With the pinch of a needle, cosmetic dermatologists such as Michele Green can make forehead wrinkles disappear and deep-furrowed crow’s-feet puff back out like yeasted dough. Botox is totally magic, a little unsettling, and very in demand: Green’s New York City practice has been swamped as Americans seek to give themselves a “post-pandemic” glow-up. But these days, many of her patients aren’t after eternal youth and sex appeal. When Green reviews her schedule for the week each Monday morning, she told me, “I’m just like, Oh my god.” At least a quarter of her Botox appointments are for people with a different motive entirely: They can’t stop clenching their jaw and grinding their teeth. Across the country, patients dealing with the meddlesome condition are now turning to Botox—yes, Botox. “It’s a very popular treatment” for people who grind and clench their teeth, Lauren Goodman, a L.A.-based cosmetic nurse, told me. Bruxism, the official term encompassing both behaviors, is an involuntary action that tends to happen when people are sleeping at night, for reasons including alcohol and tobacco use, sleep apnea, and stress—perhaps why the condition has soared in the United States during the pandemic. The condition is a tolerable nuisance for many people, but the symptoms can get very real: With bruxism on the rise, dentists are reporting more chipped and cracked teeth in patients, along with jaw pain and facial soreness. In the most severe cases, patients can suffer debilitating headaches and jaw dislocation. The most common treatments, such as mouth guards and lifestyle changes, only sometimes help get rid of symptoms. That’s what makes Botox so appealing for the recent flood of teeth grinders. Jaw injections relax the chewing muscles that clench and grind with up to 250 pounds of force—potentially relieving pain and preventing dental issues in the process. It’s not as though every teeth grinder in America is hotfooting it to their nearest Botox clinic, but the procedure seems to have blown up since the start of the pandemic. Five dentists and cosmetic experts told me they’d noticed an increase in teeth grinders and clenchers getting Botox. People who have exhausted more traditional routes are “really just committed to alleviating their pain,” said Samantha Rawdin, a prosthodontist in New York City. “If that means getting a needle to the face, so be it.” But even if Botox has some upsides, it’s hardly the permanent, sure-thing solution that dentists and patients have long searched for. That’s been the narrative all along with bruxism: Because there are so many possible causes, treatments are an educated dice roll—and none of them is universally effective. “I don’t tell my patients I can treat them,” Gilles Lavigne, a dentistry professor at the University of Montreal, told me. “I tell them I can help them manage their condition.” So, how do we still not always know how to handle this incredibly common ailment? Botox has been creeping onto the teeth-grinding stage since long before the pandemic. Although it has gained noticeable traction over the past few years, research on the efficacy of Botox stretches back to the late 1990s. In the years since, researchers have also discovered that the injections, which temporarily paralyze the masseter muscles responsible for grinding and clenching, can reduce the frequency and intensity of bruxism. It’s one of a slew of non-cosmetic Botox uses that have been identified since the drug hit the market in 1989: Injections also treat issues such as excessive underarm sweating, acne, and migraines. Botox for bruxism hasn’t been FDA approved, so it’s still considered off-label—but anyone with a Botox license can legally inject a willing teeth grinder. And at least in theory, Botox has some advantages over other bruxism treatments. Night guards might prevent you from gnashing your teeth into smithereens while you sleep, but they can be ineffective at stopping the behavior and can even make it worse—especially if you have sleep apnea, Jamison Spencer, a dentist and sleep-apnea expert based in Boise, Idaho, told me. Minimally invasive regimes such as yoga, meditation, cognitive behavioral therapy, and physical therapy are hit or miss. Muscle relaxers can be helpful for some patients, but those aren’t universally popular among the dentists I spoke with, some of whom cited America’s opioid crisis as a concern. When less invasive treatments don’t work, Botox might be “the next frontier,” Leena Palomo, a professor at New York University’s College of Dentistry, told me. Grinders and clenchers seem to be learning about the injections from a variety of sources. Rita Mizrahi, an oral surgeon in New York who offers Botox for bruxism, told me that her patients are typically referred by their regular dentists. Others discover jaw Botox in online forums such as Reddit and the beauty network RealSelf, where often anonymous discussions of the procedure abound. And some are reading mainstream-media testimonials or hearing about it from friends or family—particularly as more and more Americans embrace Botox for cosmetic purposes. At its best, the procedure can really help certain teeth grinders: Studies have indicated that Botox can decrease pain levels. One RealSelf reviewer described trying night guards, stress relief, and cutting out caffeine before getting jaw injections. “Thank goodness for something like Botox to come along in this day and age,” they wrote four months after getting the procedure. The procedure comes with some cosmetic changes too: Grinding and clenching all night can be a workout, which might lead to enlarged chewing muscles and a square, boxy face. The injections slim the jawline for many patients, giving it “more of a V-shape,” Green said. But Botox has some real downsides—and plenty of dentists are still hesitant to recommend it. For starters, it’s expensive and impermanent. The procedure typically costs at least $1,000; is not covered by medical or dental insurance; and usually won’t last for more than four months. “This isn’t a onetime thing and you’re good,” Mizrahi said. And like most of the other treatments available, jaw Botox attacks teeth-grinding and clenching symptoms, but not the cause. Because people still need to chew, the masseter muscle isn’t totally immobilized—meaning that patients “will just grind with less power,” Lavigne said. And all of the risks associated with the cosmetic use of Botox apply here too, such as bruising at the injection site, headaches, allergic reactions, and less desirable changes in facial expressions due to misplaced Botox. One RealSelf reviewer experienced no improvement in jaw pain but the unfortunate onset of a creepy grin that resembled a “chucky doll smile.” Another said that their headaches disappeared after the procedure, but so did their cheeks: “I couldn’t recognize myself in the mirror and looked like I had aged 10 years within a couple of months.” That grinders and clenchers are more frequently turning to Botox is hardly a pure success story. Early mentions of teeth gnashing exist in the Bible, yet we still don’t really understand how to make it stop. I know firsthand how frustrating that feels. In January, after trying (and failing) to open wide enough for a crispy chicken tender, I was finally motivated to see a dentist—who gave me a night guard so I’d quit slamming my teeth together. I meditate like it’s my job, I don’t have sleep apnea or take medications of any sort, and yet I still gnaw on that hunk of plastic like it’s gristle. My jaw doesn’t lock anymore but it’s still tense most mornings. I’m priced out of getting Botox—so, like many teeth grinders, I’m stuck in medical purgatory. Teeth grinding isn’t like a broken arm, where cause and effect are obvious and fixable. “Because the origin of [jaw] pain is not singular, you have to attack it from various modalities,” Mizrahi told me: “All the things that potentially contribute to the pain have to be addressed,” and that can involve fields far outside dentistry. Even dentists themselves aren’t always equipped with all the information: “We get virtually no bruxism education” in dental school, Spencer, the sleep-apnea researcher from Idaho, said. With all these roadblocks, many patients never find out why they’re clenching or grinding, says Alan Glaros, an emeritus professor of dentistry at the University of Missouri at Kansas City, who’s been researching the issue for more than 40 years. That’s partially because it’s a difficult problem to not only treat, but also study. Bruxism’s many causes intersect “a lot of disciplines,” such as dentistry, sleep health, and psychology, which muddies the research process. Each field is studying the behavior, but the results will only ever tell part of the story. “People act as if this is all solved, but it’s not,” Glaros told me. So for now, mouth guards, meditation, and Botox are what we have. The treatment, in all likelihood, isn’t going anywhere. “As people get to know others who have responded well, I predict that we’re going to see an uptick,” Palomo said. Grinders and clenchers will keep chomping on their plastic night guards or forking up thousands of dollars a year for temporary injections, all in a maybe-successful attempt to quell their pain. If only Botox could banish bruxism like it does stubborn wrinkles. from https://ift.tt/K2fxayE Check out http://natthash.tumblr.com
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It is a truth universally acknowledged among health experts that official COVID-19 data are a mess right now. Since the Omicron surge last winter, case counts from public-health agencies have become less reliable. PCR tests have become harder to access and at-home tests are typically not counted. Official case numbers now represent “the tip of the iceberg” of actual infections, Denis Nash, an epidemiologist at the City University of New York, told me. Although case rates may seem low now, true infections may be up to 20 times higher. And even those case numbers are no longer available on a daily basis in many places, as the CDC and most state agencies have switched to updating their data once a week instead of every day. How, then, is anyone supposed to actually keep track of the COVID-19 risk in their area—especially when cases are expected to increase this fall and winter? Using newer data sources, such as wastewater surveillance and population surveys, experts have already noticed potential signals of a fall surge: Official case counts are trending down across the U.S., but Northeast cities such as Boston are seeing more coronavirus in their wastewater, and the CDC reports that this region is a hot spot for further-mutated versions of the Omicron variant. Even if you’re not an expert, you can still get a clearer picture of how COVID-19 is hitting your community in the weeks ahead. You’ll simply need to understand how to interpret these alternate data sources. The problem with case data goes right to the source. Investment in COVID-19 tracking at the state and local levels has been in free fall, says Sam Scarpino, a surveillance expert at the Rockefeller Foundation’s Pandemic Prevention Initiative. “More recently, we’ve started to see lots of states sunsetting their reporting,” Scarpino told me. Since the Pandemic Prevention Initiative and the Pandemic Tracking Collective started publishing a state-by-state scorecard of breakthrough-case reporting in December 2021, the number of states with a failing grade has doubled. Scarpino considers this trend a “harbinger of what’s coming” as departments continue to shift resources away from COVID-19 reporting. [Read: Warning signs about the first post-pandemic winter] Hospitalization data don’t suffer from the same reporting problems, because the federal government collects information directly from thousands of facilities across the country. But “hospitalizations often lag behind cases by a matter of weeks,” says Caroline Hugh, an epidemiologist and volunteer with the People’s CDC, an organization providing COVID-19 data and guidance while advocating for improved safety measures. Hospitalizations also don’t necessarily reflect transmission rates, which still matter if you want to stay safe. Some studies suggest, for example, that long COVID might now be more likely than hospitalization after an infection. For a better sense of how much the coronavirus is circulating, many experts are turning to wastewater surveillance. Samples from our sewage can provide an advanced warning of increased COVID-19 spread because everyone in a public-sewer system contributes data; the biases that hinder PCR test results don’t apply. As a result, Hugh and her colleagues at the People’s CDC consider wastewater trends to be more “consistent” than constantly fluctuating case numbers. When Omicron first began to wreak havoc in December 2021, “the wastewater data started to rise very steeply, almost two weeks before we saw the same rise” in case counts, Newsha Ghaeli, the president and a co-founder of the wastewater-surveillance company Biobot Analytics, told me. Biobot is now working with hundreds of sewage-sampling sites in all 50 states, Ghaeli said. The company’s national and regional dashboard incorporates data from every location in its network, but for more local data, you might need to go to a separate dashboard run by the CDC or by your state health department. Some states have wastewater surveillance in every county, while others have just a handful of sites. If your location is not represented, Ghaeli said, “the wastewater data from communities nearby is still very applicable.” And even if your county does have tracking, checking up on neighboring communities might be good practice. “A surge in a state next door … could very quickly turn into a surge locally,” Ghaeli explained. [Read: The BA.5 wave is what COVID normal looks like] Ghaeli recommends watching how coronavirus levels in wastewater shift over time, rather than homing in on individual data points. Look at both “directionality” and “magnitude”: Are viral levels increasing or decreasing, and how do these levels compare with earlier points in the pandemic? A 10 percent uptick when levels are low is less concerning than a 10 percent uptick when the virus is already spreading widely. Researchers are still working to understand how wastewater data correlate with actual infections, because every community has unique waste patterns. For example, big cities differ from rural areas, and in some places, environmental factors such as rainfall or nearby agriculture may interfere with coronavirus tracking. Still, long-term-trend data are generally thought to be a good tool that can help sound the alarm on new surges. Wastewater data can help you figure out how much COVID-19 is spreading in a community and can even track all the variants circulating locally, but they can’t tell you who’s getting sick. To answer the latter question, epidemiologists turn to what Nash calls “active surveillance”: Rather than relying on the COVID-19 test results that happen to get reported to a public-health agency, actively seek out and ask people whether they recently got sick or tested positive. Nash and his team at CUNY have conducted population surveys in New York City and at the national level. The team’s most recent survey (which hasn’t yet been peer-reviewed), conducted from late June to early July, included questions about at-home test results and COVID-like symptoms. From a nationally representative survey of about 3,000 people, Nash and his team found that more than 17 percent of U.S. adults had COVID-19 during the two-week period—about 24 times higher than the CDC’s case counts at that time. Studies like these “capture people who might not be counted by the health system,” Nash told me. His team found that Black and Hispanic Americans and those with low incomes were more likely to get sick during the survey period, compared with the national estimate. The CDC and Census Bureau take a similar approach through the ongoing Household Pulse Survey. [Kyle Harper: Not everyone can afford to “learn to live with” COVID-19] These surveys are “a goldmine of data,” though they need to be “carefully designed,” Maria Pyra, an epidemiologist and volunteer with the People’s CDC, told me. By showing the gap between true infections and officially reported cases, surveys like Nash’s can allow researchers to approximate how much COVID-19 is really spreading. Survey results may be delayed by weeks or months, however, and are typically published in preprints or news reports rather than on a health agency’s dashboard. They might also be biased by who chooses to respond or how questions are worded. Scarpino suggested a more timely option: data collected from cellphone locations or social media. The Delphi Group at Carnegie Mellon University, for example, provides data on how many people are Googling coldlike symptoms or seeking COVID-related doctor visits. While such trends aren’t a perfect proxy for case rates, they can be a helpful warning that transmission patterns are changing. Readers seeking to monitor COVID-19 this fall should “look as local as you can,” Scarpino recommended. That means examining county- or zip-code-level data, depending on what’s available for you. Nash suggested checking multiple data sources and attempting to “triangulate” between them. For example, if case data suggest that transmission is down, do wastewater data say the same thing? And how do the data match with local behavior? If a popular community event or holiday happened recently, low case numbers might need to be taken with a grain of salt. “We’re heading into a period where it’s going to be increasingly harder to know what’s going on with the virus,” Nash told me. Case numbers will continue to be undercounted, and dashboards may be updated less frequently. Pundits on Twitter are turning to Yankee Candle reviews for signs of surges. Helpful sources still exist, but piecing together the disparate data can be exhausting—after all, data reporting and interpretation should be a job for our public-health agencies, not for concerned individuals. [Read: The plan to stop every respiratory virus at once] Rather than accept this fragmented data status quo, experts would like to see improved public-health systems for COVID-19 and other diseases, such as monkeypox and polio. “If we get better at collecting and making available local, relevant infectious-disease data for decision making, we’re going to lead healthier, happier lives,” Scarpino said. from https://ift.tt/yf0TL1I Check out http://natthash.tumblr.com In the fall of 1988, Matthew Farrow, a 5-year-old boy with a rare blood disorder, received the world’s first transplant of umbilical-cord blood from a newborn sibling. It worked: Farrow was cured. This miraculous outcome broke open a whole new field in medicine—and, not long after, a whole new industry aimed at getting expecting parents to bank their baby’s umbilical-cord blood, just in case. These days, in fact, being pregnant means being bombarded at the doctor’s office and on Instagram with ads touting cord blood as too precious to waste. For several hundred dollars upfront, plus a storage fee of $100 to $200 every year, the banks’ ads proclaim, you could save your child’s life. Cord-blood banking has been likened to a “biological insurance policy.” In the U.S., the two biggest private cord blood banks are Cord Blood Registry and ViaCord. Together, they have collected more than 1 million units. But only a few hundred units of this privately banked cord blood have ever been used in transplant, the great majority by families who chose to bank because they already had a child with a specific and rare disorder treatable with transplant. For everyone else, the odds of using privately banked cord blood are minuscule—so minuscule that the American Academy of Pediatrics (AAP) recommends against private banking. It does make an exception for families with that disease history. “But that’s a rare circumstance,” says Steve Joffe, a pediatric oncologist and ethicist at the University of Pennsylvania, “and not one that anybody is going to build a successful business model around.” ViaCord and Cord Blood Registry do offer free services for families in which someone has already been diagnosed with a condition treatable with cord blood. In general, the companies reiterated to me, cord blood does save lives and they are simply providing an option for families who want it. But the marketing also gives the impression of much more expansive uses for cord blood. The private banks’ websites list nearly 80 diseases treatable with transplant—an impressive number, though many are extremely uncommon or closely related to one another. (For example: refractory anemia, refractory anemia with ringed sideroblasts, refractory anemia with excess blasts, refractory anemia with excess blasts in transformation.) They have also recently taken to highlighting the promise of still-unproven treatments: Temporary infusions of cord blood, they say, could eventually treat more common conditions such as cerebral palsy and autism. Video testimonials feature parents talking excitedly about the potential of cord blood for their children. But the evidence isn’t there yet—and may never appear. Nonetheless, says Paul Knoepfler, a stem-cell scientist at UC Davis, “the cord-blood companies seem to be trying to expand their base of potential customers.” The initial exuberance around cord blood came from a real place. The blood left over in umbilical cords is replete with cells that have the special ability to turn into any kind of blood, including red blood cells, which carry oxygen, and white blood cells, which make up the immune system. Adults have stem cells in their bone marrow and blood—which can also be used for transplant—but those in a baby’s umbilical cord are more immunologically naive. That means they are less likely to go awry and attack a recipient’s body. “They don’t cause as much havoc,” says Karen Ballen, an oncologist at the University of Virginia. This allows doctors to use cord blood that matches only four out of six immunological markers. Because cord blood is so valuable, publicly run banks have been collecting donations since the 1990s. Despite amassing fewer units overall, public banks worldwide have provided 30 times as many units of blood for treatment—and saved more lives—than private ones, because they are accessible by any patient in need. Although the AAP recommends against private banking, it does recommend donating to public banks. One appeal of private banking, though, as the companies highlight, is that the cells in a baby’s umbilical cord are a perfect match for them in later childhood or adulthood. But this is usually irrelevant: In most of the diseases that can be cured by a cord-blood transplant, doctors would, for medical reasons, not use the patient’s own cells. In cases of inherited disorders such as sickle cell anemia, for example, a child’s own cord-blood stems have the same problematic mutation. For children with one of many types of leukemia, the concern is that cord blood could contain leukemia-precursor cells that cause the cancer to reappear; in addition, donor blood-stem cells are better because they can mop up remaining leukemia cells. Doctors would “never” use banked cord blood from a child with these types of leukemia, says Joanne Kurtzberg, a pediatrician and cord-blood pioneer at Duke University, who helped treat Farrow when he was a young boy. When privately banked cord blood is used in transplants, it is more likely to go to a sibling. Genetically, siblings have about a 25 percent chance of being perfect matches for each other. The chances of finding a suitable match among unrelated bone-marrow or cord-blood donors from a public bank, on the other hand, range from 29 to 79 percent, depending on one’s ethnic background. (The majority of donors are white, so it’s highest for white patients.) In any case, not banking a matched sibling’s cord blood doesn’t foreclose the possibility of a transplant, because that sibling can still donate bone marrow. “I often encounter families who have some guilt around not storing the cord blood, and I will point out, ‘Well, your donor child that matches our patient is still here,’” says Ann Haight, a pediatric hematologist and oncologist at Emory University. Even if a baby’s cord blood is banked, there’s no guarantee that it will contain enough cells for transplant. In fact, most may not: Public banks only keep 5 to 40 percent of their donations, as the rest don’t meet their standards. Private banks will save much smaller samples, which they argue serve a different purpose. Whereas public banks are looking for large samples that are mostly likely to be used for transplant, says Kate Giradi, the director of medical and scientific affairs at ViaCord, “when families are banking with us, this is that child’s only cord, so our threshold is way lower.” Another reason to bank these smaller samples, a spokesperson for Cord Blood Registry pointed out, is that they can still be used for experimental infusions treating conditions such as cerebral palsy and autism. (About 80 percent of units released by CBR have been used this way, as have about half from ViaCord.) The private banks partner with researchers, such as Kurtzberg at Duke, who are running clinical trials to test these treatments. The theory goes that cells from cord blood can make it to the brain, where they might have some neuroprotective role—but the mechanism remains unknown, and the effects are not entirely clear. As Kurtzberg told me, “The therapy is not proven.” The current state of cord-blood science might be summed up thus: Proven uses are very uncommon, and unproven uses are, well, unproven. Of course, a future discovery could lead to a real breakthrough in the use of stem cells from cord blood—an idea private banks trade on. Who knows what might be in store for cord blood later, when your baby is 30, 50, 70 years old? In a recent Cord Blood Registry survey of new parents, a spokesperson told me by email, 45 percent named “belief in future treatments” as the primary reason for banking their child’s cord blood and tissue. Knoepfler, the stem-cell scientist, notes that scientists have been excited for decades about the promise of stem cells. But translating interesting results in the lab to a doctor’s office, he says, “is really much harder than many of us realized. I include myself in that.” Medical discoveries have actually changed the ways cord blood is used over years, but they have so far resulted in less use of cord blood. In the past several years, doctors have refined a protocol to use half-matched donors in transplants. Doctors generally get more cells from these donors than from an infant’s banked cord blood, which means the transplants “take” more quickly and the patient spends less time in the hospital. For this reason, cord blood has been falling out of favor. Public banks have started scaling down their collections; the New York Blood Center, which had launched the world’s first public bank, recently stopped collecting new donations. How cord blood gets used in the future is still unknown. More than 30 years ago after Kurtzberg first treated Farrow, she is still in touch with him. He’s 39 now, and doing well. Having watched cord banking grow and evolve over the years, she remains a proponent of public banking and the possibilities ahead. When it comes to private banks, however, she says, “I don’t think it's a necessity. I think it’s nice to have if you can do it.” There isn’t much harm in private banking, after all, as long as parents can afford the several thousand dollars over their child’s lifetime. Afford might be the key word here. The ads for cord-blood banking feel a lot like those for any number of “nice to have” baby products aimed at anxious parents, be they organic diapers or BPA-free wooden toys tailored to your child’s age and cognitive development. If anything, the stakes of cord-blood banking are higher than anything else you might choose to buy. The opportunity only comes around “once in a lifetime,” and it could literally save your child’s life—even if the chances of that are very, very small. “It’s playing to parental guilt and the desire for parents to have healthy children and do whatever they can for their kids,” says Timothy Caulfield, a health-law professor at the University of Alberta who has studied cord-blood banks. “There’s a huge market based on exactly that.” It’s telling, perhaps, that Cord Blood Registry ran a giveaway of $20,000 worth of baby products this summer. The curated package of luxury “baby essentials” resembled the registry of parents who want the best for their kid, and can afford it. Included were a Snoo smart bassinet ($1,695), an Uppababy stroller and car seat ($1,400), Coterie diapers ($100 for a month’s supply, guaranteed to be “free of fragrance, lotion, latex, rubber, dyes, alcohol, heavy metals, parabens, phthalates, chlorine bleaching, VOCs, and optical brighteners”), and, of course, a lifetime of cord-blood and tissue banking ($11,860). from https://ift.tt/2oBKHPX Check out http://natthash.tumblr.com This article was originally published in Undark Magazine. Ten years ago, 12-year-old Rory Staunton dove for a ball in gym class and scraped his arm. He woke up the next day with a 104-degree Fahrenheit fever, so his parents took him to the pediatrician and eventually the emergency room. It was just the stomach flu, they were told. Three days later, Rory died of sepsis after bacteria from the scrape infiltrated his blood and triggered organ failure. “How does that happen in a modern society?” his father, Ciaran Staunton, asked me. Each year in the United States, sepsis kills more than a quarter million people—more than stroke, diabetes, or lung cancer. One reason for all this carnage is that if sepsis is not detected in time, it’s essentially a death sentence. Consequently, much research has focused on catching sepsis early, but the condition’s complexity has plagued existing clinical support systems—electronic tools that use pop-up alerts to improve patient care—with low accuracy and high rates of false alarm. That may soon change. Back in July, Johns Hopkins researchers published a trio of studies in Nature Medicine and npj Digital Medicine showcasing an early-warning system that uses artificial intelligence. The system caught 82 percent of sepsis cases and significantly reduced mortality. While AI—in this case, machine learning—has long promised to improve health care, most studies demonstrating its benefits have been conducted using historical data sets. Sources told me that, to the best of their knowledge, when used on patients in real time, no AI algorithm has shown success at scale. Suchi Saria, the director of the Machine Learning and Healthcare Lab at Johns Hopkins University and the senior author of the studies, said in an interview that the novelty of this research is how “AI is implemented at the bedside, used by thousands of providers, and where we’re seeing lives saved.” The Targeted Real-Time Early Warning System scans through hospitals’ electronic health records—digital versions of patients’ medical histories—to identify clinical signs that predict sepsis, alert providers about at-risk patients, and facilitate early treatment. Leveraging vast amounts of data, TREWS provides real-time patient insights and a unique level of transparency in its reasoning, according to the Johns Hopkins internal-medicine physician Albert Wu, a co-author of the study. Wu says that this system also offers a glimpse into a new age of medical electronization. Since their introduction in the 1960s, electronic health records have reshaped how physicians document clinical information; nowadays, however, these systems primarily serve as “an electronic notepad,” he added. With a series of machine-learning projects on the horizon, both from Johns Hopkins and other groups, Saria says that using electronic records in new ways could transform health-care delivery, providing physicians with an extra set of eyes and ears—and helping them make better decisions. It’s an enticing vision, but one in which Saria, the CEO of the company developing TREWS, has a financial stake. This vision also discounts the difficulties of implementing any new medical technology: Providers might be reluctant to trust machine-learning tools, and these systems might not work as well outside controlled research settings. Electronic health records also come with many existing problems, from burying providers under administrative work to risking patient safety because of software glitches. Saria is nevertheless optimistic. “The technology exists; the data is there,” she says. “We really need high-quality care-augmentation tools that will allow providers to do more with less.” Currently, there’s no single test for sepsis, so health-care providers have to piece together their diagnoses by reviewing a patient’s medical history, conducting a physical exam, running tests, and relying on their own clinical impressions. Given such complexity, over the past decade, doctors have increasingly leaned on electronic health records to help diagnose sepsis, mostly by employing a rules-based criteria—if this, then that. One such example, known as the SIRS criteria, says a patient is at risk of sepsis if two of four clinical signs—body temperature, heart rate, breathing rate, white-blood-cell count—are abnormal. This broadness, although helpful for catching the various ways sepsis might present itself, triggers countless false positives. Take a patient with a broken arm: “A computerized system might say, ‘Hey, look, fast heart rate, breathing fast.’ It might throw an alert,” says Cyrus Shariat, an ICU physician at Washington Hospital in California. The patient almost certainly doesn’t have sepsis but would nonetheless trip the alarm. These alerts also appear on providers’ computer screens as a pop-up, which forces them to stop whatever they’re doing to respond. So, despite these rules-based systems occasionally reducing mortality, there’s a risk of alert fatigue, where health-care workers start ignoring the flood of irritating reminders. According to M. Michael Shabot, a surgeon and the former chief clinical officer of Memorial Hermann Health System, “It’s like a fire alarm going off all the time. You tend to be desensitized. You don’t pay attention to it.” [Read: The burnout crisis in American medicine] Already, electronic records aren’t particularly popular among doctors. In a 2018 survey, 71 percent of physicians said that the records greatly contribute to burnout, and 69 percent said that they take valuable time away from patients. Another 2016 study found that, for every hour spent on patient care, physicians have to devote two extra hours to electronic health records and desk work. James Adams, the chair of the Department of Emergency Medicine at Northwestern University, calls electronic health records a “congested morass of information.” But Adams also says that the health-care industry is at an inflection point to transform the files. An electronic record doesn’t have to simply involve a doctor or nurse putting data in, he says; instead, it “needs to transform to be a clinical-care-delivery tool.” With their universal deployment and real-time patient data, electronic records could warn providers about sepsis and various other conditions—but that will require more than a rules-based approach. What doctors need, according to Shabot, is an algorithm that can integrate various streams of clinical information to offer a clearer, more accurate picture when something’s wrong. Machine-learning algorithms work by looking for patterns in data to predict a particular outcome, like a patient’s risk of sepsis. Researchers train the algorithms on existing data sets, which helps the algorithms create a model for how that world works and then make predictions on new data sets. The algorithms can also actively adapt and improve over time, without the interference of humans. TREWS follows this general mold. The researchers first trained the algorithm on historical electronic-records data so that it could recognize early signs of sepsis. After this testing showed that TREWS could have identified patients with sepsis hours before they actually got treatment, the algorithm was deployed inside hospitals to influence patient care in real time. Saria and Wu published three studies on TREWS. The first tried to determine how accurate the system was, whether providers would actually use it, and if use led to earlier sepsis treatment. The second went a step further to see if using TREWS actually reduced patient mortality. And the third interviewed 20 providers who tested the tool on what they thought about machine learning, including what factors facilitate versus hinder trust. In these studies, TREWS monitored patients in the emergency department and inpatient wards, scanning through their data—vital signs, lab results, medications, clinical histories, and provider notes—for early signals of sepsis. (Providers could do this themselves, Saria says, but it might take them about 20 to 40 minutes.) If the system suspected organ dysfunction based on its analysis of millions of other data points, it flagged the patient and prompted providers to confirm sepsis, dismiss the alert, or temporarily pause the alert. “This is a colleague telling you, based upon data and having reviewed all this person’s chart, why they believe there’s reason for concern,” Saria says. “We very much want our frontline providers to disagree, because they have ultimately their eyes on the patient.” And TREWS continuously learns from these providers’ feedback. Such real-time improvements, as well as the diversity of data TREWS considers, are what distinguish it from other electronic-records tools for sepsis. In addition to these functional differences, TREWS doesn’t alert providers with incessant pop-up boxes. Instead, the system uses a more passive approach, with alerts arriving as icons on the patient list that providers can click on later. Initially, Saria was worried this might be too passive: “Providers aren’t going to listen. They’re not going to agree. You’re mostly going to get ignored.” However, clinicians responded to 89 percent of the system’s alerts. One physician interviewed for the third study described TREWS as less “irritating” than the previous rules-based system. Saria says that TREWS’s high adoption rate shows that providers will trust AI tools. But Fei Wang, an associate professor of health informatics at Weill Cornell Medicine, is more skeptical about how these findings will hold up if TREWS is deployed more broadly. Although he calls these studies first-of-a-kind and thinks their results are encouraging, he notes that providers can be conservative and resistant to change: “It’s just not easy to convince physicians to use another tool they are not familiar with,” Wang says. Any new system is a burden until proven otherwise. Trust takes time. TREWS is further limited because it only knows what’s been inputted into the electronic health record—the system is not actually at the patient’s bedside. As one emergency-department physician put it, in an interview for the third study, the system “can’t help you with what it can’t see.” And even what it can see is filled with missing, faulty, and out-of-date data, according to Wang. But Saria says that TREWS’s strengths and limitations complement those of health-care providers. Although the algorithm can analyze massive amounts of clinical data in real time, it will always be limited by the quality and comprehensiveness of the electronic health record. The goal, Saria adds, is not to replace physicians, but to partner with them and augment their capabilities. The most impressive aspect of TREWS, according to Zachary Lipton, an assistant professor of machine learning and operations research at Carnegie Mellon University, is not the model’s novelty, but the effort it must have taken to deploy it on 590,736 patients across five hospitals over the course of the study. “In this area, there is a tremendous amount of offline research,” Lipton says, but relatively few studies “actually make it to the level of being deployed widely in a major health system.” It’s so difficult to perform research like this “in the wild,” he adds, because it requires collaborations across various disciplines, from product designers to systems engineers to administrators. As such, by demonstrating how well the algorithm worked in a large clinical study, TREWS has joined an exclusive club. But this uniqueness may be fleeting. Duke University’s Sepsis Watch algorithm, for one, is currently being tested across three hospitals following a successful pilot phase, with more data forthcoming. In contrast with TREWS, Sepsis Watch uses a type of machine learning called deep learning. Although this can provide more powerful insights, how the deep-learning algorithm comes to its conclusions is unexplainable—a situation that computer scientists call the black-box problem. The inputs and outputs are visible, but the process in between is impenetrable. On the one hand, there’s the question of whether this is really a problem: Doctors don’t always know how drugs work, Adams says, “but at some point, we have to trust what the medicine is doing.” Lithium, for example, is a widely used, effective treatment for bipolar disorder, but nobody really understands exactly how it works. If an AI system is similarly useful, maybe interpretability doesn’t matter. Wang suggests that that’s a dangerous conclusion. “How can you confidently say your algorithm is accurate?” he asks. After all, it’s difficult to know anything for sure when a model’s mechanics are a black box. That’s why TREWS, a simpler algorithm that can explain itself, might be a more promising approach. “If you have this set of rules,” Wang says, “people can easily validate that everywhere.” Indeed, providers trusted TREWS largely because they could see descriptions of the system’s process. Of the clinicians interviewed, none fully understood machine learning, but that level of comprehension wasn’t necessary. In machine learning, although the specific algorithmic design is important, the results have to speak for themselves. By catching 82 percent of sepsis cases and reducing time to antibiotics by 1.85 hours, TREWS ultimately reduced patient deaths. “This tool is, No. 1, very good; No. 2, received well by clinicians; and No. 3, impacts mortality,” Adams says. “That combination makes it very special.” However, Shariat, the ICU physician at Washington Hospital in California, was more cautious about these findings. For one, these studies only compared patients with sepsis who had the TREWS alert confirmed within three hours to those who didn’t. “They’re just telling us that this alert system that we’re studying is more effective if someone responds to it,” Shariat says. A more robust approach would have been to conduct a randomized controlled trial—the gold standard of medical research—where half of patients got TREWS in their electronic record while the other half didn’t. Saria says that randomization would have been difficult to do given patient-safety concerns, and Shariat agrees. Even so, he says that the absence “makes the data less rigorous.” Shariat also worries that the sheer volume of alerts, with about two out of three being false positives, might contribute to alert fatigue—and potentially overtreatment with fluids and antibiotics, which can lead to serious medical complications such as pulmonary edema and antibiotic resistance. Saria acknowledges that TREWS’s false-positive rate, although lower than that of existing electronic-health-record systems, could certainly improve, but says it will always be crucial for clinicians to continue to use their own judgment. [Read: Will probiotics ever live up to the hype?] The studies also have a conflict of interest: Saria is entitled to revenue distribution from TREWS, as is Johns Hopkins. “If this goes prime time, and they sell it to every hospital, there’s so much money,” Shariat says. “It’s billions and billions of dollars.” Saria maintains that these studies went through rigorous internal and external review processes to manage conflicts of interest, and that the vast majority of study authors don’t have a financial stake in this research. Regardless, Shariat says it will be crucial to have independent validation to confirm these findings and ensure the system is truly generalizable. The Epic Sepsis Model, a widely used algorithm that scans through electronic records but doesn’t use machine learning, is a cautionary example here, according to David Bates, the chief of general internal medicine at Brigham and Women’s Hospital. He explains that the model was developed at a few health systems with promising results before being deployed at hundreds of others. The model then deteriorated, missing two-thirds of patients with sepsis and having a concerningly high false-positive rate. “You can’t really predict how much the performance is going to degrade,” Bates says, “without actually going and looking.” Despite the potential drawbacks, Orlaith Staunton, Rory’s mother, told me that TREWS could have saved her son’s life. “There was complete breakdown in my son’s situation,” she said; none of his clinicians considered sepsis until it was too late. An early-warning system that alerted them about the condition, she added, “would make the world of difference.” After Rory’s death, the Stauntons started the organization End Sepsis to ensure that no other family would have to go through their pain. In part because of their efforts, New York State mandated that hospitals develop sepsis protocols, and the CDC launched a sepsis-education campaign. But none of this will ever bring back Rory, Ciaran Staunton said: “We will never be happy again.” This research is personal for Saria as well. Almost a decade ago, her nephew died of sepsis. By the time it was discovered, there was nothing his doctors could do. “It all happened too quickly, and we lost him,” she says. That’s precisely why early detection is so important—life and death can be mere minutes away. “Last year, we flew helicopters on Mars,” Saria says, “but we’re still freaking killing patients every day.” from https://ift.tt/RSnmkXo Check out http://natthash.tumblr.com On one level, the world’s response to the coronavirus pandemic over the past two and half years was a major triumph for modern medicine. We developed COVID vaccines faster than we’d developed any vaccine in history, and began administering them just a year after the virus first infected humans. The vaccines turned out to work better than top public-health officials had dared hope. In tandem with antiviral treatments, they’ve drastically reduced the virus’s toll of severe illness and death, and helped hundreds of millions of Americans resume something approximating pre-pandemic life. And yet on another level, the pandemic has demonstrated the inadequacy of such pharmaceutical interventions. In the time it took vaccines to arrive, more than 300,000 people died of COVID-19 in America alone. Even since, waning immunity and the semi-regular emergence of new variants have made for an uneasy détente. Another 700,000 Americans have died over that period, vaccines and antivirals notwithstanding. For some pandemic-prevention experts, the takeaway here is that pharmaceutical interventions alone simply won’t cut it. Though shots and drugs may be essential to softening a virus’s blow once it arrives, they are by nature reactive rather than preventive. To guard against future pandemics, what we should focus on, some experts say, is attacking viruses where they’re most vulnerable, before pharmaceutical interventions are even necessary. Specifically, they argue, we should be focusing on the air we breathe. “We’ve dealt with a lot of variants, we’ve dealt with a lot of strains, we’ve dealt with other respiratory pathogens in the past,” Abraar Karan, an infectious-disease physician and global-health expert at Stanford, told me. “The one thing that’s stayed consistent is the route of transmission.” The most fearsome pandemics are airborne. [Read: The plan to stop every respiratory virus at once] Numerous overlapping efforts are under way to stave off future outbreaks by improving air quality. Many scientists have long advocated for overhauling the way we ventilate indoor spaces, which has the potential to transform our air in much the same way that the advent of sewer systems transformed our water. Some researchers are similarly enthusiastic about the promise of germicidal lighting. Retrofitting a nation’s worth of buildings with superior ventilation systems or germicidal lighting is likely a long-term mission, though, requiring large-scale institutional buy-in and probably a considerable amount of government funding. Meanwhile, a more niche subgroup has zeroed in on what is, at least in theory, a somewhat simpler undertaking: designing the perfect mask. Two and a half years into this pandemic, it’s hard to believe that the masks widely available to us today are pretty much the same masks that were available to us in January 2020. N95s, the gold standard as far as the average person is concerned, are quite good: They filter out at least 95 percent of .3-micron particles—hence N95—and are generally the masks of preference in hospitals. And yet, anyone who has worn one over the past two and a half years will know that, lucky as we are to have them, they are not the most comfortable. At a certain point, they start to hurt your ears or your nose or your whole face. When you finally unmask after a lengthy flight, you’re liable to look like a raccoon. Most existing N95s are not reusable, and although each individual mask is pretty cheap, the costs can add up over time. They impede communication, preventing people from seeing the wearer’s facial expressions or reading their lips. And because they require fit-testing, the efficacy for the average wearer probably falls well short of the advertised 95 percent. In 2009, the federal government published a report with 28 recommendations to improve masks for health-care workers. Few seem to have been taken. These shortcomings are part of what has made efforts to get people to wear masks an uphill battle. What’s more,Over the course of the pandemic, several new companies have submitted new mask designs to NIOSH, the federal agency tasked with certifying and regulating masks,. Few, if any, have so far been certified. The agency appears to be overworked and underfunded. In addition, Joe and Kim Rosenberg, who in the early stages of the pandemic launched a mask company that applied unsuccessfully for NIOSH approval, told me the certification process is somewhat circular: A successful application requires huge amounts of capital, which in turn require huge amounts of investment, but investors generally like to see data showing that the masks work as advertised in, say, a hospital, and masks cannot be tested in a hospital without prior NIOSH approval. (NIOSH did not respond to a request for comment.) New products aside, there do already exist masks that outperform standard N95s in one way or another. Elastomeric respirators are reusable masks that you outfit with replaceable filters. Depending on the filter you use, the mask can be as effective as an N95 or even more so. When equipped with HEPA-quality filters, elastomerics filter out 99.97 percent of particles. And they come in both half-facepiece versions (which cover the nose and mouth) and full-facepiece versions (which also cover the eyes). Another option are PAPRs, or powered air-purifying respirators—hooded, battery-powered masks that cover the wearer’s entire head and constantly blow HEPA-filtered air for the wearer to breathe. Given the challenges of persuading many Americans to wear even flimsy surgical masks during the past couple of years, though, the issues with these superior masks—the current models, at least—are probably disqualifying as far as widespread adoption would go in future outbreaks. Elastomerics generally are bulky, expensive, limit range of motion, obscure the mouth, and require fit testing to ensure efficacy. PAPRs have a transparent facepiece and in many cases don’t require fit testing, but they’re also bulky, currently cost more than $1,000 each, and, because they’re battery-powered, can be quite noisy. Neither, let me assure you, is the sort of thing you’d want to wear to the movie theater. [Read: Is it time to start masking again?] The people who seem most fixated on improving masks are a hodgepodge of biologists, biosecurity experts, and others whose chief concern is not another COVID-like pandemic but something even more terrifying: a deliberate act of bioterrorism. In the apocalyptic scenarios that most worry them—which, to be clear, are speculative—bioterrorists release at least one highly transmissible pathogen with a lethality in the range of, say, 40 to 70 percent. (COVID’s is about 1 percent.) Because this would be a novel virus, we wouldn’t yet have vaccines or antivirals. The only way to avoid complete societal collapse would be to supply essential workers with PPE that they can be confident will provide infallible protection against infection—so-called perfect PPE. In such a scenario, N95s would be insufficient, Kevin Esvelt, an evolutionary biologist at MIT, told me: “70-percent-lethality virus, 95 percent protection—wouldn’t exactly fill me with confidence.” Existing masks that use HEPA filters may well be sufficiently protective in this worst-case scenario, but not even that is a given, Esvelt told me. Vaishnav Sunil, who runs the PPE project at Esvelt’s lab, thinks that PAPRs show the most promise, because they do not require fit testing. At the moment, the MIT team is surveying existing products to determine how to proceed. Their goal, ultimately, is to ensure that the country can distribute completely protective masks to every essential worker, which is firstly a problem of design and secondly a problem of logistics. The mask Esvelt’s team is looking for might already be out there, just selling for too high a price, in which case they’ll concentrate on bringing that price down. Or they might need to design something from scratch, in which case, at least initially, their work will mainly consist of new research. More likely, Sunil told me, they’ll identify the best available product and make modest adjustments to improve comfort, breathability, useability, and efficacy. Esvelt’s team is far from the only group exploring masking’s future. Last year, the federal government began soliciting submissions for a mask-design competition intended to spur technological development. The results were nothing if not creative: Among the 10 winning prototypes selected in the competition’s first phase were a semi-transparent mask, an origami mask, and a mask for babies with a pacifier on the inside. In the end, the questions of how much we should invest in improving masks and how we should actually improve them boil down to a deeper question about which possible future pandemic concerns you most. If your answer is a bioengineered attack, then naturally you’ll commit significant resources to perfecting efficacy and improving masks more generally, given that, in such a pandemic, masks may well be the only thing that can save us. If your answer is SARS-CoV-3, then you might worry less about efficacy and spend proportionally more on vaccines and antivirals. This is not a cheery choice to make. But it is an important one as we inch our way out of our current pandemic and toward whatever waits for us down the road. [Read: The pandemic’s legacy is already clear] For the elderly and immunocompromised, super-effective masks could be useful even outside a worst-case scenario. But more traditional public-health experts, who don’t put as much stock in the possibility of a highly lethal, deliberate pandemic, are less concerned about perfecting efficacy for the general public. The greater gains, they say, will come not from marginally improving the efficacy of existing highly effective masks but from getting more people to wear highly effective masks in the first place. “It’s important to make masks easier for people to use, more comfortable and more effective,” Linsey Marr, an environmental engineer at Virginia Tech, told me. It wouldn’t hurt to make them a little more fashionable either, she said. Also important is reusability, Jassi Pannu, a fellow at the Johns Hopkins Center for Health Security, told me, because in a pandemic stockpiles of single-use products will almost always run out. Stanford’s Karan envisions a world in which everyone in the country has their own elastomeric respirator—not, in most cases, for everyday use, but available when necessary. Rather than constantly replenishing your stock of reusable masks, you would simply swap out the filters in your elastomeric (or perhaps it will be a PAPR) every so often. The mask would be transparent, so that a friend could see your smile, and relatively comfortable, so that you could wear it all day without it cutting into your nose or pulling on your ears. When you came home at night, you would spend a few minutes disinfecting it. Karan’s vision might be a distant one. America’s tensions over masking throughout the pandemic give little reason to hope for any unified or universal uptake in future catastrophes. And even if that happened, everyone I spoke with agrees that masks alone are not a solution. They’re almost certainly the smallest part of the effort to ensure that the air we breathe is clean, to change the physical world to stop viral transmission before it happens. Even so, making and distributing millions of masks is almost certainly easier than installing superior ventilation systems or germicidal lighting in buildings across the country. Masks, if nothing else, are the low-hanging fruit. “We can deal with dirty water, and we can deal with cleaning surfaces,” Karan told me. “But when it comes to cleaning the air, we’re very, very far behind.” from https://ift.tt/wikG92F Check out http://natthash.tumblr.com I am still afraid of catching COVID. As a young, healthy, bivalently boosted physician, I no longer worry that I’ll end up strapped to a ventilator, but it does seem plausible that even a mild case of the disease could shorten my life, or leave me with chronic fatigue, breathing trouble, and brain fog. Roughly one in 10 Americans appears to share my concern, including plenty of doctors. “We know many devastating symptoms can persist for months,” the physician Ezekiel Emanuel wrote this past May in The Washington Post. “Like everyone, I want this pandemic nightmare to be over. But I also desperately fear living a debilitated life of mental muddle or torpor.” Recently, I’ve begun to think that our worries might be better placed. As the pandemic drags on, data have emerged to clarify the dangers posed by COVID across the weeks, months, and years that follow an infection. Taken together, their implications are surprising. Some people's lives are devastated by long COVID; they’re trapped with perplexing symptoms that seem to persist indefinitely. For the majority of vaccinated people, however, the worst complications will not surface in the early phase of disease, when you’re first feeling feverish and stuffy, nor can the gravest risks be said to be “long term.” Rather, they emerge during the middle phase of post-infection, a stretch that lasts for about 12 weeks after you get sick. This period of time is so menacing, in fact, that it really ought to have its own, familiar name: medium COVID. Just how much of a threat is medium COVID? The answer has been obscured, to some extent, by sloppy definitions. A lot of studies blend different, dire outcomes into a single giant bucket called “long COVID.” Illnesses arising in as few as four weeks, along with those that show up many months later, have been considered one and the same. The CDC, for instance, suggested in a study out last spring that one in five adults who get the virus will go on to suffer any of 26 medical complications, starting at least one month after infection, and extending up to one year. All of these are called “post-COVID conditions, or long COVID.” A series of influential analyses looking at U.S. veterans described an onslaught of new heart, kidney, and brain diseases (even among the vaccinated) across a similarly broad time span. The studies’ authors refer to these, grouped together, as “long COVID and its myriad complications.” But the risks described above might well be most significant in just the first few weeks post-infection, and fade away as time goes on. When scientists analyzed Sweden’s national health registry, for example, they found that the chance of developing pulmonary embolism—an often deadly clot in the lungs—was a startling 32 times higher in the first month after testing positive for the virus; after that, it quickly diminished. The clots were only two times more common at 60 days after infection, and the effect was indistinguishable from baseline after three to four months. A post-infection risk of heart attack and stroke was also evident, and declined just as expeditiously. In July, U.K. epidemiologists corroborated the Swedish findings, showing that a heightened rate of cardiovascular disease among COVID patients could be detected up to 12 weeks after they got sick. Then the hazard went away. This is all to be expected, given that other respiratory infections are known to cause a temporary spike in patients’ risk of cardiovascular events. Post-viral blood clots, heart attacks, and strokes tend to blow through like a summer storm. A very recent paper in the journal Circulation, also based on U.K. data, did find that COVID’s effects are longer-lasting, with a heightened chance of such events that lasts for almost one full year. But even in that study, the authors see the risk fall off most dramatically across the first two weeks. I’ve now read dozens of similar analyses, using data from many countries, that agree on this basic point: The greatest dangers lie in the weeks, not months, after a COVID infection. [Read: Long COVID could be a ‘mass deterioration event’] Yet many have inferred that COVID’s dangers have no end. “What’s particularly alarming is that these are really life-long conditions,” Ziyad Al-Aly, the lead researcher on the veterans studies, told the Financial Times in August. A Cleveland Clinic cardiologist has suggested that catching SARS-CoV-2 might even become a greater contributor to cardiovascular disease than being a chronic smoker or having obesity. But if experts who hold this assumption are correct—and the mortal hazards of COVID really do persist for a lifetime (or even many months)—then it’s not yet visible at the health-system level. By the end of the Omicron surge last winter, one in four Americans—about 84 million people—had been newly infected with the coronavirus. This was on top of 103 million pre-Omicron infections. Yet six months after the surge ended, the number of adult emergency-room visits, outpatient appointments, and hospital admissions across the country were all slightly lower than they were at the same time in 2021, according to an industry report released last month. In fact, emergency-room visits and hospital admissions in 2021 and 2022 were lower than they’d been before the pandemic. In other words, a rising tide of long-COVID-related medical conditions, affecting nearly every organ system, is nowhere to be found. If mild infections did routinely lead to fatal consequences at a delay of months or years, then we should see it in our death rates, too. The number of excess deaths in the U.S.—meaning those that have occured beyond historic norms—should still be going up, long after case rates fall. Yet excess deaths in the U.S. dropped to zero this past April, about two months after the end of the winter surge, and they have stayed relatively low ever since. Here, as around the world, overall mortality rates follow acute-infection rates, but only for a little while. A second wave of deaths—a long-COVID wave—never seems to break. Even the most familiar maladies of “long COVID”—severe fatigue, cognitive difficulties, and breathing trouble—tend to be at their worst during the medium post-infection phase. An early analysis of symptom-tracking data from the U.K., the U.S., and Sweden found that the proportion of those experiencing COVID’s aftereffects decreased by 83 percent four to 12 weeks after illness started. The U.K. government also reported much higher rates of medium COVID, relative to long COVID: In its survey, 11 percent of people who caught the virus experienced lingering issues such as weakness, muscle aches, and loss of smell, but that rate had dropped to 3 percent by 12 weeks post-infection. The U.K. saw a slight decline in the number of people reporting such issues throughout the spring and summer; and a recent U.S. government survey found that about half of Americans who had experienced any COVID symptoms for three months or longer had already recovered. This slow, steady resolution of symptoms fits with what we know about other post-infection syndromes. A survey of adolescents recovering from mononucleosis, which is caused by Epstein-Barr virus, found that 13 percent of subjects met criteria for chronic fatigue syndrome at six months, but that rate was nearly halved at one year, and nearly halved again at two. An examination of chronic fatigue after three different infections—EBV, Q fever, and Ross River virus—identified a similar pattern: frequent post-infection symptoms, which gradually decreased over months. [Read: It’s not just long COVID] The pervasiveness of medium COVID does nothing to negate the reality of long COVID—a calamitous condition that can shatter people’s lives. Many long-haulers experience unremitting symptoms, and their cases can evolve into complex chronic syndromes like ME/CFS or dysautonomia. As a result, they may require specialized medical care, permanent work accommodations, and ongoing financial support. Recognizing the small chance of such tragic outcomes could well be enough to make some people try to avoid infection or reinfection with SARS-CoV-2 at all costs. But if you’re like me, and trying to calibrate your behaviors to meet some personally acceptable level of COVID risk, then it helps to keep in mind the difference between the virus’s medium- and long-term complications. Medium COVID may be time-limited, but it is far from rare—and not always mild. It can mean a month or two of profound fatigue, crushing headaches, and vexing chest pain. It can lead to life-threatening medical complications. It needs recognition, research, and new treatments. For millions of people, medium COVID is as bad as it gets. from https://ift.tt/soKghPm Check out http://natthash.tumblr.com Of all the nicknames I have for my cat Calvin—Fluffernutter, Chonk-a-Donk, Fuzzy Lumpkin, Jerky McJerkface—Bumpus Maximus may be the most apt. Every night, when I crawl into bed, Calvin hops onto my pillow, purrs, and bonks his head affectionately against mine. It’s adorable, and a little bit gross. Tiny tufts of fur jet into my nose; flecks of spittle smear onto my cheeks. Just shy of a decade ago, cuddling a cat this aggressively would have left me in dire straits. From early childhood through my early 20s, I nursed a serious allergy that made it impossible for me to safely interact with most felines, much less adopt them. Just a few minutes of exposure was enough to make my eyes water and clog my nasal passages with snot. Within an hour, my throat would swell and my chest would erupt in crimson hives. Then, sometime in the early 2010s, my misery came to an abrupt and baffling end. With no apparent interventions, my cat allergy disappeared. Stray whiffs of dander, sufficient to send my body into conniptions mere months before, couldn’t even compel my nose to twitch. My body just up and decided that the former bane of its existence was suddenly totally chill. What I went through is, technically speaking, “completely weird,” says Kimberly Blumenthal, an allergist and immunologist at Massachusetts General Hospital. Some allergies do naturally fade with time, but short of allergy shots, which don’t always work, “we think of cat allergy as a permanent diagnosis,” Blumenthal told me. One solution that’s often proposed? “Get rid of your cat.” My case is an anomaly, but its oddness is not. Although experts have a broad sense of how allergies play out in the body, far less is known about what causes them to come and go—an enigma that’s becoming more worrying as rates of allergy continue to climb. Nailing down how, when, and why these chronic conditions vanish could help researchers engineer those circumstances more often for allergy sufferers—in ways that are actually under our control, and not just by chance. All allergies, at their core, are molecular screwups: an immune system mistakenly flagging a harmless substance as dangerous and attacking it. In the classic version, an allergen, be it a fleck of almond or grass or dog, evokes the ire of certain immune cells, prompting them to churn out an antibody called IgE. IgE drags the allergen like a hostage over to other defensive cells and molecules to rile them up too. A blaze of inflammation-promoting signals, including histamine, end up getting released, sparking bouts of itching, redness, and swelling. Blood vessels dilate; mucus floods out in gobs. At their most extreme, these reactions get so gnarly that they can kill. Just about every step of this chain reaction is essential to produce a bona fide allergy—which means that intervening at any of several points can shut the cascade down. People whose bodies make less IgE over time can become less sensitive to allergens. The same seems to be true for those who start producing more of another antibody, called IgG4, that can counteract IgE. Some people also dispatch a molecule known as IL-10 that can tell immune cells to cool their heels even in the midst of IgE’s perpetual scream. All this and more can eventually persuade a body to lose its phobia of an allergen, a phenomenon known as tolerance. But because there is not a single way in which allergy manifests, it stands to reason that there won’t be a single way in which it disappears. “We don’t fully understand how these things go away,” says Zachary Rubin, a pediatrician at Oak Brook Allergists, in Illinois. [Read: What they aren’t telling you about hypoallergenic dogs] Tolerance does display a few trends. Sometimes, it unfurls naturally as people get older, especially as they approach their 60s (though allergies can appear in old age as well). Other diagnoses can go poof amid the changes that unfold as children zip through the physiological and hormonal changes brought on by toddlerhood, adolescence, and the teen years. As many as 60 to 80 percent of milk, wheat, and egg allergies can peace out by puberty—a pattern that might also be related to the instability of the allergens involved. Certain snippets of milk and egg proteins, for instance, can unravel in the presence of heat or stomach acid, making the molecules “less allergenic,” and giving the body ample opportunity to reappraise them as benign, says Anna Nowak-Węgrzyn, a pediatric allergist and immunologist at NYU Langone Health. About 80 to 90 percent of penicillin allergies, too, disappear within 10 years of when they’re first detected, more if you count the ones that are improperly diagnosed, as Blumenthal has found. Other allergies are more likely to be lifers without dedicated intervention--among them, issues with peanuts, tree nuts, shellfish, pollen, and pets. Part of the reason may be that some of these allergens are super tough to neutralize or purge. The main cat allergen, a protein called “Fel d 1” that’s found in feline saliva, urine, and gland secretions, can linger for six months after a cat vacates the premises. It can get airborne, and glom on to surfaces; it’s been found in schools and churches and buses and hospitals, “even in space,” Blumenthal told me. [Read: The next weird way we’re changing cats] For hangers-on like these, allergists can try to nudge the body toward tolerance through shots or mouth drops that introduce bits of an allergen over months or years, basically the immunological version of exposure therapy. In some cases, it works: Dosing people with Fel d 1 can at least improve a cat allergy, but it’s hardly a sure hit. Researchers haven’t even fully sussed out how allergy shots induce tolerance—just that “they work well for a lot of patients,” Rubin told me. The world of allergy research as a whole is something of a Wild West: Some people are truly, genuinely, hypersensitive to water touching their skin; others have gotten allergies because of organ transplants, apparently inheriting their donor’s sensitivity as amped-up immune cells hitched a ride. Part of the trouble is that allergy can involve just about every nook and cranny of the immune system; to study its wax and wane, scientists have to repeatedly look at people’s blood, gut, or airway to figure out what sorts of cells and molecules are lurking about, all while tracking their symptoms and exposures, which doesn’t come easy or cheap. And fully disentangling the nuances of bygone allergies isn’t just about better understanding people who are the rule. It’s about delving into the exceptions to it too. How frustratingly little we know about allergies is compounded by the fact that the world is becoming a more allergic place. A lot of the why remains murky, but researchers think that part of the problem can be traced to the perils of modern living: the wider use of antibiotics; the shifts in eating patterns; the squeaky-cleanness of so many contemporary childhoods, focused heavily on time indoors. About 50 million people in the U.S. alone experience allergies each year—some of them little more than a nuisance, others potentially deadly when triggered without immediate treatment. Allergies can diminish quality of life. They can limit the areas where people can safely rent an apartment, or the places where they can safely dine. They can hamper access to lifesaving treatments, leaving doctors scrambling to find alternative therapies that don’t harm more than they help. But if allergies can rise this steeply with the times, maybe they can resolve rapidly too. New antibody-based treatments could help silence the body’s alarm sensors and quell IgE’s rampage. Some researchers are even looking into how fecal transplants that port the gut microbiome of tolerant people into allergy sufferers might help certain food sensitivities subside. Anne Liu, an allergist and immunologist at Stanford, is also hopeful that “the incidence of new food allergies will decline over the next 10 years,” as more advances come through. After years of advising parents against introducing their kids to sometimes-allergenic substances such as milk and peanuts too young, experts are now encouraging early exposures, in the hopes of teaching tolerance. And the more researchers learn about how allergies naturally abate, the better they might be able to safely replicate fade-outs. One instructive example could come from cases quite opposite to mine: longtime pet owners who develop allergies to their animals after spending some time away from them. That’s what happened to Stefanie Mezigian, of Michigan. After spending her entire childhood with her cat, Thumper, Mezigian was dismayed to find herself sneezing and sniffling when she visited home the summer after her freshman year of college. Years later, Mezigian seems to have built a partial tolerance up again; she now has another cat, Jack, and plans to keep felines in her life for good—both for companionship and to wrangle her immune system’s woes. “If I go without cats, that seems to be when I develop problems,” she told me. It’s a reasonable thought to have, Liu told me. People in Mezigian’s situation probably have the reactive IgE bopping around their body their entire life. But maybe during a fur-free stretch, the immune system, trying to be “parsimonious,” stops making molecules that rein in the allergy, she said. The immune system is nothing if not malleable, and a bit diva-esque: Set one thing off kilter, and an entire network of molecules and cells can revamp its approach to the world. I may never know why my cat allergy ghosted me. Maybe I got infected by a virus that gently rewired my immune system; maybe my hormone levels went into flux. Maybe it was the stress, or joy, of graduating college and starting grad school; maybe my diet or microbiome changed in just the right way, at just the right time. Perhaps it’s pointless to guess. Allergy, like the rest of the immune system, is a hot, complicated mess—a common fixture of modern living that many of us take for granted, but that remains, in so many cases, a mystery. All I can do is hope my cat allergy stays gone, though there’s no telling if it will. “I have no idea,” Nowak-Węgrzyn told me. “I’m just happy for you. Go enjoy your cats.” from https://ift.tt/jNUQW8V Check out http://natthash.tumblr.com As a pulmonary specialist, I spend most of my clinical time in the hospital—which, during pandemic surges, has meant many long days treating critically ill COVID-19 patients in the ICU. But I also work in an outpatient clinic, where I also treat those same sorts of patients after they’re discharged: people who survived weeks-long hospitalizations but have been dealing ever since with lung damage. Such patients often face the same social and economic factors that made them vulnerable to COVID-19 to begin with, and they require attentive care. Patients like these undoubtedly suffer what researchers have been calling post-acute sequelae of SARS-CoV-2, or PASC—which, according to one highly publicized recent CDC study, afflicts some 20 percent of COVID-19 survivors ages 18 to 64. Other studies have yielded lower estimates of the condition also called long COVID, and while differences in study methodology account for some of this variability, there’s a more fundamental issue eluding efforts to uncover the one “true” estimate of the likelihood of this condition. Quite simply, long COVID isn’t any one thing. [From the April 2021 issue: Unlocking the mysteries of long COVID] The wide spectrum of conditions that fall under the umbrella of long COVID impedes researchers’ ability to interpret estimates of national prevalence based on surveys of symptoms, which conflate different problems with different causes. More importantly, however, an incomplete and constrained perspective on what long COVID is or isn’t limits Americans’ understanding of who is suffering and why, and of what we can do to improve patients’ lives today. The cases of long COVID that turn up in news reports, the medical literature, and in the offices of doctors like me fall into a few rough (and sometimes overlapping) categories. The first seems most readily explainable: the combination of organ damage, often profound physical debilitation, and poor mental health inflicted by severe pneumonia and resultant critical illness. This serious long-term COVID-19 complication gets relatively little media attention despite its severity. The coronavirus can cause acute respiratory distress syndrome, the gravest form of pneumonia, which can in turn provoke a spiral of inflammation and injury that can end up taking down virtually every organ. I have seen many such complications in the ICU: failing hearts, collapsed lungs, failed kidneys, brain hemorrhages, limbs cut off from blood flow, and more. More than 7 million COVID-19 hospitalizations occurred in the United States before the Omicron wave, suggesting that millions could be left with damaged lungs or complications of critical illness. Whether these patients’ needs for care and rehabilitation are being adequately (and equitably) met is unclear: Ensuring that they are is an urgent priority. Recently, a second category of long COVID has made headlines. It includes the new onset of recognized medical conditions—like heart disease, a stroke, or a blood clot—after a mild COVID-19 infection. It might seem odd that an upper respiratory tract infection could trigger a heart attack. Yet this pattern has been well described after other common respiratory-virus infections, particularly influenza. Similarly, various types of infections can lead to blood clots in the legs, which can travel (dangerously) to the lungs. Respiratory infections are not hermetically sealed from the rest of the body; acute inflammation arising in one location can sometimes have consequences elsewhere. But mild COVID-19 is so common that measuring the prevalence of such complications—which also regularly occur in people without COVID-19—can be tricky. Well-controlled investigations are needed to disentangle causation and correlation, particularly because social disadvantage is associated both with COVID exposure and illnesses of basically every organ system. Some such studies, which analyzed giant electronic-health-record databases, have suggested that even mild COVID-19 is at least correlated with a startlingly wide spectrum of seemingly every illness, including diabetes, asthma, and kidney failure; basically every type of heart disease; alcohol-, benzodiazepine-, and opioid-use disorders; and much more. To be clear, this research generally suggests that such complications occur far less often after mild COVID-19 cases than severe ones, and the extent to which the coronavirus causes each such complication remains unclear. In other words, we can surmise that at least some of these complications (particularly vascular complications, which have been well-described in many studies) are likely a consequence of COVID-19, but we can’t say with certainty how many. And more importantly, we don’t yet understand why some people with mild COVID recover easily while others go on to experience such complications. However, an estimated 81 percent of Americans have now been infected at least once, so the public-health ramifications are large even if COVID causes only some of the aforementioned recognized diseases, and even if our individual risk of complications after a mild infection is modest. Regardless of cause, patients who do develop any such chronic diseases require attentive, ongoing medical care—a challenge in a nation where 30 million are uninsured and even more underinsured. Another category of long COVID is something rather more quotidian, if still very distressing for those experiencing it: respiratory symptoms that last longer than expected after an acute upper-respiratory infection caused by the coronavirus, but that are not associated with lung damage, critical illness, or a new diagnosis like a heart attack or diabetes. Symptoms such as shortness of breath and chest pain are common months after run-of-the-mill pneumonia unconnected to the coronavirus, for instance, while many patients who contract non-COVID-related upper respiratory infections subsequently report a protracted cough or a lingering loss of their sense of smell. That a COVID-related airway infection sometimes has similar consequences only stands to reason. [Read: Long-haulers are fighting for their future] However, none of these may be what most people think of when long COVID is invoked. Some may even argue that such syndromes are not, in fact, long COVID at all, even if they cause long-term suffering. “Long Covid is not a condition for which there are currently accepted objective diagnostic tests or biomarkers,” wrote Steven Phillips and Michelle Williams in the New England Journal of Medicine. “It is not blood clots, myocarditis, multisystem inflammatory disease, pneumonia, or any number of well-characterized conditions caused by Covid-19.” Instead, for some the term may invoke a chronic illness—a complex of numerous unexplained, potentially debilitating symptoms—even among those who may barely have felt sick with COVID in the acute phase. Symptoms may vary widely, and include severe fatigue, cognitive issues often described as brain fog, shortness of breath, “internal tremors,” gastrointestinal problems, palpitations, dizziness, and many other issues around the body—all typically following a mild acute respiratory infection. If the other forms of long COVID seem more easily explainable, this type is often characterized as a medical mystery. Teasing apart which kind of long COVID a person has is important, both to advance our understanding of the illness and to best care for people. Yet lumping and splitting varieties of long COVID into categories is not easy. A given patient’s case might have features of more than one of the types that I’ve described here. Some patient advocates and researchers have tended to exclude patients in the first category—that is, survivors of protracted critical illness—from their conception of COVID long-haulers. I would argue that, insofar as we define long COVID as lasting damage and symptoms imposed by SARS-CoV-2, the full variety of severe long-term manifestations should be included in its scope. “Clinical phenotyping” studies now under way may eventually help scientists and doctors better understand the needs of different types of patients, but patients in all categories deserve better care today. The biological mechanisms by which an acute coronavirus upper respiratory infection might lead to a bewildering range of chronic, burdensome symptoms even in the aftermath of mild infections are debated. Some scientists, for instance, believe that the virus causes an autoimmune disease akin to lupus. Meanwhile, one group of researchers has argued that even a mild respiratory infection from SARS-CoV-2 causes tiny clots to block tiny blood vessels all over the body, depriving tissues of oxygen throughout the body. Still others believe that the coronavirus causes a chronic infection, as such viruses as HIV or hepatitis C do. Meanwhile, some have emphasized the possibility of structural brain damage. While some published studies have provided support for each theory, none has been adequately validated as a central unifying thesis. Each is, however, worth continuing to explore. A recently published investigation, conducted at the National Institutes of Health, suggests that clinicians and scientists should consider additional possibilities as potential drivers of symptoms for at least some patients. The researchers found far higher levels of physical symptoms and mental distress among subjects who had had COVID (many with long COVID) than among those who had not. Yet symptoms could not be explained by basically any test results: Researchers found effectively no substantive differences in markers of inflammation or immune activation, in objective neurocognitive testing, or in heart, lung, liver, or kidney function. And yet these patients were suffering from such symptoms as fatigue, shortness of breath, concentration and memory problems, chest pain, and more. Notably, researchers did not identify viral persistence in the bodies of patients reporting troublesome symptoms. What this means in practice is that there are some people suffering from long COVID symptoms without evidence of structural damage to the body, autoimmunity, or chronic infection. Psychosocial strain and suffering, moreover, appears common in this population. Even pointing this out is sensitive territory—it leads some people to wrongly suggest that long COVID is less severe or concerning than those suffering from it describe, or even to question the reality of the illness. And, understandably, the invocation of psychosocial factors as potential contributing factors to suffering for some individuals may make patients feel as though they are being second-guessed. The reality, though, is that psychosocial strain is an important driver of physical symptoms and suffering—one that clinicians should treat with empathy. All suffering, after all, is ultimately produced and perceived in one place: our brain. Severe depression, for instance, can inflict debilitating and severe physical symptoms of every sort, including crushing fatigue and withering brain fog, and is itself linked to having had COVID-19. And notably, a recent study in JAMA Psychiatry found that pre-infection psychosocial distress—e.g. depression, anxiety, or loneliness—was associated with a 30–50 percent increase in the risk of long COVID among those infected, even after adjustment for various factors. A false separation of brain and body has long plagued medicine, but it does not reflect biological reality: After all, diverse neuropsychiatric processes are associated with numerous “physical” changes, ranging from reduced blood flow to the brain to high (or low) levels of the stress hormone cortisol. Illnesses of any cause that result in protracted time off one’s feet can also instigate (likely in conjunction with other factors) reversible cardiovascular deconditioning, wherein the blood volume contracts and the amount of blood ejected by the heart with each squeeze falls--changes that can lead to a racing heart rate or faintness when standing, as decades of studies have shown. Diverse neurological symptoms can also be produced by a glitch in the function rather than the structure of the brain—or what has been described as problems of brain “software” rather than “hardware”—resulting in conditions known as functional neurological disorders. Similar glitches, known as functional respiratory disorders, can disturb our breathing patterns or cause shortness of breath, even when our lungs are structurally normal. My point is not to speculate on some overarching hypothesis to explain all symptoms among all patients with long COVID. The whole point is that there’s unlikely to be just one. And there is still much to learn. Research is underway to better understand this spectrum of illnesses, and their causes. But whichever diverse factors might be contributing to patients’ symptoms, we can take steps—both among clinicians and as a society—to improve lives now. Social supports can be as important as medical interventions: For those unable to work, qualification for disability assistance should not depend on a particular lab or lung-function test result. All patients with long-COVID symptoms deserve and require high-quality medical care without onerous cost barriers that may bankrupt them, which further compounds suffering. Universal healthcare is, that is to say, desperately needed to respond to this pandemic and its aftermath. Additionally, while no specific long-COVID medications have emerged, some treatments may be helpful for improving certain symptoms regardless of the specific type of illness, such as physical rehabilitative treatments for those with shortness of breath or reduced exercise tolerance. Ensuring universal access to such specialized rehabilitative care is essential as we enter the next stage of this pandemic. So is helping patients avoid the emerging cottage industry of dodgy providers hawking unproven long-COVID therapies. Health-care professionals also need more education about the broad spectrum of COVID-19-related issues, both to improve care and reduce stigmatization of patients with all types of this illness. [Read: The pandemic after the pandemic] Doctors and scientists still have much to learn about symptoms that continue—or first turn up—months or weeks after an initial COVID infection. What’s clear today is that long COVID can be many different things. That may confound our efforts to categorize it and discuss its implications, but the sheer variety should not get in the way of care for all who are suffering. from https://ift.tt/ifZAo93 Check out http://natthash.tumblr.com This fall, unlike the one before it, and the one before that, America looks almost like its old self. Schools and universities are in session; malls, airports, and gyms are bustling with the pre-holiday rush; handwashing is passé, handshakes are back, and strangers are packed together on public transport, nary a mask to be seen. On its surface, the country seems ready to enjoy what some might say is our first post-pandemic winter. Americans are certainly acting as if the crisis has abated, and so in that way, at least, you could argue that it has. “If you notice, no one’s wearing masks,” President Joe Biden told 60 Minutes in September, after proclaiming the pandemic “over.” Almost no emergency protections against the virus are left standing; we’re dismantling the few that are. At the same time, COVID is undeniably, as Biden says, “a problem.” Each passing day still brings hundreds of deaths and thousands of hospitalizations; untold numbers of people continue to deal with long COVID, as more join them. In several parts of the country, health-care systems are struggling to stay afloat. Local public-health departments, underfunded and understaffed, are hanging by a thread. And a double surge of COVID and flu may finally be brewing. So we can call this winter “post-pandemic” if we want. But given the policy failures and institutional dysfunctions that have accumulated over the past three years, it won’t be anything like a pre-pandemic winter, either. The more we resist that reality, the worse it will become. If we treat this winter as normal, it will be anything but. By now, we’ve grown acquainted with the variables that dictate how a season with SARS-CoV-2 will go. In our first COVID winter, the vaccines had only just begun their trickle out into the public, while most Americans hadn’t yet been infected by the virus. In our second COVID winter, the country’s collective immunity was higher, but Omicron sneaked past some of those defenses. On the cusp of our third COVID winter, it may seem that SARS-CoV-2 has few plot twists left to toss us. But the way in which we respond to COVID could still sprinkle in some chaos. During those first two winters, at least a few virus-mitigating policies and precautions remained in place—nearly all of which have since come down, lowering the hurdles the virus must clear, at a time when America’s health infrastructure is facing new and serious threats. The nation is still fighting to contain a months-long monkeypox outbreak; polio continues to plague unvaccinated sectors of New York. A riot of respiratory viruses, too, may spread as temperatures cool and people flock indoors. Rates of RSV are rising; flu returned early in the season from a nearly three-year sabbatical to clobber Australia, boding poorly for us in the north. Should flu show up here ahead of schedule, Americans, too, could be pummeled as we were around the start of 2018, “one of the worst seasons in the recent past,” says Srinivasan Venkatramanan, an infectious-disease modeler at the University of Virginia and a member of the COVID-19 Scenario Modeling Hub. [Read: Fauci addresses ‘The pandemic is over’] The consequences of this infectious churn are already starting to play out. In Jackson, Mississippi, health workers are watching SARS-CoV-2 and other respiratory viruses tear through children “like nothing we’ve ever seen before,” says Charlotte Hobbs, a pediatric-infectious-disease specialist at the University of Mississippi Medical Center. Flu season has yet to go into full swing, and Hobbs is already experiencing one of the roughest stretches she’s had in her nearly two decades of practicing. Some kids are being slammed with one virus after the other, their sicknesses separated by just a couple of weeks—an especially dangerous prospect for the very youngest among them, few of whom have received COVID shots. The toll of doctor visits missed during the pandemic has ballooned as well. Left untreated, many people’s chronic conditions have worsened, and some specialists’ schedules remain booked out for months. Add to this the cases of long COVID that pile on with each passing surge of infections, and there are “more sick people than there used to be, period,” says Emily Landon, an infectious-disease physician at the University of Chicago. That’s with COVID case counts at a relative low, amid a massive undercount. Even if a new, antibody-dodging variant doesn’t come banging on the nation’s door, “the models predict an increase in infections,” Venkatramanan told me. (In parts of Europe, hospitalizations are already making a foreboding climb.) And where the demand for care increases, supply does not always follow suit. Health workers continue to evacuate their posts. Some have taken early retirement, worried that COVID could exacerbate their chronic conditions, or vice versa; others have sought employment with better hours and pay, or left the profession entirely to salvage their mental health. A wave of illness this winter will pare down forces further, especially as the CDC backs off its recommendations for health-care workers to mask. At UAB Hospital, in Birmingham, Alabama, “we’ve struggled to have enough people to work,” says Sarah Nafziger, an emergency physician and the medical director for employee health. “And once we get them here, we have a hard time getting them to stay.” [Read: The strongest sign that Americans should worry about flu this winter] Clinical-laboratory staff at Deaconess Hospital, in Indiana, who are responsible for testing patient samples, are feeling similar strain, says April Abbott, the institution’s microbiology director. Abbott’s team has spent most of the past month below usual minimum-staffing levels, and has had to cut some duties and services to compensate, even after calling in reinforcements from other, already shorthanded parts of the lab. “We’re already at this threshold of barely making it,” Abbott told me. Symptoms of burnout have surged as well, while health workers continue to clock long hours, sometimes amid verbal abuse, physical attacks, and death threats. Infrastructure is especially fragile in America’s rural regions, which have suffered hospital closures and an especially large exodus of health workers. In Madison County, Montana, where real-estate values have risen, “the average nurse cannot afford a house,” says Margaret Bortko, a nurse practitioner and the region’s health officer and medical director. When help and facilities aren’t available, the outcome is straightforward, says Janice Probst, a rural-health researcher at the University of South Carolina: “You will have more deaths.” In health departments, too, the workforce is threadbare. As local leaders tackle multiple infectious diseases at once, “it’s becoming a zero-sum game,” says Maria Sundaram, an epidemiologist at the Marshfield Clinic Research Institute. “With limited resources, do they go to monkeypox? To polio? To COVID-19? To influenza? We have to choose.” Mati Hlatshwayo Davis, the director of health in St. Louis, told me that her department has shrunk to a quarter of the size it was five years ago. “I have staff doing the jobs of three to five people,” she said. “We are in absolute crisis.” Staff have left to take positions as Amazon drivers, who “make so much more per hour.” Looking across her state, Hlatshwayo Davis keeps watching health directors “resign, resign, resign.” Despite all that she has poured into her job, or perhaps because of it, “I can’t guarantee I won’t be one of those losses too.” This winter is unlikely to be an encore of the pandemic’s worst days. Thanks to the growing roster of tools we now have to combat the coronavirus—among them, effective vaccines and antivirals—infected people are less often getting seriously sick; even long COVID seems to be at least a bit scarcer among people who are up-to-date on their shots. But considering how well our shots and treatments work, the plateau of suffering at which we’ve arrived is bizarrely, unacceptably high. More than a year has passed since the daily COVID death toll was around 200; nearly twice that number—roughly three times the daily toll during a moderate flu season—now seems to be a norm. Part of the problem remains the nation’s failed approach to vaccines, says Avnika Amin, a vaccine epidemiologist at Emory University: The government has repeatedly championed shots as a “be-all and end-all” strategy, while failing to rally sufficient uptake. Boosting is one of the few anti-COVID measures still promoted, yet the U.S. remains among the least-vaccinated high-income countries; interest in every dose that’s followed the primary series has been paltry at best. Even with the allure of the newly reformulated COVID shot, “I’m not really getting a good sense that people are busting down the doors,” says Michael Dulitz, a health worker in Grand Forks, North Dakota. Nor can vaccines hold the line against the virus alone. Even if everyone got every shot they were eligible for, Amin told me, “it wouldn’t make COVID go away.” [Read: America created its own booster problems] The ongoing dry-up of emergency funds has also made the many tools of disease prevention and monitoring more difficult to access. Free at-home tests are no longer being shipped out en masse; asymptomatic testing is becoming less available; and vaccines and treatments are shifting to the private sector, putting them out of reach for many who live in poor regions or who are uninsured and can least afford to fall ill. It doesn’t help, either, that the country’s level of preparedness lays out as a patchwork. People who vaccinate and mask tend to cluster, Amin told me, which means that not all American experiences of winter will be the same. Less prominent, less privileged parts of the country will quietly bear the brunt of outbreaks. “The biggest worry is the burden becoming unnoticed,” Venkatramanan told me. Without data, policies can’t change; the nation can’t react. “It’s like flying without altitude or speed sensors. You’re looking out the window and trying to guess.” There’s an alternative winter the country might envision—one unencumbered by the policy backslides the U.S. has made in recent months, and one in which Americans acknowledge that COVID remains not just “a problem” but a crisis worth responding to. In that version of reality, far more people would be up-to-date on their vaccines. The most vulnerable in society would be the most protected. Ventilation systems would hum in buildings across the country. Workers would have access to ample sick leave. Health-care systems would have excesses of protective gear, and local health departments wouldn’t want for funds. Masks would come out in times of high transmission, especially in schools, pharmacies, government buildings, and essential businesses; free tests, boosters, and treatments would be available to all. No one would be asked to return to work while sick—not just with COVID but with any transmissible disease. SARS-CoV-2 infections would not disappear, but they would remain at more manageable levels; cases of flu and other cold-weather sicknesses that travel through the air would follow suit. Surveillance systems would whir in every state and territory, ready to detect the next threat. Leaders might even set policies that choreograph, rather than simply capitulate to, how Americans behave. We won’t be getting that winter this year, or likely any year soon. Many policies have already reverted to their 2019 status quo; by other metrics, the nation’s well-being even seems to have regressed. Life expectancy in the U.S. has fallen, especially among Native Americans and Alaskan Natives. Institutions of health are beleaguered; community-outreach efforts have been pruned. The pandemic has also prompted a deterioration of trust in several mainstays of public health. In many parts of the country, there’s worry that the vaccine hesitancy around COVID has “spread its tentacles into other diseases,” Hobbs told me, keeping parents from bringing their kids in for flu shots and other routine vaccines. Mississippi, once known for its stellar rate of immunizing children, now consistently ranks among those with the fewest young people vaccinated against COVID. “The one thing we do well is vaccinate children,” Hobbs said. That the coronavirus has reversed the trend “has astounded me.” In Montana, sweeping political changes, including legislation that bans employers from requiring vaccines of any kind, have made health-care settings less safe. Fewer than half of Madison County’s residents have received even their primary series of COVID shots, and “now a nurse can turn down the Hepatitis B series,” Bortko told me. Health workers, too, feel more imperiled than before. Since the start of the pandemic, Bortko’s own patients of 30 years, “who trusted me with their lives,” have pivoted to “yelling at us about vaccination concerns and mask mandates and quarantining and their freedoms,” she told me. “We have become public enemy No. 1.” [Read: The pandemic’s soft closing] At the same time, many people with chronic and debilitating conditions are more vulnerable than they were before the pandemic began. The policies that protected them during the pandemic’s height are gone—and yet SARS-CoV-2 is still here, adding to the dangers they face. The losses have been written off, Bortko told me: Cases of long COVID in Madison County have been dismissed as products of “risk factors” that don’t apply to others; deaths, too, have been met with a shrug of “Oh, they were old; they were unhealthy.” If, this winter, COVID sickens or kills more people who are older, more people who are immunocompromised, more people of color, more essential and low-income workers, more people in rural communities, “there will be no press coverage,” Hlatshwayo Davis said. Americans already expect that members of these groups will die. It’s not too late to change course. The winter’s path has not been set: Many Americans are still signing up for fall flu and COVID shots; we may luck out on the viral evolution front, too, and still be dealing largely with members of the Omicron clan for the next few months. But neither immunity nor a slowdown in variant emergence is a guarantee. What we can count on is the malleability of human behavior—what will help set the trajectory of this winter, and others to come. The U.S. botched the pandemic’s beginning, and its middle. That doesn’t mean we have to bungle its end, whenever that truly, finally arrives. from https://ift.tt/ZnXkLur Check out http://natthash.tumblr.com |
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