. But the yerba mate that fits American culture has no leaves, no straws, and no gourd. Instead, it is an ingredient mixed into canned and bottled energy drinks. This style of yerba mate is convenient and fast, and requires no swapping of spit. Although carbonated, canned yerba mate has been around since the 1920s, the demand for it is new. Today, “people want more natural products and simpler ingredient lists,” says Martín Caballero, an editor at BevNET who grew up drinking yerba mate when visiting family in Argentina. “So using yerba mate as an energy caffeine source has been something we’ve seen more of.” Like, a lot more: In 2021, the Coca-Cola Company launched Honest Yerba Mate; Perrier now has an “Energize” line featuring yerba mate, and the start-up Guru sells an organic energy drink “inspired by Amazonia’s powerful botanicals.” (For the record, yerba mate doesn’t actually grow in the Amazon.) At least one company has directly felt the difference between marketing real yerba mate and the diluted stuff. Guayakí, founded in 1996, built its entire business around working with indigenous communities in Paraguay to sustainably grow the plant. At first, the company sold only tea bags and loose-leaf yerba mate, but in the mid-2000s, it shifted its focus to selling yerba-mate energy drinks. Adding bubbles and sugar paid off, as did an ambitious marketing campaign targeting college students: Over the past decade, Guayakí has likely introduced more Americans to yerba mate than all previous marketing efforts combined. And although I admire their efforts and business philosophy, their canned “Classic Gold” tastes an awful lot like watered-down Diet Coke. But perhaps that’s the strategy. [Read: Always have three beverages] These days, it’s easy to find young influencers promoting the canned version of yerba mate—or, as they often call it, “yerb.” Meanwhile, I’ve mostly given up my role as an ambassador for old-school yerba mate. My friends and colleagues just aren’t interested in sharing a green, bitter drink. But my baby couldn’t be more excited about it. Every morning, we offer her our gourd and silver straw (after sucking up the warm water so she doesn’t get jacked up on caffeine), and she grins before placing la bombilla between her tiny lips. I like to think she loves it for the same reason I do: not for the taste, but for the intimacy and ritual. from https://ift.tt/JUmMZLj Check out http://natthash.tumblr.com 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.” from https://ift.tt/XNybj68 Check out http://natthash.tumblr.com |
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