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Tag: gastrointestinal symptoms

  • Beware the Ozempic Burp

    Beware the Ozempic Burp

    On the November morning when the sulfur burps began, Derron Borders was welcoming prospective students at the graduate school where he works in New York. Every few minutes, no matter how hard he tried to stop, another foul-smelling cloud escaped his mouth. “Burps that taste and smell like rotten eggs—I think that’s what I typed in Google,” he told me.

    Eventually, Borders learned that his diabetes medication was to blame. Sulfur burps appear to be a somewhat rare side effect of semaglutide, tirzepatide, and other drugs in their class, known as GLP-1 receptor agonists. Over the past several years, these medications have become more popular under the brand names Ozempic, Wegovy, and Mounjaro, as a diabetes treatment and a weight-loss drug. And as prescription numbers rise, a strange and unpleasant side effect has been growing more apparent too.

    GLP-1 receptor agonists are well known to cause gastrointestinal symptoms, including abdominal pain, diarrhea, and vomiting. In clinical trials of semaglutide for weight loss, 44 percent of participants experienced nausea and 31 percent had diarrhea. (The same conditions afflicted only about one-sixth of participants who received a placebo.) Burping, a.k.a. “eructation,” showed up in about 9 percent of those who got the drug, versus less than 1 percent of those who took a placebo. The FDA lists eructation as a possible side effect for semaglutide and tirzepatide alike.

    But I couldn’t find any information in the clinical-trial reports or FDA fact sheets about sulfur burps in particular, and neither Novo Nordisk nor Eli Lilly, the companies that make these drugs, responded to my inquiries. Laura Davisson, the director of medical weight management at West Virginia University Health Sciences, told me that more than 1,000 of her clinic’s patients are currently on a GLP-1 receptor agonist, and about one-fifth experience sulfur burps at first. For all but a handful of these patients, she said, the issue goes away after a few months. Holly Lofton, an obesity-medicine specialist at NYU, guesses that it affects just 2 percent of her patients.

    Experts aren’t sure why taking GLP-1 receptor agonists might lead to having smelly burps, but they have some theories. Davisson proposed that semaglutide boosts the number of bacteria in patients’ digestive tracts that produce hydrogen sulfide, a gas that can be expelled from either end of the digestive tract, and that smells (as Borders found) like rotten eggs. She also noted that the drugs slow down digestion, which could give the stomach more time to break down food and produce gas. In this situation, Lofton told me, the putrid air may escape most readily up through the mouth, because it’s lighter than the liquids and semi-solids that also fill the stomach. “Whatever’s on top will come up,” she said.

    Read: We’ve had a cheaper, more potent Ozempic alternative for decades

    Eating more than usual while on the medications seems to be a common trigger. Davisson said that certain foods, such as dairy, may also lead to more odorous emissions. “Sometimes it’s a matter of trial and error,” she said. “Some tips that we give people are things like: Don’t eat really heavy meals; don’t eat large portions at once; don’t eat right before bed.” In addition to these behavioral approaches, Craig Gluckman, a gastroenterologist at UCLA Health, told me he recommends antacids and anti-gas medications to patients with GLP-1-agonist-related sulfur burps. (Online, apple-cider vinegar is commonly recommended as a fix, but Gluckman said he would not recommend it.)

    The providers I spoke with said that, in general, patients tend to experience sulfur burps when they’re first starting an Ozempic-like drug, or raising their dose. That was the case for Crystal Garcia, an HR administrator in Texas who started taking semaglutide from a compounding pharmacy after her doctor told her she was prediabetic. (Garcia vlogs about her experience with weight-loss drugs.) Three months later, while out to breakfast at a restaurant, Garcia’s family started to complain about a gross and eggy smell. Garcia figured that the smell was coming from the food, but it lingered in the car after the meal. The family wondered whether Garcia’s young son had had an accident. “I was like, it could not be me. There’s no way,” she told me. But when she burped again, she was forced to change her mind.

    Many patients are unaware that sulfur burps are a possible side effect of their medication until they start, well, burping sulfur. For a while, Borders had no idea that his diabetes medicine might be the culprit; when he saw a physician’s assistant to discuss his issue, “Ozempic didn’t even come up,” he said. The side effect is relatively new to physicians. Earlier GLP-1 agonists didn’t seem to produce sulfur burps so frequently, Lofton said. In her practice, the phenomenon wasn’t really apparent until Ozempic hit the American market in 2018, and even then, she learned about it only from her patients. “I’d never heard of sulfur burps before I started prescribing this medicine,” she said.

    Read: Ozempic is about to be old news

    Though the sulfur burps are (physically) harmless, some patients do stop taking their diabetes or weight-loss drugs because of them, Lofton told me. But most, including Garcia and Borders, end up sticking with their program. As bad as the side effects may be, patients think the drugs’ benefits are worth it. “I have had a patient say that her burps smelled like poop,” Davisson said. But even then, she did not want to stop the medication.

    Rachel Gutman-Wei

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  • Norovirus Is Almost Impossible to Stop

    Norovirus Is Almost Impossible to Stop

    In one very specific and mostly benign way, it’s starting to feel a lot like the spring of 2020: Disinfection is back.

    “Bleach is my friend right now,” says Annette Cameron, a pediatrician at Yale School of Medicine, who spent the first half of this week spraying and sloshing the potent chemical all over her home. It’s one of the few tools she has to combat norovirus, the nasty gut pathogen that her 15-year-old son was recently shedding in gobs.

    Right now, hordes of people in the Northern Hemisphere are in a similarly crummy situation. In recent weeks, norovirus has seeded outbreaks in several countries, including the United Kingdom, Canada, and the United States. Last week, the U.K. Health Security Agency announced that laboratory reports of the virus had risen to levels 66 percent higher than what’s typical this time of year. Especially hard-hit are Brits 65 and older, who are falling ill at rates that “haven’t been seen in over a decade.”

    Americans could be heading into a rough stretch themselves, Caitlin Rivers, an infectious-disease epidemiologist at Johns Hopkins University, told me, given how closely the U.S.’s epidemiological patterns tend to follow those of the U.K. “It does seem like there’s a burst of activity right now,” says Nihal Altan-Bonnet, a norovirus researcher at the National Institutes of Health. At her own practice, Cameron has been seeing the number of vomiting and diarrhea cases among her patients steadily tick up. (Other pathogens can cause gastrointestinal symptoms as well, but norovirus is the most common cause of foodborne illness in the United States.)

    To be clear, this is more a nauseating nuisance than a public-health crisis. In most people, norovirus triggers, at most, a few miserable days of GI distress that can include vomiting, diarrhea, and fevers, then resolves on its own; the keys are to stay hydrated and avoid spreading it to anyone vulnerable—little kids, older adults, the immunocompromised. The U.S. logs fewer than 1,000 annual deaths out of millions of documented cases. In other high-income countries, too, severe outcomes are very rare, though the virus is far more deadly in parts of the world with limited access to sanitation and potable water.

    Still, fighting norovirus isn’t easy, as plenty of parents can attest. The pathogen, which prompts the body to expel infectious material from both ends of the digestive tract, is seriously gross and frustratingly hardy. Even the old COVID standby, a spritz of hand sanitizer, doesn’t work against it—the virus is encased in a tough protein shell that makes it insensitive to alcohol. Some have estimated that ingesting as few as 18 infectious units of virus can be enough to sicken someone, “and normally, what’s getting shed is in the billions,” says Megan Baldridge, a virologist and immunologist at Washington University in St. Louis. At an extreme, a single gram of feces—roughly the heft of a jelly bean—could contain as many as 5.5 billion infectious doses, enough to send the entire population of Eurasia sprinting for the toilet.

    Unlike flu and RSV, two other pathogens that have bounced back to prominence in recent months, norovirus mainly targets the gut, and spreads especially well when people swallow viral particles that have been released in someone else’s vomit or stool. (Despite its “stomach flu” nickname, norovirus is not a flu virus.) But direct contact with those substances, or the food or water they contaminate, may not even be necessary: Sometimes people vomit with such force that the virus gets aerosolized; toilets, especially lidless ones, can send out plumes of infection like an Air Wick from hell. And Altan-Bonnet’s team has found that saliva may be an unappreciated reservoir for norovirus, at least in laboratory animals. If the spittle finding holds for humans, then talking, singing, and laughing in close proximity could be risky too.

    Read: Whatever happened to toilet plumes?

    Once emitted into the environment, norovirus particles can persist on surfaces for days—making frequent hand-washing and surface disinfection key measures to prevent spread, says Ibukun Kalu, a pediatric infectious-disease specialist at Duke University. Handshakes and shared meals tend to get dicey during outbreaks, along with frequently touched items such as utensils, door handles, and phones. One 2012 study pointed to a woven plastic grocery bag as the source of a small outbreak among a group of teenage soccer players; the bag had just been sitting in a bathroom used by one of the girls when she fell sick the night before.

    Once a norovirus transmission chain begins, it can be very difficult to break. The virus can spread before symptoms start, and then for more than a week after they resolve. To make matters worse, immunity to the virus tends to be short-lived, lasting just a few months even against a genetically identical strain, Baldridge told me.

    Day cares, cruise ships, schools, restaurants, military training camps, prisons, and long-term-care facilities can be common venues for norovirus spread. “I did research with the Navy, and it just goes through like wildfire,” often sickening more than half the people on tightly packed ships, says Robert Frenck, the director of the Vaccine Research Center at Cincinnati Children’s Hospital. Households, too, are highly susceptible to spread: Once the virus arrives, the entire family is almost sure to be infected. Baldridge, who has two young children, told me that her household has weathered at least four bouts of norovirus in the past several years.

    (A pause for some irony: In spite of norovirus’s infectiousness, scientists did not succeed in culturing it in labs until just a few years ago, after nearly half a century of research. When researchers design challenge trials to, say, test new vaccines, they still need to dose volunteers with norovirus that’s been extracted from patient stool, a gnarly practice that’s been around for more than 50 years.)

    Norovirus spread doesn’t have to be a foregone conclusion. Some people do get lucky: Roughly 20 percent of European populations, for instance, are genetically resistant to common norovirus strains. “So you can hope,” Frenck told me. For the rest of us, it comes down to hygiene. Altan-Bonnet recommends diligent hand-washing, plus masking to ward off droplet-borne virus. Sick people should isolate themselves if they can. “And keep your saliva to yourself,” she told me.

    Read: The stomach-flu mystery

    Rivers and Cameron have both managed to halt the virus in their homes in the past; Cameron may have pulled it off again this week. The family fastidiously scrubbed their hands with hot water and soap, donned disposable gloves when touching shared surfaces, and took advantage of the virus’s susceptibility to harsh chemicals and heat. When her son threw up on the floor, Cameron sprayed it down with bleach; when he vomited on his quilt, she blasted it twice in the washing machine on the sanitizing setting, then put it through the dryer at a super high temp. Now a couple of days out from the end of their son’s sickness, Cameron and her husband appear to have escaped unscathed.

    Norovirus isn’t new, and this won’t be the last time it hits. In a lot of ways, “this is back to basics,” says Samina Bhumbra, the medical director of infection prevention at Riley Children’s Hospital. After three years of COVID, the world has gotten used to thinking about infections in terms of airways. “We need to recalibrate,” Bhumbra told me, “and remember that other things exist.”

    Katherine J. Wu

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  • Is COVID a Common Cold Yet?

    Is COVID a Common Cold Yet?

    At the start of the coronavirus pandemic, one of the worst things about SARS-CoV-2 was that it was so new: The world lacked immunity, treatments, and vaccines. Tests were hard to come by too, making diagnosis a pain—except when it wasn’t. Sometimes, the symptoms of COVID got so odd, so off-book, that telling SARS-CoV-2 from other viruses became “kind of a slam dunk,” says Summer Chavez, an emergency physician at the University of Houston. Patients would turn up with the standard-issue signs of respiratory illness—fever, coughing, and the like—but also less expected ones, such as rashes, diarrhea, shortness of breath, and loss of taste or smell. A strange new virus was colliding with people’s bodies in such unusual ways that it couldn’t help but stand out.

    Now, nearly three years into the crisis, the virus is more familiar, and its symptoms are too. Put three sick people in the same room this winter—one with COVID, another with a common cold, and the third with the flu—and “it’s way harder to tell the difference,” Chavez told me. Today’s most common COVID symptoms are mundane: sore throat, runny nose, congestion, sneezing, coughing, headache. And several of the wonkier ones that once hogged headlines have become rare. More people are weathering their infections with their taste and smell intact; many can no longer remember when they last considered the scourge of “COVID toes.” Even fever, a former COVID classic, no longer cracks the top-20 list from the ZOE Health Study, a long-standing symptom-tracking project based in the United Kingdom, according to Tim Spector, an epidemiologist at King’s College London who heads the project. Longer, weirder, more serious illness still manifests, but for most people, SARS-CoV-2’s symptoms are getting “pretty close to other viruses’, and I think that’s reassuring,” Spector told me. “We are moving toward a cold-like illness.”

    That trajectory has been forecast by many experts since the pandemic’s early days. Growing immunity against the coronavirus, repeatedly reinforced by vaccines and infections, could eventually tame COVID into a sickness as trifling as the common cold or, at worst, one on par with the seasonal flu. The severity of COVID will continue to be tempered by widespread immunity, or so this thinking goes, like a curve bending toward an asymptote of mildness. A glance at the landscape of American immunity suggests that such a plateau could be near: Hundreds of millions of people in the U.S. have been vaccinated multiple times, some even quite recently with a bivalent shot; many have now logged second, third, and fourth infections with the virus. Maybe, just maybe, we’re nearing the level of cumulative exposure at which COVID gets permanently more chill. Then again? Maybe not—and maybe never.

    Read: What does it mean to care about COVID anymore?

    The recent trajectory of COVID, at least, has been peppered with positive signs. On average, symptoms have migrated higher up the airway, sparing several vulnerable organs below; disease has gotten shorter and milder, and rates of long COVID seem to be falling a bit. Many of these changes roughly coincided with the arrival of Omicron in the fall of 2021, and part of the shift is likely attributable to the virus itself: On the whole, Omicron and its offshoots seem to prefer infecting cells in the nose and throat over those in the lungs. But experts told me the accumulation of immune defenses that preceded and then accompanied that variant’s spread are almost certainly doing more of the work. Vaccination and prior infection can both lay down protections that help corral the virus near the nose and mouth, preventing it from spreading to tissues elsewhere. “Disease is really going to differ based on the compartment that’s primarily infected,” says Stacey Schultz-Cherry, a virologist at St. Jude Children’s Research Hospital. As SARS-CoV-2 has found a tighter anatomical niche, our bodies have become better at cornering it.

    With the virus largely getting relegated to smaller portions of the body, the pathogen is also purged from the airway faster and may be less likely to be passed to someone else. On the individual level, a sickness that might have once unfurled into pneumonia now gets subdued into barely perceptible sniffles and presents less risk to others; on the population scale, rates of infection, hospitalization, and death go down.

    This is how things usually go with respiratory viruses. Repeat tussles with RSV tend to get progressively milder; post-vaccination flu is usually less severe. The few people who catch measles after getting their shots are less likely to transmit the virus, and they tend to experience such a trivial course of sickness that their disease is referred to by a different name, “modified” measles, says Diane Griffin, a virologist and an immunologist at Johns Hopkins University.

    It’s good news that the median case of COVID diminished in severity and duration around the turn of 2022, but it’s a bit more sobering to consider that there hasn’t been a comparably major softening of symptoms in the months since. The full range of disease outcomes—from silent infection all the way to long-term disability, serious disease, and death—remains in play as well, for now and the foreseeable future, Schultz-Cherry told me. Vaccination history and immunocompromising conditions can influence where someone falls on that spectrum. So too can age as well as other factors such as sex, genetics, underlying medical conditions, and even the dose of incoming virus, says Patricia García, a global-health expert at the University of Washington.

    New antibody-dodging viral variants could still show up to cause more severe disease even among the young and healthy, as occasionally happens with the flu. The BA.2 subvariant of Omicron, which is more immune-evasive than its predecessor BA.1, seemed to accumulate more quickly in the airway, and it sparked more numerous and somewhat gnarlier symptoms. Data on more recent Omicron subvariants are still being gathered, but Shruti Mehta, an epidemiologist at Johns Hopkins, says she’s seen some hints that certain gastrointestinal symptoms, such as vomiting, might be making a small comeback.

    Read: Will we get Omicron’d again?

    All of this leaves the road ahead rather muddy. If COVID will be tamed one day into a common cold, that future definitely hasn’t been realized yet, says Yonatan Grad, an epidemiologist at Harvard’s School of Public Health. SARS-CoV-2 still seems to spread more efficiently and more quickly than a cold, and it’s more likely to trigger severe disease or long-term illness. Still, previous pandemics could contain clues about what happens next. Each of the past century’s flu pandemics led to a surge in mortality that wobbled back to baseline after about two to seven years, Aubree Gordon, an epidemiologist at the University of Michigan, told me. But SARS-CoV-2 isn’t a flu virus; it won’t necessarily play by the same epidemiological rules or hew to a comparable timeline. Even with flu, there’s no magic number of shots or past infections that’s known to mollify disease—“and I think we know even less about how you build up immunity to coronaviruses,” Gordon said.

    The timing of when and how those defenses manifest could matter too. Almost everyone has been infected by the flu or at least gotten a flu shot by the time they reach grade school; SARS-CoV-2 and COVID vaccines, meanwhile, arrived so recently that most of the world’s population met them in adulthood, when the immune system might be less malleable. These later-in-life encounters could make it tougher for the global population to reach its severity asymptote. If that’s the case, we’ll be in COVID limbo for another generation or two, until most living humans are those who grew up with this coronavirus in their midst.

    COVID may yet stabilize at something worse than a nuisance. “I had really thought previously it would be closer to common-cold coronaviruses,” Gordon told me. But severity hasn’t declined quite as dramatically as she’d initially hoped. In Nicaragua, where Gordon has been running studies for years, vaccinated cohorts of people have endured second and third infections with SARS-CoV-2 that have been, to her disappointment, “still more severe than influenza,” she told me. Even if that eventually flips, should the coronavirus continue to transmit this aggressively year-round, it could still end up taking more lives than the flu does—as is the case now.

    Wherever, whenever a severity plateau is reached, Gordon told me that our arrival to it can be confirmed only in hindsight, “once we look back and say, ‘Oh, yeah, it’s been about the same for the last five years.’” But the data necessary to make that call are getting harder to collect as public interest in the virus craters and research efforts to monitor COVID’s shifting symptoms hit roadblocks. The ZOE Health Study lost its government funding earlier this year, and its COVID-symptom app, which engaged some 2.4 million regular users at its peak, now has just 400,000—some of whom may have signed up to take advantage of newer features for tracking diet, sleep, exercise, and mood. “I think people just said, ‘I need to move on,’” Spector told me.

    Mehta, the Johns Hopkins epidemiologist, has encountered similar hurdles in her COVID research. At the height of the Omicron wave, when Mehta and her colleagues were trying to find people for their community studies, their rosters would immediately fill up past capacity. “Now we’re out there for weeks” and still not hitting the mark, she told me. Even weekly enrollment for their long-COVID study has declined. Sign-ups do increase when cases rise—but they drop off especially quickly as waves ebb. Perhaps, in the view of some potential study volunteers, COVID has, ironically, become like a common cold, and is thus no longer worth their time.

    For now, researchers don’t know whether we’re nearing the COVID-severity plateau, and they’re worried it will get only more difficult to tell. Maybe it’s for the best if the mildness asymptote is a ways off. In the U.S. and elsewhere, subvariants are still swirling, bivalent-shot uptake is still stalling, and hospitalizations are once more creeping upward as SARS-CoV-2 plays human musical chairs with RSV and flu. Abroad, inequities in vaccine access and quality—and a zero-COVID policy in China that stuck around too long—have left gaping immunity gaps. To settle into symptom stasis with this many daily deaths, this many off-season waves, this much long COVID, and this pace of viral evolution would be grim. “I don’t think we’re quite there yet,” Gordon told me. “I hope we’re not there yet.”

    Katherine J. Wu

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