When Tess Camp was pregnant with her second child, she knew she would need to get to the hospital fast when the baby came. Her first labor had been short for a first-time mother (seven hours), and second babies tend to be in more of a hurry. Even so, she was not prepared for what happened: One day, at 40 weeks, she started feeling what she thought was just pregnancy back pain. Then her water broke, and 12 minutes later, she was holding a baby in her arms. Needless to say, she didn’t make it into the hospital in time. But the first contraction after Camp’s water broke at home had been so intense—“immediate horrific pain; I could barely talk”—that she and her husband rushed into the car. He drove through town like a madman, running red lights. They were turning into the ER when she saw the baby’s head between her legs. Her husband tore out of the car, yelling for help. A security guard ran over to a terrified Camp in the passenger’s seat, and in that moment, her son slipped out and into the security guard’s hands. His umbilical cord was wrapped around his neck. An ER nurse finally appeared to take the baby—still blue and limp—and resuscitated him right on the curb. What Camp experienced is called “precipitous labor,” when a baby is born after fewer than three hours of regular contractions. It is uncommon but not entirely rare, occurring in about 3 percent of deliveries, usually in second, third, or later labors. Having had a previous fast birth, like Camp did, increases the chances of a precipitous labor. But otherwise, doctors can’t predict for sure who will have one, especially among first-time moms with no previous birth experience. Like many topics in pregnancy and childbirth, precipitous labor remains understudied. Counterintuitively, perhaps, an extremely fast labor is not always a better one. It can even be a terrible one. “It felt like being hit by a truck and dragged along behind,” says Stephanie Spitzer-Hanks, a doula and childbirth-class instructor who had precipitous labors with her two children. “People would tell me I was lucky, and I don’t feel like that. I tell my students, ‘I don’t really wish for you to have this kind of labor.’” In normal labor, each contraction gradually opens the cervix and prods the baby out. In a precipitous labor, the cervix still has to open just as wide, and the baby still has to move just as far—but in much less time. It’s like running the length of a marathon at the punishing pace of a sprint. Babies born through precipitous labor tend to do just fine, but the process can be traumatic for the mother’s body. In the normal course of labor, says Tamika Auguste, an ob-gyn at MedStar Washington Hospital Center, the back-and-forth movement of the baby’s head during contractions stretches the perineum, a layer of tissue especially likely to tear in childbirth. In one study, precipitous labor multiplied the odds of a severe third-degree perineal tear by 25 and the odds of postpartum hemorrhaging by almost 35. (Precipitous labor is also responsible for one of the most horrifying case reports I have ever come across, whose title contains the phrase “severed external anal sphincter.”) Even for ER doctors, “a precipitous delivery is right up there with some of the most stressful events that we managed,” says Joelle Borhart, an emergency-medicine doctor also at MedStar Washington Hospital Center. Precipitous labor can happen so fast that even if the mother makes it to the hospital, there is sometimes no time to transfer her from the ER to the labor-and-delivery unit. ER staff are trained in childbirth, but it’s not what they do on a daily basis. Borhart says the emergency department at her large hospital in Washington, D.C., gets about one case a month. Brian Sharp, an emergency-medicine physician at UW Health—a large academic hospital in Madison, Wisconsin—told me his hospital averages a little over once a year; the smaller community site where he also works just had their first case of precipitous labor in years. The rarity of these events means that hospitals aren’t always the most prepared. When Camp arrived with her baby almost born at the entrance of the ER, the hospital sent out the wrong code, mistakenly suggesting that there had been an abduction. No one from labor and delivery came to meet her, because they were counting babies to make sure none had gone missing. The hospital later reviewed her case, Camp told me, to figure how to improve the response in future situations. All of this means that precipitous labor can be psychologically distressing too. When Bryn Huntpalmer, who runs the podcast The Birth Hour and a childbirth course, talks with postpartum mothers, “more times than not, the person who shares their precipitous labor has that shell-shocked view of it.” Some of the mothers I interviewed talked about feeling out of control and deeply disconnected from their bodies. “I couldn’t get words out. I couldn’t open my eyes. I couldn't control what my arms were doing,” says Shannon Burke, who had a precipitous labor with her second child. “I couldn’t do anything.” For many people, the experience of childbirth is an experience of ceding control, of letting our most animal instincts take over. But in normal labor, this is at least a gradual process; you can joke and laugh and walk in the early phases, and only hours in, when you’ve mentally prepared yourself, do the screaming and vomiting take over. Burke remembers her 24-hour first labor fondly, in fact; she had spent the early phase at home with her mother and sister, readying the house for the baby. With her precipitous labor, she had no time for any of that. She plunged straight into full-blown pain. “There’s no buildup to prepare your mind and body,” Huntpalmer, the podcaster who herself went through precipitous labor, told me. “Everything was so compressed.” But in talking about her experience—and talking since on The Birth Hour with hundreds of women about their experiences--she ultimately came to see her precipitous labor as affirming, too: Her body knew what to do. “It was so hands-off from my midwife. I was able to just kind of do it all myself,” she says. Emily Geller, who delivered her second baby during a precipitous labor in a car, told me the same. She had what she felt was an unnecessary C-section with her first child, so she wanted a natural vaginal birth this time—and she did have one, just faster than she planned. It was empowering, she said, to know that she could do it after all. When Camp got pregnant with her third child, though, she did not want to give birth in the car again. Her husband was terrified too—he kept saying he was going to rent a trailer so they could spend the final weeks of her pregnancy sleeping in the hospital parking lot. “It’s $150 a week to rent a trailer,” she remembers him telling her. They didn’t do that, but she did schedule an induction at 39 weeks. Her daughter was born after two pushes. from https://ift.tt/LXJO2Ef Check out http://natthash.tumblr.com
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On Tuesday, two men at a museum in the Netherlands lifted a black sheet off a table to reveal a cantaloupe-size globe of overcooked meat perspiring under a bell jar. This was no ordinary spaghetti topper: It was a woolly-mammoth meatball, created by an Australian lab-grown-meat company called Vow. The meatball, made using real mammoth DNA, supposedly smelled like cooked crocodile meat, and in press photos, it looked oddly furry, like it had been coughed up by a cat or rolled around by a dung beetle. Still, meat from a long-extinct behemoth that lived during the Ice Age—how could I not want to try it? Although some on Twitter were clearly grossed out, many others were also intrigued. “Bet it tastes better than Ikeas,” one user wrote. Disappointingly, the meatball was not made for consumption. Because it contains proteins that haven’t been eaten in thousands of years, the scientists who made it aren’t sure it would be safe. It was a marketing ploy cooked up by a creative agency that worked with Vow. I eventually realized that I wanted the meatball for the same reasons I wanted the Doritos Locos Taco, KFC’s Double Down Sandwich, and Van Leeuwen’s ranch-flavored ice cream: sheer, dumb novelty. This was stunt marketing 101 applied to the future of food, and I was the sucker falling for it.
George Pappou, Vow’s CEO and founder, told me that the meatball was meant to “start a conversation about the food that we’re going to eat tomorrow being different from the food that we eat today.” Although the stunt drew attention toward Vow—I am writing this, and you are reading this, after all—the company doesn’t have any products on the market yet, only plans to introduce lab-made Japanese quail to diners in Singapore later this year. So what did it accomplish, exactly? “I don’t think of this one so much as a stunt as a demonstration,” Lang said. “It’s an exaggeration of the physical capabilities of new science.” Because lab-grown meat is still meat, just without animal husbandry and slaughter, it’s often held up as the future of sustainable, ethical carnivory. Beef or chicken made in this way probably won’t be widely available at your grocery store anytime soon, but according to an estimate by McKinsey, the industry as a whole could be worth $25 billion by 2030. Lab-grown meat—or “cultivated” meat, as the industry likes to call it—is made by growing animal cells in a large tank until they form a sizable lump of tissue. Then it’s seasoned and processed in much the same way as conventional meat, forming foods such as patties, nuggets, and meatballs. Vow’s meatball was grown from sheep cells that were engineered to contain a short mammoth DNA sequence, sourced from publicly available data. As a result, the cells produced the mammoth version of myoglobin, a protein that contributes to the metallic, “meaty” taste of muscle. Theoretically, this process can be used to create meat from any animal whose cells are readily available or whose DNA has been sequenced. Think of DNA as essentially an IKEA manual for building tissue. Even animals whose sequences are incomplete can be partly resurrected: Gaps in the woolly-mammoth DNA were filled in using sequences from elephants, like using Billy-bookcase instructions to build a Kallax shelf. Growing the mammoth meat, in a relatively small amount, was “ridiculously easy and fast,” Ernst Wolvetang, a scientist who worked with Vow, told the Guardian. The same could eventually be said of any type of cultivated meat if the industry can surmount the significant cost and efficiency-related challenges involved in scaling up.
Imagine the stunts that could be possible then: nuggets for every dinosaur in Jurassic Park, even human meatballs. Already, a few companies besides Vow are pursuing more exotic fare: The New York–based Primeval Foods plans to release cultivated lion burgers, ground meat, and sausages, followed by meat from giraffes and zebras, founder and CEO Yilmaz Bora told me. Diners are always looking for something new, so food “must go beyond the current beef, chicken, and pork dishes and come without the expense of nature and animals,” he said. Using stunt marketing to raise awareness about the potential of cultivated meat isn’t a guarantee that people will want to eat those products if they ever become widely available. Sometimes the creations are too gross to even consider seriously, such as Hellmann’s “mayo-nog” or Oscar Mayer’s “cold dogs,” which were, uh, hot-dog-flavored ice-cream weiners on a stick. Yet unlike these stunts, people don’t have the same frame of reference for a meatball made of cultivated mammoth meat. “The risk is that it’s off-putting,” Michael Cohen, a marketing professor at NYU, told me. Or enticing. If the mammoth meatball made you think They can do that?, then perhaps it will have done some good. If not, then it was, at the very least, a valid attempt to engage with the science. “The meatball thing was a very well-crafted marketing activity for a product”—lab-grown meat as a category—“that I think is going to have very low adoption,” Lang said. A majority of Americans have “food neophobia,” a reluctance to adopt new foods, he said; many don’t even eat seafood. Still, in the past five months, the FDA granted its first two approvals to lab-grown chicken products, clearing a regulatory pathway for even more cultivated goods. If the technology is ever able to scale, perhaps foods like mammoth meatballs will no longer be seen as a stunt. Eventually, they might just be dinner. from https://ift.tt/HdAo0if Check out http://natthash.tumblr.com The pandemic initiated a slew of transformations, and though many have not stuck, one indisputably has: Telehealth is booming in America. This golden age of electronic engagement has one massive benefit—doctors are more accessible than ever. Unfortunately, this virtue is also proving to be telehealth’s biggest problem. For patients, being able to reach their doctors by video visit, phone call, or email is incredibly convenient, but physicians have been overwhelmed by the constant communication. This cost is now being shifted back to the patients, and almost every interaction with a doctor, no matter how casual, counts as some form of “visit” now. At the start of the pandemic, telehealth was lauded as the beginning of a revolution in medicine. Patients quickly became adept at using online portals to reach their doctors, frequently writing to them with quick questions or concerns in between visits. But when in-person visits largely resumed, this higher volume of online messaging did not go away. In fact, it did not even seem to decrease. And though a video appointment and office visit might be interchangeable in a doctor’s daily schedule, busy physicians found themselves with little time to respond to those smaller communications. To stay above water, some doctors and health systems have started charging for many of their responses. These in-between interactions, once considered a standard part of care, are being reframed as separate services, many of which warrant additional charges. Having an informal relationship with your doctor is now just fiction: You get the care that you pay for. When Jed Jacobsohn got COVID for the first time in May, he began gathering information. How long should he quarantine for? How could his two young children stay healthy? He decided to give his doctor a quick call, and after five minutes, he hung up satisfied, he told me. Next thing he knew, he had a $180 bill. His satisfaction evaporated. For a patient, five minutes is fleeting; for a doctor, five minutes on the phone generates a chunk of associated work, including reviewing the patient’s chart, updating notes, and putting in orders for medications, tests, or referrals. Most doctors work for health systems that use “relative value units” to calculate how they get compensated. “You can think of them like productivity points,” A Jay Holmgren, an assistant professor at UC San Francisco who researches asynchronous messaging, told me. In order to get paid, doctors must get a certain amount of work done. Since March 2020, billing for both synchronous telehealth (that is, video visits) and asynchronous telehealth (emails and other online messages) has been allowed for the majority of providers, Holmgren told me. One explanation for billing for messages is that health systems were recognizing the time spent responding as work and ensuring that physicians could answer queries without working outside of their hours, reducing their patient load, or taking a pay cut. For those who work in private practice, billing for messaging can function as self-accountability. When Reed Wilson, a doctor in internal medicine and cardiology, used to run a private practice, he rarely had time left by the end of his long workdays to answer or respond to calls or online messages. He worried that they would get pushed aside. “That’s why I had the administrative fee,” Wilson told me. “I was providing a service.” Of course, both health systems and private practices are also businesses, which benefit from new revenue streams Being billed painfully large amounts of money for seemingly small increments of health care is nothing new. So why does the idea of a $180 bill for a phone call hit so hard? Part of the resistance can be attributed to the distinction between cost and value, Jeremy Greene, a doctor and researcher at Johns Hopkins who also wrote a book on telemedicine, told me. Jacobsohn, for instance, had really only phoned his physician to be responsible and avoid using Twitter or Google as his only source of information. Telehealth can certainly be a good substitute for an in-person visit, but if a quick phone call with a doctor simply affirms what a patient already knows, paying the bill might feel like a waste of money—especially if the patients themselves are coughing up the cash. Although Jacobsohn paid a particularly high amount because of his insurance plan, even if an insurance company is footing the bill, being charged might still rankle. Calling your doctor or emailing them has long been part of standard care; paying for it is new. The disconnect between patients’ past expectations and new reality comes down to the hidden costs of care. At the same time, though a five-minute phone call is more work for a doctor than many patients realize, it can also feel less fulfilling than another type of visit. For some, feeling truly seen by their doctor requires actually seeing their doctor (whether that’s in person or on a video call).
Ultimately, these bills for all encounters with a doctor are a more honest representation of how medicine works now than one in which a friendly doctor can field questions as a complimentary service. The field has long been shifting toward corporatization, and away from the more genteel norms once associated with care. This latest trend is edging out one of the remaining areas that had not been made fully transactional. Yes, being a doctor means cultivating meaningful, intimate relationships with patients. But, like so many other jobs, being a doctor is becoming more and more standardized. from https://ift.tt/z7M5Qgb Check out http://natthash.tumblr.com Among the many difficulties imposed upon America by the pandemic, the scourge of anti-vaccine sentiment—and the preventable deaths caused as result—ranks among the most frustrating, especially for infectious-disease doctors like me. People who are hospitalized with COVID-19 rarely refuse therapy, but acceptance of vaccines to help prevent infection has been considerably more limited. Seventy percent of Americans have received the initial complement of vaccine injections, and many fewer have received the boosters designed to address viral variants and confer additional protection. Why are so many people resistant to this potentially lifesaving treatment? Some explanations are unique to our era—the awful weaponization of science in a deeply partisan political environment during the age of social media, for instance. But the concept of vaccine hesitancy is not new. Such hesitancy is, in a larger sense, a rejection of science—a phenomenon that far predates the existence of vaccines. One of the earliest documented controversies in science denialism comes from the field of astronomy. In the third century B.C., the Greek astronomer Aristarchus of Samos proposed a heliocentric model of the universe. The idea that the Earth and planets might revolve around the sun, rather than the other way around, was shocking at the time, and Aristarchus’s theory was quickly rejected in favor of models such as those put forth by Aristotle and Ptolemy, both of whom insisted that the Earth was the center of the universe. The fact that Aristotle and Ptolemy remain better known today than Aristarchus shows the force of the rejection. It would be some 2,000 years before the notion was seriously reconsidered. In the 1530s, the Polish astronomer Nicolaus Copernicus developed his own heliocentric model based on astronomical observations. Copernicus is remembered today primarily for this perspective-changing discovery. But it’s worth noting that he delayed publication of his findings until 1543, the year of his death, perhaps for fear of scorn or religious objections. In the early 17th century, Galileo Galilei, the Italian astronomer known as the “father of modern astronomy,” recognized that explaining the celestial changes in the position of stars and sun over time required that the Earth revolve around the sun. Galileo fully and publicly supported the Copernican theory of a heliocentric universe, and condemnation from the Vatican was swift and harsh. He was tried by the Inquisition and threatened with excommunication if he did not recant. Rather than incur the wrath of the pope, he finally agreed that he was wrong. He spent the remainder of his life under house arrest. It would be another 180 years before the Church admitted that Galileo was right. Rejections of scientific advances are found throughout the history of medicine. There have been four great advances in medicine over the past 200 years: anesthesia, antisepsis, antibiotics, and immunization. Not every advance was met with resistance. When the benefits of the advance have been obvious, there has tended to be little hesitation. Anesthesia and its cousin, analgesia, for instance, were rapidly accepted; they relieved pain, and the advantages were readily appreciated. Antisepsis had a stormier path to public acceptance. In the 19th century, English and Irish physicians recognized that puerperal sepsis (a dangerous infection in a mother after delivery of a baby) was likely a contagious condition that was spread from patient to patient either by the medical staff or the local environment. They suggested that improving hygiene would reduce the high rates of mortality that puerperal sepsis caused. In 1843, Oliver Wendell Holmes Sr., a physician (and one of The Atlantic’s founders), presented a paper to the Boston Society for Medical Improvement titled “The Contagiousness of Puerperal Fever.” Holmes suggested that unwashed hands among the medical and nursing staff were responsible for transmitting puerperal fever. This did not sit well with the establishment. A prestigious Philadelphia obstetrician, Charles D. Meigs, declared Holmes’s findings to be nonsense and suggested that an increased number of cases among any physician was just bad luck. The physician who is most frequently recognized with establishing the contagious nature of this infection is a Hungarian obstetrician, Ignaz Semmelweis. He noted that patients in the Vienna General Hospital who were cared for by physicians had a higher incidence of postpartum sepsis than those who were cared for by midwives. Semmelweis realized that physicians performed autopsies, whereas midwives did not, and that physicians did not wash their hands or clothing before moving from an autopsy to a delivery. (It was routine for them to attend deliveries in their bloodstained clothing, having come directly from the autopsy suite.) When he suggested simple hygiene measures such as handwashing, he was derided and eventually run out of town. The medical establishment was unwilling to accept that physicians—rather than bad air or host weaknesses—were responsible for spreading infections and harming patients. Science denialism can work in the other direction too. When antibiotics, especially penicillin, were first introduced, they were rightly appreciated as miracle drugs. In the pre-antibiotic era, the leading cause of death among children was infectious diseases. The use of antibiotics was astoundingly successful against many, but not all, childhood diseases. The downside for this enthusiasm for treatment came when patients demanded antibiotics for conditions—such as viruses—that didn’t actually necessitate them. Fifty years ago, telling a patient that they had a virus and that penicillin was therefore of no use led to disappointment, disbelief, and even arguments from patients requesting antibiotics for simple colds. Many doctors gave in because it was simpler than spending time fighting with a patient. A consequence of the more indiscriminate use of antibiotics—which represents its own mini-genre of science denialism—has been increased bacterial resistance. But of the four great advances, none has so broadly helped humanity, or suffered more from science denialism, than immunization. Most, but not all, of the vaccines that scientists have developed since the first immunizations in the 18th century have been developed against viruses. Of all viral infections, the most feared may well have been smallpox. Over the course of the 20th century alone, an estimated 300 million people died of smallpox. Smallpox is highly contagious and spares no age group or class. Its common form has an estimated overall mortality of roughly 30 percent, but the mortality of hemorrhagic smallpox—a more severe form of the disease—approaches 100 percent. Smallpox is also wildly contagious, a characteristic that is most evident when a previously unexposed population is exposed. Smallpox was unknown in the Americas before European explorers brought cases to the New World. The disease decimated the Indigenous populations of North America and South America as a result. The early concept of immunization to prevent smallpox may have begun more than 1,000 years ago, in China. The history is contested, but some documents show that children would be made to inhale material from a ground-up, mature smallpox lesion scraped off of the body of the infected—a level of exposure that could trigger a person’s immune response to smallpox without causing a full-blown infection. A later technique, which involved scratching the skin of an uninfected individual with material from another person’s lesion, was observed by the wife of the English ambassador to Istanbul, who then brought this procedure to Europe. She was so impressed that she had her children immunized. Subsequently, an experiment was done in which six prisoners in London were immunized. Despite exposure to smallpox, none of them became ill. Like many advances in medicine, smallpox immunization was met with some resistance, including worry that immunization might inadvertently spread the disease to others. This was an understandable reaction; the live smallpox virus was used, and a small percentage of inoculated individuals did develop full-blown disease and die. In 1721, there was an outbreak of smallpox in Boston. The writer and clergyman Cotton Mather urged widespread immunization but had only moderate success because of resistance from the local population. (History complicates even the views of those who embrace science: Mather was also an ardent defender of the Salem witch trials.) Years later, a well-known case of immunization resistance occurred in Philadelphia. During an outbreak of smallpox in 1736, Benjamin Franklin’s 4-year-old son, Francis, became infected and died. Francis had not been immunized despite an opportunity to do so, and Franklin said he regretted the decision for the rest of his life. In the generations that followed, scientists built off of these earlier methods and eventually developed a stable and widely available smallpox vaccine. The global eradication of smallpox as a result remains one of the greatest accomplishments in the history of medicine. The last case of naturally occurring smallpox was reported more than 40 years ago. Even so, vaccine hesitancy has persisted. In America, new vaccines for other diseases have continued to prompt their own waves of skepticism and hostility. And although science denialism is not pervasive in the way it once was centuries ago, it still rears its ugly head. The arrival of the COVID-19 vaccines brought pernicious vaccine sentiments into the spotlight. The reasons for this vehemence are many. For instance, some people who might accept the efficacy of a vaccine have such a fear of injections that they simply avoid seeking medical care until absolutely necessary. But this represents a minority of those who reject the vaccines. A more common—and more insidious—force that pushes people away from lifesaving vaccines appears to be swelling distrust in expertise, which is both a political and cultural phenomenon. Vaccine resistance can be peddled by influential people in both liberal and conservative circles, but throughout the pandemic, right-wing anti-government organizations and television personalities in particular have promoted a stew of outrageous conspiracy theories about vaccines. Run-of-the-mill misinformation remains a problem too. Some people continue to believe that the COVID-19 vaccine will infect you and make you sick—this is not the case. Finally, of course, there are concerns about known and unknown side effects from the vaccination. Like many vaccines, the COVID shots are linked to serious health effects in extremely rare circumstances; for instance, Moderna’s and Pfizer’s mRNA shots are associated with a very small risk of heart inflammation. It is virtually impossible to prove that some side effect will not ever occur. But hundreds of millions of people have safely received the COVID vaccine in the United States alone. Perhaps the greatest disservice to vaccination has been the fraudulent claim that childhood vaccines cause autism. This claim was originally published in an otherwise respected medical journal in the 1990s, and has since been fully retracted. (The author lost his medical license.) Nevertheless, many people still believe this and have put their children at risk for serious illness as a result. Our advances in science over the past two centuries have truly been extraordinary, but our society still suffers from the forces that reject reason and prevent our ability to take full advantage of discoveries that protect us all. And we need to push back against those who endanger others because they see opportunities for fame or profit in spreading dangerous disinformation. Until that happens, our species will continue to understand the world around us in fits and starts—with too many people dying, even when we know how to save them. from https://ift.tt/BI3HLd2 Check out http://natthash.tumblr.com Last December, during a Christmas Eve celebration with my in-laws in California, I observed what I now realize was the future of COVID for older people. As everyone crowded around the bagna cauda, a hot dipping sauce shared like fondue, it was clear that we, as a family, had implicitly agreed that the pandemic was over. Our nonagenarian relatives were not taking any precautions, nor was anyone else taking precautions to protect them. Endive spear in hand, I squeezed myself in between my 94-year-old grandfather-in-law and his spry 99-year-old sister and dug into the dip. We all knew that older people bore the brunt of COVID, but the concerns seemed like a relic from earlier in the pandemic. The brutal biology of this disease meant that they disproportionately have fallen sick, been hospitalized, and died. Americans over 65 make up 17 percent of the U.S. population, but they have accounted for three-quarters of all COVID deaths. As the death count among older people began to rise in 2020, “a lot of my patients were really concerned that they were being exposed without anyone really caring about them,” Sharon Brangman, a geriatrician at SUNY Upstate University Hospital, told me. But even now, three years into the pandemic, older people are still in a precarious position. While many Americans can tune out COVID and easily fend off an infection when it strikes, older adults continue to face real threats from the illness in the minutiae of their daily life: grocery trips, family gatherings, birthday parties, coffee dates. That is true even with the protective power of several shots and the broader retreat of the virus. “There is substantial risk, even if you’ve gotten all the vaccines,” Bernard Black, a law professor at Northwestern University who studies health policy, told me. More than 300 people still die from COVID each day, and the overwhelming majority of them are older. People ages 65 and up are currently hospitalized at nearly 11 times the rate of adults under 50. Compounding this sickness are all the ways that, COVID aside, this pandemic has changed life for older adults. Enduring severe isolation and ongoing caregiver shortages, they have been disproportionately harmed by the past few years. Not all of them have experienced the pandemic in the same way. Americans of retirement age, 65 and older, are a huge population encompassing a range of incomes, health statuses, living situations, and racial backgrounds. Nevertheless, by virtue of their age alone, they live with a new reality: one in which life has become more dangerous—and in many ways worse—than it was before COVID. The pandemic was destined to come after older Americans. Their immune systems tend to be weaker, making it harder for them to fight off an infection, and they are more likely to have comorbidities, which further increases their risk of severe illness. The precarity that many of them already faced going into 2020--poverty, social isolation and loneliness, inadequate personal care—left them poorly equipped for the arrival of the novel coronavirus. More than 1 million people lived in nursing homes, many of which were densely packed and short on staff when COVID tore through them. A major reason older people are still at risk is that vaccines can’t entirely compensate for their immune systems. A study recently published in the journal Vaccines showed that for vaccinated adults ages 60 and over, the risk of dying from COVID versus other natural causes jumped from 11 percent to 34 percent within a year of completing their primary shot series. A booster dose brings the risk back down, but other research shows that it wears off too. A booster is a basic precaution, but “not one that everyone is taking,” Black, a co-author of the study, told me. Booster uptake among older Americans for the reengineered “bivalent” shots is the highest of all age groups, but still, nearly 60 percent have not gotten one. For every COVID death, many more older people develop serious illness. Risk increases with age, and people older than 70 “have a substantially higher rate of hospitalizations” than those ages 60 to 69, Caitlin Rivers, an epidemiologist at Johns Hopkins University, told me. Unlike younger people, most of whom fully recover from a bout with COVID, a return to baseline health is less guaranteed for older adults. In one study, 32 percent of adults over 65 were diagnosed with symptoms that lasted well beyond their COVID infection. Persistent coughs, aches, and joint pain can linger long after serious illness, together with indirect impacts such as loss of muscle strength and flexibility, which can affect older people’s ability to be independent, Rivers said. Older COVID survivors may also have a higher risk of cognitive decline. In some cases, these ailments could be part of long COVID, which may be more prevalent in older people. Certainly, some older adults are able to make a full recovery. Brangman said she has “old and frail” geriatric patients who bounced back after flu-like symptoms, and younger ones who still experience weakness and fatigue. Still, these are not promising odds. The antiviral Paxlovid was supposed to help blunt the wave of old people falling sick and ending up in the hospital—and it can reduce severe disease by 50 to 90 percent. But unfortunately, it is not widely used; as of July, just a third of Americans 80 or older took Paxlovid. The reality is that as long as the virus continues to be prevalent, older Americans will face these potential outcomes every time they leave their home. That doesn’t mean they will barricade themselves indoors, or that they even should. Still, “every decision that we make now is weighing that balance between risk and socialization,” Brangman said. Long before the pandemic, the threat of illness was already very real for older people. Where America has landed is hardly a new way of life but rather one that is simply more onerous. “One way to think about it is that this is a new risk that’s out there” alongside other natural causes of death, such as diabetes and heart failure, Black said. But it’s a risk older Americans can’t ignore, especially as the country has dropped all COVID precautions. Since Christmas Eve, I have felt uneasy about how readily I normalized putting so little effort into protecting my nonagenarian loved ones, despite knowing what might happen if they got sick. For older people, who must contend with the peril of attending similar gatherings, “there’s sort of no good choice,” Black said. “The world has changed.” But this new post-pandemic reality also includes insidious effects on older people that aren’t directly related to COVID itself. Those who put off nonemergency visits to the doctor earlier in the pandemic, for example, risked worsening their existing health conditions. The first year of the pandemic plunged nearly everyone into isolation, but being alone created problems for older adults that still persist. Before the pandemic, the association between loneliness and higher mortality rates, increased cardiovascular risks, and dementia among older adults was already well established. Increased isolation during COVID amplified this association. The consequences of isolation were especially profound for older adults with physical limitations, Naoko Muramatsu, a community-health professor at the University of Illinois at Chicago, told me. When caregivers or family members were unable to visit, people who required assistance for even the smallest tasks, such as fetching the mail and getting dressed, had no options. “If you don’t walk around and if you don’t do anything, we can expect that cognitive function will decline,” Muramatsu said; she has observed this firsthand in her research. One Chinese American woman, interviewed in a survey of older adults living alone with cognitive impairment during the pandemic, described the debilitating effect of sitting at home all day.“I am so useless now,” she told the interviewer. “I am confused so often. I forget things.” Even older adults who have weathered the direct and indirect effects of the pandemic still face other challenges that COVID has exacerbated. Many have long relied on personal caregivers or the staff at nursing facilities. These workers, already scarce before the pandemic, are even more so now because many quit or were affected by COVID themselves. “Long-term care has been in a crisis situation for a long time, but it’s even worse now,” Muramatsu said, noting that many home care workers are older adults themselves. Nursing homes nationwide now have nearly 200,000 fewer employees compared with March 2020, which is especially concerning as the proportion of Americans over age 65 explodes. Older people won’t have one single approach to contending with this sad reality. “Everybody is trying to figure out what is the best way to function, to try to have some level of everyday life and activity, but also keep your risk of getting sick as low as possible,” Brangman said. Some of her patients are still opting to be cautious, while others consider this moment their “only chance to see grandchildren or concerts or go to family gatherings.” Either way, older Americans will have to wrestle with these decisions without so many of their peers who have died from COVID. Again, many of these people did not have it great before the pandemic, even if the rest of the country wasn’t paying attention. “We often don’t provide the basic social support that older people need,” Kenneth Covinsky, a clinician-researcher at the UCSF Division of Geriatrics, said. Rather, ageism, the willful ignorance or indifference to the needs of older people, is baked into American life. It is perhaps the main reason older adults were so badly affected by the pandemic in the first place, as illustrated by the delayed introduction of safety precautions in nursing homes and the blithe acceptance of COVID deaths among older adults. If Americans couldn’t bring themselves to care at any point over the past three years, will they ever? from https://ift.tt/T2cHyE9 Check out http://natthash.tumblr.com Last week, the ongoing debate about COVID-19’s origins acquired a new plot twist. A French evolutionary biologist stumbled across a trove of genetic sequences extracted from swabs collected from surfaces at a wet market in Wuhan, China, shortly after the pandemic began; she and an international team of colleagues downloaded the data in hopes of understanding who—or what—might have ferried the virus into the venue. What they found, as The Atlantic first reported on Thursday, bolsters the case for the pandemic having purely natural roots: The genetic data suggest that live mammals illegally for sale at the Huanan Seafood Wholesale Market—among them, raccoon dogs, a foxlike species known to be susceptible to the virus—may have been carrying the coronavirus at the end of 2019. But what might otherwise have been a straightforward story on new evidence has rapidly morphed into a mystery centered on the origins debate’s data gaps. Within a day or so of nabbing the sequences off a database called GISAID, the researchers told me, they reached out to the Chinese scientists who had uploaded the data to share some preliminary results. The next day, public access to the sequences was locked—according to GISAID, at the request of the Chinese researchers, who had previously analyzed the data and drawn distinctly different conclusions about what they contained. [Read: The strongest evidence yet that an animal started the pandemic] Yesterday evening, the international team behind the new Huanan-market analysis released a report on its findings—but did not post the underlying data. The write-up confirms that genetic material from raccoon dogs and several other mammals was found in some of the same spots at the wet market, as were bits of SARS-CoV-2’s genome around the time the outbreak began. Some of that animal genetic material, which was collected just days or weeks after the market was shut down, appears to be RNA—a particularly fast-degrading molecule. That strongly suggests that the mammals were present at the market not long before the samples were collected, making them a plausible channel for the virus to travel on its way to us. “I think we’re moving toward more and more evidence that this was an animal spillover at the market,” says Ravindra Gupta, a virologist at the University of Cambridge, who was not involved in the new research. “A year and a half ago, my confidence in the animal origin was 80 percent, something like that. Now it’s 95 percent or above.” For now, the report is just that: a report, not yet formally reviewed by other scientists or even submitted for publication to the journal—and that will remain the case as long as this team continues to leave space for the researchers who originally collected the market samples, many of them based at the Chinese Center for Disease Control and Prevention, to prepare a paper of their own. And still missing are the raw sequence files that sparked the reanalysis in the first place—before vanishing from the public eye. Every researcher I asked emphasized just how important the release of that evidence is to the origins investigation: Without data, there’s no base-level proof—nothing for the broader scientific community to independently scrutinize to confirm or refute the international team’s results. Absent raw data, “some people will say that this isn’t real,” says Gigi Gronvall, a senior scholar at the Johns Hopkins Center for Health Security, who wasn’t involved in the new analysis. Data that flicker on and off publicly accessible parts of the internet also raise questions about other clues on the pandemic’s origins. Still more evidence might be out there, yet undisclosed. Transparency is always an essential facet of research, but all the more so when the stakes are so high. SARS-CoV-2 has already killed nearly 7 million people, at least, and saddled countless people with chronic illness; it will kill and debilitate many more in the decades to come. Every investigation into how it began to spread among humans must be “conducted as openly as possible,” says Sarah Cobey, an infectious-disease modeler at the University of Chicago, who wasn’t involved in the new analysis. The team behind the reanalysis still has copies of the genetic sequences its members downloaded earlier this month. But they’ve decided that they won’t be the ones to share them, several of them told me. For one, they don’t have sequences from the complete set of samples that the Chinese team collected in early 2020—just the fraction that they spotted and grabbed off GISAID. Even if they did have all of the data, the researchers contend that it’s not their place to post them publicly. That’s up to the China CDC team that originally collected and generated the data. Part of the international team’s reasoning is rooted in academic decorum. There isn’t a set-in-stone guidebook among scientists, but adhering to unofficial rules on etiquette smooths successful collaborations across disciplines and international borders—especially during a global crisis such as this one. Releasing someone else’s data, the product of another team’s hard work, is a faux pas. It risks misattribution of credit, and opens the door to the Chinese researchers’ findings getting scooped before they publish a high-profile paper in a prestigious journal. “It isn’t right to share the original authors’ data without their consent,” says Niema Moshiri, a computational biologist at UC San Diego and one of the authors of the new report. “They produced the data, so it’s their data to share with the world.” If the international team released what data it has, it could potentially stoke the fracas in other ways. The World Health Organization has publicly indicated that the data should come from the researchers who collected them first: On Friday, at a press briefing, Tedros Adhanom Ghebreyesus, the WHO’s director-general, admonished the Chinese researchers for keeping their data under wraps for so long, and called on them to release the sequences again. “These data could have and should have been shared three years ago,” he said. And the fact that it wasn’t is “disturbing,” given just how much it might have aided investigations early on, says Gregory Koblentz, a biodefense expert at George Mason University, who wasn’t involved in the new analysis. Publishing the current report has already gotten the researchers into trouble with GISAID, the database where they found the genetic sequences. During the pandemic, the database has been a crucial hub for researchers sharing viral genome data; founded to provide open access to avian influenza genomes, it is also where researchers from the China CDC published the first whole-genome sequences of SARS-CoV-2, back in January 2020. A few days after the researchers downloaded the sequences, they told me, several of them were contacted by a GISAID administrator who chastised them about not being sufficiently collaborative with the China CDC team and warned them against publishing a paper using the China CDC data. They were in danger, the email said, of violating the site’s terms of use and would risk getting their database access revoked. Distributing the data to any non-GISAID users—including the broader research community—would also be a breach. This morning, hours after the researchers released their report online, many of them found that they could no longer log in to GISAID—they received an error message when they input their username and password. “They may indeed be accusing us of having violated their terms,” Moshiri told me, though he can’t be sure. The ban was instated with absolutely no warning. Moshiri and his colleagues maintain that they did act in good faith and haven’t violated any of the database’s terms—that, contrary to GISAID’s accusations, they reached out multiple times with offers to collaborate with the China CDC, which has “thus far declined,” per the international team’s report. GISAID didn’t respond when I reached out about the data’s disappearing act, its emails to the international team, and the group-wide ban. But in a statement released shortly after I contacted the database—one that echoes language in the emails sent to researchers—GISAID doubled down on accusing the international team of violating its terms of use by posting “an analysis report in direct contravention of the terms they agreed to as a condition to accessing the data, and despite having knowledge that the data generators are undergoing peer review assessment of their own publication.” GISAID also “strongly” suggested “that the complete and updated dataset will be made available as soon as possible,” but gave no timeline. Why, exactly, the sequences were first made public only so recently, and why they have yet to reappear, remain unclear. In a recent statement, the WHO said that access to the data was withdrawn “apparently to allow further data updates by China CDC” to its original analysis on the market samples, which went under review for publication at the journal Nature last week. There’s no clarity, however, on what will happen if the paper is not published at all. When I reached out to three of the Chinese researchers—George Gao, William Liu, and Guizhen Wu—to ask about their intentions for the data, I didn’t receive a response. “We want the data to come out more than anybody,” says Saskia Popescu, an infectious-disease epidemiologist at George Mason University and one of the authors on the new analysis. Until then, the international team will be fielding accusations, already flooding in, that it falsified its analyses and overstated its conclusions. Researchers around the world have been raising questions about these particular genetic sequences for at least a year. In February 2022, the Chinese researchers and their close collaborators released their analysis of the same market samples probed in the new report, as well as other bits of genetic data that haven’t yet been made public. But their interpretations deviate pretty drastically from the international team’s. The Chinese team contended that any shreds of virus found at the market had most likely been brought in by infected humans. “No animal host of SARS-CoV-2 can be deduced,” the researchers asserted at the time. Although the market had perhaps been an “amplifier” of the outbreak, their analysis read, “more work involving international coordination” would be needed to determine the “real origins of SARS-CoV-2.” When reached by Jon Cohen of Science magazine last week, Gao described the sequences that fleetingly appeared on GISAID as “[n]othing new. It had been known there was illegal animal dealing and this is why the market was immediately shut down.” There is, then, a clear divergence between the two reports. Gao’s assessment indicates that finding animal genetic material in the market swabs merely confirms that live mammals were being illegally traded at the venue prior to January 2020. The researchers behind the new report insist that the narrative can now go a step further—they suggest not just that the animals were there, but that the animals, several of which are already known to be vulnerable to SARS-CoV-2, were there, in parts of the market where the virus was also found. That proximity, coupled with the virus’s inability to persist without a viable host, points to the possibility of an existing infection among animals, which could spark several more. The Chinese researchers used this same logic of location—multiple types of genetic material pulled out of the same swab—to conclude that humans were carrying around the virus at Huanan. The reanalysis confirms that there probably were infected people at the market at some point before it closed. But they were unlikely to be the virus’s only chauffeurs: Across several samples, the amount of raccoon-dog genetic material dwarfs that of humans. At one stall in particular—located in the sector of the market where the most virus-positive swabs were found—the researchers discovered at least one sample that contained SARS-CoV-2 RNA, and was also overflowing with raccoon-dog genetic material, while containing very little DNA or RNA material matching the human genome. That same stall was photographically documented housing raccoon dogs in 2014. The case is not a slam dunk: No one has yet, for instance, identified a viral sample taken from a live animal that was swabbed at the market in 2019 before the venue was closed. Still, JHU’s Gronvall told me, the situation feels clearer than ever. “All of the science is pointed” in the direction of Huanan being the pandemic’s epicenter, she said. To further untangle the significance of the sequences will require—you guessed it—the now-vanished genetic data. Some researchers are still withholding their judgment on the significance of the new analysis, because they haven’t gotten their hands on the genetic sequences themselves. Others are also wondering whether more data could yet emerge, given how long this particular set went unshared. “This is an indication to me in recent days that there is more data that exists,” Maria Van Kerkhove, the WHO’s COVID-19 technical lead, told me. Which means that she and her colleagues haven’t yet gotten the fullest picture of the pandemic’s early days that they could—and that they won’t be able to deliver much of a verdict until more information emerges. The new analysis does bolster the case for market animals acting as a conduit for the virus between bats (SARS-CoV-2’s likeliest original host, based on several studies on this coronavirus and others) and people; it doesn’t, however, “tell us that the other hypotheses didn’t happen. We can’t remove any of them,” Van Kerkhove told me. More surveillance for the virus needs to be done in wild-animal populations, she said. Having the data from the market swabs could help with that, perhaps leading back to a population of mammals that might have caught the virus from bats or another intermediary in a particular part of China. At the same time, to further investigate the idea that SARS-CoV-2 first emerged out of a laboratory mishap, officials need to conduct intensive audits and investigations of virology laboratories in Wuhan and elsewhere. Last month, the U.S. Department of Energy ruled that such an accident was the likelier catalyst of the coronavirus outbreak than a natural spillover from wild animals to humans. The ruling echoed earlier judgments from the FBI and a Senate minority report. But it contrasted with the views of four other agencies, plus the National Intelligence Council, and it was made with “low confidence” and based on “new” evidence that has yet to be declassified. [Read: The lab leak will haunt us forever] The longer the investigation into the virus’s origins drags on, and the more distant the autumn of 2019 grows in our rearview, “the harder it becomes,” Van Kerkhove told me. Many in the research community were surprised that new information from market samples collected in early 2020 emerged at all, three years later. Settling the squabbles over SARS-CoV-2 will be especially tough because the Huanan market was so swiftly shut down after the outbreak began, and the traded animals at the venue rapidly culled, says Angela Rasmussen, a virologist at the University of Saskatchewan and one of the researchers behind the new analysis. Raccoon dogs, one of the most prominent potential hosts to have emerged from the new analysis, are not even known to have been sampled live at the market. “That evidence is gone now,” if it ever existed, Koblentz, of George Mason University, told me. For months, Chinese officials were even adamant that no mammals were being illegally sold at the region’s wet markets at all. So researchers continue to work with what they have: swabs from surfaces that can, at the very least, point to a susceptible animal being in the right place, at the right time, with the virus potentially inside it. “Right now, to the best of my knowledge, this data is the only way that we can actually look,” Rasmussen told me. It may never be enough to fully settle this debate. But right now, the world doesn’t even know the extent of the evidence available—or what could, or should, still emerge. from https://ift.tt/1IRPcKF Check out http://natthash.tumblr.com For three years now, the debate over the origins of the coronavirus pandemic has ping-ponged between two big ideas: that SARS-CoV-2 spilled into human populations directly from a wild-animal source, and that the pathogen leaked from a lab. Through a swirl of data obfuscation by Chinese authorities and politicalization within the United States, and rampant speculation from all corners of the world, many scientists have stood by the notion that this outbreak—like most others—had purely natural roots. But that hypothesis has been missing a key piece of proof: genetic evidence from the Huanan Seafood Wholesale Market in Wuhan, China, showing that the virus had infected creatures for sale there. This week, an international team of virologists, genomicists, and evolutionary biologists may have finally found crucial data to help fill that knowledge gap. A new analysis of genetic sequences collected from the market shows that raccoon dogs being illegally sold at the venue could have been carrying and possibly shedding the virus at the end of 2019. It’s some of the strongest support yet, experts told me, that the pandemic began when SARS-CoV-2 hopped from animals into humans, rather than in an accident among scientists experimenting with viruses. The findings won’t fully silence the entrenched voices on either side of the origins debate. But the new analysis may offer some of the clearest and most compelling evidence that the world will ever get in support of an animal origin for the virus that, in just over three years, has killed nearly 7 million people worldwide. [Read: The lab leak will haunt us forever] The genetic sequences were pulled out of swabs taken in and near market stalls around the pandemic’s start. They represent the first bits of raw data that researchers outside of China’s academic institutions and their direct collaborators have had access to. Late last week, the data were quietly posted by researchers affiliated with the country’s Center for Disease Control and Prevention, on an open-access genomic database called GISAID. By almost pure happenstance, scientists in Europe, North America, and Australia spotted the sequences, downloaded them, and began an analysis. The samples were already known to be positive for the coronavirus, and had been scrutinized before by the same group of Chinese researchers who uploaded the data to GISAID. But that prior analysis, released as a preprint publication in February 2022, asserted that “no animal host of SARS-CoV-2 can be deduced.” Any motes of coronavirus at the market, the study suggested, had most likely been chauffeured in by infected humans, rather than wild creatures for sale. The new analysis, led by Kristian Andersen, Edward Holmes, and Michael Worobey—three prominent researchers who have been looking into the virus’s roots—shows that that may not be the case. Within about half a day of downloading the data from GISAID, the trio and their collaborators discovered that several market samples that tested positive for SARS-CoV-2 were also coming back chock-full of animal genetic material—much of which was a match for the common raccoon dog. Because of how the samples were gathered, and because viruses can’t persist by themselves in the environment, the scientists think that their findings could indicate the presence of a coronavirus-infected raccoon dog in the spots where the swabs were taken. Unlike many of the other points of discussion that have been volleyed about in the origins debate, the genetic data are “tangible,” Alex Crits-Christoph, a computational biologist and one of the scientists who worked on the new analysis, told me. “And this is the species that everyone has been talking about.” Finding the genetic material of virus and mammal so closely co-mingled—enough to be extracted out of a single swab—isn’t perfect proof, Lakdawala told me. “It’s an important step; I’m not going to diminish that,” she said. Still, the evidence falls short of, say, isolating SARS-CoV-2 from a free-ranging raccoon dog or, even better, uncovering a viral sample swabbed from a mammal for sale at Huanan from the time of the outbreak’s onset. That would be the virological equivalent of catching a culprit red-handed. But “you can never go back in time and capture those animals,” says Gigi Gronvall, a senior scholar at the Johns Hopkins Center for Health Security. And to researchers’ knowledge, “raccoon dogs were not tested at the market and had likely been removed prior to the authorities coming in,” Andersen wrote to me in an email. He underscored that the findings, although an important addition, are not “direct evidence of infected raccoon dogs at the market.” Still, the findings don’t stand alone. “Do I believe there were infected animals at the market? Yes, I do,” Andersen told me. “Does this new data add to that evidence base? Yes.” The new analysis builds on extensive previous research that points to the market as the source of the earliest major outbreak of SARS-CoV-2: Many of the earliest known COVID-19 cases of the pandemic were clustered roughly in the market’s vicinity. And the virus’s genetic material was found in many samples swabbed from carts and animal-processing equipment at the venue, as well as parts of nearby infrastructure, such as storehouses, sewage wells, and water drains. Raccoon dogs, creatures commonly bred for sale in China, are also already known to be one of many mammal species that can easily catch and spread the coronavirus. All of this left one main hole in the puzzle to fill: clear-cut evidence that raccoon dogs and the virus were in the exact same spot at the market, close enough that the creatures might have been infected and, possibly, infectious. That’s what the new analysis provides. Think of it as finding the DNA of an investigation’s main suspect at the scene of the crime. The findings don’t rule out the possibility that other animals may have been carrying SARS-CoV-2 at Huanan. Raccoon dogs, if they were infected, may not even be the creatures who passed the pathogen on to us. Which means the search for the virus’s many wild hosts will need to plod on. “Do we know the intermediate host was raccoon dogs? No,” Andersen wrote to me, using the term for an animal that can ferry a pathogen between other species. “Is it high up on my list of potential hosts? Yes, but it’s definitely not the only one.” On Tuesday, the researchers presented their findings at a hastily scheduled meeting of the World Health Organization’s Scientific Advisory Group for the Origins of Novel Pathogens, which was also attended by several of the Chinese researchers responsible for the original analysis, according to multiple researchers who were not present but were briefed about it before and after by multiple people who were there. Shortly after the meeting, the Chinese team’s preprint went into review at a Nature Research journal—suggesting that a new version was being prepared for publication. (I reached out to the WHO for comment and will update this story when I have more information.) At this point, it’s still unclear why the sequences were posted to GISAID last week. They also vanished from the database shortly after appearing, without explanation. When I emailed George Gao, the former China CDC director-general and the lead author on the original Chinese analysis, asking for his team’s rationale, I didn’t immediately receive a response. Given what was in the GISAID data, it does seem that raccoon dogs could have been introduced into and clarified the origins narrative far sooner—at least a year ago, and likely more. China has, for years, been keen on pushing the narrative that the pandemic didn’t start within its borders. In early 2020, a Chinese official suggested that the novel coronavirus may have emerged from a U.S. Army lab in Maryland. The notion that a dangerous virus sprang out from wet-market mammals echoed the beginnings of the SARS-CoV-1 epidemic two decades ago—and this time, officials immediately shut down the Huanan market, and vehemently pushed back against assertions that live animals being sold illegally in the country were to blame; a WHO investigation in March 2021 took the same line. “No verified reports of live mammals being sold around 2019 were found,” the report stated. But just three months later, in June 2021, a team of researchers published a study documenting tens of thousands of mammals for sale in wet markets in Wuhan between 2017 and late 2019, including at Huanan. The animals were kept in largely illegal, cramped, and unhygienic settings—conditions conducive to viral transmission—and among them were more than 1,000 raccoon dogs. Holmes himself had been at the market in 2014 and snapped a photo at Stall 29, clearly showing a raccoon dog in a cage; another set of images from the venue, captured by a local in December 2019 and later shared on Weibo, caught the animals on film as well—right around the time that the first recorded SARS-CoV-2 infections in humans occurred. And yet, Chinese researchers maintained their stance. As Jon Cohen reported for Science magazine last year, scientists from several of China’s largest academic institutions posted a preprint in September 2021 concluding that a massive nationwide survey of bats—the likeliest original source of the coronavirus before it jumped into an intermediate host, such as raccoon dogs, and then into us—had turned up no relatives of SARS-CoV-2. The implication, the team behind the paper asserted, was that relatives of the coronavirus were “extremely rare” in the region, making it unlikely that the pandemic had started there. The findings directly contradicted others showing that cousins of SARS-CoV-2 were indeed circulating in China’s bats. (Local bats have also been found to harbor viruses related to SARS-CoV-1.) The original Chinese analysis of the Huanan market swabs, from February 2022, also stuck with China’s party line on the pandemic. One of the report’s graphs suggested that viral material at the market had been mixed up with genetic material of multiple animal species—a data trail that should have led to further inquiry or conclusions, but that the Chinese researchers appear to have ignored. Their report noted only humans as being linked to SARS-CoV-2, stating that its findings “highly” suggested that any viral material at the market came from people (at least one of whom, presumably, picked it up elsewhere and ferried it into the venue). The Huanan market, the study’s authors wrote, “might have acted as an amplifier” for the epidemic. But “more work involving international coordination” would be needed to suss out the “real origins of SARS-CoV-2.” The wording of that report baffled many scientists in Europe, North America, and Australia, several of whom had, almost exactly 24 hours after the release of the China CDC preprint, published early versions of their own studies, concluding that the Huanan market was the pandemic’s probable epicenter—and that SARS-CoV-2 might have made its hop into humans from the venue twice at the end of 2019. Itching to get their hands on China CDC’s raw data, some of the researchers took to regularly trawling GISAID, occasionally at odd hours—the only reason that Florence Débarre, an evolutionary biologist at the French National Centre for Scientific Research, spotted the sequences pinging onto the server late last Thursday night with no warning or fanfare. Within hours of downloading the data and starting their own analysis, the researchers found their suspicions confirmed. Several surfaces in and around one stall at the market, including a cart and a defeathering machine, produced virus-positive samples that also contained genetic material from raccoon dogs—in a couple of cases, at higher concentrations than of human genomes. It was Stall 29—the same spot where Holmes had snapped the photo of the raccoon dog, nearly a decade before. Slam-dunk evidence for a raccoon-dog host—or another animal—could still emerge. In the hunt for the wild source of MERS, another coronavirus that caused a deadly outbreak in 2012, researchers were eventually able to identify the pathogen in camels, which are thought to have caught their initial infection from bats—and which still harbor the virus today; a similar story has played out for Nipah virus, which hopscotched from bats to pigs to us. [Read: Bird flu leaves the world with an existential choice] Proof of that caliber, though, may never turn up for SARS-CoV-2. (Nailing wild origins is rarely simple: Despite a years-long search, the wild host for Ebola still has not been definitively pinpointed.) Which leaves just enough ambiguity to keep debate about the pandemic’s origins running, potentially indefinitely. Skeptics will likely be eager to poke holes in the team’s new findings—pointing out, for instance, that it’s technically possible for genetic material from viruses and animals to end up sloshed together in the environment even if an infection didn’t take place. Maybe an infected human visited the market and inadvertently deposited viral RNA near an animal’s crate. But an infected animal, with no third-party contamination, still seems by far the most plausible explanation for the samples’ genetic contents, several experts told me; other scenarios require contortions of logic and, more important, additional proof. Even prior to the reveal of the new data, Gronvall told me, “I think the evidence is actually more sturdy for COVID than it is for many others.” The strength of the data might even, in at least one way, best what’s available for SARS-CoV-1: Although scientists have isolated SARS-CoV-1-like viruses from a wet-market-traded mammal host, the palm civet, those samples were taken months after the outbreak began—and the viral variants found weren’t exactly identical to the ones in human patients. The versions of SARS-CoV-2 tugged out of several Huanan-market samples, meanwhile, are a dead ringer for the ones that sickened humans with COVID early on. The debate over SARS-CoV-2’s origins has raged for nearly as long as the pandemic itself—outlasting lockdowns, widespread masking, even the first version of the COVID vaccines. And as long as there is murkiness to cling to, it may never fully resolve. While evidence for an animal spillover has mounted over time, so too have questions about the possibility that the virus escaped from a laboratory. When President Joe Biden asked the U.S. intelligence community to review the matter, four government agencies and the National Intelligence Council pointed to a natural origin, while two others guessed that it was a lab leak. (None of these assessments were made with high confidence; a bill passed in both the House and the Senate would, 90 days after it becomes a law, require the Biden administration to declassify underlying intelligence.) If this new level of scientific evidence does conclusively tip the origins debate toward the animal route, it will be, in one way, a major letdown. It will mean that SARS-CoV-2 breached our borders because we once again mismanaged our relationship with wildlife—that we failed to prevent this epidemic for the same reason we failed, and could fail again, to prevent so many of the rest. from https://ift.tt/gwUAfWm Check out http://natthash.tumblr.com Bad things happen to a human body in zero gravity. Just look at what happens to astronauts who spend time in orbit: Bones disintegrate. Muscles weaken. So does immunity. “When you go up into space,” says Saïd Mekari, who studies exercise physiology at the University of Sherbrooke, in Canada, “it’s an accelerated model of aging.” Earthbound experiments mimicking weightlessness have revealed similar effects. In the 1970s, Russian scientists immersed volunteers in bathtubs covered in a large sheet of waterproof fabric, enabling them to float without being wet. In some of these studies, which lasted up to 56 days, subjects developed serious heart problems and struggled to control their posture and leg movements. Weightlessness hurts us because our bodies are fine-tuned to gravity as we experience it here on Earth. It tugs at us from birth to death, and still our intestines stay firmly coiled in their stack, blood flows upward, and our spine is capable of holding up our head. Unnatural contortions can throw things off: People have died from hanging upside down for too long. But as a general rule, the constant push of g-force on our body is a part of life that we rarely notice. Or at least, that’s what scientists have always thought. But there is another possibility: that gravity itself is making some people sick. A new, peer-reviewed theory suggests that the body’s relationship with gravity can go haywire, causing a disorder that has long been a troubling mystery: irritable bowel syndrome. This is a rogue idea that is far from widely accepted, though one that at least some experts say can’t be dismissed outright. IBS is a very common ailment, affecting up to an estimated 15 percent of people in the United States, and the symptoms can be brutal. People who have IBS experience abdominal pain and gas, feel bloated, and often have diarrhea, constipation, or both. But no exact cause of IBS has been pinned down. There’s evidence behind many competing theories, such as early-life stress, diet, and even gut infections, but none have emerged as the sole explanation. That is a problem for patients—it’s difficult to treat a condition when you don’t know what to target. Brennan Spiegel, a gastroenterologist at Cedars-Sinai Medical Center, in Los Angeles, has a different idea: People with IBS are hypersensitive to gravity as a result of any number of factors—stress, weight gain, a change in the gut microbiome, bad sleep patterns, or another behavior or injury. The idea came to him after watching a relative confined to a nursing-home bed develop classic symptoms of IBS. “We’re upright organisms,” he told me. “We’re not really supposed to be lying flat for that long.” The hypothesis, published late last year in The American Journal of Gastroenterology, is just that, a hypothesis. Spiegel hasn’t conducted any experiments or patient surveys that point to a “mismatch” in our body’s reaction to gravity as the cause of IBS, though the mechanics are all based in firm science. But part of what makes the theory so alluring is that it might encompass all of the other conventional explanations for the disease. “It’s meant to be a new way of thinking about old ideas,” he said. So exactly how would someone’s relationship with gravity get off-kilter? Consider serotonin, a chemical that carries messages from the brain to the body. Spiegel sees serotonin as an “anti-gravity substance” because of the role it plays in so many important bodily functions influenced by g-force, such as blood flow. Serotonin can cause blood vessels to narrow, slowing circulation. It can make certain muscles contract or relax. It’s also crucial to digestion, helping with bowel function, getting rid of irritating foods, and regulating how much we eat. Without serotonin, gravity would turn our intestines into a “flaccid sac,” Spiegel writes. Because 95 percent of the body’s serotonin is produced in the gut, if levels spike or plummet from factors such as stress, then the chemical’s possible handling of gravity would be thrown into chaos, affecting digestion. The result, he theorizes, is IBS. Other parts of our body that respond to gravity can also be in on the problem. We are hardwired to react negatively to situations in which the pull of gravity might harm us; walk to the edge of a cliff and your body will tell you something. The amygdala in our brain is key to fear responses, and stress of various kinds can cause it to go into overdrive. Spiegel thinks that when stress taxes the amygdala, a person begins overreacting to potential threats, including from gravity. The digestive issues that make up IBS are a manifestation of that overreaction. Sure enough, people with IBS have been shown to have a hyperactive amygdala. That is hardly anything close to proof. The thought that this painful and prolonged condition could be a gravity disorder is a major stretch, relying on a renegade interpretation of basic biology. “People just think I’m crazy,” Spiegel said. Many of his fellow doctors are not sold on the idea. The gravity hypothesis is another in a long parade of unconvincing theories about IBS, Emeran Mayer, a gastroenterologist at UCLA, told me. He’s heard them all: “It doesn’t exist; it’s a hysterical trait of neurotic housewives; it’s abnormal electrical activity in the colon.” He added, “I don’t think there’s any other disease that has gone through these peaks of attention-grabbing new theories.” Spiegel’s idea has clear holes. If a faulty reaction to gravity triggers IBS, says David C. Kunkel, a gastroenterologist at UC San Diego, then you would expect to see higher rates of IBS among populations living at sea level versus at high altitudes, where g-force is slightly weaker. But that doesn’t seem to be the case: About a quarter of Peruvians live high in the mountains and most Icelanders live at sea level, yet both countries have high rates of IBS. Likewise, IBS rates appear to decrease with age, “which would not be expected if the disease was caused by a constant gravitational force,” Kunkel told me. Spiegel is aware that the gravity hypothesis has little support in the field and no proof. But the gravity hypothesis has some logic behind it. The fact that the weightlessness of space travel can drastically change the body lends credence to the idea that other shifts in our relationship to gravity could do the same, says Declan McCole, a biomedical scientist at UC Riverside. And the gut may be particularly sensitive to gravity changes. McCole has found that weightlessness made epithelial cells—which line the gut and stop invaders from entering the body—easier to evade. So if our internal chemistry can change in a way that makes us hypersensitive to gravity, then, to McCole, it stands to reason that such a shift could hit the gut hard. He’s less sure of whether that hypersensitivity exists. If it does, then why haven’t we identified any chemicals that help handle gravity, as we have for fear or sex drive or hunger? That molecule may indeed turn out to be serotonin, but right now there’s no proof. The gravity hypothesis really matters only if it is meaningful for people with IBS. And that’s not guaranteed. Tying the very real pain of IBS to such a fantastical idea may seem closer to mythology than medicine, leaving patients feeling dismissed or belittled. Or they may throw up their hands in despair and prepare for a lifetime of pain: If the immovable force of gravity is the enemy, then why bother fighting? But if there is some truth to it, then the hypothesis could also provide a possible starting place for treatments. Some of Spiegel’s suggestions are already common, such as weight loss and medications that decrease serotonin, but he also advocates for some gravity-specific therapies. “I do talk about it with my patients,” Spiegel said. “I recommend certain yoga poses; I recommend tilt tables.” People who have IBS may balk at his more radical ideas, such as moving to a higher altitude or farther from the equator. The gravity hypothesis may never be anything more than a hypothesis. We have a long way to go before truly knowing whether the human body can develop a hypersensitivity to gravity that can make us ill, or whether some of us are better equipped to handle gravity than others. But the weight of evidence is enough to make us think twice before ignoring the idea that our body’s relationship to gravity can go awry—including for those of us not coping with IBS. If gravity might contribute to IBS, why not other ailments too? And then, why can’t it also be harnessed for good? Mekari and his colleagues recently found that lying at a six-degree downward angle sped up response times to cognition tests—pointing to a possible link between gravity and executive functioning. Antigravity treadmills, which help astronauts prepare for weightlessness, are being studied for the treatment of cerebral palsy, Parkinson’s disease, and sports injuries. All of these unknowns about gravity can feel haunting. Life on Earth has changed a lot since its first forms appeared about 4 billion years ago, but through it all, gravity has seemingly remained constant—perhaps the single thing that connects every organism that has ever lived. What if there’s still much we have to learn about what it’s doing to us? After all, right now your body is coping with gravity, just as it has been for every other second of your life. Perhaps it would be weirder if gravity wasn’t doing anything to us over time. “Every fiber in our body is straining to manage this force,” Spiegel said. You don’t need to spend 56 days in a bathtub to figure that out. from https://ift.tt/76EwLkc Check out http://natthash.tumblr.com To be a newborn in the year 2023—and, almost certainly, every year that follows—means emerging into a world where the coronavirus is ubiquitous. Babies might not meet the virus in the first week or month of life, but soon enough, SARS-CoV-2 will find them. “For anyone born into this world, it’s not going to take a lot of time for them to become infected,” maybe a year, maybe two, says Katia Koelle, a virologist and infectious-disease modeler at Emory University. Beyond a shadow of a doubt, this virus will be one of the very first serious pathogens that today’s infants—and all future infants—meet.
[Read: Is COVID a common cold yet?] That future crossroads might not sound all that different from where the world is currently. With vaccines now common in most countries and the virus so transmissible, a significant majority of people have some degree of immunity. And in recent months, the world has begun to witness the consequences of that shift. The flux of COVID cases and hospitalizations in most countries seems to be stabilizing into a seasonal-ish sine wave; disease has gotten, on average, less severe, and long COVID seems to be somewhat less likely among those who have recently gotten shots. Even the virus’s evolution seems to be plodding, making minor tweaks to its genetic code, rather than major changes that require another Greek-letter name. But today’s status quo may be more of a layover than a final destination in our journey toward COVID’s final form. Against SARS-CoV-2, most little kids have fared reasonably well. And as more babies have been born into a SARS-CoV-2-ridden world, the average age of first exposure to this coronavirus has been steadily dropping—a trend that could continue to massage COVID-19 into a milder disease. Eventually, the expectation is that the illness will reach a stable nadir, at which point it may truly be “another common cold,” says Rustom Antia, an infectious-disease modeler at Emory. The full outcome of this living experiment, though, won’t be clear for decades—well after the billions of people who encountered the coronavirus for the first time in adulthood are long gone. The experiences that today’s youngest children have with the virus are only just beginning to shape what it will mean to have COVID throughout a lifetime, when we all coexist with it from birth to death as a matter of course. At the beginning of SARS-CoV-2’s global tear, the coronavirus was eager to infect all of us, and we had no immunity to rebuff its attempts. But vulnerability wasn’t just about immune defenses: Age, too, has turned out to be key to resilience. Much of the horror of the disease could be traced to having not only a large population that lacked protection against the virus—but a large adult population that lacked protection against the virus. Had the entire world been made up of grade-schoolers when the pandemic arrived, “I don’t think it would have been nearly as severe,” says Juliet Pulliam, an infectious-disease modeler at Stellenbosch University, in South Africa. Across several viral diseases--polio, chicken pox, mumps, SARS, measles, and more—getting sick as an adult is notably more dangerous than as a kid, a trend that’s typically exacerbated when people don’t have any vaccinations or infections to those pathogens in their rearview. The manageable infections that strike toddlers and grade-schoolers may turn serious when they first manifest at older ages, landing people in the hospital with pneumonia, brain swelling, even blindness, and eventually killing some. When scientists plot mortality data by age, many curves bend into “a pretty striking J shape,” says Dylan Morris, an infectious-disease modeler at UCLA. The reason for that age differential isn’t always clear. Some of kids’ resilience probably comes from having a young, spry body, far less likely to be burdened with chronic medical conditions that raise severe disease risk. But the quick-wittedness of the young immune system is also likely playing a role. Several studies have found that children are much better at marshaling hordes of interferon—an immune molecule that armors cells against viruses—and may harbor larger, more efficient cavalries of infected-cell-annihilating T cells. That performance peaks sometime around grade school or middle school, says Janet Chou, a pediatrician at Boston Children’s Hospital. After that, our molecular defenses begin a rapid tumble, growing progressively creakier, clumsier, sluggish, and likelier to launch misguided attacks against the tissues that house them. By the time we’re deep into adulthood, our immune systems are no longer sprightly, or terribly well calibrated. When we get sick, our bodies end up rife with inflammation. And our immune cells, weary and depleted, are far less unable to fight off the pathogens they once so easily trounced. Whatever the explanations, children are far less likely to experience serious symptoms, or to end up in the hospital or the ICU after being infected with SARS-CoV-2. Long COVID, too, seems to be less prevalent in younger cohorts, says Alexandra Yonts, a pediatrician at Children’s National Hospital. And although some children still develop MIS-C, a rare and dangerous inflammatory condition that can appear weeks after they catch the virus, the condition “seems to have dissipated” as the pandemic has worn on, says Betsy Herold, the chief of pediatric infectious disease at the Children’s Hospital at Montefiore, in the Bronx. Should those patterns hold, and as the age of first exposure continues to fall, COVID is likely to become less intense. The relative mildness of childhood encounters with the virus could mean that almost everyone’s first infection—which tends, on average, to be more severe than the ones that immediately follow—could rank low in intensity, setting a sort of ceiling for subsequent bouts. That might make concentrating first encounters “in the younger age group actually a good thing,” says Ruian Ke, an infectious-disease modeler at Los Alamos National Laboratory. COVID will likely remain capable of killing, hospitalizing, and chronically debilitating a subset of adults and kids alike. But the hope, experts told me, is that the proportion of individuals who face the worst outcomes will continue to drop. That may be what happened in the aftermath of the 1918 flu pandemic, Antia, of Emory, told me: That strain of the virus stuck around, but never caused the same devastation again. Some researchers suspect that something similar may have even played out with another human coronavirus, OC43: After sparking a devastating pandemic in the 19th century, it’s possible that the virus no longer managed to wreak much more havoc than a common cold in a population that had almost universally encountered it early in life. Such a fate for COVID, though, isn’t a guarantee. The virus’s propensity to linger in the body’s nooks and crannies, sometimes causing symptoms that last many months or years, could make it an outlier among its coronaviral kin, says Melody Zeng, an immunologist at Cornell University. And even if the disease is likely to get better than what it is now, that is not a very high bar to clear. Some small subset of the population will always be naive to the virus—and it’s not exactly a comfort that in the future, that cohort will almost exclusively be composed of our kids. Pediatric immune systems are robust, UCLA’s Morris told me. But “robust is not the same as infallible.” Since the start of the pandemic, more than 2,000 Americans under the age of 18 have died from COVID—a small fraction of total deaths, but enough to make the disease a leading cause of death for children in the U.S. MIS-C and long COVID may not be common, but their consequences are no less devastating for the children who experience them. Some risks are especially concentrated among our youngest kids, under the age 5, whose immune defenses are still revving up, making them more vulnerable than their slightly older peers. There’s especially little to safeguard newborns just under six months, who aren’t yet eligible for most vaccines—including COVID shots—and who are rapidly losing the antibody-based protection passed down from their mothers while they were in the womb. A younger average age of first infection will also probably increase the total number of exposures people have to SARS-CoV-2 in a typical lifetime—each instance carrying some risk of severe or chronic disease. Ke worries the cumulative toll that this repetition could exact: Studies have shown that each subsequent tussle with the virus has the potential to further erode the functioning or structural integrity of organs throughout the body, raising the chances of chronic damage. There’s no telling how many encounters might push an individual past a healthy tipping point. Racking up exposures also won’t always bode well for the later chapters of these children’s lives. Decades from now, nearly everyone will have banked plenty of encounters with SARS-CoV-2 by the time they reach advanced age, Chou, from Boston Children’s Hospital, told me. But the virus will also continue to change its appearance, and occasionally escape the immunity that some people built up as kids. Even absent those evasions, as their immune systems wither, many older people may not be able to leverage past experiences with the disease to much benefit. The American experience with influenza is telling. Despite a lifetime of infections and available vaccines, tens of thousands of people typically die annually of the disease in the United States alone, says Ofer Levy, the director of the Precision Vaccines Program at Boston Children’s Hospital. So even with the expected COVID softening, “I don’t think we’re going to reach a point where it’s, Oh well, tra-la-la,” Levy told me. And the protection that immunity offers can have caveats: Decades of research with influenza suggest that immune systems can get a bit hung up on the first versions of a virus that they see, biasing them against mounting strong attacks against other strains; SARS-CoV-2 now seems to be following that pattern. Depending on the coronavirus variants that kids encounter first, their responses and vulnerability to future bouts of illness may vary, says Scott Hensley, an immunologist at the University of Pennsylvania. [Read: Are our immune systems stuck in 2020?] Early vaccinations—that ideally target multiple versions of SARS-CoV-2—could make a big difference in reducing just about every bad outcome the virus threatens. Severe disease, long COVID, and transmission to other children and vulnerable adults all would likely be “reduced, prevented, and avoided,” Chou told me. But that’s only if very young kids are taking those shots, which, right now, isn’t at all the case. Nor are they necessarily getting protection passed down during gestation or early life from their mothers, because many adults are not up to date on COVID shots. Some of these issues could, in theory, end up moot. A hundred or so years from now, COVID could simply be another common cold, indistinguishable in practice from any other. But Morris points out that this reality, too, wouldn’t fully spare us. “When we bother to look at the burden of the other human coronaviruses, the ones who have been with us for ages? In the elderly, it’s real,” he told me. One study found that a nursing-home outbreak of OC43—the purported former pandemic coronavirus—carried an 8 percent fatality rate; another, caused by NL63, killed three out of the 20 people who caught it in a long-term-care facility in 2017. These and other “mild” respiratory viruses also continue to pose a threat to people of any age who are immunocompromised. SARS-CoV-2 doesn’t need to follow in those footsteps. It’s the only human coronavirus against which we have vaccines—which makes the true best-case scenario one in which it ends up even milder than a common cold, because we proactively protect against it. Disease would not need to be as inevitable; the vaccine, rather than the virus, could be the first bit of intel on the disease that kids receive. Tomorrow’s children probably won’t live in a COVID-free world. But they could at least be spared many of the burdens we’re carrying now. from https://ift.tt/BdbPWwj Check out http://natthash.tumblr.com Elizabeth often met her husband, Mitch, after work at the same restaurant in Lower Manhattan. Mitch was usually there by the time she arrived, swirling his drink and joking with a waiter. Elizabeth and Mitch had been friends before becoming romantically involved and bantered back and forth without missing a beat. Anyone looking at their table might well have envied them, never suspecting that Elizabeth dreaded these pleasant get-togethers. Elizabeth, a tall, elegant woman, told me about those evenings in a composed, confiding tone, which only makes her story more uncanny. (Both her name and Mitch’s have been changed to protect their privacy.) Once the meal was over, Mitch would invariably give her a wary, skeptical look and say, “Now you’ll go to your place and I’ll go to mine.” Hearing these words, Elizabeth would nod meekly, then duck into the bathroom for a minute before running out. She’d cross the street, wait for Mitch to emerge—making sure that he was headed in the right direction—and then hurry home to wait for him. It always struck her how normal Mitch appeared. It was herself she barely recognized: the nervous, frazzled woman hiding behind lampposts, following a man who looked so at ease in the world. Then, with a burst of speed, she managed to get back to their apartment a few minutes before he did. Arriving home, Mitch always gave her the same cheerful greeting: “Hey, honey, how are you?” He had already forgotten their rendezvous. The nightmare would officially begin after Mitch had made himself comfortable. Without any warning, he’d look up from a magazine or the TV, stare at Elizabeth, and ask her to leave. Calmly at first, he’d order her out of her own home. When she tried to convince him that she was home, he’d scoff. How could it be her home, when he lived there? Although he sensed that they knew each other, he had forgotten they were married. Moreover, he felt threatened by her presence. When Mitch first began to act this way, Elizabeth had done her best to plead her case. She’d point to things in the apartment and remind him of where they came from. “Look,” she’d say. “Our wedding picture, see?” Unfazed, Mitch would reply. “Yeah? You must have planted it there.” “But look, I can tell you everything that’s in the closet or anywhere else in the house. We’ve lived here 15 years, me and you, remember?” “So you’ve been snooping around my apartment. Now stop touching my things and get out before I call the cops.” Some evenings, when she stalled, he flew into a rage, grabbed her by the neck like a stray cat, and pushed her out the front door, where she sat all night in the hallway. But Mitch wasn’t predictable—sometimes he seemed perfectly normal in the evenings; at other times, he magnanimously let her remain. But as his episodes grew more frequent and his recalcitrance more extreme, her exile in the hallway became almost a nightly routine. She took to carrying a spare key in her pocket and would let herself in when she thought Mitch had fallen asleep. Mitch had Alzheimer’s. I met Elizabeth in 2016, when I was a volunteer at an Alzheimer’s organization in New York City. I’ve remained in touch with her since, even after Mitch’s eventual death from the disease, in 2020. Although Mitch had already been diagnosed by the time Elizabeth and I began discussing her case, she was surprised at the turn his condition had taken. Many people with dementia experience occasional delusions and hallucinations, but relatively few become as fixated as Mitch did on the fact that a spouse is an imposter. I once asked Elizabeth why she thought she continued to argue with Mitch when she knew it wouldn’t do any good. She chuckled. “The thing is, he had an answer for everything. No matter what I said or could prove, he had an explanation. I just couldn’t let it go.” When patients with dementia have an answer for everything, caregivers get caught in a loop. It’s surprisingly hard not to be goaded by a patient’s responses. Even if the answers are nonsensical, the patient’s ability to provide them suggests that we’re still dealing with a functional mind. Indeed, the part of the mind that helps patients produce a steady stream of answers remains intact. It was this part—what the neuroscientist Michael Gazzaniga has termed the “left-brain interpreter”—that Mitch was now leaning on. The “interpreter” is an unconscious process responsible for sweeping inconsistencies and confusion under the rug. When things don’t add up, when our expectations are flipped, when our environment suddenly changes, the left-brain interpreter provides explanations that help us make sense of things. For instance, patients feeling anxious or afraid because of memory loss or confusion will come up with explanations for their disorientation. They’ll blame the aide for misplacing a purse or insist that people are conspiring against them. When they feel internal discord, their unconscious mind searches for an external source, and this source gives shape to their paranoia. So when Mitch was confronted by evidence that Elizabeth was his wife, which contradicted his impression that she was someone else, his left-brain interpreter found explanations for that evidence—for instance, that it had been planted in his apartment. This is partly why so many patients are adept at coming up with quick (albeit wrong) answers and rationalizations for their warped views. The mind’s propensity to create believable narratives is all too human. In a 1962 study that would surely be considered unethical today, the psychologists Stanley Schachter and Jerry Singer administered epinephrine to their subjects. Epinephrine, a synthetic hormone that narrows blood vessels, can produce anxiety, shakiness, and sweating. Some participants were then informed that they had been given a vitamin that had no side effects. The others were told that the pill could produce a racing heart, tremors, and flushing. Those who knew about the possible side effects immediately attributed their discomfort to the drug. Those unaware of possible side effects and who experienced agitation blamed their environment, even thinking that the other participants were responsible. We evidently have a tendency to find reasons for what disturbs us rather than remain in the dark. This need to ascertain cause and effect is yet another function of the left-brain interpreter, and it plays out in many ways. For example, we’ll assign reasons to our feelings despite often not knowing their true cause. We’ll twist facts, defend misconceptions, and opt to believe whatever makes sense of what’s happening around us. So when patients argue, caregivers may find it difficult to distinguish pathology from the mind’s normal tendency to resist what it doesn’t know. At one of our meetings, Elizabeth described a particularly unsettling moment with Mitch. One evening, amid a harrowing confrontation, instead of throwing her out, Mitch suddenly relaxed and turned on the TV. He flipped through the channels, then stopped on the opening credits to the movie Doctor Zhivago and, hearing its music, reached for her hand. “Imagine,” Elizabeth said softly, looking at me, “we’re holding hands.” The perpetuation of the sweet Mitch is what kept her off-balance. Because alongside the man who didn’t recognize her was the man who might stroke her hair and ask how she put up with him. Alongside the man who threw her out was the man who made a video for their anniversary in which he confessed how lost he’d be without her. If that Mitch did not exist—if Elizabeth had had only the delusional Mitch to deal with—her left-brain interpreter would have had less to contend with. Instead, her brain was badgered by inconsistency and uncertainty. When we think of Alzheimer’s, we usually think of it as erasing the self. But what happens in most cases is that the self splinters into different selves; some we recognize, others we don’t. In fact, the self, or, more accurately, “self-representation” in the brain, is not, as the philosopher Patricia Churchland phrased it, an “all-or-nothing affair.” Instead, our “self” is distributed throughout the brain, which can make Alzheimer’s even more complicated than is generally believed. If the self is, in some sense, already fragmented, its gradual erosion can remain unnoticed behind the ebb and flow of a person’s familiar personality. Cases, of course, vary, and quite commonly Alzheimer’s doesn’t get rid of the self as much as it brings parts of it to the fore. For Elizabeth, Mitch was still Mitch. A loved one’s identity doesn’t evaporate when change occurs. One reason for this may be our unconscious belief in what the psychologist Paul Bloom refers to as the “essential self.” Early in our development, we attribute to other people a permanent “deep-down self.” And though our understanding of people becomes more complex as we grow older, our belief in a “true” or “real” self persists. When experimental philosophers, interested in how we define the self, asked participants to consider what happens when a hypothetical brain transplant affects a subject’s cognitive abilities, personality, and memory, most participants continued to believe that the subject’s “true self” remained intact. Only in those cases where the subject began to behave in morally uncharacteristic ways—kleptomania, criminality, pedophilia, or engaging in other abhorrent behaviors—did participants conclude that the “true self” had been radically altered. Bloom explains that we’re more likely to associate the “good” qualities in people with their true selves—“good,” of course, as defined by our own values. In this sense, another person’s “true” self is an extension of what we hold dear. So if the essential self is intuitively equated with the moral self, then the cognitive problems attending dementia can seem peripheral as long as changes in behavior do not run “deep enough” to redefine a husband or a father. The reason Elizabeth kept arguing with Mitch was that she was appealing to the “real” Mitch, the “good” Mitch, the one “still in there,” the one who, in the past, would have come to her aid. For caregivers, the idea of a “real self” can be a double-edged sword. If, on the one hand, it encourages us to argue with afflicted loved ones in the hope of breaking through to their “real selves,” it can also be a source of great frustration. If, on the other hand, we start to doubt the existence of an essential self, how can we account for the person we’re caring for? Who is it that we are suffering and sacrificing for? As Mitch’s cognitive capacity ebbed, so too did his confusion. He became calmer—and so did Elizabeth. Even so, Elizabeth told me that he could still, on occasion, become upset. One day when Mitch was filling in a coloring book, an activity he previously would have found beneath him, he looked up and said, “I think there’s something wrong with me.” “Well, honey,” Elizabeth said gently, “you have something called Alzheimer’s, and that’s okay, I’m here for you.” Mitch furrowed his brow. “No, that’s not it. I don’t have that. Why would you even say that?” Telling me this, Elizabeth reprimanded herself: “I felt awful upsetting him.” But her response was only natural. When Mitch sensed something was wrong, she thought, for a moment, that she had glimpsed the old Mitch, the true Mitch. So she had confided in him as she had in the past, hoping he’d understand. This article has been excerpted from Dasha Kiper’s new book, Travelers to Unimaginable Lands: Stories of Dementia, the Caregiver, and the Human Brain. When you buy a book using a link on this page, we receive a commission. 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