Health | The Atlantichttps://www.theatlantic.com/health/2024-03-18T12:34:48-04:00Copyright 2024 by The Atlantic Monthly Group. All Rights Reserved.tag:theatlantic.com,2024:50-677791<p dir="ltr">When Steve Edsel was a boy, his adoptive parents kept a scrapbook of newspaper clippings in their bedroom closet. He would ask for it sometimes, poring over the headlines about his birth. Headlines like this: “Mother Deserts Son, Flees From Hospital,” <em>Winston-Salem Journal,</em> December 30, 1973.</p><p dir="ltr">The mother in question was 14 years old, “5 feet 6 with reddish brown hair,” and she had come to the hospital early one morning with her own parents. They gave names that all turned out to be fake. And by 8 o’clock that evening, just hours after she gave birth, they were gone. In a black-and-white drawing of the mother, based on nurses’ recollections, she has round glasses and sideswept bangs. Her mouth is grimly set.</p><p dir="ltr">The abandoned boy was placed in foster care with a local couple, the Edsels, who later adopted him. Steve knew all of this growing up. His parents never tried to hide his origins, and they always gave him the scrapbook when he asked. It wasn’t until he turned 14, though, that he really began to wonder about his birth mom. “I’m 14,” he thought at the time. “This is how old she was when she had me.”</p><p dir="ltr">Steve began looking for her in earnest in his 20s, but the paper trail quickly ran cold. When he turned 40, he told his wife, Michelle, that he wanted to give the search one last go. This was in 2013. AncestryDNA had started selling mail-in test kits the previous year, so he bought one. His matches at first seemed unpromising—some distant relatives—but when he began posting in a Facebook group for people seeking out biological family, he got connected to a genetic genealogist named CeCe Moore. Moore specializes in finding people via distant DNA matches, a technique made famous in 2018 when it led to the <a href="https://www.theatlantic.com/science/archive/2018/04/golden-state-killer-east-area-rapist-dna-genealogy/559070/?utm_source=feed">capture of the Golden State Killer</a>. But back then, genetic genealogy was still new, and Moore was one of its pioneers. She volunteered to help Steve.</p><p dir="ltr">Within just a couple of weeks, she had narrowed down the search to two women, cousins of the same age. On Facebook, Steve could see that one cousin had four kids, and she regularly posted photos of them, beautiful and smiling. They looked well-off, their lives picture-perfect— “like a storybook,” Steve says. The other woman was unmarried; she didn’t have kids. She was not friends with her immediate family on Facebook, and she had moved halfway across the country from them. One evening—a Saturday, Steve clearly remembers—Moore asked to speak with him by phone.</p><p dir="ltr">She confirmed what he had already suspected: His birth mom was the second woman. But Moore had another piece of news too. She had unexpectedly figured out something about his biological father as well.<em> It looks like your parents are related.</em> Steve didn’t know what to say. <em>Do you understand what I mean?</em> He said he thought so. <em>Either your mom’s father or your mom’s brother is your father.</em> A sea of emotions rose to a boil inside him: anger, hurt, worthlessness, disgust, shame, and devastation all at once. In his years of wondering about his birth, he had never, ever considered the possibility of incest. Why would he? What were the chances?</p><hr class="c-section-divider"><p dir="ltr">In 1975, around the time of Steve’s birth, a psychiatric textbook put the frequency of incest at one in a million.</p><p dir="ltr">But this number is almost certainly a dramatic underestimate. The stigma around openly discussing incest, which often involves child sexual abuse, has long made the subject difficult to study. In the 1980s, <a href="https://www.hup.harvard.edu/books/9780674002708">feminist scholars argued</a>, based on the testimonies of victims, that incest was far more common than recognized, and in recent years, DNA has offered a new kind of biological proof. Widespread genetic testing is uncovering case after secret case of children born to close biological relatives—providing an unprecedented accounting of incest in modern society.</p><p dir="ltr">The geneticist Jim Wilson, at the University of Edinburgh, was shocked by the frequency he found in the U.K. Biobank, an anonymized research database: One in 7,000 people, according to his unpublished analysis, was born to parents who were first-degree relatives—a brother and a sister or a parent and a child. “That’s way, way more than I think many people would ever imagine,” he told me. And this number is just a floor: It reflects only the cases that resulted in pregnancy, that did not end in miscarriage or abortion, and that led to the birth of a child who grew into an adult who volunteered for a research study.</p><p dir="ltr">Most of the people affected may never know about their parentage, but these days, many are stumbling into the truth after AncestryDNA and 23andMe tests. Steve’s case was one of the first Moore worked on involving closely related parents. She now knows of well over 1,000 additional cases of people born from incest, the significant majority between first-degree relatives, with the rest between second-degree relatives (half-siblings, uncle-niece, aunt-nephew, grandparent-grandchild). The cases show up in every part of society, every strata of income, she told me.</p><p data-id="injected-recirculation-link" dir="ltr"><i>[<a href="https://www.theatlantic.com/science/archive/2018/07/dna-test-misattributed-paternity/562928/?utm_source=feed">Read: When a DNA Test Shatters Your Identity</a>]</i></p><p dir="ltr">Neither AncestryDNA nor 23andMe informs customers about incest directly, so the thousand-plus cases Moore knows of all come from the tiny proportion of testers who investigated further. This meant, for example, uploading their DNA profiles to a third-party genealogy site to analyze what are known as “runs of homozygosity,” or ROH: long stretches where the DNA inherited from one’s mother and father are identical. For a while, one popular genealogy site instructed anyone who found high ROH to contact Moore. She would call them, one by one, to explain the jargon’s explosive meaning. Unwittingly, she became the keeper of what might be the world’s largest database of people born out of incest.</p><p dir="ltr">In the overwhelming majority of cases, Moore told me, the parents are a father and a daughter or an older brother and a younger sister, meaning a child’s existence was likely evidence of sexual abuse. She had no obvious place to send people reeling from such revelations, and she was not herself a trained therapist. After seeing many of these cases, though, she wanted people to know they were not alone. Moore ended up creating a private and invite-only support group on Facebook in 2016, and she tapped Steve and later his wife, Michelle, to become admins, too. The three of them had become close in the months and years after the search for his birth mom, as they navigated the emotional fallout together.</p><p dir="ltr">One day this past January, Michelle, who also works as Moore’s part-time assistant, told me she had spoken with four new people that week, all of them with ROH high enough to have parents who were first-degree relatives. She used to dread these calls. “I would stumble over my words,” she told me. But not anymore. She tells the shaken person on the line that they can join a support group full of people who are living the same reality. She tells them they can talk to her husband, Steve.</p><hr class="c-section-divider"><p dir="ltr">When Steve first discovered the truth about his biological parents, a decade ago, he had no support group to turn to, and he did not know what to do with the strange mix of emotions. He was genuinely happy to have found his birth mom. He had never looked like his adoptive parents, but in photos of her and her family, he could see his eyes, his chin, and even the smirky half-grin that his face naturally settles into.</p><p dir="ltr">But he radiated with newfound anger, too, on her behalf. He could not know the exact circumstances of his conception, and his DNA test alone could not determine whether her older brother or her father was responsible. But Steve could not imagine a consensual scenario, given her age. The bespectacled 14-year-old girl who disappeared from the hospital had remained frozen in time in his mind, even as he himself grew older, got married, became a stepdad. He felt protective of that young girl. </p><p dir="ltr">As badly as he wanted to know his birth mom, he worried she would not want to know him. Would his sudden reappearance dredge up traumatic memories—memories she had perhaps been trying to outrun her whole adult life, given how far she had moved and how little she seemed connected to her family? A religious man, Steve prayed over it and settled on handwriting a letter. He included a couple of paragraphs about his life, some photos, and a message that he loved her. He left out what he knew about his paternity. And he took care to send the letter by certified mail, so that he could confirm its receipt and so that it would not accidentally fall into anyone else’s hands.</p><p dir="ltr">She never responded. But Steve knew that she had received it: The post office sent him the green slip that she had signed upon delivery, and he scrutinized her signature—her actual name, written by her actual hand. At 40 years old, he touched for the first time something his mother had just touched, held something she had just held. He put the slip inside the pages of his Bible.</p><p dir="ltr">Steve had never faulted his mother for leaving him at the hospital, and finding out about his paternity made him even more understanding. But the revelation also made him struggle with who he was. Did it mean that something was wrong with him, written into his DNA from the moment of his conception? On a <a href="https://podcasts.apple.com/us/podcast/ep-1-the-secret-one/id1572201167?i=1000526354990">podcast</a> later, he admitted to feeling like trash, “like something that somebody had just thrown away.” Those first six months after his discovery were the hardest six months of his life.</p><hr class="c-section-divider"><p dir="ltr">Across human cultures, incest between close family members is one of the most universal and most deeply held taboos. A common explanation is biological: Children born from related parents are more likely to develop health complications, because their parents are more likely to be carriers of the same recessive mutations. From the 1960s to the ’80s, a <a href="https://publications.aap.org/pediatrics/article-abstract/40/1/55/43627/CHILDREN-OF-INCEST">handful</a> <a href="https://www.sciencedirect.com/science/article/abs/pii/S0022347682803478">of</a> <a href="https://karger.com/hhe/article-abstract/21/2/108/158742/A-Study-of-Children-of-Incestuous-Matings">studies</a> following a few dozen children born of incest documented high rates of infant mortality and congenital conditions.</p><p dir="ltr">But in the past, healthy children born from incestuous unions would have never come to the attention of doctors. As widespread DNA testing has uncovered orders of magnitude more people whose parents are brother and sister or parent and child, it’s also shown that plenty of those people are perfectly healthy. “There is a large element of chance in whether incest has a poor outcome,” according to Wilson, the geneticist. It depends on whether those runs of homozygosity contain recessive disease-causing mutations. All of us have some of these runs in our DNA—usually less than 1 percent of the genome in Western populations, higher in cultures where cousin marriage is common. But that number is about 25 percent, Wilson said, in people born from first-degree relatives. While the odds of a genetic disease are much higher, the outcome is far from predetermined.</p><p dir="ltr">Still, these numbers make people wonder. Steve was born with a heart murmur, which required open-heart surgery at ages 13 and 18, though he does not know for sure the cause; heart defects are among the more common birth defects in the general population. He and Michelle were also never able to have children together. Others in the Facebook group have shared their struggles with autoimmune diseases, fibromyalgia, eye problems, and so on—though these are often hard to definitively link to incest. Health problems arising from incest might manifest in any number of ways, depending on exactly which mutations are inherited. “When I go to the doctor and they ask me my family history, I wonder: <em>How much do I need to go into it?</em>” says Mandy, another member of the group. (I am identifying some people by first name only, so they can speak freely about their family and medical histories.) How much experience would a typical doctor have with incest, anyway?</p><p dir="ltr">After Mandy first learned that her father was her mother’s uncle, she went looking for stories about other people like her. All she could find were “gross fantasies” online and medical-journal articles about health problems. She felt very lonely. “<em>I don’t have anybody I can talk to about this</em>,” she remembers thinking. “<em>Nobody knows what to say.</em>” When she found the Facebook group, she could see that she was far from the only one like her. She watched the others cycle, too, through the stages of denial, anger, bargaining, depression, and acceptance.</p><p dir="ltr">She does not know exactly what happened between her biological parents, but her mother was 17, and her mother’s uncle was in his 30s. The discovery, for all the hurt that it surfaced, has helped Mandy reconcile some of her childhood experiences. Unlike Steve, she was raised by her biological mother, and she believed her mother’s husband to be her biological father. He mostly ignored her, but her mother was cruel. She treated Mandy differently than she did her younger brothers. “At least now I have more of an answer as to why,” Mandy told me. “I wasn’t a bad kid and unlovable.”</p><p dir="ltr">Kathy was also raised by her mother, though she had an early inkling that her dad was not her biological dad. Their blood types were incompatible, and she heard rumors about her mother and grandfather. Although her mother’s family was violent and chaotic, she was close to her dad’s family, especially her granny on that side. “They’ve been my rock,” she told me. By the time Kathy took a DNA test confirming that her dad was not her biological dad, she had spent a lifetime distancing herself from her biological family and embracing one with whom she shared no DNA.</p><p dir="ltr">Hers was, in some ways, the opposite journey of adoptees such as Steve, who wanted so badly to know his biological family. But the two of them have become close. Kathy remembers how angry he used to be on his mother’s behalf. She told him that she used to be angry too, but she had to leave it behind. “It’s not going to bring me any peace. It’s not going to bring my mother any peace,” she recalled saying. And it wouldn’t undo what had been done to his mother by her father or her brother so many years ago.</p><hr class="c-section-divider"><p dir="ltr">In the end, Steve was able to identify his biological father, though not through any particular feat of genetic sleuthing. One day, two and a half years after his DNA test, he logged in to AncestryDNA and saw a parent match. It was his mother’s older brother. From the site, he could see that his father-uncle had logged in once, presumably seen that Steve was his son, and—even after Steve sent him a message—never logged back on again.</p><p dir="ltr">By then, his initial anger had started to dissipate. He still felt deeply for his birth mom. Michelle says that her husband has always been a sensitive guy—she makes fun of him for crying at movies—but he’s become even more empathetic. The feelings of worthlessness he initially struggled with has given way to a sense of purpose; he and Michelle now spend hours on the phone talking with others in the support group.</p><p dir="ltr">Steve has still never spoken to his birth mother. He tried writing to her a second time, sending a journal about his life—but she returned it unopened. He messages her occasionally on Facebook, sending photos of grandkids and puppies he’s raised. Every year, he wishes her a happy birthday. She has not replied, but she has also not blocked him.</p><p dir="ltr">When the journal came back unopened, Steve decided to try messaging his mother’s cousin—the other woman he’d initially thought could be his birth mom. He yearned for some kind of connection with someone in his biological family. He wrote to the cousin about his mom—but not his dad—and she actually replied. She told him that she and his mom had been close as children, Steve recounted, but she did not know about a pregnancy. To her, it had seemed like her cousin one day “fell off the face of the Earth,” he says. She agreed to read his journal, and the two of them soon began speaking on the phone about their families.</p><p dir="ltr">Months later, Steve felt like he could finally share the truth about his biological father, and the cousin again accepted him for who he was. They met for the first time in 2017 when she was visiting a nearby town, and she later invited Steve and Michelle to Thanksgiving. Last year, she extended another invitation to a large family gathering. Steve’s immediate biological family was not there, but hers was, and they all knew about him and his mom and his dad. They greeted him with hugs, and they took photos together as a family. “It felt like a relief,” he told me, like a burden had been lifted from him. In this family, he was not a secret. </p>Sarah Zhanghttp://www.theatlantic.com/author/sarah-zhang/?utm_source=feedIllustration by the Atlantic; Sources: The Herald Sun; Courtesy of Steve EdselDNA Tests Are Uncovering the True Prevalence of Incest2024-03-18T11:52:55-04:002024-03-18T12:34:48-04:00People are discovering the truth about their biological parents with DNA—and learning that incest is far more common than many think.tag:theatlantic.com,2024:50-677736<p>The irony undergirding the new wave of obesity drugs is that they initially weren’t created for obesity at all. The weight loss spurred by Ozempic, a diabetes drug in the class of so-called GLP-1 agonists, gave way to Wegovy—the same drug, repackaged for obesity. Zepbound, another medication, soon followed. Now these drugs have a new purpose: heart health.</p><p></p><p>On Friday, the FDA <a href="https://www.fda.gov/news-events/press-announcements/fda-approves-first-treatment-reduce-risk-serious-heart-problems-specifically-adults-obesity-or">approved the use of Wegovy</a> for reducing the risk of heart attack, stroke, and death in adults who are overweight and have cardiovascular disease. The move had been anticipated since the publication of a landmark trial in the fall, which showed the <a href="https://www.theatlantic.com/health/archive/2023/11/ozempic-wegovy-obesity-drugs-benefits/676011/?utm_source=feed">drug’s profound effects on cardiovascular health</a>. The decision could usher in a new era where GLP-1 drugs become mainstream, opening up access to millions of Americans who previously didn’t qualify for Wegovy.</p><p>Some of the obstacles stopping people from getting the drug may also begin to crumble. Insurance companies commonly deny coverage of Wegovy because obesity is seen as a cosmetic concern rather than a medical one, but that argument may not hold up for cardiovascular disease. “This new FDA indication is HUGE,” Katherine Saunders, an obesity-medicine physician at Weill Cornell Medicine, told me in an email. Wegovy may soon be within reach for many more Americans—that is, if they can find it.</p><p></p><p>In practice, Wegovy is maddeningly hard to get hold of. Shortages of injectable semaglutide, the active ingredient in Wegovy and Ozempic, have been ongoing since <a href="https://www.accessdata.fda.gov/scripts/drugshortages/dsp_ActiveIngredientDetails.cfm?AI=Semaglutide%20Injection&st=c">March 2022</a>; currently, most doses of Wegovy are in limited supply. As the popularity of semaglutide has skyrocketed, demand has completely outstripped the capacity of its manufacturer, Novo Nordisk. The drug comes in <a href="https://www.reuters.com/business/healthcare-pharmaceuticals/novo-nordisk-ceo-confident-catalent-will-overcome-wegovy-production-problems-2023-08-25/">injection pens</a> containing a glass vial; “these are not easy products to make,” Lars Fruergaard Jørgensen, the CEO of Novo Nordisk, said in August. In response to the shortages, the company withheld its supply of lower Wegovy doses last year. Because treatment on the medication must begin in low doses, this meant that new patients who wanted to start on Wegovy functionally couldn’t. In January, the company began “more than doubling the amount of the lower-dose strengths” of the drug, a Novo Nordisk spokesperson told me, and it plans to gradually increase overall supply throughout the rest of the year.</p><p>The ongoing shortages have left providers and patients feeling stuck. “It is devastating to prescribe a lifesaving medication for a patient and then find out it’s not covered or we can’t locate supply,” Saunders said. Doctors are scrambling to make do with what’s available. Ivania Rizo, an endocrinologist at Boston Medical Center, told me she has had to turn to older GLP-1 drugs such as Saxenda to <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10338283/">“bridge”</a> patients to higher doses of Wegovy, although now that <a href="https://www.fiercepharma.com/pharma/obesity-drug-shortage-expands-saxenda-novo-nordisk-warns-limited-supply-2023-and-beyond">is in shortage</a> too. Patients can spend each day calling pharmacy after pharmacy in search of one with Wegovy in stock, Rizo said. In desperation, some have turned to <a href="https://www.nytimes.com/2023/05/16/well/live/ozempic-alternatives-semaglutide.html">versions of the drug</a> that are custom-made by compounding pharmacies with little oversight, despite the <a href="https://www.fda.gov/drugs/postmarket-drug-safety-information-patients-and-providers/medications-containing-semaglutide-marketed-type-2-diabetes-or-weight-loss">FDA expressing concerns</a> about them. The shots are supposed to be taken weekly, but others have attempted to stretch their doses beyond that.</p><p>That the new FDA approval could very mainstream obesity drugs may create long-needed pressure to help resolve these shortages. It makes clear that Wegovy is a lifesaving medication not only for people with obesity but also for those with cardiovascular disease—the leading cause of death in the U.S.—putting the impetus on Novo Nordisk to ramp up production. But in the short term, the access issues may persist. “The new approval is very likely to worsen shortages, because the demand for Wegovy will continue to climb—now at an even faster pace,” Saunders said.</p><p>If patients think they’re stuck now, they’re about to feel entrenched. Wegovy is the only obesity drug that has been approved to reduce the risk of heart attacks, but none of its competitors is easily available either. Supplies of certain dosages of Eli Lilly’s Mounjaro, a diabetes drug whose active ingredient is sold for obesity as Zepbound, are <a href="https://www.accessdata.fda.gov/scripts/drugshortages/dsp_ActiveIngredientDetails.cfm?AI=Tirzepatide%20Injection&st=c">limited</a>, and <a href="https://www.fiercepharma.com/pharma/eli-lilly-mounts-clinical-and-commercial-case-tirzepatide-mounjaro-zepbound-come-their-own">shortages</a> are expected later this year. “We need supply to increase dramatically,” Saunders said. Both <a href="https://www.manufacturingdive.com/news/novo-nordisk-manufacturing-glp-1-kalundborg-denmark/699551/">Novo Nordisk</a> and <a href="https://www.manufacturingdive.com/news/eli-lilly-to-grow-production-for-weight-loss-drugs-in-2024-earnings-Q4-concord-north-carolina-plant/706885/#:~:text=To%20keep%20up%20with%20demand,and%20be%20operational%20in%202027.">Eli Lilly</a> have invested heavily in expanding production capacity, but some of the new plants won’t open until 2029.</p><p></p><p>For all of its advantages, the FDA approval has a sobering effect on the unrelenting hype around GLP-1s. So much of the excitement around obesity drugs has focused on the future, as dozens of pharmaceutical companies develop more powerful drugs, and commentators imagine a world without obesity. In the process, the issues of the present have gone overlooked. More drugs won’t make much of a difference if the drugs themselves are out of reach.</p>Yasmin Tayaghttp://www.theatlantic.com/author/yasmin-tayag/?utm_source=feedIllustration by The Atlantic. Source: Getty.The Ozempic Revolution Is Stuck2024-03-12T18:17:00-04:002024-03-13T13:24:43-04:00Millions more Americans are now eligible for obesity drugs. But the injections remain maddeningly hard to find.tag:theatlantic.com,2024:50-677735<p>Measles seems poised to make a comeback in America. Two adults and two children staying at a migrant shelter in Chicago have gotten sick with the disease. A sick kid in Sacramento, California, may have exposed hundreds of people to the virus at the hospital. Three other people were diagnosed in Michigan, along with seven from the same elementary school in Florida. As of Thursday, <a href="https://www.cdc.gov/measles/cases-outbreaks.html">17 states</a> have reported cases to the CDC since the start of the year. (For comparison, that total was 19, plus the District of Columbia, for all of 2023, and just 6 for 2022.) “We’ve got this pile of firewood,” Matthew Ferrari, the director of the Center for Infectious Disease Dynamics at Penn State, told me, “and the more outbreaks that keep happening, the more matches we’re throwing at it.”</p><p>Who’s holding the matchbook? There’s an easy answer to who’s at fault. One of the nation’s political parties, and not the other, <a href="https://www.theatlantic.com/ideas/archive/2022/01/human-sacrifice-ritual-mass-vaccination/621355/?utm_source=feed">turned against vaccines</a> to some extent during the pandemic, leading to <a href="https://www.theatlantic.com/health/archive/2022/12/covid-deaths-anti-vaccine-republican-voters/672575/?utm_source=feed">voter disparities in death rates</a>. One party, and not the other, has a presumptive presidential candidate who threatens to <a href="https://nymag.com/intelligencer/article/trump-school-funding-vaccine-mandates.html">punish</a> any school that infringes on parental rights by requiring immunizations. And one party, but not the other, appointed a <a href="https://www.theatlantic.com/health/archive/2024/02/florida-measles-outbreak-school-children-vaccination/677539/?utm_source=feed">vaccine-skeptical surgeon general</a> in Florida who recently sidestepped standard public-health advice in the middle of an outbreak. The message from Republicans, as <em>The Washington Post</em>’s Alexandra Petri joked in a recent column, can sound like this: <a href="https://www.washingtonpost.com/opinions/2024/03/08/measles-resurgence-magazine-profile-satire/">“We want measles <em>in</em> the schools and books <em>out</em> of them!”</a></p><p>But the politics of vaccination, however grotesque it may be in 2024, obscures what’s really going on. It’s true that vaccine attitudes have become more polarized. Conservative parents in particular may be opting out of school vaccine requirements in higher numbers than they were before. In the blood-red state of Idaho, for example, <a href="https://apnews.com/article/vaccines-waivers-schools-measles-idaho-e7015d8fd38ec80802eeae350755a402">more than 12 percent</a> of kindergartners received exemptions from the rules for the 2022–23 school year, a staggering rate of refusal that is up by half from where it was just a few years ago. Politicized recalcitrance is unfortunate, to say the least, and it can be deadly. Even so, America’s political divides are simply not the cause of any recent measles outbreak. The virus has returned amid a swirl of global health inequities. Any foothold that it finds in the U.S. will be where hyperlocal social norms, not culture-war debates, are causing gaps in vaccine access and acceptance. The more this fact is overlooked, the more we’re all at risk.</p><p>Consider where the latest measles cases have been sprouting up: By and large, the recent outbreaks have been a blue-state phenomenon. (Idaho has so far been untouched; the same is true for Utah, with the nation’s third-highest school-vaccine-exemption rate.) Zoom into the county level, and you’ll find that the pattern is repeated: Measles isn’t picking on Republican communities; if anything, it seems to be avoiding them. The recent outbreak in Florida unfolded not in a conservative area such as Sarasota, where vaccination coverage has been lagging, but rather in Biden-friendly Broward County, at a school where <a href="https://www.miamiherald.com/news/local/education/article285751501.html">97 percent</a> of the students have received at least one MMR shot. Similarly, the recent cases in Michigan turned up not in any of the state’s MAGA-voting, <a href="https://www.michigan.gov/mdhhs/-/media/Project/Websites/mdhhs/Adult-and-Childrens-Services/Children-and-Families/Immunization-Information/School-Waiver-Information/Kindergarten-Immunization-Waivers-by-County.pdf">vaccine-forgoing</a> areas but among the diverse and relatively left-wing populations in and around Ann Arbor and Detroit.</p><p>Stepping back to look at the country as a whole, one can’t even find a strong connection—or, really, any consistent link at all—between U.S. measles outbreaks, year to year, and U.S. children’s vaccination rates. Sure, the past three years for which we have student-immunization data might seem to show a pattern: Starting in the fall of 2020, the average rate of MMR coverage for incoming kindergarteners did drop, if only by a little bit, from 93.9 to 93.1 percent; at the same time, the annual number of reported measles cases went up almost tenfold, from 13 to 121. But stretch that window back one more year, and the relationship appears to be reversed. In 2019, America was doing great in terms of measles vaccination—across the country, 95.2 percent of kindergartners were getting immunized, according to the CDC—and yet, in spite of this fantastic progress, measles cases were exploding. More than 1,200 Americans got sick with the disease that year, as measles took its greatest toll in a generation.</p><p>It’s not that our high measles-vaccination coverage didn’t matter then or that our slightly lower coverage doesn’t matter now. Vaccination rates <em>should</em> be higher; this is always true. In the face of such a contagious disease, 95 percent would be good; 99 percent much better. When fewer people are protected, more people can get sick. In Matthew Ferrari’s terms, a dropping immunization rate means the piles of firewood are getting bigger. If and when the flames do ignite, they could end up reaching farther, and burning longer, than they would have just a year or two ago. In the midst of any outbreak large enough, where thousands are affected, children will die.</p><p data-id="injected-recirculation-link"><i>[<a href="https://www.theatlantic.com/health/archive/2023/02/us-covid-vaccine-obsession-future-variants/672933/?utm_source=feed">Read: The good news about vaccine hesitancy</a>]</i></p><p>Despite America’s <a href="https://www.theatlantic.com/health/archive/2023/02/us-covid-vaccine-obsession-future-variants/672933/?utm_source=feed">fevered national conversation about vaccines</a>, however, rates of uptake simply haven’t changed that much. Even with the <a href="https://www.pbs.org/newshour/show/measles-outbreak-raises-concerns-about-drop-in-vaccinations">recent divot</a> in our national vaccine rates, the country remains in broad agreement on the value of immunity: 93 percent of America’s kindergartners are getting measles shots, a rate that has barely budged for decades. The sheer resilience of this norm should not be downplayed or ignored or, even worse, reimagined as a state of grace from which we’ve fallen. Our protection remains strong. In Florida, the surgeon general’s lackadaisical response to the crisis at the Broward County elementary school did not produce a single extra case of the disease, in spite of <a href="https://www.theguardian.com/us-news/2024/mar/03/florida-measles-outbreak-preventable">grim</a> <a href="https://www.scientificamerican.com/article/florida-surgeon-general-risks-making-a-dangerous-measles-outbreak-much-worse/">predictions</a> to the contrary, almost certainly thanks to how many kids are already vaccinated.</p><p>At the same time, however, measles has been thriving overseas. Its reemergence in America is not a function of the nation’s political divides, but of the disease’s global prevalence. Europe had almost 60,000 cases last year, up from about 900 in 2022. The World Health Organization reports that the number of reported cases around the world surged to <a href="https://www.cbsnews.com/news/measles-cases-rose-worldwide-2023-who/">306,000</a>, after having dropped to a record low of 123,000 in 2021. As the pandemic has made apparent, our world is connected via pathogens: Large outbreaks in other countries, where vaccination coverage may be low, have a tendency to seed tiny outbreaks in the U.S., where coverage has been pretty high, but narrow and persistent cracks in our defenses still remain. (In 2022, more than half of the world's unvaccinated infants were concentrated in just <a href="https://www.cdc.gov/mmwr/volumes/72/wr/mm7246a3.htm">10 countries</a>; some of these are measles hotspots at this moment.) This also helps explain why so many Americans got measles in 2019. That was a catastrophic year for measles around the world, with 873,000 reported cases in total, the most since 1994. We had pretty good protection then, but the virus was everywhere—and so, the virus was here.</p><p data-id="injected-recirculation-link"><i>[<a href="https://www.theatlantic.com/health/archive/2024/02/florida-measles-outbreak-school-children-vaccination/677539/?utm_source=feed">Read: Florida’s experiment with measles</a>]</i></p><p>In high-income countries such as the U.S., Ferrari told me, “clustering of risk” tends to be the source of measles outbreaks more than minor changes in vaccine coverage overall. Even in 2019, when more than 95 percent of American kindergarteners were getting immunized, we still had pockets of exposure where protection happened to be weakest. By far the biggest outbreak from that year occurred among Hasidic Jewish populations in New York State. Measles was imported via <a href="https://www.nejm.org/doi/full/10.1056/NEJMoa1912514">Israel</a> from the hot spot of <a href="https://www.cdc.gov/mmwr/volumes/69/wr/pdfs/mm6918a3-H.pdf">Ukraine</a>, and took off within a group whose vaccination rates were much, much lower than their neighbors’. In the end, <a href="https://www.cdc.gov/mmwr/volumes/68/wr/mm6840e2.htm">more than 1,100 people</a> were infected during that outbreak, which began in October 2018 and lasted for nearly a year. “A national vaccination rate has one kind of meaning, but all outbreaks are local outbreaks,” Noel Brewer, a professor at the University of North Carolina at Chapel Hill and a member of the federal Advisory Committee on Immunization Practices, told me. “They happen on a specific street in a specific group of houses, where a group of people live and interact with each other. And those rates of vaccination in that specific place can drop well below the rate of coverage that will forestall an outbreak.”</p><p>We’ve seen this time and time again over the past decade. When bigger outbreaks do occur in the U.S., they tend to happen in tight-knit communities, where immunization norms are radically out of sync with those of the rest of American society, politics aside. In 2014, when an outbreak of nearly 400 cases took hold in Ohio, almost entirely <a href="https://www.nejm.org/doi/full/10.1056/nejmoa1602295">within the Amish community</a>, the local vaccination rate was estimated to be about 14 percent. (The statewide number for young children at that time was more than 95 percent.) In 2011 and 2017, measles broke out among the large Somali American community in Minnesota, where <a href="https://www.statnews.com/2017/05/08/measles-vaccines-somali/">anti-vaccine messaging has been intense</a>, and where immunization rates for 2-year-olds dropped from <a href="https://www.bmj.com/content/357/bmj.j2378">92 percent</a> 20 years ago to <a href="https://sahanjournal.com/health/measles-mmr-vaccine-minnesota-department-of-health-outreach-somali/">35 percent</a> in 2021. An outbreak from the end of 2022, affecting 85 people in and around Columbus, Ohio, may well be <a href="https://sahanjournal.com/health/measles-mmr-vaccine-minnesota-department-of-health-outreach-somali/">linked</a> to the nation’s second-biggest community of Somalis.</p><p>Care must be taken in how these outbreaks are discussed. In Minnesota, for example, state health officials have avoided calling out the Somali community, <a href="https://sahanjournal.com/health/measles-mmr-vaccine-minnesota-department-of-health-outreach-somali/">for fear of stigmatizing</a>. But another sort of trouble may arise when Americans overlook exactly who’s at risk, and exactly why. Experts broadly agree that the most effective way to deal with local outbreaks is with local interventions. Brewer pointed out that during the 2019 outbreak in New York, for example, nurses who belonged to local Jewish congregations took on the role of vaccine advocates. In Minnesota, the Department of Health has brought on more Somali staff, who coordinate with local Somali radio and TV stations to share its message. Yet these efforts can be obscured by news coverage of the crisis that points to a growing anti-science movement and parents giving up on vaccination all across the land. When measles spread among New York’s orthodox Jews, <em>The New York Times</em> reported on “<a href="https://www.nytimes.com/2019/06/13/nyregion/measles-outbreak-new-york.html">an anti-vaccine fervor on the left</a> that is increasingly worrying health authorities.” When the virus hit Columbus, <em>NBC News</em> noted that it was “happening as resistance to school vaccination requirements is <a href="https://www.nbcnews.com/health/health-news/cdc-director-warns-vaccine-misinformation-public-health-threat-rcna61245">spreading across the country</a>.”</p><p>Two different public-health responses can be undertaken in concert, the experts told me: You treat the problem at its source, and you also take the chance to highlight broader trends. A spate of measles cases in one community becomes an opportunity for pushing vaccination everywhere. “That’s always an important thing for us to do,” Ferrari said. Even so, the impulse to <em>nationalize</em> the problem will have its own, infelicitous effects. First, it’s meaningfully misleading. By catastrophizing subtle shifts in vaccination rates, we frighten many parents for no reason. By insisting that every tiny outbreak is a product of our national politics, we distract attention from the smaller measures that can and should be taken—well ahead of any upsurge of disease—to address hyperlocal vaccination crises. And by exaggerating the scale of our divisions—by asserting that we’ve seen a <a href="https://www.cbsnews.com/news/anti-vaccine-science-politics-2024/">dangerous shift</a> on a massive scale, or an <a href="https://nymag.com/intelligencer/2022/10/how-vaccine-skeptics-took-over-the-republican-party.html">anti-vaccine takeover</a> of the Republican Party—we may end up worsening the very problem that worries us the most.</p><p>We are a highly vaccinated nation, our politics notwithstanding. Telling people otherwise only fosters more division; it feeds the feeling that taking or refusing measles shots is an important mode of self-expression. It further polarizes health behavior, which can only widen the cracks in our defenses. “We have become quite militant and moralistic about vaccination,” Brewer told me, “and we probably would do well to be less absolute.” Measles outbreaks overseas are growing; measles outbreaks here will follow. Their specific causes ought not be ignored.</p>Daniel Engberhttp://www.theatlantic.com/author/daniel-engber/?utm_source=feedIllustration by The AtlanticThe Return of Measles2024-03-12T15:55:00-04:002024-03-12T18:04:25-04:00Cases are creeping up in America, and not because of politics. <strong> </strong>tag:theatlantic.com,2024:50-677689<p>Recently, a photo of rice left me confused. The rice itself looked tasty enough—fluffy, well formed—but its oddly fleshy hue gave me the creeps. According to the scientists who’d developed it, each pink-tinged grain was seeded with muscle and fat cells from a cow, imparting a nutty, umami flavor.</p><p></p><p>In one sense, this “<a href="https://www.eurekalert.org/news-releases/1033922">beef rice</a>” was just another example of lab-grown meat, touted as a way to eat animals without the ethical and environmental impacts. Though not yet commercially available, the rice was developed by researchers in Korea as a nutrition-dense food that can be produced sustainably, at least more so than beef itself. Although it has a more brittle texture than normal rice, it can be cooked and served in the same way. Yet in another sense, this rice was entirely different. Lab-grown meat aims to replicate conventional meat in every dimension, including taste, nutrition, and appearance. Beef rice doesn’t even try.</p><p></p><p>Maybe that’s a good thing. Lab-grown meat, also widely known as cultivated meat, has long been heralded as <a href="https://www.nytimes.com/2013/08/06/science/a-lab-grown-burger-gets-a-taste-test.html">the future of food</a>. But so far, the goal of perfectly replicating meat as we know it—toothy, sinewy, and sometimes bloody—has proved impractical and expensive. Once-abundant <a href="https://agfundernews.com/preliminary-agfunder-data-point-to-78-decline-in-cultivated-meat-funding-in-2023-investors-blame-general-risk-aversion#:~:text=With%20Finless%20Foods%20rumored%20to,seafood%20companies%20trying%20to%20raise">funding has dried up</a>, and this week, Florida moved toward becoming the <a href="https://floridaphoenix.com/2024/03/06/florida-now-poised-to-become-the-first-state-in-the-nation-to-ban-lab-grown-meat/">first state to ban sales of cultivated meat</a>. It seems unlikely that whole cuts of cultivated meat will be showing up on people’s plates anytime soon—but maybe something like beef rice could. The most promising future of lab-grown meat may not look like meat at all, at least as we’ve always known it.</p><p></p><p>The promise of cultivated meat is that you can have your steak and eat it too. Unlike the meatless offerings at your grocery store, cultivated meat <em>is </em>meat—just created without killing any animals. But the science just isn’t there yet. Companies have more or less figured out the first step, taking a sample of cells from a live animal or egg and propagating them in a tank filled with a nutrient-rich broth. Though not cheaply: By one estimate, creating a slurry of cultivated cells costs <a href="https://thecounter.org/lab-grown-cultivated-meat-cost-at-scale/">$17 a pound or more to produce</a>.</p><p></p><p>The next step has proved prohibitively challenging: coaxing that sludge of cells to mature into different types—fat, muscle, connective tissue—and arranging them in a structure resembling a solid cut of meat. Usually, the cells need a three-dimensional platform to guide their growth, known as a scaffold. “It’s something that is very easy to get wrong and hard to get right,” Claire Bomkamp, a senior scientist at the Good Food Institute, a nonprofit supporting meat alternatives, told me. So far, a few companies have served up proofs of concept: In June, the United States <a href="https://www.reuters.com/business/retail-consumer/upside-foods-good-meat-receive-final-usda-approval-sell-cultivated-meat-2023-06-21/#:~:text=The%20FDA%20issued%20its%20approvals,Good%20Meat%20in%20March%202023.">approved the sale of cultivated chicken</a> from Upside Foods and Good Meat. However, it is <a href="https://www.bloomberg.com/news/articles/2024-02-01/upside-foods-lab-grown-meat-is-off-the-menu-at-bar-crenn-its-sole-venue?sref=BGQFqz7X">virtually impossible to come by</a> now.</p><p></p><p>The basic science of lab-grown meat can be used for more than just succulent chicken breasts and medium-rare steaks. Cells grown in a tank function essentially like ground meat, imparting a <a href="https://gfi.org/solutions/hybrids-blends-nutrition-taste-cost-sustainability/">meaty flavor and mouthfeel</a> to whatever they are added to, behaving more like an ingredient or a seasoning than a food product. Hybrid meat products, made by mixing a small amount of cultivated-meat cells with other ingredients, are promising because they would be <a href="https://www.google.com/url?q=https://www.wired.com/story/hybrid-meat-blended-burgers-upside-foods-ivy-farm-technologies/&sa=D&source=docs&ust=1709915770812857&usg=AOvVaw0trhsimERxcA_QQalND6Gd">more cost-effective</a> than entire lab-grown steaks or chicken breasts but meatier than purely plant-based meat.</p><p></p><p>Already, the start-up SciFi Foods is producing what has been described as a “<a href="https://www.foodnavigator-usa.com/Article/2022/07/13/scifi-foods-claims-industry-first-for-cultivated-beef-says-immediate-future-is-hybrid-for-cell-cultured-meat">fatty meat paste</a>” that is intended to be mixed with plant-based ingredients to make burgers. Only small amounts are needed to make the burgers beefy; each <a href="https://www.foodnavigator-usa.com/Article/2022/07/13/scifi-foods-claims-industry-first-for-cultivated-beef-says-immediate-future-is-hybrid-for-cell-cultured-meat">costs less than $10</a> to make, according to the company—still considerably more than a normal beef patty, but the prices should come down over time. Maybe it sounds weird, but that’s not so different from imitation crab—which doesn’t contain much or any crab at all. A similar premise underlies the <a href="https://www.theatlantic.com/health/archive/2023/02/plant-based-meat-lab-grown-animal-fat-flavor/673190/?utm_source=feed">plant-based bacon laced with cultivated pork fat</a> that I tried last year. Was it meat? I’m not sure. Did it taste like it? Absolutely.</p><p></p><p>Meat can be so much more than what we’ve always known. “We don’t have to make meat the same way that it’s always come out of an animal,” Bomkamp said. “We can be a little bit more expansive in what our definition of meat is.” Beef rice, which essentially uses rice as a miniature scaffold to grow cow cells, falls into this category. It isn’t particularly meaty—only 0.5 percent of each grain is cow—but the scientists who developed it say the proportion could change in future iterations. It’s framed as a way to feed people in “underdeveloped countries, during war, and in space.”</p><p></p><p>Eventually, cultivated meat could impart a whiff of meatiness to blander foods, creating new, meat-<em>ish</em> products in the process that are more sustainable than regular meat and more nutritious than plants. Beef rice is one option; <a href="https://www.psu.edu/news/institutes-energy-and-environment/story/growing-impact-podcast-probes-world-cellular-agriculture/">meat grown on </a><a href="https://www.psu.edu/news/institutes-energy-and-environment/story/growing-impact-podcast-probes-world-cellular-agriculture/">mushroom</a> roots is in development. Even stranger foods are possible. Bomkamp envisions using the technology to make thin sheets of seafood—combining elements of salmon, tuna, and shrimp—to wrap around a rainbow roll of sushi. In this scenario, cultivated meat probably won’t save the planet from climate change and animal suffering. “It wouldn’t serve its original function of being a direct replacement for commercial meat,” Daniel Rosenfeld, who studies perceptions of cultivated meat at UCLA, told me. But at the very least, it could provide another dinner option.</p><p>Of course, it’s in the interest of the cultivated-meat industry to suggest that cultivated meat isn’t just outright doomed. No doubt some vegetarians would cringe at the thought, as would some dedicated carnivores. But considering how much meat Americans eat, it’s not hard to imagine a future in which cultivated cells satisfy people searching for a new kind of meat product. Imagine the salad you could make with chicken cells grown inside arugula, or bread baked with bacon-infused wheat. But should those prove too difficult to produce, I’d happily take a bowl of beef rice, in all its flesh-tinged glory.</p>Yasmin Tayaghttp://www.theatlantic.com/author/yasmin-tayag/?utm_source=feedIllustration by Katie Martin. Source: Getty.Everything Can Be Meat2024-03-08T12:29:00-05:002024-03-11T15:00:22-04:00The most promising future of lab-grown meat may not look like meat at all.tag:theatlantic.com,2024:39-677471<p><i>Photographs by Fumi Nagasaka</i></p><p data-flatplan-paragraph="true"><small><i data-stringify-type="italic">This article was featured in the One Story to Read Today newsletter. </i><i data-stringify-type="italic"><a data-event-element="inline link" data-sk="tooltip_parent" data-stringify-link="https://www.theatlantic.com/newsletters/sign-up/one-story-to-read-today/" delay="150" href="https://www.theatlantic.com/newsletters/sign-up/one-story-to-read-today/?utm_source=feed" rel="noopener noreferrer" target="_blank">Sign up for it here</a></i><i data-stringify-type="italic">.</i></small></p><p class="dropcap">T<span class="smallcaps">hey call it</span> the Purge.</p><p>You have experienced, in a modest way, something like it in the waning days of a bad cold, when your lungs finally expel their accumulated gunk. The rattle in your chest quiets. Your sinuses clear. You smell again: the animal sweetness of your children’s hair, the metallic breeze stirring a late-summer night. Your body, which oozed and groaned under the yoke of illness, is now a perfectly humming machine. Living is easy—everything is easy. How wonderful it is to breathe, simply breathe.</p><aside class="callout-placeholder" data-source="magazine-issue"></aside><p>Imagine, though, that you had never been able to simply breathe. Imagine that mucus—thick, copious, dark—had been accumulating since the moment you were born, thwarting air and trapping microbes to fester inside your lungs. That you spent an hour each day physically pounding the mucus out of your airways, but even then, your lung function would spiral only downward, in what amounted to a long, slow asphyxiation. This was what it once meant to be born with cystic fibrosis.</p><p>Then, in the fall of 2019, a new triple combination of drugs began making its way into the hands of people with the genetic disease. Trikafta corrects the misshapen protein that causes cystic fibrosis; this molecular tweak thins mucus in the lungs so it can be coughed up easily. In a matter of hours, patients who took it began to cough—and cough and cough and cough in what they later started calling the Purge. They hacked up at work, at home, in their car, in bed at night. It’s not that they were sick; if anything, it was the opposite: They were becoming well. In the days that followed, their lungs were cleansed of a tarlike mucus, and the small tasks of daily life that had been so difficult became unthinkingly easy. They ran up the stairs. They ran after their kids. They ran 10Ks. They <a href="https://www.cff.org/community-posts/2021-09/because-trikafta-i-am-training-my-first-marathon">ran marathons</a>.</p><p>Cystic fibrosis once all but guaranteed an early death. When the disease was first identified, in the 1930s, most babies born with CF died in infancy. The next decades were a grind of incremental medical progress: A child born with CF in the ’50s could expect to live until age 5. In the ’70s, age 10. In the early 2000s, age 35. With Trikafta came a quantum leap. Today, those who begin taking the drug in early adolescence, a <a href="https://cysticfibrosisnewstoday.com/news/cf-patients-kaftrio-trikafta-may-enjoy-near-normal-lifespan/#:~:text=In%20a%20scenario%20where%20treatment,on%20best%20supportive%20care%20alone">recent study</a> projected, can expect to survive to age 82.5—an essentially normal life span.</p><p>CF was one of the first diseases to be traced to a specific gene, and Trikafta is one of the first drugs designed for a specific, inherited mutation. It is not a cure, and it doesn’t work for all patients. But a substantial majority of the 40,000 Americans with CF have now lived through a miracle—a thrilling but disorienting miracle. Where they once prepared for death, they now have to prepare for life. “It’s like the opposite of a terminal diagnosis,” Jenny Livingston told me.</p><p>Jenny spent her 20s in and out of the hospital for CF-related lung infections. During her frequent weeks-long stays, she made some of her best friends in the CF ward, only to watch them succumb, one by one, to the disease that she knew would eventually kill her too. More than anything, she hoped to live long enough to see her daughter graduate from high school.</p><p data-id="injected-recirculation-link"><i>[<a href="https://www.theatlantic.com/magazine/archive/2020/12/the-last-children-of-down-syndrome/616928/?utm_source=feed">From the December 2020 issue: Sarah Zhang on the last children of Down syndrome</a>]</i></p><p>Today, Jenny is 36. Four years into taking Trikafta, she’s the healthiest she’s been in her adult life. Her daughter is 14, a lanky high-school freshman. They’re both obsessed with Harry Styles, and after Jenny started on Trikafta, they flew together <a href="https://www.tiktok.com/@jenny.lungsnroses/video/7028613348631678254">to see him live</a>—twice. They learned to hunt deer with Jenny’s partner, Randy. They often go up into the aspen- and fir-topped mountains that overlook their little town in central Utah. Jenny’s last hospitalization—four years ago, just before she started Trikafta—is now more distant in time than her daughter’s future graduation.</p><p>Having lived one life defined by cystic fibrosis, Jenny wonders: What is she going to do with her second life?</p><p class="dropcap"><span class="smallcaps">Jenny was born </span>in 1987, the youngest of her parents’ five children together and the third to have cystic fibrosis. Given the family history, the doctors knew to test her as an infant, wrapping her forearm in plastic until a sheen of sweat appeared on her skin: the classic “sweat test” for cystic fibrosis. The faulty protein in CF cannot control the balance of salt and water in the body, which results in mucus that is unusually thick and sweat that is unusually salty. In medieval Europe, centuries before anyone understood why, a <a href="https://www.cuimc.columbia.edu/news/legacy-changing-medicine-cystic-fibrosis">proverb</a> foretold the fate of children with salt on their skin: “Woe to the child who tastes salty from a kiss on the brow, for he is cursed and soon will die.”</p><p>The 1980s, suffice it to say, were not the Middle Ages. By the time Jenny was born, her two older sisters with cystic fibrosis—Shannan, 8, and Teresa, 7—were on a strict schedule of mucus-clearing chest therapy and medications that had kept them alive past toddlerhood. Shannan wasn’t diagnosed until she was 13 months old. “I knew when she was born that there was something wrong,” their mother, Lisa, told me. As a newborn, Shannan projectile vomited and blew out her diapers constantly. When she got older, she was often so insatiably hungry that she would cry when a spoon scraped the bottom of a near-empty food jar. She scarfed down five pancakes at a time. In the baby photos in Lisa’s scrapbook, she is all skinny legs and big, swollen belly—a classic sign of malnutrition.</p><p>Shannan <i>was</i> starving, it turned out. Food was passing through her body undigested because her pancreas had been damaged as a result of thick mucus blocking the ducts that release digestive enzymes. Cystic fibrosis was originally named, in fact, for the fibrous cysts that a 1930s pathologist saw in the pancreases of babies who had died. An early epiphany helped doctors overcome the malfunctioning pancreas, though: The missing enzymes could be replaced with pills. By the time of Shannan’s diagnosis, CF was known as a disease of the lungs, in which sticky mucus made fertile ground for bacteria, and the cycle of infection and scarring, infection and scarring would eventually cause the lungs to fail.</p><p>Lisa relayed the news of Shannan’s diagnosis over the phone to her husband, Tom, who was at work. As she repeated the doctor’s words, their awful meaning sank in. Their daughter would not live long. They would watch her die. In that moment, the two of them broke down on the phone, the physical distance between them collapsed by grief.</p><p>Shannan died when she was 14. “I remember the sound of her oxygen machine more than her voice,” Jenny told me. The rumble and puff of the machine had run in the background of their home, punctuated by chronic coughs from all three girls with CF. But neither Teresa nor Jenny was ever as sick as Shannan was in childhood—due perhaps to chance or to being diagnosed and starting treatments earlier in life. Even when they were newborns, their mother coaxed applesauce sprinkled with enzymes into their mouth, so they could absorb nutrients from their milk.</p><p>Not long after Shannan died, Lisa and Tom divorced—their marriage had been strained even before the loss of their daughter—and they both eventually remarried. Despite the upheavals in her family, Jenny remembers her childhood as quite normal. Yes, she had to take the enzymes with every meal, and she had to clear her lungs of mucus every day—first by having her parents pound on her chest and back and later by using an oscillating vest that shook her body. As inhaled CF drugs were developed, they were added to her daily regimen. She went to the hospital for annual preventive “tune-ups,” but she was never sick enough to need emergency hospitalizations, and CF did not seem to hold her back.</p><p>Lisa thinks of Jenny as her sassy daughter. Her youngest was always stubborn, always a go-getter. Through the Make-A-Wish Foundation, she was able to get a horse, which she entered in local shows and rode through the foothills just outside town. In the summer, the salt from the dried sweat on her arms became crystals that glimmered in the sun, a subtle reminder of the disease still inside her. The invincibility of youth, however, made her think she had perhaps escaped her oldest sister’s fate.</p><p>At 19, Jenny married a local boy she had fallen in love with, and at 21, she was shocked to find herself pregnant: “A very, very happy surprise.” She had always longed to be a mother. As a young girl, she once drew a picture proclaiming that she would grow up to have six children. The drawing “broke my heart,” says her stepmother, Candy. Even if Jenny lived long enough, cystic fibrosis often causes fertility issues—in many women, thickened cervical mucus is thought to prevent pregnancy, and in almost all men, sperm ducts <a href="https://www.cff.org/managing-cf/fertility-men-cf">never develop</a> because of blockages that occur in utero. And at the time, doctors often recommended against pregnancy for health reasons.</p><p>But Jenny pushed the worries out of her mind. She was simply happy. She set up a crib and painted the nursery. In retrospect, the fevers and shortness of breath she began to feel were not just the normal discomforts of pregnancy, but she didn’t clock it then. She had an uneventful labor, and gave birth to a healthy baby girl. They named her Morgan.</p><p class="dropcap"><span class="smallcaps">The trouble started </span>in the following months. Six weeks after giving birth, Jenny went back to work. Between nursing and soothing and diapering a newborn, she could no longer keep up her treatment routine. She sometimes also skipped medications when she couldn’t afford them with the pay from her job as a bank teller and her husband’s as a welder.</p><p>Then she caught a bug. It was 2009, the year of swine flu, so it could have been that or a more mundane cold, but either way, it triggered something deep in her lungs. She started feeling short of breath. By the time she got to a CF specialist at a hospital two hours away, in Salt Lake City, she could not walk from the car to the front door. She was too weak to stand for her lung-function test. She collapsed into her hospital bed, and for the next several days, she was unable to use the toilet or shower on her own. Convinced that she would die 100 miles from her three-month-old daughter, she had a terrible revelation: “This is why they said ‘Don’t have kids.’ ”</p><p>This was Jenny’s first CF pulmonary exacerbation, when lung function plummets from an acute infection. Doctors inserted her first PICC line, a catheter that runs from the upper arm to the heart, delivers antibiotics, and stays in place longer than an IV. She recovered, but just months later, she was back in the hospital with another exacerbation. Then another and another, and on this went for the next several years. Jenny counted for me the PICC-line scars still visible as white dots on each arm—at least 10 on the left, 16 on the right. When the veins in her arms started to reject PICC lines, doctors placed a port under her right collarbone for easy access to her central vein.</p><figure class="full-width"><img alt="2 photos: patients in scrubs with cucumber slices on eyes and face masks lie upside down on hospital bed; woman in hospital bed with blonde toddler in pink onesie" height="340" src="https://cdn.theatlantic.com/media/img/posts/2024/03/Zhang_2/470e00bd8.png" width="928">
<figcaption class="caption"><em>Left</em>: As a child, during one of her preventive “tune-ups,” Jenny (<em>center</em>) passed the time in the hospital doing avocado face masks with her sister Teresa and Kara Hansen, another CF patient. <em>Right</em>: Jenny’s daughter, Morgan, visiting her at the hospital in 2011. (Courtesy of Jenny Livingston)</figcaption>
</figure><p>Each infection scarred her lungs; each exacerbation eroded her lung function. The disease that had been a minor plot point in her life became one of its major storylines, and the people in the hospital became recurring characters. At the University of Utah’s CF center, she met Warren, one of her best friends, whom she came to know so well, she could identify his cough through the hospital walls. He was “so dang funny,” Jenny said, unafraid of joking about the death that would befall them both. Where she was a rule follower, he was a troublemaker. Once, he commandeered a hospital floor scrubber, waving at patients in their rooms as he drove past. Another time, he managed to procure a bootleg copy of <i>The Avengers</i>. Stuck in the hospital over the film’s opening weekend, he and the other CF patients organized a movie night. James brought his Xbox to play the bootleg DVD. Heather (“the biggest Swiftie”) and Angie (“gorgeous, tall blonde”) joined too. They found a waiting room with a TV, and the nurses passed around microwave popcorn.</p><p>Jenny and her friends made sure to sit several feet apart. People with cystic fibrosis have had to <a href="https://healthmatch.io/blog/6-feet-apart-how-cystic-fibrosis-research-helped-establish-social-distancing">practice</a> social distancing since long before COVID, because they are considered a danger to one another. Their lungs harbor destructive and often antibiotic-resistant bacteria that can become impossible to uproot once established. Certain names are spoken with an air of doom: <i>Burkholderia cepacia</i>, <i>Pseudomonas aeruginosa</i>. When doctors in the 1990s realized that people with CF were infecting and killing one another by simply gathering, they stopped allowing patients to go within several feet of one another unmasked. Camps for children with cystic fibrosis, which Jenny still <a href="https://cysticfibrosisnewstoday.com/forums/forums/topic/cf-camp-memories/">remembers fondly</a>, were all shut down. In the hospital, she once again found a community in the disease that was taking over her life. But many of those friendships ended too soon: Of the five people at the <i>Avengers</i> movie night, Jenny is the only one alive today. Warren, James, Heather, and Angie have all died.</p><p>As Jenny struggled with her health, the new reality of chronic illness took a toll on her marriage. She and her husband eventually divorced. After a particularly harrowing hospitalization in 2012, her doctors encouraged her to stop working and go on disability. Something in her life had to give, they told her, or it would be her body. Her disease and her daughter became her whole world.</p><p>Even as a young child, Morgan could sense when her mom was heading toward another exacerbation. If she noticed that Jenny was more tired than usual or coughing more than usual, she began to dread their coming separation. When she was 3 years old, she asked, “Do all mommies live in the hospital sometimes?” When she was 6, after Warren’s death, she asked, “Can you die from CF?” She understood that their existence together was fragile.</p><p>Jenny answered truthfully: Yes. But she assured her daughter that she was taking care of herself as best she could. Still, she made plans for what was probably inevitable. If she died, her daughter would live with her aunt and uncle. If she died, she wanted a funeral just like Warren’s, with music, candy, and an open mic for everyone to share their favorite memories.</p><p class="dropcap"><span class="smallcaps">A cure for </span>cystic fibrosis had supposedly been imminent since 1989, when Jenny turned 2. That year, scientists identified the recessive gene behind cystic fibrosis, which encodes a protein called CFTR that controls the flow of salt and water. The discovery seemed so explosive that a Reuters reporter rushed to publish the scoop more than two weeks before the scientific papers were due to come out; two press conferences followed.</p><p>In the decades after, however, researchers came to understand the wide gulf between identifying a genetic problem and knowing how to solve it. Early attempts in the ’90s at using gene therapy to fix mutations failed again and again, both for CF and for other genetic conditions that once seemed tantalizingly close to a cure.</p><p>Then, CF researchers changed tack: Instead of correcting the gene, why not correct the mutated protein itself with small fixer molecules? This had never been done before—with any disease—but the nonprofit Cystic Fibrosis Foundation deemed the strategy promising enough to strike an unusual venture-philanthropy agreement with a company that would attempt it, which was eventually bought by Vertex Pharmaceuticals. The foundation funded the research in return for a share of the revenue.</p><p>The move paid off. In 2012, Vertex released a drug called Kalydeco that worked stunningly well—improving lung function and erasing many symptoms in the small group of CF patients who could take it. That was the catch: The FDA approved Kalydeco only for the roughly 4 percent of people with CF who carried a rare and specific mutation. Still, it provided a jolt of optimism. Kalydeco was the first drug ever tailored to a person’s inherited genetic mutation, and the breakthrough portended a new age of “personalized medicine.” It also inspired other patient-advocacy groups to copy the venture-philanthropy model. In 2014, the Cystic Fibrosis Foundation sold the rights to royalties from Kalydeco and future Vertex CF drugs for $3.3 billion, which it could invest in new research.</p><p>After Kalydeco, the next CF mutation to target was obvious. About 1,700 unique mutations have been found in people with CF, but some 90 percent of patients—including Jenny—carry at least one copy of a mutation, known as F508del, that leaves their protein channels too seriously distorted for Kalydeco alone to correct. Fixing this shape would be a much bigger task. In 2013, Jenny joined the clinical trial for a two-drug combination from Vertex, made up of Kalydeco plus a second fixer molecule. It failed to especially improve her symptoms, though it did work enough to stabilize her falling lung function. “It seemed to push pause,” she said. She stopped getting sicker, but she was still sick. The research went on.</p><p>A few years later, word began spreading of a forthcoming three-drug combination from Vertex. In clinical trials, neither patients nor doctors are told who is on the placebo and who is on the experimental drug. But in this trial, everyone could tell. The triple combo made patients’ lung function jump by a shocking 10 percentage points. Overnight, they woke up smelling for the first time the distinctive scent of their home. They could even taste their sweat becoming less salty. This was Trikafta.</p><p>In the fall of 2019, Trikafta was <a href="https://www.fda.gov/news-events/press-announcements/fda-approves-new-breakthrough-therapy-cystic-fibrosis">approved</a> by the FDA just 10 days before a large annual gathering of CF experts in Nashville. Doctors who attended told me the atmosphere was electric. Jenny happened to be there to speak on an unrelated panel, and she remembers seeing the geneticist Francis Collins walk onstage with a guitar. Collins is best known as the longtime director of the National Institutes of Health, where he <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2931629/">oversaw</a> the sequencing of the human genome in the ’90s (he has since <a href="https://www.nih.gov/farewell-dr-francis-collins#:~:text=Collins%2C%20M.D.%2C%20Ph.,confirmed%20by%20the%20U.S.%20Senate">retired</a> from the NIH). But he had made his name in 1989 as one of the scientists who <a href="https://www.science.org/doi/10.1126/science.2772644">discovered</a> the gene for cystic fibrosis.</p><p>In those long years when progress was halting, Collins, who is also an amateur musician, wrote a song to inspire a gathering of CF researchers. He sang “<a href="https://directorsblog.nih.gov/2019/11/01/singing-dare-to-dream/">Dare to Dream</a>” again that day in Nashville, his baritone raspier with age. When he got to the verse that he had rewritten for this occasion—“That triple treatment has taken 30 years”—cheers broke out in the convention center. In the crowd were people who had waited their whole career, even their whole life, for this moment. <i>We dare to dream, dare to dream.</i> As they swayed to the music, perhaps no one quite understood the magnitude and velocity of the change to come.</p><p class="dropcap"><span class="smallcaps">Jenny received her </span>first box of Trikafta on November 17, 2019, at the end of yet another two-week hospital stay. She had gotten sick again in Nashville. Actually, she had been fighting off a cold before she left, and despite assiduously staying in her hotel room to keep up her treatment routine, she felt an infection settling into her lungs. At the conference, she heard a lot about Trikafta, but she didn’t expect to get it so quickly. CF centers were being inundated with calls from patients asking for the new drug.</p><p>In the hospital in Utah, she recorded a video that she sent to her sister with CF, Teresa, who now lived in Ohio. She is sitting on her hospital bed. “My Trikafta is here,” she says, her voice shaking and her eyes tearing up. The miracle drug she had been promised her whole life was now in her hands.</p><p>Teresa was also able to start the drug not long after. For her, Trikafta’s impact was immediate and unmistakable. The Purge started on the drive back from the doctor’s visit where she took the first dose. The mucus coming up was so thin that she was confused; it was nothing like the sticky gunk she’d had to work so hard to cough up. A month later, she went back for a sweat test, and her salt level was normal. Based on the results, you would not know she had cystic fibrosis.</p><figure><img alt="photo: red-haired woman sits cross-legged on armchair in living room inhaling from medical apparatus with long gray tubes" height="864" src="https://cdn.theatlantic.com/media/img/posts/2024/03/Zhang_3/414429f97.png" width="665">
<figcaption class="caption">Though Trikafta has dramatically improved Jenny’s CF symptoms, she still uses a vest and inhaled treatments to prevent lung infections and other complications from the disease. (Fumi Nagasaka for <em>The Atlantic</em>)</figcaption>
</figure><p>“I think of it like, ‘Oh, back when I used to have CF,’ ” Teresa said on a recent call with Jenny and me. “I don’t feel like I have CF. I feel completely normal.” She has been able to stop using her vest and inhaled medications, freeing up that time for her adopted children and the farm where she lives with her family. Before Trikafta, every small exertion was a negotiation with her lungs. Should she go upstairs? How many breaths would that take? Now she’s running around milking the goats, trimming their hooves, throwing 30 bales of hay into the barn.</p><p>On that same call, the sisters got to talking about an upcoming trip to see their grandmother, and Teresa asked Jenny a question that would have been inconceivable before Trikafta: Could they stay in the same hotel room? To avoid infecting each other with the bacteria in their lungs, the two had not shared a room since Teresa left Utah 15 years earlier. At family gatherings, they kept their distance. They didn’t even touch the same serving utensils, sending their partners to get their food. Now, Jenny told her sister, “I would totally stay in the same hotel room.”</p><p>When Jenny started Trikafta, it took her longer than it took Teresa to notice much change. She didn’t have the dramatic capital-<i>P</i> Purge because, she thinks, the hospitalization had already temporarily cleared her lungs. But two months after she started the drug, when a snowstorm blanketed their town, her family drove out to their favorite sledding hill. Jenny had never liked sledding; she would stand in the cold while everyone else ran around having fun, their easy breaths turning into white puffs in the air. This time, her nephew called out and she jogged over.</p><p>It wasn’t until she got to him that she realized she had jogged <i>up</i>—all the way to the top of the hill. “I don’t run, and I don’t climb hills. And I just ran up a hill and felt super fine,” she says in a video she took right after. “I’m going to see if I can do it again. Ready?”</p><p>“Yes,” her daughter, Morgan, answers next to her. They take off. “Mom!” Morgan shouts a few seconds later, as the distance between them grows larger. “You’re beating me, Mom!” At the top of the hill, Jenny looks back to see Morgan still catching up.</p><p>Jenny went down the hill and ran back up again, simply to prove that she could. “At one point, I just plopped up here on my bum and cried,” she told me during my visit in October, pointing to the spot on the hill where it had all hit her. In front of us, big gray mountains jutted into the blue sky. The sledding hill, she admitted, did not look that impressive. But for all of Morgan’s life, Jenny had been on the sidelines. She’d watch as Morgan swam in the lake or rode her bike, her low-grade fever making her too tired to join. That day on the hill, they finally ran together.</p><p>From there, Jenny began noticing changes in her body, big and small. The tips of her fingers, which had always been slightly swollen and round—a sign of low oxygen—thinned out as her lungs improved. She didn’t need as many enzyme pills to digest her meals. Her chronic cough disappeared. She hadn’t realized how much she had always suppressed her laughter to avoid triggering her cough. Now she can laugh—big belly laughs that match the warmth of her personality. “Oh my gosh, my laugh drives her crazy,” she told me in the car, laughing, after picking up Morgan from school. “That’s because you laugh at stuff that’s not funny,” her daughter shot back. Jenny laughed again.</p><p class="dropcap"><span class="smallcaps">Trikafta had effects </span>that even doctors did not anticipate. In the months after the drugs became widely available, some patients unexpectedly got pregnant; the drug that thins lung mucus, it turns out, also thins cervical mucus. Then, patients started <i>trying</i> to get pregnant. The drug made many people with CF feel so healthy that they no longer worried about the physical toll of pregnancy and parenthood or the agony of leaving behind young children. Doctors began speaking of a Trikafta baby boom.</p><p>Doors opened to other once-impossible futures. A 22-year-old told me he decided to train as an aircraft mechanic, a job that would have been far too physically demanding when he was being hospitalized multiple times a year. One woman started dating. “I don’t want to fall in love with somebody, knowing that I’m not going to be around very long,” she had thought. Now she and her boyfriend have been together for four years. A father who was being evaluated for a lung transplant before Trikafta felt healthy enough to spend the summer of 2020 tearing down and rebuilding his family’s deck, and now expects his CF lungs to see him through graduations and grandkids.</p><p>Trikafta is a lifelong medication, and it is not meant to undo organ damage that has already occurred. But the earlier treatment begins, the healthier one stays. A handful of pregnant women have now used Trikafta to treat their unborn children with cystic fibrosis. Last fall, I corresponded with one such expecting mother, who does not have CF but whose son was diagnosed by genetic testing. She started Trikafta at 26 weeks. When her son was born in October, his lungs and pancreas were perfectly healthy.</p><p>Officially, Trikafta is approved in the U.S. for patients as young as 2. Unofficially, some parents give their newborns Trikafta, either indirectly through breast milk or directly by grinding up the pills into tiny doses. So long as they stay on the medication, these children may never experience any of the physical ravages of the disease. Recently, Make-A-Wish announced that children with CF would <a href="https://wish.org/cf-update#">no longer</a> automatically be eligible for the program, because “life-changing advances” had radically improved the outlook for them.</p><p>CF centers these days are unusually quiet. Fewer patients need once-routine weeks-long hospitalizations. Instead of thinking about lung function, more and more are worrying about the maladies that come with middle and old age—colon cancer, high cholesterol, heart disease. Obesity has been a confounding <a href="https://www.sciencedirect.com/science/article/pii/S2214623721000284">new issue</a>. Before Trikafta, patients were usually underweight, and they were told to cram as many calories in as possible, by whatever means possible. Every additional pound was a small victory. One patient described microwaving pints of Ben & Jerry’s to drink mixed with heavy cream; when even that failed to make her gain weight, she got a feeding tube. Now people on Trikafta worry about getting too many calories.</p><p>In February, Vertex <a href="https://investors.vrtx.com/news-releases/news-release-details/vertex-announces-positive-results-pivotal-trials">announced</a> the results of a clinical trial for a next-generation triple-combination therapy, which may be even more effective than Trikafta. All of these changes have made for an existential moment for doctors, too: The disease they were trained to treat is no longer the disease most of their patients have.</p><p class="dropcap"><span class="smallcaps">Doctors told me </span>they could think of only one other comparable breakthrough in recent memory: the arrival of powerful HIV drugs in the 1990s. Like Trikafta, those drugs were not a cure, but they transformed AIDS from a terminal illness into a manageable chronic one. Young men got up from their deathbed, newly strong and hale. AIDS hospices emptied—and then went bankrupt.</p><p>This was a remarkable turn of events. But it elicited a complicated mix of emotions, not all of them joyful. Some patients who were no longer dying grew depressed, anxious, and even suicidal at the thought of living. This phenomenon became known as “Lazarus syndrome.”</p><p>Death is an end, after all. Life comes with problems: Patients who spent lavishly during what were supposed to be their last days now had no money to live on. Those who stayed with a lover in sickness found that they could not actually stand them in health. They fretted about insurance and paperwork and chores, everyday annoyances that would no longer be obliterated by imminent death. In 1996, the writer Andrew Sullivan, who is HIV-positive, described life after the advent of the HIV drugs in his essay “<a href="https://www.nytimes.com/1996/11/10/magazine/when-plagues-end.html">When Plagues End</a>”:</p><blockquote>
<p>When you have spent several years girding yourself for the possibility of death, it is not so easy to gird yourself instead for the possibility of life. What you expect to greet with the euphoria of victory comes instead like the slow withdrawal of an excuse. And you resist it.</p>
<p>The intensity with which you had learned to approach each day turns into a banality, a banality that refuses to understand or even appreciate the experience you have just gone through.</p>
</blockquote><p>For some HIV patients, their reversal of fortune seemed unreal. “He doesn’t trust what’s happening to him,” one doctor said about a patient who had made a dramatic recovery, yet found himself in psychological distress.</p><p>Doubts like these crept into the minds of many people on Trikafta, too. What if the new drug stopped working? Or had horrible side effects? Or stopped being covered by insurance? Trikafta’s <a href="https://www.cbsnews.com/colorado/news/patients-doctors-worry-trikafta-no-longer-available-colorado/">sticker price</a> is more than $300,000 a year. Insurance typically covers most of that cost—minus what can be significant co-pays and deductibles—and Vertex offers co-pay assistance. But patients’ lives ultimately depend on decisions made by nameless bureaucrats in rooms far away: Insurance plans can suddenly change what they cover, and in 2022, Vertex announced that it would substantially reduce its financial assistance.</p><p>A 43-year-old woman I interviewed asked not to be named, because she feared that speaking about her improved health would cause her to lose disability benefits, which would also get her kicked off the government insurance that pays for Trikafta. Her health has not improved as dramatically as others’ has, and she still has frequent infections and occasional bleeding in her lungs. If she returns to work but her health declines, it could take a long time to get back on disability—time she would have to go without Trikafta. She would also need a job with health insurance good enough to cover the expensive drug—but could she even get one as a 40-something with no recent employment history?</p><p>For other patients, new health granted new independence, which could be scary too. As a child, Patrick Allen Brown was sick enough to miss long stretches of school. His parents didn’t expect him to do chores, let alone support himself with a job one day. So much of his life was spent in the hospital that movies became his way of understanding the outside world. In his teens and 20s, he drank heavily.</p><p>After Trikafta restored Brown’s physical health, he was no longer a chronically ill adult who lived with his parents. He was a pretty healthy adult who still lived with his parents. He was 32, and hadn’t finished college. Now he had to budget, commit to a career. He decided to get sober. When one of his parents needed back surgery recently, their roles flipped: He became the caretaker. Brown has now graduated from culinary school and found work as a chef, but he feels as if he is still catching up to his peers.</p><figure class="full-width"><img alt="2 photos: sunlit hill with trees, fence, and partially cloudy blue sky; red-haired woman hugs blonde girl looking at camera with sky and mountains in background" height="353" src="https://cdn.theatlantic.com/media/img/posts/2024/03/Zhang_4/c1c5001bc.png" width="928">
<figcaption class="caption">Two months after Jenny began taking Trikafta, she found that she was able to run up a local sledding hill for the first time. Jenny and Morgan often go up into the aspen- and fir-topped mountains that overlook their town in central Utah. (Fumi Nagasaka for <em>The Atlantic</em>)</figcaption>
</figure><p>The great blossoming of possibilities on Trikafta also dredged up regret about decisions too late to undo. Kara Hansen, 41, has a daughter who was adopted, and she had always wanted another child. But in 2016, she had to be repeatedly hospitalized: in April, then again in May, July, and August. She gave up on having a second child—how could she, if she couldn’t even guarantee living for the daughter she already had? Then, in 2018, she joined the original trial for Trikafta, becoming one of the first people in the world to experience its miraculous effects. If she had known her health would improve so dramatically and hold steady six years on, she would have tried to get pregnant, but she feels like it’s too late now. To plan for such a miracle would have been foolish, but to live in its unexpected aftermath can still be painful.</p><p class="dropcap"><span class="smallcaps">After a year </span>on Trikafta, Jenny told Teresa something that she acknowledged sounded “insane” but that her sister understood immediately: “To no longer be actively dying kind of sucks,” she said. The certainty of dying young, she realized, had been a security blanket. She’d never worried about retirement, menopause, or the loneliness of outliving a parent or a partner.</p><p>Cystic fibrosis had defined her adult life. Now what? For so long, she’d just been trying to see her daughter graduate from high school. Now she faced seeing Morgan go off and live her own life. What then? Jenny had become active in patient advocacy, and soon after the start of the pandemic, she volunteered to moderate an online patient forum on mental health for her CF center in Utah. It went so well that her longtime social worker at the center felt compelled to give some career advice: Try social work.</p><p data-id="injected-recirculation-link"><i>[<a href="https://www.theatlantic.com/magazine/archive/2022/10/kids-glasses-vision-increased-nearsightedness-myopia/671244/?utm_source=feed">From the October 2022 issue: Sarah Zhang on why so many kids need glasses now</a>]</i></p><p>Jenny enrolled in an online master’s program in 2022, and this past fall she chose a practicum with a hospice agency. Having watched the death of so many friends and contemplated her own, she felt prepared to shepherd people through the sadness and awkwardness and even humor that accompany the end of life. She understood, too, the small dignities that mean the world when your body is no longer up to the task of living. One hospice patient, she noticed, often had trouble understanding conversations because his hearing aids were never charged correctly. She got the situation fixed, and on a recent visit, he wanted to listen to music, playing for her the favorite songs of his youth. On another man’s shelf, she recognized a birding book, and she made plans for a window feeder to bring birds to him.</p><p>Jenny doesn’t share the details of her life with patients, but in their experiences with death, she has seen her own refracted. One hospice patient, a devout elderly woman, was estranged from her adult son, who no longer believed. Jenny herself grew up religious—Mormon, in her case—but she is not anymore. Her family is still Mormon, as is virtually everyone in the town she has lived in since childhood, which has 3,500 people, several Mormon churches, and a Mormon temple. She is liberal, whereas most of her relatives voted for Donald Trump.</p><p>Still, Jenny has made a point of staying close to her large, tight-knit family. Knowing she would die young had long ago clarified that she wanted to leave with no regrets, no grudges, and no words left unsaid to the people she loved. In the foothills outside town one day, she pointed in the direction of her house, her brother’s house, her mom’s house, her dad and stepmom’s house, all minutes away from one another.</p><p class="dropcap"><span class="smallcaps">Although Trikafta looks </span>to be a very safe drug for most people, it does have side effects. It can cause cataracts as well as liver injury. More perplexing, Trikafta may affect the brain.</p><p>For Jenny, starting Trikafta coincided with a wave of intense insomnia, brain fog, and anxiety. For months, she could sleep only two or three hours a night. She’d lose her phone and find it in the freezer. Her lungs were so much healthier, but her brain was going haywire. Soon, she realized that other CF patients had begun sharing stories online of depression, anger, or suicidal thoughts that emerged at the same time they started taking Trikafta.</p><p>Doctors sometimes chalked up these symptoms to the existential unease of no longer dying, or the fear and isolation everyone felt in the early days of the pandemic. But Jenny’s doctor took the side effects she reported seriously enough to suggest that she halve her Trikafta dose, and soon after, they subsided. (Some of her CF symptoms did return, but they were muted enough that she could pare down her regimen of treatments.)</p><p>The link between Trikafta and these symptoms in the brain is still not fully proven or understood. “We’ve done an in-depth analysis of the preclinical data, clinical data, and real-world-evidence data, and we don’t find any causal relationship,” Fred Van Goor, a vice president and the head of CF research at Vertex, told me in January. And an <a href="https://www.atsjournals.org/doi/full/10.1164/rccm.202308-1525OC">analysis</a> co-authored by the company’s scientists last year found similar rates of depression and suicidality in CF patients with or without Trikafta. But in November, a group of scientists published a <a href="https://pubmed.ncbi.nlm.nih.gov/37655981/">review</a> arguing that the possible neuropsychiatric effects of Trikafta deserved a “serious research effort.” The protein behind CF is found in cells throughout the body, including the brain. Trikafta could be acting on the brain directly, the authors hypothesized, or it could be acting indirectly via changes to inflammation throughout the body or specifically in the gut. The drug may affect different subsets of patients differently, says Anna Georgiopoulos, a psychiatrist at Massachusetts General Hospital who co-authored the review. She believes that neuropsychiatric side effects afflict only a “small minority” of people on Trikafta, but says that studies are needed to know exactly how many.</p><p>In the meantime, some patients have quit Trikafta altogether, their neuropsychiatric symptoms too debilitating even on a lower dose. “Physically I was feeling the best I’ve ever felt,” says Aimee Lecointre of her time on the drug, but mentally, “I felt on the verge of a panic attack almost every day.” The contradiction confused her: How could she be so anxious and depressed when her health was getting so much better? When she finally decided to try stopping Trikafta, the nervous energy that had filled her body all day long dissipated. But her CF symptoms came back. During our phone conversation, she paused every few minutes to cough.</p><p>She and Jenny have known each other for years, going back to their mutual hospitalizations. The three of us were supposed to meet over apple-cider floats when I was in Utah, but Lecointre had health issues come up at the last minute, the kind of disruption that happens all the time for people with a chronic illness. For a while, her Instagram feed filled with people on Trikafta whose lives were transforming while hers stayed the same; she had to delete social media from her phone. She still feels sad, sometimes, that Trikafta didn’t work out for her. But she was able to go back to one of Vertex’s two-drug combos, and although it is less effective than Trikafta, she feels so much better. There is more to cope with, but the coping is easier.</p><p class="dropcap"><span class="smallcaps">For another group </span>of CF patients, Trikafta simply does not work. About 10 percent <a href="https://pharmacy.ucsf.edu/news/2019/12/rare-cystic-fibrosis-mutations-limit-benefits-targeted-drugs">lack</a> the F508del mutation that the triple combination was specifically designed to fix. Over time, though, scientists have found that some less common mutations are similar enough to F508del that those who carry them still benefit from Trikafta. And in late 2020, word got out that the FDA would soon approve the drug for additional mutations.</p><p>Gina Ruiz remembers waiting and waiting for the list of new mutations that fall. She had spent the past year watching her peers on Trikafta be handed what she thought of as a “reverse Uno card”—reverse weight loss, reverse lung decline, reverse CF—while her own health continued to worsen. She was sitting in a car when she saw the list, and she scrolled through the <a href="https://investors.vrtx.com/news-releases/news-release-details/vertex-announces-fda-approvals-trikaftar">177 new mutations</a> hoping to find hers. She was crushed when she did not. Ruiz and most people in the 10 percent have mutations that leave their CFTR protein too garbled or incomplete to correct with any combination of fixer molecules. Treating these mutations will require a different strategy altogether.</p><p>The Cystic Fibrosis Foundation continues to fund research into a cure for all, and scientists, including those at Vertex, are once again exploring genetic therapies, applying the lessons of past failures. But a genetic-therapy breakthrough specific to CF is still years, if not decades, away. After Vertex created that first drug for the 4 percent, the path toward Trikafta was clear. After Trikafta, terra incognita.</p><p>Ruiz is wary of getting her hopes up again. At age 29, she can no longer work. She lives with her parents. Her lung function has fallen to 30 percent. And in December, her weight reached a new low of 89 pounds. “I went to Target last night and I was beyond exhausted,” she told me the following month. Her knees hurt too, another complication of CF. As she’s watched her peers on Trikafta get married and chase after toddlers, her own world has shrunk. Halfway through the store, she got so tired that she had to rest in a chair in the home-goods section before she could go on.</p><p>Other patients with rare mutations told me the CF communities they once relied on for support have become quiet, as the 90 percent have gotten on with their lives. “It’s extremely isolating,” says Steph Hansen, who was steeling herself for another hospitalization when we spoke in January. She describes it as a one-two punch: Her health is no better, yet she has lost the community that once buoyed her. She’s connected with a handful of other patients who can’t take Trikafta, but CF is already a rare disease, and they are the rarest of the rare.</p><figure class="full-width"><img alt="photo of group of 12 people standing in line, some hugging, on grassy field with mountains and sky in distance" height="714" src="https://cdn.theatlantic.com/media/img/posts/2024/03/Zhang_5/c709bf5e3.png" width="928">
<figcaption class="caption">Jenny has made a point of staying close to her large, tight-knit family; knowing she would die young clarified that she wanted to leave without any grudges. (Fumi Nagasaka for <em>The Atlantic</em>)</figcaption>
</figure><p>The F508del mutation is <a href="https://www.smithsonianmag.com/science-nature/tracking-origins-cystic-fibrosis-ancient-europe-180970238/">most common</a> in people of European ancestry, so people with mutations ineligible for Trikafta in the U.S. are <a href="https://www.kumc.edu/about/news/news-archive/trikafta-2021.html">disproportionately</a> Black or Latino. Globally, the proportion of people ineligible is higher in Latin America, Asia, and Africa, where diagnosis and treatment for CF also <a href="https://www.sciencedirect.com/science/article/pii/S1569199322000315">lag</a>. In most developing countries, even eligible patients cannot get Trikafta—because Vertex currently does not sell its expensive drug outside a few dozen countries, concentrated in Europe and the English-speaking world. (Vertex says it has a pilot program that “provides Trikafta at no cost to people with CF in certain lower income countries.”) Its patents also block other companies from making a cheaper generic version. In early 2023, activists asked four countries to revoke or suspend patents for Trikafta in a coordinated campaign. One of the countries was India, where <i>The New York Times</i> <a href="https://www.nytimes.com/2023/02/07/health/cystic-fibrosis-drug-trikafta.html">wrote</a> about a father named Seshagiri Buddana. His son would have been able to take Trikafta if he lived in the U.S., but he died in December 2022 one day before he would have turned 9.</p><p>All of this weighs on Jenny. What makes her different from those who have died, other than the luck of being born at the right time, in the right place, with the right mutations?</p><p class="dropcap"><span class="smallcaps">Two days after </span>my visit to Utah, Jenny’s father, Tom, had a heart attack while chopping firewood. He felt short of breath, and a trip to the hospital revealed that his major arteries were 90 percent blocked.</p><p>When Jenny texted me the news, she said she had been replaying our recent conversations about life and death. She was glad to feel, upon learning her father might die, that nothing between the two of them was left unsaid or unresolved. I thought of what Tom had told me in his living room. Before we had gone over to his house that day, Jenny had warned me that her dad was a jokester, not a man prone to earnest reflection. But when the conversation shifted to the impact of Trikafta, he turned to me, completely serious. “I was going to bury my kids. And I’m not. They get to bury me, which is the way it’s supposed to be.”</p><p>We all fell silent for a moment, as we felt the weight he had been carrying all those years. After burying his eldest daughter at 14, Tom could no longer watch movies in which children die. In Jenny’s years of sickness, he had often driven her two hours to the hospital in Salt Lake City, but he rarely set foot inside. Hospitals are places where people go to be born or to die, he’d say, and all my children have already been born.</p><p>After his heart attack, Tom needed an emergency quintuple-bypass surgery. He did well, and came home to recover. He spent the time rethinking his priorities. Just before falling ill, he had skipped a family outing to an amusement park to work. Now he regretted it. He’s become more open about his emotions; still a jokester, he’s taken to saying that his heart has been opened in more ways than one since the surgery.</p><p>It’s interesting, Jenny says. Her father has lived a longer and very different life from her own, but she recognizes what he is going through. People die from this, he started saying. <i>I</i> could have died from this. He got close enough to see death’s shadow, only to be pulled back to a life whose familiarity suddenly felt unfamiliar. What would he do with his unexpected life? “Hey,” Jenny told her dad. “I get it.”</p><hr><p><small><i>This article appears in the </i><a href="https://www.theatlantic.com/magazine/toc/2024/04/?utm_source=feed"><i>April 2024</i></a><i> print edition with the headline “After the Miracle.”</i></small></p>Sarah Zhanghttp://www.theatlantic.com/author/sarah-zhang/?utm_source=feedFumi Nagasaka for The AtlanticBefore she started taking Trikafta, in 2019, Jenny Livingston hoped more than anything to survive long enough to see her daughter graduate from high school.The Cystic-Fibrosis Breakthrough That Changed Everything2024-03-07T07:00:00-05:002024-03-07T13:12:56-05:00The disease once guaranteed an early death—but a new treatment has given many patients a chance to live decades longer than expected. What do they do now?tag:theatlantic.com,2024:50-677666<p>On June 3, 2021, a roughly 60-year-old man in the riverside city of Magdeburg, Germany, received his first COVID vaccine. He opted for Johnson & Johnson’s shot, popular at that point because unlike Pfizer’s and Moderna’s vaccines, it was one-and-done. But that, evidently, was not what he had in mind. The following month, he got the AstraZeneca vaccine. The month after that, he doubled up on AstraZeneca and added a Pfizer for good measure. Things only accelerated from there: In January 2022, he received at least 49 COVID shots.</p><p></p><p>A few months later, employees at a local vaccination center thought to themselves, <em>Huh, wasn’t that guy in here yesterday? </em>and alerted the police. By that point, the German Press Agency reported, the man had been vaccinated as many as <a href="https://apnews.com/article/covid-health-germany-europe-document-forgery-120b2c4db8aa71ffeadf766a9829910b">90 times</a>. And still he was not done. As of November, he said he’d received 217 COVID shots—<em>217</em>!</p><p></p><p>That’s according to a <a href="https://www.thelancet.com/journals/laninf/article/PIIS1473-3099(24)00134-8/fulltext#sec1">new </a><a href="https://www.thelancet.com/journals/laninf/article/PIIS1473-3099(24)00134-8/fulltext#sec1">paper</a> published in <em>The Lancet</em>. After German researchers learned of the man from newspaper articles, they managed to contact him via the public prosecutor investigating the case. He was “very interested” in participating in a study, Kilian Schober, an immunologist at <a href="https://www.mikrobiologie.uk-erlangen.de/forschung/forschergruppen-arbeitsgruppen/ag-dr-k-schober/">Uniklinikum Erlangen</a> and a co-author on the paper, <a href="https://www.fau.eu/2024/03/05/news/research/researchers-investigate-immune-response-of-a-man-who-received-217-covid-vaccinations/">said in a statement</a>. They pieced together his vaccination timeline through interviews and medical records, and collected blood and saliva samples to examine the immunological effects of “hypervaccination.”</p><p></p><p>The man’s identity hasn’t been revealed, and in the paper he’s referred to only as “HIM” (seemingly an acronym, though what it stands for is not specified). He is hardly the world’s only hypervaccinated person. A retired postman in India had reportedly received 12 shots by January 2022 and told <em>The New York Times</em>, “I still want more.” A New Zealand man, meanwhile, <a href="https://www.theguardian.com/world/2021/dec/13/new-zealand-authorities-investigate-claims-man-received-10-covid-vaccinations-in-one-day">allegedly</a> racked up 10 in a single day. But pause for a moment and consider the sheer logistics of HIM’s feat. In all, he received his 217 vaccinations over the course of just under two and a half years, which comes out to an average of seven and a half shots a month, although the distribution was far from even. For several weeks in early 2022, he received two shots nearly every day. He seems to have had a strong preference for the Pfizer and Moderna vaccines, but he also got at least one shot of AstraZeneca and Sanofi-GSK and, of course, Johnson & Johnson.</p><p></p><p><em>Why? </em>you might wonder. The paper itself elides this question, saying only that he did so “deliberately and for private reasons.” Perhaps the most obvious explanation would be extreme, probably pathological COVID anxiety. News reports from April 2022 offer another possible explanation: that he did so to sell the vaccination cards. But German prosecutors did not bring charges once HIM’s scheme was uncovered, and he continued getting unnecessary shots.</p><p></p><p>Getting 217 COVID shots is very much not the public-health guidance in Germany or anywhere else. Yet the strategy seemingly panned out: HIM has never contracted COVID, researchers concluded based on antigen tests, PCR tests, and bloodwork. “If you ask immunologists, we might have predicted that it would be not beneficial to do this,” Cindy Leifer, an immunologist at Cornell University who wasn’t involved with the <em>Lancet</em> study, told me. They might have expected the constant action to exhaust the immune system, leaving it vulnerable to actual viral threats. But such worries came to nothing.</p><p></p><p>Still, immunologists cautioned against inferring any strong causal connection. He avoided the virus; he got vaccinated 217 times. He did not necessarily avoid the virus <em>because </em>he got vaccinated 217 times. In fact, the authors wrote, although hypervaccination seems to have increased the quantity of antibodies and T cells that HIM’s body produced to fend off the virus—even after 216 shots, the 217th still produced a modest increase—it had no real effect on the <em>quality </em>of the immune response. “He would have been just as well protected if he had gotten a normal number of three to four vaccinations,” Schober told me.</p><p></p><p>Nor did hypervaccination lead to any adverse effects. By shot 217, one might have expected to see some of the <a href="https://www.cdc.gov/coronavirus/2019-ncov/vaccines/safety/adverse-events.html">rare side effects</a> associated with the vaccines, such as myocarditis, pericarditis, or Guillain-Barré Syndrome, but as far as researchers could tell, HIM was completely fine. Remarkably, he didn’t even report feeling minor side effects from any of his 217 shots. On some level, this makes total sense: As Schober reasonably pointed out, HIM probably would not have gotten all those shots if each one had knocked him out for a day. Fair, but still: 217 shots and no side effects? How?</p><p></p><p>If nothing else, HIM is one hell of an advertisement for the vaccines. Worried about side effects from your third booster? Well, this guy’s gotten more than 200, and he’s a-okay. Travis Kelce has been <a href="https://www.nbcsports.com/nfl/profootballtalk/rumor-mill/news/travis-kelce-responds-to-mr-pfizer-label-from-aaron-rodgers">called</a> Mr. Pfizer, but he’s got nothing on HIM. Scientifically, things are somewhat murkier. The results of the HIM study were largely unsurprising, researchers told me, but the mysteries at the margins—such as the absence of any side effects—are a good reminder that four years after the pandemic began, immunology is still, as my former colleague Ed Yong wrote, “<a href="https://www.theatlantic.com/health/archive/2020/08/covid-19-immunity-is-the-pandemics-central-mystery/614956/?utm_source=feed">where intuition goes to die</a>.”</p><p></p><p>At the end of the paper, the authors are very clear: “We do not endorse hypervaccination as a strategy to enhance adaptive immunity.” The takeaway, Leifer said, should not be <em>the more shots, the better</em>.<em> </em>Schober told me he even tried to personally convey this message to HIM after his 216th shot. “From the bottom of my heart as a medical doctor, I really told him that he shouldn’t get vaccinated again,” Schober said.</p><p></p><p>HIM seemed to take this advice seriously. Then he went and got shot No. 217 anyway.</p>Jacob Sternhttp://www.theatlantic.com/author/jacob-stern/?utm_source=feedThe Atlantic. Source: Getty.Pfizer Couldn’t Pay for Marketing This Good2024-03-06T16:36:00-05:002024-03-08T16:12:33-05:00Well now we know what happens when someone gets 217 COVID shots.tag:theatlantic.com,2024:50-677645<p data-flatplan-paragraph="true"><small><i data-stringify-type="italic">This article was featured in the One Story to Read Today newsletter. </i><i data-stringify-type="italic"><a data-event-element="inline link" data-sk="tooltip_parent" data-stringify-link="https://www.theatlantic.com/newsletters/sign-up/one-story-to-read-today/" delay="150" href="https://www.theatlantic.com/newsletters/sign-up/one-story-to-read-today/?utm_source=feed" rel="noopener noreferrer" target="_blank">Sign up for it here</a></i><i data-stringify-type="italic">.</i></small></p><p dir="ltr">When scientists first created the class of drugs that includes Ozempic, they told a tidy story about how the medications would work: The gut releases a hormone called GLP-1 that signals you’re full, so a drug that mimics GLP-1 could do the exact same thing, helping people eat less and lose weight.</p><p dir="ltr">The rest, as they say, is history. The GLP-1 revolution birthed semaglutide, which became Ozempic and Wegovy, and tirzepatide, which became Mounjaro and Zepbound—blockbuster drugs that are rapidly changing the face of obesity medicine. The drugs work as intended: as powerful modulators of appetite. But at the same time that they have become massive successes, the original science that underpinned their development has fallen apart. The fact that they worked was “serendipity,” Randy Seeley, an obesity researcher at the University of Michigan, told me. (Seeley has also consulted for and received research funding from companies that make GLP-1 drugs.)</p><p dir="ltr">Now scientists are beginning to understand why. In recent years, studies have shown that GLP-1 from the gut breaks down quickly and has little effect on our appetites. But the hormone and its receptors are naturally present in <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4888559/">many parts of the brain</a> too. These brain receptors are likely the reason the GLP-1 drugs can curb the desire to eat—but also, anecdotally, <a href="https://www.theatlantic.com/health/archive/2023/05/ozempic-addictive-behavior-drinking-smoking/674098/?utm_source=feed">curb other desires</a> as well. The weight-loss drugs are ultimately drugs for the brain.</p><p dir="ltr">Obesity medications differ in a key way from the natural molecule they’re meant to mimic: They last a lot longer. GLP-1 released in the gut has a half-life of just minutes in the bloodstream, whereas semaglutide and tirzepatide have half-lives measured in days. This is by design. Both drugs were specifically engineered to resist degradation, so that they need to be injected only once a week. (The <a href="https://investor.lilly.com/news-releases/news-release-details/amylin-and-lilly-announce-fda-approval-byettatm-exenatide">very first GLP-1 drug</a> on the market, exenatide, had to be injected <a href="https://pubmed.ncbi.nlm.nih.gov/24435322/">twice a day</a> when it was released, in 2005—the field has come a long way.) The medications are also given at levels much higher than natural GLP-1 ever reaches in the bloodstream; Seeley tends to put it at five times as high, but he said even that may be a gross underestimate.</p><p data-id="injected-recirculation-link" dir="ltr"><i>[<a href="https://www.theatlantic.com/health/archive/2024/02/ozempics-muscle-loss-problem/677326/?utm_source=feed">Read: Ozempic makes you lose more than fat</a>]</i></p><p dir="ltr">By indiscriminately flooding the body with long-lasting molecules, the injections likely allow engineered GLP-1 drugs to penetrate parts of the body that the natural gut hormone cannot—namely, deep in the brain. First-generation GLP-1 drugs including exenatide, which are far less powerful than the current crop, have been shown to cross the blood-brain barrier and tickle areas important for appetite and nausea. Exactly what Ozempic <a href="https://www.theatlantic.com/health/archive/2023/04/ozempic-wegovy-mounjaro-weight-loss-drug-development-access/673627/?utm_source=feed">and its successors</a> do is still less clear, but they are so effective that many scientists think they must be reaching far, directly or indirectly.</p><p dir="ltr">All of this matters because the brain, as we now know, has its own GLP-1 system, parallel to and largely separate from whatever is going on in the gut. Neurons in the hindbrain, sitting at the base of the skull, <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3275387/">secrete their own GLP-1</a>, while receptors listening to them are found throughout the brain. In animal experiments, hitting those receptors indeed suppresses appetite.</p><p dir="ltr">It took a long time for scientists to appreciate the extent of GLP-1 in the brain, Karolina Skibicka, a neuroscientist at Penn State, told me. When she published her first <a href="https://www.jneurosci.org/content/jneuro/32/14/4812.full.pdf">study</a>, in 2012, on a GLP-1 drug’s impact on the dopamine reward system, she had to spend two years going back and forth with skeptical reviewers. At the time, she said, “the idea was considered so wild.” (Skibicka has received research funding from the Novo Nordisk Foundation, which has a majority ownership in but whose grants are commercially independent from Novo Nordisk, the manufacturer of Ozempic.) Since then, in a series of clever experiments using rodents, scientists have been able to show that GLP-1 drugs likely act on the brain. They don’t seem to work, for example, to suppress appetite in mice whose <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4038572/">brain GLP-1 receptors have been genetically erased</a>. Moreover, the effects of GLP-1 extend <a href="https://pubmed.ncbi.nlm.nih.gov/27030669/">beyond food</a>: Rodents given the drugs will drink less alcohol and use less cocaine. Anecdotally, too, people on GLP-1 medications have reported spontaneously quitting drinking, smoking, shopping, and other addictive and compulsive behaviors.</p><p data-id="injected-recirculation-link" dir="ltr"><i>[<a href="https://www.theatlantic.com/health/archive/2023/05/ozempic-addictive-behavior-drinking-smoking/674098/?utm_source=feed">Read: Did scientists accidentally invent an anti-addiction drug?</a>]</i></p><p dir="ltr">A more refined understanding of how GLP-1 works in the brain could help improve the current injections. <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9821052/">Nausea and vomiting</a> are among the most common side effects and would seem to go hand in hand with a lack of appetite. But these symptoms appear to be governed by distinct systems in the brain, Scott Kanoski, a neuroscientist at the University of Southern California, told me. In fact, scientists have been able to find brain areas in rodents where GLP-1 analogues can suppress appetite without causing nausea, which hints at the possibility of developing drugs that do the same.</p><p>Even as scientists zero in on the likely mechanisms of these weight-loss drugs, they are encountering new and baffling questions. Tirzepatide, for example, activates receptors for a second hormone called GIP, and this is often <a href="https://www.theatlantic.com/health/archive/2024/01/why-you-will-stop-losing-weight-ozempic/677148/?utm_source=feed">cited as a potential explanation</a> for its slightly superior efficacy over semaglutide, which acts on GLP-1 alone. But just last month, Amgen <a href="https://www.reuters.com/business/healthcare-pharmaceuticals/promising-early-data-details-amgen-weight-loss-drug-published-2024-02-05/">released data</a> on a new drug that activates GLP-1 receptors, <em>blocks</em> GIP receptors, and still helps people lose weight. How can two drugs with opposite actions on GIP have the same outcome?</p><p dir="ltr">Scientists are perplexed, but they are not shocked. For years and years, promising findings in rats and mice did not translate into real-world treatments for obesity. Drugs based on other, seemingly important hormones—ghrelin (the “hunger hormone”) and leptin (the “satiety hormone”)—were <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5364444/">never able to achieve</a> the spectacular clinical results of GLP-1. The latest drugs succeeded not because we fully understood the hormone they’re based on but because we got lucky. And drug development, for all the careful research required, does sometimes come down to luck.</p><p data-id="injected-recirculation-link" dir="ltr"><i>[<a href="https://www.theatlantic.com/health/archive/2024/01/why-you-will-stop-losing-weight-ozempic/677148/?utm_source=feed">Read: The Ozempic plateau</a>]</i></p><p dir="ltr">In the end, gut GLP-1 could still be important—just not for appetite regulation. The stuff that is produced by the gut, specifically in the end of the small intestine and the colon, makes up most of the GLP-1 produced in the body, Daniel Drucker, an endocrinologist at Mount Sinai Hospital in Toronto, told me. It also tends to spike during gut infections. Drucker now thinks that GLP-1 in the gut is primarily responsible for controlling inflammation. (He has consulted for and received research funding from companies making GLP-1 drugs.) Other scientists have explored using GLP-1 drugs to <a href="https://www.thelancet.com/pdfs/journals/eclinm/PIIS2589-5370(21)00259-5.pdf">treat inflammatory gut disease</a>, such as ulcerative colitis and Crohn’s. But they’ve run into a bit of a dilemma: Many people with these conditions are already underweight, and GLP-1 drugs are just too good at making people lose more weight.</p>Sarah Zhanghttp://www.theatlantic.com/author/sarah-zhang/?utm_source=feedIllustration by The Atlantic. Source: Getty.The Science Behind Ozempic Was Wrong2024-03-05T12:58:17-05:002024-03-08T16:10:23-05:00The weight-loss effects of GLP-1 drugs have little to do with the gut.tag:theatlantic.com,2024:50-677600<p>Last Friday, in a bathroom at the Newark airport, I encountered a phrase I hadn’t seen in a long time: <span class="smallcaps">Stop the spread</span><em>.</em> It accompanied an automatic hand-sanitizing station, which groaned weakly when I passed my hand beneath it, dispensing nothing. Presumably set up in the early pandemic, the sign and dispenser had long ago become relics. Basically everyone seemed to ignore them. Elsewhere in the terminal, I spotted prompts to <span class="smallcaps">maintain a safe distance</span> and <span class="smallcaps">reduce overcrowding</span>, while maskless passengers sat elbow-to-elbow in waiting areas and mobbed the gates.</p><p>Beginning in 2020, COVID signage and equipment were everywhere. Stickers indicated how to stand six feet apart. Arrows on the grocery-store floor directed shopping-cart traffic. Plastic barriers enforced distancing. <span class="smallcaps">Masks required</span> signs dotted store windows, before they were eventually replaced by softer pronouncements such as <span class="smallcaps">masks recommended</span> and <span class="smallcaps">masks welcome</span>. Such messages—<a href="https://www.theatlantic.com/health/archive/2022/07/covid-spread-air-disinfect-sanitize-hygiene-theater/661507/?utm_source=feed">some more helpful than others</a>—became an unavoidable part of navigating pandemic life.</p><p></p><p>Four years later, the coronavirus has not disappeared—but the health measures are gone, and so is most daily concern about the pandemic. Yet much of this COVID signage remains, impossible to miss even if the messages are ignored or outdated. In New York, where I live, notices linger in the doorways of apartment buildings and stores. A colleague in Woburn, Massachusetts, sent me a photo of a sign reminding park-goers to gather in groups of 10 or less; another, in Washington, D.C., showed me stickers on the floors of a bookstore and pier bearing faded reminders to stay six feet apart. “These are artifacts from another moment that none of us want to return to,” Eric Klinenberg, a sociologist at NYU and the author of <a href="https://bookshop.org/p/books/2020-the-year-the-world-cracked-open-eric-klinenberg/20095577?ean=9780593319482"><em>2020: One City, Seven People, and the Year Everything Changed</em></a>, told me. All these flyers, signs, and stickers make up the “ghost architecture” of the pandemic, and they are still haunting America today.</p><p></p><p>That some COVID signage persists makes sense, considering how much of it once existed. According to the <a href="https://covid-signage.net/map">COVID-19 Signage Archive</a>, one store in Key West <a href="https://covid-signage.net/?sign=4076978434">had</a><a href="https://covid-signage.net/?sign=4076978434"> a</a><a href="https://covid-signage.net/?sign=4076978434"> reminder to mask up</a> during the initial Omicron wave: <span class="smallcaps">Do not wear it above chin or below nose</span>. In the summer of 2021, a placard at a Houston grocery store indicated that the shopping carts had been <a href="https://covid-signage.net/?sign=3256534203">“sanitizd</a><a href="https://covid-signage.net/?sign=3256534203">.”</a><a href="https://covid-signage.net/?sign=3256534203"> </a>And in November 2020, you could have stepped on a <a href="https://covid-signage.net/?sign=1154907306">customized welcome mat</a> in Washington, D.C., that read <span class="smallcaps">Thank you for practicing 6 ft social distancing</span>. Eli Fessler, a software engineer and linguist who launched the crowdsourced archive in December 2020, wanted “to preserve some aspect of [COVID signage] because it felt so ephemeral,” he told me. The gallery now comprises nearly 4,000 photos of signs around the world, including submissions he received as <a href="https://covid-signage.net/?sign=1429956928">recently as this past October</a>: a <span class="smallcaps">keep safe distance</span> sign in Incheon, South Korea.</p><p></p><p>No doubt certain instances of ghost architecture can be attributed to forgetfulness, laziness, or apathy. Remnants of social-distancing stickers on some New York City sidewalks appear too tattered to bother scraping away; outdoor-dining sheds, elaborately constructed but now barely used, are a hassle to dismantle. A faded decal posted at a restaurant near my home in Manhattan depicts social-distancing guidelines for <a href="https://www.nyc.gov/assets/mome/pdf/NYC-TAKE-OUT-GUIDELINES-11X17.pdf">ordering takeout alcohol</a> that haven’t been relevant since 2020. “There’s a very human side to this,” Fessler said. “We forget to take things down. We forget to update signs.”</p><p></p><p>But not all of it can be chalked up to negligence. Signs taped to a door can be removed as easily as they are posted; plastic barriers can be taken down. Apart from the ease, ghost architecture should have disappeared by now because spotting it is never pleasant. Even in passing, the signs can awaken uncomfortable memories of the early pandemic. The country’s overarching response to the pandemic is what Klinenberg calls the “will not to know”—a conscious denial that COVID changed life in any meaningful way. Surely, then, some examples are left there on purpose, even if they evoke bad memories.</p><p>When I recently encountered the <span class="smallcaps">masks required</span> sign that’s still in the doorway of my local pizza shop, my mind flashed back to more distressing times: <em>Remember when that was a thing?</em> The sign awakened a nagging voice in my brain reminding me that I used to mask up and encourage others to do the same, filling me with guilt that I no longer do so. Perhaps the shop owner has felt something similar. Though uncomfortable, the signs may persist because taking them down requires engaging with their messages head-on, prompting a round of fraught self-examination: <em>Do I no longer believe in masking? Why not?</em> “We have to consciously and purposely say we no longer need this,” Klinenberg told me.</p><p>Outdated signs are likely more prevalent in places that embraced public-health measures to begin with, namely bluer areas. “I would be surprised to see the same level of ghost architecture in Florida, Texas, or Alabama,” Klinenberg said. But ghost architecture seems to persist everywhere. A colleague sent a photo of a floor sticker in a Boise, Idaho, restaurant that continues to thank diners for practicing social distancing. These COVID callbacks are sometimes even virtual: An outdated <a href="https://www.thepalmshotel.com/health-and-safety">website</a> for a Miami Beach spa still encourages guests to physically distance and to “swipe your own credit card.”</p><p>Most of all, the persistence of ghost architecture directly reflects the failure of public-health messaging to clearly state what measures were needed, and when. Much of the signage grew out of garbled communication in the first place: <a href="https://covid-signage.net/?sign=3765532065">“Six feet” directives</a>, for example, <a href="https://www.theatlantic.com/health/archive/2022/06/covid-numbers-outdated-two-doses-six-feet/661366/?utm_source=feed">far outlasted the point</a> when public-health experts knew it was a faulty benchmark for stopping transmission.</p><p></p><p>The rollback of public-health precautions has been just as chaotic. Masking policy has <a href="https://www.theatlantic.com/health/archive/2023/02/covid-mask-guidelines-fight-cochrane-review/673039/?utm_source=feed">vacillated wildly</a> since the arrival of vaccines; although the federal COVID emergency declaration <a href="https://www.cdc.gov/coronavirus/2019-ncov/your-health/end-of-phe.html#:~:text=The%20federal%20COVID%2D19%20PHE,ended%20on%20May%2011%2C%202023.">officially ended last May</a>, there was no corresponding call to end public-health measures across the country. Instead, individual policies <a href="https://nashp.org/state-tracker/states-covid-19-public-health-emergency-declarations/">lapsed at different times in different states</a>, and in some cases were setting-specific: California didn’t end its mask requirement <a href="https://www.cdph.ca.gov/Programs/OPA/Pages/NR23-014.aspx">for high-risk environments</a> such as nursing homes until last April. Most people still don’t know how to think about COVID, Klinenberg said, and it’s easier to just leave things as they are.</p><p></p><p>If these signs are the result of confusing COVID messaging, they are also adding to the problem. Prompts to wash or sanitize your hands are generally harmless. In other situations, however, ghost architecture can perpetuate misguided beliefs, such as thinking that keeping six feet apart is protective in a room full of unmasked people, or that <a href="https://www.theatlantic.com/health/archive/2023/02/covid-mask-guidelines-fight-cochrane-review/673039/?utm_source=feed">masks alone are foolproof against COVID</a>. To people who must still take precautions for health reasons, the fact that signs are still up, only to be ignored, can feel like a slap in the face. The downside to letting ghost architecture persist is that it sustains uncertainty about how to behave, during a pandemic or otherwise.</p><p></p><p>The contradiction inherent in ghost architecture is that it both calls to mind the pandemic and reflects a widespread indifference to it. Maybe people don’t bother to take the signs down because they assume that nobody will follow them anyway, Fessler said. Avoidance and apathy are keeping them in place, and there’s not much reason to think that will change. At this rate, COVID’s ghost signage may follow the same trajectory as the defunct Cold War–era nuclear-fallout-shelter signs that lingered on New York City buildings for <a href="https://www.reuters.com/article/us-new-york-nuclear/new-york-removes-misleading-nuclear-fallout-shelter-signs-idUSKBN1EL0SF/">more than half a century</a>, at once misleading observers and reminding them that the nuclear threat, though diminished, is still present.</p><p></p><p>The signs I saw at the Newark airport seemed to me hopelessly obsolete, yet they still stoked unease about how little I think about COVID now, even though the virus is still <a href="https://www.theatlantic.com/health/archive/2024/02/covid-anniversary-flu-isolation-cdc/677588/?utm_source=feed">far deadlier</a> than the flu and other common respiratory illnesses. Passing another <span class="smallcaps">stop the spread</span> hand-sanitizing station, I put my palm under the dispenser, expecting nothing. But this time, a dollop of gel squirted into my hand.</p><p></p>Yasmin Tayaghttp://www.theatlantic.com/author/yasmin-tayag/?utm_source=feedIllustration by Matteo Giuseppe Pani. Source: Getty.The Pandemic’s ‘Ghost Architecture’ Is Still Haunting Us2024-02-29T13:04:00-05:002024-03-11T10:46:41-04:00“Stand six feet apart” signs are outdated, ignored, and everywhere.tag:theatlantic.com,2024:50-677588<p>Four years after what was once the “novel coronavirus” was declared a pandemic, COVID remains the most dangerous infectious respiratory illness regularly circulating in the U.S. But a glance at the United States’ most prominent COVID policies can give the impression that the disease is just another seasonal flu. COVID vaccines are now reformulated annually, and <a href="https://www.theatlantic.com/health/archive/2023/01/annual-seasonal-covid-vaccine-shots-federal-regulation/672854/?utm_source=feed">recommended</a> in the autumn for everyone over the age of six months, just like flu shots; tests and treatments for the disease are steadily being commercialized, like our armamentarium against flu. And the CDC is <a href="https://www.washingtonpost.com/health/2024/02/13/covid-isolation-guidelines-cdc-change/">reportedly</a> considering more flu-esque isolation guidance for COVID: Stay home ’til you’re feeling better and are, for at least a day, fever-free without meds.</p><p></p><p>These changes are a stark departure from the earliest days of the crisis, when public-health experts excoriated public figures—among them, former President Donald Trump—for <a href="https://www.forbes.com/sites/tommybeer/2020/09/10/all-the-times-trump-compared-covid-19-to-the-flu-even-after-he-knew-covid-19-was-far-more-deadly/?sh=6737c97f9d2f">evoking flu</a> to <a href="https://www.vox.com/science-and-health/2020/3/13/21176735/covid-19-coronavirus-worse-than-flu-comparison">minimize</a> COVID deaths and <a href="https://apnews.com/article/virus-outbreak-donald-trump-ap-fact-check-anthony-fauci-flu-fe474f0c15f76adf324791a2cfc1e2bb">dismiss</a> <a href="https://www.washingtonpost.com/politics/2020/10/06/210000-deaths-later-trump-reverts-comparing-coronavirus-flu/">mitigation strategies</a>. COVID might still carry a bigger burden than flu, but COVID policies are getting more flu-ified.</p><p></p><p data-id="injected-recirculation-link"><i>[<a href="https://www.theatlantic.com/health/archive/2023/01/annual-seasonal-covid-vaccine-shots-federal-regulation/672854/?utm_source=feed">Read: The flu-ification of COVID policy is almost complete</a>]</i></p><p></p><p>In some ways, as the population’s immunity has increased, COVID <em>has</em> become more flu-like, says Roby Bhattacharyya, a microbiologist and an infectious-disease physician at Massachusetts General Hospital. Every winter seems to bring a COVID <a href="https://biobot.io/data/">peak</a>, but the virus is now much less likely to hospitalize or kill us, and <a href="https://www.theatlantic.com/health/archive/2024/01/long-covid-dropping-risk-incidence/677183/?utm_source=feed">somewhat less likely to cause long-term illness</a>. People develop symptoms <a href="https://www.thelancet.com/journals/lanmic/article/PIIS2666-5247(23)00005-8/fulltext">sooner after infection</a>, and, especially if they’re vaccinated, are less likely to be as sick for as long. COVID patients are no longer overwhelming hospitals; those who do develop severe COVID tend to be those made more vulnerable by age or other health issues.</p><p></p><p>Even so, COVID and the flu are nowhere near the same. SARS-CoV-2 still spikes in non-winter seasons and simmers throughout the rest of the year. In 2023, COVID hospitalized <a href="https://covid.cdc.gov/covid-data-tracker/#trends_cumulativehospitalizations_select_00">more than 900,000 Americans</a> and killed 75,000; the <a href="https://www.cdc.gov/flu/about/burden/index.html">worst flu season of the past decade</a> hospitalized 200,000 fewer people and resulted in 23,000 fewer deaths. A <a href="https://www.cdc.gov/nchs/covid19/pulse/long-covid.htm">recent CDC survey</a> reported that more than 5 percent of American adults are currently experiencing long COVID, which cannot be fully prevented by vaccination or treatment, and for which there is no cure. Plus, scientists simply understand much less about the coronavirus than flu viruses. Its patterns of spread, its evolution, and the durability of our immunity against it all may continue to change.</p><p></p><p>And yet, the CDC and White House continue to fold COVID in with other long-standing seasonal respiratory infections. When the nation’s authorities start to match the precautions taken against COVID with those for flu, RSV, or common colds, it implies “that the risks are the same,” Saskia Popescu, an epidemiologist at the University of Maryland, told me. Some of those decisions are “not completely unreasonable,” says Costi Sifri, the director of hospital epidemiology at UVA Health, especially on a case-by-case basis. But taken together, they show how bent America has been on treating COVID as a run-of-the-mill disease—making it impossible to manage the illness whose devastation has defined the 2020s.</p><p></p><p>Each “not completely unreasonable” decision has trade-offs. <a href="https://www.theatlantic.com/health/archive/2023/01/annual-seasonal-covid-vaccine-shots-federal-regulation/672854/?utm_source=feed">Piggybacking COVID vaccines onto flu shots</a>, for instance, is convenient: Although COVID-vaccination rates still lag those of flu, they <a href="https://www.theatlantic.com/health/archive/2023/08/respiratory-virus-season-covid-flu-rsv-vaccine-shots/675174/?utm_source=feed">might be even lower</a> if no one could predict when shots might show up. But such convenience may come at the cost of protecting Americans against COVID’s year-round threat. Michael Osterholm, an epidemiologist at the University of Minnesota School of Public Health, told me that a once-a-year vaccine policy is “dead wrong … There is no damn evidence this is a seasonal virus yet.” Safeguards against infection and milder illness start to fade within months, leaving people who dose up in autumn potentially more susceptible to exposures by spring. That said, experts are still torn on the benefits of administering the same vaccine more than once a year—especially to a public that’s largely unwilling to get it. Throughout the pandemic, immunocompromised people have been able to get extra shots. And today, an advisory committee to the CDC <a href="https://www.cdc.gov/vaccines/acip/meetings/downloads/slides-2024-02-28-29/06-COVID-Wallace-508.pdf">voted</a> to <a href="https://yourlocalepidemiologist.substack.com/p/98b18572-b151-412b-bc4c-352badef74a5">recommend</a> that older adults once again get an additional dose of the most recently updated COVID vaccine in the coming months. Neither is a pattern that flu vaccines follow.</p><p></p><p data-id="injected-recirculation-link"><i>[<a href="https://www.theatlantic.com/health/archive/2023/08/respiratory-virus-season-covid-flu-rsv-vaccine-shots/675174/?utm_source=feed">Read: Fall’s vaccine routine didn’t have to be this hard</a>]</i></p><p></p><p>Dropping the current COVID-isolation guideline—which has, since the end of 2021, recommended that people cloister for five days—may likewise be dangerous. Many Americans have long abandoned this isolation timeline, but given how new COVID is to both humanity and science, symptoms alone don’t yet seem enough to determine when mingling is safe, Popescu said. (The dangers are even tougher to gauge for infected people who never develop fevers or other symptoms at all.) Researchers don’t currently have a clear picture of how long people can transmit the virus once they get sick, Sifri told me. For most respiratory illnesses, fevers show up relatively early in infection, which is generally when people pose the most transmission risk, says Aubree Gordon, an epidemiologist at the University of Michigan. But although SARS-CoV-2 <a href="https://www.thelancet.com/journals/lanres/article/PIIS2213-2600(22)00226-0/fulltext">adheres</a> to this same rough timeline, <a href="https://www.nejm.org/doi/full/10.1056/nejmc2202092">infected people</a> can <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9981266/">shed</a> the virus <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9045443/">after their symptoms</a> begin to resolve and are “definitely shedding longer than what you would usually see for flu,” Gordon told me. (Asked about the specifics and precise timing of the update, a CDC spokesperson told me that there were “no updates to COVID guidelines to announce at this time,” and did not respond to questions about how flu precedents had influenced new recommendations.)</p><p></p><p>At the very least, Emily Landon, an infectious-disease physician at the University of Chicago, told me, recommendations for <em>all </em>respiratory illnesses should tell freshly de-isolated people to mask for several days when they’re around others indoors; she would support some change to isolation recommendations with this caveat. But if the CDC aligns the policy fully with its flu policy, it might not mention masking at all.</p><p></p><p data-id="injected-recirculation-link"><i>[<a href="https://www.theatlantic.com/health/archive/2023/02/rules-asymptomatic-covid-have-changed/673233/?utm_source=feed">Read: No one really knows how much COVID is silently spreading … again</a>]</i></p><p></p><p>Several experts told me symptom-based isolation might also remove remaining incentives to test for the coronavirus: There’s little point if the guidelines for all respiratory illnesses are essentially the same. To be fair, Americans have already been testing less frequently—in some cases, to <em>avoid </em>COVID-specific requirements to stay away from work or school. And Osterholm and Gordon told me that, at this point in the pandemic, they agree that keeping people at home for five days isn’t sustainable—especially without paid sick leave, and particularly not for health-care workers, who are in short supply during the height of respiratory-virus season.</p><p></p><p>But the less people test, the less they’ll be diagnosed—and the less they’ll benefit from antivirals such as Paxlovid, which work best when administered early. Sifri worries that this pattern could yield another parallel to flu, for which many providers <a href="https://www.theguardian.com/world/2015/jan/09/cdc-bad-flu-season-doctors-avoid-prescribing-tamiflu">hesitate</a> to <a href="https://news.vumc.org/2023/11/13/study-finds-antiviral-treatment-is-largely-underused-in-children-with-influenza/">prescribe</a> Tamiflu, <a href="https://www.center4research.org/tamiflu-not-tamiflu/">debating</a> its effectiveness. Paxlovid use is already <a href="https://publichealth.jhu.edu/2024/why-more-people-should-be-prescribed-paxlovid-for-covid">shaky</a>; both antivirals may end up chronically underutilized.</p><p></p><p>Flu-ification also threatens to further stigmatize long COVID. Other respiratory infections, including flu, have been <a href="https://medicine.wustl.edu/news/long-flu-has-emerged-as-a-consequence-similar-to-long-covid-19/">documented</a> triggering long-term illness, but potentially at lower rates, and to different degrees than SARS-CoV-2 currently does. Folding this new virus in with the rest could make long COVID seem all the more negligible. What’s more, fewer tests and fewer COVID diagnoses could make it much harder to connect any chronic symptoms to this coronavirus, keeping patients out of long-COVID clinics—or reinforcing a false portrait of the condition’s rarity.</p><p></p><p>The U.S. does continue to treat COVID differently from flu in a few ways. Certain COVID products remain <a href="https://aspr.hhs.gov/newsroom/Pages/FreeTestsSchools-29Nov23.aspx">more</a> <a href="https://www.hhs.gov/about/news/2023/02/07/readout-of-hhs-secretary-becerras-meeting-with-pharmacy-ceos-on-covid-19-therapeutics-commercialization.html">available</a>; some <a href="https://www.theatlantic.com/health/archive/2023/09/covid-infection-surge-universal-masking-return/675239/?utm_source=feed">precautions</a> in health-care settings remain stricter. But these differences, too, will likely continue to fade, even as COVID’s burden persists. Tests, vaccines, and treatments are slowly commercializing; as demand for them drops, supply may too. And several experts told me that they wouldn’t be surprised if hospitals, too, soon flu-ify their COVID policies even more, for instance by allowing recently infected employees to return to work <a href="https://www.cdc.gov/flu/professionals/infectioncontrol/healthcaresettings.htm">once they’re fever-free</a>.</p><p></p><p>Early in the pandemic, public-health experts hoped that COVID’s tragedies would prompt a rethinking of <em>all </em>respiratory illnesses. The pandemic showed what mitigations could do: During the first year of the crisis, isolation, masking, distancing, and shutdowns brought flu transmission to a near halt, and may have <a href="https://www.theatlantic.com/health/archive/2024/02/flu-vaccine-pandemic-change-yamagata-trivalent/677350/?utm_source=feed">driven an entire lineage</a> of the virus <a href="https://www.theatlantic.com/science/archive/2023/04/yamagata-flu-transmission-lineage-extinction/673662/?utm_source=feed">to extinction</a>—something “that never, in my wildest dreams, did I ever think would be possible,” Landon told me.</p><p></p><p>Most of those measures weren’t sustainable. But America’s leaders blew right past a middle ground. The U.S. could have built and maintained systems in which everyone had free access to treatments, tests, and vaccines for a longer list of pathogens; it might have invested in widespread ventilation improvements, or enacted universal sick leave. American homes might have been stocked with <a href="https://www.theatlantic.com/health/archive/2022/03/covid-test-all-respiratory-viruses/622959/?utm_source=feed">tests for a multitude of infectious microbes</a>, and masks to wear when people started to cough. Vaccine requirements in health-care settings and schools might have expanded. Instead, “we seem to be in a more 2019-like place than a future where we’re preventing giving each other colds as much as we could,” Bhattacharyya told me.</p><p></p><p data-id="injected-recirculation-link"><i>[<a href="https://www.theatlantic.com/health/archive/2022/03/covid-test-all-respiratory-viruses/622959/?utm_source=feed">Read: Next winter, what if we test for even more viruses?</a>]</i></p><p><br>
That means a return to a world in which <a href="https://www.cdc.gov/flu/about/burden/index.html">tens of thousands</a> of Americans die each year of flu and RSV, as they did in the 2010s. With COVID here to stay, every winter for the foreseeable future will layer on yet another respiratory virus—and a particularly deadly, disabling, and transmissible one at that. The <a href="https://www.theatlantic.com/health/archive/2023/11/flu-season-winter-sickness-covid/676173/?utm_source=feed">math</a> is simple: “The risk has overall increased for everyone,” Landon said. That straightforward addition could have inspired us to expand our capacity for preserving health and life. Instead, our tolerance for suffering seems to be the only thing that’s grown.</p>Katherine J. Wuhttp://www.theatlantic.com/author/katherine-j-wu/?utm_source=feedIllustration by The Atlantic. Source: lesichkadesign / Getty.Why Are We Still Flu-ifying COVID?2024-02-28T14:22:58-05:002024-02-28T15:18:01-05:00The diseases are nowhere near the same.tag:theatlantic.com,2024:50-677539<p>The state of Florida is trying out a new approach to measles control: No one will be forced to not get sick.</p><p>Joseph Ladapo, the state’s top health official, announced this week that the <a href="https://www.nbcnews.com/health/health-news/measles-outbreak-florida-elementary-school-rcna139637">six cases of the disease</a> reported among students at an elementary school in Weston, near Fort Lauderdale, do not merit <a href="http://www.leg.state.fl.us/statutes/index.cfm?App_mode=Display_Statute&URL=1000-1099/1003/Sections/1003.22.html#:~:text=declare%20a%20communicable%20disease%20emergency">emergency action</a> to prevent unvaccinated students from attending class. Temporary exclusions of that kind while an outbreak is ongoing are part of the <a href="https://www.nyc.gov/site/doh/about/press/pr2019/commissioner-orders-all-yeshivas-to-exclude-unvaccinated-students.page">normal</a> public-health <a href="https://www.nbcnews.com/storyline/measles-outbreak/clark-county-keeps-800-students-out-school-due-measles-outbreak-n980491">response</a> to measles clusters, as a means of both protecting susceptible children and preventing further viral spread. But Ladapo is going his own way. “Due to the high immunity rate in the community, as well as the burden on families and educational cost of healthy children missing school,” he said in a <a href="https://www.nbcmiami.com/news/local/florida-surgeon-general-measles-vaccinations-outbreak/3239826/">letter</a> released on Tuesday, the state’s health department “is deferring to parents or guardians to make decisions about school attendance.”</p><p>That decision came off as brazen, even for an administration that has made <a href="https://www.vanityfair.com/news/2023/03/desantis-antivax-florida-trump">systematic efforts</a> to <em>lower</em> vaccination rates among its constituents over the past two years. Ladapo’s letter acknowledges the benefits of vaccination, as well as the fact that vulnerable children are “normally recommended” to stay home. Still, it doesn’t bother giving local parents the bare-minimum advice that all kids who are able should get their MMR (measles, mumps, and rubella) shots, Dorit Reiss, a professor and vaccine-policy expert at UC Law San Francisco, told me: “I wouldn’t have expected him, in the middle of a measles outbreak, to be willing to sacrifice children in this way.”</p><p>The Florida Department of Health has not responded to a request for comment on Ladapo’s future plans, should this situation worsen. For the moment, though, he has chosen to lower the guardrails from their standard height. It’s an escalation of his, and Florida’s, broader push against established norms in public health, especially as they relate to vaccination. So what happens now?</p><p>At least in any immediate sense, Ladapo’s decision may not do much harm. In fact, there’s good reason to believe that its effects will end up being minimal. Parents who have children at the school, Manatee Bay Elementary, <a href="https://www.cbsnews.com/miami/news/florida-department-of-health-investigates-broward-countys-multiple-measles-cases/">have until today</a> to decide whether to pull out those kids for the next three weeks. Many seem to have already done so: About 200 students and six teachers have been <a href="https://www.nbcnews.com/video/florida-superintendent-says-elementary-school-is-safe-amid-measles-outbreak-204624965971">absent</a>, according to local news reports. In the meantime, Broward County Public Schools’ superintendent said yesterday that just <a href="https://www.miamiherald.com/news/local/education/article285751501.html">33 students</a> out of the school’s nearly 1,100 were still unvaccinated. Given those two facts—some degree of self-imposed isolation, and 97 percent of the community now having some level of immune protection—the virus will have a hard time spreading no matter what the rules for attendance might be.</p><p>Disease modeling, too, suggests that the risk of a larger outbreak is low. For a <a href="https://digitalcommons.library.tmc.edu/cgi/viewcontent.cgi?article=1398&context=childrenatrisk">study</a> released in 2019, a team of researchers based at Newcastle University and the University of Pittsburgh simulated thousands of measles outbreaks at schools in Texas, the most populous state to allow nonmedical exemptions from routine vaccine requirements. The researchers looked at the extent to which a policy of sequestering unvaccinated kids would help to reduce the outbreaks’ size. In the median outcome, even without any school-wide interventions, they found that an initial case of measles spreads only to a small handful of people. Adding in the rule that unvaccinated kids must stay at home has no effect on transmission. When the school’s vaccination rates are assumed to be unusually low, the rule reduces the outbreak’s size by one case.</p><p>Not all of the modeling outcomes are so rosy. For the very worst-case scenarios, in which a case of measles emerges in a school where unvaccinated kids happen to be clustered, the study found that forced suspensions have dramatic benefits. A major outbreak in the Dallas–Fort Worth area, for example, might end up infecting 477 people in the absence of any interventions, according to the model. When unvaccinated kids are kept from going to school, that number drops by 95 percent.</p><p>Hypothetical models can’t tell us what will happen in a real-life school with real-life kids, like the one in Weston, Florida. But given Manatee Bay Elementary’s reported vaccination rate, it’s fair to assume that Ladapo’s policy won’t be catastrophic. Indeed, it may well end up sparing a few dozen families from the fairly serious inconvenience of being out of school without having much effect at all on the outbreak’s final size.</p><p>But is the sparing of that inconvenience worth the risks that still remain? (And how should one value the time of a parent who could have vaccinated their child but chose not to?) As Reiss points out, if this policy leads to even one more case in the current outbreak, it will have put one more kid at risk of hospitalization, long-term complications, or even death. Worst-case outbreak scenarios <em>do</em> occur from time to time, as we all know well by now, and the Weston outbreak getting much worse is certainly within the realm of possibility. Any public-health authority would have to weigh these odds in the face of a six-case cluster, and surely almost every statewide health authority would choose to err on the side of caution. In Florida, though, the scale appears to tip the other way: Ladapo has rolled the dice on doing less.</p><p>That’s been his way since the very day he was appointed by Governor Ron DeSantis, in September 2021. Just hours after he was <a href="https://health.wusf.usf.edu/health-news-florida/2021-09-22/floridas-new-surgeon-general-says-hes-done-with-fear-over-covid">introduced</a>, the state ended mandatory quarantines for low-risk students who had been exposed to COVID. The following March, just a few weeks after being <a href="https://news.wfsu.org/state-news/2022-02-23/despite-democrat-pushback-ladapo-now-has-senate-approval-to-continue-as-floridas-top-doctor">confirmed</a> into the job, Ladapo <a href="https://www.nytimes.com/2022/03/07/us/florida-covid-vaccine-kids.html">announced</a> that Florida would be “the first state to officially recommend against the COVID-19 vaccines for healthy children.” He continued to scale up from there: That fall, he <a href="https://www.floridahealth.gov/newsroom/2022/10/20220512-guidance-mrna-covid19-vaccine.pr.html">recommended against the use of mRNA vaccines</a> by any men under the age of 40. A year later, in October 2023, his office warned everyone under the age of 65 about the risks of getting <a href="https://www.floridahealth.gov/newsroom/2023/10/20231023-booster-covid19.pr.html">an mRNA-based COVID booster</a>. And then, finally, just last month, Ladapo came out with a warning that mRNA-based COVID vaccines “<a href="https://www.floridahealth.gov/newsroom/2024/01/20240103-halt-use-covid19-mrna-vaccines.pr.html">are not appropriate for use in human beings</a>.”</p><p data-id="injected-recirculation-link"><i>[<a href="https://www.theatlantic.com/ideas/archive/2021/03/the-curious-case-of-floridas-pandemic-response/618360/?utm_source=feed">Read: The curious case of Florida’s pandemic response</a>]</i></p><p>The man’s commitment to undermining vaccination is truly unparalleled among leading public-health officials. “As a surgeon general he stands alone,” Reiss told me. Yet Ladapo’s policy activism, however grotesque it might seem, has been bizarrely ineffective in practice. Take his March 2022 move to lead the way on <em>not</em> vaccinating young people against COVID. Media coverage of that announcement dwelled on reasonable concerns that this policy would <a href="https://www.cnn.com/2022/03/08/politics/florida-covid-19-vaccine-desantis/index.html">dampen immunization rates</a>; vaccine experts said it was a dangerous and irresponsible move that would “<a href="https://www.theguardian.com/us-news/2022/mar/08/florida-children-vaccination-coronavirus">cause more people to die</a>.” In practice, though, it seems to have done almost nothing. At the time of Ladapo’s announcement, 24.2 percent of Florida’s kids and 66.3 percent of its teenagers had received at least one dose of a COVID vaccine. (The corresponding national numbers at the time were somewhat higher.) By the end of the year, and in spite of Ladapo’s contrarian guidance, Florida’s vaccination numbers for these age groups were up by about four and three points, respectively—which is almost exactly the same amount, percentage-wise, as the increases in those numbers seen across the country.</p><p>Or compare Florida’s experience to that of Nevada, a state that had very similar child and teen vaccination rates in March 2022: 23.1 percent and 64.0 percent. Through the end of 2022, while Ladapo was discouraging his constituents from getting shots, that state’s Democratic governor was engaged in a <a href="https://www.nevadaappeal.com/news/2021/dec/13/sisolak-announces-effort-vaccinate-ages-5-11-nevad/">large-scale effort</a> to do the opposite. Yet the results were essentially the same: Nevada’s rates increased by pretty much the same amount as Florida’s.</p><p>For all of Ladapo’s efforts to dampen his state’s enthusiasm for <a href="https://www.commonwealthfund.org/blog/2022/two-years-covid-vaccines-prevented-millions-deaths-hospitalizations">life-saving interventions</a>, Florida’s age-adjusted rates of death from COVID do not appear to have increased relative to the rest of the country, at least according to reported numbers. In this way, one of the nation’s loudest and most powerful voices of vaccine skepticism seems to be shouting into the wind. His proclamations and decisions to this point have been exquisitely effective at producing outrage but embarrassingly feeble when it comes to changing outcomes. Even taken on its own terms, as a means of changing public-health behavior, Ladapo’s anti-vaccine activism has been a demonstrable failure.</p><p data-id="injected-recirculation-link"><i>[<a href="https://www.theatlantic.com/health/archive/2023/02/us-covid-vaccine-obsession-future-variants/672933/?utm_source=feed">Read: The good news about vaccine hesitancy</a>]</i></p><p>Perhaps this week’s decision to relax the rules on fighting measles will mark just one more step along that path: Once again, Florida’s surgeon general will have taken an appalling stance that ends up having no effect. But then again, now could be different. By the time Ladapo got around to undermining COVID shots, more than two-thirds of the state’s population, and 91 percent of its seniors, were already fully vaccinated. The damage he could have done was limited. But the measles outbreak in Weston is unfolding in real time. More such outbreaks are <a href="https://www.nytimes.com/2024/02/01/opinion/health/measels-europe-vaccination.html">nearly guaranteed</a> to occur in the U.S. in the months ahead. Reiss worries that Ladapo’s new idea, of choosing not to separate out unvaccinated kids during a school outbreak, could end up spreading to other jurisdictions. “If this becomes a precedent, that becomes a bigger problem,” she told me.</p><p>For the first time since taking office, Ladapo may finally have a real opportunity to make a difference through his vaccination policy. That’s a problem.</p>Daniel Engberhttp://www.theatlantic.com/author/daniel-engber/?utm_source=feedAndrew West / The News Press / USA Today NetworkFlorida’s Experiment With Measles2024-02-22T17:43:00-05:002024-02-23T08:16:39-05:00How far can the state go before a serious outbreak hits?tag:theatlantic.com,2024:50-677510<p>In my childhood home, an often-repeated phrase was “All disease begins in the gut.” My dad, a health nut, used this mantra to justify his insistence that our family eat rice-heavy meals, at the exact same time every day, to promote regularity and thus overall health. I would roll my eyes, dubious that his enthusiasm for this practice was anything more than fussiness.</p><p></p><p>Now, to my chagrin, his obsession has become mainstream. Social-media testimonials claim that improving your “gut health” not only helps with stomach issues such as bloating and pain but also leads to benefits beyond the gastrointestinal system (easing problems including, but not limited to, <a href="https://www.tiktok.com/t/ZT8KXqdsm/">itching</a>, <a href="https://www.tiktok.com/t/ZT8KVaVpM/">puffy face, slow-growing </a><a href="https://www.tiktok.com/t/ZT8KVaVpM/">hair, low energy</a>, <a href="https://www.tiktok.com/t/ZT8KVuKMn/">acne</a>, <a href="https://www.tiktok.com/t/ZT8KVg8cg/">weight gain</a>, and <a href="https://www.tiktok.com/t/ZT8KV7JP2/">anxiety</a>). You can now find a staggering range of products claiming to support digestive health: Joining traditionally gut-friendly fermented foods such as yogurt and sauerkraut are “probiotic” or “prebiotic” teas, cookies, gummies, supplements, powders, and even sodas.</p><p></p><p>The reality is less straightforward. Maintaining the health of the gastrointestinal tract, like the health of any body part, is always a good idea. But expecting certain foods and products to overhaul gut health is unrealistic, as is believing that they will guarantee greater overall well-being. Those claims are “a little bit premature,” Karen Corbin, an investigator at the AdventHealth Research Institute of Metabolism and Diabetes, told me. Obsessing over it just isn’t worth the trouble, and can even do more harm than good. “Gut health” cookies, after all, are still cookies.</p><p></p><p>In my dad’s defense, your gut does matter for your health. A massive microbial civilization lives <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5837012/#:~:text=Bacteria%20form%20the%20majority%20of,small%20intestine%20and%20stomach4.">mostly along the large intestine</a>, helping the body get the most out of food. Broadly, a healthy gut is one where the different segments of this population—numerous species of bacteria, fungi, and viruses—live in harmony. An unhealthy one implies a disturbance of the peace: One group may grow too powerful, or an <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2653718/">invading microbe</a> may throw things off-balance, leading to problems including <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5114849/">gastroenteritis</a> and a <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5695238/#:~:text=The%20role%20of%20commensal%20microbes,increase%20susceptibility%20to%20systemic%20infection.">compromised immune system</a>.</p><p></p><p>Diet in particular has a profound impact on the gut—and how it subsequently makes you feel. “Food can have effects on the microbiome, which can then secondarily affect the host,” Purna Kashyap, a gastroenterologist at the Mayo Clinic, told me. The effects of food on a person and their microbes, he added, are generally congruent; fast food, for example, is “bad for both of us.” Neglect to feed your microbiome and the balance of microbes could tip into disarray, resulting in an imbalanced gut and corresponding bloating, stomach pain, and problems with bowel movements.</p><p></p><p>Fermented foods such as yogurt and kimchi, long considered good for digestive health, are known as “probiotics” because they contain live bacteria that take up residence in your gut. Other foods are considered “prebiotic” because they feed the microbes already in your gut—mostly fiber, because it isn’t digested in the stomach. Getting more fiber improves regularity and supports a more normal GI system, Corbin said.</p><p></p><p>But the fundamental problem with the gut-health obsession is that “there’s no clear definition of a healthy gut microbiome,” Corbin said. The makeup and balance of people’s microbiomes vary based on numerous factors, including genes, diet, environment, and even pets. This means that a treatment that works to rebalance one gut might not work for another. It also means that a product promoting a healthy gut doesn’t mean anything concrete. The idea that achieving gut health, however it’s defined, can solve stomach-related issues is misguided; <a href="https://www.mountsinai.org/health-library/symptoms/abdominal-pain">many diseases</a> can cause abdominal distress.</p><p></p><p>Less certain is how much gut health is responsible for benefits <em>beyond</em> the gastrointestinal tract. No doubt the microbiome is connected to other parts of the body; recent research has suggested that it has a role in <a href="https://www.utsouthwestern.edu/newsroom/articles/year-2023/aug-intestinal-bacteria-weight-gain.html">weight gain</a>, <a href="https://www.thelancet.com/journals/ebiom/article/PIIS2352-3964(23)00092-0/fulltext#secsectitle0010">depression</a>, and even <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9903080/#:~:text=Recent%20findings%20have%20shown%20that,ncRNA)%20through%20the%20gut%20microbiome.">cancer</a>, supporting the idea that having a healthy gut could lead to other benefits. But the mechanisms underpinning them are largely unknown. Which microbes are involved? What are they doing? There are “a lot of tall claims based on animal studies that the microbiome influences diabetes or obesity or whatever,” and the translatability of those studies to humans is “really unlikely,” Daniel Freedberg, a gastroenterologist at Columbia University, told me. Until scientists can show definitively that microbe X leads to outcome Y, Corbin said, any relationships between the gut and overall health are “just correlations.”</p><p></p><p>None of this is to say that paying more attention to your digestive health is a bad idea. Especially for people diagnosed with gastrointestinal problems like IBS or Crohn’s disease, it can be essential. For everyone else, pursuing a healthy gut with food and supplements can be a nonspecific process with poorly defined goals. The food industry has capitalized on interest in probiotics and prebiotics—as well as lesser-known <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9027423/#:~:text=Therefore%2C%20the%20term%20postbiotic%20appropriately,microbes%2C%20such%20as%20cell%20walls.">postbiotics</a> and <a href="https://pubmed.ncbi.nlm.nih.gov/31965850/">synbiotics</a>—making products such as <a href="https://thecoconutcult.com/">“insanely probiotic”</a><a href="https://thecoconutcult.com/"> yogurt</a>, probiotic-fortified chocolate and spaghetti, and prebiotic sodas. Particularly with probiotics, the specifics are lacking. Which bacteria, and how many of them, actually make it past the stomach into the colon isn’t well understood. “A lot of probiotics are unlikely to contain viable bacteria, and probably very few of them are really making it through to the colon,” Freedberg said.</p><p></p><p>Prebiotics are generally more important, although the source matters. Prebiotic fiber is “one of the most important things that determines what bacteria are there,” Freedberg told me, but getting small amounts from fiber-fortified products isn't going to make a huge difference. The soda brands Poppi and Olipop largely contain inulin, a type of fiber that’s common in food manufacturing for its slightly sweet taste, Freedberg explained, though it probably doesn’t contain a lot, otherwise it would become “sludgy.” Olipop contains about nine grams of fiber per can, roughly the same amount as <a href="https://www.dietaryguidelines.gov/resources/2020-2025-dietary-guidelines-online-materials/food-sources-select-nutrients/food-0">one cup of cooked lima</a><a href="https://www.dietaryguidelines.gov/resources/2020-2025-dietary-guidelines-online-materials/food-sources-select-nutrients/food-0"> beans</a>.</p><p></p><p>Of course, any product that is inherently unhealthy won’t magically become good for you the moment fiber or live bacteria are added to it. With desserts and salty snacks, no amount of fiber “is going to overcome the issue” that they are full of sugar or salt, Corbin said. Concerns about medium aside, though, gut-health products elicited a shrug from her: Buying foods containing additional prebiotic fiber is a “reasonable approach,” so long as they’re healthy to begin with. If probiotics make a patient feel “fantastic,” Freedberg said, “I’m not going to rock the boat.” Prebiotic and probiotic products may help to a degree, but don’t expect them to overhaul an unhealthy gut one soda at a time. All of the experts I spoke with said that people concerned about their gut health should eat a lot of fruits, vegetables, whole grains, and legumes, and cut out junk that won’t feed their microbiome. In other words, a basic healthy diet is more than enough to achieve good gut health.</p><p></p><p>My dad’s gut-health mantra was <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8452999/#:~:text=More%20than%202000%20years%20ago,and%20inflammatory%20disorders%20%5B5%5D.">apparently borrowed from Hippocrates</a>, suggesting that people have been obsessing over the digestive system for thousands of years with the belief that it is the key to overall health. The draw of this idea is its simplicity: Proposing that the body’s many ills can be collapsed into a single mega-ailment makes treatment seem refreshingly uncomplicated compared with the medical interventions needed to address individual problems. That the proposed treatments are easy and self-administrable—sipping fibrous soda, popping bacteria-packed pills—adds to the appeal.</p><p>But perhaps what is most compelling about the idea is that there is some truth to it. Lately, research on the microbiome has seen some promising advances. A large study published in 2022 showed <a href="https://www.nature.com/articles/s41467-022-34502-3">significantly elevated levels</a> of certain bacteria in people with depressive symptoms. Another <a href="https://www.nature.com/articles/s41467-023-38778-x?utm_campaign=related_content&utm_source=HEALTH&utm_medium=communities">study</a>, co-authored by Corbin in 2023, was one of the first to show, in a human clinical trial, that a high-fiber diet shifts the microbiome in a way that could promote weight loss. This moment is especially confusing because we are finally beginning to understand the gut’s connections to the rest of the body, and how eating certain foods can soothe it. Much more is known about the gut than in the days of Hippocrates, but still far less than the gut influencers on social media would have you believe.</p>Yasmin Tayaghttp://www.theatlantic.com/author/yasmin-tayag/?utm_source=feedIllustration by Matteo Giuseppe Pani. Source: Getty.‘Gut Health’ Has a Fatal Flaw2024-02-20T13:44:00-05:002024-02-21T11:51:25-05:00The obsession with digestion has gone too far.tag:theatlantic.com,2024:50-677415<p><small><em>This article was originally published by </em><a href="https://knowablemagazine.org/content/article/health-disease/2024/where-did-bed-bugs-come-from-how-to-get-rid-of-them">Knowable Magazine</a><em>.</em></small></p><p>The stories have become horribly familiar: houses so overrun by bedbugs that the bloodsucking insects pile an <a href="https://www.youtube.com/watch?v=dutu022h-hU">inch deep</a> on the floor. An airport <a href="https://www.kiro7.com/news/trending/hawaii-airport-closed-multiple-gates-deep-clean-after-bed-bug-discovery/T7DIU4O26NASRAAZUFW27CGCLU/">shutting down gates for deep cleaning</a> after the parasites were spotted. Fear and loathing during Fashion Week 2023 in Paris, with bedbug-detection dogs working overtime when the insects turned up in movie theaters and trains.</p><p>For reasons that almost certainly have to do with global travel and poor pest management, bedbugs have resurfaced with a vengeance in 50 countries since the late 1990s. But recently, the resurgence has brought an added twist: When exterminators swarm out to hunt these pests, they might encounter not just one but two different kinds of bugs.</p><p>Besides the common bedbug, <em>Cimex lectularius</em>, which has always made its home in the Northern Hemisphere, there are now sightings of its relative, the tropical bedbug, <em>Cimex hemipterus</em>, in temperate regions. Historically, this species didn’t venture that far from the equator, write the entomologists Stephen Doggett and Chow-Yang Lee in the <a href="https://www.annualreviews.org/doi/10.1146/annurev-ento-120220-015010">2023 issue of the <em>Annual Review of Entomology</em></a>. But in recent years, tropical bedbugs have turned up in the United States, Sweden, Italy, Norway, Finland, China, Japan, France, Central Europe, Spain—“even in Russia, which would have once been unthinkable,” says Lee, a professor of urban entomology at UC Riverside.</p><p>Like the common bedbug, the tropical version has grown resistant to many standard pesticides—to the point where some experts say they wouldn’t bother spraying should their own home become infested. It has been estimated that the fight against bedbugs is costing the world economy billions annually.</p><p>This all adds up to a sobering new reality: For many people, bedbugs are becoming a fact of life again, much as they used to be throughout humanity’s history. But as scientists race to find new strategies to combat these pests—everything from microfabricated surfaces that entrap the insects to fungal spores that invade and kill them—they also learn more about the often-bizarre biology of bedbugs, which might one day reveal the parasite’s Achilles’ heel.</p><p>Genomics shows that bedbugs emerged 115 million years ago, before the dinosaurs went extinct. When the first humans appeared and moved into caves, the ancestors of today’s bedbugs were ready and waiting. It is thought that these insects initially fed on <a href="https://knowablemagazine.org/content/article/living-world/2018/betting-bats-genetic-treasures">bats</a>. But bats reduce their blood circulation during their sleeplike torpor state, likely making it harder for the bloodsucking parasite to feed. Presumably, then, at least some bedbug ancestors happily switched to humans.</p><p>Since then, the bugs have followed humankind across the globe, tagging along on ancient shipping routes and modern plane rides. Preserved bedbugs were found in the quarters used by workers in ancient Egypt some 3,550 years ago.</p><p>Bedbugs can survive a year or more without feeding. About as big as flattened apple seeds, they squeeze into tiny cracks in walls or in the joints of bed frames during the day; they crawl out at night, attracted by a sleeper’s exhaled carbon dioxide and body warmth. At the turn of the 20th century, an estimated <a href="https://www.researchgate.net/publication/372234325_Battling_Bed_Bugs_Through_the_Ages_A_Historical_Journey_of_Control_Strategies_Part_1_Pre-Insecticides">75 percent of homes in the U.K. contained bedbugs</a>. Bizarre prescriptions for remedies have circulated down the years, including a recipe for “cat juice” in a pest-control guide from 1725. The formula called for suffocating and skinning a cat, roasting it on a spit, mixing the drippings with egg yolk and oil, and smearing the concoction into crevices around the bed.</p><p>DDT (dichlorodiphenyltrichloroethane) and the pesticides that followed helped bring a few decades’ worth of respite from the 1940s to the 1990s—enough that most people forgot about the insects and didn’t recognize them when they reappeared around the turn of the millennium.</p><p>Doggett and Lee hypothesize that the bloodsuckers’ comeback started in areas of Africa, where common and tropical bedbugs naturally coexist, and where DDT (and, later, other insecticides) were sprayed in bedrooms against malaria-carrying mosquitoes. Initially, this would have killed the majority of bedbugs too. But some resistant ones survived and multiplied.</p><p data-id="injected-recirculation-link"><i>[<a href="https://www.theatlantic.com/magazine/archive/2021/12/animals-adapting-climate-change/620532/?utm_source=feed">Read: Animals of the future</a>]</i></p><p>Bedbugs suck up more than three times their body weight in blood. As they do, they also take in any viruses or other infectious agents that might circulate in the body of their prey, such as hepatitis B and HIV. They have never been found to transmit these pathogens in the wild—but this doesn’t mean that the parasites are benign. “Bedbugs produce some of the most irritating bites of all insects,” says Doggett, a medical entomologist at Westmead Hospital, in Sydney, Australia. “If I receive one, I don’t sleep, as I react so badly. If there are lots of bedbugs, the bites are horrendous.” There have been cases where people have accidentally set mattresses on fire in desperate attempts to chase off the bugs, sometimes <a href="https://www.washingtonpost.com/news/post-nation/wp/2017/12/10/a-woman-tried-to-kill-bed-bugs-with-alcohol-and-set-a-fire-that-left-10-without-a-home/">burning down their home in the process</a>.</p><p>Humans aren’t the only ones to react so strongly. The <em>Cimicidae</em> family, to which bedbugs belong, comprises about 100 species. Almost all prefer to bite nonhuman animals, such as <a href="https://knowablemagazine.org/content/article/living-world/2022/learning-about-birds-their-genomes">birds</a>. Biologists have observed cliff-swallow chicks jumping to their death from heavily infested nests rather than enduring the bites.</p><p>Infestations in which hundreds of bugs may descend upon a bed at night can cause a human sleeper to become anemic. Victims can even develop insomnia, anxiety, and <a href="https://knowablemagazine.org/content/article/health-disease/2022/how-antidepressants-changed-ideas-depression">depression</a>. They may find themselves shunned by friends, blacklisted by landlords, and—being sleep-deprived—more prone to car accidents and problems at work.</p><p data-id="injected-recirculation-link"><i>[<a href="https://www.theatlantic.com/health/archive/2014/10/bed-bug-madness-the-psychological-toll-of-the-blood-suckers/381447/?utm_source=feed">Read: The psychological toll of bedbugs</a>]</i></p><p>Indirectly, at least, bedbugs may cause human deaths. Doggett has noticed that some people in Africa are giving up the bed nets that protect them from mosquitoes and life-threatening malaria infections because bedbugs hide in them. “In some regions, malaria cases are on the rise, and we think that bedbugs are contributing to this,” he says.</p><p>By now, bedbug resistance has been reported against most of the prevalent insecticides, including organochlorines, organophosphates, carbamates, neonicotinoids, aryl pyrroles, and pyrethroids. Some of today’s bedbug strains tolerate pesticide doses that are many thousands of times higher than those that used to consistently kill them. Resistant bedbugs have either developed gene mutations that prevent pesticides from binding effectively to their cells or they produce enzymes that quickly break down the toxins in their body. Others are growing thicker exoskeletons that the poisons can’t easily penetrate.</p><p>An investigation some years back into a hospital in Cleveland discovered that new bedbugs showed up in the facility every 2.2 days on average. And tropical bedbugs seem just as happy in our modern indoors as the common variety does. “Heating and air-conditioning have made our living environments more standardized,” Lee says. “If a tropical bedbug happens to be introduced to a house in Norway, it can now survive there even in winter.”</p><p>Currently, the only bedbug sprays that still tend to work are certain combination products that blend different classes of pesticides. But it’s only a matter of time before these, too, will fail, experts say: Reports of resistance have already been documented. More and more, exterminators incorporate nonchemical approaches such as heat treatments, in which trained professionals warm up rooms to more than 120 degrees Fahrenheit for several hours. They sometimes sprinkle a floury dust called diatomaceous earth around rooms, which clings to those bugs that hide from the heat in wall cracks or under mattresses. The dust abrades the insect’s exoskeleton, dehydrating it to death.</p><p>Such measures—combined with more awareness—have helped plateau, or even partly reverse, the spread of bedbugs in some places. In New York City, for example, bedbug complaints <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9135212/#:~:text=Bed%20bug%20complaints%20have%20significantly,decrease%20over%20the%20same%20period.">fell by half</a> from 2014 to 2020, from 875 complaints a month to 440, on average. To be sure, that’s still 14 complaints a day.</p><p>But although effective, nonchemical methods tend to work slowly. “It’s very common that an elimination takes one to two or even three months,” says Changlu Wang, an entomologist at Rutgers University. Meanwhile, residents must keep living in their infested quarters.</p><p>Nonchemical measures may also be expensive, because they can require laborious steps such as sealing cracks in walls and physically removing bugs by vacuuming. Although a quick (but increasingly futile) spraying of pesticides may cost a few hundred dollars, mechanical eradications can run as high as several thousand dollars. This puts effective bedbug control out of many people’s reach, making them vulnerable to entrenched infestations that can spread through communities.</p><p>The result is that the epidemic has shifted to the poor, says Michael Levy, an epidemiologist at the University of Pennsylvania: “While many cities now have bedbug policies, very few provide much assistance to those who cannot afford treatment.” A 2016 report on 2,372 low-income apartment units in 43 buildings across four New Jersey cities found that 3.8 percent to 29.5 percent were infested with bedbugs.</p><p>The northward spread of tropical bedbugs complicates matters further. Although the two species look alike, tropical bedbugs have more hair on their legs, which allows them to climb out of many of the smooth-walled traps that are used to monitor homes. This means that infestations could stay undetected longer, Lee says. And the larger a population grows, the harder it is to get rid of.</p><p>To fight back, researchers find inspiration in traditional wisdom. In the Balkan region, homeowners used to spread the leaves of the bean plant <em>Phaseolus vulgaris L.</em> around their beds. The leaves possess tiny hooks on their surface that trap the bugs. Now scientists at UC Irvine are developing a “physical insecticide” in the shape of a synthetic material sporting sharply curved microstructures that mimic those on the bean leaves. These irreversibly impale the feet of the bedbugs, Catherine Loudon, a biology professor at UC Irvine, wrote in a 2022 paper in <a href="https://academic.oup.com/icb/article/62/5/1186/6591576"><em>Integrative and Comparative Biology</em></a>: “The bugs are unable to get away once they are pierced.”</p><p>Other recent approaches are also rooted in nature. Scientists have found, for example, that essential oils can repel bedbugs. However, the effect is mostly temporary. Certain fungal spores, on the other hand, work permanently. “Basically, the spores go into the body of the bedbug and kill it,” Wang says. At least one product containing the insect-killing fungus <em>Beauveria bassiana</em> is now available in the United States.</p><p data-id="injected-recirculation-link"><i>[<a href="https://www.theatlantic.com/health/archive/2014/12/a-better-bedbug-trap/384123/?utm_source=feed">Read: A better bed bug trap</a>]</i></p><p>Researchers continue to be fascinated by the biology of this insect, particularly its sex life. Although female bedbugs possess a normal set of genitalia, the males typically mate by stabbing a needle-sharp penis straight into the female’s abdomen to inject sperm. They usually do this just after a female bedbug has fed, because this makes her too engorged to protect herself.</p><p>Having to cope with these frequent injuries has led female bedbugs to evolve the only immunity organ in the insect kingdom, says Klaus Reinhardt, a zoologist at the Dresden University of Technology, in Germany. They have also evolved a remarkably elastic material that covers the parts of their abdomen most likely to be stabbed. “It resembles one of those self-sealing injection bottles that close up again when you pull the needle,” Reinhardt says.</p><p>Although this knowledge will likely do little to combat these pests directly, answering another question might: Why don’t bedbugs stay on their host’s body, as lice do? As it turns out, bedbugs don’t like our smell. Certain <a href="https://www.nature.com/articles/s41598-021-01981-1">lipids in human skin repel the bugs</a>, according to a 2021 study in <em>Scientific Reports</em>. This makes them retreat to daytime hiding places, marking their trails with pheromones.</p><p>Already, exterminators try to trap bedbugs with fake trail markings. And one day, we might deter the insects from spreading by treating suitcases with smells they despise.</p><p>But for now, caution remains the best approach. Experts advise that travelers check accommodations for bedbug-defecation stains: on mattress seams and furniture, and behind headboards. (The insects poop as frequently as a few dozen times after every blood meal, often right next to their victims.) Suitcases should be kept in the hotel bathtub or wrapped in a plastic bag. Upon arrival back home, the luggage’s contents should be put into the clothes dryer for at least 30 minutes at the highest setting, or into a very cold freezer for several days.</p><p>If bedbugs do invade a home, “the biggest mistake is to try and get rid of them on one’s own,” Doggett says. “The average person doesn’t appreciate how challenging it is to control bedbugs and will use supermarket insecticides that are labeled for bedbugs but don’t work. The infestation will spread, and the costs escalate.”</p>Ute Eberlehttp://www.theatlantic.com/author/ute-eberle/?utm_source=feedIllustration by The Atlantic. Source: animatedfunk; Paul Campbell / Getty.The ‘Unthinkable’ New Reality About Bedbugs2024-02-10T08:00:00-05:002024-02-12T15:17:57-05:00Another, much stronger species is headed north.tag:theatlantic.com,2024:50-677411<p>No medication in the history of modern weight loss has inspired as much awe as the latest class of obesity drugs. Wegovy and Zepbound are so effective that they are often likened to “<a href="https://www.barrons.com/articles/obesity-weight-loss-drugs-food-beverage-stocks-8f84b3cf">magic</a><a href="https://www.barrons.com/articles/obesity-weight-loss-drugs-food-beverage-stocks-8f84b3cf">”</a> and “<a href="https://www.cnbc.com/2023/10/14/obesity-medicine-euphoria-warning-experts-tackle-miracle-drugs.html">miracles</a>.” Indeed, the weekly injections, which belong to a broader class known as GLP-1s, can lead to weight loss of 20 percent or more, fueling hype about a future in which many more millions of Americans take them. Major food companies including <a href="https://agfundernews.com/from-glp-1-companion-foods-to-natures-ozempic-what-the-new-breed-of-weight-loss-drugs-means-for-the-food-industry">Nestlé</a> and <a href="https://www.reuters.com/business/retail-consumer/snack-maker-conagra-may-tweak-portions-weight-loss-drugs-alter-appetites-2023-10-05/">Conagra</a> are considering tailoring their products to suit GLP-1 users. Underlying all this excitement is a huge assumption: They work for everyone.</p><p></p><p>But for a lot of people, they just <em>don’t</em>. Anita, who lives in Arizona, told me she “took it for granted” that she would lose weight on a GLP-1 drug because “the people around me who were on it were just dropping weight like mad.” Instead, she didn’t shed any pounds. Likewise, Kathryn, from Florida, hasn’t lost any weight since starting the medication in October. “I was really hoping this was something that would be a game changer for me, but it feels like it was just a lot of wasted money,” she told me. (I’m identifying both Anita and Kathryn by their first name only to allow them to speak openly about their health issues.)</p><p></p><p>Some people can’t tolerate the side effects of the drugs and have to stop taking them. Others simply don’t respond. For some, the strength of the dose, or length of the treatment, does not seem to make a difference. Appetites might remain robust; the “<a href="https://www.pbs.org/newshour/health/patients-say-drugs-like-ozempic-help-with-food-noise-heres-what-that-means">food chatter</a>” in the brain may stay noisy. Together, both groups of less successful GLP-1 users account for a not-insignificant share of patients on these drugs—potentially up to a third. “We don’t really know why it happens, [but] we know it does happen,” Louis Aronne, an obesity-medicine specialist at Weill Cornell Medical College, told me. Despite the promise of a so-called Ozempic revolution, lots of “No-zempics” have been left behind.</p><p>Of the two biggest reasons some people don’t lose weight on GLP-1 drugs—side effects and nonresponse—the former is much more straightforward. The GLP-1 drugs Wegovy and Zepbound (which contain the active ingredients semaglutide and tirzepatide, respectively), are known for causing potentially gnarly gastrointestinal symptoms, such as nausea and vomiting, although most people’s reactions are mild and temporary. Yet some have it far worse. Severe, albeit uncommon, side effects include pancreatitis, severe gastrointestinal distress, low blood sugar, and even hair loss, which “can push people off” the drugs, Steven Heymsfield, a professor who studies obesity at Louisiana State University, told me. In one of the <a href="https://newsroom.clevelandclinic.org/2023/11/11/international-clinical-trial-finds-that-semaglutide-reduced-cardiovascular-events-by-20-in-adults-with-overweight-or-obesity-who-dont-have-diabetes/">biggest studies</a> of semaglutide, encompassing more than 17,000 people over about five years, nearly 17 percent of patients discontinued the medication because of side effects.</p><p></p><p>Far more mysterious are the people who tolerate the drugs but respond weakly to them—or sometimes not at all. Researchers have known this might happen since these drugs were in early <a href="https://www.nejm.org/doi/full/10.1056/NEJMoa2032183">clinical</a> <a href="https://pubmed.ncbi.nlm.nih.gov/30293770/">trials</a>. About 14 percent of people who took semaglutide for obesity saw minimal impacts of less than 5 percent weight loss <a href="https://www.nejm.org/doi/full/10.1056/NEJMoa2032183">in one study</a>, as did 9 to 15 percent of people who took tirzepatide in a <a href="https://www.nejm.org/doi/full/10.1056/NEJMoa2206038">similar one</a>. In her own experience working with patients, “somewhere between a quarter and a third” are nonresponders, Fatima Cody Stanford, an obesity-medicine specialist at Harvard, told me, adding that it can take up to three months to determine whether the drug is working or not. That the same medication at the same dosage can lead to dramatic weight loss in one person and hardly any in another “remains confounding,” Aronne told me.</p><p></p><p>The broad explanation is that it has something to do with genetics. The drugs work by masquerading as the appetite-suppressing hormone GLP-1 and binding to its receptor, like a key fitting into a lock. Although the lock’s overall shape is generally consistent from person to person, its nooks and crannies can vary because of genetic differences. “For some people, that key just won’t fit right,” Eduardo Grunvald, an obesity-medicine doctor at UC San Diego Health, told me. In other cases, genes may limit the effects of these drugs after they bind to GLP-1 receptors. One possibility is that people metabolize the drugs differently: Some patients may break them down too quickly for them to take effect; others may process them too slowly, potentially building up such high levels of the medications that they become toxic, Heymsfield said.</p><p></p><p>For No-zempic patients, perhaps the most consequential impact of individual variation is on the propensity for obesity itself. “We are all very different from a genetic standpoint, in terms of our risk of weight gain,” Grunvald said. Numerous factors can drive obesity, including diet, environment, stress, and—most pertinent to GLP-1 drugs—altered brain function.</p><p></p><p>GLP-1 drugs target a pathway that regulates appetite and insulin levels. Some cases of obesity can be caused by a disruption in that particular mechanism, in which case GLP-1s can indeed be wondrous. But “not everyone has dysfunction in this particular pathway,” Stanford said. When that is the case, the drugs won’t be very effective. A different <a href="https://www.thelancet.com/journals/eclinm/article/PIIS2589-5370(23)00059-7/fulltext#secsectitle0055">pathway</a>, for example, controls the absorption of fat from food; another increases energy expenditure. In these people, GLP-1s might tamp down appetite to a degree, maybe leading to some weight loss, but a different drug may be required to treat obesity at its root. “It is not all about food intake,” Stanford said.</p><p></p><p>That’s not to say that No-zempics are out of options. They might have better success switching from one GLP-1 to the other, or even stacking them, Heymsfield said. Some patients who don’t respond to GLP-1s at all can get better results with <a href="https://www.niddk.nih.gov/health-information/weight-management/prescription-medications-treat-overweight-obesity">older drugs</a> that work on different obesity pathways, Aronne said. One, called Qsymia, a combination of the <a href="https://www.ncbi.nlm.nih.gov/books/NBK482165/#:~:text=Phentermine%20was%20first%20introduced%20in,with%20exercise%20and%20caloric%20restriction.">decades-old drugs</a> phentermine and topiramate, can lead to an average weight loss of 14 percent body weight at its highest dose. If medications don’t work, bariatric surgery remains a <a href="https://www.theatlantic.com/health/archive/2023/04/weight-loss-surgeons-arent-worried-about-ozempic/673853/?utm_source=feed">powerful option</a>, one that may even be growing in popularity. Last year, the number of <a href="https://www.medtechdive.com/news/procedure-volumes-capital-spending-trends-survey/703865/">bariatric surgeries performed in the U.S. grew</a> despite the boom in GLP-1 usage, a trend that <a href="https://www.healthcaredive.com/news/glp-1s-medtech-executives-q3/698865/">some expect to continue</a>, because so many people don’t tolerate the drugs.</p><p></p><p>The intense hype around the game-changing nature of GLP-1s makes it easy to forget that they are, in fact, just drugs. “Every drug that’s ever been made” works in some people and not in others, Heymsfield said; there’s no reason to think GLP-1s would be any different. Remembering that they are in an early stage of development has a sobering effect. Eventually, obesity drugs may leave fewer people behind. The category is expanding rapidly: By one count, more than <a href="https://www.statnews.com/2023/09/12/new-weight-loss-drug-tracker-novo-nordisk-eli-lilly/">90 new drug candidates</a> are in development.</p><p></p><p>They are evolving to attack obesity from multiple fronts, which, at least in theory, widens their net of potential users. In an <a href="https://www.nejm.org/doi/full/10.1056/NEJMoa2301972">early study</a> on an experimental candidate named retatrutide—called a triple agonist because it acts on GLP-1 as well as two other targets involved in obesity, GIP and glucagon receptors—<em>100 percent</em> of people on the highest dose lost 5 percent or more of their body weight. New candidates are also expected to have fewer side effects. They have to, Heymsfield said, because the competition is so steep that any new drug has to be “as good with less side effects, or better.”</p><p></p><p>But no matter how good these drugs get, it’s unrealistic to think that they’ll become a one-size-fits-all treatment for everyone with obesity. The disease is simply too complex, with too many drivers, for a single type of medication to treat it. More than 200 different drugs exist for treating high blood pressure alone; in comparison, Aronne said, regulating weight is “far more complicated.” The future, rife with options, holds promise that No-zempics may find a way forward. Yet considering all the unknowns about obesity and what causes it, that may not be enough to guarantee that they will see the results they want.</p>Yasmin Tayaghttp://www.theatlantic.com/author/yasmin-tayag/?utm_source=feedKatie MartinOzempic Can Turn Into No-zempic2024-02-09T13:51:00-05:002024-02-13T10:57:28-05:00The obesity-drug revolution is leaving lots of people behind.tag:theatlantic.com,2024:50-677371<p data-flatplan-paragraph="true"><small><i data-stringify-type="italic">This article was featured in the One Story to Read Today newsletter. </i><i data-stringify-type="italic"><a data-event-element="inline link" data-sk="tooltip_parent" data-stringify-link="https://www.theatlantic.com/newsletters/sign-up/one-story-to-read-today/" delay="150" href="https://www.theatlantic.com/newsletters/sign-up/one-story-to-read-today/?utm_source=feed" rel="noopener noreferrer" target="_blank">Sign up for it here</a></i><i data-stringify-type="italic">.</i></small></p><p dir="ltr">Imagine an older man goes in to see his doctor. He’s 72 years old and moderately overweight: 5-foot-10, 190 pounds. His blood tests show high levels of triglycerides. Given his BMI—27.3—the man qualifies for taking semaglutide or tirzepatide, two of the wildly popular injectable drugs for diabetes and obesity that have produced dramatic weight loss in clinical trials. So he asks for a prescription, because his 50th college reunion is approaching and he’d like to get back to his freshman-year weight.</p><p dir="ltr">He certainly <em>could</em> use these drugs to lose weight, says Thomas Wadden, a clinical psychologist and obesity researcher at the University of Pennsylvania, who recently laid out this <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10748770/">hypothetical</a> in an academic paper. But should he? And what about the tens of millions of Americans 65 and older who aren’t simply trying to slim down for a cocktail party, but live with diagnosable obesity? Should they be on Wegovy or Zepbound?</p><p dir="ltr">Already, seniors make up 26.6 percent of the people who have been prescribed these and other GLP-1 agonists, including Ozempic, since 2018, according to a <a href="https://www.medrxiv.org/content/10.1101/2024.01.18.24301500v1">report</a> from Truveta, which draws data from a large network of health-care systems. In the coming years, that proportion could rise even higher: The bipartisan Treat and Reduce Obesity Act, <a href="https://wenstrup.house.gov/updates/documentsingle.aspx?DocumentID=407634">introduced</a> in Congress last July, would allow Medicare to cover drug treatments for obesity among its roughly 50 million Part D enrollees above the age of 65; in principle, about two-fifths of that number would qualify as patients. Even if this law doesn’t pass (and it’s been introduced half a dozen times since 2012), America’s retirees will continue to be prescribed these drugs for diabetes in enormous numbers, and they’ll be losing weight on them as well. One way or another, the Boomers will be giving shape to our Ozempic Age.</p><p dir="ltr">Economists say the cost to Medicare of giving new drugs for obesity to just a fraction of this aging generation would be staggering—<a href="https://www.nejm.org/doi/full/10.1056/NEJMp2300516">$13.6 billion</a> a year, according to an estimate published in <em>The New England Journal of Medicine</em> last March. But the health effects of such a program might also be unsettling. Until recently, the very notion of prescribing any form of weight loss whatsoever to an elderly patient—i.e., someone 65 or older—was considered suspect, even dangerous. “Advising weight loss in obese older adults is still shunned in the medical community,” the geriatric endocrinologist Dennis Villareal and his co-authors wrote in a 2013 “review of the controversy” for a medical journal. More than a decade later, clinicians are still struggling to reach consensus on safety, Villareal told me.</p><p dir="ltr">Ample research shows that interventions for seniors with obesity can resolve associated complications. Wadden helped run a <a href="https://onlinelibrary.wiley.com/doi/10.1038/oby.2006.84">years-long, randomized trial</a> of dramatic calorie reduction—using liquid meal replacements, in part—and stringent exercise advice for thousands of overweight adults with type 2 diabetes. “Clearly the people who were older did have benefits in terms of improved glycemic control and blood-pressure control,” he told me. Other, smaller studies led by Villareal find that older people who succeed at losing weight through diet and exercise end up <a href="https://www.nejm.org/doi/10.1056/NEJMoa1616338">feeling more robust</a>.</p><p dir="ltr">Such outcomes are significant on their own terms, says John Batsis, who treats and studies geriatric obesity at the UNC School of Medicine. “When we talk about older adults, we really need to be thinking about what’s important to older adults,” he told me. “It’s for them to be able to get on the floor and play with their grandchildren, or to be able to walk down the hallway without being completely exhausted.” But weight loss can also have adverse effects. When a person addresses their obesity through dieting alone, as much as 25 percent of the weight they lose derives from loss of muscle, bone, and other fat-free tissue. For seniors who, through natural aging, are already near the threshold of developing a functional impairment, a sudden drop like this could be enfeebling. Wadden’s trial found that, among the people who were on the weight-loss program for more than a decade, their risk of fracture to the hip, shoulder, upper arm, or pelvis increased by <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5685890/">39 percent</a>. An analogous <a href="https://www.medscape.com/viewarticle/997679">increase</a> has turned up in studies of patients who undergo bariatric surgery, Batsis told me.</p><p data-id="injected-recirculation-link" dir="ltr"><i>[<a href="https://www.theatlantic.com/health/archive/2024/02/ozempics-muscle-loss-problem/677326/?utm_source=feed">Read: Ozempic makes you lose more than fat</a>]</i></p><p dir="ltr">The effect of dieting on muscle and bone can be attenuated, but not prevented, through resistance training. And obesity itself—which is associated with higher bone density, but perhaps also reduced bone <em>quality</em>—may pose its own fracture risks, Batsis said. But even when a weight-loss treatment benefits an older patient, what happens when it ends? People tend to regain fat, but they don’t recover bone and muscle, Debra Waters, the director of gerontology research at the University of Otago, in New Zealand, told me. That makes the long-term effects of these interventions for older adults very murky. “What happens when they’re 80? Are they going to have really poor bone quality, and be at higher risk of fracture? We don’t know,” Waters said. “It’s a pretty big gamble to take, in my opinion.”</p><p dir="ltr">Villareal told me that doctors should apply “the general principle of starting slow and going slow” when their older patients are trying to lose weight. But that approach doesn’t necessarily square with the rapid and remarkable weight loss seen in patients who are taking semaglutide or tirzepatide, which may produce a greater proportional loss of muscle and bone. (For semaglutide, it appears to be about 40 percent.)</p><p dir="ltr">Then again, when given to laboratory animals, GLP-1 drugs seem to tamp down inflammation in the brain; they’re now in clinical trials to see whether they might <a href="https://www.reuters.com/business/healthcare-pharmaceuticals/after-weight-loss-alzheimers-may-be-next-frontier-drugs-like-ozempic-2023-05-08/">slow the progression</a> of Alzheimer’s disease and dementia. Their multiple established benefits could also help seniors address several chronic problems—diabetes, obesity, <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9657108/">fatty liver disease</a>, and <a href="https://www.globenewswire.com/news-release/2023/10/10/2757941/0/en/Novo-Nordisk-will-stop-the-once-weekly-injectable-semaglutide-kidney-outcomes-trial-FLOW-based-on-interim-analysis.html">kidney disease</a>, for instance—all at once. “Such a ‘one-stop shop’ approach can lead to reduction of medication burden, adverse drug events, hypoglycemic episodes, medication costs, and treatment nonadherence,” one team of geriatricians <a href="https://journals.sagepub.com/doi/full/10.1177/2040622319862691">proposed</a> in 2019.</p><p dir="ltr">Overall, Batsis remains optimistic. “As a clinician, I’m very excited about these medications,” he told me. As a scientist, though, he’s inclined to wait and see. It’s surely true that <em>some</em> degree of weight loss is a great idea for <em>some</em> older patients. “But the million-dollar question is: What’s the sweet spot? How much weight is really enough? Is it 5 to 10 percent? Or is it 25 percent? We don’t know.” Waters said that if Medicare is going to pay for people’s Wegovy, then it should also cover scans of their body composition, to help predict how weight loss might affect their muscles and bones. Wadden said he thinks that treatments should be limited to people who have specific, weight-related complications. For everyone else—as for the hypothetical 72-year-old man who is prepping for his college reunion—he counsels prudence.</p><p dir="ltr">To some extent, such advice is beside the point. Older people are already on Ozempic, and they’re already on Trulicity, and some of them are already taking GLP-1 drugs as a treatment for obesity. Truveta reported that the patients in its member health-care systems who are over 65 have received 281,000 prescriptions for GLP-1 drugs across the past five years. Given the network’s size, one can assume that at least 1 million seniors, overall, have already tried these medications. Millions more will try them in the years to come. If we still have questions about their use, mass experience will start providing answers.</p>Daniel Engberhttp://www.theatlantic.com/author/daniel-engber/?utm_source=feedIllustration by Ben Kothe / The Atlantic. Sources: Peter Dazeley; JakeOlimb / Getty.Older Americans Are About to Lose a Lot of Weight2024-02-07T07:00:00-05:002024-02-08T08:55:09-05:00People over 65 make up a sizable portion of Americans on GLP-1 drugs. That might be trouble.tag:theatlantic.com,2024:50-677353<p>GoFundMe started as a crowdfunding site for underwriting “<a href="https://kffhealthnews.org/news/gofundme-ceo-gigantic-gaps-in-health-system-showing-up-in-crowdfunding/">ideas and dreams</a>,” and, as GoFundMe’s co-founders, Andrew Ballester and Brad Damphousse, once put it, “<a href="https://www.theatlantic.com/magazine/archive/2019/11/gofundme-nation/598369/?utm_source=feed">for life’s important moments</a>.” In the early years, it funded honeymoon trips, graduation gifts, and church missions to overseas hospitals in need. Now GoFundMe has become a go-to for patients trying to escape medical-billing nightmares.<br>
<br>
<a href="https://onlinelibrary.wiley.com/doi/full/10.1002/nvsm.1777">One study found</a> that, in 2020, the number of U.S. campaigns related to medical causes—about 200,000—was 25 times higher than the number of such campaigns on the site in 2011. More than 500 campaigns are currently dedicated to asking for financial help for treating people, mostly kids, with spinal muscular atrophy, a neurodegenerative genetic condition. The recently approved gene therapy for young children with the condition, by the drugmaker Novartis, costs about $2.1 million for the single-dose treatment.</p><p></p><p>Perhaps the most damning aspect of all this is that paying for expensive care with crowdfunding is no longer seen as unusual; instead, it is being normalized as part of the health system, like getting blood work done or waiting on hold for an appointment. Need a heart transplant? <a href="https://www.mlive.com/news/grand-rapids/2018/11/incoming_congresswomans_tweet.html">Start a GoFundMe</a> in order to <a href="https://kffhealthnews.org/news/no-cash-no-heart-transplant-centers-require-proof-of-payment/">get on the waiting list</a>. Resorting to GoFundMe when faced with bills has become so accepted that in some cases, patient advocates and hospital financial-aid officers recommend crowdfunding as an alternative to being sent to collections. My inbox and the <a href="https://kffhealthnews.org/news/tag/bill-of-the-month/">Bill of the Month project</a> (run by <em>KFF Health News</em>, where I am the senior contributing editor, and NPR) have become a kind of complaint desk for people who can’t afford their medical bills, and I’m gobsmacked every time a patient tells me they’ve been advised that GoFundMe is their best option.</p><p></p><p>GoFundMe itself acknowledges the reliance of patients on the company’s platform. Ari Romio, a spokesperson for the company, said that “medical expenses” is the most common category of fundraiser it hosts. But she declined to say what proportion of campaigns are medically related, because people starting a campaign self-select the purpose of the fundraiser. They might choose the family or travel category, she said, if a child needs to go to a different state for treatment, for example. So although the company has estimated in the past that <a href="https://onlinelibrary.wiley.com/doi/full/10.1002/nvsm.1777">a third</a> of the funds raised on the site are medical-related, that could be an undercount. </p><p></p><p>Andrea Coy of Fort Collins, Colorado, turned to GoFundMe in 2021 as a last resort after an air-ambulance bill tipped her family’s finances over the edge. Her son Sebastian, then a year old, had been admitted with pneumonia to a local hospital and then transferred urgently by helicopter to Children’s Hospital Colorado in Denver when his oxygen levels dropped. REACH, the air-ambulance transport company that contracted with the hospital, was out-of-network, and billed the family nearly $65,000 for the ride—more than $28,000 of which Coy’s insurer, UnitedHealthcare, paid. Even so, REACH continued sending Coy’s family bills for the remaining balance, and later began regularly calling Coy to try to collect, enough that she felt the company was harassing her, she told me.</p><p></p><p>Coy made multiple calls to her company’s human-resources department, REACH, and UnitedHealthcare for help in resolving the case. She applied to various patient groups for financial assistance and was rejected again and again. Eventually, she got the outstanding balance knocked down to $5,000, but even that was more than she could afford on top of the $12,000 the family owed out-of-pocket for Sebastian’s actual treatment.</p><p></p><p>That’s when a hospital financial-aid officer suggested she try GoFundMe. But, as Coy said, “I’m not an influencer or anything like that,” so the appeal “offered only a bit of temporary relief—we’ve hit a wall.” They have gone deep into debt and hope to climb out of it.</p><p></p><p>In an emailed response, a spokesperson for REACH noted that they could not comment on a specific case because of patient-privacy laws, but that, if the ride occurred before the federal No Surprises Act went into effect, the bill was legal. (That act protects patients from such air-ambulance bills and has been in force since January 1, 2022.) But the spokesperson added, “If a patient is experiencing a financial hardship, we work with them to find equitable solutions.” What is “equitable”—and whether that includes seeking an additional $5,000, beyond a $28,000 insurance payment, for transporting a sick child—is subjective, of course. </p><p></p><p>In many respects, research shows, GoFundMe <a href="https://www.sciencedirect.com/science/article/abs/pii/S0277953623002095">tends to perpetuate socioeconomic disparities</a> that already affect medical bills and debt. If you are famous or part of a circle of friends who have money, your crowdfunding campaign is much more likely to succeed than if you are middle-class or poor. When the family of the former Olympic gymnast Mary Lou Retton started a fundraiser on another platform, *spotfund, for her recent ICU stay at a time when she was uninsured, <a href="https://www.theguardian.com/sport/2023/oct/23/mary-lou-retton-released-from-hospital-but-has-long-road-ahead-in-recovery">nearly $460,000 in donations</a> quickly poured in. (Although Retton said she could not get affordable insurance because of her preexisting condition—dozens of orthopedic surgeries—the Affordable Care Act <a href="https://kffhealthnews.org/news/article/mary-lou-retton-uninsured-aca-olympic-gymnast-missed-bar/">prohibits insurers</a> from refusing to cover people because of their prior medical histories, or charging them abnormally high rates.)</p><p></p><p>And given the price of American health care, even the most robust fundraising can feel inadequate. If you’re looking for help to pay for a $2 million drug, even tens of thousands is a drop in the bucket.</p><p></p><p>Rob Solomon, <a href="https://www.linkedin.com/pulse/introducing-gofundmes-next-ceo-rob-solomon%3FtrackingId=Qv0nAaRVnDijrucK6WlmMA%253D%253D/?trackingId=Qv0nAaRVnDijrucK6WlmMA%3D%3D">the CEO of the platform</a> from 2015 to <a href="https://techcrunch.com/2020/01/29/gofundme-ceo-rob-solomon-is-stepping-down-will-be-replaced-by-tim-cadogan-ceo-of-openx/">March 2020</a>, who was named one of <em>Time</em> magazine’s <a href="https://time.com/collection/health-care-50/">50 most influential people</a> in health care, has <a href="https://kffhealthnews.org/news/gofundme-ceo-gigantic-gaps-in-health-system-showing-up-in-crowdfunding/">said</a> that he “would love nothing more than for ‘medical’ to not be a category on GoFundMe.” He told <em>KFF Health News</em> that “the system is terrible. It needs to be rethought and retooled. Politicians are failing us. Health-care companies are failing us. Those are realities.”</p><p></p><p>But despite the noble ambitions of its original vision, GoFundMe is a privately held for-profit company. In 2015, the founders sold a majority stake to a venture-capital investor group led by Accel Partners and Technology Crossover Ventures. And when I asked about medical bills being the most common reason for GoFundMe campaigns, the company’s current CEO, Tim Cadogan, sounded less critical than his predecessor of the health system, whose high prices and financial cruelty have arguably made his company famous.</p><p></p><p>“Our mission is to help people help each other,” he said. “We are not, and cannot, be the solution to complex, systemic problems that are best solved with meaningful public policy.”</p><p></p><p>And that’s true. Despite the site’s hopeful vibe, most campaigns generate only a small fraction of the money owed. Almost all of the medical-expense campaigns in the U.S. fell short of their goal, and some raised little or no money, a 2017 study from the University of Washington found. The average campaign made it to just about 40 percent of the target amount, and there is evidence that yields—measured as a percent of their target—have gotten worse over time. </p><p></p><p>Carol Justice, a recently retired civil servant and a longtime union member in Portland, Oregon, turned to GoFundMe after she faced a mammoth unexpected bill for bariatric surgery at Oregon Health & Science University.</p><p></p><p>She had expected to pay about $1,000, the amount left in her deductible, after her health insurer paid the $15,000 cap on the surgery. She didn’t understand that a cap meant she would have to pay the difference if the hospital, which was in-network, charged more.</p><p></p><p>And it did, leaving her with a bill of $18,000, to be paid all at once or in monthly $1,400 increments. “That’s more than my mortgage,” she told me. “I was facing filing for bankruptcy or losing my car and my house.” She made numerous calls to the hospital’s financial-aid office, many unanswered, and received only unfulfilled promises that “we’ll get back to you” about whether she qualified for help.</p><p></p><p>So, Justice said, her health coach—provided by the city of Portland—suggested starting a GoFundMe. The campaign yielded about $1,400, just one monthly payment, including $200 from the health coach and $100 from an aunt. She dutifully sent each donation directly to the hospital.</p><p></p><p>In an emailed response, the hospital system said that it couldn’t discuss individual cases, but that “financial assistance information is readily available for patients, and can be accessed at any point in a patient’s journey with OHSU. Starting in early 2019, OHSU worked to remove barriers for patients most in need by providing a quick screening for financial assistance that, if a certain threshold is met, awards financial assistance without requiring an application process.”</p><p></p><p>This particular tale has a happy-ish ending. In desperation, Justice went to the hospital and planted herself in the financial-aid office, where she had a tearful meeting with a hospital representative who determined that—given her finances—she wouldn’t have to pay the bill.</p><p></p><p>“I’d been through the gamut and just cried,” she said. She told me that she would like to repay the people who donated to her GoFundMe. But so far, the hospital won’t give the $1,400 back.</p><p></p><p></p>Elisabeth Rosenthalhttp://www.theatlantic.com/author/elisabeth-rosenthal/?utm_source=feedMatteo Giuseppe PaniGoFundMe Is a Health-Care Utility Now2024-02-05T13:23:30-05:002024-02-05T16:25:42-05:00Resorting to crowdfunding to pay medical bills has become so routine, in some cases health professionals recommend it.tag:theatlantic.com,2024:50-677350<p>In Arnold Monto’s ideal vision of this fall, the United States’ flu vaccines would be slated for some serious change—booting a major ingredient that they’ve consistently included since 2013. The component isn’t dangerous. And it made sense to use before. But to include it again now, Monto, an epidemiologist and a flu expert at the University of Michigan, told me, would mean vaccinating people “against something that doesn’t exist.”</p><p></p><p>That probably nonexistent something is Yamagata, a lineage of influenza B viruses that <a href="https://www.theatlantic.com/science/archive/2023/04/yamagata-flu-transmission-lineage-extinction/673662/?utm_source=feed">hasn’t been spotted by global surveyors since March of 2020</a>, shortly after COVID mitigations sent flu transmission plummeting to record lows. “And it isn’t for lack of looking,” Kanta Subbarao, the director of the WHO’s Collaborating Centre for Reference and Research on Influenza, told me. In a last-ditch attempt to find the missing pathogen, a worldwide network of monitoring centers tested <a href="https://cdn.who.int/media/docs/default-source/influenza/who-influenza-recommendations/vcm-southern-hemisphere-recommendation-2024/202309_recommendation.pdf?sfvrsn=2c2cbebd_8&download=true">nearly 16,000</a> influenza B virus samples collected from February to August of last year. Not a single one of them came up Yamagata. “The consensus is that it’s gone,” Cheryl Cohen, the head of South Africa’s Centre for Respiratory Diseases and Meningitis, told me. Officially removing an ingredient from flu vaccines will codify that sentiment, effectively publishing Yamagata’s obituary.</p><p></p><p data-id="injected-recirculation-link"><i>[<a href="https://www.theatlantic.com/science/archive/2023/04/yamagata-flu-transmission-lineage-extinction/673662/?utm_source=feed">Read: The flu may never be the same</a>]</i></p><p></p><p><a href="https://cdn.who.int/media/docs/default-source/influenza/who-influenza-recommendations/vcm-northern-hemisphere-recommendation-2023-2024/202302_seasonal_recommendation_a.pdf?sfvrsn=42612ae5_3&download=true">Last year around this time</a>, Subbarao told me, the WHO was already gently suggesting that the world might want to drop Yamagata from vaccines; by September, the agency had grown <a href="https://cdn.who.int/media/docs/default-source/influenza/who-influenza-recommendations/vcm-southern-hemisphere-recommendation-2024/202309_recommendation.pdf?sfvrsn=2c2cbebd_8&download=true">insistent</a>, describing the ingredient as “no longer warranted” and urging that “every effort should be made to exclude it as soon as possible.” The following month, an advisory committee to the FDA <a href="https://www.fda.gov/advisory-committees/advisory-committee-calendar/vaccines-and-related-biological-products-advisory-committee-october-5-2023-meeting-announcement">unanimously voted</a> to speedily adopt that same change.</p><p></p><p>But the switch from a four-flu vaccine to a trivalent one, guarding against only three, isn’t as simple as ordering <em>the usual, please, just hold the Yams.</em> Trivalent vaccines require their own licensure, which some manufacturers may have allowed to lapse—or never had at all; manufacturers must also adhere to the regulatory pipelines specific to each country. “People think, ‘They change the strains every season; this should be no big deal,’” Paula Barbosa, the associate director of vaccine policy at the International Federation of Pharmaceutical Manufacturers and Associations, which represents vaccine manufacturers, told me. This situation is not so simple: “They need to change their whole manufacturing process.” At the FDA advisory-committee meeting in October, an industry representative cautioned that companies might need <a href="https://www.fda.gov/media/172764/download">until the 2025–26 season</a> to fully transition to trivalents in the Northern Hemisphere, a timeline that Barbosa, too, considers realistic. The South could take until 2026.</p><p></p><p>In the U.S., though, where experts such as Monto have been pushing for expedient change, a Yamagata-less flu vaccine could be coming this fall. When I reached out to CSL Seqirus and GSK, two of the world’s major flu-vaccine producers, a spokesperson from each company told me that their firm was on track to deliver trivalent vaccines to the U.S. in time for the 2024–25 flu season, should the relevant agencies recommend and request it. (The WHO’s annual meeting to recommend the composition of the Northern Hemisphere’s flu vaccine isn’t scheduled until the <a href="https://www.who.int/news-room/events/detail/2024/02/19/default-calendar/who-consultation-on-the-composition-of-influenza-virus-vaccines-for-use-in-the-2024-2025-northern-hemisphere-influenza-season">end of February</a>; an FDA advisory meeting on the same topic will follow shortly after.) Sanofi, another vaccine producer, was less definitive, but told me that, with sufficient notice from health authorities, its plans would allow for trivalent vaccines this year, “if there is a definitive switch.” AstraZeneca, which makes the FluMist nasal-spray vaccine, told me that it was “engaging with the appropriate regulatory bodies” to coordinate the shift to a trivalent vaccine “as soon as possible.”</p><p></p><p>Quadrivalent flu vaccines are relatively new. Just over a decade ago, the world relied on immunizations that included two flu A strains (H1N1 and H3N2), plus one B: either Victoria <em>or </em>Yamagata, whichever scientists predicted might be the bigger scourge in the coming flu season. “Sometimes the world got it wrong,” Mark Jit, an epidemiologist at the London School of Hygiene & Tropical Medicine, told me. To hedge their bets, experts eventually began to recommend simply sticking in both. But quadrivalent vaccines typically cost more to manufacture, experts told me. And although several countries, including the U.S., quickly transitioned to the heftier shots, many nations—especially those with fewer resources—<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8143996/">never did</a>.</p><p></p><p>Now “the extra component is a waste,” Vijay Dhanasekaran, a virologist at the University of Hong Kong, told me. It’s pointless to ask people’s bodies to mount a defense against an enemy that will never attack. Trimming Yamagata out of flu-vaccine recipes should also make them cheaper, Dhanasekaran said, which could improve global access. Plus, continuing to manufacture Yamagata-focused vaccines raises the small but serious risk that the lineage could be inadvertently reintroduced to the world, Subbarao told me, as companies grow gobs of the virus for their production pipeline. (Some vaccines, such as FluMist, also immunize people with live-but-weakened versions of flu viruses.)</p><p></p><p>Some of the researchers I spoke with for this article weren’t ready to rule out the possibility—however slim—that Yamagata is still biding its time somewhere. (Victoria, a close cousin of Yamagata, and the other B lineage that pesters people, once went mostly quiet for about a decade, before <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4715237/">roaring back in the early aughts</a>.) But most experts, at this point, are quite convinced. The past couple of flu seasons have been heavy enough to offer even a rather rare lineage the chance to reappear. “If it had been circulating in any community, I’m pretty sure that global influenza surveillance would have detected it by now,” Dhanasekaran said. Plus, even before the pandemic began, Yamagata had been the wimpiest of the flu bunch, Jit told me: slow to evolve, crummy at transmitting, and <a href="https://www.theatlantic.com/science/archive/2023/04/yamagata-flu-transmission-lineage-extinction/673662/?utm_source=feed">already dipping in prevalence</a>. When responses to the pandemic starved <em>all</em> flu viruses of hosts, he said, this lineage was the likeliest to be lost.</p><p></p><p data-id="injected-recirculation-link"><i>[<a href="https://www.theatlantic.com/science/archive/2021/02/covid-19-flu-season/617924/?utm_source=feed">Read: The pandemic broke the flu</a>]</i></p><p></p><p>Eventually, companies may return to including four types of flu in their products, swapping in, say, another strain of H3N2, the <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7144439/">most severe and fastest-evolving of the bunch</a>—a change that Subbarao and Monto both told me might actually be preferable. But incorporating a second H3N2 is even more of a headache than returning to a trivalent vaccine: Researchers would likely first need to run clinical trials, experts told me, to ensure that the new components played nicely with each other and conferred additional benefits.</p><p></p><p>For the moment, a slimmed-down vaccine is the quickest way to keep up with the flu’s current antics. And in doing so, those vaccines will also reflect the strange reality of this new, COVID-modified world. “A whole lineage of flu has probably been eliminated through changes in human behavior,” Jit told me. Humanity may not have intended it. But our actions against one virus may have forever altered the course of another.</p>Katherine J. Wuhttp://www.theatlantic.com/author/katherine-j-wu/?utm_source=feedIllustration by The Atlantic. Source: Getty.Flu Shots Need to Stop Fighting ‘Something That Doesn’t Exist’2024-02-05T09:45:57-05:002024-02-09T14:34:32-05:00One type of flu virus has gone missing for so long, it doesn’t make sense to vaccinate against it.tag:theatlantic.com,2024:50-677336<p data-flatplan-paragraph="true"><small><i data-stringify-type="italic">This article was featured in the One Story to Read Today newsletter. </i><i data-stringify-type="italic"><a data-event-element="inline link" data-sk="tooltip_parent" data-stringify-link="https://www.theatlantic.com/newsletters/sign-up/one-story-to-read-today/" delay="150" href="https://www.theatlantic.com/newsletters/sign-up/one-story-to-read-today/?utm_source=feed" rel="noopener noreferrer" target="_blank">Sign up for it here</a></i><i data-stringify-type="italic">.</i></small></p><p>About four years ago, a new patient came to see me for a psychiatric consultation because he felt stuck. He’d been in therapy for 15 years, despite the fact that the depression and anxiety that first drove him to seek help had long ago faded. Instead of working on problems related to his symptoms, he and his therapist chatted about his vacations, house renovations, and office gripes. His therapist had become, in effect, an expensive and especially supportive friend. And yet, when I asked if he was considering quitting treatment, he grew hesitant, even anxious. “It’s just baked into my life,” he told me.</p><p></p><p>Among those who can afford it, regular psychotherapy is often viewed as a lifelong project, like working out or going to the dentist. Studies suggest that most therapy clients can measure their treatments in months instead of years, but a solid chunk of current and former patients <em>expect </em>therapy to last indefinitely. Therapists and <a href="https://www.nytimes.com/2021/04/13/style/couples-therapy.html">clients</a> alike, along with <a href="https://www.buzzfeed.com/eleanorbate/celebs-talk-about-therapy">celebrities</a> and <a href="https://www.allure.com/story/therapy-when-happy">media</a> <a href="https://www.businessinsider.com/can-i-go-to-therapy-if-im-not-depressed-2017-11">outlets</a>, have endorsed the idea of going to therapy for extended stretches, or when you’re feeling fine. I’ve seen this myself with friends who are basically healthy and think of having a therapist as somewhat like having a physical trainer. The problem is, some of the most commonly sought versions of psychotherapy are simply not designed for long-term use.</p><p></p><p>Therapy comes in many varieties, but they all share a common goal: to eventually end treatment because you feel and function well enough to thrive on your own. Stopping doesn’t even need to be permanent. If you’ve been going to therapy for a long time, and you’re no longer in acute distress, and you have few symptoms that bother you, consider taking a break. You might be pleasantly surprised by how much you learn about yourself.</p><p></p><p>Therapy, in both the short and long term, can be life-altering. Short-term therapy tends to be focused on a particular problem, such as a depressed mood or social anxiety. In cognitive behavioral therapy, usually used for depressive and anxiety disorders, a clinician helps a client relieve negative feelings by correcting the distorted beliefs that he has about himself. In dialectical behavior therapy, commonly used to treat borderline personality disorder, patients learn skills to manage powerful emotions, which helps improve their mood and relationships. Both treatments typically last less than a year. If you start to get rusty or feel especially challenged by life events that come your way, you simply return for another brief stint. Termination is expected and normal.</p><p></p><p data-id="injected-recirculation-link"><i>[<a href="https://www.theatlantic.com/family/archive/2023/02/short-term-therapy-mental-health-care-affordability-accessibility/673012/?utm_source=feed">Read: What’s the smallest amount of therapy that’s still effective?</a>]</i></p><p></p><p>Some types of therapy, such as psychodynamic therapy and psychoanalysis, are designed to last for several years—but not forever. The main goal of these therapies is much more ambitious than symptom relief; they aim to uncover the unconscious causes of suffering and to change a client’s fundamental character. At least one well-regarded study found that <a href="https://www.cambridge.org/core/journals/psychological-medicine/article/abs/outcome-of-short-and-longterm-psychotherapy-10-years-after-start-of-treatment/E2F5B69FED541530B13A818CEE06D739">long-term therapy</a> is both highly effective and superior to briefer treatment for people diagnosed with a clinically significant psychiatric illness; other <a href="https://bmcpsychiatry.biomedcentral.com/articles/10.1186/s12888-023-04895-6">papers</a> have shown less conclusive evidence for long-term therapy. And few studies compare short and extended treatment for clients with milder symptoms.</p><p></p><p>In fact, there’s reason to believe that talk therapy in the absence of acute symptoms may sometimes cause harm. Excessive self-focus—easily facilitated in a setting in which you’re literally paying to talk about your feelings—can increase your anxiety, especially when it substitutes for tangible actions. If your neurotic or depressive symptoms are relatively mild (meaning they don’t really interfere with your daily functioning), you might be better served by spending less time in a therapist’s office and more time connecting with friends, pursuing a hobby, or volunteering. Therapists are trained to use the tools they’ve learned for certain types of problems, and many of the stress-inducing minutiae of daily life are not among them. For example, if you mention to your therapist that you’re having trouble being efficient at work, he might decide to teach you a stress-reduction technique, but your colleagues or boss might provide more specific strategies for improving your performance.</p><p></p><p>One of my childhood friends, whose parents were both psychoanalysts, went to weekly therapy appointments while we were growing up. He was a happy, energetic kid, but his parents wanted him and his sister to be better acquainted with their inner lives, to help them deal with whatever adversity came their way. My friend and his sister both grew up to be successful adults, but also highly anxious and neurotic ones. I imagine their parents would say the kids would have been worse without the therapy—after all, mental illness ran in their family. But I can find no substantial clinical evidence supporting this kind of “preventive” psychotherapy.</p><p></p><p data-id="injected-recirculation-link"><i>[<a href="https://www.theatlantic.com/health/archive/2019/01/existential-therapy-you-can-ask-big-questions/579292/?utm_source=feed">Read: What it’s like to visit an existential therapist</a>]</i></p><p></p><p>Beginning therapy in the first place is, to be clear, a privilege. Therapy is not covered by many insurance plans, and a very large number of people who could benefit from it can’t afford it for any duration. Only <a href="https://www.nami.org/mhstats">47 percent</a> of Americans with a psychiatric illness received any form of treatment in 2021; in fact, federal estimates suggest that the United States is several thousand mental-health professionals short, a gap that is likely to <a href="https://bhw.hrsa.gov/data-research/projecting-health-workforce-supply-demand">grow</a> in the coming years. Stopping therapy when you’re ready opens up space for others who might need this scarce service more than you do.</p><p></p><p>I do not mean to suggest that a therapy vacation should be considered lightly, or that it’s for everyone. If you have a serious mental-health disorder, such as major depression or bipolar disorder, you should discuss with your mental-health provider whether ending therapy is appropriate for your individual situation. (Keep in mind that your therapist might not be ready to quit when you are. Aside from a financial incentive to continue treatment, parting with a charming, low-maintenance patient is not so easy.) My rule of thumb is that you should have minimal to no symptoms of your illness for six months or so before even considering a pause. Should you and your therapist agree that stopping is reasonable, a temporary break with a clear expiration date is ideal. At any time, if you’re feeling worse, you can always go back.</p><p></p><p>Psychiatrists do something similar with psychiatric meds: For example, when I prescribe a depressed patient an antidepressant, and then they remain stable and free of symptoms for several years, I usually consider tapering the medication to determine whether it’s still necessary for the patient’s well-being. I would do this only for patients who are at a low risk of relapse—for example, people who’ve had just one or two episodes, rather than many over a lifetime. Pausing therapy should be even less risky: The beautiful thing about therapy is that, unlike a drug, it equips you with new knowledge and skills, which you carry with you when you leave.</p><p></p><p data-id="injected-recirculation-link"><i>[<a href="https://www.theatlantic.com/health/archive/2019/08/can-you-just-got-therapy-once/596359/?utm_source=feed">Read: The quick therapy that actually works</a>]</i></p><p></p><p>About a year after my patient and I first talked about ending therapy, I ran into him in a café. He told me that stopping had taken him six months, but now he was thriving. Maybe you, like my patient, are daunted by the idea of quitting cold turkey. If so, consider taking a vacation from treatment instead. It might be the perfect way to see how far you’ve really come.</p><p><iframe frameborder="no" height="200" scrolling="no" src="https://player.megaphone.fm/ATL9636107890" width="100%"></iframe><em>Subscribe here: <a href="https://podcasts.apple.com/us/podcast/radio-atlantic/id1258635512">Apple Podcasts</a> | <a href="https://open.spotify.com/playlist/4PgNKjRJJWlaV6zuNr69BO">Spotify</a> | <a href="https://www.youtube.com/@TheAtlantic/podcasts">YouTube</a> | <a href="https://podcasts.google.com/feed/aHR0cHM6Ly9mZWVkcy5tZWdhcGhvbmUuZm0vcmFkaW9hdGxhbnRpYw">Google Podcasts</a> | <a href="https://pca.st/ccxU">Pocket Casts</a></em></p>Richard A. Friedmanhttp://www.theatlantic.com/author/richard-friedman/?utm_source=feedGettyPlenty of People Could Quit Therapy Right Now2024-02-05T07:30:00-05:002024-02-26T12:39:55-05:00Except in rare cases, treatment shouldn’t last forever.tag:theatlantic.com,2024:50-677326<p>The newest and much-hyped obesity drugs are, at their core, powerful appetite suppressants. When you eat fewer calories than you burn, the body starts scavenging itself, breaking down fat, of course, but also muscle. About a quarter to a third of the weight shed is lean body mass, and most of that is muscle.</p><p>Muscle loss is not inherently bad. As people lose fat, they need less muscle to support the weight of their body. And the muscle that goes first tends to be <a href="https://pubmed.ncbi.nlm.nih.gov/10102702/">low quality and streaked with fat</a>. Doctors grow concerned when people start to feel weak in everyday life—while picking up the grandkids, for example, or shoveling the driveway. Taken further, the progressive loss of muscle can make patients, especially elderly ones who already have less muscle to spare, <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4269139/">frail and vulnerable to falls</a>. People trying to slim down from an already healthy weight, who have less fat to spare, may also be prone to losing muscle. “You have to pull calories from somewhere,” says Robert Kushner, an obesity-medicine doctor at Northwestern University, who was also an investigator in a <a href="https://www.nejm.org/doi/pdf/10.1056/nejmoa2032183">key trial</a> for one of these drugs.</p><p>Kushner worries about patients who start with low muscle mass and go on to become super responders to the drugs, losing significantly more than the average 15 to 20 percent of their body weight. The more these patients lose, the more likely their body is breaking down muscle. “I watch them very carefully,” he told me. The impacts of losing muscle may go beyond losing just strength. Muscle cells are major consumers of energy; they influence insulin sensitivity and absorb some <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8074531/">80 percent of the glucose</a> flooding into blood after a meal. Extreme loss might alter these metabolic functions of muscle too.</p><p>Exactly how all of this will affect people on Wegovy and Zepbound, which are still relatively novel obesity drugs, is too early to say. (You may have heard these same two drugs referred to as Ozempic and Mounjaro, respectively, which are their names when sold for diabetes.) These drugs cause a proportion of muscle loss <a href="https://link.springer.com/article/10.1007/s13679-023-00534-z">higher</a> than diet and exercise alone, though roughly on par with bariatric surgery. Lifestyle changes can blunt the loss, but pharmaceutical companies are on the hunt for new drug combinations that could build muscle while burning fat.</p><p>The arrival of powerful weight-loss drugs has moved the field beyond simple <em>weight loss</em>, Melanie Haines, an endocrinologist at Massachusetts General Hospital, told me. That challenge is largely solved. Instead of fixating on the number of pounds lost, researchers, doctors, and ultimately patients can focus on where those pounds are coming from.</p><hr class="c-section-divider"><p>Doctors currently offer two pieces of standard and unsurprising advice to protect people taking obesity drugs against muscle loss: Eat a high-protein diet, and do resistance training. These recommendations are perfectly logical, but their effectiveness against these drugs specifically is unclear, John Jakicic, a professor of physical activity and weight management at the University of Kansas Medical Center, told me. He is now surveying patients to understand their real-world behavior on these drugs.</p><p>Fatigue, for example, is a common side effect. “When you’re tired, and you’re fatigued, do you really feel like exercising?” he said. Haines wonders the same about eating enough protein. The drugs are so good at suppressing appetite, she said, that some people might not be able to stomach enough food to get adequate protein. (Food companies have started<a href="https://www.wsj.com/business/retail/ozempic-and-a-protein-shake-food-makers-prep-weight-loss-drug-side-dishes-ff36abf7?mod=itp_wsj"> pitching</a> high-protein snacks and shakes to people on obesity drugs.)</p><p data-id="injected-recirculation-link"><i>[<a href="https://www.theatlantic.com/health/archive/2024/01/why-you-will-stop-losing-weight-ozempic/677148/?utm_source=feed">Read: The Ozempic plateau</a>]</i></p><p>If patients stop taking Wegovy and Zepbound—and about <a href="https://www.wired.com/story/ozempic-wegovy-quitting-weight-loss/">half of patients</a> do stop within a year, at least in real-world studies of people taking this class of drugs for diabetes—the weight regained <a href="https://pubmed.ncbi.nlm.nih.gov/38093678/">comes back</a> as fat more than muscle, says Tom Yates, a physical-activity professor at the University of Leicester. Muscle mass tends not to entirely recover. It’s “almost as if you’re better off staying where you are than going through cycles of weight loss,” he told me.</p><p>Yet, he pointed out, the U.K. recommends Wegovy for a <a href="https://www.nice.org.uk/guidance/ta875/chapter/1-Recommendations">maximum of two years</a>. In the U.S., patients who can’t afford the steep out-of-pocket price have been forced to stop when insurance companies abruptly <a href="https://www.nytimes.com/2024/01/26/business/obesity-drugs-insurance-north-carolina.html">cut off coverage</a> or <a href="https://www.newsweek.com/ozempic-mounjaro-price-increase-patients-quit-unaffordable-1863384">a manufacturer’s discount coupon expires</a>. These policies are likely to trigger cycles of weight loss and gain that lead, ultimately, to net muscle loss.</p><hr class="c-section-divider"><p>Meanwhile, drug companies are already thinking about the next generation of weight-loss therapies. “Wouldn’t it be great to have another mechanism that's moving away from just appetite regulation?” Haines said. Companies are testing ways to preserve—perhaps even enhance—muscle during weight loss by combining Wegovy or Zepbound with a second muscle-boosting drug. Such a combination could, in theory, allow patients to lose fat and gain muscle at the same time.</p><p>Years ago, scientists first became interested in potential muscle-enhancing drugs that <a href="https://www.technologyreview.com/2007/10/18/271042/mimicking-the-massively-muscular/">mimic mutations</a> found in certain breeds of almost comically ripped dogs and <a href="https://breeds.okstate.edu/cattle/belgian-blue-cattle.html">cattle</a>. At the time, they hoped to treat muscle-wasting diseases. The drugs never quite worked for that purpose, but the <a href="https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2774903">trial</a> for one such drug, an antibody called bimagrumab, found that patients also lost fat in addition to gaining lean mass. A start-up <a href="https://www.fiercebiotech.com/biotech/versanis-bio-snags-70m-to-test-ex-novartis-muscle-drug-support-from-ex-novartis-ceo-joe">acquired the drug</a> and began testing it for weight loss <a href="https://www.versanisbio.com/news/versanis-bio-announces-completion-of-enrollment-of-the-believe-phase-2b-study-in-patients-with-obesity/">in combination with semaglutide</a>, the active ingredient in Wegovy, or Ozempic. And last year, Eli Lilly, the maker of Zepbound, <a href="https://investor.lilly.com/news-releases/news-release-details/lilly-completes-acquisition-versanis-bio">snapped up that company</a> for up to $1.9 billion—in hopes of making its own combination therapy.</p><p data-id="injected-recirculation-link"><i>[<a href="https://www.theatlantic.com/health/archive/2023/12/obesity-drugs-ozempic-pills-injections/676359/?utm_source=feed">Read: Are you sure you want an Ozempic pill? </a>]</i></p><p>Pairing bimagrumab with an existing obesity drug could potentially maximize the weight loss from both. Losing weight tends to <a href="https://www.theatlantic.com/health/archive/2024/01/why-you-will-stop-losing-weight-ozempic/677148/?utm_source=feed">get harder</a> over time; as you lose muscle, your body burns fewer calories. A drug that minimizes that muscle loss—or even flips it into muscle gain—could help patients boost the amount of energy their body expends, while Wegovy or Zepbound suppresses calories consumed. The mechanisms of how this might actually work in the body still need to be understood, though. <a href="https://onlinelibrary.wiley.com/doi/pdf/10.1002/jcsm.12205">Previous</a> <a href="https://pubmed.ncbi.nlm.nih.gov/31397289/">studies</a> of bimagrumab found that patients grew more muscle, but they didn’t necessarily become faster or stronger. Haines, who is planning a small study of her own with bimagrumab, is most interested in how the combination affects not the structural but the metabolic functions of muscle.</p><p>Bimagrumab is the furthest along of several drugs that tinker with the same pathway for muscle growth. The biotech company Regeneron recently published promising <a href="https://diabetesjournals.org/diabetes/article/72/Supplement_1/207-OR/149796/207-OR-Myostatin-Inhibition-Synergizes-with-GLP-1R">data</a> on two of its muscle-enhancing antibodies paired with semaglutide in primates; a <a href="https://investor.regeneron.com/static-files/7dfdabe2-05d1-4145-b5c5-342cec0ce9c4">trial in humans</a> is due to begin later this year. The start-up Scholar Rock is testing another antibody called <a href="https://www.clinicaltrialsarena.com/news/scholar-rock-sma-drug-investigated-obesity-trial/?cf-view">apitegromab</a>. Other companies are interested in combining the obesity drugs with different potential muscle boosters that work by mimicking certain hormones such as <a href="https://www.biospace.com/article/releases/bioage-labs-announces-plans-for-phase-2-trial-of-first-in-class-apelin-receptor-agonist-bge-105-azelaprag-co-administered-with-tirzepatide-for-treatment-of-obesity-in-collaboration-with-lilly-s-chorus-organization/">apelin</a> or <a href="https://ir.verupharma.com/news-events/press-releases/detail/189/veru-reports-muscle-data-from-5-clinical-studies-of">testosterone</a>. If they succeed, the next generation of drugs could help sculpt a more muscular body, not just a smaller one. Eating less can only do so much to better your health.</p>Sarah Zhanghttp://www.theatlantic.com/author/sarah-zhang/?utm_source=feedIllustration by The Atlantic. Sources: Artem Hvozdkov; MirageC / Getty.Ozempic Makes You Lose More Than Fat2024-02-02T09:33:46-05:002024-02-02T12:29:01-05:00Existing weight-loss drugs can cause muscle loss, but the next generation could allow patients to gain muscle instead.tag:theatlantic.com,2024:50-677307<p>Scott Napper, a biochemist and vaccinologist at the University of Saskatchewan, can easily envision humanity’s ultimate doomsday disease. The scourge would spread fast, but the progression of illness would be slow and subtle. With no immunity, treatments, or vaccines to halt its progress, the disease would eventually find just about every single one of us, spreading via all manner of body fluids. In time, it would kill everyone it infected. Even our food and drink would not be safe, because the infectious agent would be hardy enough to survive common disinfectants and the heat of cooking; it would be pervasive enough to infest our livestock and our crops. “Imagine if consuming a plant could cause a fatal, untreatable neurodegenerative disorder,” Napper told me. “Any food grown within North America would be potentially deadly to humans.”</p><p></p><p>This nightmare illness doesn’t yet exist. But for inspiration, Napper needs to look only at the very real contagion in his own lab: chronic wasting disease (CWD), a highly lethal, highly contagious neurodegenerative disease that is devastating North America’s deer, elk, and other cervids.</p><p></p><p data-id="injected-recirculation-link"><i>[<a href="https://www.theatlantic.com/science/archive/2023/12/deer-chronic-wasting-disease-decline/676962/?utm_source=feed">Read: An incurable disease is coming for deer</a>]</i></p><p></p><p>In the half century since it was <a href="https://www.aphis.usda.gov/aphis/ourfocus/wildlifedamage/programs/nwrc/sa_spotlight/accomplishments_chronic_wasting_disease">discovered</a> in a captive deer colony in Colorado, CWD has worked its way into <a href="https://www.usgs.gov/centers/nwhc/science/expanding-distribution-chronic-wasting-disease">more than 30 U.S. states and four Canadian provinces</a>, as well as South Korea and several countries in Europe. In some captive herds, the disease has been detected in <a href="https://pubmed.ncbi.nlm.nih.gov/21598099/">more than 90 percent</a> of individuals; in the wild, Debbie McKenzie, a biologist at the University of Alberta, told me, “we have areas now where more than 50 percent of the bucks are infected.” And CWD kills indiscriminately, gnawing away at deer’s brains until the tissue is riddled with holes. “The disease is out of control,” Dalia Abdelaziz, a biochemist at the University of Calgary, told me.</p><p></p><p>What makes CWD so formidable is its cause: infectious misfolded proteins called prions. Prion diseases, which include mad cow disease, have long been known as terrifying and poorly understood threats. And CWD is, in many ways, “the most difficult” among them to contend with—more transmissible and widespread than any other known, Marcelo Jorge, a wildlife biologist at the University of Georgia, told me. Scientists are quite certain that CWD will be impossible to eradicate; even limiting its damage will be a challenge, especially if it spills into other species, which could include us. CWD is already a perfect example of how dangerous a prion disease can be. And it has not yet hit the ceiling of its destructive potential.</p><hr class="c-section-divider"><p>Among the world’s known infectious agents, prions are an anomaly, more like zombies than living entities. Unlike standard-issue microbes—viruses, bacteria, parasites, fungi—prions are just improperly folded proteins, devoid of genetic material, unable to build more of themselves from scratch, or cleave themselves in two. To reproduce, they simply find properly formed proteins that share their base composition and convert those to their aberrant shape, through mostly mysterious means. And because prions are slightly malformed versions of molecules that our bodies naturally make, they’re difficult to defend against. The immune system codes them as benign and ignores them, even as disease rapidly unfolds. “This is an entirely new paradigm of infectious disease,” Napper told me. “It’s a part of your own body that’s turning against you.”</p><p></p><p>And yet, we’ve managed to keep many prion diseases in check. <a href="https://www.ninds.nih.gov/health-information/disorders/kuru">Kuru</a>, once common in the highlands of Papua New Guinea, was transmitted through local rituals of funerary cannibalism; the disease fizzled out after people stopped those practices. Mad cow disease (more formally known as bovine spongiform encephalopathy) was <a href="https://www.cdc.gov/prions/bse/control-measures.html">contained</a> by culling infected animals and eliminating the suspected source, <a href="https://www.aphis.usda.gov/aphis/ourfocus/animalhealth/animal-disease-information/cattle-disease-information/cattle-bse/cattle-bse">cow feed made with infected tissues</a>. Even scrapie, a highly contagious prion disease of sheep and goats, is limited to livestock, making it feasible to pare down infected populations, or <a href="https://iowaagriculture.gov/sites/default/files/animal-industry/pdf/Scrapie/Genetics%20of%20Scrapie%20122120.pdf">breed</a> them toward genetic resistance.</p><p></p><p data-id="injected-recirculation-link"><i>[<a href="https://www.theatlantic.com/health/archive/2015/02/insomnia-that-kills/384841/?utm_source=feed">Read: Insomnia that kills</a>]</i></p><p></p><p>CWD, meanwhile, is a fixture of wild animals, many of them migratory. And whereas most other prion diseases primarily keep quarters in the central nervous system, CWD “gets in pretty much every part of the body,” Jorge told me. Deer then pass on the molecules, often through direct contact; they’ll shed prions in their saliva, urine, feces, reproductive fluids, and even antler velvet long before they start to show symptoms. Candace Mathiason, a pathobiologist at Colorado State University, and her colleagues have found that <a href="https://pubmed.ncbi.nlm.nih.gov/32817706/">as little as 100 nanograms of saliva</a> can seed an infection. Her studies <a href="https://pubmed.ncbi.nlm.nih.gov/34960698/">suggest</a> that deer can also pass prions <a href="https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0071844">in utero</a> from doe to growing fawn.</p><p></p><p>Deer also <a href="https://pubmed.ncbi.nlm.nih.gov/30355150/">ingest</a> prions from their environment, where the molecules can linger in soil, on trees, and on hunting bait for years or decades. A team led by Sandra Pritzkow, a biochemist at UTHealth Houston, has found that <a href="https://pubmed.ncbi.nlm.nih.gov/25981035/">plants can take up prions from the soil, too</a>. And unlike the multitude of microbes that are easily done in by UV, alcohol, heat, or low humidity, prions are so structurally sound that they can survive nearly any standard environmental assault. In laboratories, scientists must blast their equipment with temperatures of about 275 degrees Fahrenheit for 60 to 90 minutes, under extreme pressure, to rid it of prions—or drench their workspaces with bleach or sodium hydroxide, at concentrations high enough to rapidly corrode flesh.</p><p></p><p>Infected deer are also frustratingly difficult to detect. The disease typically takes <a href="https://veterinaryresearch.biomedcentral.com/articles/10.1186/s13567-021-00986-y">years</a> to fully manifest, while the prions infiltrate the brain and steadily destroy neural tissue. The molecules kill insidiously: “This isn’t the kind of disease where you might get a group of deer that are all dead around this watering hole,” Jorge told me. Deer drift away from the herd; they forage at odd times. They become braver around us. They drool and urinate more, stumble about, and begin to lose weight. Eventually, a predator picks them off, or a cold snap freezes them, or they simply starve; in all cases, though, the disease is fatal. Because of CWD, deer populations in many parts of North America are declining; “there is definitely some concern that local populations will disappear,” McKenzie told me. Researchers worry the disease will soon overwhelm caribou in Canada, imperiling the Indigenous communities who rely on them for food. Hunters and farmers, too, are losing vital income. Deer are unlikely to go extinct, but the disease is depriving their habitats of key grazers, and their predators of food.</p><p></p><p data-id="injected-recirculation-link"><i>[<a href="https://www.theatlantic.com/ideas/archive/2023/09/hunting-benefits-conservation/675196/?utm_source=feed">Read: America needs hunting more than it knows</a>]</i></p><p></p><p>In laboratory experiments, CWD has proved <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9316268/">capable</a> of infecting rodents, sheep, goats, cattle, raccoons, ferrets, and primates. But so far, jumps into non-cervid species don’t seem to be happening in the wild—and although <a href="https://www.frontiersin.org/articles/10.3389/fimmu.2023.1156451/full">people eat an estimated 10,000 CWD-infected cervids each year</a>, no human cases have been documented. Still, lab experiments indicate that human proteins, at least <a href="https://pubmed.ncbi.nlm.nih.gov/35996016/">when expressed by mice</a>, could be susceptible to CWD too, Sabine Gilch, a molecular biologist at the University of Calgary, told me. </p><p></p><p>And the more prions transmit, and the more hosts they find themselves in, the more opportunities they may have to infect creatures in new ways. Prions don’t seem to evolve as quickly as many viruses or bacteria, Gilch told me. But “they’re not as static as we would like them to be.” She, McKenzie, and other researchers have detected a <a href="https://pubmed.ncbi.nlm.nih.gov/34310662/">multitude</a> of <a href="https://www.mdpi.com/1999-4915/14/7/1390">CWD strains</a> bopping around in the wild—each with its own propensity for interspecies spread. With transmission so unchecked, and hosts so numerous, “this is kind of like a ticking time bomb,” Surachai Supattapone, a biochemist at Dartmouth, told me.</p><hr class="c-section-divider"><p>The world is unlikely to ever be fully rid of CWD; even the options to slow its advance are so far limited. Efforts to survey for infection depend on funding and researchers’ time, or the generosity of local <a href="https://besjournals.onlinelibrary.wiley.com/doi/full/10.1002/2688-8319.12203">hunters</a> for samples; environmental decontamination is still <a href="https://ucalgary.ca/news/veterinary-medicine-prof-receives-425m-grant-develop-tools-stop-chronic-wasting-disease">largely experimental</a> and tricky to do at scale; treatments—which don’t yet exist—would be nearly impossible to administer en masse. And culling campaigns, although sometimes quite effective, especially at the edges of the disease’s reach, often spark public backlash.</p><p></p><p>Deer that carry certain genetic variants do seem less susceptible to prions, and progress more slowly to full-blown disease and death. But because <a href="https://www.mdpi.com/1999-4915/14/7/1390">none so far</a> seems able to fully block infection, or completely curb shedding, prolonging life may simply prolong transmission. “Once an animal gets infected,” Abdelaziz told me, there’s almost a “hope it dies right away.” Even if sturdier prion resistance is someday found, “it’s probably just a matter of time until prions start to adapt to that as well,” Gilch said.</p><p></p><p>Vaccines, in theory, could help, and in recent years, several research groups—including Napper’s and Abdelaziz’s—have made breakthroughs in overcoming the immune system’s inertia in attacking proteins that look like the body’s own. Some strategies try to target the problematic, invasive prions only; others are going after <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10140515/">both the prion and the native, properly folded protein</a>, so that the vaccine can do double duty, waylaying the infectious invader and starving it of reproductive fodder. (So far, <a href="https://www.frontiersin.org/articles/10.3389/fmolb.2017.00019/full">lab animals</a> seem to do mostly fine even when they’re bred to lack the native prion protein, whose function is still mostly mysterious.) In early trials, both teams’ vaccines have <a href="https://www.tandfonline.com/doi/full/10.1080/19336896.2017.1367083">produced</a> <a href="https://www.sciencedirect.com/science/article/pii/S0021925820311078">promising</a> immune responses in cervids. But neither team yet fully knows how effective their vaccines are at cutting down on shedding, how long that protection might last, or whether these strategies will work across cervid species. One of Napper’s vaccine candidates, for instance, seemed to <a href="https://linkinghub.elsevier.com/retrieve/pii/S0264410X18314257">hasten the progression of disease in elk</a>.</p><p></p><p>Vaccines for wildlife are also <a href="https://doi.org/10.3389/fimmu.2023.1156451">tough to deliver</a>, especially the multiple doses likely needed in this case. “It’s not like you can just run around injecting every elk and deer,” Napper told me. Instead, he and other researchers plan to compound their formula with a salty apple-cider slurry that he hopes wild cervids might eat with some regularity. “The deer absolutely love it,” he said.</p><p></p><p>Should any CWD vaccines come to market, though, they will almost certainly be the first prion vaccines that clear the experimental stage. That could be a boon for more than just deer. Another prion disease may spill over from one species to another; others may arise spontaneously. CWD is not, and may never be, the prion disease that most directly affects us. But it is, for now, the most urgent—and the one from which we have the most to lose, and maybe gain.</p>Katherine J. Wuhttp://www.theatlantic.com/author/katherine-j-wu/?utm_source=feedIllustration by Joanne Imperio / The AtlanticDeer Are Beta-Testing a Nightmare Disease2024-02-01T08:00:00-05:002024-02-01T12:25:33-05:00Prion diseases are poorly understood, and this one is devastating.tag:theatlantic.com,2024:50-677310<p>There’s something fundamentally excessive about winter sports. Instead of curling up with a book or Netflix when the weather turns cold, winter athletes wrestle with inordinate layers and high-tech gear just to make it through the day without frostbite. They sprint across ice with knives strapped to their feet and hurtle down mountains at speeds generally reserved for interstate highways. They fall off ski lifts—<a href="https://www.theguardian.com/us-news/2024/jan/29/lake-tahoe-gondola-woman-trapped">or are trapped overnight in them</a>. Show me an experienced winter recreationalist, and I’ll show you someone who has slipped, skidded, and crashed their way to a broken tailbone or torqued knee, and more likely than not a concussion or two.</p><p>But over the past few years, climate change, social media, and a pandemic-era obsession with the outdoors have combined to make these already intense sports even more extreme. Seasoned athletes have long considered bunny slopes and indoor ice rinks to be mere gateways to backcountry skiing (zooming through the tree line on untouched powder—and sometimes jumping out of a helicopter to get there) or “wild” ice skating over remote glaciers and freshly frozen lakes. Now a growing crowd of beginners has started to follow them—and the consequences can be fatal.</p><p>Since the rise of remote work enabled an exodus from big cities in 2020 and 2021, a <a href="https://nsaa.org/webdocs/Media_Public/IndustryStats/historical_skier_visits_thru_22-23.pdf">record number</a> of people have visited U.S. ski areas each winter. Resorts can be so crowded that people wait 45 minutes for a chair lift that, four years ago, might have only had a three-minute line. No wonder skiers are searching farther and farther afield to get their fix. Greg Poschman, the county commissioner chairman of Colorado’s Pitkin County, told me that in just the past few seasons, he’s seen more people up in the backcountry and out on frozen lakes and rivers than he has in a lifetime living near Aspen. That sentiment is echoed by athletes and officials across the United States. All it takes is a sufficiently impressive stunt posted to social media, and once-deserted corners of the natural world will be inundated with hobbyists a few days later.</p><p>In the wilderness, or even the “sidecountry” just outside resort bounds, athletes are exposed to dangers that are rare in more controlled settings. Miles from civilization, no one is policing the landscape for holes in the ice, buried rocks and twigs, and surprise cliffs, not to mention avalanches and <a href="https://upnorthlive.com/news/local/anglers-warned-of-river-dangers">ice dams</a>. Perhaps most crucially, pushing out farther from roads and services means being farther from rescue when things go wrong. “You may be doing something that’s a low-risk sport”—ice-skating, snowshoeing, and the like—“but the consequences are very high,” Poschman said.</p><p data-id="injected-recirculation-link"><i>[<a href="https://www.theatlantic.com/photo/2018/01/the-insanity-of-downhill-ice-cross-racing/551273/?utm_source=feed">Photos: The insanity of downhill ice cross racing</a>]</i></p><p>Even sports that have never relied on curated resorts to thrive are becoming more treacherous. Kale Casey, a five-time Team USA co-captain for sled-dog sports, told me that unpredictable winter seasons are forcing teams away from traditional routes across Alaska that have become unsafe. Portions of the famous roughly 1,000-mile <a href="https://www.travelalaska.com/explore-alaska/articles/all-about-iditarod">Iditarod race</a> have been rerouted. Mushers are strategically running certain portions of races at night so their dogs—bred for temperatures around –20 degrees—don’t overheat. As the planet warms, and snow coverage of Alaska’s tundra contracts, other winter sports are converging with the mushers on the little snow that’s left. This season, five dogs have been hit and killed by people riding snowmobiles (known locally as snow machines); five more dogs were also injured in these collisions. “During the lockdown, there wasn’t a snow machine available in Alaska,” Casey told me. “Everybody bought them—and they’ve got to go places. Where do they go? They go where we go.”</p><p>Climate change isn’t just pushing winter athletes into more crowded or remote territory. It’s also making that territory less predictable. From across the Northern Hemisphere, the near-identical refrain I heard went something like this: As recently as five years ago, the snow season used to begin sometime around Thanksgiving. It started slowly, with the odd storm or two, building up ice and snowpack gradually as temperatures fell. On a given day, you could be fairly certain of the quality of whatever frigid surface you were skiing on, climbing up, or skating over. And if the weather wasn’t good, well, the snow and ice would be there for you the next day.</p><p>But now everyone I spoke with—whether in Iceland or in alpine California—said the first storms don’t come until January. The weather is unpredictable: Record-setting blizzards are interspersed with snow-melting rain. A dry early season followed by rain and wet snow is the <a href="https://www.wired.com/story/snow-sports-are-becoming-more-dangerous/">perfect recipe for avalanches</a>, Poschman said. Shannon Finch, who was an avalanche-rescue dog handler in Utah for 12 years before turning to heli-ski guiding, told me that even experts are now “perplexed, confused, and getting caught off guard” in environments they’d previously navigated with ease. Her dog, Lēif, struggled in these new conditions: When someone is buried by an avalanche, their scent is less likely to rise through wetter snow and warmer air temperatures. Consequently, Lēif needed to cover considerably more ground before making a rescue. </p><p>The shorter seasons also create havoc for a uniquely human reason: FOMO. “People are chomping at the bit to get out there” and are willing to take greater risks for good snow or ice, Travis White, who runs a tourism fishing business in the Upper Peninsula of Michigan, told me. The result is that even a relatively leisurely activity such as ice fishing suddenly becomes an extreme sport. With fewer waterways icing over, more people from places that no longer freeze regularly are suddenly crowding onto just a few lakes. These newcomers aren’t around to watch the water slowly freeze; they don’t know where to watch out for eddies and currents that may make the ice unstable, or how to avoid the most recently frozen patches, which are also the most dangerous. </p><p>Stories of <a href="https://www.mlive.com/news/saginaw-bay-city/2024/01/fisherman-dies-after-falling-through-ice-on-saginaw-bay.html">ice fishers</a>, <a href="https://www.nbcnews.com/news/us-news/ice-skater-72-dies-group-6-plunges-frozen-california-reservoir-rcna15438">figure skaters</a>, and <a href="https://abc13.com/teen-uses-hockey-stick-ice-rescue-pennsylvania-pa-news/11523355/#:~:text=Pennsylvania%20%2D%2D%20A%20Pennsylvania%20teenager,they%20heard%20screams%20for%20help">hockey players</a> falling in—even dying—abound. Incidents on the snow are common too. Earlier this month, <a href="https://www.outsideonline.com/outdoor-adventure/snow-sports/why-the-hell-did-23-skiers-require-rescue-near-killington-resort/">23 people needed rescuing</a> in Killington, Vermont, after ducking a boundary rope to ski and snowboard out-of-bounds on a particularly good powder day—the kind that’s getting vanishingly rare in the Northeast.</p><p data-id="injected-recirculation-link"><i>[<a href="https://www.theatlantic.com/business/archive/2015/02/how-skiing-went-from-the-alps-to-the-masses/385691/?utm_source=feed">Read: How skiing went from the Alps to the masses</a>]</i></p><p>White, like many of the other winter enthusiasts I spoke with, also blames social media for the extreme lengths people go to in his sport. Inexperienced ice fishers might see a cool spot posted on Instagram and find it easily, thanks to geolocation. The same goes for wild ice-skating, snowmobiling, and backcountry skiing. Athletes also worry that impressive, engagement-oriented stunts posted online could inspire inexperienced people to try extreme moves in those remote sites. “The only thing that I see on social media is people jumping off cliffs on their skis,” Ben Graves, a Colorado-based outdoor educator and an avid backcountry skier, told me. But only a tiny fraction of skiers who can find said cliffs are good enough to jump off them with something approximating safety.</p><p>That fraction could soon get even smaller. Ívar Finnbogason, a manager at Icelandic Mountain Guides, is deeply concerned by the decline in skill he’s witnessed over the past decade. He stepped away from a career as an ice climber when he became a father, in part because of the danger but mostly because waiting and waiting for the right conditions meant that he simply couldn’t train effectively. “That’s no way for you as an athlete—as someone with ambition—to build up your momentum,” he told me.</p><p>By the end of the century, snow and ice may be so scarce that only the most well-resourced and committed athletes can even attempt these new extremes. With just a degree or two Celsius more warming, much of the Northern Hemisphere can expect <a href="https://www.theatlantic.com/science/archive/2024/01/winter-snow-loss-climate-change/677078/?utm_source=feed">massive snow loss</a>. If this happens, the only way to reach the snow might be with a helicopter or a days-long hike.</p><p data-id="injected-recirculation-link"><i>[<a href="https://www.theatlantic.com/science/archive/2024/01/winter-snow-loss-climate-change/677078/?utm_source=feed">Read: The threshold at which snow starts irreversibly disappearing</a>]</i></p><p>A dramatic collapse in winter sports might well result in fewer accidents. But we would also lose something intrinsically human. For many winter-recreation devotees, these sports are more than just activities to pass the time. They are a way of life, dating as far back as <a href="https://www.mabeyski.com/news/the-history-of-skiing/">8000 B.C.E.</a> Perhaps those who test their skills against the strength of Mother Nature have it right. Maybe now is the time for winter athletes to take their passions to dangerous new heights, before they lose the option forever.</p>Talia Barringtonhttp://www.theatlantic.com/author/talia-barrington/?utm_source=feedDominic Ebenbichler / ReutersRisking Their Lives to Ski While They Can2024-01-31T14:49:33-05:002024-02-05T13:47:58-05:00Winter sports are gnarlier than ever.tag:theatlantic.com,2024:50-677252<p data-flatplan-paragraph="true"><small><i data-stringify-type="italic">This article was featured in the One Story to Read Today newsletter. </i><i data-stringify-type="italic"><a data-event-element="inline link" data-sk="tooltip_parent" data-stringify-link="https://www.theatlantic.com/newsletters/sign-up/one-story-to-read-today/" delay="150" href="https://www.theatlantic.com/newsletters/sign-up/one-story-to-read-today/?utm_source=feed" rel="noopener noreferrer" target="_blank">Sign up for it here</a></i><i data-stringify-type="italic">.</i></small></p><p>On Tuesday, curiosity finally got the best of me. How potent could Panera’s Charged Lemonades <em>really</em> be? Within minutes of my first sip of the hyper-caffeinated drink in its strawberry-lemon-mint flavor, I understood why <a href="https://www.theatlantic.com/technology/archive/2023/12/panera-charged-lemonade-ai-existential-risk/676984/?utm_source=feed">memes</a> have likened it to an illicit drug. My vision sharpened; sweat slicked my palms.</p><p>Laced with more caffeine than a typical energy drink, Panera’s Charged Lemonade has been implicated in two wrongful-death lawsuits since it was introduced in 2022. Though both customers who died had health issues that made them sensitive to caffeine, a third lawsuit this month alleges that the lemonade gave an otherwise healthy 27-year-old lasting heart problems. Following the second death, Panera <a href="https://abcnews.go.com/GMA/Food/3rd-lawsuit-panera-bread-alleges-caffeinated-lemonade-led/story?id=106577795#:~:text=Following%20the%20December%20suit%2C%20a,one%20of%20the%20company's%20products.%22">denied</a> that the drink was the cause, but in light of the lawsuits, it has added <a href="https://www.nrn.com/news/panera-bread-updates-store-warnings-after-student-dies-drinking-charged-lemonade">warnings about the drink</a>, <a href="https://www.verywellhealth.com/panera-lemonade-8414700">reduced its caffeine content</a>, and removed the option for <a href="https://www.nrn.com/news/panera-bread-removes-its-controversial-charged-lemonades-self-serve-area-some-stores">customers to serve themselves</a>.</p><p></p><p>All the attention on Panera’s Charged Lemonade has resurfaced an age-old question: <a href="https://www.washingtonpost.com/wellness/2023/12/06/panera-caffeine-lawsuits-deaths-risks/">How much caffeine is too much?</a> You won’t find a simple answer anywhere. Caffeine consumption is widely considered to be beneficial because it mostly is—boosting alertness, productivity, and even mood. But there is a point when guzzling caffeine tips over into uncomfortable, possibly unhealthy territory. The problem is that defining this point in discrete terms is virtually impossible. In the era of extreme caffeine, this is a dangerous way to live.</p><p></p><p>Most people don’t have to worry about dying after drinking a Charged Lemonade. The effects, though uncomfortable, usually seem to be minor. After drinking half of mine, I was so wired that I couldn’t make sense of the thoughts ricocheting around my brain for the next few hours. Caffeine routinely leads to jitteriness, nervousness, sweating, insomnia, and rapid heartbeat. If mild, such symptoms can be well worth the benefits.</p><p></p><p>But consuming too much caffeine can have serious health impacts. High doses—more than <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6247400/">1,000 milligrams a day</a>—can result in a state of intoxication known as <em>caffeinism</em>. The symptoms can be severe: People can “develop seizures and life-threatening irregularities of the heartbeat,” and some die, David Juurlink, a toxicology professor at the University of Toronto who also works at the Ontario Poison Centre, told me. “It’s one of the dirty little secrets, I’m afraid, of caffeine.” Juurlink said he occasionally gets calls about people, typically high-school or college students, who have ingested multiple caffeine pills on a dare or in a suicide attempt.</p><p></p><p>You’re unlikely to ingest that much caffeine from beverages alone, yet the increasing availability of highly caffeinated products makes it more of a possibility than ever before. Besides Panera’s Charged Lemonade, dozens of energy drinks contain similar amounts of caffeine, and some come in <a href="https://sporked.com/article/best-ghost-energy-drink-flavors/">candy-inspired flavors</a> such as Bubblicious and Sour Patch Kids. Less potent but highly snackable products include <a href="https://www.businessinsider.com/review-of-new-go-cubes-formula-2017-3">c</a><a href="https://www.businessinsider.com/review-of-new-go-cubes-formula-2017-3">affeinated coffee cubes</a>, energy chews, <a href="https://www.xomarshmallow.com/products/caffeinated-marshmallows-latte-edition-set-of-12">marshmallows</a>, mints, <a href="https://preworkoutpops.com/products/variety-pack?variant=40738762850358">ice pops</a>, and even <a href="https://trymeloair.com/collections/caffeine-vapes-diffusers">vapes</a>. Consumed quickly and in rapid succession, these foods can lead to potentially toxic caffeine intake “because your body hasn’t had time to tell you to stop,” Jennifer Temple, a professor at the University of Buffalo who studies caffeine use, told me.</p><p></p><p>More than ever, we need a way to track our caffeine consumption, but we don’t seem to have any good options. In all of the lawsuits against Panera, the basic argument is this: Had the company more adequately warned customers of the drink’s caffeine content, perhaps no one would have been hurt. But most of us just aren’t used to thinking about caffeine in numerical terms the way we do with calories and alcohol by volume (ABV). Caffeine intake is generally something that’s not measured but <em>experienced</em>: I know, for example, that a double espresso from the office coffee machine will give me the shakes. But even though I knew how much caffeine is in a Charged Lemonade, I had no idea how much of it I could drink before having the same reaction.</p><p> </p><p>The FDA does have a recommended daily caffeine limit of 400 milligrams, the equivalent of about four or five cups of coffee. “Based on the relevant science and information available,” a spokesperson told me, consuming that much each day “does not raise safety concerns” for most adults, except for people who are pregnant or nursing, or have concerns related to their health conditions or the medication they take. The agency, however, doesn’t require food labels to note caffeine content, though some companies include that information voluntarily.</p><p></p><p>But the numbers are helpful only up to a point. The FDA’s daily recommendation is a “rough guideline” that can’t be used as a universal standard, because “it’s not safe for everybody,” Temple said. For one person, 237 milligrams could mean a trip to the hospital; for another, that would just be breakfast. The effect of a given caffeine dose “varies tremendously from person to person based upon their historical pattern of use and also their genetics,” Juurlink told me.</p><p></p><p>Although people generally aren’t aware of the amounts of caffeine they consume, they tend to develop a good sense of how much they can handle, Temple said. But usually, this knowledge is product-specific; when trying a new caffeine product, the effect can be hard to predict. Part of the problem is that the amount of caffeine in products varies dramatically, even among drinks that may seem similar: A 12-ounce Americano from McDonald’s contains <a href="https://www.caffeineinformer.com/mccafe-coffee-caffeine-content">71 milligrams</a> of caffeine, but the same drink at Starbucks contains 150 milligrams. The caffeine in popular energy drinks ranges from 75 milligrams (Ocean Spray Cran-Energy) to 316 milligrams (Redline Xtreme), according to the <a href="https://www.cspinet.org/caffeine-chart">Center for Science in the Public Interest</a>.</p><p></p><p>Contrast this with alcohol, which tends to be served in conventional units regardless of brand: a can of beer, a glass of wine, or a shot of liquor, all of which have roughly the same ability to intoxicate. Having a standard unit to gauge consumption isn’t foolproof—consuming too much alcohol is still far too easy—but it is nevertheless helpful for thinking about how much you’re ingesting, as well as the differences between beverages. Without such a metric for caffeine, consuming new beverages takes on a daredevil quality. Sipping the Charged Lemonade felt like venturing into the Wild West of caffeine.</p><p></p><p>The reason we aren’t good at thinking about caffeine is that historically, we’ve never really had to think that hard about it. Sure, one too many espressos might have occasionally put someone over the edge, but caffeine was consumed and sold in amounts that didn’t require as much thought or caution. “A generation ago, you didn’t have all these energy drinks,” so people didn’t grow up learning about safe caffeine consumption the way they may have done for alcohol, Darin Detwiler, a food-policy expert at Northeastern University, told me.</p><p></p><p>Compounding the concern is the fact that energy drinks are popular with kids, who are more susceptible to caffeine’s effects because they’re smaller. Kids tend to drink even more when drinks are labeled as highly caffeinated, Temple said, and the fact that they contain huge amounts of sugar to mask the bitter taste of caffeine adds to their appeal. Last year, a child reportedly went into cardiac arrest after drinking a can of Prime Energy—prompting Senator Chuck Schumer to <a href="https://www.npr.org/2023/07/11/1186818826/logan-paul-ksi-prime-energy-drink-caffeine">call on the FDA</a> to investigate its “eye-popping caffeine content.”</p><p></p><p>Nothing else in our daily diet is quite like caffeine. Certainly people swear by it, and its benefits are clear: <a href="https://www.theatlantic.com/family/archive/2023/02/coffee-caffeine-happiness-health-benefits/673158/?utm_source=feed">Research shows</a> that it can improve cognitive performance, speed up reaction time, and boost logical reasoning, and it may even reduce the risk of <a href="https://www.mayoclinic.org/healthy-lifestyle/nutrition-and-healthy-eating/expert-answers/coffee-and-health/faq-20058339">Parkinson’s, diabetes</a>, liver disease, and <a href="https://www.theatlantic.com/health/archive/2016/06/coffeeeeeeee/487181/?utm_source=feed">cancer</a>. But for a substance so ubiquitous that it’s called <a href="https://www.camh.ca/en/health-info/mental-illness-and-addiction-index/caffeine#:~:text=Caffeine%20is%20the%20most%20widely,of%20adults%20regularly%20consume%20caffeine.">the most widely used drug in the world</a>, our grasp of how to maximize its benefits is feeble at best. Even the most seasoned coffee drinkers sometimes unintentionally get too wired; as new, more highly caffeinated products become available, instances of caffeine drinkers overdoing it will probably become more common. Perhaps the best we can do is learn how much of each drink we can handle, one super-charged sip at a time.</p>Yasmin Tayaghttp://www.theatlantic.com/author/yasmin-tayag/?utm_source=feedIllustration by Ben Kothe / The Atlantic. Source: Getty.Caffeine’s Dirty Little Secret2024-01-26T06:00:00-05:002024-02-08T11:10:47-05:00“How much is too much?” is an impossible question.tag:theatlantic.com,2024:50-677242<p>In the weeks after she caught COVID, in May 2022, Lauren Shoemaker couldn’t wait to return to her usual routine of skiing, backpacking, and pregaming her family’s eight-mile hikes with three-mile jogs. All went fine in the first few weeks after her infection. Then, in July, hours after finishing a hike, Shoemaker started to feel off; two days later, she couldn’t make it to the refrigerator without feeling utterly exhausted. Sure it was a fluke, she tried to hike again—and this time, was out of commission for months. Shoemaker, an ecologist at the University of Wyoming, couldn’t do her alpine fieldwork; she struggled to follow a movie with a complex plot. She was baffled. Exercise, the very thing that had reliably energized her before, had suddenly become a trigger for decline.</p><p>For the majority of people, exercise is scientifically, physiologically, psychologically good. It boosts immunity, heart function, cognition, mood, energy, even life span. Doctors routinely prescribe it to patients recovering from chronic obstructive pulmonary disease and heart attacks, managing metabolic disease, or hoping to <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3258000/">stave off cognitive decline</a>. Conditions that worsen when people strive for fitness are very rare. Post-exertional malaise (PEM), which affects Shoemaker and most other people with long COVID, just happens to be one of them.</p><p>PEM, first described decades ago as a hallmark of myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), is now understood to <a href="https://portlandpress.com/biochemsoctrans/article-abstract/46/3/547/67402/Metabolic-abnormalities-in-chronic-fatigue?redirectedFrom=fulltext">fundamentally alter</a> the body’s ability to <a href="https://www.hindawi.com/journals/jar/2016/2497348/">generate and use energy</a>. For people with PEM, just about any form of physical, mental, or emotional exertion—in some cases, activities no more intense than answering emails, folding laundry, or digesting a particularly rare steak—can spark a debilitating wave of symptoms called a crash that may take weeks or months to abate. Simply sitting upright for too long can leave Letícia Soares, a long-hauler living in Brazil, temporarily bedbound. When she recently moved into a new home, she told me, she didn’t bother buying a dining table or chairs—“it just felt useless.”</p><p data-id="injected-recirculation-link"><i>[<a href="https://www.theatlantic.com/health/archive/2024/01/long-covid-dropping-risk-incidence/677183/?utm_source=feed">Read: How much less to worry about long COVID now</a>]</i></p><p>When it comes to PEM, intense exercise—designed to boost fitness—is “absolutely contraindicated,” David Putrino, a physical therapist who runs a long-COVID clinic at Mount Sinai, in New York, told me. And yet, the idea that exertion could undo a person rather than returning them to health is so counterintuitive that some clinicians and researchers still endorse its potential benefits for those with PEM; it’s dogma that Shoemaker heard repeatedly after she first fell ill. “If exercise could cure this,” she told me, “I would have been cured so quickly.”</p><p>The problem is, there’s no consensus about what people who have PEM should do instead. Backing off physical activity too much might start its own downward spiral, as people lose muscle mass and strength in a phenomenon called deconditioning. Navigating the middle ground between deconditioning and crashing is “where the struggle begins,” Denyse Lutchmansingh, a pulmonary specialist at Yale, told me. And as health experts debate which side to err on, millions of long-haulers are trying to strike their own balance.</p><hr class="c-section-divider"><p>Though it’s now widely accepted that PEM rejiggers the body’s capacity for strain, scientists still aren’t sure of the precise biological causes. Some studies have found <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8198768/">evidence</a> of <a href="https://journal.chestnet.org/article/S0012-3692(23)00502-0/fulltext">impaired blood flow</a>, <a href="https://linkinghub.elsevier.com/retrieve/pii/S0012369221002567">stymieing the delivery of oxygen to cells</a>; others have discovered <a href="https://www.nature.com/articles/s41467-023-44432-3">broken mitochondria</a> struggling to process raw fuel into power. A few have seen hints of excessive inflammation, and immune cells aberrantly attacking muscles; others point to issues with recovery, perhaps via a slowdown in the clearance of lactate and other metabolic debris.</p><p>The nature of the crashes that follow exertion can be <a href="https://www.frontiersin.org/articles/10.3389/fneur.2020.01025/full">varied, sprawling, and strange</a>. They might appear hours or days after a catalyst. They can involve flu-like coughs or sore throats. They may crater a patient’s cognitive capacity or plague them with insomnia for weeks; they can leave people feeling so fatigued and pained, they’re almost unable to move. Some of Shoemaker’s toughest crashes have saddled her with tinnitus, numbness, and extreme sensitivity to sound and light. Triggers can also change over time; so can people’s symptoms—even the length of the delay before a crash.</p><p>But perhaps the worst part is what an accumulation of crashes can do. Rob Wüst, who studies skeletal-muscle physiology at Amsterdam University Medical Center, told me that his team has found an unusual amount of muscle damage <a href="https://www.nature.com/articles/s41467-023-44432-3">after exertion</a> in people with PEM that may take months to heal. People who keep pushing themselves past their limit could watch their baseline for exertion drop, and then drop again. “Every time you PEM yourself, you travel a little further down the rabbit hole,” Betsy Keller, an exercise physiologist at Ithaca College, told me.</p><p data-id="injected-recirculation-link"><i>[<a href="https://www.theatlantic.com/health/archive/2022/09/mecfs-chronic-fatigue-syndrome-doctors-long-covid/671518/?utm_source=feed">Read: Long COVID has forced a reckoning for one of medicine’s most neglected diseases</a>]</i></p><p>Still, the goal of managing PEM has never been to “just lay in a bed all day and don’t do anything,” Lily Chu, the vice president of the International Association for Chronic Fatigue Syndrome/Myalgic Encephalomyelitis (IACFS/ME), told me. In the 1960s, a group of scientists found that <a href="https://www.ahajournals.org/doi/10.1161/CIRCULATIONAHA.119.041046">three weeks of bed rest</a> slashed healthy young men’s <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2655009/">capacity for exertion</a> by nearly 30 percent. (The participants eventually trained themselves back to baseline.) Long periods of bed rest were once commonly prescribed for recovery from heart attacks, says Prashant Rao, a sports cardiologist at Beth Israel Deaconess Medical Center, in Massachusetts. But now too much rest is actively avoided, because “there’s a real risk of spiraling down, and symptoms worsening,” Rao told me. “I really fear for that, even for people with PEM.”</p><p>There is no rulebook for threading this needle, which has led researchers to approach treatments and rehabilitation for long COVID in <a href="https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2809670">different ways</a>. Some clinical trials that involve exercise as an intervention explicitly exclude people with PEM. “We did not feel like the exercise program we designed would be safe for those individuals,” Johanna Sick, a physiologist at the University of Vienna who is helping run <a href="https://clinicaltrials.gov/study/NCT06073002">one such trial</a>, told me.</p><p>Other researchers <a href="https://karger.com/res/article/101/6/593/829151/Outpatient-Pulmonary-Rehabilitation-in-Patients">hold out hope</a> that activity-based interventions may still help long-haulers, and are <a href="https://clinicaltrials.gov/study/NCT05846126">keeping</a> <a href="https://clinicaltrials.gov/study/NCT05094622?tab=table">patients</a> with PEM in experiments. But some of those decisions have been controversial. The government-sponsored RECOVER trial <a href="https://www.washingtonpost.com/wellness/2023/05/22/long-covid-treatment-exercise-trial/">was heavily criticized last year</a> for its plan to enroll long-haulers in an exercise study. Scientists have since revised the trial’s design to reroute participants with moderate to severe PEM to another intervention, according to Adrian Hernandez, the Duke cardiologist leading the trial. The details are still being finalized, but the plan is to instead look at pacing, a strategy for monitoring activity levels to ensure that people stay below their crash threshold, Janna Friedly, a physiatrist at the University of Washington who’s involved in the trial, told me.</p><p>Certain experimental regimens can be light enough—stretching, recumbent exercises—to be tolerable by many (though not all) people with PEM. <a href="https://clinicaltrials.gov/study/NCT06172803">Some researchers</a> are trying to <a href="https://workwellfoundation.org/wp-content/uploads/2023/01/HRM-Factsheet.pdf">monitor participants’ heart rate</a>, and having them perform only activities that keep them in a low-intensity zone. But even when patients’ limitations are taken into account, crashes can be hard to avoid, Tania Janaudis-Ferreira, a physiotherapist at McGill University, in Quebec, told me. She recently wrapped a <a href="https://clinicaltrials.gov/study/NCT05298878">clinical trial</a> in which, despite tailoring the regimen to each individual, her team still documented several mild to moderate crashes among participants with PEM.</p><p data-id="injected-recirculation-link"><i>[<a href="https://www.theatlantic.com/health/archive/2023/04/long-covid-symptoms-invisible-disability-chronic-illness/673773/?utm_source=feed">Read: Long COVID is being erased—again</a>]</i></p><p>Just how worrisome crashes are is another matter of contention. Pavlos Bobos, a musculoskeletal-health researcher at the University of Western Ontario, told me that he’d like to see more evidence of harm before ruling out exercise for long COVID and PEM. Bruno Gualano, a physiologist at the University of São Paulo, told me that even though crashes seem temporarily damaging, he’s not convinced that exercise worsens PEM in the long term. But Putrino, of Mount Sinai, is adamant that crashes set people back; most other experts I spoke with agreed. And several researchers told me that, because PEM seems to upend basic physiology, reduced activity may not be as worrisome for people with the condition as it is for those without.</p><p>For Shoemaker, the calculus is clear. “Coming back from being deconditioned is honestly trivial compared to recovering from PEM,” she told me. She’s willing to wait for evidence-based therapies that can safely improve her PEM. “Whatever we figure out, if I could get healthy,” she told me, “then I can get back in shape.”</p><hr class="c-section-divider"><p>At this point, several patients and researchers told me, most exercise-based trials for long COVID seem to be at best a waste of resources, and at worst a recipe for further harm. PEM is not new, nor are the interventions being tested. Decades of research on ME/CFS have already shown that traditional exercise therapy <a href="https://www.ncf-net.org/library/Reporting%20of%20Harms.pdf">harms</a> more often than it helps. (Some researchers insisted that more PEM studies are needed in long-haulers—just in case the condition diverges substantially from its manifestation in ME/CFS.) And although a subset of long-haulers could be helped by exercise, experts don’t yet have a great way to safely distinguish them from the rest.</p><p>Even pacing, although often recommended for <em>symptom</em> <em>management</em>, is not generally considered to be a reliable <em>treatment</em>, which is where most long-COVID patient advocates say funds should be focused. Ideally, Putrino and others told me, resources should be diverted to trials investigating drugs that might address PEM’s roots, such as the antiviral Paxlovid, which could clear lingering virus from long-haulers’ tissues. Some researchers are also hopeful about <a href="https://journal.chestnet.org/article/S0012-3692(22)00890-X/fulltext">pyridostigmine</a>, a medication that might enhance the delivery of oxygen to tissues, as well as <a href="https://link.springer.com/article/10.1007/s10238-022-00871-8">certain</a> <a href="https://www.sciencedirect.com/science/article/pii/S104366182200305X?casa_token=Y_shWADqex4AAAAA:E6SB4WdGjwmaEUcPUK6W-u2FkAwyhy_I5HU4Vv4ZCGZ9IrnrVl0jJjOwtDdH6Hit0v7fJOohVF0">supplements</a> that might support mitochondria on the fritz.</p><p>Those interventions are still experimental—and Putrino said that no single one is likely to work for everyone. That only adds to the challenge of studying PEM, which has been shrouded in <a href="https://nap.nationalacademies.org/catalog/19012/beyond-myalgic-encephalomyelitischronic-fatigue-syndrome-redefining-an-illness">disbelief</a> for decades. Despite years of research on ME/CFS, Chu, of the IACFS/ME, told me that many people with the condition have encountered medical professionals who suggest that they’re just anxious, even lazy. It doesn’t help that there’s not yet a blood test for PEM; to diagnose it, doctors must ask their patients questions and trust the answers. Just two decades ago, researchers and physicians <a href="https://www.qmul.ac.uk/wiph/media/the-wolfson-institute-of-population-health-wiph/documents/3.cbt-therapist-manual.pdf">speculated</a> that PEM stemmed from an irrational fear of activity; some routinely prescribed therapy, antidepressants, and just pushing through, Chu said. <a href="https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(11)60096-2/fulltext">One highly publicized 2011 study</a>, since <a href="https://www.statnews.com/2016/09/21/chronic-fatigue-syndrome-pace-trial/">widely criticized as shoddy science</a>, appeared to support those claims—influencing treatment recommendations from top health authorities such as the CDC.</p><p>The CDC and other organizations <a href="https://www.statnews.com/2017/09/25/chronic-fatigue-syndrome-cdc/">have since</a> <a href="https://www.cdc.gov/me-cfs/pdfs/systematic-review/file1-final-report-mecfs-systematic-review-508.pdf">reversed</a> their <a href="https://www.cdc.gov/me-cfs/treatment/index.html">position</a> on exercise and cognitive behavioral therapy as PEM treatments. Even so, many people with long COVID and ME/CFS are still routinely told to blow past their limits. All of the long-haulers I spoke with have encountered this advice, and learned to ignore it. Fighting those calls to exercise can be exhausting in its own right. As <a href="https://www.theatlantic.com/health/archive/2023/07/chronic-fatigue-long-covid-symptoms/674834/?utm_source=feed">Ed Yong wrote in <em>The Atlantic</em></a> last year, American society has long stigmatized people who don’t push their way through adversity—even if that adversity is a medically documented condition that cannot be pushed through. Reconceptualizing the role of exercise in daily living is already a challenge; it is made all the more difficult when being productive—even overworked—is prized above all else.</p><p data-id="injected-recirculation-link"><i>[<a href="https://www.theatlantic.com/health/archive/2023/07/chronic-fatigue-long-covid-symptoms/674834/?utm_source=feed">Read: Fatigue can shatter a person</a>]</i></p><p>Long-haulers know that tension intimately; some have had to battle it within themselves. When Julia Moore Vogel, a researcher at Scripps, developed long COVID in the summer of 2020, she was at first determined to grit her way through. She took up Pilates and strength training, workouts she at the time considered gentle. But the results were always the same: horrific migraines that relegated her to bed. She now does physical therapy to keep herself moving in safe and supervised amounts. When Vogel, a former competitive runner, started her program, she was taken aback by how little she was asked to do—sometimes just two reps of chin tucks. “I would always laugh because I would be like, ‘These are not exercises,’” she told me. “I’ve had to change my whole mental model about what exercise is, what exertion is.”</p>Katherine J. Wuhttp://www.theatlantic.com/author/katherine-j-wu/?utm_source=feedChris Sorensen / Gallery Stock‘If Exercise Could Cure This, I Would Have Been Cured So Quickly’2024-01-25T12:17:06-05:002024-01-26T16:02:42-05:00Striving for fitness is usually healing. But for most people with long COVID, it can be toxic. <strong> </strong>tag:theatlantic.com,2024:50-677215<p>These days, the options for dietary supplements are virtually limitless. And whatever substance you want to ingest, you can find it in gummy form. Omega-3? You bet. Vitamin C? Absolutely. Iron? Calcium? Zinc? Yes, yes, and yes. There are peach collagen rings and strawberry-watermelon fiber rings. There are brambleberry probiotic gummies and “tropical zing” gummy worms that promise to put you in “an upbeat mood.” There are libido gummies and menopause gummies. There are gummies that claim to boost your metabolism, to reinforce your immune system, to strengthen your hair, your skin, your nails. For kids, there are <em>Transformers</em> multivitamin gummies and <em>My Little Pony</em> multivitamin gummies.</p><p></p><p>I could go on. A simple search for gummy vitamins on the CVS website turns up more than 50 results. This is the golden age of gummies, and that can seem like a great thing. Who wouldn’t rather eat a peach ring than pop a pill? But if the notion that something healthy can taste exactly like candy seems too good to be true, that’s because it is.</p><p></p><p>Gummy supplements are a relatively new phenomenon, but gummy candies are not. Starch-based Turkish delight has been around since the late 18th century. In 1860s England, some of the earliest gummies were <a href="https://www.bbc.com/news/uk-england-35100612">popularly known</a> as “unclaimed babies” (because they were shaped like infants, many more of which apparently were unclaimed back then). In the 1920s, the German confectioner Hans Riegel founded Haribo and created the gelatin-based gummy bears still consumed around the world today. It would be <a href="https://www.google.com/url?q=https://thehustle.co/04282022-gummy-bears/&sa=D&source=docs&ust=1705612271560593&usg=AOvVaw1rZXd2gA3iCiRdnl35QMsa">another 60 years</a>, though, before Haribo gummies arrived on American shores. In the decades that followed, gummy sweets became ubiquitous, taking almost every shape imaginable: worms, frogs, sharks, snakes, watermelons, doughnuts, hamburgers, french fries, bacon, Coke bottles, bracelets, Band-Aids, brains, teeth, eyeballs, genitalia, soldiers, mustaches, Legos, and, as in days of old, <a href="https://sourpatchkids.com/">children</a>.</p><p></p><p>Only in the late 1990s and early 2000s, though, did the supplement industry begin experimenting with gummies. The driving principle was not a new one: As Mary Poppins put it, “A spoonful of sugar makes the medicine go down.” <em>Flintstones</em> multivitamins have been around in their hard, chewable form <a href="https://www.flintstonesvitamins.com/faq#:~:text=When%20did%20Flintstones%E2%84%A2%20Vitamins,8%20years%20later%2C%20in%201968.">since 1968</a>; even if superior to pills, they basically taste like sweet, vaguely chemical chalk.</p><p></p><p>Gummy vitamins, on the contrary, are virtually indistinguishable from the treats they’re modeled on. You could pop men’s multis at the movies the same way you could Sour Patch Kids. (Or Starburst gummies, or Skittles gummies, or Jolly Rancher gummies—pretty much every non-chocolate candy now comes in gummy form.) Which is probably why they’ve become so popular, says Tod Cooperman, the president of ConsumerLab, a watchdog site that reviews supplements. When he founded ConsumerLab in 1999, gummy supplements hardly existed. Adult gummy vitamins didn’t hit the market <a href="https://www.nytimes.com/2017/02/28/well/eat/vitamins-gone-gummy.html#:~:text=Gummy%20vitamins%20and%20supplements%20originally,marketing%20gummy%20products%20to%20adults.">until 2012</a>. Now, Nina Puch, a scientist who formulates gummies for the food and pharmaceutical consulting company Knechtel, told me, three-quarters of the gummies she designs are supplements rather than candies. Gummy supplements are everywhere. They’re a rapidly expanding $7 billion–plus industry, and by 2027 that figure is <a href="https://www.wsj.com/articles/gummy-vitamins-are-surging-in-popularity-are-they-healthy-or-just-candy-11665486949">projected</a> to double.</p><p></p><p>But what makes gummy supplements appealing also makes them concerning. The reason they taste as good as candy, it turns out, is because on average, they can contain just as much sugar as <a href="https://www.wsj.com/articles/gummy-vitamins-are-surging-in-popularity-are-they-healthy-or-just-candy-11665486949">candy</a> does. The earliest gummy supplements, Cooperman told me, were basically just candy with vitamins sprayed on. They’ve come a long way since then: The active ingredients are now carefully integrated into the gummy itself by scientists such as Puch, and done so in a way that preserves as much of the gummy’s flavor and consistency as possible. But the nutritional essentials haven’t changed much—the average gummy vitamin <a href="https://www.uclahealth.org/news/should-you-take-gummy-vitamins#:~:text=Most%20gummy%20vitamins%20contain%20between,36%20grams%20for%20men%20daily.">contains</a> about the same amount of sugar in a serving as one Sour Patch Kid does.</p><p></p><p>A little extra sugar is not the end of the world. But there’s also the danger of overdoses. Especially for children, it’s important that medicines and supplements not taste <em>too </em>good, Cora Breuner, a professor of pediatrics at the University of Washington, told me. Consumed in excess, many of the vitamins and nutrients delivered in supplements can be toxic. They have to strike an appropriate balance, neither tasting so bad that kids refuse to take them nor so good that they’ll want too much. Most gummy supplements seemingly fail the latter test, and not without consequences. Annual calls to Poison Control for pediatric melatonin overdoses have risen 530 percent over the past decade, in part, experts <a href="https://www.theatlantic.com/health/archive/2023/05/melatonin-kids-overdose/674104/?utm_source=feed">suggested to me</a> last year, because of the hormone’s increased availability in gummy form. The overdose numbers are <a href="https://www.nbcnews.com/health/health-news/fda-takes-first-step-protect-children-medications-look-taste-candy-rcna122744">also up</a> for multivitamins.</p><p></p><p>The risk of overdose can be greatly mitigated by simply taking care to store gummies where kids can’t get them. The more significant problem, Cooperman told me, is that gummies are simply a less reliable delivery mechanism than the alternatives. Vitamins and many other compounds degrade far faster in gummies’ half-liquid, half-solid state than in traditional pill or capsule form, he said, because gummies offer less protection from heat, light, moisture, and other contaminants.</p><p></p><p>To compensate, supplement makers will in many cases load their products with far more of a substance than advertised on the packaging. Some overage is to be expected with all supplements, but the margins for many gummy supplements are gargantuan. “Gummy vitamins were the most likely form to contain much more of an ingredient than listed,” ConsumerLab <a href="https://www.consumerlab.com/reviews/multivitamin-review-comparisons/multivitamins/">wrote</a> in its 2023 review of multivitamins and multiminerals. Of the four gummy supplements reviewed, three contained nearly twice as much of the relevant substance as they were supposed to, and the fourth contained only around three-quarters as much.</p><p></p><p>A <a href="https://jamanetwork.com/journals/jama/article-abstract/2804077">recent analysis</a> of melatonin and CBD gummies yielded similar results: Some contained as much as 347 percent the amount of those substances stated on the label. Because the FDA generally does not regulate supplements as drugs, such wild variability is accepted in a way that it isn’t for actual pharmaceuticals. (In 2020, the FDA <a href="https://www.formularywatch.com/view/is-medicine-delivered-via-gummies-the-future-">granted</a> the first-ever Investigational New Drug Application for a gummy medication, though no such product appears to have come to market.) “If you have something that you need a specific amount of every time you take it, gummies are not the way to go,” says Pieter Cohen, a doctor at Cambridge Health Alliance, in Somerville, Massachusetts, and the lead author of the melatonin-CBD research. Taking too much of a supplement is generally not as dangerous as taking too much of a prescription drug, but, as Breuner noted, many supplements taken in sufficient excess can still be toxic. When I asked Cooperman what advice he had for people trying to navigate all of this, his answer was simple: “Don’t buy a gummy.”</p><p></p><p>Perhaps the rise of gummy supplements was inevitable. The supplement industry has become so big in part because it can promote its products as, say, boosting the immune system or supporting healthy bones, without subjecting them to the strict regulatory demands imposed on pharmaceuticals. Supplements blur the line between food and drug, and gummy supplements—designed and marketed on the premise that healthy stuff can and should taste as good as candy—only intensify that blurring. Cohen, for one, thinks the distinction is worth preserving. Calcium supplements should not go down as easy as Haribos. That may be a bitter pill to swallow, but not everything can taste like candy.</p>Jacob Sternhttp://www.theatlantic.com/author/jacob-stern/?utm_source=feedGettyGummy Vitamins Are Just Candy2024-01-22T15:40:00-05:002024-01-25T17:22:25-05:00The false promise of sweet, chewy supplementstag:theatlantic.com,2024:50-677183<p>Compared with the worst days of the pandemic—when vaccines and antivirals were nonexistent or scarce, when <a href="https://www.nytimes.com/interactive/2021/world/covid-cases.html">more than 10,000 people</a> around the world were dying each day, when long COVID largely went unacknowledged even as <a href="https://www.theatlantic.com/health/archive/2020/06/covid-19-coronavirus-longterm-symptoms-months/612679/?utm_source=feed">countless people fell chronically ill</a>—the prognosis for the average infection with this coronavirus has clearly improved.</p><p></p><p>In the past four years, the likelihood of severe COVID has massively dropped. Even now, as the United States barrels through what may be its second-largest wave of SARS-CoV-2 infections, rates of death <a href="https://public.tableau.com/app/profile/benjamin.renton/viz/InsideMedicineCOVID-19MetricsDashboard/Dashboard1?publish=yes">remain near their all-time low</a>. And although tens of thousands of Americans are still being hospitalized with COVID each week, emergency rooms and intensive-care units are no longer routinely being forced into crisis mode. Long COVID, too, appears to be a less common outcome of new infections than it once was.</p><p></p><p data-id="injected-recirculation-link"><i>[<a href="https://www.theatlantic.com/health/archive/2023/02/long-covid-cases-treatment-chronic-illness-emergency/673032/?utm_source=feed">Read: The future of long COVID</a>]</i></p><p></p><p>But where the drop in severe-COVID incidence is clear and prominent, the drop in long-COVID cases is neither as certain nor as significant. Plenty of new cases of <a href="https://www.cdc.gov/nchs/covid19/pulse/long-covid.htm">the chronic condition</a> are still appearing with each passing wave—even as millions of people who developed it in years past continue to suffer its long-term effects.</p><p></p><p>In a way, the shrinking of severe disease has made long COVID’s dangers more stark: Nowadays, “long COVID to me still feels like the biggest risk for most people,” Matt Durstenfeld, a cardiologist at UC San Francisco, told me—in part because it does not spare the young and healthy as readily as severe disease does. Acute disease, by definition, eventually comes to a close; as a chronic condition, long COVID means debilitation that, for many people, may never fully end. And that lingering burden, more than any other, may come to define what living with this virus long-term will cost.</p><hr class="c-section-divider"><p>Most of the experts I spoke with for this story do think that the average SARS-CoV-2 infection is less likely to unfurl into long COVID than it once was. Several studies and <a href="https://www.cdc.gov/nchs/covid19/pulse/long-covid.htm">data</a> sets support this idea; physicians running clinics told me that, anecdotally, they’re seeing that pattern play out among their patient rosters too. The number of referrals coming into Alexandra Yonts’s long-COVID clinic at Children’s National, in Washington, D.C., for instance, has been steadily dropping in the past year, and the waitlist to be seen has shortened. The situation is similar, other experts told me, among adult patients at Yale and UCSF. Lisa Sanders, an internal-medicine physician who runs a clinic at Yale, told me that more recent cases of long COVID appear to be less debilitating than ones that manifested in 2020. “People who got the earliest versions definitely got whacked the worst,” she said.</p><p></p><p>That’s reflective of how our relationship to COVID has changed overall. In the same way that immunity can guard a body against COVID’s most severe, acute forms, it may also protect against certain kinds of long COVID. (Most experts consider <em>long COVID</em> to be <a href="https://www.theatlantic.com/health/archive/2023/02/long-covid-cases-treatment-chronic-illness-emergency/673032/?utm_source=feed">an umbrella term</a> for many related but separate syndromes.) Once wised up to a virus, our defenses become strong and fast-acting, more able to keep infection from spreading and lingering, as it might in some long-COVID cases. Courses of illness also tend to end more quickly, with less viral buildup, giving the immune system less time or reason to launch a campaign of friendly fire on other tissues, another potential trigger of chronic disease.</p><p></p><p>In line with that logic, a glut of <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9566528/">studies</a> has shown that <a href="https://www.cambridge.org/core/journals/antimicrobial-stewardship-and-healthcare-epidemiology/article/effectiveness-of-covid19-vaccine-in-the-prevention-of-postcovid-conditions-a-systematic-literature-review-and-metaanalysis-of-the-latest-research/A0B115B5D3AA60846799857B801D116E">vaccination</a>—especially recent and <a href="https://www.bmj.com/content/383/bmj-2023-076990">repeated</a> vaccination—can <a href="https://publications.aap.org/pediatrics/article/doi/10.1542/peds.2023-064446/196419/Vaccine-Effectiveness-Against-Long-COVID-in?autologincheck=redirected&utm_source=substack&utm_medium=email">reduce</a> a person’s chances of developing long COVID. “There is near-universal agreement on that,” Ziyad Al-Aly, the chief of research at the VA St. Louis Health Care System and a clinical epidemiologist at Washington University in St. Louis, told me. Some experts think that antiviral use may be making a dent as well, by decreasing the proportion of COVID cases that progress to severe disease, a risk factor for certain types of long COVID. Others have pointed to the possibility that more recent <a href="https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(22)00941-2/fulltext">variants</a> of the <a href="https://www.ijidonline.com/article/S1201-9712(23)00702-6/fulltext">virus</a>—some of them maybe less likely to penetrate deeply into the lungs or affect certain especially susceptible organs—may be less apt to trigger chronic illness too.</p><p></p><p>But consensus on any of these points is lacking—especially on just how much, if at all, these interventions help. Experts are divided even on the effect of vaccines, which have the most evidence to back their protective punch: Some studies find that they trim risk by <a href="https://jamanetwork.com/journals/jama/article-abstract/2794072">15 percent</a>, others up to <a href="https://www.cambridge.org/core/journals/antimicrobial-stewardship-and-healthcare-epidemiology/article/effectiveness-of-covid19-vaccine-in-the-prevention-of-postcovid-conditions-a-systematic-literature-review-and-metaanalysis-of-the-latest-research/A0B115B5D3AA60846799857B801D116E">about 70 percent</a>. Paxlovid, too, has become a point of contention: Although some analyses have shown that taking the antiviral early in infection <a href="https://jamanetwork.com/journals/jamainternalmedicine/fullarticle/2802878">helps prevent</a> long COVID, others have found <a href="https://onlinelibrary.wiley.com/doi/full/10.1002/jmv.29333">no effect at all</a>. Any implication that we’ve tamed long COVID exaggerates how positive the overall picture is. Hannah Davis, one of the leaders of the Patient-Led Research Collaborative, who developed long COVID during the pandemic’s first months, told me that she’s seen how the most optimistic studies get the most attention from the media and the public. With a topic as unwieldy and challenging to understand as this, Davis said, “we still see overreactions to good news, and underreactions to bad news.”</p><p></p><p>That findings are all over the place on long COVID isn’t a shock. The condition still lacks a universal definition or a standard method of diagnosis; when recruiting patients into their studies, research groups can rely on <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10176974/">distinct</a> <a href="https://www.cdc.gov/coronavirus/2019-ncov/long-term-effects/index.html">sets</a> of criteria, inevitably yielding disparate and seemingly contradictory sets of results. With vaccines, for instance, the more wide-ranging the set of potential long-COVID symptoms a study looks at, the less effective shots may appear—simply because “vaccines don’t work on everything,” Al-Aly told me.</p><p></p><p>Studying long COVID has also gotten tougher. The less attention there is on COVID, “the less likely people are to associate long-term symptoms with it,” Priya Duggal, an infectious-disease epidemiologist at Johns Hopkins University, told me. Fewer people are testing for the virus. And some physicians still “don’t believe in long COVID—that’s what I hear a lot,” Sanders told me. The fact that fewer new long-COVID cases are appearing before researchers and clinicians could be in part driven by fewer diagnoses being made. Al-Aly worries that the situation could deteriorate further: Although long-COVID research is still chugging along, “momentum has stalled.” Others <a href="https://www.nature.com/articles/d41586-023-03225-w">share his concern</a>. Continued public disinterest, Duggal told me, could dissuade journals from publishing high-profile papers on the subject—or deter politicians from setting aside funds for future research.</p><hr class="c-section-divider"><p>Even if new cases of long COVID are less likely nowadays, the incidence rates haven’t dropped to zero. And rates of recovery are slow, low, and still murky. At this point, “people are entering this category at a greater rate than people are exiting this category,” Michael Peluso, a long-COVID researcher at UCSF, told me. The <a href="https://www.cdc.gov/nchs/covid19/pulse/long-covid.htm">CDC’s Household Pulse Survey</a>, for instance, shows that the proportion of American adults reporting that they’re currently dealing with long COVID has held steady—about 5 to 6 percent—for more than a year (though the numbers <em>have </em>dropped since 2021). Long COVID remains one of the most debilitating chronic conditions in today’s world—and full recovery <a href="https://www.mdpi.com/2077-0383/12/3/741">remains</a> <a href="https://www.nature.com/articles/s41467-022-29513-z">uncommon</a>, especially, it seems, for those who have been dealing with the disease for the longest.</p><p></p><p>Exact numbers on recovery are tricky to come by, for the same reasons that it’s difficult to pin down how effective preventives are. Some studies report rates <a href="https://www.bmj.com/content/380/bmj-2022-072529">far more optimistic</a> than <a href="https://www.thelancet.com/journals/lanepe/article/PIIS2666-7762(23)00143-6/fulltext">others</a>. David Putrino, a physical therapist who runs a long-COVID clinic at Mount Sinai Health System, where he and his colleagues have seen more than 3,000 long-haulers since the pandemic’s start, told me his best estimates err on the side of the prognosis being poor. About 20 percent of Putrino’s patients fully recover within the first few months, he told me. Beyond that, though, he routinely encounters people who experience only partial symptom relief—as well as a cohort that, “no matter what we think to try,” Putrino told me, “we can’t even seem to stop them from deteriorating.” Reports of higher recovery rates, Putrino and other experts said, might be conflating improvement with a return to baseline, or mistakenly assuming that people who stop responding to follow-ups are better, rather than just done participating.</p><p></p><p data-id="injected-recirculation-link"><i>[<a href="https://www.theatlantic.com/health/archive/2023/04/long-covid-symptoms-invisible-disability-chronic-illness/673773/?utm_source=feed">Read: Long COVID is being erased—again</a>]</i></p><p></p><p>Davis also worries that recovery rates could drop<em>.</em> Some researchers and clinicians have noticed that today’s new long-COVID patients are more likely than earlier patients to come in with certain <a href="https://www.nature.com/articles/s41598-023-36995-4">neurological symptoms</a>—among them, <a href="https://www.nature.com/articles/s41579-022-00846-2">brain fog and dizziness</a>—that have been linked to slower recovery trajectories, Lekshmi Santhosh, a pulmonary specialist at UCSF, told me.</p><p></p><p>In any case, recovery rates are still modest enough that long-COVID clinics across the country—even ones that have noted a dip in demand—remain very full. Currently, Putrino’s clinic has a waitlist of three to six months. The same is true for clinical trials investigating potential treatments. One, run by Peluso, that is <a href="https://classic.clinicaltrials.gov/ct2/show/NCT05877508">investigating monoclonal-antibody therapy</a> has a waitlist that is “hundreds of people deep,” Peluso told me: “We do not have the problem of not being able to find people who want to participate.”</p><p></p><p>Any decrease in long-COVID incidence may not last, either. Viral evolution could always produce a new variant or subvariant with higher risks of chronic issues. The protective effects of vaccination may also be quite temporary, and the fewer people who keep up to date with their shots, the more porous immunity’s safety net may become. In this way, kids—though seemingly less likely to develop long COVID overall—may remain worryingly vulnerable, Yonts told me, because they’re born entirely susceptible, and immunization rates in the youngest age groups remain extremely low. And yet, little kids who get long COVID may need to live with it the longest. Some of Yonts’s patients have barely started grade school and have already been sick for three-plus years—half of their lives so far, or more.</p><p></p><p>Long COVID can also manifest after <a href="https://www.nature.com/articles/s41591-022-02051-3">repeat infections</a> of SARS-CoV-2—and although several experts told me they think that each subsequent exposure poses less incremental risk, any additional exposure is worrisome. People all over the world are being exposed, over and over again, as the pathogen spreads with blistering speed, more or less year-round, in populations that have mostly dropped mitigations and are mostly behind on annual shots (where they’re available). Additional infections can worsen the symptoms of people living with long COVID, or yank them out of remission. Long COVID’s inequities may also widen as marginalized populations, less likely to receive vaccines or antivirals and more likely to be exposed to the virus, continue to develop the condition at higher rates.</p><p></p><p>There’s no question that COVID-19 has changed. The disease is more familiar; the threat of severe disease, although certainly not vanished, is quantitatively less now. But dismissing the dangers of the virus would be a mistake. Even if rates of new long-COVID cases continue to drop for some time, Yonts pointed out, they will likely stabilize somewhere. These risks will continue to haunt us and incur costs that will keep adding up. Long COVID may not kill as directly as severe, acute COVID has. But people’s lives still depend on avoiding it, Putrino told me—“at least, their life as they know it right now.”</p>Katherine J. Wuhttp://www.theatlantic.com/author/katherine-j-wu/?utm_source=feedIllustration by The Atlantic. Source: Getty.How Much Less to Worry About Long COVID Now2024-01-18T12:39:37-05:002024-01-18T16:44:42-05:00New cases seem to be less common nowadays, but that change is not as comforting as it sounds.tag:theatlantic.com,2024:50-677161<p>This year, I’m going to get into shape. It does not matter that I’ve made this same resolution every year for more than a decade, or that I gave up after a month each time. In 2024, I mean it. Unlike years past, my motivation is not aesthetic but utilitarian: I want to get fit so I stop feeling like garbage. As I enter my late 30s, I’m struggling with the health issues that come with the terrain—<a href="https://www.fda.gov/drugs/special-features/high-blood-pressure-understanding-silent-killer">high blood pressure</a>, <a href="https://www.ninds.nih.gov/health-information/disorders/back-pain#:~:text=Age%3A%20The%20first%20attack%20of,not%20properly%20support%20the%20spine.">lower-back pain</a>, and <a href="https://medlineplus.gov/ency/article/003998.htm">persistently achy joints</a>. On top of those, I’m a new mom, chronically sleep-deprived and exhausted. My six-month-old son saps all my energy but also steels my resolve to protect it.</p><p></p><p>With all my new motivation, I first had to find a workout regime. Scrolling through social media for inspiration, I saw athletes of every variety across my feed. There were people sweating it out at a <a href="https://sealfit.com/">Navy SEAL–style workout</a>, a <a href="https://www.hithouse.com/">Muay Thai–inspired kickboxing class</a>, and a <a href="https://conbody.com/">workout designed and taught by former inmates</a>. Yoga isn’t just yoga anymore; it can be <a href="https://www.theatlantic.com/health/archive/2015/04/bikram-so-hot-in-herre/391047/?utm_source=feed">hot</a>, <a href="https://antigravityfitness.com/">aerial</a>, <a href="https://www.instagram.com/acroyogala/?hl=en">acrobatic</a>, <a href="https://www.instagram.com/namasdrake/">Drake</a>, and even <a href="https://www.nygoatyoga.com/">goat</a>. Personal trainers shout commands through media including YouTube, <a href="https://www.getsupernatural.com/">VR headsets</a>, and, uh, <a href="https://www.theatlantic.com/health/archive/2020/01/mirror-mirror-workout-wall/604699/?utm_source=feed">mirrors</a>. You can work out alone or in a group (or alone in a group, if <a href="https://www.theatlantic.com/magazine/archive/2019/12/the-tribe-of-peloton/600748/?utm_source=feed">Peloton</a> is your thing). For the graceful, there is barre; for the nerds, there is a <a href="https://www.theconqueror.events/lotr8/?gad_source=1&gclid=Cj0KCQiAnfmsBhDfARIsAM7MKi0ld9afIDKeZOPvQRFfcNC83Z-PaOSry362GmNVUvDKjFWcuxL74DAaAnJzEALw_wcB"><em>Lord of the Rings</em></a><a href="https://www.theconqueror.events/lotr8/?gad_source=1&gclid=Cj0KCQiAnfmsBhDfARIsAM7MKi0ld9afIDKeZOPvQRFfcNC83Z-PaOSry362GmNVUvDKjFWcuxL74DAaAnJzEALw_wcB">–themed </a><a href="https://www.theconqueror.events/lotr8/?gad_source=1&gclid=Cj0KCQiAnfmsBhDfARIsAM7MKi0ld9afIDKeZOPvQRFfcNC83Z-PaOSry362GmNVUvDKjFWcuxL74DAaAnJzEALw_wcB">app</a> that logs exercise as movement from the Shire to Mordor.</p><p></p><p>We are living in a golden age of fitness: With workouts to accommodate every skill level, interest, time commitment, and social capacity, it should be easier than ever for novices to find one and get started. But it’s not. Instead of finding a workout that suited me, choice overload left me even more inert, and less motivated, than I was when I started my search. If you’re serious about committing to a fitness regime, choosing one isn’t just about moving your body. It could shape your future schedule, lifestyle, and even identity. To others, the way you exercise might say something about who you are, whether that’s a <a href="https://www.womensrunning.com/culture/became-marathon-maniac/">marathon maniac</a> or a <a href="https://www.instagram.com/explore/tags/pelotonmom/">#PelotonMom</a>. To the exercise newbie, this can make the stakes feel dauntingly high.</p><p></p><p>The stakes <em>are </em>high. Exercise will lead to results only if you do it consistently, potentially spending hours on it each week. It’s essential to pick right. I was never fitter than when I played in a basketball league in my early 20s and was held accountable for going to games and practice. Since then, I’ve only dabbled in activities—like kickboxing, spinning, and something called <a href="https://go.dancechurch.com/">Dance Church</a>. None of them stuck. In the search for the ideal workout, baseline criteria include practical concerns such as location and affordability. No matter how exciting the class, a gym that’s out of the way or prohibitively expensive is not one you will attend regularly. Then there is what I call doability—as in, <em>Can my body do that?</em> Answering honestly can eliminate unlikely options, such as the <a href="https://www.healthline.com/nutrition/300-workout-review">grueling</a> <a href="https://www.healthline.com/nutrition/300-workout-review">circuit</a> that turned actors into Spartans for the movie <a href="https://www.theatlantic.com/culture/archive/2014/03/why-gay-guys-love-300/358908/?utm_source=feed"><em>300</em></a>. Being too pragmatic, however, can also stifle fitness aspirations. If your goal is an eight-pack, the “<a href="https://fortune.com/well/2023/08/28/lazy-girl-workouts-tips-tricks/">lazy-girl workout</a>” probably isn’t going to cut it.</p><p></p><p>Ruling out options based on practicality only whittles the list down so much. The next step is harder: figuring out what you actually want to do. For a goal as broad as “get in shape,” you can drive yourself crazy trying to find the answer. Picking a workout that ticks all the boxes is virtually impossible, because there will always be other options that seem better. At first, streaming <a href="https://www.theatlantic.com/health/archive/2020/06/yoga-with-adriene-pandemic/612964/?utm_source=feed">Yoga With Adriene</a> in my living room seemed like a cheap, enjoyable, and physically demanding option, but it lacked a social component to hold me accountable. Programs inspired by high-intensity interval training (HIIT), such as F45, promise to get people ripped—fast!—but exercising under a constant deadline is my idea of hell. I found flaws in workouts as varied as rock climbing, rugby, Orangetheory, Tabata, <a href="https://poolfit.tv/water-workout-blog/aqua-tabata-deep-shallow">Aqua Tabata</a>, and Tabata-style spinning.</p><p></p><p>Adding to the gravity of the decision is what it signals about who you are. Personal fitness is rarely personal these days. Stereotypes inform the culture of certain workouts and how their adherents are seen: Indoor rock climbing is associated with <a href="https://www.vice.com/en/article/k7ew5z/climbing-trend-millennial-men-bouldering">tech bros</a>, running with intensely driven morning people, weight lifting with gym rats. Many boutique workouts come with even more distinct personality types, perpetuated by the communities they spawn in real life and on social media. Perhaps the most recognizable is the CrossFit Bro, an aggressive, bandanna-wearing jock who can’t stop talking about CrossFit. Pure Barre and SoulCycle call to mind lithe, athleisure-clad smoothie drinkers; Peloton, the kind of person who can afford a Peloton.</p><p></p><p>New identities can also form by virtue of the lifestyle shifts that these workouts can bring about. Friendships are nurtured by sweat spilled during class; exercise may even shift eating habits. For some, fitness programs become so embedded in daily life that they begin to resemble <a href="https://www.theatlantic.com/health/archive/2017/06/the-church-of-crossfit/531501/?utm_source=feed">institutionalized religion</a>. In an extreme case of life imitating exercise, a couple who met at CrossFit got married and served a <a href="https://www.thecut.com/swellness/2016/07/crossfit-wedding-games-paleo.html">paleo cake at their wedding</a>, which was held during a CrossFit competition. Because exercise is so good at fostering community, the search for a workout is sometimes described as <a href="https://www.latimes.com/health/la-he-fitness-social-clubs-20180324-htmlstory.html">finding</a><a href="https://www.latimes.com/health/la-he-fitness-social-clubs-20180324-htmlstory.html"> “your tribe.”</a></p><p></p><p data-id="injected-recirculation-link"><i>[<a href="https://www.theatlantic.com/health/archive/2017/06/the-church-of-crossfit/531501/?utm_source=feed">Read: The church of CrossFit</a>]</i></p><p></p><p>These stereotypes are not always true, of course, and they can also be aspirational. Embarrassed as I am to admit it, I would love to be a smoothie girl. But the notion of joining a <em>tribe </em>makes pedaling on a stationary bike or joining a rock-climbing gym feel much more consequential than the activities themselves. I was getting nowhere in my own fitness search, so I turned to experts for a reality check. Selecting from a multitude of fitness options is “quite a dilemma,” Sarah Ullrich-French, a kinesiology professor at Washington State University, told me, but the way out is to focus on what feels good, physically and psychologically. Fitness identities, however palpable, only have to mean something if you want them to. If the stereotype of the intensely focused predawn runner inspires you to get up for a morning jog, lean into it. But if it seems like an annoying downside to running, it’s okay to treat it as such. Pay attention to workouts that bring up anxiety and dread; even if you aspire toward a certain identity, “negative associations and feelings will often win over our goals and what we think we should do,” Ullrich-French said.</p><p></p><p>Part of my problem was having a goal that was too diffuse. Theoretically any workout could help me <em>get fit</em>, but if I refined my ambition to, say, “getting up the stairs to work without heaving,” doing so would narrow my options to exercises that optimize stamina and strength. Instead of immediately signing up for a weekly running club, start with small, attainable goals, such as taking the time to stretch each morning, Adam Makkawi, an assistant professor of medicine at Columbia University, told me. Small goals are easier to achieve, and can help make more workout options a real possibility.</p><p></p><p>My biggest mistake was to treat choosing a workout as an intellectual endeavor, sort of like shopping for a new vacuum by reading endless online reviews. Test several options, and when you’ve found one that you like, customize its intensity and frequency until it suits you, Catherine Sabiston, a professor of kinesiology and physical education at the University of Toronto, told me. The likelihood that you’ll stick to it, she added, boils down to competency—how well you feel you can accomplish a task—and enjoyment, both of which can be known only through experience.</p><p></p><p>Choice overload is real, but it can also be a powerful excuse to stay inert. Although a little self-reflection about fitness identities can be helpful, fixating on them can rule out perfectly viable options. In this spirit, I compiled a list of doable, challenging, and conceivably fun workouts to try—and even mustered up excitement for a fitness identity that brought me joy. This week, I begin my search in earnest, embarking on a virtual <em>Lord of the Rings</em> running journey across the rugged terrain of Middle Earth.</p>Yasmin Tayaghttp://www.theatlantic.com/author/yasmin-tayag/?utm_source=feedIllustration by Ben Kothe / The AtlanticThere Are Too Many Ways to Exercise2024-01-18T07:00:00-05:002024-01-22T15:45:24-05:00Choosing a workout regimen has become a workout in and of itself.