Bird flu, at this point, is somewhat of a misnomer. The virus, which primarily infects birds, is circulating uncontrolled around much of the world, devastating not just birds but wide swaths of the animal kingdom. Foxes, bobcats, and pigs have fallen ill. Grizzly bears have gone blind. Sea creatures, including seals and sea lions, have died in great numbers. But none of the sickened animals has raised as much concern as mink. In October, a bird-flu outbreak erupted at a Spanish mink farm, killing thousands of the animals before the rest were culled. It later became clear that the virus had spread between the animals, picking up a mutation that helped it thrive in mammals. It was likely the first time that mammal-to-mammal spread drove a huge outbreak of bird flu. Because mink are known to spread certain viruses to humans, the fear was that the disease could jump from mink to people. No humans got sick from the outbreak in Spain, but other infections have spread from mink to humans before: In 2020, COVID outbreaks on Danish mink farms led to new mink-related variants that spread to a small number of humans. As mammals ourselves, we have good reason to be concerned. Outbreaks on crowded mink farms are an ideal scenario for bird flu to mutate. If, in doing so, it picks up the ability to spread between humans, it could potentially start another global pandemic. “There are many reasons to be concerned about mink,” Tom Peacock, a flu researcher at Imperial College London, told me. Right now, mink are a problem we can’t afford to ignore. For two animals with very different body types, mink and humans have some unusual similarities. Research suggests that we share similar receptors for COVID, bird flu, and human flu, through which these viruses can gain entry into our bodies. The numerous COVID outbreaks on mink farms during the early pandemic, and the bird-flu outbreak in Spain, gravely illustrate this point. It’s “not surprising” that mink can get these respiratory diseases, James Lowe, a veterinary-medicine professor at the University of Illinois at Urbana-Champaign, told me. Mink are closely related to ferrets, which are so well known for their susceptibility to human flu that they’re the go-to model for flu research. Mink wouldn’t get sick as often, and wouldn’t be as big an issue for humans, if we didn’t keep farming them for fur in the perfect conditions for outbreaks. Many barns used to raise mink are partially open-air, making it easy for infected wild birds to come in contact with the animals, sharing not only air but potentially food. Mink farms are also notoriously cramped: The Spanish farm, for example, kept tens of thousands of mink in about 30 barns. Viral transmission would be all but guaranteed in those conditions, but the animals are especially vulnerable. Because mink are normally solitary creatures, they face significant stress in packed barns, which may further predispose them to disease, Angela Bosco-Lauth, a biomedical-sciences professor at Colorado State University, told me. And because they’re often inbred so their coats look alike, an entire population may share a similar genetic susceptibility to disease. The frequency of outbreaks among mink, Bosco-Lauth said, “may actually have less to do with the animals and more to do with the fact that we raise them in the same way … we would an intensive cattle farm or chickens.” So far, there’s no evidence that mink from the Spanish farm spread bird flu to humans: None of the workers tested positive for the virus, and since then, no other mink farms have reported outbreaks. “We’re just not very susceptible” to bird flu, Lowe said. Our bird-flu receptors are tucked deep in our lungs, but when we’re exposed, most of the virus gets caught in the nose, throat, and other parts of the upper respiratory tract. This is why bird-flu infection is less common in people but is often pneumonia-level severe when it does happen. Indeed, a few humans have gotten sick and died from bird flu in the 27 years that the current strain of bird flu, known as H5N1, has circulated. This month, a girl in Cambodia died from the virus after potentially encountering a sick bird. The more virus circulating in an environment, the higher the chances a person will get infected. “It’s a dose thing,” Lowe said. But our susceptibility to bird flu could change. Another mink outbreak would give the virus more opportunities to keep mutating. The worry is that this could create a new variant that’s better at binding to the human flu receptors in our upper respiratory tract, Stephanie Seifert, a professor at Washington State University who studies zoonotic pathogens, told me. If the virus gains the ability to infect the nose and throat, Peacock, at Imperial College London, said, it would be better at spreading. Those mutations “would worry us the most.” Fortunately, the mutations that arose on the Spanish mink farm “were not as bad as many of us worried about,” he added, “but that doesn’t mean that the next time this happens, this will also be the case.” Because mink carry the receptors for both bird flu and human flu, they could serve as “mixing vessels” for the viruses to combine, researchers wrote in 2021. (Ferrets, pigs, and humans share this quality too.) Through a process called reassortment, flu viruses can swap segments of their genome, resulting in a kind of Frankenstein pathogen. Although viruses remixed in this way aren’t necessarily more dangerous, they could be, and that’s not a risk worth taking. “The previous three influenza pandemics all arose due to mixing between avian and human influenza viruses,” Peacock said. While there are good reasons to be concerned about mink, it is hard to gauge just how concerned we should be—especially given what we still don’t know about this changing virus. After the death of the young girl in Cambodia, the World Health Organization called the global bird flu situation “worrying,” while the CDC maintains that the risk to the public is low. Lowe said “it’s certainly not very risky” that bird flu will spill over into humans, but is worth keeping an eye on. H5N1 bird flu is not new, he added, and it hasn’t affected people en masse yet. But the virus has already changed in ways that make it better at infecting wild birds, and as it spreads in the wild, it may continue to change to better infect mammals, including humans. “We don’t understand enough to make strong predictions of public-health risk,” Jonathan Runstadler, an infectious-diseases professor at Tufts University, told me. As bird flu continues to spread among birds and in domestic and wild animal populations, it will only become harder to control. The virus, formally seasonal, is already present year-round in parts of Europe and Asia, and it is poised to do the same in the Americas. Breaking the chain of transmission is vital to preventing another pandemic. An important step is to avoid situations where humans, mink, or any other animal could be infected with both human and bird flu at the same time. Since the COVID outbreaks, mink farms have generally beefed up their biosecurity: Farm workers are often required to wear masks and protective gear, such as disposable overalls. To limit the risk to mink—and other susceptible hosts—farms need to reduce their size and density, reduce contact between mink and wild birds, and monitor the virus, Runstadler said. Some nations, including Mexico, Ecuador, have recently embraced bird-flu vaccines for poultry in light of the outbreaks. H5N1 vaccines are also available for humans, though they aren’t readily available. Still, one of the most obvious options is to shut mink farms down. “We probably should have done that after SARS-CoV-2,” Bosco-Lauth, at Colorado State, said. Doing so is controversial, however, because the global mink industry is valuable, with a huge market in China. Denmark, which produces up to 40 percent of the world’s mink pelts, temporarily banned mink breeding in 2020 after a spate of COVID outbreaks, but the ban expired last month, and farms are returning, albeit in a limited capacity. But mink are far from the only animal that poses a bird-flu risk to humans. “Frankly, with what we’re seeing with other wildlife species, there really aren’t any mammals that I would discount at this point in time,” Bosco-Lauth said. Any mammal species repeatedly infected by the virus is a potential risk, including marine mammals, such as seals. But we should be most concerned about the ones humans frequently come into close contact with, especially animals that are raised in high density, such as pigs, Runstadler said. This doesn’t pose just a human public-health concern, he said, but the potential for “ecological disruption.” Bird flu can be a devastating disease for wildlife, killing animals swiftly and without mercy. Whether bird flu makes the jump into humans, it isn’t the last virus that will threaten us—or mink. The era we live in has become known as the “Pandemicine,” as my colleague Ed Yong has called it, one defined by the regular spillover of viruses into humans, caused by our disruption of the normal trajectories of viral movement in nature. Mink may never pass bird flu to us. But that doesn’t mean they won’t be a risk the next time a novel influenza or coronavirus comes around. Doing nothing about mink essentially means choosing luck as a public-health strategy. Sooner or later, it will run out. from https://ift.tt/R902Anh Check out http://natthash.tumblr.com
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In the early days of the pandemic, one of the scariest and most surprising features of SARS-CoV-2 was its stealth. Initially assumed to transmit only from people who were actively sick—as its predecessor SARS-CoV did—the new coronavirus turned out to be a silent spreader, also spewing from the airways of people who were feeling just fine. After months of insisting that only the symptomatic had to mask, test, and isolate, officials scrambled to retool their guidance; singing, talking, laughing, even breathing in tight quarters were abruptly categorized as threats. Three years later, the coronavirus is still silently spreading—but the fear of its covertness again seems gone. Enthusiasm for masking and testing has plummeted; isolation recommendations have been pared down, and may soon entirely disappear. “We’re just not communicating about asymptomatic transmission anymore,” says Saskia Popescu, an infectious-disease epidemiologist and infection-prevention expert at George Mason University. “People think, What’s the point? I feel fine.” Although the concern over asymptomatic spread has dissipated, the threat itself has not. And even as our worries over the virus continue to shrink and be shunted aside, the virus--and the way it moves between us—is continuing to change. Which means that our best ideas for stopping its spread aren’t just getting forgotten; they’re going obsolete. [Read: A negative COVID test has never been so meaningless] When SARS-CoV-2 was new to the world and hardly anyone had immunity, symptomless spread probably accounted for most of the virus’s spread—at least 50 percent or so, says Meagan Fitzpatrick, an infectious-disease transmission modeler at the University of Maryland’s School of Medicine. People wouldn’t start feeling sick until four, five, or six days, on average, after being infected. In the interim, the virus would be xeroxing itself at high speed in their airway, reaching potentially infectious levels a day or two before symptoms started. Silently infected people weren’t sneezing and coughing—symptoms that propel the virus more forcefully outward, increasing transmission efficiency. But at a time when tests were still scarce and slow to deliver results, not knowing they had the virus made them dangerous all the same. Precautionary tests were still scarce, or very slow to deliver results. So symptomless transmission became a norm, as did epic superspreading events. Now, though, tests are more abundant, presymptomatic spread is a better-known danger, and repeated rounds of vaccination and infection have left behind layers of immunity. That protection, in particular, has slashed the severity and duration of acute symptoms, lowering the risk that people will end up in hospitals or morgues; it may even be chipping away at long COVID. At the same time, though, the addition of immunity has made the dynamics of symptomless transmission much more complex. On an individual basis, at least, silent spread could be happening less often than it did before. One possible reason is that symptoms are now igniting sooner in people’s bodies, just three or so days, on average, after infection—a shift that roughly coincided with the rise of the first Omicron variant and could be a quirk of the virus itself. But Aubree Gordon, an infectious-disease epidemiologist at the University of Michigan, told me that faster-arriving sicknesses are probably being driven in part by speedier immune responses, primed by past exposures. That means that illness might now coincide with or even precede the peak of contagiousness, shortening the average period in which people spread the virus before they feel sick. In that one very specific sense, COVID could now be a touch more flulike. Presymptomatic transmission of the flu does seem to happen on occasion, says Seema Lakdawala, a virologist at Emory University. But in general, “people tend not to hit their highest viral levels until after they develop symptoms,” Gordon told me. Coupled with more population-level immunity, this arrangement could be working in our favor. People might be less likely to pass the virus unwittingly to others. And thanks to the defenses we’ve collectively built up, the pathogen itself is also having more trouble exiting infected bodies and infiltrating new ones. That’s almost certainly part of the reason that this winter hasn’t been quite as bad as past ones have, COVID-wise, says Maia Majumder, an infectious-disease modeler at Harvard Medical School and Boston Children’s Hospital. That said, a lot of people are still undoubtedly catching the coronavirus from people who aren’t feeling sick. Infection per infection, the risk of superspreading events might now be lower, but at the same time people have gotten chiller about socializing without masks and testing before gathering in groups—a behavioral change that’s bound to counteract at least some of the forward shift in symptoms. Presymptomatic spread might be less likely nowadays, but it’s nowhere near gone. Multiply a small amount of presymptomatic spread by a large number of cases, and that can still seed … another large number of cases. [Read: You probably have an asymptomatic infection right now] There could be some newcomers to the pool of silent spreaders, too—those who are now transmitting the virus without ever developing symptoms at all. With people’s defenses higher than they were even a year and a half ago, infections that might have once been severe are now moderate or mild; ones that might have once been mild are now unnoticeable, says Seyed Moghadas, a computational epidemiologist at York University. At the same time, though, immunity has probably transformed some symptomless-yet-contagious infections into non-transmissible cases, or kept some people from getting infected at all. Milder cases are of course welcome, Fitzpatrick told me, but no one knows exactly what these changes add up to: Depending on the rate and degree of each of those shifts, totally asymptomatic transmission might now be more common, less common, or sort of a wash. Better studies on transmission patterns would help cut through the muck; they’re just not really happening anymore. “To get this data, you need to have pretty good testing for surveillance purposes, and that basically has stopped,” says Yonatan Grad, an infectious-disease epidemiologist at Harvard’s School of Public Health. Meanwhile, people are just straight-up testing less, and rarely reporting any of the results they get at home. For many months now, even some people who are testing have been seeing strings of negative results days into bona-fide cases of COVID—sometimes a week or more past when their symptoms start. That’s troubling on two counts: First, some legit COVID cases are probably getting missed, and keeping people from accessing test-dependent treatments such as Paxlovid. Second, the disparity muddles the start and end of isolation. Per CDC guidelines, people who don’t test positive until a few days into their illness should still count their first day of symptoms as Day 0 of isolation. But if symptoms might sometimes outpace contagiousness, “I think those positive tests should restart the isolation clock,” Popescu told me, or risk releasing people back into society too soon. [Read: People are fed up with rapid tests] American testing guidelines, however, haven’t undergone a major overhaul in more than a year—right after Omicron blew across the nation, says Jessica Malaty Rivera, an infectious-disease epidemiologist at Boston Children’s Hospital. And even if the rules were to undergo a revamp, they wouldn’t necessarily guarantee more or better testing, which requires access and will. Testing programs have been winding down for many months; free diagnostics are once again growing scarce. Through all of this, scientists and nonscientists alike are still wrestling with how to define silent infection in the first place. What counts as symptomless depends not just on biology, but behavior—and our vigilance. As worries over transmission continue to falter and fade, even mild infections may be mistaken for quiet ones, Grad told me, brushed off as allergies or stress. Biologically, the virus and the disease may not need to become that much more muted to spread with ease: Forgetting about silent spread may grease the wheels all on its own. from https://ift.tt/LrjzFIn Check out http://natthash.tumblr.com The lab-leak theory lives! Or better put: It never dies. In response to new but unspecified intelligence, the U.S. Department of Energy has changed its assessment of COVID-19’s origins: The agency, which had previously been undecided on the matter, now rates a laboratory mishap ahead of a natural spillover event as the suspected starting point. That conclusion, first reported over the weekend by The Wall Street Journal, matches up with findings from the FBI, and also a Senate Minority report out last fall that called the pandemic, “more likely than not, the result of a research-related incident.” Then again, the new assessment does not match up with findings from elsewhere in the federal government. In mid-2021, when President Biden asked the U.S. intelligence community for a 90-day review of the pandemic’s origins, the response came back divided: Four agencies, plus the National Intelligence Council, guessed that COVID started (as nearly all pandemics do) with a natural exposure to an infected animal; three agencies couldn’t decide on an answer; and one blamed a laboratory accident. DOE’s revision, revealed this week, means that a single undecided vote has flipped into the lab-leak camp. If you’re keeping count—and, really, what else can one do?—the matter still appears to be decided in favor of a zoonotic origin, by an updated score of 5 to 2. The lab-leak theory remains the outlier position. Are we done? No, we aren’t done. None of these assessments carries much conviction: Only one, from the FBI, was made with “moderate” confidence; the rest are rated “low,” as in, hmm we’re not so sure. This lack of confidence—as compared with the overbearing certainty of the scientists and journalists who rejected the possibility of a lab leak in 2020—will now be fodder for what could be months of Congressional hearings, as House Republicans pursue evidence of a possible “cover-up.” But for all the Sturm und Drang that’s sure to come, the fundamental state of knowledge on COVID’s origins remains more or less unchanged from where it was a year ago. The story of a market origin matches up with recent history and an array of well-established facts. But the lab-leak theory also fits in certain ways, and—at least for now—it cannot be ruled out. Putting all of this another way: ¯\_(ツ)_/¯. That’s not to say that it’s a toss-up. All of the agencies agree, for instance, that SARS-CoV-2 was not devised on purpose, as a weapon. And several bits of evidence have come to light since Biden ordered his review—most notably, a careful plot of early cases from Wuhan, China, that stamps the city’s Huanan market complex as the outbreak’s epicenter. Many scientists with relevant knowledge believe that COVID started in that market—but their certainty can waver. In that sense, the consensus on COVID’s origins feels somewhat different from the one on humans’ role in global warming, though the two have been pointedly compared. Climate experts almost all agree, and they also feel quite sure of their position. The central ambiguity, such as it is, of COVID’s origin remains intact and perched atop a pair of improbable-seeming coincidences: One concerns the Huanan market, and the other has to do with the Wuhan Institute of Virology, where Chinese researchers have specialized in the study of bat coronaviruses. If COVID really started in the lab, one position holds, then it would have to be a pretty amazing coincidence that so many of the earliest infections happened to emerge in and around a venue for the sale of live, wild animals … which happens to be the exact sort of place where the first SARS-coronavirus pandemic may have started 20 years ago. But also: If COVID really started in a live-animal market, then it would have to be a similarly amazing coincidence that the market in question happened to be across the river from the laboratory of the world’s leading bat-coronavirus researcher … who happened to be running experiments that could, in theory, make coronaviruses more dangerous. [Read: The lab-leak theory meets its perfect match] One might argue over which of these coincidences is really more surprising; indeed, that’s been the major substance of this debate since 2020, and the source of endless rancor. In theory, further studies and investigations would help resolve some of this uncertainty—but these may never end up happening. A formal inquiry into the pandemic’s origin, set up by the World Health Organization, had intended to revisit its claim from early 2021 that a laboratory source was “extremely unlikely.” Now that project has been shelved in the face of Chinese opposition, and the Wuhan Institute of Virology has long since stopped responding to requests for information from its U.S.-based research partners and the NIH, according to an inspector general’s report from the Department of Health and Human Services. In the meantime, the smattering of facts that have been introduced into the lab-leak debates over the past two years, have been, at times, maddeningly opaque—like the unnamed, “new intelligence” that swayed the Department of Energy. (For the record, The New York Times reports that each of the agencies investigating the pandemic’s origin had access to this same intelligence; only DOE changed its assessment to favor the lab-leak explanation as a result.) We’re only told that certain fresh and classified information has changed the minds of some (but only some) unnamed analysts who now believe (with limited assurance) that a laboratory origin is most likely. Well, great, I guess that settles it. [Read: Bird flu leaves the world with an existential choice] When more specific information does crop up, it tends to vary in the telling over time; or else it’s promptly pulverized by its partisan opponents. The Journal’s reporting, for instance, mentions a finding by U.S. intelligence that three researchers at the Wuhan Institute of Virology became ill in November 2019, in what could have been the initial cluster of infection. But how much is really known about those sickened scientists? The specifics vary with the source. In one telling, a researcher’s wife was sickened, too, and died from the infection. Another adds the seemingly important fact that the researchers were “connected with gain-of-function research on coronaviruses.” But the unnamed current and former U.S. officials who pass along this sort of information can’t even seem to settle on its credibility. Or consider the reporting, published last October by ProPublica and Vanity Fair, on a flurry of Chinese Community Party communications from the fall of 2019. These were interpreted by Senate researcher Toy Reid to mean that the Wuhan Institute of Virology had undergone a major biosafety crisis that November—just when the COVID outbreak would have been emerging. Critics ridiculed the story, calling it a “train wreck” premised on a bad translation. In response ProPublica asked three more translators to verify Reid’s reading, and claimed they “all agreed that his version was a plausible way to represent the passage,” and that the wording was ambiguous. Maybe this is just what happens when you’re trapped inside an information vacuum: Any scrap of data that happens to float by will push you off in new directions. from https://ift.tt/8XuFZfJ Check out http://natthash.tumblr.com For the past few weeks, my daily existence has been scored by the melodies of late winter: the drip of melting ice, the soft rustling of freshly sprouted leaves—and, of course, the nonstop racket of sneezes and coughs. The lobby of my apartment building is alive with the sounds of sniffles and throats being cleared. Every time I walk down the street, I’m treated to the sight of watery eyes and red noses. Even my work Slack is rife with illness emoji, and the telltale pings of miserable colleagues asking each other why they feel like absolute garbage. “It’s not COVID,” they say. “I tested, like, a million times.” Something else, they insist, is making them feel like a stuffed and cooked goose. That something else might be the once-overlooked common cold. After three years of largely being punted out of the limelight, a whole glut of airway pathogens—among them, adenovirus, RSV, metapneumovirus, parainfluenza, common-cold coronaviruses, and rhinoviruses galore—are awfully common again. And they’re really laying some people out. The good news is that there’s no evidence that colds are actually, objectively worse now than they were before the pandemic started. The less-good news is that after years of respite from a bunch of viral nuisances, a lot of us have forgotten that colds can be a real drag. [Read: The pandemic broke the flu … again] Once upon a time—before 2020, to be precise—most of us were very, very used to colds. Every year, adults, on average, catch two to three of the more than 200 viral strains that are known to cause the illnesses; young kids may contract half a dozen or more as they toddle in and out of the germ incubators that we call “day cares” and “schools.” The sicknesses are especially common during the winter months, when many viruses thrive amid cooler temps, and people tend to flock indoors to exchange gifts and breath. When the pandemic began, masks and distancing drove several of those microbes into hiding—but as mitigations have eased in the time since, they’ve begun their slow creep back. For the majority of people, that’s not really a big deal. Common-cold symptoms tend to be pretty mild and usually resolve on their own after a few days of nuisance. The virus infiltrates the nose and throat, but isn’t able to do much damage and gets quickly swept out. Some people may not even notice they’re infected at all, or may mistake the illness for an allergy—snottiness, drippiness, and not much more. Most of us know the drill: “Sometimes, it’s just congestion for a few days and feeling a bit tired for a while, but otherwise you’ll be just fine,” says Emily Landon, an infectious-disease physician at the University of Chicago. As a culture, we’ve long been in the habit of dismissing these symptoms as just a cold, not enough of an inconvenience to skip work or school, or to put on a mask. (Spoiler: The experts I spoke with were adamant that we all really should be doing those things when we have a cold.) The general infectious-disease dogma has always been that colds are a big nothing, at least compared with the flu. But gentler than the flu is not saying much. The flu is a legitimately dangerous disease that hospitalizes hundreds of thousands of Americans each year, and, like COVID, can sometimes saddle people with long-term symptoms. Even if colds are generally less severe, people can end up totally clobbered by headaches, exhaustion, and a burning sore throat; their eyes will tear up; their sinuses will clog; they’ll wake up feeling like they’ve swallowed serrated razor blades, or like their heads have been pumped full of fast-hardening concrete. It’s also common for cold symptoms to stretch out beyond a week, occasionally even two; coughs, especially, can linger long after the runny nose and headache resolve. At their worst, colds can lead to serious complications, especially in the very young, very old, and immunocompromised. Sometimes, cold sufferers end up catching a bacterial infection on top of their viral disease, a one-two punch that can warrant a trip to the ER. “The fact of the matter is, it’s pretty miserable to have a cold,” Landon told me. “And that’s how it’s always been.” [Read: Don’t worry, it’s not COVID] As far as experts can tell, the average severity of cold symptoms hasn’t changed. “It’s about perception,” says Jasmine Marcelin, an infectious-disease physician at the University of Nebraska Medical Center. After skipping colds for several years, “experiencing them now feels worse than usual,” she told me. Frankly, this was sort of a problem even before COVID came onto the scene. “Every year, I have patients who call me with ‘the worst cold they’ve ever had,’” Landon told me. “And it’s basically the same thing they had last year.” Now, though, the catastrophizing might be even worse, especially since pandemic-brain started prompting people to scrutinize every sniffle and cough. There’s still a chance that some colds this season might be a shade more unpleasant than usual. Many people falling sick right now are just coming off of bouts with COVID, flu, or RSV, each of which infected Americans (especially kids) by the millions this past fall and winter. Their already damaged tissues may not fare as well against another onslaught from a cold-causing virus. It’s also possible that immunity, or lack thereof, could be playing a small role. Many people are now getting their first colds in three-plus years, which means population-level vulnerability might be higher than it normally is this time of year, speeding the rate at which viruses spread and potentially making some infections more gnarly than they’d otherwise be. But higher-than-usual susceptibility seems unlikely to be driving uglier symptoms en masse, says Roby Bhattacharyya, an infectious-disease physician and microbiologist at Massachusetts General Hospital. Not all cold-causing viruses leave behind good immunity—but many of those that do are thought to prompt the body to mount relatively durable defenses against truly severe infections, lasting several years or more. Plus, for a lot of viruses going around right now, the immunity question is largely moot, Landon told me. So many different pathogens cause colds that a recent exposure to one is unlikely to do much against the next. A person could catch half a dozen colds in a five-year time frame and not even encounter the same type of virus twice. [Read: Maybe consider not kissing that baby] It’s also worth noting that what some people are categorizing as the worst cold they’ve ever had might actually be a far more menacing virus, such as SARS-CoV-2 or a flu virus. At-home rapid tests for the coronavirus often churn out false-negative results in the early days of infection, even after symptoms start. And although the flu can sometimes be distinguished from a cold by its symptoms, they’re often pretty similar. The illnesses can only be definitively diagnosed with a test, which can be difficult to come by.
from https://ift.tt/3qB81WX Check out http://natthash.tumblr.com Last month, at a dining table in a sunny New York City hotel suite, I found myself thrown completely off guard by a strip of fake bacon. I was there to taste a new kind of plant-based meat, which, like most Americans, I’ve tried before but never truly craved in the way that I’ve craved real meat. But even before I tried the bacon, or even saw it, I could tell it was different. The aroma of salt, smoke, and sizzling fat rising from the nearby kitchen seemed unmistakably real. The crispy bacon strips looked the part too—tiger-striped with golden fat and presented on a miniature BLT. Then crunch gave way to satisfying chew, followed by a burst of hickory and the incomparable juiciness of animal fat. I knew it wasn’t real bacon, but for a moment, it fooled me. The bacon was indeed made from plants, just like the burger patties you can buy from companies such as Impossible Foods and Beyond Meat. But it had been mixed with real pork fat. Well, kind of. What marbled the meat had not come from a butchered pig but a living hog whose fat cells had been sampled and grown in a vat. This lab-grown fat, or “cultivated fat,” was made by Mission Barns, a San Francisco start-up, with one purpose: to win people over to plant-based meat. And a lot of people need to be won over, it seems. The plant-based-meat industry, which a few years ago seemed destined for mainstream success, is now struggling. Once the novelty of seeing plant protein “bleed” wore off, the high price, middling nutrition, and just-okay flavor of plant-based meat has become harder for consumers to overlook, food analysts told me. In 2021 and 2022, many of the fast-food chains that had once given plant-based meat a national platform—Burger King, Dunkin’, McDonald’s--lost interest in selling it. In the past four months, the two most visible plant-based-meat companies, Beyond Meat and Impossible Foods, have each announced layoffs. Meanwhile, the future of meat alternatives—lab-grown meat that is molecularly identical to the real deal—is at least several years away, lodged between science fiction and reality. But we can’t wait until then to eat less meat; it’s one of the single best things that regular people can do for the climate, and also helps address concerns about animal suffering and health. Lab-grown fat might be the bridge. It is created using the same approach as lab-grown meat, but it’s far simpler to make and can be mixed into existing plant-based foods, Elysabeth Alfano, the CEO of the investment firm VegTech Invest, told me. As such, it’s likely to become commercially available far sooner—maybe even within the next few years. Maybe all it will take to save fake meat is a little animal fat. Animal fat is culinary magic. It creates the juiciness of a burger, and leaves a buttery coat on the tongue. Its absence is the reason that chicken breasts taste so bland. Fat, the chef Samin Nosrat wrote in Salt, Fat, Acid, Heat, is “a source of both rich flavor and of a particular desired texture.” The fake meat on the market now is definitely lacking in the flavor and texture departments. Most products approximate meatiness using a concoction of plant oils, flavorings, binders, and salt, which is certainly meatier than the bean burgers that came before it, but is far from perfect: The food blog Serious Eats, for instance, has pointed out off-putting flavor notes, at least prior to cooking, including coconut and cat food. On a molecular level, plant fat is ill-equipped to mimic its animal counterpart. Coconut oil, common in plant-based meat, is solid at room temperature but melts under relatively low heat, so it spills out into the pan while cooking. As a result, the mouthfeel of plant-based meat tends to be more greasy than sumptuous. Replacing those plant oils with cultivated animal fat, which keeps its structure when heated, would maintain the flavor and juiciness people expect of real meat, Audrey Gyr, the start-up innovation specialist at the Good Food Institute, a nonprofit that advocates for plant-based substitutes, told me. In a sense, the technique of using animal fat to flavor plants is hardly new. Chicken schmaltz has long lent rich nuttiness to potato latkes; rendered guanciale is what gives a classic amatriciana its succulence. Plant-based bacon enhanced with pork fat follows from the same culinary tradition, but it’s very high-tech. Fat cells sampled from a live animal are grown in huge bioreactors and fed with plant-derived sugars, proteins, and other growth components. In time, they multiply to form a mass of fat cells: a soft, pale solid with robust flavor, the same white substance you might see encircling a pork chop or marbling a steak. Out of the bioreactor, the fat “looks a little bit like margarine,” Ed Steele, a co-founder of the London-based cultivated-fat company Hoxton Farms, told me. It is a complicated process, but far easier than engineering cultivated meat, which involves many cell types that must be coaxed into rigid muscle fibers. Fat involves one type of cell and is most useful as a formless blob. Just as in the human body, all it takes is time, space, and a steady drip of sugars, oils, and other fats, Eitan Fischer, CEO of Mission Barns, told me. The bacon I’d tried at the tasting had been constructed by layering cultivated fat with plant-based protein, curing and smoking the loaf, then slicing it into bacon-like strips. Mixing just 10 percent cultivated fat with plant-based protein by mass, Steele said, can make a product taste and feel like the real thing. Already, cultivated-fat products are within sight. Mission Barns plans to incorporate its cultivated fat into its own plant-based products; Hoxton Farms hopes to sell its fat directly to existing plant-based-meat manufacturers. Other companies, such as the Belgian start-up Peace of Meat, the Berlin-based Cultimate Foods, and Singapore’s fish-focused ImpacFat, are also working on their own versions of cultivated fat. In theory, the fat can be mixed into virtually any type of plant-based meat—nuggets, sausages, paté. In the U.S., a path to market is already being cleared. Last November, cultivated chicken from the California start-up Upside Foods received FDA clearance; now it’s waiting on additional clearance from the Department of Agriculture. Pending its own regulatory approvals, Mission Barns says it is ready to launch its products in a few supermarkets and restaurants, which also include a convincingly porky plant-based meatball I also tried at the tasting. (Due to the pending approval, I had to sign a liability waiver before digging in.) I left the tasting with animal fat on my lips and a new conviction in my mind: At the right price, I’d buy this bacon over the regular stuff. Because cultivated fat can be made without harming animals—the fat cells in the bacon I tasted came from a happily free-ranging pig named Dawn, a PR rep for Mission Barns told me—it may appeal to flexitarians like myself who just want to eat less meat. Although there’s no guarantee it would taste as good at home as it did when prepared by Mission Barns’s private chef, with its realistic texture and flavor, cultivated fat could solve the main issue plaguing plant-based meat: It just doesn’t taste that good. Cultivated fat is “the next step in making environmentally friendly foods more palatable to the average consumer,” Jennifer Bartashus, a packaged-food analyst at Bloomberg Intelligence, told me. But cultivated fat still faces some of the same problems that have turned America off plant-based meat. The current products for sale are not particularly healthy, and cultivated fat would not change that fact. Building consumer trust and familiarity may also be an issue. Some people are leery of plant-based products because they’re confused about what they’re made of. The more complex notion of cultivated fat may be just as unappetizing, if not more so. “We still don’t know exactly how consumers are going to feel about cultivated fat,” Gyr said. Certainly, finding a catchy name for these products would help, but I have struggled to find a term less clunky than “plant-based meat flavored with cultivated animal fat” to describe what I ate. Unless cultivated-fat companies really nail their marketing, they could go the way of “blended meat”—mixtures of plant-based protein and real meat introduced by three meat companies in 2019, which was “a bit of a marketing failure,” Gyr said. Above all, though, is the price relative to that of traditional meat. Plant-based meat’s higher cost has partly been blamed for the industry’s slump, and products containing cultivated fat, in all likelihood, will not be cheaper in the near future. Neither founder I spoke with shared specific numbers; Fischer, of Mission Barns, said only that the company’s small production scale makes it “fairly expensive” compared with traditional meat products, while Steele said his hope is that companies using Hoxton Farms’ cultivated fat in their plant-based-meat recipes won’t have to spend more than they do now. Despite these obstacles, cultivated fat is promising for the flagging plant-based-meat industry because of the fact that it is absolutely delicious. Cultivated fat could “lead to a new round of innovation that will pull consumers back in,” Bartashus said. After all, plant-based and real meat could reach cost parity around 2026, at which point even more companies might want to get in on meat alternatives. Cultivated fat might warm us up to the future of fully cultivated meat. With enough time, lab-grown chicken breasts could become as boring as regular chicken breasts. Enthusiasm about cultivated fat, and fake meat in general, has a distinctly techno-optimist flavor, as if persuading all meat eaters to embrace plants gussied up in bacon grease will be easy. “Eventually our goal is to outcompete current conventional meat prices, whether it’s meatballs or bacon,” Fischer said. But even as the problems with eating meat have only become clearer, meat consumption in the U.S. has continued to rise. Globally, meat consumption in countries such as India and China is expected to skyrocket in the coming years. At the very least, cultivated fat provides consumers with another option at a time when eating a steak for one meal and then opting for plant-based meat the next can count as a win. Since the tasting, I’ve often thought about why eating the bacon left me feeling so perplexed. When I gnawed on the crispy golden edge of one of the strips, I knew I was eating real bacon fat, but my brain still wrestled with the idea that it had not come directly from a piece of pork. I’ve only ever known a world where animal fat comes from slaughtered animals. That is changing. If cultivated fat can tide the plant-based-meat industry over until lab-grown meat becomes a reality, these new products will have done their part. In the meantime, we may come to find that they’re already good enough. from https://ift.tt/FN07rpQ Check out http://natthash.tumblr.com In one very specific and mostly benign way, it’s starting to feel a lot like the spring of 2020: Disinfection is back. “Bleach is my friend right now,” says Annette Cameron, a pediatrician at Yale School of Medicine, who spent the first half of this week spraying and sloshing the potent chemical all over her home. It’s one of the few tools she has to combat norovirus, the nasty gut pathogen that her 15-year-old son was recently shedding in gobs. Right now, hordes of people in the Northern Hemisphere are in a similarly crummy situation. In recent weeks, norovirus has seeded outbreaks in several countries, including the United Kingdom, Canada, and the United States. Last week, the U.K. Health Security Agency announced that laboratory reports of the virus had risen to levels 66 percent higher than what’s typical this time of year. Especially hard-hit are Brits 65 and older, who are falling ill at rates that “haven’t been seen in over a decade.” Americans could be heading into a rough stretch themselves, Caitlin Rivers, an infectious-disease epidemiologist at Johns Hopkins University, told me, given how closely the U.S.’s epidemiological patterns tend to follow those of the U.K. “It does seem like there’s a burst of activity right now,” says Nihal Altan-Bonnet, a norovirus researcher at the National Institutes of Health. At her own practice, Cameron has been seeing the number of vomiting and diarrhea cases among her patients steadily tick up. (Other pathogens can cause gastrointestinal symptoms as well, but norovirus is the most common cause of foodborne illness in the United States.) To be clear, this is more a nauseating nuisance than a public-health crisis. In most people, norovirus triggers, at most, a few miserable days of GI distress that can include vomiting, diarrhea, and fevers, then resolves on its own; the keys are to stay hydrated and avoid spreading it to anyone vulnerable—little kids, older adults, the immunocompromised. The U.S. logs fewer than 1,000 annual deaths out of millions of documented cases. In other high-income countries, too, severe outcomes are very rare, though the virus is far more deadly in parts of the world with limited access to sanitation and potable water. Still, fighting norovirus isn’t easy, as plenty of parents can attest. The pathogen, which prompts the body to expel infectious material from both ends of the digestive tract, is seriously gross and frustratingly hardy. Even the old COVID standby, a spritz of hand sanitizer, doesn’t work against it—the virus is encased in a tough protein shell that makes it insensitive to alcohol. Some have estimated that ingesting as few as 18 infectious units of virus can be enough to sicken someone, “and normally, what’s getting shed is in the billions,” says Megan Baldridge, a virologist and immunologist at Washington University in St. Louis. At an extreme, a single gram of feces—roughly the heft of a jelly bean—could contain as many as 5.5 billion infectious doses, enough to send the entire population of Eurasia sprinting for the toilet. Unlike flu and RSV, two other pathogens that have bounced back to prominence in recent months, norovirus mainly targets the gut, and spreads especially well when people swallow viral particles that have been released in someone else’s vomit or stool. (Despite its “stomach flu” nickname, norovirus is not a flu virus.) But direct contact with those substances, or the food or water they contaminate, may not even be necessary: Sometimes people vomit with such force that the virus gets aerosolized; toilets, especially lidless ones, can send out plumes of infection like an Air Wick from hell. And Altan-Bonnet’s team has found that saliva may be an unappreciated reservoir for norovirus, at least in laboratory animals. If the spittle finding holds for humans, then talking, singing, and laughing in close proximity could be risky too. [Read: Whatever happened to toilet plumes?] Once emitted into the environment, norovirus particles can persist on surfaces for days—making frequent hand-washing and surface disinfection key measures to prevent spread, says Ibukun Kalu, a pediatric infectious-disease specialist at Duke University. Handshakes and shared meals tend to get dicey during outbreaks, along with frequently touched items such as utensils, door handles, and phones. One 2012 study pointed to a woven plastic grocery bag as the source of a small outbreak among a group of teenage soccer players; the bag had just been sitting in a bathroom used by one of the girls when she fell sick the night before. Once a norovirus transmission chain begins, it can be very difficult to break. The virus can spread before symptoms start, and then for more than a week after they resolve. To make matters worse, immunity to the virus tends to be short-lived, lasting just a few months even against a genetically identical strain, Baldridge told me. Day cares, cruise ships, schools, restaurants, military training camps, prisons, and long-term-care facilities can be common venues for norovirus spread. “I did research with the Navy, and it just goes through like wildfire,” often sickening more than half the people on tightly packed ships, says Robert Frenck, the director of the Vaccine Research Center at Cincinnati Children’s Hospital. Households, too, are highly susceptible to spread: Once the virus arrives, the entire family is almost sure to be infected. Baldridge, who has two young children, told me that her household has weathered at least four bouts of norovirus in the past several years. (A pause for some irony: In spite of norovirus’s infectiousness, scientists did not succeed in culturing it in labs until just a few years ago, after nearly half a century of research. When researchers design challenge trials to, say, test new vaccines, they still need to dose volunteers with norovirus that’s been extracted from patient stool, a gnarly practice that’s been around for more than 50 years.) Norovirus spread doesn’t have to be a foregone conclusion. Some people do get lucky: Roughly 20 percent of European populations, for instance, are genetically resistant to common norovirus strains. “So you can hope,” Frenck told me. For the rest of us, it comes down to hygiene. Altan-Bonnet recommends diligent hand-washing, plus masking to ward off droplet-borne virus. Sick people should isolate themselves if they can. “And keep your saliva to yourself,” she told me. [Read: The stomach-flu mystery] Rivers and Cameron have both managed to halt the virus in their homes in the past; Cameron may have pulled it off again this week. The family fastidiously scrubbed their hands with hot water and soap, donned disposable gloves when touching shared surfaces, and took advantage of the virus’s susceptibility to harsh chemicals and heat. When her son threw up on the floor, Cameron sprayed it down with bleach; when he vomited on his quilt, she blasted it twice in the washing machine on the sanitizing setting, then put it through the dryer at a super high temp. Now a couple of days out from the end of their son’s sickness, Cameron and her husband appear to have escaped unscathed. Norovirus isn’t new, and this won’t be the last time it hits. In a lot of ways, “this is back to basics,” says Samina Bhumbra, the medical director of infection prevention at Riley Children’s Hospital. After three years of COVID, the world has gotten used to thinking about infections in terms of airways. “We need to recalibrate,” Bhumbra told me, “and remember that other things exist.” from https://ift.tt/wQcZWOj Check out http://natthash.tumblr.com For many Americans, wearing a mask has become a relic. But fighting about masks, it seems, has not. Masking has widely been seen as one of the best COVID precautions that people can take. Still, it has sparked ceaseless arguments: over mandates, what types of masks we should wear, and even how to wear them. A new review and meta-analysis of masking studies suggests that the detractors may have a point. The paper—a rigorous assessment of 78 studies—was published by Cochrane, an independent policy institution that has become well known for its reviews. The review’s authors found “little to no” evidence that masking at the population level reduced COVID infections, concluding that there is “uncertainty about the effects of face masks.” That result held when the researchers compared surgical masks with N95 masks, and when they compared surgical masks with nothing. On Twitter, longtime critics of masking and mandates held this up as the proof they’d long waited for. The Washington Free Beacon, a conservative outlet, quoted a researcher who has called the analysis the “scientific nail in the coffin for mask mandates.” The vaccine skeptic Robert Malone used it to refute what he called “self-appointed ‘experts’” on masking. Some researchers weighed in with more nuanced interpretations, pointing out limitations in the review’s methods that made it difficult to draw firm conclusions. Even the CDC director, Rochelle Walensky, pushed back against the paper in a congressional testimony this week, citing its small sample size of COVID-specific studies. The argument is heated and technical, and probably won’t be resolved anytime soon. But the fact that the fight is ongoing makes clear that there still isn’t a firm answer to among the most crucial of pandemic questions: Just how effective are masks at stopping COVID? An important feature of Cochrane reviews is that they look only at “randomized controlled trials,” considered the gold standard for certain types of research because they compare the impact of one intervention with another while tightly controlling for biases and confounding variables. The trials considered in the review compared groups of people who masked with those who didn’t in an effort to estimate how effective masking is at blunting the spread of COVID in a general population. The population-level detail is important: It indicates uncertainty about whether requiring everyone to wear a mask makes a difference in viral spread. This is different from the impact of individual masking, which has been better researched. Doctors, after all, routinely mask when they’re around sick patients and do not seem to be infected more often than anyone else. “We have fairly decent evidence that masks can protect the wearer,” Jennifer Nuzzo, an epidemiologist at Brown University, told me. “Where I think it sort of falls apart is relating that to the population level.” The research on individual masking generally shows what we have come to expect: High-quality masks provide a physical barrier between the wearer and infectious particles, if worn correctly. For instance, in one study, N95 masks were shown to block 57 to 90 percent of particles, depending on how well they fit; cloth and surgical masks are less effective. The caveat is that much of that support came from laboratory research and observational studies, which don’t account for the messiness of real life. That the Cochrane review reasonably challenges the effectiveness of population-level masking doesn’t mean the findings of previous studies in support of masking are moot. A common theme among criticisms of the review is that it considered only a small number of studies by virtue of Cochrane’s standards; there just aren’t that many randomized controlled trials on COVID and masks. In fact, most of those included in the review are about the impact of masking on other respiratory illnesses, namely the flu. Although some similarities between the viruses are likely, Nuzzo explained on Twitter, COVID-specific trials would be ideal. The handful of trials in the review that focus on COVID don’t show strong support for masking. One, from Bangladesh, which looked at both cloth and surgical masks, found a 9 percent decrease in symptomatic cases in masked versus unmasked groups (and a reanalysis of that study found signs of bias in the way the data were collected and interpreted); another, from Denmark, suggested that surgical masks offered no statistically significant protection at all. Criticisms of the review posit that it might have come to a different conclusion if more and better-quality studies had been available. The paper’s authors acknowledge that the trials they considered were prone to bias and didn’t control for inconsistent adherence to the interventions. “The low to moderate certainty of evidence means our confidence in the effect estimate is limited, and that the true effect may be different from the observed estimate of the effect,” they concluded. If high-quality masks worn properly work well at an individual level, after all, then it stands to reason that high-quality masks worn properly by many people in any situation should indeed provide some level of protection. Tom Jefferson, the review’s lead author, did not respond to a request for comment. But in a recent interview about the controversy, he stood by the practical implications of the new study. “There’s still no evidence that masks are effective during a pandemic,” he said. Squaring all of this uncertainty with the support for masking and mandates early in the pandemic is difficult. Evidence for it was scarce in the early days of the pandemic, Nuzzo acknowledged, but health officials had to act. Transmission was high, and the costs of masking were seen as low; it was not immediately clear how inconvenient and unmanageable masks could be, especially in settings such as schools. Mask mandates have largely expired in most places, but it doesn’t hurt most people to err on the side of caution. Nuzzo still wears a mask in high-risk environments. “Will that prevent me from ever getting COVID? No,” she said, but it reduces her risk—and that’s good enough. What is most frustrating about this masking uncertainty is that the pandemic has presented many opportunities for the U.S. to gather stronger data on the effects of population-level masking, but those studies have not happened. Masking policies were made on sound but limited data, and when decisions are made that way, “you need to continually assess whether those assumptions are correct,” Nuzzo said—much like how NASA collects huge amounts of data to prepare for all the things that could go wrong with a shuttle launch. Unfortunately, she said, “we don’t have Houston for the pandemic.” Obtaining stronger data is still possible, though it won’t be easy. A major challenge of studying the effect of population-level masking in the real world is that people aren’t good at wearing masks, which of course is a problem with the effectiveness of masks too. It would be straightforward enough if you could guarantee that participants wore their masks perfectly and consistently throughout the study period. But in the real world, masks fit poorly and slip off noses, and people are generally eager to take them off whenever possible. Ideally, the research needed to gather strong data—about masks, and other lingering pandemic questions—would be conducted through the government. The U.K., for example, has funded large randomized controlled trials of COVID drugs such as molnupiravir. So far, that doesn’t seem to have happened in the U.S. None of the new studies on masking included in the Cochrane review were funded by the U.S. government. “The fact that we never as a country really set up studies to answer the most pressing questions is a failure,” said Nuzzo. What the CDC could do is organize and fund a research network to study COVID, much like the centers of excellence the agency has for fields such as food safety and tuberculosis. The window of opportunity hasn’t closed yet. The Cochrane review, for all of its controversy, is a reminder that more research on masking is needed, if only to address whether pro-mask policies warrant the rage they incite. You would think that the policy makers who encouraged masking would have made finding that support a priority. “If you’re going to burn your political capital, it’d be nice to have the evidence to say that it’s necessary,” Nuzzo said. At this point, even the strongest possible evidence is unlikely to change some people’s behavior, considering how politicized the mask debate has become. But as a country, the lack of conclusive evidence leaves us ill-prepared for the next viral outbreak—COVID or otherwise. The risk is still low, but bird flu is showing troubling signs that it could make the jump from animals to humans. If it does, should officials be telling everyone to mask up? That America has never amassed good evidence to show the effect of population-level masking for COVID, Nuzzo said, has been a missed opportunity. The best time to learn more about masking is before we are asked to do it again. from https://ift.tt/KzxAVEF Check out http://natthash.tumblr.com In the early spring of 2020, the condition we now call long COVID didn’t have a name, much less a large community of patient advocates. For the most part, clinicians dismissed its symptoms, and researchers focused on SARS-CoV-2 infections’ short-term effects. Now, as the pandemic approaches the end of its third winter in the Northern Hemisphere, the chronic toll of the coronavirus is much more familiar. Long COVID has been acknowledged by prominent experts, national leaders, and the World Health Organization; the National Institutes of Health has set up a billion-dollar research program to understand how and in whom its symptoms unfurl. Hundreds of long-COVID clinics now freckle the American landscape, offering services in nearly every state; and recent data hint that well-vetted drugs to treat or prevent long COVID may someday be widespread. Long COVID and the people battling it are commanding more respect, says Hannah Davis, a co-founder of the Patient-Led Research Collaborative, who has had long COVID for nearly three years: Finally, many people “seem willing to understand.” But for all the ground that’s been gained, the road ahead is arduous. Long COVID still lacks a universal clinical definition and a standard diagnosis protocol; there’s no consensus on its prevalence, or even what symptoms fall under its purview. Although experts now agree that long COVID does not refer to a single illness, but rather is an umbrella term, like cancer, they disagree on the number of subtypes that fall within it and how, exactly, each might manifest. Some risk factors—among them, a COVID hospitalization, female sex, and certain preexisting medical conditions—have been identified, but researchers are still trying to identify others amid fluctuating population immunity and the endless slog of viral variants. And for people who have long COVID now, or might develop it soon, the interventions are still scant. To this day, “when someone asks me, ‘How can I not get long COVID?’ I can still only say, ‘Don’t get COVID,’” says David Putrino, a neuroscientist and physical therapist who leads a long-COVID rehabilitation clinic at Mount Sinai’s Icahn School of Medicine. As the world turns its gaze away from the coronavirus pandemic, with country after country declaring the virus “endemic” and allowing crisis-caliber interventions to lapse, long-COVID researchers, patients, and activists worry that even past progress could be undone. The momentum of the past three years now feels bittersweet, they told me, in that it represents what the community might lose. Experts can’t yet say whether the number of long-haulers will continue to increase, or offer a definitive prognosis for those who have been battling the condition for months or years. All that’s clear right now is that, despite America’s current stance on the coronavirus, long COVID is far from being beaten. Despite an influx of resources into long-COVID research in recent months, data on the condition’s current reach remain a mess—and scientists still can’t fully quantify its risks. Recent evidence from two long-term surveys have hinted that the pool of long-haulers might be shrinking, even as new infection rates remain sky-high: Earlier this month, the United Kingdom’s Office for National Statistics released data showing that 2 million people self-reported lingering symptoms at the very start of 2023, down from 2.3 million in August 2022. The U.S. CDC’s Household Pulse Survey, another study based on self-reporting, also recorded a small drop in long-COVID prevalence in the same time frame, from about 7.5 percent of all American adults to roughly 6. Against the massive number of infections that have continued to slam both countries in the pandemic’s third year and beyond, these surveys might seem to imply that long-haulers are leaving the pool faster than newcomers are arriving. Experts cautioned, however, that there are plenty of reasons to treat these patterns carefully—and to not assume that the trends will be sustained. It’s certainly better that these data aren’t showing a sustained, dramatic uptick in long-COVID cases. But that doesn’t mean the situation is improving. Throughout the pandemic, the size of the long-COVID pool has contracted or expanded for only two reasons: a change in the rate at which people enter, or at which they exit. Both figures are likely to be in constant flux, as surges of infections come and go, masking habits change, and vaccine and antiviral uptake fluctuates. Davis pointed out that the slight downward tick in both studies captured just a half-year stretch, so the downward slope could be one small portion of an undulating wave. A few hours spent at the beach while the tide is going out wouldn’t be enough to prove that the ocean is drying up. [Read: We’re bungling the COVID wind-down] Recent counts of new long-COVID cases might also be undercounts, as testing slows and people encounter more challenges getting diagnosed. That said, it’s still possible that, on a case-by-case basis, the likelihood of any individual developing long COVID after a SARS-CoV-2 infection may have fallen since the pandemic’s start, says Deepti Gurdasani, a clinical epidemiologist at Queen Mary University of London and the University of New South Wales. Population immunity—especially acquired via vaccination—has, over the past three years, better steeled people’s bodies against the virus, and strong evidence supports the notion that vaccines can moderately reduce the risk of developing long COVID. Treatments and behavioral interventions that have become more commonplace may have chipped away at incidence as well. Antivirals can now help to corral the virus early in infection; ventilation, distancing, and masks—when they’re used—can trim the amount of virus that infiltrates the body. And if overall exposure to the virus can influence the likelihood of developing long COVID, that could help explain why so many debilitating cases arose at the very start of the pandemic, when interventions were few and far between, says Steven Deeks, a physician researcher at UC San Francisco. There’s not much comfort to derive from those individual-level stats, though, when considering what’s happening on broader scales. Even if immunity makes the average infected person less likely to fall into the long-COVID pool, so many people have been catching the virus that the inbound rate still feels like a flood. “The level of infection in many countries has gone up substantially since 2021,” Gurdasani told me. The majority of long-COVID cases arise after mild infections, the sort for which our immune defenses fade most rapidly. Now that masking and physical distancing have fallen by the wayside, people may be getting exposed to higher viral doses than they were a year or two ago. In absolute terms, then, the number of people entering the long-COVID pool may not really be decreasing. Even if the pool were getting slightly smaller, its size would still be staggering, an ocean of patients with titanic needs. “Anecdotally, we still have an enormous waitlist to get into our clinic,” Putrino told me. Deeks told me that he’s seen another possible reason for optimism: People with newer cases of long COVID might be experiencing less debilitating or faster-improving disease, based on what he’s seen. “The worst cases we’ve seen come from the first wave in 2020,” he said. But Putrino isn’t so sure. “If you put an Omicron long-COVID patient in front of me, versus one from the first wave, I wouldn’t be able to tell you who was who,” he said. The two cases would also be difficult to compare, because they’re separated by so much time. Long COVID’s symptoms can wax, wane, and qualitatively change; a couple of years into the future, some long-haulers who’ve just developed the condition may be in a spot that’s similar to where many veterans with the condition are now. [Read: The flu-ification of COVID policy is almost complete] Experts’ understanding of how often people depart the long-COVID pool is also meager. Some long-haulers have undoubtedly seen improvement—but without clear lines distinguishing short COVID from medium and long COVID, entry and exit into these various groups is easy to over- or underestimate. What few data exist on the likelihood of recovery or remission is inconsistent, and not always rosy: Investigators of RECOVER, a large national study of long COVID, have calculated that about two-thirds of the long-haulers in their cohort do not return to baseline health. Putrino, who has worked with hundreds of long-haulers since the pandemic began, estimates that although most of his patients experience at least some benefit from a few months of rehabilitation, only about one-fifth to one-quarter of them eventually reach the point of feeling about as well as they did before catching the virus, while the majority hit a middling plateau. A small minority of the people he has treated, he told me, never seem to improve at all. Letícia Soares, a long-hauler in Brazil who caught the virus near the start of the pandemic, falls into that final category. Once a disease ecologist who studied parasite transmission in birds, she is now mostly housebound, working when she is able as a researcher for the Patient-Led Research Collaborative. Her days revolve around medications and behavioral modifications she uses for her fatigue, sleeplessness, and chronic pain. Soares no longer has the capacity to cook or frequently venture outside. And she has resigned herself to this status quo until the treatment landscape changes drastically. It is not the life she pictured for herself, Soares told me. “Sometimes I think the person I used to be died in April of 2020.” Even long-haulers who have noticed an improvement in their symptoms are wary of overconfidence. Some absolutely do experience what could be called recovery—but for others, the term has gotten loaded, almost a jinx. “If the question is, ‘Are you doing the things you were doing in 2019?’ the answer is largely no,” says JD Davids, a chronic-illness advocate based in New York. For some, he told me, “getting better” has been more defined by a resetting of expectations than a return to good health. Relapses are also not uncommon, especially after repeat encounters with the virus. Lisa McCorkell, a long-hauler and a co-founder of the Patient-Led Research Collaborative, has felt her symptoms partly abate since she first fell ill in the spring of 2020. But, she told me, she suspects that her condition is more likely to deteriorate than further improve—partly because of “how easy it is to get reinfected now.” Last week, in his State of the Union address, President Joe Biden told the American public that “we have broken COVID’s grip on us.” Highlighting the declines in the rates of COVID deaths, the millions of lives saved, and the importance of remembering the more than 1 million lost, Biden reminded the nation of what was to come: “Soon we’ll end the public-health emergency.” When the U.S.’s state of emergency was declared nearly three years ago, as hospitals were overrun and morgues overflowed, the focus was on severe, short-term disease. Perhaps in that sense, the emergency is close to being over, Deeks told me. But long COVID, though slower to command attention, has since become its own emergency, never formally declared; for the millions of Americans who have been affected by the condition, their relationship with the virus does not yet seem to be in a better place. [Read: Trying to stop long COVID before it even starts] Even with many more health-care providers clued into long COVID’s ills, the waiting lists for rehabilitation and treatment remain untenable, Hannah Davis told me. “I consider myself someone who gets exceptional care compared to other people,” she said. “And still, I hear from my doctor every nine or 10 months.” Calling a wrap on COVID’s “emergency” phase could worsen that already skewed supply-demand ratio. Changes to the nation’s funding tactics could strip resources—among them, access to telehealth; Medicaid coverage; and affordable antivirals, tests, and vaccines—from vulnerable populations, including people of color, that aren’t getting their needs met even as things stand, McCorkell told me. And as clinicians internalize the message that the coronavirus has largely been addressed, attention to its chronic impacts may dwindle. At least one of the country's long-COVID clinics has, in recent months, announced plans to close, and Davis worries that more could follow soon. Scientists researching long COVID are also expecting new challenges. Reduced access to testing will complicate efforts to figure out how many people are developing the condition, and who’s most at risk. Should researchers turn their scientific focus away from studying causes and cures for long COVID when the emergency declaration lifts, Davids and others worry that there will be ripple effects on the scientific community’s interest in other, neglected chronic illnesses, such as ME/CFS (myalgic encephalomyelitis or chronic fatigue syndrome), a diagnosis that many long-haulers have also received. The end of the U.S.’s official crisis mode on COVID could stymie research in other ways as well. At Johns Hopkins University, the infectious-disease epidemiologists Priya Duggal, Shruti Mehta, and Bryan Lau have been running a large study to better understand the conditions and circumstances that lead to long COVID, and how symptoms evolve over time. In the past two years, they have gathered online survey data from thousands of people who both have and haven’t been infected, and who have and haven’t seen their symptoms rapidly resolve. But as of late, they’ve been struggling to recruit enough people who caught the virus and didn’t feel their symptoms linger. “I think that the people who are suffering from long COVID will always do their best to participate,” Duggal told me. That may not be the case for individuals whose experiences with the virus were brief. A lot of them “are completely over it,” Duggal said. “Their life has moved on.” Kate Porter, a Massachusetts-based marketing director, told me that she worries about her family’s future, should long COVID fade from the national discourse. She and her teenage daughter both caught the virus in the spring of 2020, and went on to develop chronic symptoms; their experience with the disease isn’t yet over. “Just because the emergency declaration is expiring, that doesn’t mean that suddenly people are magically going to get better and this issue is going to go away,” Porter told me. After months of relative improvement, her daughter is now fighting prolonged bouts of fatigue that are affecting her school life—and Porter isn’t sure how receptive people will be to her explanations, should their illnesses persist for years to come. “Two years from now, how am I going to explain, ‘Well, this is from COVID, five years ago’?” she said. A condition that was once mired in skepticism, scorn, and gaslighting, long COVID now has recognition—but empathy for long-haulers could yet experience a backslide. Nisreen Alwan, a public-health researcher at the University of Southampton, in the U.K., and her colleagues have found that many long-haulers still worry about disclosing their condition, fearing that it could jeopardize their employment, social interactions, and more. Long COVID could soon be slated to become just one of many neglected chronic diseases, poorly understood and rarely discussed. Davis doesn’t think that marginalization is inevitable. Her reasoning is grim: Other chronic illnesses have been easier to push to the sidelines, she said, on account of their smaller clinical footprint, but the pool of long-haulers is enormous—comprising millions of people in the U.S. alone. “I think it’s going to be impossible to ignore,” she told me. One way or another, the world will have no choice but to look. from https://ift.tt/aJDXy41 Check out http://natthash.tumblr.com I grew up in a nonstick-pan home. No matter what was on the menu, my dad would reach for the Teflon-coated pan first: nonstick for stir-fried vegetables, for reheating takeout, for the sunny-side-up eggs, garlic fried rice, and crisped Spam slices that constituted breakfast. Nowadays, I’m a much fussier cook: A stainless-steel pan is my kitchen workhorse. Still, when I’m looking to make something delicate, such as a golden pancake or a classic omelet, I can’t help but turn back to that time-tested fave. And what a dream it is to use. Nonstick surfaces are so frictionless that fragile crepes and scallops practically lift themselves off the pan; cleaning up sticky foods, such as oozing grilled-cheese sandwiches, becomes no more strenuous than rinsing a plate. No wonder 70 percent of skillets sold in the U.S. are nonstick. Who can afford to mangle a dainty snapper fillet or spend time scrubbing away crisped rice? All of this convenience, however, comes with a cost: the unsettling feeling that cooking with a nonstick pan is somehow bad for you. My dad had a rule that we could only use a soft, silicon-edged spatula with the pan, born of his hazy intuition that any scratches on the coating would cause it to leach into our food and make us sick. Many home cooks have lived with these fears since at least the early 2000s, when we first began to hear about problems with Teflon, the substance that makes pans nonstick. Teflon is produced from chemicals that are part of an enormous family of chemicals known as perfluoroalkyl and polyfluoroakyl substances, or PFAS, and research has linked exposure to them to many health conditions, including certain cancers, reproductive issues, and high cholesterol. And that is about all we know: In kitchens over the past two decades, the same questions around safety have lingered unanswered amid the aromas of sizzling foods and, perhaps, invisible clouds of Teflon fumes. It is objectively ridiculous that the safety of one of the most common household items in America remains such a mystery. But the reality is that it is nearly impossible to measure the risks of PFAS from nonstick cookware—and more important, it’s probably pointless to try. That’s because PFAS have for many decades imparted a valuable stain- and water-resistance to many types of surfaces, including carpets, car seats, and raincoats. At this point, the chemicals are also ubiquitous in the environment, particularly in the water supply. Last June, the Environmental Protection Agency established new safety guidelines for the level of certain PFAS in drinking water; a study published around the same time showed that millions of deaths are correlated with PFAS exposure. By the Environmental Working Group’s latest count, PFAS have contaminated more than 2,850 sites in 50 states and two territories—an “alarming” level of pervasiveness, researchers wrote in a National Academies of Sciences, Engineering, and Medicine report last year. But something about nonstick pans has generated the biggest freak-out. This is not surprising, given their exposure to food and open flames. After all, people do not heat up and consume raincoats (as far as I know). Since research into their health effects began, certain types of PFAS have been flagged as more dangerous than others. Two of them, PFOA and PFOS, were voluntarily phased out by manufacturers for several reasons, including the fact that they were deemed dangerous to the immune system; now many nonstick pans specify that their coatings are PFOA free. (If you’re confused by all the acronyms, you aren’t the only one.) But other types of PFAS are still used in these coatings, and their risks to humans aren’t clear. Teflon claims that any flakes of nonstick coating you might ingest are inert, but public studies backing up that claim are difficult to find. In the absence of relevant data, everyone seems to have a different take on nonstick pans. The FDA, for example, allows PFAS to be used in nonstick cookware, but the EPA says that exposure to them can lead to adverse health effects, and last year proposed labeling certain members of the group as “hazardous substances.” According to the CDC, the health effects of low exposure to these chemicals are “uncertain.” Food experts are similarly undecided on nonstick pans: A writer for the culinary site Serious Eats said he “wouldn’t assume they’re totally safe,” whereas a Wirecutter review said they “seem to be safe”—if used correctly. That’s about the firmest answer you’re going to get regarding the safety of nonstick cookware. “In no study has it been shown that people who use nonstick pans have higher levels” of PFAS, says Jane Hoppin, a North Carolina State University epidemiologist and a member of a National Academies of Sciences, Engineering, and Medicine committee to study PFAS. But she also told me that, with regard to the broader research on PFAS-related health risks, “I haven’t seen anybody say it’s safe to use.” Certainly, more research could be done on PFAS, given the lack of relevant studies. There is no research, for example, showing that people who use nonstick pans are more likely to get sick. The one study on exposure from nonstick pans mentioned in the report that Hoppin and others published last year found inconclusive results after measuring gaseous PFAS released from heated nonstick pans, though the researchers tested only a few pans. Another study in which scientists used nonstick pans to cook beef and pork—and an assortment of more glamorous meats including chicken nuggets—and then measured the PFAS levels likewise failed to reach a conclusion, because too few meat samples were used. More scientists could probably be convinced to pursue rigorous research in this field if PFAS exposure came only from nonstick pans. Investigating the risks would be tough, perhaps impossible: Designing a rigorous study to test the risks of PFAS exposure would likely involve forcing unwitting test subjects to breathe in PFAS fumes or eat from flaking pans. But given that we are exposed to PFAS in so many other ways—drinking water being chief among them—what would be the point? “They’re in dental floss, and they’re in your Gore-Tex jacket, and they’re in your shoes,” Hoppin said. “The relative contribution of any one of those things is minor.” As long as PFAS keep proliferating in the environment, we might never fully know exactly what nonstick pans are doing to us. The best we can do for now is decide what level of risk we’re willing to accept in exchange for a slippery pan, based on the information available. And that information is frustratingly vague: Most nonstick products come with a disclosure of the types of PFAS they contain and the types they do not. Sometimes they also include instructions to avoid high heat, especially above 500 degrees Fahrenheit. Hoppin recommends throwing nonstick pans away once they start flaking; in general, it seems worth it to use the pans only when essential. There is likewise a dearth of guidance on breathing in the fumes from an overheated pan, though breathing in PFAS fumes in industrial settings has been known to cause flulike symptoms. If you’re concerned, Hoppin said, you could use any of the growing number of nonstick alternatives, including ceramic and carbon-steel cookware. (Her preference is well-seasoned cast iron.) Still, perhaps it’s time to accept that exposure to PFAS is inevitable, much like exposure to microplastics and other carcinogens. At this point, so many harmful substances are all around us that there doesn’t seem to be any point in trying to limit them in individual products, though such efforts are underway for raincoats and period underwear. “What we really need to do is remove these chemicals from production,” Hoppin said. The hope is that doing so would broadly reduce our exposure to PFAS, and there’s evidence that it would work: After PFOS was phased out in the early 2000s, its levels in human blood declined significantly. But until PFAS are more tightly regulated, we’ll continue our endless slide through nonstick limbo, with our grasp of the cookware’s safety remaining slippery at best. I’ve tried to cut down on my nonstick-pan use for sheer peace of mind. Many professional chefs reject nonstick pans as unnecessary if you know the proper technique; French chefs, after all, were flipping omelets long before the first Teflon pan was invented--by a French engineer—in 1954. Fancying myself a purist, I recently attempted to cook an omelet using All-Clad stainless steel, following a set of demanding instructions involving ungodly amounts of butter and a moderate amount of heat. Unlike my resolve to avoid nonstick pans, the eggs stuck. from https://ift.tt/u4MQ5Dd Check out http://natthash.tumblr.com A few weeks ago, a three-inch square of plastic and metal began, slowly and steadily, to upend my life. The culprit was my new portable carbon-dioxide monitor, a device that had been sitting in my Amazon cart for months. I’d first eyed the product around the height of the coronavirus pandemic, figuring it could help me identify unventilated public spaces where exhaled breath was left to linger and the risk for virus transmission was high. But I didn’t shell out the $250 until January 2023, when a different set of worries, over the health risks of gas stoves and indoor air pollution, reached a boiling point. It was as good a time as any to get savvy to the air in my home. I knew from the get-go that the small, stuffy apartment in which I work remotely was bound to be an air-quality disaster. But with the help of my shiny Aranet4, the brand most indoor-air experts seem to swear by, I was sure to fix the place up. When carbon-dioxide levels increased, I’d crack a window; when I cooked on my gas stove, I’d run the range fan. What could be easier? It would basically be like living outside, with better Wi-Fi. This year, spring cleaning would be a literal breeze! The illusion was shattered minutes after I popped the batteries into my new device. At baseline, the levels in my apartment were already dancing around 1,200 parts per million (ppm)—a concentration that, as the device’s user manual informed me, was cutting my brain’s cognitive function by 15 percent. Aghast, I flung open a window, letting in a blast of frigid New England air. Two hours later, as I shivered in my 48-degree-Fahrenheit apartment in a coat, ski pants, and wool socks, typing numbly on my icy keyboard, the Aranet still hadn’t budged below 1,000 ppm, a common safety threshold for many experts. By the evening, I’d given up on trying to hypothermia my way to clean air. But as I tried to sleep in the suffocating trap of noxious gas that I had once called my home, next to the reeking sack of respiring flesh I had once called my spouse, the Aranet let loose an ominous beep: The ppm had climbed back up, this time to above 1,400. My cognitive capacity was now down 50 percent, per the user manual, on account of self-poisoning with stagnant air. By the next morning, I was in despair. This was not the reality I had imagined when I decided to invite the Aranet4 into my home. I had envisioned the device and myself as a team with a shared goal: clean, clean air for all! But it was becoming clear that I didn’t have the power to make the device happy. And that was making me miserable. CO2 monitors are not designed to dictate behavior; the information they dole out is not a perfect read on air quality, indoors or out. And although carbon dioxide can pose some health risks at high levels, it’s just one of many pollutants in the air, and by no means the worst. Others, such as nitrogen oxide, carbon monoxide, and ozone, can cause more direct harm. Some CO2-tracking devices, including the Aranet4, don’t account for particulate matter—which means that they can’t tell when air’s been cleaned up by, say, a HEPA filter. “It gives you an indicator; it’s not the whole story,” says Linsey Marr, an environmental engineer at Virginia Tech. Still, because CO2 builds up alongside other pollutants, the levels are “a pretty good proxy for how fresh or stale your air is,” and how badly it needs to be turned over, says Paula Olsiewski, a biochemist and an indoor-air-quality expert at the Johns Hopkins Center for Health Security. The Aranet4 isn’t as accurate as, say, the $20,000 research-grade carbon-dioxide sensor in Marr’s lab, but it can get surprisingly close. When Jose-Luis Jimenez, an atmospheric chemist at the University of Colorado at Boulder, first picked one up three years ago, he was shocked that it could hold its own against the machines he used professionally. And in his personal life, “it allows you to find the terrible places and avoid them,” he told me, or to mask up when you can’t. That rule of thumb starts to break down, though, when the terrible place turns out to be your home—or, at the very least, mine. To be fair, my apartment’s air quality has a lot working against it: two humans and two cats, all of us with an annoying penchant for breathing, crammed into 1,000 square feet; a gas stove with no outside-venting hood; a kitchen window that opens directly above a parking lot. Even so, I was flabbergasted by just how difficult it was to bring down the CO2 levels around me. Over several weeks, the best indoor reading I sustained, after keeping my window open for six hours, abstaining from cooking, and running my range fan nonstop, was in the 800s. I wondered, briefly, if my neighborhood just had terrible outdoor air quality—or if my device was broken. Within minutes of my bringing the meter outside, however, it displayed a chill 480. [Read: The plan to stop every respiratory virus at once] The meter’s cruel readings began to haunt me. Each upward tick raised my anxiety; I started to dread what I’d learn each morning when I woke up. After watching the Aranet4 flash figures in the high 2,000s when I briefly ignited my gas stove, I miserably deleted 10 wok-stir-fry recipes I’d bookmarked the month before. At least once, I told my husband to cool it with the whole “needing oxygen” thing, lest I upgrade to a more climate-friendly Plant Spouse. (I’m pretty sure I was joking, but I lacked the cognitive capacity to tell.) In more lucid moments, I understood the deeper meaning of the monitor: It was a symbol of my helplessness. I’d known I couldn’t personally clean the air at my favorite restaurant, or the post office, or my local Trader Joe’s. Now I realized that the issues in my home weren’t much more fixable. The device offered evidence of a problem, but not the means to solve it. Upon hearing my predicament, Sally Ng, an aerosol chemist at Georgia Tech, suggested that I share my concerns with building management. Marr recommended constructing a Corsi-Rosenthal box, a DIY contraption made up of a fan lashed to filters, to suck the schmutz out of my crummy air. But they and other experts acknowledged that the most sustainable, efficient solutions to my carbon conundrum were mostly out of reach. If you don’t own your home, or have the means to outfit it with more air-quality-friendly appliances, you can only do so much. “And I mean, yeah, that is a problem,” said Jimenez, who’s currently renovating his home to include a new energy-efficient ventilation device, a make-up-air system, and multiple heat pumps. Many Americans face much greater challenges than mine. I am not among the millions living in a city with dangerous levels of particulate matter in the air, spewed out by industrial plants, gas-powered vehicles, and wildfires, for whom an open window could risk additional peril; I don’t have to be in a crowded office or a school with poor ventilation. Since the first year of the pandemic—and even before—experts have been calling for policy changes and infrastructural overhauls that would slash indoor air pollution for large sectors of the population at once. But as concern over COVID has faded, “people have moved on,” Marr told me. Individuals are left on their own in the largely futile fight against stale air. [Read: Put your face in airplane mode] Though a CO2 monitor won’t score anyone victories on its own, it can still be informative: “It’s nice to have an objective measure, because all of this is stuff you can’t really see with the naked eye,” says Abraar Karan, an infectious-disease physician at Stanford, who’s planning to use the Aranet4 in an upcoming study on viral transmission. But he told me that he doesn’t let himself get too worked up over the readings from his monitor at home. Even Olsiewski puts hers away when she’s cooking on the gas range in her Manhattan apartment. She already knows that the levels will spike; she already knows what she needs to do to mitigate the harms. “I use the tools I have and don’t make myself crazy,” she told me. (Admittedly, she has a lot of tools, especially in her second home in Texas—among them, an induction stove and an HVAC with ultra-high-quality filters and a continuously running fan. When we spoke on the phone, her Aranet4 read 570 ppm; mine, 1,200.) I’m now aiming for my own middle ground. Earlier this week, I dreamed of trying and failing to open a stuck window, and woke up in a cold sweat. I spent that day working with my (real-life) kitchen window cracked, but I shut it when the apartment got too chilly. More important, I placed my Aranet4 in a drawer, and didn’t pull it out again until nightfall. When my spouse came home, he marveled that our apartment, once again, felt warm. from https://ift.tt/IL8vpqO Check out http://natthash.tumblr.com |
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