Years ago, just after I finished my psychiatry residency, a beloved supervisor called to say she had some bad news. At a routine checkup, she had glanced at her chest X-ray up on the viewing box while waiting for her doctor to come into the room. She was a trauma surgeon before becoming a psychiatrist and had spent years reading chest X-rays, so she knew that the coin-size lesion she saw in her lung was almost certainly cancer, given her long history of smoking. We had dinner soon after. She was still more than two years away from the end of her life and felt physically fine—vital, even. That’s why I was so surprised when she said she had no desire to spend whatever time she had left on exotic travel or other new adventures. She wanted her husband, her friends, her family, dinner parties, and the great outdoors. “Just more Long Island sunsets. I don’t need Bali,” she told me. At the end of life, you might expect people to feel regret for all the things they wanted to do and never made time for. But I have yet to know a patient or friend who, facing the blunt fact of their own mortality, had anything close to a bucket list. This squares with some recent research that shows that people tend to prefer familiar experiences more when they are reminded that their days are limited. The people I know even regretted the novelty they’d chased along the way, whether it was recreational-drug use or dating exciting people who they knew weren’t relationship material. Deathbed pronouncements can have limited applications for the rest of life, but this pattern suggests that novelty is perhaps overrated. Chasing the high of new sensations simply isn’t appealing for many people, and can sometimes even be bad for our health. I suspect that’s because, too often, the pursuit of novelty requires sacrificing the things we already know we love. It’s a common misconception that people who don’t have a taste for the newest, sexiest experience are dull, incurious, and unimaginative. A 2002 study found that people will switch away from their favorite, habitual choices when they know others are watching in order to avoid being judged as narrow-minded. And yet, Warren Buffett notoriously eats breakfast at the same fast-food restaurant every day and sticks to a strict work schedule. Taylor Swift’s music can be redundant and predictable. Barack Obama is famous for his strict morning exercise regime and daily reading time. Even when they’re not facing death, many people just don’t seem to like novelty that much. In 2017, a poll by a British soup company found that 77 percent of U.K. workers had consumed the exact same lunch every day for nine months and that one in six people had done so for at least two years. You might think it’s just a matter of convenience or economic exigency (the study didn’t say), but I’m not so sure; wealthy people I know partake in similar behavior, even if they do it at a fancy restaurant. Consider, too, that when people lose a pet, many run out and get a replacement of the same breed with a similar temperament. They repeatedly date people with the same quirks and problems. They return to a favorite vacation spot. They listen to the same musical artists and styles time and again. [Read: The people who eat the same meal every day] Research shows that humans have an intrinsic preference for things and people they are familiar with, something called the mere exposure effect. Several studies have shown that people who listen to unfamiliar songs repeatedly grow fonder of the songs they hear most by the end of the experiment, even if they did not initially like them very much. You don’t even have to be aware that you’re growing used to something for the effect to work. This tendency toward repetition may seem natural, even lazy, but it runs counter to much of our history. We, along with other animals, evolved to be exquisitely sensitive to novel experiences. Way back in the Paleolithic era, there was a clear survival advantage to being attuned to new situations, which could lead someone to a potential mate or a piece of mastodon, or reveal a deadly threat. Nowadays, though, with every conceivable reward—food, sex, drugs, emotional validation, you name it—either a click, tap, or ChatGPT query away, conventional novelty-seeking has lost much of its adaptive advantage. As Arthur Brooks has written in The Atlantic, novelty can be fun and exciting. New and unexpected experiences activate the brain’s reward pathway more powerfully than familiar ones, leading to greater dopamine release and a more intense sense of pleasure. But on its own, excitement won’t bring about enduring happiness. Human beings habituate rapidly to what is new. To achieve a lifetime of stimulation, you would have to embark on an endless search for the unfamiliar, which would inevitably lead to disappointment. Worse, the unfettered pursuit of novelty can lead to harm through excessive thrill-seeking—including antisocial behavior such as reckless driving—particularly when the novelty seeker has poor impulse control and a disregard for others. [Read: Don’t approach life like a picky eater] There’s a better way. Research shows that when novelty-seeking is paired with persistence, people are far more likely to be happy, probably because they are able to achieve something meaningful. You might, for example, take a variety of courses in college or try different summer internships if you’re not yet sure what interests you. When one really clicks, you should explore it in depth; it might even become a lifelong passion. This principle relates to less consequential pleasures, too: If you’re checking out a new neighborhood joint, consider ordering different things during your first few visits, then picking your favorite and sticking with it. Novelty-seeking is most valuable when you use it as a tool to discover the things and people you love—and once you find them, go deep and long with those experiences and relationships. The siren call that tells you there might be a new and better version of what you already have is likely an illusion, driven by your brain’s relentless reward pathway. When in doubt, pick a beloved activity over an unfamiliar one. This golden rule of novelty may help explain why some people at the end of their life regret having spent so much time exploring new things, even if they once brought fleeting pleasure. Age, too, might partly explain this feeling, because older people tend to be less open to new experiences. But that’s probably not the whole story. My colleagues who treat children and adolescents have mentioned that, in the face of life-threatening diagnoses, even young people prefer the familiar. They do so not only because the familiar is known and safe, but because it is more meaningful to them. After all, things become familiar to us because we choose them repeatedly—and we do that because they are deeply rewarding. Imagine, just for a moment, that your death is near. What might you miss out on if you put your bucket list on hold? Sure, you won’t make it to Bali or Antarctica. But maybe instead you could fit in one last baseball game with your kids, one last swim in the ocean, one last movie with your beloved, one last Long Island sunset. If you prioritize the activities and people you already love, you won’t reach the end of your life wishing you’d made more time for them. from https://ift.tt/vO1i5Ws Check out http://natthash.tumblr.com
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In March 2020, Yamagata’s trail went cold. The pathogen, one of the four main groups of flu viruses targeted by seasonal vaccines, had spent the first part of the year flitting across the Northern Hemisphere, as it typically did. As the seasons turned, scientists were preparing, as they typically did, for the virus to make its annual trek across the equator and seed new outbreaks in the globe’s southern half. That migration never came to pass. As the new coronavirus spread, pandemic-mitigation measures started to squash flu-transmission rates to record lows. The drop-off was so sharp that several flu lineages may have gone extinct, among them Yamagata, which hasn’t been definitively detected in more than three years despite virologists’ best efforts to root it out. [Read: The pandemic broke the flu] Yamagata’s disappearance could still be temporary. “Right now, we’re all just kind of holding our breath,” says Adam Lauring, a virologist at the University of Michigan Medical School. The virus might be biding its time in an isolated population, escaping the notice of tests. But the search has stretched on so fruitlessly that some experts are ready to declare it officially done. “It’s been missing for this long,” says Vijaykrishna Dhanasekaran, a virologist at Hong Kong University. “At this point, I would really think it’s gone.”
Yamagata, in many ways, has long been an underdog among underdogs. The lineage is one of two in a group called influenza B viruses, and it’s slower to evolve and transmit, and is thus sometimes considered less troublesome, than its close cousin Victoria. As a pair, the B’s are also commonly regarded as the wimpier versions of flu. To be fair, the competition is stiff. Flu B’s are constantly being compared with influenza A viruses—the group that contains every flu subtype that has caused a pandemic in our recent past, including the extraordinarily deadly outbreak of 1918. Seasonal flu epidemics, too, tend to be heavily dominated by flu A’s, especially H3N2 and H1N1, two notably tough-to-target strains that feature prominently in each year’s vaccine. Even H5N1, the flavor of avian influenza that’s been devastating North America’s wildlife, is a member of the pathogen’s A team. [Read: Eagles Are Falling, Bears Are Going Blind] B viruses, meanwhile, don’t have a particularly daunting résumé. “To our knowledge, there has never been a B pandemic,” says John Paget, an infectious-disease epidemiologist at the Netherlands Institute for Health Services Research. Only once every seven seasons or so does a B virus dominate. And although A and B viruses sometimes tag-team the winter, causing twin outbreaks spaced out by a few weeks, these seasons often open with a major flu A banger and then close out with a more muted B coda. The reasons underlying these differences are still pretty murky, though scientists do have some hints. Whereas flu A viruses are known as especially speedy shape-shifters, constantly spawning genetic offshoots that vie to outcompete one another, flu B’s evolve at oddly plodding rates. Their sluggish approach makes it easier for our immune system to recognize the viruses when they reappear, resulting in longer-lasting protection, more effective vaccines, and fewer reinfections than are typical with the A’s. Those molecular differences also seem to drive differences in how and when the viruses spread. The A’s tend to trouble people repeatedly from birth to death, and are great at globe-trotting. But B’s, perhaps because immunity against them is easier to come by, more often concentrate among kids, many of whom have never encountered the viruses before—and who are usually more resilient to respiratory viruses and travel less than adults, keeping outbreaks mostly regional. That might also help explain why B epidemics so frequently lag behind A’s: Slower pathogen evolution facing off with more durable host immunity add up to less rapid B spread, while their A colleagues rush ahead. Our bodies also seem to mount rather fiery defenses against A viruses, steeling them against other infections in the weeks that follow and deepening the disadvantage against any B’s trailing behind. All of that means flu B has a hard time catching humans off guard. The virus’s host preferences, too, make flu A viruses more dangerous. Those lineages are great at hopscotching among a whole menagerie of species—most infamously, pigs and wild, water-loving birds—sometimes undergoing rapid bursts of evolution as they go. But flu B’s seem to almost exclusively infect humans, igniting only the rare and fast-resolving outbreak in a limited number of other species—a few seals here, a handful of pigs there. Spillovers from wild creatures into humans are the roots of global outbreaks. And so, with its zoonotic bent, “influenza A will always be the main focus” of concern, says Carolien van de Sandt, a virologist at the Peter Doherty Institute for Infection and Immunity, in Melbourne. Even among some scientists, Yamagata and Victoria register as little more than literal B-list blips.
Flu lineages have dipped into relative obscurity before only to come roaring back. After the end of the H2N2 pandemic of the late 1950s, H1N1 appeared to flame out—only to reemerge nearly two decades later to greet a population full of young people whose immune systems hadn’t glimpsed it before. And as recently as the 1990s, the B lineage Victoria underwent a years-long ebb in most parts of the world, before ricocheting back to prominence in the early 2000s. As far as researchers can tell, Victoria is alive and well; during the globe’s most recent winter seasons, the lineage appears to have ignited late-arriving outbreaks in several countries, including in South Africa, Malaysia, and various parts of Europe. But based on the viral sequences that researchers have isolated from people sick with flu, Yamagata is still nowhere to be found, says Saverio Caini, a virologist at the cancer research center ISPRO, in Italy. The lineage was already teetering on a precipice before the pandemic began, van de Sandt told me. Yamagata and Victoria, which splintered apart in the early 1980s, are still closely related enough that they often compete for the same hosts. And just prior to 2020, Victoria, the more diverse and fleet-footed of the two B lineages, had been reliably edging out its cousin, pushing Yamagata’s prevalence down, down, down. That trend, coupled with several years of use of a well-matched Yamagata strain in the seasonal flu vaccine, meant that Yamagata “had already decreased in incidence and circulation,” van de Sandt said. With the odds so steeply stacked, the addition of pandemic mitigations may have been the final factor that snuffed the lineage out. Recently, a few countries—including China, Pakistan, and Belize—have tentatively reported possible Yamagata infections. But there’s been no conclusive genetic proof, several experts told me. Several parts of the world, including the United States, regularly use flu vaccines containing active flu viruses that can trip the same viral tests that the wild, disease-causing pathogens do. “So the reports could be contaminations,” van de Sandt said. Scientists would need to scour the virus’s genetic sequences to distinguish infection from injection; those data, however, haven’t emerged. Should the Yamagata dry spell continue, researchers may want to start considering snipping the lineage out of vaccines altogether, perhaps as early as the middle or end of this year. Doing so would punt the world back to the early 2010s, when flu shots were trivalent—designed to protect people against two A viruses, H3N2 and H1N1, plus either Victoria or Yamagata, depending on which lineage researchers forecasted would surge more. (They were often wrong.) Or maybe the space once used for Yamagata could feasibly be filled with another flavor of H3N2, the fastest mutator of the bunch. But purging Yamagata from the vaccine would be a gamble. If Yamagata is not gone for good, van de Sandt worries that booting it from the vaccine would leave the world vulnerable to a massive and deadly outbreak. Even Dhanasekaran, who is among the researchers who are fairly confident that we’ve seen the last of Yamagata, told me he doesn’t want to rule out the possibility that the virus is cloistering in an immunocompromised person with a chronic infection, and it’s unclear if it could reemerge from such a hiding place. The only thing scientists can do for now is be patient, says Jayna Raghwani, a computational biologist at the University of Oxford. “If we don’t see it in successive seasons for another two to three years, that will be more convincing,” she told me. If Yamagata’s death knell has actually rung, though, it will have reverberating effects. There’s no telling, for instance, how other flu lineages might be affected by their colleague’s supposed retirement. Perhaps Victoria, which can swap genetic material with Yamagata, will evolve more slowly without its partner. At the same time, Victoria may have an easier time infecting people now that it no longer needs to compete as often for hosts. If Yamagata has gone to pasture, “there won’t be a ceremony declaring the world Yamagata free,” Lauring told me. And it’s easy, he points out, to forget things we don’t see. But even if Yamagata seems gone for now, the effects of its demise will be significant enough that it can’t be forgotten—not just yet. from https://ift.tt/8ziGPUV Check out http://natthash.tumblr.com All of a sudden, Ozempic is everywhere. The weight-loss drug that it contains, semaglutide, is a potent treatment for obesity, and Hollywood and TikTok celebrities have turned it into a sensation. In just a few months, the medication has been branded as “revolutionary” and “game-changing,” with the power to permanently alter society’s conceptions of fatness and thinness. Certainly, a drug like semaglutide could be all of those things: Never in the history of medicine has one so safely led to such dramatic weight loss in so many people. But let’s not get ahead of ourselves. As weight-loss medications go, Ozempic is far from perfect. Though the drug has profound impacts, it requires weekly injections, a tolerance for uncomfortable side effects, and the stamina—not to mention the budget—for long-term treatment. (Ozempic has somehow become a catchall term for semaglutide but technically that product has gotten FDA sign-off only as a diabetes medication. A larger dose of semaglutide, marketed as Wegovy, has been approved for weight loss.) Made by the Danish drugmaker Novo Nordisk, semaglutide dominates the U.S. weight-loss market right now, but its reign might be short-lived. The colossal demand for these drugs has spurred a competition in the pharmaceutical industry to develop even more potent and powerful medications. The first of them could become available as soon as this summer. For all its hype, semaglutide is the stepping stone and not the final destination of a new class of obesity drugs. Just how good they get, and how quickly, will go a long way in determining whether this pharmaceutical revolution actually meets its full promise. In a sense, semaglutide hardly represents a major step forward in science. Diet drugs are nothing new, and even the category of pharmaceuticals that these new products belong to, called “GLP-1 agonists,” has been around for several years. These drugs mimic the hormone GLP-1 (glucagon-like peptide one) and bind to its receptor in the body. This triggers a sense of fullness associated with having just eaten, and also slows the release of food from the stomach. (It also increases insulin secretion, keeping blood sugar in check, which is why Ozempic is still intended as a diabetes drug.) Already, these pharmaceuticals have gotten better over time: A daily injection called liraglutide and sold as Saxenda, which was approved by the FDA in 2014 for obesity, leads to the loss of 5 to 10 percent of a person’s body weight in most cases. But one reason semaglutide took off in a way that liraglutide didn’t is that it can lead to weight loss of up to 20 percent. “Now you have a shot that’s once a week instead of every day, you’re making dramatic improvements, and people notice more,” Angela Fitch, the president of the Obesity Medicine Association and the chief medical officer of the obesity-care start-up Knownwell, told me. But not everyone who takes these drugs can achieve that level of weight loss. More than 60 percent of those on Wegovy experience smaller changes, in part because the drug can’t account for the complex drivers of obesity that aren’t related to food. The next generation of drugs is reaching for more. The first leap forward is Mounjaro, known generically as tirzepatide, a diabetes drug from Eli Lilly that the FDA is expected to approve for weight loss this year. In one study, it led to 20 percent or more weight loss in up to 57 percent of people who took the highest dose; The Wall Street Journal recently called it the “King Kong” of weight-loss drugs. People on Mounjaro tend to lose more weight more quickly and generally have a “better experience” than those on Wegovy, Keith Tapper, a biotech analyst at BMO Capital Markets, told me. It’s also cheaper, though by no means cheap, at roughly $980 for the highest-dose option, he said; a dose of Wegovy costs about $1,350. These leaps in potency are happening on the molecular level. Like semaglutide, Mounjaro mimics the effects of GLP-1, but it also hits receptors for another hormone—GIP. That leads to even more weight loss by further attenuating focus on food and potentially also increasing the activity of a fat-burning enzyme, said Tapper. So-called dual-agonist drugs “offer a step change” in both weight loss and blood-sugar control, he added. And why stop at two receptors when so many others are involved in regulating hunger? “This area is exploding in terms of research and testing different combinations of hormones,” which are still poorly understood, Shauna Levy, a professor specializing in bariatric surgery at Tulane University School of Medicine, told me. Eli Lilly has another drug in the works that targets three receptors; one from the drugmaker Amgen works by “putting the brakes” on the GIP receptor and “putting the gas” on GLP-1’s, a company spokesperson told me. Several other companies have already joined what some have dubbed a “race” to develop the next great obesity drug, in which Lilly, Pfizer, Amgen, Structure Therapeutics, and Viking Therapeutics are expected to be the front-runners, said Tapper. The potency of weight-less drugs is not the only factor that will determine the shape of their future trajectory. Wegovy and Mounjaro injections are tolerable for most people, but they are less convenient than a pill. Making oral versions of these drugs isn’t as easy as packing everything into a capsule, though. Semaglutide is a molecule that gets chewed up in the stomach. For this reason, the semaglutide pill Rybelsus, which is already approved for diabetes, leads to far less dramatic weight loss than its injectable kin. But drugmakers are undeterred by this complication, because a pill even more powerful than semaglutide would no doubt have many customers. In January, Pfizer’s CEO Albert Bourla said that an oral weight-loss drug “unlocks the market,” which he estimated could eventually be worth $90 billion. Pfizer doesn’t have any weight-loss drugs yet but is developing a twice-daily GLP-1 agonist pill; Eli Lilly also has an oral version in the works. Tapper expects those drugs to become available in 2026, and a similar offering from Structure Therapeutics is likely to follow the next year. Drugmakers will also likely vie to create drugs with fewer side effects. Novo Nordisk notes that gastrointestinal issues are common with semaglutide; accounts of horrible nausea, constipation, and vomiting have proliferated online. As one actor put it to New York Magazine, people on Ozempic are “shitting their brains out.” With Wegovy, more serious issues, such as pancreatitis, thyroid cancer, and kidney failure, are also possible but are considered rare. Although nothing to scoff at, side effects tend to subside with prolonged treatment and can usually be managed with help from a doctor, said both Fitch and Levy, who regularly prescribe semaglutide to patients with obesity. It’s possible, Levy added, that people experiencing really terrible effects may be getting their drugs from shady compounding pharmacies or even from other countries. The fact that people are turning to sketchy outlets to get weight-loss drugs underscores the biggest issue with them: access. Medicare and most private insurance companies don’t cover anti-obesity drugs. (Such drugs are classified as “cosmetic” by the Centers for Medicare and Medicaid Services, and thus don’t qualify for coverage.) “I am hopeful that the price will come down with more competition,” Fitch told me. But there’s no guarantee that will happen: Competition typically makes a product cheaper over time, but research suggests that isn’t always the case in pharmaceuticals. Even if the drugs do become cheaper, they may not become cheap enough. The oral forms of these drugs, some of which could be available by 2026, are expected to cost about $500 a month, Tapper said. By 2030, the cost of obesity drugs could come down to about $350 a month, according to a recent Morgan Stanley analysis, which would still be out of reach for many Americans. Levy estimates that the next five years will bring about a “huge explosion” of next-gen obesity drugs. In that case, the market will likely expand to accommodate a variety of drugs with different price points and efficacies. Some people may aim to lose 20 or more percent of their body weight; some may be content with less. The market is so diverse that it will likely “support a broad range of options,” said Tapper, such as cheaper, lower-dose oral drugs for people who have milder medical issues, and more expensive injectables for those with more severe medical concerns. That opens up the possibility that medically mediated weight loss could soon be an option for a far greater proportion of people. Regardless of how much these drugs’ costs may decrease, they will always add up if people are paying out of pocket for them. They are meant to be taken long term: Once a person stops taking Wegovy, the weight tends to come right back. The current crop of weight-loss medications are essentially maintenance drugs, much like the cholesterol-busting drug Lipitor, which is taken daily to treat long-term disease. But Lipitor, unlike obesity drugs, is generally covered by insurance. Unless obesity drugs receive the same kind of coverage, no level of improvement will lead them to deliver on what Ozempic is promising us now. from https://ift.tt/k0Ktx89 Check out http://natthash.tumblr.com Colleen Kennedy, a retired medical assistant, was prepared for the annihilation of chemotherapy and radiation treatment for stage-three lung cancer. She hadn’t expected the hiccup fits that started about halfway through her first treatment round. They left her gasping for air and sent pain ricocheting through her already tender body. At times, they triggered her gag reflex and made her throw up. After they subsided, she felt tired, sore, breathless—as if she’d just finished a tough workout. They were, Kennedy, now 54, told me, “nothing compared to what we would consider normal hiccups at all.” They lasted for nearly a year. Hiccups are one of the most common bodily experiences that humans (and, rats, squirrels, rabbits, cats, dogs, and horses) have; even fetuses get them. When we hiccup, the diaphragm involuntarily contracts and the vocal cords snap closed, producing the eponymous “hic” sound. These spasms usually disappear within a few minutes. Compared with cancer’s existential threat and the brutal reality of treating it, hiccups are innocuous, banal, and unserious. But these two experiences are, peculiarly, connected. As many as 40 percent of cancer patients deal with bouts of hiccups during their illness. For a smaller subset—about one in 10—those spells last for more than 48 hours. Chronic hiccups interrupt almost every aspect of life. They disrupt concentration and conversations. They shake a person awake. Eating, drinking, and swallowing can feel like choking. Often, chest aches linger long after a hiccupping fit subsides. And they are difficult to treat. Doctors have some off-label prescriptions at their disposal, but none has been rigorously tested—none has been proved to work any better than home remedies. Kennedy tried to eradicate her hiccups with deep, forceful inhales and by drinking water from the far rim of a glass; she also trained herself to exhale before drinking or eating to limit the amount of air she swallowed. “Sometimes it worked, but most times it didn’t,” she said. Many try chiropractice or acupuncture. Others recruit household items: sugar, lemons, vinegar, a pencil, a cold spoon. Only one hiccup drug has ever been approved by the Food and Drug Administration. [Read: The two technologies changing the future of cancer treatment] In popular culture, hiccups are a joke: In a Looney Tunes bit from 1942, Daffy Duck’s hiccups send his hat bouncing. In a 2005 episode of Foster’s Home For Imaginary Friends, Bloo tries everything to cure his hiccups—he pours a box of sugar into his mouth, breathes into a brown paper bag, drinks hot sauce, eats peanut butter, gets scared, takes small sips and big gulps, stands on his head, brushes his teeth while singing, swallows a lemon. Nothing works. In 1937’s Snow White and the Seven Dwarfs, Dopey accidentally swallows a bar of soap and starts hiccuping bubbles. In 1970’s Aristocats, Uncle Waldo gets hiccups from drinking too much. In 1975’s Monty Python and the Holy Grail, a hiccuping guard is commanded by the king to get a drink to rid him of his ailment. In a 1992 episode of The Simpsons, a man who’s been hiccupping for 45 years gives this four-second interview to the local Springfield TV news: “Hic—kill me—hic—kill me—hic—kill me.” In medicine, hiccups are a conundrum. “There’s really no benefit to a hiccup, as far as anyone knows,” Aminah Jatoi, a Mayo Clinic oncologist who studies hiccups, told me. A transient symptom that appears and disappears randomly, hiccups are nearly impossible to study with rigor. Experiments on treatments are, accordingly, a nightmare to orchestrate. To date, only a handful of randomized, controlled trials have studied pharmacological treatments for hiccups; none recruited more than 40 patients. Most studies rely on storytelling: single-patient case reports, limited case series, and analyses of databases of doctor’s notes. What we do know: A sudden temperature shift can bring hiccups on, as can drinking alcohol, eating spicy food, and getting excited or stressed. High blood sugar can be to blame. So can low sodium or electrolytes. Many drugs—including steroids, chemotherapy agents, benzodiazepines, opioids, nicotine, antibiotics, anesthesia, and anti-nausea and blood-pressure medicines—are linked with hiccups. Some drugs used to treat intractable hiccups can cause hiccups. In one case study, a patient’s hiccups were incited by a hair brushing against the eardrum; in another, from 1988, the culprit was an ant crawling around the eardrum. The medical conditions associated with hiccups range the body’s entire upper half: stroke, brain injury, meningitis, multiple sclerosis, ear infection, rhinitis, goiters, sore throat, pneumonia, bronchitis, asthma, tuberculosis, fluid in the lungs or heart, bloating, gas, pregnancy, hernias, ulcers, liver disease, kidney disease. And cancer. [Derek Thompson: The surprising reason for the decline in cancer mortality] Experts offer two main explanations for the cancer-hiccup connection. In one, cancers that invade the chest, throat, or head (that is, anything along the route of a hiccup) provoke them. In the other, medications prescribed to cancer patients— including chemotherapy drugs, steroids, and opioids—set them off. Regardless of whether cancer itself is to blame or whether they’re a side effect of treatment, hiccups add another layer of misery to the experience. One study published in 2022 showed that hiccups were a major detriment to the quality of life of about one in 20 of the cancer patients surveyed. Among those with hiccups, almost one in three said they struggled to relax or recreate; a smaller portion said they couldn’t enjoy meals. In another study of 320 cancer patients, hiccups sent one in 10 to the hospital for help. Other research suggests that upwards of three-quarters of hiccup-struck patients deal with the spasms without medical intervention. In a survey of 90 cancer-health-care providers with experience with hiccups, 40 percent rated their patients’ hiccup severity as worse than their nausea and vomiting. Even so, experts say, hiccups remain an aside for both patients and practitioners. Given the rapidity of physician visits—on average about 23 minutes, by one measure, for patients with cancer—hiccups may simply fall too low on a list of preoccupations to warrant mention, but “I think part of what happens is patients feel a little embarrassed bringing it up,” Jatoi said. Or “the patient may want to be a ‘good’ patient and not complain,” says Thomas Smith, an oncologist and palliative-medicine specialist at Johns Hopkins—perhaps because they fear their doctors will modify their treatment course if they speak up about any negative side effects. Oncologists, for their part, don’t consistently or directly ask about hiccups in the way that they screen for pain, nausea, and trouble breathing. “I don’t know of a single symptom-assessment scale in use that has a line for hiccups,” Smith told me. Some brush off patients who do complain of the spasms. “My doctors just shook their heads like I was joking when I told them I got the hiccups all the time,” one patient wrote to Mayo Clinic hiccup researchers. [Uri Bram: The cure for hiccups exists] And so hiccups are relegated to the category of “orphan” symptoms—prevalent, distressing, characteristically unaddressed. Other such symptoms include muscle cramps, itchiness, muscle twitching, restless legs syndrome, loss or distortion of taste, dry mouth, and sweating. The success of palliative care depends on alleviating orphan symptoms: Every hiccup or itch or tingling foot, every flush of sweat or bout of constipation tethers patients to a raw state of awareness. “It’s a common reminder that you have chemotherapy, which is a constant reminder you have cancer, which is a constant reminder you’re facing your mortality,” Smith said. Treating hiccups offers medical relief in the form of escape. “It may make it possible for patients to have a few hours where they don’t think about cancer.” Jatoi said she often warns patients who are about to start a potentially hiccup-inducing regimen. “That helps patients speak up,” she said, which is a step toward finding relief. Oncologists can try prescribing a muscle-spasm treatment, for example, an off-label use that seems to help some patients. They might tweak the chemotherapy regimen to swap in drugs less likely to cause hiccups. The one treatment for hiccups that the FDA has approved—chlorpromazine, an antipsychotic first synthesized 72 years ago—can come with serious side effects, which research has shown to include low blood pressure and delirium. In the absence of clinically proven solutions, most hiccup sufferers are shepherded toward home remedies—breath-holding; drinking through hard-to-suck straws; swallowing spoonfuls of sugar, peanut butter, or vinegar. “None of them have been tested to see how effective they are,” Smith said. But without solid alternatives, he added, they’re worth trying. After all, unlike the hiccups themselves, “they’re completely harmless.” from https://ift.tt/DJToFG0 Check out http://natthash.tumblr.com |
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