Health | The Atlantic

The ‘Cuteservative’ in Chief

2026-10-31T10:00:00-04:00

Inside a podcast studio at Turning Point USA’s headquarters last month, a former witch sat in a pink velvet armchair, telling Alex Clark about the demon that stalked her house. Even though this self-described witch, known on TikTok as @yourspiritualbigsis, had only ever used her powers for good, she believed that practicing sorcery had made her vulnerable to satanic forces. The demon—10, maybe 15 feet tall, whose face had “divots” for eyes—had tormented her, she said, until she spoke the name “Jesus” out loud and became a Christian.

Clark, whose Culture Apothecary is one of America’s top wellness podcasts, told her guest that she was going to ask “counter questions,” as she does with everyone she interviews. In this case: If the spells she was doing were technically producing good—helping people make money, get pregnant, pass a test—why is that evil? How can Christians tell whether someone has the spiritual gift of prophecy or they’re harnessing dark power? Clark wasn’t concerned about whether sorcery was real—“It is real,” she said—but when her guest brought up the occult sacrifice of babies procured through a sex-trafficking network supported by the government and Hollywood, Clark had no further questions.

This was just another day in the studio. Since 2024, when she launched her podcast with a mission to “heal a sick culture” and to do so “physically, emotionally, and spiritually,” Clark has welcomed a wild array of guests, united only by their willingness to contradict conventional wisdom and generally accepted facts. Listening to Culture Apothecary, you might hear a regenerative farmer recommend the subcutaneous fat of a “healthy, happy pig” as a miracle skin-care ingredient, a chiropractor talk about testing muscle strength using “homeopathically charged frequencies,” the self-described Christian nationalist Doug Wilson suggest spanking as a form of biblical discipline for children, or leaders in the “Make America Healthy Again” movement disavow vaccines and industrial agriculture.

On the podcast, Clark positions herself not as an expert but as a question-asking woman of the people. Depending on who you talk with—and I spoke with Clark’s colleagues, her critics, her close friends, her mom—she’s either a powerful force connecting everyday women to the GOP or an agent of chaos. She has been the Republican commentator posting bikini photos while her peers post pictures in cardigans and the single 33-year-old podcasting about child-rearing. By her own account, she is also the contributor at TPUSA, the late Charlie Kirk’s conservative organization, who causes the nonprofit the most trouble with the Trump administration.

Maggie Shannon for The Atlantic

Alex Clark and a former witch, known on TikTok as @yourspiritualbigsis, during a taping of her podcast, Culture Apothecary, in September

Clark grew up in an evangelical, conservative home in southern Indiana. After high school, she worked at Sephora and took classes at a community college, and planned to transfer to a four-year school for fashion merchandising and journalism. But then she started an internship at a Louisville, Kentucky, radio station, which led to a full-time job as an anchor and the unofficial Millennial-woman correspondent for a morning show. She had always loved pop culture and politics, and came to TPUSA in 2019 so that she could air her conservative views while discussing Dancing With the Stars. Even before Robert F. Kennedy Jr. and Donald Trump teamed up, she pivoted to podcasting about wellness because she thought that talking about organic food, herbal medicine, and suspicions about vaccines could bring more women into the GOP. When the MAHA movement came to Washington, Clark’s own profile rose, and soon she had the attention of some of the most powerful men in the country.

But recently, MAHA and MAGA have started to drift apart. MAHA is failing to draw hordes of voters to Republicans; the Trump administration has failed MAHA on many of the issues Clark cares about. As the rift widens, Clark is stretching to keep a foot on each side and figuring out, if she does have to choose one, how to take her audience of MAHA moms and conservative young women along with her.

Between tapings, Clark ate takeout from a seed-oil-free restaurant as she reviewed podcast transcripts and a spreadsheet of upcoming episodes, reacting to them with facial expressions worthy of a mime. Her team member took notes while she dictated episode titles (“He Was Gay, Then Everything Changed” and “Acetaminophen Before Age 4: What Parents Should Know”). The whole time, she exuded the energy of someone who had incredible gossip to share. The minute I stepped away to check out a rack of Culture Apothecary sweatshirts (Trust Farms, Not Pharma), Clark shrieked. “We’re all peeing our pants, screaming, crying, throwing up,” she said, her eyes wide and made even more dramatic by false lashes. Taylor Swift had just announced a new single. She looked for clues in Swift’s post and predicted that the music video would debut later that week at the MTV Video Music Awards. (She was right.)

Like many 30-something women, she is devoted to Taylor Swift, and, however unfiltered Clark can sometimes seem, like Swift, she aims to make every detail of her world matter. Her studio’s forest-green wallpaper includes illustrations of her preferred remedies for America’s ailing culture: raw milk, steak, butter, wildflowers, hair bows, the Bible. Her podcast-planning spreadsheet is in that same bespoke shade of green, which she developed with graphic designers. (She calls it “Forks, Washington,” after the town made famous in Twilight.) Even her off-the-cuff X posts can be seen as part of her brand—a girl speaking her mind, even if that includes insinuating that Candace Owens performed oral sex on Vladimir Putin. The ads she writes for the show might seem borderline nonsensical—in one ad for a clean-beauty company, for reasons that I do not understand, she includes a monologue about a taxidermied possum who wears a cheerleading uniform and is named Gerald—but according to Clark, that strategy tends to bring high returns for her sponsors. What listener is going to want to skip those?

Not the “Cuteservatives,” as Clark calls her fandom. They keep tabs on her personal life, too, and at the TPUSA Women’s Leadership Summit in June, she orchestrated an announcement for them. “There’s one thing I haven’t told you guys,” she said. The stage lights went out, and when they came back on, she was standing beside Vance Voetberg, the bespectacled author of the MAHA fitness Substack Running on Butter. On her finger was a diamond ring. “I’m engaged!” The crowd screamed. Later, on Instagram, she described him as her “‘BUTTER’ half.” She has since released a steady stream of content about their small summer wedding at his family home in rural Washington State: a recipe for the prosciutto butter they served, details about the outfits she picked for Voetberg and her maid of honor, and a two-hour interview with her new husband, in which she revealed that she walked down the aisle to Swift’s “You Are In Love” and gifted all of her guests a Jaspr, perhaps the most aesthetically pleasing air purifier in existence.

Maggie Shannon for The Atlantic

Clark and Caroline Lanier, a social-media admin, check out what was probably, if Clark’s obsessions are any indication, a post about Taylor Swift.

Clark is also, like Swift, a woman of distinct eras. For most of her life, she was focused not on health but pop culture. MTV was banned in her childhood home, but when she saw Britney Spears’s “I’m a Slave 4 U” music video at a sleepover, “I was absolutely mesmerized,” she said. She idolized Spears, Christina Aguilera, and Jessica Simpson. She was also so conservative “that she’d make Rush Limbaugh look like a liberal,” her high-school radio and TV teacher, Timothy Dench, told me.

She knew even then that she wanted an audience made up of young women. She dreamed about being a fashion writer at Teen Vogue or Seventeen, but got the job on a local radio show. Listeners knew her as a fast-food connoisseur and the “Chicken Nugget Princess”—she ate nuggets at least once a day and would peel off the skin, eat that, then turn to the meat. By 2019, she was co-hosting an Indianapolis morning show, but her superiors were telling her to stop bringing up politics on air and on Twitter. She imagined a show that would combine her passions for the GOP and for pop culture—“TMZ and Fox News if they had a baby,” she told me—and pitched it to Charlie Kirk at TPUSA as a way to show women that Republicans could be cool. POPlitics became TPUSA’s first show.

Clark’s wellness era started around 2020. She was skeptical of the COVID shot and never got it, and, after watching the Hulu series Dopesick, became convinced that Big Pharma’s misdeeds were the greatest true-crime story ever told. Practically overnight, she emptied out her fridge and began her transformation into someone who keeps a tiny vial of unrefined sea salt in her purse, sits in front of red light every day, and makes a morning smoothie with six different types of powder, glyphosate-free oats, aloe-vera juice, Cowboy Colostrum, collagen, creatine, strawberries, cherries, pineapple, peaches, and an entire avocado.

And she noticed that her audience was moving toward wellness with her. Whenever she had a guest on to talk about why, say, women should be suspicious of the pill, viewership spiked, so she met with Kirk about rebranding her show around health. “If we are the ones championing these issues, we will grab all the female voters,” she remembers telling him in July 2024. Two weeks before Culture Apothecary was scheduled to debut, she watched RFK Jr. endorse Trump live at a rally in Glendale, Arizona. The crowd was so electric it reminded her of Swift’s Eras Tour.

A month later, Clark got a standing ovation at the Capitol. Her speech at a Senate roundtable, on behalf of Millennial mothers outraged by food and pharmaceutical corporations harming their children, cemented her as MAHA’s big sister. Sponsors and listeners flocked to Culture Apothecary, and Clark, who now had the attention of both stay-at-home moms and powerful politicians, became the person most visibly fusing MAHA and MAGA for women.

Over the past year, that union has gotten shakier. Trump’s accord with MAHA—his promise to let RFK Jr. “run wild” on health and food—has been one defining force in his second administration, and the health secretary has managed to remake federal vaccine policy, change the food pyramid, and extract some voluntary commitments from companies about food dye. But many MAHA supporters feel like they were owed more—especially when it came to regulating food and pesticides. The disillusionment has gotten bad enough that one of MAHA’s top leaders, Calley Means, resigned from the Trump administration less than two weeks before the midterms, reportedly out of frustration that the government wasn’t advancing MAHA’s food policy.

Maggie Shannon for The Atlantic

Clark’s bookshelf at her home

Clark, meanwhile, keeps getting angrier. In January, she and other MAHA activists were abruptly disinvited from an event at the Department of Health and Human Services—which they believe was because MAHA had recently launched a petition to fire the head of the EPA. Someone later sent Clark a picture of the check-in table: On the front page of the “Not Permitted List” was her photograph. (In response to a request for comment, HHS referred me to the White House, which did not comment on the disinvitation; a spokesperson told me, “The MAHA coalition has never been stronger or more empowered.”) After the White House and the Supreme Court both came down in favor of the weed killer glyphosate, the chemical that MAHA hates most, Clark headlined a rally outside the Supreme Court Building, wearing a camo jacket that read: I TURN INTO ERIN BROCKOVICH WHEN I’M ANGRY.

Clark thinks that Trump is a true MAHA believer (despite his love of McDonald’s) and that he’s getting hemmed in by those around him. Before the April rally, Trump met with her and other MAHA leaders, and he kept talking about making an executive order about vaccines. According to Clark, what he described was so extreme that if she shared the details, they would “make him look bad right before midterms.” She believes that his advisers steered him away from it. (Trump did later issue an executive order reducing the number of diseases included in the childhood-vaccination schedule. The White House spokesperson wrote in an email that “President Trump wants to execute on ideas that are durable, long-lasting, and hold up in court to ensure the permanence” of the MAHA movement.) Clark still loves the president, but “I have zero stomach for conservative commentators that all they do is blow the Trump admin,” she said. “Sorry to be crass.” As a Republican, she’d be sad if the GOP loses this cycle, but as a MAHA leader, “then I’d kind of get to flex an ‘I told you so’” about the party needing her audience’s vote.

Clark’s own career doesn’t necessarily hinge on the White House’s approval or MAHA’s political viability. Her wellness episodes were doing well before the MAHA label existed, and she’s proved that she has an instinct for where the conservative movement is going and how to get American women—even those who don’t think of themselves as political—to follow it. Maybe this election will mark the end of an era for MAHA. But Clark is already entering a new one herself.

After a day of taping, Clark took me back to her apartment in Scottsdale, Arizona, where she now lives with her butter half. It still looked like a Millennial girl’s Barbie Dreamhouse: maximalist floral wallpaper, a brocade velvet shower curtain, black-and-white striped accent chairs. A Jaspr air purifier hummed in the corner, and on the floor, her Pekingese, Mochi, ate raw rabbit and organic pumpkin puree from his dog bowl and drank glass-bottled, micro-plastic-tested Loonen water.

Voetberg had homemade cookies and raw milk waiting for us. He is a national-champion fiddle player and competitive runner, who grew up homeschooled and one of 10 kids. He’d been a fan of Clark’s podcast for years, and after lobbying mutual friends to set them up, he and Clark had their first date last fall, got engaged over Memorial Day weekend, and got married at the end of August. They’d just returned from their Bora-Bora honeymoon. “We have sex now!” She laughed and leaned over their glasses of raw milk to kiss him.

Clark’s primary goal in life was always to get married and have a family. When, at 23, she appeared on the Fox dating show Coupled, she was so earnest about looking for a husband that the producers told her she needed to relax, she said. Over the years, being single became an occupational hazard. Groypers, the followers of the alt-right leader Nick Fuentes, would DM her pictures of empty egg cartons and tell her that she was useless because she wasn’t married with kids; feminists criticized her for being an unmarried career woman who told other women to focus on their families.

Now that she’s married, she told me, she will not be a tradwife who embodies a pioneer-esque domestic crunchiness: A nail artist comes to her house every two weeks, and she “wouldn’t last five seconds living more than 10 minutes away from a Sephora.” Nor does she plan to adhere to strict domestic gender roles. Voetberg told me that he takes the lead on household chores; he made those cookies and stepped in to cook chili for dinner while Clark was busy talking with me. She has said she will put family first, but she also wants a career. Between that and her choice to continue using the last name Clark professionally, some people on the right call her a closet feminist. She is not, she told me, and believes that feminism has been a “net negative.” Voetberg chimed in to say that he could see how people might think that she has benefited from the movement. But Clark kept returning to the idea that, overall, feminism had badly served women by pushing them to prioritize their careers over motherhood.

Maggie Shannon for The Atlantic

Alex Clark and her husband, Vance Voetberg, at home with their dog, Mochi

Her latest Culture Apothecary series—“Wife School”—certainly has gone well beyond any feminist’s comfort zone. In these interviews, she asked married Christian women about how to be a good biblical wife. Guests had tips on household organization but also on giving one’s husband input while still allowing him to be the family’s final decision maker. In one particularly controversial episode, the Christian writer Tilly Dillehay said that, for the health of a marriage, women should have sex with their husbands even when they do not want to.

If part of MAHA’s success was that it could speak to people across the political spectrum, the issues Clark is now exploring almost certainly don’t. Over chili, Voetberg said that he thought aspects of first-wave feminism had been good. Like the right to vote, I suggested.

“Don’t get her started on that,” Voetberg said.

“I’m not gonna advocate to repeal the Nineteenth!” Clark replied, although some people in the MAGAverse insist that the Nineteenth Amendment was a mistake that should, like Roe, be corrected. I asked whether they’d vote as a family, and they started talking about landownership, which was once attached to suffrage, and how the question of who should vote in America was a “giant, giant topic,” as Voetberg put it. Clark joked—maybe?—that she’d love it if she needed her husband’s permission to open a bank account, as American women once did. (Later, she wrote in an email that she and Voetberg had not consciously adopted household voting as a practice—“We just automatically vote the same.”)

When she has kids—and she wants to be pregnant before January—she said that she may look at her newborn and decide to never do another interview again. But her current plan is to keep working. Her audience loved “Wife School,” she said, and she is sensing another groundswell like the one she saw toward health—this one toward human connection, in community and family. Championing those issues could be another way to grab female voters: Moms of all political persuasions can probably agree that, as a recent Culture Apothecary episode argued, “babies don’t need all that STUFF!”—even if many of them are not quite ready to give their husbands the final say on their family decisions, finances, or sex lives.

Knowing how seriously to take Clark’s more provocative stances can be difficult. If Taylor Swift is one of Clark’s idols, so is 1980s and ’90s Howard Stern: He was clever and funny, and wasn’t afraid to be shocking. (“I’m not saying, as a Christian, that I agree with the type of content he was doing,” she said.) For similar reasons, she admires the early days of the sex-and-dating podcast Call Her Daddy, when the hosts graphically detailed their own exploits. “I don’t ever want people to feel comfortable,” Clark said—and her more MAHA-leaning listeners might not be, if she doubles down on a conservative vision of family and femininity. But, she told me, “I love controversy.” It keeps people listening. “Whether you listen to me because you love me, or listen to me because you hate me,” she said, “you’re still a fan either way.”

Foie Gras Is Tearing D.C. Apart

2026-10-31T09:48:10-04:00

In Washington, D.C., voters are thinking more than they usually would about ducks. The most contentious question on the ballot in the nation’s capital this midterm-election cycle is a referendum on foie gras, the extra-fatty liver delicacy made by overfeeding ducks (and sometimes geese) through a tube stuck down their esophagus. Selling foie gras has been banned in New York City, Pittsburgh, California, India, and Brazil; Target won’t stock it. On Tuesday, D.C. residents will decide: Should their restaurants still be able to serve it?

In the lead-up to the election, anti-foie-gras advocates have imported Olivia Gray, a four-and-a-half-pound male duck from Maryland, to act as their mascot. A Capitol Hill restaurant has countered with a foie-gras tasting menu. A local publication predicted this week that the year’s hottest Halloween costumes would be foie gras–related. Residents are debating the usual moral quandaries of this issue: Is force-feeding ducks a practice so cruel it should be banned? Do people have the right to eat whatever they find delicious? But the real reason the ballot initiative is tearing D.C. apart is that it’s become a proxy for arguments about democracy.

The referendum, known as Initiative 86, would ban “force-feeding a bird for the purpose of enlarging the bird’s liver beyond normal size” within the district, as well as the sale or importation of any products resulting from such practices. It amassed more valid signatures from D.C. residents than any other ballot initiative in the city’s history—more, even, than Initiative 71, the referendum on recreational cannabis that, when passed in 2014, made it possible to (legally) buy a joint four blocks from the White House. Everyone I spoke with, including foie-gras fans, expects Initiative 86 to pass. Ballot measures tend to do well here, and proponents are essentially asking voters to choose duck happiness over a food they’ve probably never eaten.

The pro-ban side, headed by a group called Pro-Animal DC, has spent more than $470,000 lobbying for Initiative 86 to pass. Most of that money was spent this summer on hiring people to collect all of those signatures, a spokesperson for the organization told me. Supporters have been hanging SAVE THE DUCKS posters at Metro stops around the city. Olivia the duck has been making frequent appearances, including co-hosting a panel at George Washington University’s law school. Meghan Abrego, who bought Olivia on eBay when he was just an egg (and Abrego thought he was female), told me that she’s feeling optimistic heading into Election Day. The real question, she said, is not whether the ban will pass, but “What states will pick it up next?”

The anti-ban contingent is not formally organized. Few people seem eager to be targeted as pro–foie gras activists: Bart Hutchins, a local chef who has become the face of the opposition to Initiative 86, told me he has received death threats and has been followed to his car since writing an op-ed opposing the ban in The Washington Post. Hutchins co-owns Butterworth’s, the Capitol Hill restaurant serving the foie-gras tasting menu in protest of the referendum. He told me that the two farms that produce virtually all U.S. foie gras are run ethically; when he has visited the farm he procures Butterworth’s livers from, he said, the ducks don’t actually seem to mind gavage much. Sales from the tasting menu will benefit Hutchins’s Foie Gras Legal Defense Fund, which he says will be put toward mounting a challenge should the ban pass and financially supporting chefs who are fined for continuing to serve the dish, as he intends to do.

This fight is a microcosm of questions about money in politics and what powerful forces might really be behind a grassroots movement. Hutchins and his allies have argued that animal-rights groups are trying to, effectively, force their political views down District residents’ gullets: The initiative is mostly funded by the national organization Pro-Animal Future, which is based in Oregon; Dr. Bronner’s Magic Soaps, headquartered in California, has also contributed money. (Even Olivia is not a D.C. resident.) On the opposing side, a major foie-gras producer based in New York is already rallying its lawyers to challenge the ban if it passes, Axios reported this week.

National organizations fund the activities of local chapters all the time, but D.C. is a particularly attractive city for outside interest groups to fund ballot initiatives: Because of its national prominence, initiatives that pass here are more likely to inspire similar actions across the country. And because its civic-minded voters are packed into a tiny geographic area, gathering petition signatures is easy. Six citizen initiatives have reached the D.C. ballot since 2014, and nearly 90 percent of the total funding for them came from outside the District. As much as they’re arguing about the merits of foie gras, Washingtonians are arguing about astroturfing.

Another popular argument against Initiative 86 is that no one in D.C. should be wasting any time on such a small issue in the first place. Yet I was ready to do my own civic duty. On Wednesday, I made my way to a church to meet Abrego, who was pushing Olivia the duck around in a stroller. Abrego wanted Olivia to appear at a town hall being convened there, but the church wouldn’t let Olivia in, so we stood outside. Some attendees recognized the duck and tried to pet him; D.C.’s Democratic nominee for mayor gave him a high five.

Then I headed from the church to Butterworth’s. Waiting for me were four courses of foie gras, including a Waldorf salad laid on a bed of “foie gras snow” and a “foie gras Twinkie” served with foie-gras ice cream. I’d had foie gras once before on the urging of someone who said the taste would change my life, but I’ve never understood the hype. I still found Butterworth’s version almost disgustingly rich; the duck breast, however, was a star. As I ate, Hutchins made sure I understood that his foie gras comes from ducks that live in open barns and keep to a vegetarian diet; the liver and breast on my plate may have come from the same animal, he said, which helps make farming more sustainable. A man sitting next to me, who said he was a Trump-administration staffer but didn’t volunteer his name, described himself as a foie-gras enthusiast. Nearby, another table started chanting, “Olé, olé, olé, olé; foie gras, foie gras” to the tune of the soccer anthem.

As an on-again, off-again vegetarian, I gravitate toward meat that is so thoroughly estranged from its animal origins that I could imagine it grew on a tree—like a chicken nugget. All in all, the ducks that made my meals at Butterworth’s probably had a better life than most animals I consume. Still, in the lulls in my conversation with Hutchins, my mind would sometimes flash back to Olivia in the stroller, or to the videos I’d seen earlier that day of ducks with metal tubes down their throat. Even if the birds live in an open barn and eat no meat, their livers swell up to 10 times their normal size. After about two weeks of force-feeding, the ducks get so fat they can’t really move.

Foie gras is a low-hanging source of suffering, and using a ballot initiative to bring the issue to a vote seems like a healthy-enough expression of democracy—certainly more healthy than eating as much foie gras as I did. In the Butterworth’s bathroom after my meal, I found myself staring at the rabbits on the wallpaper, feeling sick. Maybe I wasn’t built to handle that much liver. Or maybe the campaign and the backlash had both succeeded in forcing me to think about the political and moral dimensions of my food. That’s democracy at work.

Doctors Say a Rare Kind of Measles Is on the Rise

2026-10-30T07:00:00-04:00

Each October, after the last of the tobacco has been harvested and the apple jam canned, Amish communities begin celebrating the months-long “wedding season.” Twice a week, hundreds of celebrants pack into a home to watch a young couple wed and share a meal. These gatherings, however joyful, add to the worries of Roberta Devers, a home-birth midwife in Lancaster County, Pennsylvania. At her prenatal appointments, she’s been asking mothers-to-be: With all of the celebrations, how are you going to keep yourself safe from measles?

In Pennsylvania, at least 1,398 people have been infected with measles this year, according to recent estimates from the state health department; the Amish community, which has significantly lower vaccination rates than other Pennsylvanians, has been especially hard hit. Experts caution that the actual number of infections is likely much higher. “Every house that I go into, either my pregnant mama has it, her husband has it and she’s going to get it, or a family member has it,” Devers told me last week as she drove from one patient appointment to another through Lancaster County’s rolling farmland. Measles can be especially dangerous during pregnancy, leading to low birth weight, early labor, and miscarriage; one of Devers’s patients recently miscarried at 17 weeks while she was fighting a measles infection.

If more pregnant women get measles, the number of newborns who have measles will almost certainly rise too. According to the American Academy of Pediatrics, historical reports suggest that about a quarter of children born to mothers who are sick with measles in the days leading up to labor will likely acquire the disease. No data on the current rate of measles acquired in utero, which is known as congenital measles, are publicly available yet. But health-care providers working in Pennsylvania say it’s on the rise—perhaps at a scale not seen in decades, if ever.

Before the measles vaccine was licensed in 1963, roughly 95 percent of Americans contracted the disease in childhood, making them immune by the time they entered their reproductive years. But people who are of childbearing age today have lived through historically low measles rates. That means that a number of unvaccinated adults, including pregnant ones, never caught measles in childhood and are therefore not immune—and are now contracting the virus during large outbreaks. About two-thirds of the cases reported in Pennsylvania this year have been in adults ages 18 to 49, some of whom appear to be passing on the disease during childbirth.

In an October 19 advisory, the Pennsylvania Department of Health noted that congenital measles had been identified in the state for the first time in decades. “It’s gone from something we never see to something that we are now commonly seeing,” John Goldman, an infectious-disease physician at the University of Pittsburgh Medical Center in Harrisburg, told me. The Atlantic’s Tom Bartlett reported in August that an infant in Lancaster County, born to a mother who was severely ill with measles, was declared dead within 30 minutes after birth.

[Read: The measles-stricken mother who lost her newborn son]

Documenting an increase in congenital-measles cases is challenging. Case reports date back to at least the 1930s, but “no one has done any kind of systematic collection” of data, Adam J. Ratner, an infectious-disease pediatrician in New York, told me. The Pennsylvania Department of Health cannot release measles patients’ personal information, including their precise age, in order to protect their privacy, the deputy press secretary Stephanie Nojiri told me, and even if they could, no national definition for congenital measles exists to standardize tracking. Historically, doctors have diagnosed congenital measles when they observe a measles rash and other typical symptoms of the disease within the first 10 days of a newborn’s life. But that definition may unwittingly count some infants who contract measles in their first days of life outside the womb and miss counting infants with milder cases who do not present with a rash, Ratner said.

Because congenital measles has historically been so rare, doctors know very little about its effects. Measles is known to wipe a person’s immune memory, making survivors highly susceptible to infections for years to follow; a 2019 study in children found that the virus demolished anywhere from 11 to 73 percent of antibodies and memory cells. And all people who contract measles are at risk of developing a rare but almost always fatal brain inflammation, subacute sclerosing panencephalitis, that can occur a decade or more after they contract the disease. But newborns can react to viruses differently than children even a few months older, which could mean that the effects of congenital measles deviate. That dangerous brain inflammation, for example, appears to occur more commonly and more quickly in congenital cases than in cases acquired after birth.

For now, doctors are trying to pool what they do know. Ratner, who is a member of the American Academy of Pediatrics’ committee on infectious diseases, helped assemble new AAP guidance on how to treat congenital measles; he and his colleagues consulted doctors in Canada, which saw congenital-measles cases during an outbreak last year, but also had to extrapolate from how pediatricians treat measles in older children. John Goldman told me that he and other physicians had been following that guidance, as well as the Pennsylvania Department of Health’s, and recommending both vitamin A, which can help limit the severity of an infection in children with a deficiency, and a dose of antibodies, which can help prevent an infected mother from transmitting the virus to her child at all. “There’s not a lot of good data on how you treat it,” Goldman said. But, he added, Pennsylvania may soon end up with the country’s largest data set of congenital-measles cases, which could help doctors treat those cases more effectively in future outbreaks.

The best way to prevent a congenital-measles infection is, of course, to prevent a mother from getting measles before she gives birth. The best way to do that is with the measles vaccine, which is typically given shortly after a person’s first birthday. One of the few times an adult can’t get vaccinated is, crucially, during pregnancy—just when protection is most necessary.

To help shield unvaccinated pregnant women, Roberta Devers argued that the providers who interact with them most often—in many cases, midwives—should be allowed to inoculate the other members of their household. In New York, Governor Kathy Hochul has allowed licensed midwives to administer the measles vaccine as part of a recent disaster declaration responding to the state’s growing outbreak. Pennsylvania, however, does not allow vaccines to be provided by traditional midwives, many of whom study through apprenticeships rather than attending nursing school and are not licensed by the state. Christian Macedonia, a maternal-fetal-medicine physician in Lancaster County, told me that’s for good reason: Providers who have not gone through formal medical training, he said, should not be distributing shots.

But he also acknowledged that midwives are “really at the front line” of the congenital-measles crisis. In insular religious communities, such as the Amish one in Lancaster County, which have seen the largest measles outbreaks over the past couple of years, midwives may be the only medical professionals with whom families regularly interact. “We have intimate relationships with these families,” Devers said. “We want to be able to carry the vaccine, because our families started to request it.”

Devers knows that many of her patients still distrust the formal health-care system. At a recent postpartum appointment, she talked with a mother who questioned the motives of pop-up vaccination clinics—she was suspicious of the shots being offered for free. As she spoke, the mother cradled her feverish 12-week-old baby, who had measles.

Is There Anything BPC-157 Can’t Cure?

2026-10-27T07:00:00-04:00

The wellness industry loves a secret cure. I encountered dozens of them at Dave Asprey’s Beyond Biohacking Conference, held in May on several floors of a hotel in downtown Austin. There were supplements galore, of course: algae tablets for detoxification, ketones for concentration, nitric oxide for circulation. One company claimed that its capsules contained quantum energy. I saw people hooked to IV vitamin drips, sweating inside infrared saunas, and sealed in hyperbaric oxygen chambers. I watched a woman climb into a giant quartz bowl, which someone then struck with a mallet. I tried a pair of inflatable compression pants that rhythmically squeezed my legs to stimulate lymphatic drainage. I also stripped to my boxers and spent a thrillingly miserable two and a half minutes inside a cryotherapy booth.

The main attraction, though, was peptides, the short chains of amino acids now hyped as miracle drugs. In a ballroom packed with several hundred people, Asprey and a fellow health guru, Jay Campbell, extolled the many virtues of peptides, railed against restrictions on their promotion, and predicted a future in which they transform mainstream medicine. Both men are in their 50s, with shredded physiques and zero medical degrees. Asprey is best known for popularizing the trend of dumping butter and coconut oil into your coffee. Campbell made his name advocating for testosterone replacement and now bills himself as one of the world’s leading authorities on peptides. He spoke excitedly about one cutting-edge compound, called Klotho, that can “literally lower your biological age.” He told the crowd that he’s heard from women in their 70s who, after taking Klotho and the peptide FLGR242, started menstruating again. (Instead of imploring them to call their doctor, which is what the American Cancer Society recommends for postmenopausal bleeding, his advice was to “keep injecting.”) As peptides become more readily available over the next few years, Campbell anticipates that disease as we know it will come to an end, including “ontological” mutations. (I’m guessing these are mutations that afflict only philosophers.)

Campbell and Asprey have been promoting underground peptides in their books and on their podcasts for years. Lately, though, these gray-market drugs have started to gain traction with a broader audience. The most talked-about among them goes by the cryptic designation BPC‑157. It’s commonplace enough that asking questions about it immediately tags you as a tourist. BPC‑157 is a component in most of the popular peptide combos, ones with names such as Glow, Klow, and Wolverine (a reference to the comic-book superhero with self-healing powers, not the carcass-eating skunk-bear). It’s rumored to be good for stomach ailments including acid reflux, bloating, and ulcers. Also, sprained ankles. It will reportedly ameliorate arthritis, carpal tunnel syndrome, and sciatica, not to mention hernias and migraines. BPC‑157 has been said to loosen stiff shoulders and repair runner’s knee. Suffering from bursitis? Gingivitis? Road rash? Low libido? Its boosters promise that it can help with all of these conditions and more.

In recent months, BPC‑157’s profile has risen significantly, at least judging by Google searches and Instagram videos, some of which feature a creepy AI-generated character who magically restores torn ligaments. Praise from big-name podcasters such as Andrew Huberman and Joe Rogan has no doubt contributed to its popularity (Rogan declared BPC‑157 “super legit”). Reliable sales figures, though, are hard to come by. Conventional drugs that have been approved by the FDA—including GLP-1s like Ozempic, which are also peptides—are sold by multibillion-dollar global behemoths with legions of researchers and executives. Peptides like BPC‑157 are sold by … honestly, who knows? The companies pop up and disappear. The proprietor of your favorite American peptide supplier might be an enterprising undergraduate who buys in bulk from China, where many peptides are manufactured, and relabels them. A small glass vial of freeze-dried powder arrives on your doorstep; you dissolve the powder in sterile water, draw it into a syringe, and inject it into your abdomen. Peptides are usually advertised as “for research use only,” a wink-wink disclaimer that allows vendors to maintain that they’re not violating federal laws regulating drug sales. Maybe that gives you pause. Or maybe you think that these sketchy transactions are necessary because the establishment—that is, Big Pharma and the United States government—is suppressing the good stuff.

Amid the sellers of red-light panels and blue-light glasses at Beyond, I stumbled on a company marketing a drinkable version of BPC‑157. Its giveaway sticker read We Prefer Oral Peptides, with the word peptides in much smaller letters because haha sex. The representative behind the counter referred to BPC‑157 as “the soccer mom’s peptide” and nonchalantly squirted some from what was essentially a hand-soap dispenser into a tiny plastic cup, then held it out to me. I hesitated, and the peptide hung in the air, unclaimed. “Are you afraid of it?” he asked. The not-so-subtle subtext was that I shouldn’t be, that taking BPC‑157 was equivalent to trying the dissolvable herbal-tea strips a few tables down or giving the giant quartz bowl a whirl. For the record: We were in a hotel hallway and I was being encouraged—dared, really—to try a drug that isn’t FDA-approved, is prohibited by the World Anti-Doping Agency for athletes’ use, and allegedly works throughout the body via some mysterious mechanism that is not entirely predictable. I was being offered an unspecified dose, although I wouldn’t know what dose would be appropriate, because there are no agreed-upon dosing guidelines. I declined the peptide. The representative shrugged and drank it himself.

Perhaps I was being too cautious. Thousands of Americans have ingested or injected BPC‑157. That guy didn’t keel over after he swigged it. Whatever you think of their relevant credentials, Asprey and Campbell appear to be insufferably healthy middle-aged men. Robert F. Kennedy Jr., the secretary of health and human services, is on record as being “a big fan of peptides,” a casually sweeping endorsement of an entire class of drugs. Although Kennedy has stoked vaccine hesitancy for most of this century and argues that Americans are overmedicated, he has a soft spot for these particular shots. The “Make America Healthy Again” movement is officially on board too, which feels strange considering that MAHA is all about treating anything modern and artificial with suspicion. They’re the raw-milk people! They don’t even like Doritos and Coca-Cola! And yet they’ve decided that these highly processed powders, assembled by machines that link amino acids together, are somehow consistent with the nature-knows-best ethos. For MAHA, the renegade cachet of peptides is central to their appeal, and the fact that medical experts are wary of them is a plus. Under Kennedy, the FDA may soon allow six peptides, including BPC‑157, to be made in the United States, which would mean that doctors could prescribe them, and that telehealth companies such as Hims & Hers, best known for discreetly shipping men generic Viagra, could offer them for sale.

[Read: America is about to go over a peptide cliff]

Is there any evidence that BPC‑157 works? Its evangelists like to note that the peptide has several decades of peer-reviewed research behind it. Those papers, more than 200 of them, are packed with charts and citations and have been published in journals that are respectable enough, if not quite top-tier. BPC‑157 has been tested on mice, rabbits, guinea pigs, chickens, honeybees, and, above all else, rats. So many rats. These rats have endured all manner of miseries in the name of science. They have had their tendons severed, stomachs ulcerated, tails amputated, muscles crushed, bowels perforated, spinal cords compressed, blood vessels tied off. The ones that received the peptide consistently fared better, according to the studies: Their wounds closed more quickly, tendons knitted together more completely, ulcers shrank. Overall, they were more likely to survive this catalog of laboratory horrors than the unlucky controls. If the published literature is to be believed, BPC‑157 is a rodent panacea.

When you read the papers, one after another, until you’re bleary-eyed and bewildered, you start to notice some patterns. One is that very few of these studies have been conducted on humans, and humans, famously, are not rats. Another is that, as I’ve already suggested, BPC‑157 is said to work almost every time for almost everything. Behold these triumphant verbs: improves, enhances, promotes, stimulates, accelerates, restores, increases, prevents, abolishes, counteracts, heals, protects. And it seems to yield benefits regardless of the form, or method of application, or which orifice it is delivered into. Also, when you examine the list of authors, you see many of the same names crop up again and again. One name, however, appears at the top of nearly every paper: Predrag Sikirić.

Sikirić is a 72-year-old professor emeritus of pharmacology at the University of Zagreb School of Medicine, in Croatia. I emailed him. I wanted to know where this wondrous elixir, supposedly good for both heartburn and a ruptured Achilles, came from, and why we’re hearing about it only from podcasters. Precisely four minutes later, my phone buzzed. An insistent man with a thick accent wanted to know how quickly I could get on a plane.

The current global hub for BPC‑157 research is a cramped, cluttered room with a single window half-obscured by a tangle of plants. Sikirić’s laboratory is at the university’s medical school, roughly a mile north of Zagreb’s main square, near a small café where future doctors smoke cigarettes and grouse about their workload. These modest quarters are temporary; renovations are under way on a larger laboratory in the building across the street. For now, new experiments are on hold, and Sikirić and his longtime lab assistant are confined to a glorified storage closet with empty rat enclosures stacked next to boxes of small plastic tubes and bags of feed. Among the haphazard decorations—including a foam brain and a hat that reads HAPPY ANIMAL HAPPY HUMAN—hangs a collage of patent medicines from the heyday of cure-alls, back when you could make whatever claims you wished about your restorative tonic without fear of government regulators shutting you down. On a counter sits a large glass bottle of clear liquid, the letters BPC scrawled on the label in blue marker.

The peptide in that bottle is Sikirić’s life’s work. When he was still a student, inspired by the pioneering research of the endocrinologist Hans Selye, who studied the biological effects of stress, Sikirić came to believe that the body produced, in essence, some universal antidote to injury, a molecule that would cue damaged tissue to return to its normal state, regardless of what had caused the harm. He reasoned that the remedy was probably found in gastric juice, because the stomach is constantly adjusting to fresh insults. Sikirić spent the 1980s searching for it, and the decades since trying to convince the world that he found it. Along the way, his work has often drawn eye rolls from colleagues at the medical school, some of whom remain unmoved by the animal evidence he has amassed. Even those who admire Sikirić’s persistence and have known him for years, such as Miloš Judaš, the director of the university’s Croatian Institute for Brain Research, do not share his faith in the curative properties of BPC‑157 (“We are not sure whether it really works or not,” Judaš told me). Sikirić’s discussions with pharmaceutical companies have repeatedly stalled. The recognition he believed would be forthcoming from the scientific community has never materialized, despite his prolific scholarly output.

But none of that has deterred Sikirić in his effort to, as he told me, “bring BPC to mankind.” He’s just kept plugging away at this singular line of research, coaxing generations of graduate students to join him in the mission, and dreaming up new experiments to test his theory. Now the world is seeking him out. Along with reporters like me, he hears from peptide promoters eager to brag about being buddies with the discoverer of BPC‑157. How his peptide took center stage, Sikirić isn’t sure. For a long time, BPC‑157 wasn’t really known outside his lab except among readers of niche scientific journals such as Digestive Diseases and Sciences and the European Journal of Pharmacology. In the mid-2010s, it began appearing on bodybuilding forums and in biohacking guides, where it was touted as a way to speed healing and recovery. But it remained on the fringes until recently. Testimonials from Rogan and Huberman, whose health recommendations reach enormous audiences, certainly helped spread the word: Rogan swore it fixed his hurt elbow, while Huberman credited it with eliminating his back pain.

Mare Milin for The Atlantic

Predrag Sikirić has published hundreds of papers purporting to show the salutary effects of the peptide BPC⁠-157.

However it happened, Sikirić is pleased that his peptide is at last having its moment. He is gratified that BPC‑157 is flourishing on the gray market as well. “Officially, I have to be against any kind of usage without full approval,” he said. Unofficially, he’s all for it. He interprets BPC‑157’s word-of-mouth success as proof that his peptide is helping the masses. If it wasn’t, why would so many people recommend it? He is delighted, too, that the health secretary of the United States is a believer in peptides. I asked if he’s ever spoken with Kennedy, who has a habit of reaching out to researchers whose work he admires. “I would kindly reject to reply to the question,” he said. “This is good English?” (An HHS spokesperson did not respond to an inquiry about whether Kennedy had spoken with Sikirić.)

Sikirić can be at once engaging and cagey. Try to pin him down, and he launches into an unrelated anecdote. Broach a contentious topic, and he responds with a puzzling analogy. Ask about his past, and he grudgingly provides a few biographical details. Sikirić grew up in Zagreb, which was then part of Yugoslavia. His father, a lawyer, was jailed repeatedly for his opposition to the country’s ruling Communist party; his mother, an encyclopedia editor, encountered government censorship. As a child, Sikirić underwent multiple surgeries, and those hospital stays made him want to be a doctor. Medicine also offered an escape from politics: “The pain is the pain for anybody,” he said. After medical school, he worked for three years as an emergency physician in a small town, treating victims of car accidents, heart attacks, and stabbings.

But a country doctor can only do so much. The wonder drug he envisioned might help millions. Sikirić returned to the University of Zagreb to pursue this dream with a single-minded, near-manic intensity. In addition to churning out hundreds of papers, he has supervised numerous doctoral dissertations, all of them on BPC‑157. His students tell of late-night phone calls from Sikirić, eager to share an insight. He and his wife of more than 40 years don’t have children. He has no hobbies, doesn’t take vacations to the nearby coast, and works for long stretches without a break. Sikirić walks quickly, albeit at a slight angle, as if he might tip over. He drives quickly, too: When I rode with him, he sped through downtown Zagreb, braking a few feet from crossing pedestrians, half-grinning at my evident anxiety. You wouldn’t think it to look at him—baggy professorial sweater and corduroys, tightly cropped gray hair—but Sikirić is a septuagenarian in a hurry.

BPC‑157’s newfound fame has brought with it unwelcome scrutiny. Last year, a group of researchers in Poland raised concerns about BPC‑157’s safety, arguing that how it works is poorly understood and warning that it could cause neurological damage or promote tumor growth. These possibilities, they wrote, must be considered “before falling into complete admiration.” In response, Sikirić pointed to his animal studies suggesting that BPC‑157, on the contrary, inhibits tumor growth and protects against neurological damage. When I asked him about the Polish paper, he dismissed it as a bid for attention and emphasized how much it upset him. If BPC‑157 really increased the risk of cancer, Sikirić insists that he would tell the public to stop using it immediately.

One argument for BPC‑157’s safety rests on the assumption that if the body makes it, it must be safe. But does the body make it? Sikirić has asserted that his peptide is a fragment of a protein, but he’s never publicly shared key details about that protein. Several researchers have attempted to locate BPC-157’s amino-acid sequence in databases of protein and DNA sequences, to no avail. I asked William Pearson, a computational biologist who co-developed the first widely used search tool for such databases, to try to determine where BPC‑157 comes from. After hours of combing through repositories containing hundreds of millions of protein and DNA sequences, Pearson couldn’t find a match. If the peptide occurs in humans, those searches should have turned it up. He also identified no matches among proteins from other animals—including, it’s worth noting, rats.

Sikirić downplayed the failed searches. He doubts that those databases are comprehensive, though he acknowledged that he hasn’t used them himself. Sikirić told me he’s sure that BPC‑157 originates in humans because he isolated it from newborns in the ’90s. I didn’t remember seeing that study in any of his papers, but that’s because Sikirić says he never published it and doesn’t intend to (“Some things you have to keep for yourself,” he said). As for the gene behind BPC‑157, he maintains that he’s close to finding it, but won’t reveal how he is conducting that search. He likened providing such basic information to a country disclosing its nuclear secrets. The answers, he said, could be found only in his head. I asked what would happen if he got run over by a bus: “This could be huge problem.”

Sikirić believes that, like the cure-alls in his office collage, his peptide can be applied to any ailment, from minor aches to major diseases. During my stay in Zagreb, we played a little game: I named a malady and he told me whether BPC‑157 could treat it. Macular degeneration? “Yes, it could.” Gut inflammation? “This is the favorite site of activity.” Dementia? “Certainly.” COVID? “Naturally, yes.” Concussions? “We published data about it.” Anxiety? “The experiment was helpful in the mice.” Depression? “Exactly.” Heart attacks? “Any kind of condition.” Headaches? “Any kind of pain.” In Sikirić’s estimation, BPC‑157 can do no wrong. Its all-purpose goodness is fundamental to his theory: The peptide is consistently returning the body to its healthiest state. Other drugs have limitations and downsides, but not BPC‑157. He compares it to steroids, but believes it’s superior because BPC‑157 has no known toxic dose (“You could eat BPC without any harm—literally eat, like bread,” he said) and you can take it indefinitely.

Until I told him, Sikirić seemed unaware that some users report distressing side effects from BPC‑157. There’s an online support group called “Haters of BPC‑157,” in which people who believe that the peptide has harmed them commiserate and trade notes on recovery. The most common complaint appears to be anhedonia, which is a kind of emotional numbing. They say they struggle to feel pleasure after taking the peptide. Some blame themselves for using an unapproved drug. Others are angry at Sikirić (“Fuck him,” one member of the group messaged me). Sikirić told me he felt sorry that people were suffering but doesn’t believe it has anything to do with his peptide. (Predictably, he contends that BPC‑157 actually counteracts anhedonia.) Maybe the product they bought was contaminated, he argued, or maybe the cause was something else entirely. These are only anecdotes, he pointed out. And he’s right; that is all they are. But the human evidence in favor of BPC‑157 is also largely anecdotal.

Illustration by The Atlantic. Sources: Durham Peptides; Ultra Pure Bioscience; Amino Research; XL Peptides.

Peptides are usually listed as “for research use only,” a disclaimer to skirt federal laws regulating drug sales.

Sikirić takes BPC‑157 himself. Of course he does. I first suspected this when I noticed an empty plastic tube in the cup holder in his car. He was somewhat sheepish when I asked about it, and not forthcoming about how often, or for what purpose, he takes it. As a rule, it’s frowned upon for scientists to sample the merchandise, though there have been famous exceptions. Jonas Salk tested the polio vaccine on himself before it was given to millions of American children; Albert Hofmann dropped way too much acid once before biking home. I asked many of Sikirić’s colleagues and former students if they had taken BPC‑157. Several told me they would never try a drug that hadn’t been approved for human use. Others swore by it. They use it when they feel a cold coming on. They blend it into a cream and smear it on burns and diaper rash. They take it when they twist their ankle or strain their back. A bunch of them give it to their dogs. One former student, now a doctor, showed me a small tube of BPC‑157 that she carries in her purse, just in case.

This is not how drug development is supposed to work. After a promising candidate is tested on animals, it normally passes through three phases of human clinical trials, after which regulators review the evidence and make a determination. The story of why BPC‑157 hasn’t followed this path is convoluted. More than two decades ago, clinical trials began under the auspices of Pliva, a Croatian drug company, but didn’t reach the third phase. Pliva’s research institute, which was responsible for new drug development, was acquired by GlaxoSmithKline in 2006, and progress on BPC‑157 subsequently ceased. In Sikirić’s version, GSK, as it’s now known, decided to shelve the peptide because it was too effective and the company feared it would cannibalize sales of its other drugs. “Let’s just say major breakthroughs are not welcome,” he told me. Yet it’s hard to imagine a pharmaceutical company nixing an important discovery knowing that a competitor might snatch it up. A study conducted by Pliva researchers found that although BPC‑157 did hasten the healing of skin wounds in rats, the results were similar to those achieved with an already approved drug. The peptide did something, in other words, but it wasn’t a breakthrough.

Another problem may have been Sikirić himself. Two former Pliva employees involved in the BPC‑157 project told me Sikirić’s passion sometimes seemed to override his objectivity. He bristled at pushback, and his commitment bordered on obsession. As one of them put it, when it came to his peptide, “Predrag was in love.” Neither knew for sure why GSK didn’t move forward with BPC‑157 (a GSK spokesperson told me she couldn’t find anyone with knowledge about a decision made 20 years ago). But they noted that it’s far from unusual for experimental drugs to be abandoned during clinical trials; in fact, about 90 percent don’t make it all the way through the process, including ones that show some benefit in animal studies.

After GSK dropped the peptide, the rights were returned to Sikirić, allowing him to pursue BPC‑157 trials elsewhere. In 2015, a Phase 1 clinical trial was conducted in Tijuana, Mexico, but the results have never been published. The trial’s sponsor was PharmaCotherapia, a Croatian company co-owned by Sikirić that last year reported having no employees. Sikirić let me briefly review the safety findings on his laptop but declined to share the full report. The summary I read described mild adverse events among some subjects but concluded that BPC‑157 was “safe and well tolerated.” According to Sikirić, the report was never published because the trial’s principal investigator, Rufino Menchaca, a clinical neurologist, wouldn’t sign off once the trial was completed (Menchaca, through a representative, declined to speak with me). The reason for his refusal to sign isn’t entirely clear, although Sikirić told me it had to do with worry that others would steal the data if they were published. Sikirić hopes to restart clinical trials soon, again in Tijuana, looking specifically at whether BPC‑157 is a beneficial treatment for multiple sclerosis—though, in his mind, there is no question. He’s certain that the experiments will confirm his expectations.

Sikirić is so determined to vindicate BPC‑157 that he frequently sounds more like a salesman than a scientist. Money, however, doesn’t seem to be what drives him: As Sikirić will admit, he has no knack for business, and at the moment it’s shady online sellers who are getting rich from his peptide, not him. He just wants to be right, and he wouldn’t mind getting some credit, too. As I’m typing this, Sikirić is sending me yet more papers via WhatsApp even though it’s after midnight in Croatia. He needs me, and everyone else, to set aside any misgivings and agree with him that BPC‑157 is a marvel. Skepticism is taken as an insult. Too often Sikirić’s message is: Trust me. Trust me about where BPC‑157 comes from. Trust me that it works on humans, not just rats. Trust me that it’s safe.

FDA scientists don’t seem to trust him. In June, the FDA published a 68-page report that looked closely at BPC‑157 studies and found them unconvincing, arguing that they lack sufficient human-safety data and that too little is known about how or whether the peptide works. Agency researchers couldn’t tell from the literature how dosage affected outcomes. They flagged the possibility that it could provoke harmful immune-system reactions. Claims about BPC‑157 should be “interpreted with caution,” they wrote, because of troubling gaps in the literature.

But when an FDA advisory committee met in July, it more or less disregarded that report and recommended allowing BPC‑157, along with five other peptides, to be made by licensed compounding pharmacies in the United States. It probably wasn’t a coincidence that weeks before the vote, the agency had announced the appointments of eight new committee members, six of whom had ties to the wellness industry, which hopes to capitalize on a regulatory change. (An HHS spokesperson told me that “all committee members underwent the same ethics review and vetting process required of all FDA advisory committee members.”) One peptide lobbyist told me that the projected profits for BPC‑157 could be in the billions. Hims & Hers plans to start manufacturing BPC‑157 and allowing customers with a prescription to purchase it, assuming the FDA gives the green light (the company’s CEO, Andrew Dudum, told shareholders that he was “extremely excited about this category”). Although FDA officials still have to accept the committee’s recommendation, that seems like a formality, given that Kennedy oversees the agency.

[Read: The peptide boom is getting out of hand]

I have mixed feelings about the move. No, we don’t know enough about these peptides, and providing what amounts to backdoor government approval seems like a terrible idea. At the same time, if people are going to take BPC‑157, I’d rather the supply come from a licensed pharmacy than some guy with a storage unit and an overseas hookup. I kept thinking about the question the peptide representative at the Beyond conference asked me: “Are you afraid of it?” Sikirić sent me home with a small plastic tube containing a single milligram of BPC‑157. It looked like nothing, barely a few grains of fine white powder. I considered taking it, both for the sake of this story and because I have this weird twinge in my right shoulder sometimes. Instead, I sent it off to get tested. The report that came back was glowing: Unlike the gray-market peptides, many of which contain filler and God knows what else, the peptide from Sikirić’s laboratory was chemically pure, full-strength, 100 percent BPC‑157. It was the real thing—whatever that is.

This article appears in the December 2026 print edition with the headline “Mr. Peptide.”

The Evolution of the Human Brain Set It Up for Failure

2026-10-18T08:00:00-04:00

Apes don’t develop Alzheimer’s—at least, not like we do. Although we share a hefty amount of our DNA with our closest primate relatives, humans are uniquely at risk of developing the disease that can erode our sense of who we are.

When I make the diagnosis in my neurology clinic, I tell patients and family members that in most cases, doctors can’t point to a single, definitive cause of the illness. Age, genetics, health, lifestyle factors, and environmental triggers all play a role. But a growing body of research offers another dimension: We can lose our sense of self precisely because our species evolved to have one. In recent years, scientists have been comparing the brains of humans with those of other, closely related species, and teasing out how the genetics, structure, and molecular mechanisms differ. What they’re finding is that the same characteristics that support our unparalleled cognitive abilities make us susceptible to Alzheimer’s disease.

Certainly, the biological hallmarks of Alzheimer’s look different inside the human brain than in the brains of other species. Melissa Edler, a comparative neurobiologist at Kent State University, and her team have identified distinct patterns in how humans and chimpanzees accumulate amyloid plaques and tau tangles, the toxic proteins that build up in brains with Alzheimer’s. She believes that looking at multiple species is going to be crucial to understanding how this disease develops. If nonhuman primates aren’t developing Alzheimer’s, “why aren’t they?” she asked, when we spoke about her work. “What’s different about their brains?”

One answer dates back to the early 2000s, when the Swedish geneticist Svante Pääbo (who went on to win the Nobel Prize for sequencing the Neanderthal genome) wondered what might account for the profound behavioral differences between humans and other apes—after all, we build civilizations while nonhuman primates cannot, without assistance, start a fire. Pääbo and his team of international researchers collected brain, blood, and liver tissue from humans, chimpanzees, orangutans, and macaques. But instead of comparing the genes themselves, they measured the genes’ activity—effectively, how hard each gene was working to make messenger RNA, which carries instructions from DNA on how to make proteins. Gene activity in the liver and blood, they found, was roughly equivalent across the species they tested. But activity in the human brain had ramped up.

Pääbo hadn’t set out to study Alzheimer’s specifically, but his findings hinted at a link between evolution and brain disease that others have pursued more directly. In a study published in 2020, for instance, Thomas Arendt, a neuroscientist at Leipzig University, and his team looked at autopsied brain samples from people with and without Alzheimer’s disease and found nearly 300 genes whose level of activity was different in the Alzheimer’s brains. When they looked at those particular genes more closely, they found that their genetic sequences had undergone a lot of change in a short amount of time—an indication that those genes played an important role in the human brain’s rapid and distinctive evolution. “In other words,” Arendt told me recently, “Alzheimer’s disease is based on changes in the genome that are typically human.”

Other researchers, too, have gathered evidence that supports the idea that evolution and Alzheimer’s are integrally related. A group at Duke University discovered that human evolution had influenced genes involved in the production of amyloid—the main protein that forms Alzheimer’s plaques. Scientists in China and the United Kingdom found that stretches of regulatory DNA that quickly morphed as the brain was evolving are associated with Alzheimer’s risk. Researchers from the MD Anderson Cancer Center, based in Houston, found uniquely human genes that get in the way of a protein called REST, which may guard against Alzheimer’s when working properly. Other studies have presented findings along similar lines. Collectively, these results only add to Arendt’s argument—that the genetic changes that made the human brain may be the same ones that left it imperiled.

The cognitive leap that set us apart also required the human brain to grow. The parietal lobes, which rise toward the crown of the head before sloping down the rear of the brain, are conspicuously larger in humans than in nonhuman primates, as Emiliano Bruner, a senior researcher in hominid paleoneurology at the Museo Nacional de Ciencias Naturales in Madrid, has demonstrated. A structure called the precuneus, tucked along the inner wall of those lobes, is larger too. The parietal lobes help the brain stitch sight, sound, and touch together into a cohesive model of the external world. They also play a central role in our advanced, abstract cognition, allowing for self-awareness, autobiographical memory, and our sense of being the same person across time.

Bruner had been mapping out these areas when he was contacted by Heidi Jacobs, now an associate professor of radiology at Massachusetts General Hospital and Harvard Medical School, who had been studying the same anatomy. For decades, Alzheimer’s research had focused almost exclusively on a different area of the brain—the temporal lobes, its de facto memory hubs. But Jacobs’s work suggested that the parietal lobes were also implicated in the disease’s earliest stages. Bruner and Jacobs began discussing whether the enlargement of these regions could have increased their vulnerability. Soon, they came up with a theory: The parts of the brain that had expanded most dramatically during human evolution were also among the first to be assailed by Alzheimer’s.

This was no coincidence, they argued. The precuneus consumes enormous amounts of energy and generates heat that has to be carefully dissipated to keep the brain functioning at its best. It also sits in a zone where the brain’s blood supply is thinnest, which makes it vulnerable to certain conditions, some of them age-related, that impact blood flow. Myelin, the fatty coating that is crucial for fast signaling between neurons, is also particularly fragile in this area. Essentially, Bruner and Jacobs reasoned, because of the rapid and imperfect reorganization that the parietal lobes underwent during human evolution, the region doing much of the brain’s hardest cognitive work has some of the most precarious infrastructure.

“It is like putting the engine of a Ferrari into a Fiat 500,” Bruner said. “That small car will go really fast, but it’s going to get hot. And braking will be an issue.”

What Bruner calls “braking,” the Yale neuroscientist Amy Arnsten calls “regulation”—specifically, calcium regulation, which supports learning and memory. The failure of that system, Arnsten argues, may be tied to how Alzheimer’s begins.

Most neurons fire because something in the outside world activates them: a flash of light, a sound. Neurons in our most recently evolved brain regions, which help us hold an idea in our minds, or conjure a detailed plan, keep firing even after the initial stimulus is gone. Although competing theories exist, Arnsten and others consider this persistent firing to be the cellular foundation of working memory. These “delay cells” depend on calcium to keep them active, but as we age and the cells’ system falters, calcium can rise to harmful levels, triggering a chain reaction that can cause tau proteins to clump. Over time, those clumps can contribute to the tangles of fibers that are seen in patients with Alzheimer’s.

Arnsten has shown that this apparatus, as well as the damage it causes when it breaks down, increases in lockstep with hominid evolution. Marmosets have the least of it. Macaques more. Chimpanzees, more still. Humans, by far, the most. “The closer to human,” Arnsten said, “the more the Alzheimer’s pathology.”

Our bodies are no strangers to evolutionary trade-offs. Homo sapiens’ vertical spine leaves us vulnerable to herniated discs; our pelvis, narrowed by bipedalism, makes childbirth difficult. We manage these compromises as best we can. But if an evolutionary give-and-take implicates our organ of thought and reason, accepting the compromise is harder.

The suggestion that neurological fragility is the price of a highly evolved mind is not novel, the historian Michael Hagner, who’s studied our understanding of the brain as the locus of personhood, told me. In the 19th century, some physicians and social theorists believed that the overwhelming demands of modern life were overtaxing the nervous system. That inclination, to interpret our cognitive vulnerabilities as the price of progress, has persisted even as more specific diagnoses have emerged to explain our brains’ instabilities.

Therapeutic options for Alzheimer’s remain both scarce and disputed, and understanding the disease’s ties to our brain’s evolution could open new avenues toward prevention and treatment. Amy Arnsten and her colleagues, for instance, are currently developing drugs that target calcium dysregulation, aiming to intervene before the system begins to break down. For now, the notion that human cognition and Alzheimer’s susceptibility share an evolutionary origin remains theoretical, and every time I deliver an Alzheimer’s diagnosis, I am acutely aware that I can offer little to change my patient’s fate. But if losing the sense of self is uniquely human, so is the ability to consider what having one allows us to gain.

What Three Gene-Therapy Deaths Have in Common

2026-10-16T07:30:00-04:00

In recent months, news came out about several distressing cases that have underscored the risks of gene therapy, which delivers DNA to a patient’s cells to treat disease. All of these cases have one thing in common that’s not apparent at first glance.

A child in China, enrolled in a clinical trial for gene therapy, died of acute respiratory distress syndrome, in which fluid builds up in the lungs and oxygen cannot enter. In a separate clinical trial in China, a child died after clots formed in their small blood vessels, likely disrupting the delivery of oxygen to organs such as the kidneys and brain. And earlier this year, researchers reported that a 5-year-old boy treated in Philadelphia had a brain tumor that was likely caused by gene therapy. (He’s doing okay now.) In each of these cases, the gene therapies relied on a versatile but unpredictable type of virus: adeno-associated virus, or AAV for short.

AAVs are the workhorses of many of the most successful gene therapies in the world. Scientists modify them so that they can deliver a working copy of particular genes to the body, but cannot replicate and aren’t infectious. These treatments have transformed a form of spinal muscular atrophy—once the genetic disorder most responsible for infant mortality—into a survivable condition, and have been approved for a devastating enzyme deficiency, muscle-wasting disease, and hemophilia, to name a few.

The terrible outcomes AAVs can cause are rare, but they’re a real risk. So far, the treatments have been used in small patient groups—the most commonly given one has been received by about 5,000 children since 2019—and focused on diseases that dramatically affect or shorten people’s lives. But AAV-based gene therapies are being explored for prevalent ailments, including heart disease, high blood pressure, and perhaps even Alzheimer’s. As the use of gene therapy increases, so might the instances in which it goes dramatically wrong.

The modified AAVs involved in gene therapy each contain a single strand of DNA. One portion of that strand drives the virus’s ability to get inside cells, and another is the helpful human gene that’s being delivered. The viral components are more likely than the therapeutic gene to be unpredictable and can cause side effects. On occasion, for instance, instead of hanging around within cells, AAVs insert themselves into the patient’s genetic code. This seems to have been what happened to the 5-year-old who developed a brain tumor—the AAV put itself into a part of his DNA that then produced the cancer.

Hurler syndrome, the condition the boy was being treated for when he received the gene therapy at 13 months old, is progressively debilitating. The syndrome can cause problems for the skeleton, heart, lungs, and liver, and affect cognitive development; life expectancy is short. Many gene therapies are geared toward children for whom a working copy of a vital gene would promise something closer to a healthy life. “We should remember what diseases we are talking about,” Albert Rizvanov, a scientist at Kazan Federal University in Russia who studies gene therapy, told me.

For such patients, gene therapy may seem like an obvious choice. But parents are still left weighing the potential benefits of treatment against the real risks, including fatal complications.

Jo Kaur and her husband, Richie DiGeorge, faced this question not too long ago. Their son Riaan was born in 2019 weighing less than six pounds, and by the time he was three months of age, they were concerned about his eyesight. Riaan’s pediatrician suspected it was just near-sightedness, Kaur, who has written extensively online about her family’s story, told me, but her “mom radar went off.” She secured an appointment with an ophthalmologist who found that her son had cataracts in both his eyes. Riaan’s overall growth also wasn’t on track, and he was missing milestones. At 15 months old, he was diagnosed with a severe form of Cockayne syndrome, a genetic condition that causes progressive muscle weakness and nerve damage.

This diagnosis meant not just that Riaan had problems with his eyes or was growing a little slowly, but that his life would likely be short—perhaps just five to seven years. He could roll and pull his family in for cuddles, but by the time he was 6 years old, at the end of 2025, he was still unable to sit independently for more than a few minutes at a time, or stand or walk independently, or feed himself. He was so small that he was still wearing clothes for 18-month-olds.

By then, Riaan had lost a lot of nervous tissue. His brain size was about 50 percent of what would be typical for a child his age. But Kaur and DiGeorge had worked closely with scientists for years to develop a gene therapy for Cockayne syndrome. The hope was to stop or at least slow Riaan’s loss of nerve cells. “Because Cockayne syndrome is neurodegenerative, even an extended period in which Riaan simply remains where he is now would be enormously meaningful to us,” Kaur said.

The researchers developing a Cockayne-syndrome treatment for Riaan had done mouse experiments to determine whether the medication was safe and whether it worked. Some of the animals had signs of liver damage, but they also lived longer. Kaur and her husband had been involved in countless meetings and stayed up-to-date on all of the developments. Knowing the risks so intimately increased the weight of the decision to allow Riaan to receive the treatment. “We’d read all the papers, we knew the science,” she said, “but you’re still making a huge decision for your child.” She and her husband were primarily concerned about the treatment’s safety.

Ultimately, this past April, they decided to go ahead with the therapy. Riaan would be the first child in the world to receive this treatment for Cockayne syndrome. Surgeons created a small hole in his skull, inserted a catheter, and within minutes delivered the gene therapy to him. When night came, as Kaur wrote in her own account of Riaan’s procedure, she fought the urge to sneeze as he slept on her arm in the hospital. Everything seemed very delicate, and she dared not move. His head had to stay elevated and he “had so many wires,” she told me. “I didn’t want to wake him.”

The first successful gene therapy, tested back in 1990, used a nonreplicating version of a mouse virus. But that virus doesn’t readily get into all cells, so scientists kept looking for others to try. One was adenovirus—an attractive option in part because it could deliver working genes to a high number of cells. But in 1999, an 18-year-old named Jesse Gelsinger died shortly after having a severe immunological response to a therapy that used adenovirus to treat his rare metabolic disorder. Gelsinger is believed to have experienced the same acute respiratory distress syndrome that killed one of the patients in China.

In that recent trial, the Chinese company HuidaGene Therapeutics was using gene therapy to treat Duchenne muscular dystrophy. In many cases, the body weakness caused by Duchenne leads to death during a child’s teenage years, and families whose kids might benefit from gene therapy have been pushing for it. In the United States, a different AAV-based gene-therapy treatment for Duchenne, made by the company Sarepta, has been controversial in part because of concerns that it may not actually do enough for patients. But it has also been associated with deaths: Last summer, the FDA reported that it was investigating after several patients receiving Sarepta’s therapy succumbed to acute liver failure, a known risk. (After the deaths, in a public statement, HuidaGene extended condolences to the family and reiterated its focus on patient safety. Sarepta paused shipments of treatment for certain patients.)

AAVs delivered into the bloodstream are very good at reaching the liver, where they’re filtered out and can accumulate. As a result, the engineered viruses can have a harder time reaching other organ systems and tissues, including muscle. To get to those harder-to-reach parts of the body, sometimes scientists increase the amount of treatment they give. The doses of viral particles in gene therapy can vary so widely that one type of treatment might have a dose of 500 billion functional viral particles per kilogram, and another 300 trillion. (The doses in commonly used drugs tend to occupy a much narrower range.) Many patients have few other options than to risk a bigger dose, Luk Vandenberghe, who was involved in the discovery of a commonly used AAV and now directs the gene-therapy center at the Massachusetts Eye and Ear Infirmary, told me. “The alternatives can mean restarting development with a new and modified gene therapy,” he said.

Researchers have been trying to test different variants of AAV and engineering the viruses’ shells to get them to reach desired tissues in the body. But that, too, can change how the body reacts. A year ago, a child died in a clinical trial that used an AAV designed with a shell to help it reach the brain and deliver treatment for a congenital seizure disorder. The company behind the trial, Capsida, paused the clinical trial and a few months later said that the child had experienced brain swelling following the infusion. In May, it announced that it had closed the trial. (The company has “been conducting extensive nonclinical work to understand what led to the outcome” and will incorporate its findings into future work, Katherine Carlyle Smith, a Capsida spokesperson, wrote in an email.)

Despite the risks of gene therapy, the growing number of people who have received it also means that many people have benefited, without concerning side effects. “Caution is of course always top of mind, but I think the promise of gene therapy overwhelms the risks of not taking action for a lot of parents,” Kaur, Riaan’s mother, told me. She and her husband felt especially cautious about giving Riaan gene therapy, precisely because he had a life-limiting disease: “We want to maintain and preserve the life and happiness that he currently has,” she said.

Currently, Riaan is being tapered off his immunosuppressants and monitored closely. In the meantime, Kaur is observing signs that the therapy might be helping. He can sit by himself on the edge of the couch. He still needs support to stand or walk, but he wants to try more often. Kaur knows these observations are anecdotal, but Riaan’s physical therapist has also noticed the changes, she said. He has become more expressive, too—an outcome that surprised Kaur. “He would rarely say ‘mama,’ and now he says it all day long … ‘ma-ma-ma,’” she says. “It’s beautiful to hear.”

A Lab-Leak Story You Haven’t Heard

2026-10-15T10:53:31-04:00

You’ve almost certainly had RSV. Most of us catch it before we turn 2. Usually it feels like a cold: runny nose, cough, maybe a fever. But RSV (short for “respiratory syncytial virus”) can take a dangerous turn. In the United States, it puts more babies in the hospital than any other virus and kills thousands of seniors each year. Cases tend to climb as the weather cools—so, right about now.

Health Secretary Robert F. Kennedy Jr. seems to be intent on spreading the word about RSV: He brought up the virus during interviews on both CNN and Fox News in August. He could have used those appearances to remind viewers about the RSV vaccine, which the FDA first approved in 2023 and the CDC recommends for older adults and for women in the later stages of pregnancy during the fall and winter. Instead, Kennedy made two false statements. First, on CNN, he called RSV “the biggest killer of kids in this country today.” (According to the CDC, it isn’t; cancer claims more children’s lives.) His other whopper was weirder: In both appearances, he blamed RSV on a scientific experiment gone wrong, saying on Fox that it “came from a laboratory” and on CNN that it came from gain-of-function experiments, or something like them.

To be clear, RSV did not leak from a lab. But Kennedy has been repeating this fiction on podcasts for years, and he included it in his 2021 book, The Real Anthony Fauci. Even in that compendium of dubious and debunked assertions, Kennedy’s theory about RSV—which involves nonhuman primates, a military research facility, and, of course, vaccines—stands out. It’s a case study in how, as an anti-vaccine activist, he has trafficked in half truths and half-baked narratives, and how he relies on loyalists who reinforce his beliefs rather than experts who can challenge them. Kennedy could easily have consulted the historical record or reached out to subject-matter experts. Instead, as he’s done frequently during his nearly two years as health secretary, he parroted the flawed research of an activist ally.

Kennedy claims RSV originated in captive chimpanzees, and then spread to humans. On a 2023 podcast, he said scientists deliberately infected a lab worker with the virus. In The Real Anthony Fauci, he endorses a different theory, writing that the virus “entered polio vaccines at the Walter Reed Hospital laboratories in 1955” and caused a “devastating pandemic.” It’s part of his absurd argument that polio vaccines caused more harm than the potentially paralytic disease itself.

In fact, RSV’s discovery did begin in a laboratory, with chimpanzees getting the sniffles. In October 1955, 14 chimps housed at an annex of the Walter Reed Army Institute of Research in Silver Spring, Maryland, all came down with what seemed like a cold. Scientists set about determining what made them sick, swabbing their throats and taking blood samples. Researchers isolated the virus and intentionally infected another group of chimps. In February 1956, a lab worker who had contact with the second group of chimps fell ill. Tests indicated that the worker and the chimps had the same virus.

If that were all you knew, you might think Kennedy was onto something: Chimps get sick, a lab worker catches it, and a novel pathogen is thereby unleashed on humanity. It’s a compelling story and one that supports Kennedy’s thesis that scientists, rather than diligently searching for the cures to what ails us, are courting disaster with their reckless experiments.

But the real story doesn’t end there. Evidence soon emerged that RSV had been circulating in humans long before it was found at Walter Reed. In 1957, researchers at Johns Hopkins University reported that 80 percent of the children they had tested in Baltimore had antibodies to the virus by age 4. Inmates at a federal prison in Ohio had antibodies too. Those findings strongly suggested widespread, long-standing human infection rather than a virus suddenly escaping from a chimp colony. The Johns Hopkins scientists surmised that the virus might be of human origin and had been “introduced into a susceptible population of chimpanzees.”

More solid proof of that hypothesis came decades later. A study published in 2007 detected RSV proteins in preserved lung tissue from a child who died in 1931, nearly a quarter century before the chimp outbreak. The authors called it “the earliest confirmed case of RSV infection ever reported.” Other evidence points back even earlier. Descriptions of an illness researchers believe was likely RSV can be found in accounts from the 19th century. An 1819 treatise refers to an “acute suffocative catarrh”—that is, a thick buildup of mucus—that matches RSV’s characteristic symptoms. A recent analysis of genetic changes in RSV estimated that ancestors of today’s virus have been circulating for hundreds of years.

I spoke with several RSV researchers about Kennedy’s theory. None of them gave it any credence, including Philip Roane, who was a technician at Johns Hopkins in the mid-1950s and helped identify the virus in children. (Roane, who is now 98 and a microbiology professor at Howard University, wasn’t given formal credit on the 1957 paper, but he received a box of chocolates and a bottle of scotch from the lead author.) When I told Larry Anderson, a professor emeritus of infectious diseases at Emory University and a longtime RSV researcher, what Kennedy had said, I had to wait until he stopped laughing to get his answer. This isn’t a theory that researchers I spoke with—some of whom have spent decades studying RSV—take seriously.

But Kennedy still had to get that theory from somewhere, right? In The Real Anthony Fauci, Kennedy cites a 2021 article, “From Chimpanzees to Children: The Origins of RSV,” by Lyn Redwood. The relationship between Kennedy and Redwood, a nurse practitioner and anti-vaccine activist, goes back to 2005: Redwood, who believes that her son’s autism was caused by exposure to a mercury-based preservative in vaccines, was among a group of activists looking to recruit prominent figures to support their cause. Kennedy credits her with helping persuade him to take on the issue of vaccine safety.

In her article, Redwood, who is now a senior adviser to the health secretary, suggests that RSV-infected cells from Walter Reed chimpanzees might somehow have made it into the polio vaccine. The tainted vaccine, in turn, could have infected millions of children who received it in the 1950s. But that speculation rests on an obvious error: The kidney cells used to produce early polio vaccines came from monkeys, not chimpanzees. Redwood conflates the two in her article, referring to the chimps at Walter Reed as “sick monkeys.” When I contacted Redwood recently, she defended her article, saying she did not believe the evidence that RSV had been circulating among humans before 1956, even after I sent her the paper about the 1931 tissue sample. (She didn’t respond to an email noting the monkey mistake.)

As for whether RSV made it into the polio vaccine, she told me that she “just posed the question” and that anyone who claimed otherwise would be “misrepresenting my article.” In his book, Kennedy does precisely that: He cites her article when he writes that the virus spread via polio vaccines. What began as confused conjecture by Redwood was repackaged by Kennedy as simple fact.

When I asked HHS for clarification on Kennedy’s views, a spokesperson told me in an email that RSV “originated from a troop of infected chimpanzees,” and that the virus “spread to lab workers and then to the public but not through vaccination.” None of that is true—and it contradicts the (also false) account in Kennedy’s book. When it comes to rewriting medical history, the health secretary can’t even keep his fictions straight.

The Rise of the IRL Influencer

2026-10-13T08:00:00-04:00

At Café Soul, a semi-regular party in New York City, $30 buys you a chance to belt R&B hits, sip margaritas from commemorative glasses, try out Awkward Games’ icebreaker cards, and—as the ticket page promises—form “genuine connections.” When I arrived 45 minutes after the rooftop party started on a recent Saturday afternoon, the few 20- and 30-something guests were mostly sitting on mid-century-modern couches, looking at their phones. But Tionne Barmer, who dreamed up the event, promised me that, in two hours, the rooftop would be packed: People would be enjoying the Patrón-sponsored bar, trying the brown-sugar cold brew (underwritten by On the Way Coffee), using Awkward Games cards to skip small talk, and maybe even flirting. (The event was also sponsored by Tinder.) They’d have a chance to make genuine connections, which is what Barmer was really selling. “People will pay for the entertainment,” he said, “and, on the side, they get community.”

Barmer has always had a talent for bringing people together, and now he’s making a living out of it. Some people call this job “event curator”; others have started using the term community builder. People like Barmer are, in essence, professional scene-makers. They were student-body presidents, sorority leaders, slumber-party queens, that one guy in the friend group who threw the best parties—and now they organize knitting circles, silent reading parties, adult summer camps, run clubs, and life-story sharing sessions to help young adults find one another. They sell their guests the opportunity for friendship, and they sell brands access to the groups they’ve gathered, not on Instagram or TikTok, but in real life.

If Barmer and others like him can make this a full-time profession (he quit his finance job only when his side gig as a community builder could match that income), it’s in part because Americans are in desperate need of shindigs. As The Atlantic has reported, in the past three decades, pretty much every measure of socializing—hosting dinner parties, going on picnics, volunteering—has dropped by double digits; in 2023, only 4.1 percent of us managed to make it to a social event or host one on an average weekend or holiday. “Everyone wants to attend parties, but no one wants to throw them,” Ellen Cushing wrote in this magazine last year.

Planning a party is, after all, a lot of work. Umama Kibria, a co-founder of Play Social Club, grew up helping her father host picnics for their Desi community. He’d cater meals and create elaborate The Price Is Right–esque games. Although he sold tickets to cover the cost of the food, he’d spend his own money on the decor, activities, and prizes. Kibria saw how the events drained his energy and finances. When she graduated from college, she started hosting large gatherings of her own, including grown-up field days and her own Desi picnics. Unlike her dad, she charged enough to make a profit.

What really shocked her father, Kibria told me, was how she was able to find brand partners who’d contribute $10,000 sponsorships so that she could periodically host free events. Between ticket sales, affiliated codes, equity deals, and consulting gigs, she made her dad’s hobby her full-time job. If she provides her peers with the social life they crave, she realized, “people will pay.”

They really will, Joan Li, an associate principal of wellness-industry insights at the market-research firm Mintel, told me. Many Americans now see social connection as a purchasable good. Just as DoorDash offers food delivery for people who don’t have time or don’t want to cook, solo entrepreneurs and businesses offer social calendars. This so-called IRL economy is in some ways a reaction against the internet and the ills of the influencer economy: People want to get off their phones and go somewhere to make an actual friend. But the job of “community builder” is also an outgrowth of influencer culture, Brooke Erin Duffy, a communications professor at Cornell who studies influencers, told me. Because social media is now saturated with creators monetizing their followers, anyone who can get people together offline and in-person could command a premium.

That’s part of the pitch that Pie (short for “People I Enjoy”), a new platform for hosts to advertise and monetize events, is making. “Think about the value of how much influencers get paid to make a video to, hopefully, get someone for three-to-five seconds in a feed, versus sticking someone IRL in front of a logo or a product for an hour. The value is so much higher there,” Nadya Okamoto, an influencer and a co-founder of Pie, told me. The thought of Michaels sponsoring knitting circles so that the company can stick its logo in front of people for longer might give some of us pause—it certainly bummed me out—but Pie, along with platforms such as Onbrand and Offline, which match brands with events to sponsor, is pushing to build a world in which socializing is also a marketing opportunity.

Right now, Pie offers participants in its Pie Creator Club, including Barmer, an average of $445 and up to $3,500 a month to organize gatherings. The company also co-hosted a dinner this summer at which community builders swapped best practices for “communitymaxxing.” It’s currently using venture capital to pay its creators, but long-term, Pie is wagering that businesses will pay community builders like they do online influencers, for access to their guests. And some brands are already betting on this new economy: Tinder launched an “Events” section of its app this past spring, and by the end of the year, plans to feature events in 75 cities, mainly through partnerships with party organizers like Barmer.

As I wandered around Café Soul, which was part of a series that Barmer had designed to get people off their phones, signs reminded guests to LIVE IN THE MOMENT. And as the party picked up, they were doing just that: Hundreds of people formed a dance circle, then opened it up for a man in head-to-toe stone-washed denim, who dropped it low, backed it up, and gave his new friends what may be one of the most electric performances of T-Pain’s “I’m Sprung” ever given at 3 p.m. on a Saturday. But people did also have their phones out to film themselves dancing and lip-synching; one guy in plaid culottes and tiny green sunglasses was filming on a tripod. These events still need to generate online content to be financially viable, Andrew Roth, a co-founder of Offline, told me. Most people find out about these communities through social media, and companies expect that any event they sponsor will generate posts featuring their products. Still, he said, influencers get paid millions of dollars to keep us on our phones—why not reward the hosts getting us (mostly) off them? Roth described a future in which “you already have your monthly book club, and it just so happens this one you’re going to get paid for.”

This proposition is akin to an older phenomenon—the Tupperware parties of the 1950s, Duffy said, when women hosted friends in their living room and exhibited the latest and greatest in food storage. Plenty of people have also paid to socialize at their country club or local Rotary chapter; others have found ways to turn their hobbies into a business, without a venture-backed app to help them do it. At its worst, a world in which a book club is sponsored by Barefoot Wine could make people feel like their every waking moment is a marketing opportunity, even more than they already do. When I played a round of icebreaker cards with two women—who had first met, they told me, at a makeup class at Nordstrom, hosted by another so-called IRL community called Girls That Gather—I had fun, but I felt a bit like I was inhabiting a simulacrum of “community.” Yet all the hosts I spoke with seemed like they were earnestly trying to make sure that their events did not feel that way.

Many of them asked me which communities I was a part of. I’d tell them about Sundays at church and Wednesday Bible study in my living room. A couple of them told me that they were essentially trying to build a secular community from the same template: Churches give people a physical place to repeatedly congregate in a large group setting, and also offer ways for smaller groups to gather throughout the week. Safi Aziz, another full-time community builder, told me he sees events as helping fill the gap left by the decline of public institutions. “If we’re no longer gathering as much over religion” or other organizational ties, he said, “all we really have left to gather over is common interest.” (In his case, that common interest is game nights, which he runs through his company, Joust.)

But unlike these IRL communities, church doesn’t promise a great time. Authentic communities can’t be optimized, because they’re fueled by friction: showing up when it is inconvenient; being kind to one another even when Barbara is being a pain in the neck. They build trust because they ask something of you, besides just money, as the price of admission.

So far, professional community builders mostly seem to be offering people an easy way to party—and thank God for that. Even if someone goes to an event and doesn’t connect with anyone, they’ve still gathered with a group of people that weekend. That is the first step of being part of a community, and something America certainly needs.

The Best Protein Source Is Hiding in Plain Sight

2026-10-10T08:00:00-04:00

Somehow, America has yet to reach peak protein. Perhaps we never will. Even after David bars have gone viral for being bricks of essentially pure protein and Starbucks has rolled out lattes topped with “protein cold foam,” new and somehow weirder protein-laced products keep hitting shelves. You can now buy protein Honey Nut Cheerios, protein popcorn and PopCorners, protein sodas, protein ranch dressing, and protein chips. (Doritos launched a nacho-cheese-flavored version with 10 grams of protein per one-ounce serving.)

In an era of GLP-1 drugs and peptide stacks and Oura rings and self-optimization, of wellness influencers and looks-maxxers, everybody seems to be doing everything they can to eat as much protein as possible. The magical macronutrient will supposedly make you more muscular, or more toned, or thinner—or something, really anything, just better. Amid the protein frenzy, regular food seemingly doesn’t cut it anymore. Why order a simple flat white when you can instead sip a Dunkin’ Nutty Pumpkin Iced Protein Latte?

[Read: America has entered late-stage protein]

Into the fray, I would suggest a humble alternative: Have some yogurt. Calorie for calorie, Greek yogurt has more protein than Chipotle’s High Protein Low Calorie Bowl, Kraft’s new PowerMac, or yes, a Dunkin’ Nutty Pumpkin Iced Protein Latte. So do some traditional yogurts, as well as other fermented options in the dairy aisle such as skyr and kefir. And that’s if you opt for the full-fat, luscious kind (which I recommend). Nonfat Greek yogurt, which is lower in calories, is roughly as protein-dense as a David bar—with the added benefits of having just two ingredients (milk, culture) and not tasting like plastic.

Yogurt is not only full of protein but also good for your bones, your digestion, and your immune system. Yogurt is an ingredient: Eat it plain or bake with it, use it as the base of a sauce or dip, throw it in a marinade or soup. Sure, some yogurts have added sugars, but so does a Starbucks Iced Banana Protein Cream Matcha. And as far as health fads go, yogurt is typically probiotic. All things considered, yogurt may be the easiest protein of all.

[Read: Let’s not fool ourselves about yogurt]

In spite of everything it has going for it, yogurt has not been the face of the protein craze. Perhaps that’s because yogurt is not splashy or technologically innovative or referred to by a trademarked proper noun. A David bar may taste different and have distinct packaging from an RxBar or a Jacob protein bar made with beef tallow, but all plain yogurt is the same. Though some companies have released “protein-enhanced” yogurt (whatever that means), for the most part yogurt is not optimized by corporate food scientists and focus groups in the way that today’s protein-branded products are. Yogurt has been optimized in the sense that humans have consumed it for thousands of years.

Imagine wellness influencers suggesting that you dollop yogurt into a bowl and sprinkle berries on top without measuring anything. There wouldn’t be any regimen to adopt or wellness plan to pay for. There wouldn’t be any special trademarked protein products for influencers to hawk: The company behind the David bar, for instance, has sponsored Andrew Huberman and, until recently, Peter Attia was its chief science officer. The homemade parfait would all be rather mundane and boring compared with Attia’s rotation of four protein powders or the bodybuilder Chris Bumstead’s breakfast filet mignon. It wouldn’t get any views.

Protein is not just a health fad; it is a business. So is everything else in the world of wellness. Indeed, there’s something about many of these setups—which proffer the perfect low-calorie, high-protein snack to pick up on your way to work every morning; a biometric wristband to wear every night; supplements to consume every day for the rest of your life; a weight-loss drug you will inject every week—that keeps people coming back for more, giving their attention and money and energy to the endless pursuit of betterment.

Health and more broadly self-improvement are, obviously, admirable pursuits. Protein can be a way to achieve either. But obsessing over hitting those goals can become unhealthy, as most obsessions are. Have some yogurt, or don’t. You’ll probably be fine.

What We Really Know About the Russian ‘Plague’ Case

2026-10-06T13:17:40-04:00

In a world on edge still from the last pandemic, rumors of a deadly disease that could have escaped from a lab can cause some understandable distress—however speculative they might be. Late last week, reports emerged that a woman who died in a Siberian hospital may have contracted plague, or even that she had seeded a plague outbreak. The case almost immediately set off rounds of hurried speculation within Russia and abroad; officials have shared few details, inspiring elaborate theories about what killed the woman, who worked in a plague-research facility. The fervor around the case escalated on Sunday, when Axios reported that the State Department was monitoring a “suspected plague outbreak” in Russia.

So far, the evidence that the death was caused by plague or something worse is thin, in part because Russian authorities—who have a poor reputation for transparency about biosecurity—have shared few clarifications. But scientists have a good understanding of how plague works. And if the lab worker did contract plague, that is no cause for international panic.

Here’s what is actually known. Sometime in the past week, a woman who worked at the Irkutsk Anti-Plague Research Institute of Siberia and the Far East, not far from the Mongolian border, died of “pneumonia of an unknown cause,” Rospotrebnadzor, Russia’s agency for consumer protection and public health, said Sunday. Government officials have not confirmed her identity, but Russian media have reported that the woman was Daria Shipilova, a 27- or 28-year-old technician at the lab. A local official said that the hospital where she was treated has been placed under quarantine; local media, meanwhile, reported that several hospitals were under quarantine. And Igor Kobzev, the governor of the Irkutsk region, said in a statement on Friday that other people—local media later reported the number as 200—may have been in contact with a resident who contracted an “especially dangerous infection,” and were placed under medical observation. He did not identify the resident as Shipilova or say that the person had died. The public-health agency told state media that “no micro-organisms linked to her professional activity were identified in the patient’s samples” and that no contacts have experienced “health changes related to infectious pathology.” Meanwhile, an aluminum factory in the same town as the laboratory imposed a mask mandate for its more than 2,000 employees, The Wall Street Journal reported.

Plague might sound medieval, but it’s endemic among animals in many parts of the world today. Although Russia hasn’t reported any plague cases to the WHO since at least 2018, Mongolia has. An average of seven cases are recorded in the United States every year, typically from a flea bite or handling infected animals. More than 80 percent of U.S. cases are the bubonic form of the disease, which presents with swollen, pus-filled lymph nodes. Two other main forms of plague, all caused by the same bacterium, are also occasionally reported around the world: septicemic, which infects the blood, and pneumonic, which infects the lungs. Because the lab worker died of pneumonia, speculation that she’d died from plague centered on this last form.

Pneumonic plague is the sole form of the disease that can transmit between humans, but that doesn’t mean it’s particularly likely to spread. David Wagner, the executive director of Northern Arizona University’s Pathogen and Microbiome Institute, told me that the respiratory droplets that can spread pneumonic plague—not to be confused with the tinier aerosols that can spread diseases such as flu and COVID—are only released during a cough or sneeze and only travel about three to six feet. “You have to be in very close proximity to someone with pneumonic plague to contract it from them,” he said.

Because transmission between humans is relatively difficult, the Russian government’s response to the mystery death from pneumonia—placing 200 people under medical observation—is “really incongruent with what you would expect for plague,” Amesh Adalja, an infectious-disease physician at Johns Hopkins University, told me. Daniel Jernigan, the former director of the CDC’s National Center for Emerging and Zoonotic Infectious Diseases, told me that response was “above and beyond” what is typically required for plague cases. Perhaps, he said, the Russian authorities acted out of an abundance of caution; per Reuters, a local official recently said that most of the hospital workers who had been placed under quarantine have already been released.

Even if Shipilova did die of plague, fears of a larger outbreak are probably moot by now. Plague has an incubation period of only one to seven days, so anyone Shipilova might have exposed would have come down with symptoms by now, Jernigan said. Russian authorities have said that no one under medical observation has tested positive for plague. Generally speaking, the chances of a large outbreak of plague are slim. “Once you have an accurate diagnosis, it’s readily treated with multiple types of antibiotics, which is why we don’t have massive plague outbreaks and pandemics anymore,” Wagner said.

Very quickly, though, some scientists, security experts, and media outlets began speculating that whatever killed Shipilova was not traditional pneumonic plague, but a dangerous pathogen that had been somehow altered in the lab. The fear is that the pathogen could be resistant to antibiotics or other treatments, making it harder to prevent an outbreak. No evidence so far suggests that’s true or that the Irkutsk lab was modifying plague bacteria to make it more dangerous. Still, the host of unanswered questions surrounding this case has paved the way for conjectures about links to biological weapons and for conspiracy thinking about government collusion and vaccine companies set to profit off a plague pandemic.

Some Russian media outlets reported—and international outlets repeated—that the woman contracted plague after she broke a test tube containing a sample of the disease. (If that was the case, Adalja said, the lab should have followed the standard procedure of prescribing antibiotics immediately after exposure, which has not been reported.) And in the past, the Russian government has worked on bioterrorist agents and hidden the true cause of disease outbreaks. For example, Soviet officials attributed a 1979 anthrax outbreak that killed at least 64 people to contaminated meat. More than a decade later, President Boris Yeltsin admitted that the anthrax had come from a military biological-weapons facility.

The war in Ukraine has increased speculation about planned biological threats. In 2022, the Russian military began refurbishing a Soviet-era laboratory to handle deadly pathogens such as Ebola viruses, The Washington Post reported. “There’s just a standard lack of transparency from the Russian government that adds to the vacuum of information,” Adalja said.

The U.S. government, for its part, has given inconsistent signals about whether it believes that the incident has wider implications. Along with the State Department, the CDC and the Administration for Strategic Preparedness and Response are reportedly working to learn more about the death. But Secretary of State Marco Rubio downplayed the possibility of danger to reporters yesterday, saying, “I don’t think it’s cause for alarm, but it is cause for focus and a cause to just keep an eye on it.” Today, he called on Russia to be more transparent and share more information. President Trump has offered his sympathies to Russia and said that the U.S. will offer help, though he didn’t specify what form that would take. (The White House did not respond to a request for comment.)

The strong public reaction to the death in Siberia can likely be attributed to some surface-level similarities to the early days of the coronavirus pandemic—a mysterious respiratory disease, rumors of a lab leak, an initial response being handled by a secretive government. Still, the experts I spoke with were adamant that pneumonic plague would not be another COVID-19. Plague may not be totally relegated to the history books, but a major outbreak is low on the list of real threats.

When Anesthesia Goes Wrong

2026-10-05T07:30:00-04:00

Photographs by Julia Sellmann

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When Freddy Marquez was 12, he was hit by a motorcycle while biking and smashed his face into the pavement. He healed fast, but as adolescence reshaped his boyish features, the scar started to tug on his upper lip, leaving his mouth ajar. “Mom,” he said, “I’m going to high school. I don’t want to look like this.” So in September 2024, his parents found a surgeon in central Florida, where they live, to do a scar revision.

On the morning of his surgery, Freddy went into the operating room around 9. His mom, Joana Jardin, settled into a waiting-room chair, expecting to drive him home in a few hours. Noon came, then 1 o’clock, then 2, then 3. “Where is my son?” Joana began to ask. “Where is my son?” The staff couldn’t tell her anything, except that she had to wait. She watched as other parents picked up their kids from surgery and left. At 4 o’clock, she realized she was the only one in the waiting room.

When Joana finally got to see Freddy, around 5, he was barely conscious. His eyes were closed, his breaths shallow. He was just sleepy, a nurse reassured her, because he’d gotten Benadryl after a hive-like rash broke out—but not to worry, the monitors tracking his vitals showed nothing else awry. Eventually, Freddy managed to slump into a wheelchair, his eyes still closed. He was sent home.

The next day, Freddy woke up. Then he threw up. He was still drowsy and now irritable. His head hurt. Joana took him to urgent care and later to the ER, where doctors who evaluated him figured he was just recovering from surgery. But in the coming days, his symptoms became stranger and more disturbing. Freddy started losing control of the muscles in his face. He developed tremors. He choked on his saliva. He lost his balance. He felt what he could only describe as electricity coursing through his brain. “Please, Dad, pray for me,” he would cry when the “electricity” struck.

At the hospital where Freddy was finally admitted, doctors ordered two separate MRIs of his brain, and, to keep him still during the scans, they put him under anesthesia. Both times, he took hours to regain consciousness. Both times, he emerged worse than before.

Freddy lost the ability to walk. His body spasmed and twitched as his muscles took on a life of their own. When Joana saw her son in the hospital bed—eyes staring at the ceiling, limbs flailing wildly—she remembers thinking this is how people once believed you could be “possessed by a demon.”

The scans found spots of white in Freddy’s brain—signs of dying and dead neurons—but no explanation as to what had caused them. In the coming weeks, he got better and then worse, worse enough that doctors ordered yet another MRI. His parents begged the hospital not to use anesthesia again. Don’t worry, Joana remembers being told; the doctors can do it safely. They do it all the time. Joana felt that she had no choice but to trust them. As Freddy slid into unconsciousness, she once again started ticking off the hours waiting for him to wake up: 1 p.m., 2, 3, 4. “Where is my son?”

Freddy never woke up. His body went into cardiac arrest, then respiratory failure. He died on December 29, 2024, at age 14.

Julia Sellmann for The Atlantic

Photographs of Freddy Marquez, who died at 14, shortly after routine surgery under anesthesia

Julia Sellmann for The Atlantic

Freddy’s mother, Joana Jardin

Before that final MRI, in one of their last conversations, Freddy had blurted in a half plea, half accusation, “You don’t understand what is happening to me, Mommy.” He was old enough, by then, to have lost faith in his parents’ omniscience but young enough to still yearn for it. His ordeal had revealed to him that the adult world is riddled with unknowns; that the assurances of even doctors in white coats can mean very little. “I promise that I’m going to understand. Until my last breath,” his mother told him. “I’m going to understand.”

And she would, eventually. Joana did not know it then, but Freddy’s death would be linked to dozens of cases of unexplained catastrophic brain damage after routine anesthesia, all in children or young adults. Several, like Freddy, died. Others became permanently disabled.

The mystery of why Freddy died would ultimately collide with one of the greatest unsolved mysteries of medicine: How does anesthesia work in the first place? How is it that anesthesiologists can induce a state that some have called “functionally equivalent to brainstem death”—only to reverse it? This process happens 60,000 times a day in operating rooms across the United States. Yet it remains poorly understood. What happened inside Freddy’s brain, some researchers now think, may be an extreme version of what happens inside any of our brains when we slip into unconsciousness under anesthesia.

This past May, in Germany, I watched a doctor give a talk to her colleagues about two eerily similar cases almost two decades apart. One was Freddy’s. The other was that of a boy in Germany who went under anesthesia for a broken arm in 2006. Like Freddy, Ulrich “Uli” Gabriel Gobin Hernández was 14. Like Freddy, he took hours to wake up and then gradually lost control of his muscles. But unlike Freddy, Uli survived. The woman giving the talk was not Uli’s doctor. She was his mother.

Yaremy Hernández Castillo, who is soft-spoken and modest to a fault, wore a white coat with sensible sneakers as she flicked through slides of her son’s brain scans. Most of her colleagues at the cardiac-rehab hospital where she worked had no idea that she’d spent the past 20 years—outside her job as an internist—trying to decipher his condition. Early on, she had intuited that what happened to her son could be explained only by something still unknown to medical science. “Uli Gabriel, patient zero,” she came to think of him. But in the initial lonely years of her investigation, his doctors doubted her. Her own medical colleagues did too. “Everyone told me it was absurd,” she recalled to me, even as they could muster no better explanation.

These were the facts of Uli’s case: On Saturday, January 14, 2006—a beautiful day to hit the slopes—he went snowboarding near his family’s home in the Bavarian Alps. Uli took a jump way too fast and landed on his right arm; the humerus bone did not withstand the force of impact. He ended up at the local clinic, where Yaremy worked at the time, and where she trusted he was in capable hands. On weekends, the alpine-village clinic treated an influx of skiers with mangled bones.

But as the hours passed and Uli did not wake up from surgery, Yaremy began to worry. When he finally did rouse—confused, vomiting, and talking “like a drunk man”—her instincts both as a mother and as a doctor screamed that something was wrong.

The trauma surgeon came to check on Uli’s arm and declared it perfect—his own job was done. No one else seemed to share Yaremy’s growing alarm at her son’s mysterious neurological symptoms. The word she kept using to describe this period was alone. To get an MRI of Uli’s brain, Yaremy personally arranged for an ambulance to take him to a larger hospital. On the MRI, two ghostly white spots appeared in his basal ganglia.

The death of brain cells in the basal ganglia, which coordinates movements of the body, explained Uli’s symptoms, which progressed to erratic twisting, painful muscle spasms, and involuntary protrusion of the tongue. But what had caused the damage? No one knew. Uli could still walk and talk, albeit with some difficulty, and he remembered everything: the confusion, the pain, the seven dwarfs from Snow White plastered all over his pediatric hospital room, which, as a 14-year-old, he found tragically uncool. He was impatient to get better and to get out; he had tickets to a Foo Fighters show less than two weeks later. But the day of the concert came and went, and Uli remained stuck in the hospital, his symptoms unresolved, their underlying cause still unknown. The tests that doctors ran all came back negative.

Had his anesthesiologist made a mistake? Yaremy couldn’t dismiss the possibility. How does a perfectly healthy kid become so sick from routine anesthesia, other than because of a terrible mistake? Malpractice could give grief a direction and a shape, suggesting a person to blame (a doctor) and a means of redress (a lawsuit). Friends kept telling Yaremy to sue. In the end, she did, filing a lawsuit against Uli’s anesthesiologist, Ludwig Düthorn, a senior colleague whom she regularly passed in the hallways of their clinic. At the very least, she figured, the lawsuit could help uncover what had really happened.

At the clinic, Yaremy began to avoid the ICU, where Düthorn worked, unsure of what to say about the tragedy that had rattled both of their lives. Düthorn, too, was haunted by the case. He replayed the surgery in his mind, searching for any hint of the debacle to come. Uli’s blood pressure had dipped briefly—but that wasn’t uncommon during anesthesia, and would not have been enough to cause this level of brain damage. Düthorn had counteracted the drop with a routine dose of noradrenaline, and that had worked as intended. All of Uli’s other vitals were unremarkable. All of the dosages had been double-checked by a nurse.

Afterward, whenever Düthorn had to anesthetize a healthy young boy, he would think of Uli. “I was personally devastated,” he told me. “I thought, I did the anesthesia. It is my fault. But on the other hand, I could find no mistake.”

Julia Sellmann for The Atlantic

Uli was an active kid, skiing at 3 years old and playing soccer in elementary school.

The death or serious injury of a healthy child from anesthesia is so unusual as to be universally shocking to doctors these days. Anesthesia is known to pose risks to the elderly or ill, but even then it is far safer than it once was.

In the 19th century, as many as one out of 2,500 patients died under chloroform, then a popular anesthetic. But patients were willing to take the risk, because the alternative was pure, visceral horror: During the pre-anesthesia era, hospitals would put their operating rooms in towers, so as to spare other patients from all the screaming.

Like many medical breakthroughs, the discovery of anesthesia was something of an accident. Doctors became aware that ether, a popular party drug at the time, made giddy revelers insensitive to pain. They decided to give it a try in the operating theater: The first public demonstration was carried out on October 16, 1846, when a 21-year-old man under ether had a malformation removed from his neck at Massachusetts General Hospital. (The name anaesthesia, from the Greek for “without sensation,” was suggested by Oliver Wendell Holmes Sr., the eminent doctor and essayist who also gave this magazine its name, in 1857.) At the time, doctors did not understand why ether worked; that it did was good enough.

General anesthesia today is often likened, colloquially, to sleep. But what it does to the brain is stranger and frankly spookier: A patient who is merely asleep would not lie still and take a bone saw to the chest. To render someone so deeply unconscious, anesthesia shuts down multiple distinct functions in the nervous system, making a patient insensate, paralyzed, and unable to form memories. The brain under anesthesia is suppressed to such an extent that Emery Brown, an anesthesiologist at Harvard and MIT, has compared it to coma or brain-stem death.

“The key thing is that it’s reversible,” Brown told me. When anesthetics stop being administered, the patient starts to rouse within minutes. Their consciousness flips back on. The spell breaks. This total reversal has happened millions of times in millions of people, the magic of it now mundane. But Uli had needed hours to find his way back to consciousness, his brain adrift someplace too deep and too dark to return from unscathed.

In the months after his accident, Uli’s symptoms became manageable enough for him to return to school. Still, he could be unsteady on his feet. On a walk with friends and their dog one day in 2007, he took a tumble and fractured his collarbone. His mother hoped the bone would heal without surgery, but his erratic limb movements from the damage to his brain kept jostling the broken bone. Surgery became inevitable.

Wary of anesthesia, Yaremy asked his doctor to avoid the type Uli had received for his arm surgery. She had no scientific evidence to cite, but she hoped he would listen to her, as a worried mother and as a fellow doctor. He did not.

This time, Uli did not wake up for days. Yaremy thought he was going to die. She would open his eyelids to check his reflexes. Nothing. When his eyes finally stayed open on their own, Uli was delirious. He screamed whenever an unfamiliar nurse entered his room. He had trouble following conversations. His skin became hypersensitive to touch. He lost more control over his limbs. He would never again be able to play guitar in his band or impress girls with snowboarding tricks. He would never even walk or talk on his own.

Yaremy struggled to care for him at home, and she began to contemplate her life in small-town Germany. She had grown up an ocean away, in the boisterous city of Caracas. At 21, she met a German man at a disco in Venezuela, who became her husband and then Uli’s father, and who persuaded her to move to this tiny ski town, where her new in-laws ran a hotel. When she arrived—with 1-year-old Uli in her arms—she spoke little German. For a long time, she was the only foreigner in town. She missed the warmth of the Venezuelan sun and she missed her large family, who she knew would rally to help her back home.

And so, soon after the disastrous second surgery, Yaremy boarded a plane with Uli, now 17, to Caracas. Her younger child decided to stay in Germany with their father. They all planned to reunite in Venezuela later, but Yaremy knew her marriage was already over, its existing cracks widened by the new challenges of caring for their son.

The move proved, in one way, fortuitous. A few years into living in Caracas, Yaremy encountered the first hint that what had happened to her son had also happened to someone else. When picking up medication for Uli—Botox to relax his clenched muscles—she met another mother doing the same for her own son. The facts of his case sounded awfully familiar: anesthesia, delayed awakening, brain damage, loss of muscle control. The mother told Yaremy about a spate of anesthesia complications in the Venezuelan state of Carabobo in the early 2000s, which were blamed on a contaminated batch of sevoflurane, then a fairly new anesthesia drug in the country. Her son, this mother said, was one such case.

Uli, too, had gotten sevoflurane during both surgeries. The colorless and faintly sweet gas has since become one of the most widely used anesthetics worldwide. But Uli’s surgeries were two years apart and 5,000 miles away in Germany, which had had no reports of contaminated sevoflurane. Yaremy couldn’t see how the incidents in Carabobo could be connected to her son’s. Still, she filed them away in her mind.

Not long after, Yaremy began chasing down a second clue, which emerged as Uli’s malpractice case wound its way through the German legal system. The lawsuit itself was unlikely to succeed, now that Uli had suffered the same complications under a different anesthesiologist, but an expert examining the facts of the case made a crucial observation: The two symmetrical white spots in Uli’s basal ganglia, he said, looked much like the brain damage found in people with inherited mitochondrial disease.

Mitochondria are the tiny structures inside our cells that act as power generators. When they become dysfunctional, cells are first starved of energy; then they die. The most vulnerable cells are the most energy-hungry ones; neurons are particularly susceptible, especially those in the basal ganglia. In children with mitochondrial disease, neuron death can be triggered by physiological stress of any kind: fasting, illness, dehydration, and, yes, anesthesia. Perhaps the fault lay with Uli’s mitochondria too.

In 2013, Yaremy managed to secure an appointment at a leading genetic-disease lab in Houston. She boarded the plane with Uli, convinced that the answer awaited them at their destination. There, specialists ran a series of blood tests on Uli and searched his DNA for mutations that cause mitochondrial disease. “I felt like I was going to see the light,” Yaremy told me over breakfast in May. “But nothing happened.” She sighed, her shoulders tense with disappointment.

The tests found no mutations known to cause mitochondrial disease. Moreover, Uli had never exhibited other symptoms; mitochondrial dysfunction affects numerous parts of the body, including the heart and muscles, and symptoms frequently manifest in childhood. Uli had been a healthy and energetic boy: walking before age 1, skiing at 3. Yaremy wondered if her son’s reaction to sevoflurane could be caused by a novel mitochondrial mutation. Uli remembers hearing the doctor, who did not know he understood English, mention her belief dismissively to his medical students.

Yaremy and Uli returned home to Caracas, where they had been building a new life. Uli enrolled at Venezuela’s largest university; using an eye-tracking device to communicate, he graduated with a degree in modern languages. Yaremy worked her way up to professor of medicine at the same university.

Then, in the mid-2010s, Venezuela’s petroleum-dependent economy cratered. Public hospitals lacked equipment as basic as disposable gloves; inflation soared to more than 1 million percent. Even with her connections, Yaremy began to struggle to obtain Uli’s medications. She decided in 2018 to uproot their lives once again, taking Uli back to Germany, where he could receive more reliable care.

By then, Yaremy was closer to finding the explanation for Uli’s condition than she knew. She already held key pieces of the puzzle. But it would take a second tragedy in her family for her to realize how they fit together.

In June 2020, Yaremy got a call from her younger cousin—and Uli’s godmother—María Fernanda Pozo Castillo, or Mafer. They are close, having grown up together in Caracas. Because Yaremy is the doctor in the family, Mafer told me, everyone bugs her with their ailments. (“Yaremy, I have a headache,” she said, slipping into an imitation.) But she was calling about something much more serious. Her 13-year-old son, Matías, had just had knee surgery after a bike accident in Austin, Texas, and he’d struggled to wake up. He had gotten sevoflurane.

“Mafer, no!” Yaremy said.

Even as she began to relive the cold dread of waiting for Uli to wake up, Yaremy pulled herself into problem-solving mode. “Don’t leave the hospital without an MRI, okay?” she told her cousin. “If the doctor says it’s not necessary, it doesn’t matter. You demand an MRI.”

Mafer remembers that the doctors were reluctant to order a brain scan for her son—he’ll be kicking a ball again in three weeks, they told her. But she kept asking and asking until they acceded. Sure enough, the MRI—which was done without further anesthesia—showed two white lesions in the basal ganglia. “Same places,” Yaremy immediately said when she heard this. “Same places as Uli Gabriel.”

In the coming days, Matías started experiencing involuntary limb movement. He developed muscle contractions, even more severe than his older cousin’s, that left him screaming in pain. The contractions have persisted, even with high doses of muscle relaxant delivered straight to his spinal cord. This past summer, Matías’s pain became so excruciating that he had to be hospitalized in the ICU. His mother cares for him full-time. Before we spoke on the phone, she kept apologizing that she might need to leave at any minute to tend to him.

Yaremy was devastated for her family; so was Uli. “I wouldn’t wish it on anyone,” he told me when we met in the spring, tapping the sentence out letter by letter on a board that he uses to communicate.

Julia Sellmann for The Atlantic

Uli has been unable to walk or talk on his own since his second surgery. He uses eye-tracking devices and letter boards to communicate.

Yet amid her grief, Yaremy’s scientific mind got to work: One kid in her family? Okay, a fluke. But two? It had to be genetic. She thought of Uli’s mitochondrial-DNA test from seven years earlier. The sequencing had found no mutations known to cause disease. But the report did note some “variants of unknown significance,” including one called m.11232T>C, meaning that the 11,232nd letter of his mitochondrial genome had been altered from a T to a C. No one made much of the finding; all of us have variants of unknown significance in our genomes, most of which are of little consequence, like minor typos that do not obscure the meaning of a sentence. But maybe this mutation was, in fact, significant.

Mitochondria carry their own loop of DNA, separate from the chromosomes that make up the rest of our genome, and are inherited through the maternal line. Yaremy’s mother and Mafer’s mother are sisters, so they and their children share the same mitochondrial line.

Could a single typo in their mitochondrial DNA be responsible for all of the catastrophic brain damage in the family? And what was the connection to sevoflurane?

Yaremy now began searching for a scientist to study her family. She suspected that Uli and Matías carried the same mutation, as might other relatives. Two of her mother’s sisters, she realized, had also suffered complications after surgery that now seemed to trace back to anesthesia. Were others at risk too?

She found Julio Montoya, an expert in mitochondrial disease at the University of Zaragoza, in Spain, who saw her email in a waiting room as he was about to undergo emergency surgery for a detached retina. With his one good eye, he read it and replied immediately. He was keen to investigate.

Montoya and his colleague Eduardo Ruiz-Pesini had, it turned out, seen the m.11232T>C mutation before. In 2018, they had found it in a Venezuelan boy at a Barcelona hospital. This patient had become severely ill after surgery to remove his tonsils and adenoids—and deteriorated even further with subsequent rounds of anesthesia in later years. The Spanish team decided, along with Yaremy, to put together a formal research proposal. The boy from the Barcelona hospital would become patient one in their study; Uli became patient two, and Matías patient three.

Over the years, Yaremy had talked with colleagues in Venezuela about Uli so relentlessly that word sometimes came back to her of similar cases: nearly always kids, nearly always after routine surgery. An introvert by nature, Yaremy had to learn to badger anyone and everyone for a useful crumb of information.

She began running down some of these rumors: The wife of the son of a friend knew a neurologist who knew an anesthesiologist who knew of a boy who had fallen ill after surgery on a broken forearm. He became patient four. Patient five was the boy whose mother she’d met picking up Botox in Caracas. A physical therapist told her about a boy who’d had cleft-lip surgery—patient six. An old friend from medical school, an anesthesiologist, had examined a boy who developed symptoms after surgery for a cochlear implant. The friend had once been skeptical of Yaremy’s theory, but now he helped her gather data. This boy became the seventh and final patient in the study.

All of the patients who ended up in the study were boys, but Yaremy heard of girls affected, too. For every patient she managed to track down, she followed other trails that ran cold. Families who’d filed lawsuits were reluctant to talk; others were lacking complete medical records. The allegedly contaminated sevoflurane in Carabobo, Yaremy learned, had been widely discussed among doctors at the time, but news coverage of the events 20 years ago had disappeared from the internet as a result of the regime’s media crackdowns and poor digital recordkeeping. She managed to get hold of one newspaper article—a printout saved by the mother picking up Botox in Caracas. But she was not able to find any other families whose children had died or become disabled in Carabobo.

A haunting pattern appeared in the cases she was able to pull together. All seven patients in the study had received sevoflurane. Most of them could trace their maternal relatives to Carabobo; Yaremy’s own maternal grandmother was from the state. And all seven had the same T-to-C mutation. This mutation is extremely rare, even in Venezuela, but it is an estimated 15 times more prevalent in Carabobo, where it is believed to have originated many, many generations ago. The Spanish researchers hypothesized that this old mutation had taken on new, potentially fatal importance in the era of modern anesthesia.

General anesthesia today is usually achieved through a cocktail of drugs, both inhaled and intravenous. Of these, sevoflurane is one of the most popular, particularly for children. It is easy to administer, quick to work, and not irritating to the airways. But sevoflurane seemed to behave differently—and dangerously—in the presence of the T-to-C mutation.

To prove this, the Spanish researchers would need to collect cells with the mutation and subject them to sevoflurane in a lab. Yaremy volunteered her own. In the fall of 2024, she found a colleague to draw her blood and a lab to biopsy a ribbon of her skin. Her cells soon made it to Spain, where the team got to work.

As the lab experiments were ongoing last summer, tragic news came out of Chile. Five children there had suffered terrible outcomes after routine anesthesia; four were dead, according to an alert from the Chilean Society of Anesthesiology. All five children were Venezuelan.

The news spread within the Venezuelan diaspora. In the past decade, more than half a million Venezuelans have moved to Chile, where they have not always found themselves welcome. Now some of the parents alleged that poor medical care and discrimination had killed their children. They filed lawsuits and demanded justice on social media. In videos the parents shared of their children on Instagram and on TV, they are all bouncy and bright: a 4-year-old girl swinging in gymnastics class, a 2-year-old boy in a Messi jersey kicking a soccer ball.

Chilean investigators were able to collect genetic samples from only three cases—out of what had grown to a total of seven in the country—but all three patients had the same T-to-C mutation. One of the children who died in Chile, Yaremy later learned, was the cousin of a patient in her study. As word of the mutation spread around the world, doctors started reporting cases in the United States, Canada, Colombia, Peru, and Guyana.

“I suffered with each kid, each mother,” Yaremy told me. Even when a child survived, she saw ahead to their “lifetime of complications.” She often thinks about the boy with the cleft lip from her study, who, abandoned by his mother, lives in a poor village in Venezuela with his grandmother. His family can’t afford Botox or other treatments. In videos she has seen, his muscles are always clenched, his limbs unusable.

Back in Spain, the researchers raced to finish the experiments. They ultimately found that cells carrying the mutation were indeed hypersensitive to sevoflurane. This mutation could explain why Uli—and Matías and all the other children—had stayed unconscious for so long after surgery. The study, with Yaremy as a co-author, was the cover story of the June 2026 issue of Anesthesiology, the official journal of the American Society of Anesthesiologists. Accompanying it was an editorial written by two physician-scientists in the U.S., Richard Levy, at Stanford, and Philip Morgan, at Seattle Children’s Hospital.

I had first spoken with Levy a few months earlier, after the ASA issued an alert—following up on the one in Chile—about terrible complications from anesthesia, primarily sevoflurane, in people with maternal Venezuelan ancestry. In our conversation, I asked what seemed like a basic question: How does sevoflurane work? “If you can figure that out, you have a Nobel Prize,” Levy told me. “The reality is, we don’t know.” We don’t know how any inhaled anesthetics work. But this novel mutation out of Venezuela, he and Morgan thought, might hold a clue.

Julia Sellmann for The Atlantic

More than a decade after his injury, Uli became a case study in a scientific paper, co-authored by his mother, about how anesthesia interacts with a rare mitochondrial mutation.

Anesthesia likely taps into something evolutionarily ancient in the body. A one-cell protozoan, a Venus flytrap, and a human are all susceptible to anesthesia—and two of those things don’t even have a brain.

For most of the 20th century, scientists clung to the idea that these drugs perturb the fatty membrane of living cells—a hypothesis based on how the gases behave in olive oil. But by the 1980s, a new dogma began to take hold: Anesthetics bind to proteins on the surface of brain cells, which interrupts their signaling. This is best understood in a drug called propofol, which is a common anesthetic but not an inhaled one; the milky-white liquid is delivered via IV. In an elegant set of experiments in the 2000s, scientists identified propofol’s primary target as a protein called the GABA receptor. Yet the same experiment, when repeated with a common inhaled anesthetic, failed to find an analogous target. Decades later, it remains elusive. Maybe it doesn’t exist.

Today, the general consensus regarding the mechanism of inhaled anesthesia is that the gases bind weakly to many proteins in the brain, which together add up to complete loss of consciousness. Most practicing anesthesiologists don’t think much about this. Sevoflurane works. The proof is in the operating room every day. What more do you need?

But a group of researchers dissatisfied with the conventional wisdom on proteins, including Levy and Morgan, has been slowly building the case for an alternative hypothesis: Actually, it’s the mitochondria.

When these researchers heard about children with a mitochondrial mutation dying from anesthesia, they immediately saw the implications. Scientists have long relied on rare mutations to probe the mysteries of biology. In another Venezuelan state called Zulia, for example, families with a shared mutation for Huntington’s disease have been crucial to our understanding of the condition. Rare mutations are a kind of natural experiment.

Morgan, along with his wife and scientific collaborator, Margaret Sedensky, had once run lab experiments looking for mutations that altered sensitivity to anesthesia—though only in a tiny, transparent worm called Caenorhabditis elegans. When they induced random mutations in the worm, they found that the relevant ones were clustered in the mitochondria. Their findings didn’t make much of an impact among their fellow anesthesiologists, though. “We’re like the comic relief at our big national meeting of 15,000 anesthesiologists,” Sedensky told me. “ ‘Here come the worm doctors.’ ”

But Morgan and Sedensky kept working out the details of their theory. Inhaled anesthetics such as sevoflurane, they now argue, work by inhibiting the mitochondria, inducing a kind of temporary brownout in the brain. The bubbles used to transport brain chemicals become frozen in place, like cars that have run out of gas. They restart as soon as anesthesia is discontinued. But in some hypersensitive patients, the mitochondria could become so impaired that their brain cells die. Morgan had found some of these hypersensitive patients before, but he believes Uli’s mutation could help pinpoint more precisely how anesthesia works on mitochondria. This past summer, cells with the mutation—derived from Yaremy’s blood sample—arrived in the couple’s lab in Seattle.

Understanding how anesthesia works, Levy told me, could enable scientists to design better drugs that precisely target the brain, without lingering side effects. Though modern anesthesia drugs are generally quite safe, they are imperfect. They affect the cardiovascular system; they affect ostensibly unrelated areas of the brain, such as the region that controls nausea. And they have been linked to cognitive decline in the elderly after surgery—though the degree to which the drugs are responsible, as opposed to other factors such as the physical effects of surgery, is still being debated. How much of that can be avoided?

Before her study was published, Yaremy had someone she needed to call: Ludwig Düthorn, Uli’s anesthesiologist after the snowboarding accident. She had not seen Düthorn since testifying against him at the malpractice trial years earlier. She’d lost the suit; legally, he had already been absolved. Personally, she felt she had to apologize.

Düthorn was gratified to know what Yaremy had found, but even now, he told me, he feels a doubt gnawing at him in the operating room. Uli had a silent and novel mutation in his DNA. Could his next 14-year-old patient have a different one?

Cases like Uli’s unsettle everyone they touch. In the 2000s, Rafael Legórburu, then an anesthesiologist in Caracas, treated a young boy who would not wake up after sevoflurane—a case he now suspects was connected to this mutation. The boy suffered profound brain damage. Legórburu still finds it difficult to talk about 20 years later. “I have a scar,” he told me, “for the rest of my life.” Today he lives in Spain, where he practices aesthetic medicine, administering Botox and fillers; he says he’ll never touch sevoflurane again.

Doctors are now revisiting a number of old malpractice cases—some of which resulted in large settlements—that might be explained by the T-to-C mutation. An anesthesiologist whose hospital had settled one such case involving their patient told me they felt relieved, and vindicated. (They spoke with me on the condition of anonymity because they were not authorized by the hospital to speak publicly.) At the same time, they could not entirely shake their sense of responsibility. “It was the worst experience of my life,” they kept telling me.

A group of Venezuelan anesthesiologists—largely based in the U.S.—recently formed the Venezuelan Anesthesia Perioperative Risk society, or VAPOR, to raise awareness of the mutation among health-care workers, and to promote guidelines for screening and treating patients with maternal Venezuelan ancestry. A quarter of Venezuela’s population—8 million people—has left the country in recent years, meaning the mutation is scattered more widely than ever. Yet within Venezuela, no lab is testing for it, and anesthesiologists do not routinely have access to the specialized equipment needed to administer anesthesia without inhaled gases.

Yaremy is working with scientists to continue studying the mutation, about which many questions remain: Do other anesthetic drugs, inhaled or administered via IV, pose a danger? Are children more vulnerable, or have we simply not looked hard enough yet in adults? The oldest known patient to be affected was 31 years old.

In her own life, Yaremy has finally found a measure of stability. She and Uli live in Radolfzell, a bucolic lakeside town in southern Germany, where she works at the cardiac-rehab hospital. It’s calmer than the ICUs where she’s worked in the past. “B-O-R-I-N-G,” Uli joked, tapping out the letters in English. But the calm is welcome after years of upheaval. Uli has his own apartment and a rotating cast of full-time assistants; he works as a translator for medical records. (He is fluent in English, Spanish, and German.) He is a doting uncle to his niece and nephew, the children of his younger sibling, Levi.

The mutation still lurks in their lives. Both times after giving birth, Levi, who uses they/them pronouns, developed an infection in the uterus and needed surgery. Yaremy made sure that they did not get sevoflurane. But what about Levi’s kids, who also have the mutation? What if they’re rushed into emergency surgery on their own? Levi had closely followed the news of the children who died in Chile. “They could have been my kids,” Levi remarked as we parted ways after a family lunch by the lake. The water was a brilliant clear blue that day; so was the sky.

A few days after I left Germany, Yaremy learned about a new suspected case: a 12-year-old boy who’d had trouble waking up after surgery in Caracas. “How can this still be happening?” Uli wrote to me. “I mean what the ****!?”

Julia Sellmann for The Atlantic

Uli and Yaremy now live in the lakeside town of Radolfzell, Germany. Uli works as a translator for medical records.

Joana, Freddy Marquez’s mom, first caught wind of the suspected mutation in the summer of 2025, when she heard on social media about the children who’d died in Chile. She, too, is originally from Venezuela. And she made the connection instantly. Months earlier, when Freddy had been hospitalized, his doctors had ordered a genetic test that turned up a variant of unknown significance. Freddy had the m.11232T>C mutation as well. This information never made it into his chart for the same reason Uli’s mutation wasn’t initially taken seriously: No one understood its importance at the time.

Joana began commenting about Freddy on every related post she could find. One by one, she linked up with others who told similar stories: another mother in Florida, the family of a girl who died in Houston, Yaremy’s cousin Mafer in Austin, and so on. Joana got added to a WhatsApp group for the parents in Chile, which has since evolved into a de facto global support group for parents of children with this rare mutation. Through the group, Joana also learned of Yaremy. They spoke for the first time in February, and recognized in each other a maternal instinct that is both steely and tender. “She was in tears,” Joana told me, “and I was in tears.”

In February, Joana appeared on Instagram Live in a zebra-print shirt to talk about Freddy, alongside other affected mothers. The zebra print was a reference to the old medical adage “When you hear hoofbeats, think horses, not zebras”—meaning: think of the common explanation, not the exotic one. But sometimes, it is zebras. Freddy died because what happened to him lay just outside medical knowledge. His particular mutation is rare, but encounters with the unknown in medicine are not. Joana was asking for some humility, some openness to the possibility of zebras. Since Freddy’s death, she has made advocating for people with rare mitochondrial conditions her life’s mission.

Joana can still picture him: swimming, playing basketball, riding “like crazy” on his bike as Gordito, his Alaskan malamute, raced alongside him. “His flipping dog is now chasing me wherever I go,” she said. And Joana continues to propel herself forward. She’s cold-calling researchers. She’s going to medical conferences. She’s offering up her own cells to study. She is keeping the promise she made to Freddy before he died.

This article appears in the November 2026 print edition with the headline “Going Under.”

Are Mormons Losing Their Distinctiveness?

2026-10-04T08:00:00-04:00

Mormons have sometimes called themselves a “peculiar people,” and statistically, they have been. Compared with Protestants, Catholics, Jews, and Buddhists, Latter-day Saints have higher birth rates, higher marriage rates, and larger families. They also have a relatively high retention rate—meaning that those who are born into the Church of Jesus Christ of Latter-day Saints tend to stay members for life. But recently, all of these long-held patterns have started to shift.

The Church is not facing a crisis, exactly—more of a demographic ravine than a cliff, Jana Riess, a historian who studies the LDS faith, told me. But as of 2024, only about half of young people born into the Church stay in it—down from more than 80 percent in the 1980s. Its marriage rate has fallen 10 percent since 2011, and in the past 40 years, the number of annual recorded births per 1,000 LDS members has dropped from 25 to five, according to an analysis of Church records by the independent data scientist Alex Bass. If Latter-day Saints’ peculiarity was defined in part by their early marriages, their minivans full of kids, and their loyalty to the Church, some of that peculiarity seems to be slipping away.

The LDS Church’s birth-rate and retention problems are far from unique: People in the United States are having fewer babies and leaving religion pretty much across the board. Doug Andersen, a spokesperson for the Church, wrote to me in an email that “official church records show consistent worldwide increases in both membership and participation,” in part because a record number of converts are joining worldwide.

Still, the demographic tilt is enough of a problem that the Church’s new leader, Dallin Oaks, is taking notice. Under the previous Church prophet, mentions of family were fewer and farther between at the Church’s biannual conference. But this year, in his first conference address since becoming prophet, Oaks issued a warning: Although the Church’s marriage and birth rates were better than the U.S. average, they had declined significantly. “We are a family Church,” he said, and quoted from the 1995 “Family Proclamation,” which once hung on the walls of many LDS homes: “God’s commandment for His children to multiply and replenish the earth remains in force.”

In some ways, what’s happening to the LDS now is what happens to any religion that grows beyond a core of strong believers. Over time, the more particular edges of a faith—the meatless Fridays of Catholicism, for instance—can get sanded down until it more closely resembles mainstream American culture and mainline Protestantism, Matthew Bowman, the chair of Mormon Studies at Claremont Graduate University, told me. (The Church now discourages use of the word “Mormon” as a nickname for members of the faith, but the term is still used in proper names, such as Bowman’s title or The Book of Mormon.) To him, the demographic shifts in the LDS indicate that “the long process of assimilation is becoming more noticeable now.”

Compared with individual Protestant denominations, such as Methodism, the LDS looks like it’s doing better at retaining its young people, Justin Dyer, a religion professor at Brigham Young University, told me. But Ryan Burge, a political scientist at Washington University in St. Louis, argues that that’s not the right comparison to make, because even if someone switches from Methodist to Lutheran, they still hold pretty much the same Protestant beliefs. And Protestantism’s retention more generally, at 70 percent, far surpasses the LDS Church’s.

Lower retention may also have more ramifications for the LDS Church than it would for Methodists. Fewer young people means fewer missionaries. And fewer members means that the work of operating churches, which are volunteer-led at the local and regional levels, will fall on fewer people. In the past, the Church’s robust structure for kids (Sunday school, youth programs, regional dances, and sleepaway camps) carried young people into missionary work, which usually equated to lifelong membership, but that formula seems to be failing now, Jana Riess said. (She herself is an LDS member.) “The Church has been great at retention in the past and is doing many of the same things that used to be so successful then. So it’s understandable why leaders would be sort of wringing their hands and saying, ‘Why isn’t this enough?’”

The Church is having a particularly hard time keeping young women. In 2025, fewer than 40 percent of 18-year-old girls stayed in the faith, according to Dyer’s research. Many apostates leave because they are more liberal than the Church on issues such as same-sex marriage, but when Riess interviewed young women for her upcoming book on people who leave the faith, many of them also brought up feeling undervalued by the Church.

In LDS theology, only men can hold what is called the priesthood—the authority given by God to Joseph Smith and passed down through every generation of LDS men—which allows them to bless children and the sick, pass the sacrament, and serve in certain leadership positions. Because of this, essentially, “there is nowhere in the LDS Church where a man reports to a woman on questions of final authority, and there is nowhere in the LDS Church where a woman has final say,” Bowman said. And the 1995 Family Proclamation made clear that a wife’s role is to nurture the children. “It’s a tough position for the Church to be in,” Riess said. “It wants to remain attractive to women in a culture that has moved in a different direction, but also wants to stay pretty much on the same path of emphasizing this very particular configuration of the nuclear family.”

Many women do not mind the Church’s male priesthood, or at least accept it. “I can believe that something’s divine but also fallible at the same time,” Sophie Smith, a graduate student at BYU, told me. She believes that women already have many ways to contribute to the faith and that “whether it’s in this life or the next, it will not be a patriarchal Church.” But LDS leaders do seem to be aware of the Church’s young-women problem: Women can now direct their ward’s Sunday-school program, and recently, the Church lowered the age at which women can serve a mission from 19 to 18.

This decision has led to a record boom in missionary numbers, but it’s also “a way to keep young women in the fold and try to socialize them more deeply in the faith,” Riess said. (One refrain in LDS circles, Bowman said, is: “A missionary’s most important convert is himself or herself.”) Completing a mission at 18 also means that young women can get married sooner: They return around age 20, and “on the LDS checklist, the next check is getting married and having children,” Alyssa Beck, who leads classes for teenage girls at her ward in Los Angeles, told me.

Women who do lean into the Church’s call to motherhood may still struggle to have a big family, though. Smith has noticed those around her having fewer kids, mostly because they can’t afford more. For years, the single-family-home price in the so-called Mormon Corridor—Utah, Idaho, and Arizona—ran below the national average, but since 2020, prices have soared above that threshold, according to Bass’s analysis. “There are still people who are like, I wanna have eight kids, and that’s awesome,” Smith said. But out of necessity—because both parents need to work, and kids are expensive—many don’t.

These younger families may find less than they once did to keep them immersed in the culture of the religion. Between bazaars, choirs, plays, and road shows, congregants might have once been at their chapel four times a week; now many active members come only on Sundays, Bowman said. (And even Sunday services have been shortened from three hours to two.) As the faith has grown internationally, “the cultural apparatus that was built in Utah just wasn’t exportable,” Bowman said, and because the Church tries to keep its practices consistent across the world (whether in Kenya or Utah, every chapel uses the same teachings and Sunday-school curriculum), he believes that Church leadership pared back the social expectations of being a Latter-day Saint. That cultural loosening might be helping the Church grow internationally and simultaneously making it easier for American members to leave. (Andersen, the LDS spokesperson, said that the Church is “encouraged by increased participation of our children, youth, and young adults in the United States in the past decade.”)

For now, the Church seems to be insisting that its future is rooted in family—which will require people to heed the words of the prophet, and multiply and replenish the Earth. To do that, though, young people will need to stick around. Churches across the country, not just the LDS, are trying to figure out that particular puzzle: Recently, many younger Americans have passionately recommitted to religion, but their depth of feeling hasn’t caught on widely—at least not yet. Whether they grew up LDS, Catholic, or Baptist, many Americans seem to want churches to offer some combination of retreat from mainstream U.S. life and assimilation in it. But, as Bowman said, “that is a very, very tricky sweet spot to hit.”

MAHA Gone Mild

2026-09-30T16:45:13-04:00

The Make America Healthy Again movement has always had a split personality. Many of the movement’s leaders are fervent anti-vaccine activists whose views are at odds with scientific evidence and out of step with most Americans. At the same time, MAHA’s tenets include eating more vegetables and getting enough sleep, which is perfectly reasonable advice; it’s just hard to take seriously from people who, like Health Secretary Robert F. Kennedy Jr., wax nostalgic about catching measles.

That duality has been especially stark this month, as the midterms approach and Republicans look to MAHA for an electoral boost. At a conference two weeks ago for Children’s Health Defense, the anti-vaccine organization Kennedy founded, he told the audience that they had a “steadfast friend at the White House.” At a MAHA data summit on Monday, Kennedy previewed his plan to use a database of Americans’ health records to compare rates of autism among vaccinated and unvaccinated people. And yet, the second annual MAHA Summit, which was held yesterday in a hotel ballroom in Washington, D.C., seemed perfectly calibrated to downplay controversy.

Other high-ranking administration officials, including Vice President Vance and Medicaid chief Mehmet Oz, spoke at yesterday’s summit, lending the affair an extra layer of high-profile polish, but the event was mostly an opportunity for its roster of sponsors to tout their products and services. An executive from Walmart—one of the event’s many corporate sponsors—spoke about making food labels simpler and more transparent, though he didn’t say how his company, which sells more groceries than any other retailer, plans to do that. After being lobbed yet another softball question from the moderator, he gushed, “It means a lot for us to be here with MAHA.” Also among the sponsors was Grail, a cancer-screening company, which just last week announced that its controversial early-detection test had been recommended for approval by a Food and Drug Administration panel. Hims & Hers and Gameday Men’s Health—two wellness companies that stand to make serious money if the FDA allows gray-market peptides to be made and prescribed in the United States—also chipped in. Bloomberg reported that companies that forked over $300,000 were allowed to have “meaningful input” on the selection of panelists and topics. (In an email, an HHS spokesperson wrote that the FDA’s decisions “are made through established processes grounded in law, science, and evidence.”)

[Read: America is about to go over a peptide cliff]

The MAHA Summit was “very money-driven,” Mary Holland, who runs Children’s Health Defense and was not on the speaker list for yesterday’s conference, told me outside the ballroom. Kennedy has for years denounced corporate influence over the health agencies he now oversees, but onstage, there was no handwringing about conflicts of interest. Instead, Tony Lyons, the president of the nonprofit MAHA Center, which organized the summit, offered praise for “the investors scaling natural remedies, breakthrough technologies, next-generation devices, and cutting-edge therapies.” (Lyons is also Kennedy’s longtime publisher, and his company, Skyhorse, paid Kennedy $4 million in book advances over the past year.) Corporate convenience seemed to beat out Kennedy’s “eat real food” agenda: The conference swag bags contained two organic snack bars, a packet of electrolyte powder, potato chips fried in grass-fed-beef tallow, and a bag of dehydrated taco filling made from pinto beans and peas, all vaguely MAHA-coded but certainly nowhere to be found on the administration’s inverted food pyramid.

Plenty of Kennedy’s vocally anti-vaccine compatriots were in attendance, if not on the agenda. I spotted Mark Gorton, the president of the MAHA Institute, who, at the Children’s Health Defense conference, declared himself “the boldest anti-vaxxer in the anti-vax conference.” Del Bigtree, Kennedy’s former communications director, who once told me he’d rather his kids catch diseases such as polio and measles than get the shots that prevent them, spent most of his time chatting with his many fans in attendance. He was pleased at how large companies appear to be on board with MAHA, even if the summit steered clear of the issue—vaccines—that brought him and Kennedy together. “It really probably should be called ‘MAHA Food Summit,’” he told me. (An HHS spokesperson wrote that Kennedy “oversees an extraordinarily broad health portfolio and addresses different priorities in different settings.”)

[Read: ‘I genuinely am upset that your kids are vaccinated’]

But lest Bigtree and other anti-vaccine activists have any doubts, Kennedy has repeatedly reassured them that he is on their side. At the Children’s Health Defense conference, he went so far as to read from a manufacturer’s list of possible adverse events from a hepatitis B vaccine. In an appearance on CNN last month, Kennedy again floated a possible connection between autism and vaccines, even though researchers have found no such link.

Since Kennedy’s failed run for president in the 2024 election, he has drawn together an unlikely and seemingly uneasy coalition. Some are hard-core activists, like the guy I spoke with who was wearing a shirt that took aim at fluoride, vaccines, hospital births, aspartame, and root canals. But other attendees at the packed, invite-only event said they were there because they hoped psychedelics might be used to treat depression; because they thought that AI might improve health care; or because they were looking for answers to medical problems their doctors hadn’t been able to solve. They weren’t anti-vaxxers, and they weren’t necessarily big Kennedy fans, as a couple of them confided to me between sessions. But Kennedy and his Republican allies seem to hope they can channel these different levels of frustration with mainstream medicine and keep all of those voters under the MAHA banner. The midterms will be, among so many other things, a test of how far that banner can be stretched.

GLP-1s Are Rewriting the Story of Weight Loss and Mental Health

2026-09-29T13:25:05-04:00

Noom, the popular weight-loss app, prompts its users not only to log their meals and exercise but also to gaze at paintings. The “Mindful Art Break” feature includes images of such works as Claude Monet’s Woman With a Parasol—Madame Monet and Her Son and Franz Marc’s The Bewitched Mill, neither of which seems to have anything to do with body fat. Breath work, meditation, and lessons in cognitive-behavioral-therapy techniques are also available on the app. One user, in a testimonial the company sent me, said that Mindful Art Break helped them “contemplate something other than weight loss.”

Why, then, would a weight-loss company offer such a program? Noom launched a stand-alone emotional-health program called Noom Mood in 2023, the same year it added GLP-1s to its offerings. Then, last year, the company integrated core Mood tools into the flagship app “after seeing major overlap with weight, stress, and self-care needs,” Emily Passer, Noom’s head of communications, told me. Other weight-loss services—especially newer ones that offer GLP-1 medications—are getting into mental health too.

Mental health and weight are, of course, intimately linked. As someone who lost almost 70 pounds by strength training and getting treatment for an eating disorder more than a decade ago, I can certainly attest to the importance of mental-health support during any sort of body change. But Noom and other weight-related companies are leaning into a common strategy to entice customers: To be palatable (and successful), a weight-loss company must now profess care for its customers’ psychological health, not just for their waistline.

Wondr Health, a weight-loss platform that partners with employers, offers information about managing stress and anxiety and says that its program begins with “behavior change.” Weight Watchers, which filed for bankruptcy last year, announced in December its “fully integrated platform for the GLP-1 era,” including features related to behavioral health and community support. Kim Boyd, the company’s chief medical officer, told me that weight loss and mental health shouldn’t be treated as separate pursuits. “It’s all happening in one person, and those things are really, really connected,” she said.

“Mental well-being is a huge trend right now, and I could see how it would be good business to capitalize on it,” A. Janet Tomiyama, the director of UCLA’s Diet, Stigma, and Health Lab, told me. Other industries have done just that in recent years—see Ulta Beauty’s “feel-good” wellness initiatives and Bumble’s “interest badges” for therapy and mindfulness. The messaging is playing to widespread sentiments. In a May 2025 survey, YouGov asked U.S. adults to rank how essential various states of being or behaviors are to overall physical health; 79 percent of respondents said that “having good mental health” is essential. When the National Academy of Sports Medicine asked personal trainers in April what their goals were for their average client, mental clarity and stress relief came in just under weight loss and well ahead of athletic performance.

And yet, mental-health support from a weight-loss company might feel incongruous, in no small part because the tools of weight loss and the drive to lose weight have historically not improved people’s mood. Tomiyama said that in a 2010 study she co-authored, the stress hormone cortisol spiked when women were randomly assigned to start a diet. Plus, Tomiyama said, because many people who diet gain the weight back, they end up feeling as if they’ve failed. “We have scientific, causal evidence that diets ruin people’s mental health,” she said. “So I’m not surprised that these companies are noticing that through their customer base and realizing they have to do something about it.”

Now more than ever, though, dramatic weight loss doesn’t have to involve dieting at all. Instead of cutting calories and fighting against related hunger, people can take a GLP-1 and feel fuller from less food. One small, non-placebo-controlled study on how a GLP-1 called liraglutide affected mood and behavior suggested that the drugs significantly improved depression symptoms. The research is complicated, though: Other studies have found no significant effect on mood, and still others suggest that, at high doses, GLP-1s are linked to depressed mood, possibly because of their dopamine-dampening effects. Anecdotally, some GLP-1 users experience anhedonia. But others feel more optimistic, perhaps because, unlike dieting, the drugs can turn down the dial on so-called food noise.

The social effects of GLP-1s are also less than straightforward. On the one hand, people who are overweight or have obesity face a lot of stigma and can be treated poorly, which is famously not ideal for your mental health. So perhaps GLP-1s can improve mood simply by being an effective way to lose weight. On the other hand, Tomiyama conducted another study that found that people who lose weight through GLP-1s are socially stigmatized even more than people who have never tried to lose weight in the first place, perhaps because of perceptions that GLP-1 users opted for the “easy way out.” People who go off GLP-1s and gain weight back are stigmatized too. Boyd, from Weight Watchers, said that the mental-health-related struggle she observes most from the company’s clients is shame around GLP-1 use being seen as a cheat code. She knows of one woman who was storing her neighbor’s GLP-1 medications in her fridge because the neighbor didn’t want her husband to know she was on them.

It’s no wonder, then, that people who take these drugs might want some extra help for their mental health. In a 2024 survey of 300 GLP-1 users, 75 percent reported that they were interested in behavioral-health support, and 63 percent believed that they would achieve better health outcomes while taking GLP-1s if they also received such support. They might be right. Spencer Nadolsky, an obesity specialist who founded an online medical-weight-management platform that offers both GLP-1s and behavioral and emotional support, told me that psychological support “doesn’t necessarily lead to a lot more weight loss in general, but it improves outcomes in other realms of the weight-loss journey,” including patients’ feelings about the process and their general quality of life.

The cynical view—one I’ve taken myself—is that any gesture toward mental health by an entity selling weight loss (or anything else) is an empty marketing-and-sales tactic. How effective these interventions are at actually supporting customers’ mental health, and whether companies will continue offering them if mental-health support exits the zeitgeist, remains to be seen. But in my experience, weight loss on its own also isn’t enough to meaningfully improve mental health. When I got treatment for my binge-eating disorder, the pounds were coming off because I was eating less and because I was exercising in a way I liked. My mindset and lifestyle seemed to be changing for good because I was talking through the anxiety and depression that drove my bingeing in the first place.

I think back to the times I sat in early-2000s Weight Watchers meetings with my mom, where conversations revolved around the scale—or when a doctor told preteen me to “eat healthier” to lose weight without asking what I even knew or thought about healthy eating, or how difficult it was for me because I had a disorder. It would have been nice to have someone even pretend to care about my feelings. Hopefully, this new concern on the part of the companies will last.

Why a Sea-Lion Epidemic Is a Bad Sign for Humans

2026-09-18T11:06:00-04:00

You have likely never heard of synanthropes, though you surely know them. And they know you. Synanthropes, whose name is derived from the Greek for “together with man,” are not our pets or our herds of domesticated animals but something like our oldest frenemies: beings from which we have long sought and failed to decouple ourselves, that now reside within our communities, and that have become an ineluctable part of our lives. They include insects like bedbugs, which have evolved within urban environments to become uncommonly dependent on humans for their survival, as well as house sparrows, seagulls, blackbirds, and pigeons, all of which have adapted themselves to take advantage of cities while evading their dangers. In Singapore, synanthropic river otters have begun rampaging through local markets and aggressively pursuing tourists for food. Black bears are bathing in backyard swimming pools in California.

All of these creatures straddle the human world and the wild. And that can make them uniquely perilous to human health.

In Chile, which has a 4,000-mile-long coastline, the most conspicuous synanthrope is the South American sea lion. About 130,000 of these pinnipeds, which can weigh 660 pounds and resemble giant waterlogged chocolate Labrador retrievers, live in raucous colonies on the water’s edge. On account of their ubiquity, pretty much everyone in Chile has had some kind of run-in with the barking beasts.

“As a Chilean, you can easily see sea lions,” Victor Neira, a veterinary scientist and virologist, told me from his lab at the University of Chile in Santiago. Sea lions have long been habituated to human handouts in Chile, and many of the urban colonies they’ve established are located near fish-processing plants, where the animals gorge on fish guts, bycatch, and other detritus dumped back into the ocean. “They’re not aggressive by nature,” Neira said. “They see people all the time, so they generally just move out of the way for you.” He thought for a second and seemed to change his mind. “That being said, if you mingle with them, they will try to bite you. So usually you have to kind of run or you have to scream.”

Neira has had more than his fair share of sea-lion encounters, because he’s spent the past decade tracking novel viruses in wild and domesticated animal populations across South America to sound the alarm about potential threats to humans. The more blood and fecal samples he and his team collect from seabirds and marine mammals, the more likely they are to detect novel pathogens or viral variants that have just appeared in the region. This sort of epidemiological research is undertaken in countries across the world because scientists now recognize that synanthropes are among the most important vectors transmitting novel pathogens to human populations. The hope is that a network of scientific early-warning systems, like the one Neira and his team have designed, can give humanity a head start in identifying new pathogens and stamping them out before they explode into the next pandemic.

In December 2022, Neira discovered a disturbing anomaly in blood samples he had been routinely collecting from migratory birds in Chile. H5N1—an influenza virus that causes acute respiratory symptoms and death in birds—appeared to be circulating among pelicans, cormorants, and terns. All three species regularly cross paths with other birds and sea creatures, and the viruses they harbor, along their migration routes. Neira was terrified. In the preceding 20-plus years, H5N1 had killed tens of millions of wild birds around the world, and hundreds of millions of poultry had been culled to contain its spread. He girded himself for a devastating avian outbreak. When the viral wave arrived, though, the casualties went much further.

Neira told me that in early January 2023, clusters of dead seabirds began washing up on shore. Later that month, Neira’s team witnessed the first cases of H5N1 among Chile’s sea-lion colonies. After years during which the monthly number of sea lions stranded on land (a measure that marine biologists use to assess disease severity and death counts) never surpassed 100, January 2023 saw a sudden spike to about 250. One month later, that number had doubled, and in June, more than 4,500 stranded sea lions were observed by scientific authorities. Overall, somewhere between 10 and 25 percent of the sea-lion population in the country died in the six months after the first H5N1 case was detected among Chilean seabirds, though Neira estimates that the proportion could be double that. It was a sudden and deeply frightening mass-mortality event, caused by a virus that had gained the ability to infect and kill mammalian hosts as well as avian ones. The corpses were piling up on shore, attracting flies and other scavengers—and risking further spread of the virus. Eventually, Neira said, the Chilean government built halls to house the remains, a sign of the scale of the crisis and its lasting impacts on Chile’s ecosystem.

More epidemics were caused by novel viruses in the past two decades than in all of the 20th century, suggesting that human vulnerability to opportunistic pathogens has shifted dramatically. The H5N1-fueled mass-mortality event among Chilean sea lions is an unsettling illustration of how synanthropes are ratcheting up this risk by bringing novel viruses carried by wild and migratory animals close to humans. H5N1 is still spreading through animals worldwide, including in the United States. More than 1,000 American dairy herds have tested positive for H5N1 over the past two years; cases among poultry and cattle alike may tick up this fall during the seasonal migration of wild birds.

So far, that hasn’t translated into a major human outbreak. Since 2024, only 71 human cases of H5N1 have been reported in the U.S. Two people have died. No evidence indicates that the virus currently infecting cattle can spread between people. It’s a lucky break, given how ubiquitous H5N1 is among hundreds of wild bird species that regularly come in contact with poultry and cattle herds, which are perfectly positioned to infect human populations with opportunistic pathogens. That luck might not hold forever, though. A recent report from the World Health Organization suggests that H5N1 viruses are continuing to mix and match genetic material, and a 2024 study from Scripps Research Institute in San Diego found that the H5N1 variant circulating in U.S. cattle is only a single amino-acid mutation away from being able to efficiently infect humans.

As animal populations continue to come into closer proximity with humans, the threat posed by synanthropic viruses will only grow. Viral pathogens can now be efficiently borne from the most remote places on Earth into the heart of human metropolises. It just takes an animal to bring it from there to here.

This article has been adapted from Dan Werb’s new book, Our Wild Familiars: How Animals Are Adapting to Cities and Reshaping the Natural World.

RFK Jr.’s Brazen Reassurance to Anti-Vaxxers

2026-09-17T19:33:23-04:00

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Since becoming Health and Human Services secretary, Robert F. Kennedy Jr. has repeatedly denied that he opposes vaccines and has toned down some of his more extreme rhetoric on the subject. But in a keynote speech today at a conference for Children’s Health Defense, the anti-vaccine organization he founded, the old Kennedy was back. He complained about safety studies, floated disproven theories about a link between vaccines and autism, and all but declared himself an anti-vaxxer. “You have a strong and steadfast friend at the White House,” he told the crowd.

His choice to take the stage at the conference signaled a shift. Since becoming HHS secretary, Kennedy had distanced himself from Children’s Health Defense as he worked to convince the Senate that he held mainstream-enough views on vaccines. Children’s Health Defense, meanwhile, attempts to convince parents that vaccines are a threat to their children’s well-being. In just the past few days, CHD has used its X account to warn parents against trusting babies with health-care providers who might give them vaccines, claimed that childhood vaccines kill more children than do the diseases they prevent, and alleged that COVID vaccines were designed to cause infertility. The speakers at its conference were a who’s who of the anti-vaccine movement.

Nearly everything the organization promotes runs counter to guidance from the CDC, an agency that Kennedy leads as head of the Department of Health and Human Services. But much of Kennedy’s speech was consistent with CHD’s brand of scaremongering. He suggested that vaccines contribute to chronic disease and disorders such as autism. He bemoaned the fact that more vaccines are recommended for American children now than when he was a child. And he falsely claimed that nothing is known about their safety. “We have no idea what the risk profile is for these products,” he told the crowd.

In one of the more bizarre moments of his address, Kennedy read from the manufacturer’s list of possible adverse events for the vaccine against hepatitis B, a disease that can lead to liver failure. Among those he mentioned was anaphylaxis, an allergic reaction that occurs roughly once for every 1 million doses administered. He ignored the benefits of the vaccine, which has drastically reduced infections and is projected to have prevented millions of deaths. Instead, he implied that the vaccine was merely part of an industry “gold rush.”

The speakers surrounding Kennedy are publicly hostile to vaccination. He was introduced by Mary Holland, the CEO of Children’s Health Defense, who took over the organization after Kennedy’s departure and praised him for taking on “the corrupt medical pharmaceutical complex.” Mark Gorton, the president of a pro-Kennedy think tank called the MAHA Institute, had earlier told the crowd that vaccines are a “public-health nightmare” and that eliminating them would make the country healthier. And then there was Andrew Wakefield, known for his discredited 1998 Lancet paper that alleged a connection between autism and the MMR vaccine. Anti-vaccine activists have spent decades citing Wakefield’s faulty research in an effort to fuel fear of immunizations.

Now is a terrible time for Kennedy to return to public anti-vaccine advocacy. Pennsylvania is in the midst of a deadly measles outbreak. The official count in the state is 731 cases since April and 117 in just the past week; the real number of infections is almost certainly much higher. Four people, two of them infants, have died since mid-August. Much of the suffering has been concentrated among the state’s Amish community, where immunization rates are low, about 25 percent in Lancaster County. Before becoming HHS secretary, Kennedy praised the Amish for declining to get vaccinated, telling a crowd at an Amish country fair in 2021 that, when it comes to vaccines, “it’s so important for us to think more like the Amish think.”

Rather than speaking publicly about how low vaccination rates are the reason that measles is sickening and killing Americans, Kennedy has spent the past month squabbling with Pennsylvania’s governor, Josh Shapiro, over how to define measles-associated deaths. Under Kennedy’s leadership, the CDC has so far declined to list any deaths from Pennsylvania’s ongoing outbreak; this afternoon, while he was onstage, HHS’s official X account called the state government’s demands that the CDC do so “political blackmail.” In his speech at the conference, Kennedy’s only mention of measles was part of a complaint that deaths from the disease “get headlines” while the alleged dangers of vaccines are ignored. (An HHS spokesperson didn’t respond to a question about why Kennedy was appearing at an anti-vaccine conference during a measles outbreak.)

Kennedy reassured the crowd that research into vaccine safety was going on behind the scenes at HHS. “As I said, you have friends in the White House,” he said, “and we are doing this one day at a time.” He claimed that HHS had failed to study vaccine risks and told the audience that he was remedying that. He mentioned making use of the Vaccine Safety Datalink, a collection of Americans’ electronic health records. That database has long been a topic of fascination for Kennedy and other anti-vaccine activists who believe that it might contain hidden evidence that vaccines are harmful.

Kennedy built his reputation on being the country’s most prominent anti-vaccine activist. As HHS secretary, he has often emphasized less controversial issues, such as ultraprocessed foods and artificial dyes. Today, he took to the stage with a message for his longtime allies: He is still one of them.

This Is Your Brain on Short-Form Video

2026-09-16T15:37:46-04:00

Among the many aspects of online life accused of rotting our brains, a certain folk psychology holds that short-form video is an especially egregious driver of the decay. In an interview last month promoting his new film, in which a London couple move their tech-dependent kids to a barn without electricity, Andrew Garfield described himself as addicted to an Instagram feed full of “weird ceramics” and Japanese craftspeople. “I’ve given all of those hours to nothing,” he told Variety. “It’s genuinely enraging because we don’t have as much control over these impulses as we should.” Even Steve Chen, one of the co-founders of YouTube—home to many a recycled TikTok on its Shorts—has said that he’s wary of his kids watching too much short-form video, because of the damage it does to attention. Sometimes, when I emerge from the dark vortex of a scroll gone too long, I worry that my thoughts will permanently become as flighty as my feed.

But here’s the tricky part: Very little research exists on what short-form videos are doing to the human mind. This lack of data gives cover to tech executives, who, when faced with the potentially harmful effects of their products, can cite the difficulty of establishing any one app or feature as the cause of a person’s unraveling. Short-form video in particular is a marker of how far behind cognitive research is, compared with the relentless pace of new technology. What available studies hint at so far is at least worthy of unease, and the not-knowing is only making things worse.

Research on short-form videos and cognition is difficult to conduct. Studies on human subjects tend to be slow and expensive, and academics are wary of spending years investigating apps that could be irrelevant by the time their results are published. Plus, the federal government hasn’t prioritized funding research on potentially addictive behaviors, including gambling and social-media use. The industry could help fill in the gaps by funding or even leading research, especially given that American social-media platforms have exclusive and valuable data. But companies are not particularly motivated to bankroll research that could show detrimental effects of their wildly profitable products. So far, they have largely chosen to keep internal research private.

(Data points do creep out. In 2024, for instance, a sloppily redacted complaint in a lawsuit against TikTok revealed some of the company’s internal research, which allegedly found that compulsive usage of the app “correlates with a slew of negative mental health effects like loss of analytical skills, memory formation, contextual thinking, conversational depth, empathy, and increased anxiety.” At the time, a spokesperson for TikTok argued that the documents were outdated and that the quotes in the complaint had been cherry-picked.)

Complicating things further is the fact that much of the publicly available research on short-form video is flimsy. In a study conducted at China’s Zhejiang University that went viral last month, 56 young adults clicked through a series of short videos (not on social media) as they lay in an MRI machine. Two brain regions involved in executing cognitively demanding tasks were found to be more active when participants swiped away from videos before they were midway through, versus when they stuck around until a video’s end. Prominent social-media accounts, including one for the prediction market Polymarket, promoted the study as more proof that TikTok is making us smooth-brained. One news outlet ran the headline “Instagram Reels & TikTok Make You Dumb & Depressed.” But the study, multiple neuroscientists told me, said nothing about short-form videos, intelligence, or depression—instead, it found that brain areas involved in taking action lit up when a participant chose to take the action of skipping to the next video. Besides, the study lacked controls, equated finishing a video with enjoying it, and never established the baseline that supposedly video-addled brain activity was being compared against. (The study’s corresponding author did not respond to a request for comment.)

Stronger studies are much rarer. But they do point in the same direction as many Americans’ intuition: Increased short-form-video use appears to be associated with poorer impulse control, mental-health outcomes, and attention capacity. Researchers at the University of Bristol concluded last year that the constant context-switching inherent to watching short-form videos may degrade prospective memory: the ability to recall something you had previously intended to do. Caty Enders, a doctoral student at the University of New Mexico, has also found that students who used TikTok at a high volume had more issues with both working memory (the information you need to keep track of what you’re doing in the moment) and episodic memory (a form of long-term memory that stores past personal events, such as what you did for your tenth birthday). A 2024 study conducted at Sigmund Freud University, in Austria, found that participants who reported watching more than four hours of short-form videos a day exhibited neurological activity that indicates cognitive abnormality.

Take all these findings with a grain of salt, however. Even the highest-quality studies on short-form videos tend to be limited in their explanatory power. They’re usually small and preliminary. And Keith Robert Head, a researcher at Capella University who recently published a review article on short-form video and attention, could point me to just four good studies on the topic that had been conducted in the United States. Most of the existing research comes from China, and Enders cautioned me against applying findings across the two countries, given that social-media platforms in the U.S. are subject to much less government control and are capable of accessing more user data and personalizing feeds to a greater degree.

Psychologists and neuroscientists have reasoned that short-form video is probably an especially potent and dangerous type of social media because the constant stream of non sequiturs and bright visuals is so overstimulating, and because there’s no upper limit to how long you can spend scrolling. But no one has established whether the negative effects of short-form video are because of something specific to the medium or the fact that spending hours on TikTok displaces healthy habits such as sleeping—in which case, the videos would be no more inherently harmful than bingeing Friends. Participants in a study Enders conducted on TikTok use and memory spent an average of 133 minutes a day on the app. “If you do anything every day for 133 minutes, it will change you,” Enders said.

Uncertainty around any technology’s effects not only relieves pressure on tech companies to make targeted modifications but also leaves governments to decide policy without sufficient information. Some countries have already instituted blanket social-media bans for minors based on imperfect data—not an ideal basis on which to restrict civil liberties. And everyone else is left with the ambient and unsure sense that the apps they use are terrible for them.

The fact that so many people perceive a problem with short-form video may be reason enough for alarm. Luiz Pessoa, a neuroscientist at the University of Maryland who spoke with me about the shortcomings of the recent viral study, thinks that an attention epidemic is clearly at hand, despite scientists’ limited understanding of it. He and his teenage daughter often watch the highlight reels from Formula 1 races, and when they do, she’s also looking at her phone. “It’s obvious we’re multi-, triple-, quadruple-tasking in ways that at least 20, 30 years ago we weren’t,” he told me. You don’t have to be a neuroscientist to have reason to suspect your brain can be stretched only so thin.

Pennsylvania’s Measles Outbreak Is Enormous

2026-09-16T10:01:44-04:00

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Following America’s recent measles deaths, anti-vaccine activists have cast doubt on the virus as the culprit. They’ve pointed to a victim’s underlying health conditions or, as they did last year in Texas, blamed hospital error. But the two latest measles deaths in Pennsylvania—bringing the state’s total to four since mid-August—have made the United States’ measles crisis undeniable.

Last month, the Pennsylvania Department of Health announced two measles-associated deaths; both cases were later revealed to be infants too young to have been vaccinated. In response, Robert F. Kennedy Jr.—who was an anti-vaccine activist for decades before becoming health secretary—wrote on X that the deaths might have been “altogether fabricated.” (He later acknowledged a coroner’s conclusion that one of the deaths had been caused by measles.) Then, last weekend, an unvaccinated 40-year-old woman died in Jefferson County; immediately, people on Reddit and X insisted that her death wasn’t really caused by measles, because she’d had asthma and chronic obstructive pulmonary disease, both of which can make breathing difficult. Yesterday, state officials revealed that an unvaccinated 18-year-old died from a rare inflammatory condition of the brain and spinal cord that can be triggered by measles. Some commenters online deemed that death suspicious too.

What the armchair epidemiologists miss is that vulnerability to the infection doesn’t make a death less real. The two infants both tested positive for measles. The Lancaster County coroner’s office determined that one infant died of a ruptured spleen; however, when I spoke with that child’s parents, they told me that the mother had been extremely ill with the disease when she gave birth, the baby was not breathing when he was born, and they believed measles had killed their son. The other infant was born with a rare neurological condition, but the coroner found that measles was ultimately the cause of death. Greg Furlong, the Jefferson County coroner who investigated the 40-year-old woman’s death, told me that although the woman had conditions that made her vulnerable to measles, and was on supplemental oxygen, she was active before she contracted the virus. She cooked for her family and cleaned the house. Measles killed her in about a week. “If she wouldn’t have got the measles, would she still be alive today? I say yes,” Furlong, a Republican who is also the mayor of Summerville, said.

[Read: The measles-stricken mother who lost her newborn son]

Four deaths in roughly four weeks suggest that the state is in the midst of an enormous outbreak. The Pennsylvania health department lists total cases at 693, with 99 in the past week. But considering that measles kills about one to three of every 1,000 children it infects, the actual number is likely much larger. Milder cases are going unreported. Many who fall ill, particularly in the Amish community, aren’t getting tested; the Amish parents of the infant who died with a ruptured spleen told me that their 13 living children had all caught the virus, but they never got swabbed.

These deaths are occurring after three unvaccinated people, including two young girls, died of measles in Texas and New Mexico last year. Those were the first measles deaths in the country in a decade. The last time the United States experienced four measles deaths in a calendar year was in 1992, at the tail end of a years-long outbreak that killed more than 100 Americans. That resurgence led to a recommendation that children receive two doses of the measles, mumps, and rubella vaccine, and prompted a nationwide push to increase vaccination rates. It worked, and measles was declared eliminated in the United States in 2000. But overall kindergarten vaccination rates started declining during the coronavirus pandemic, and some areas, including Lancaster County, have fallen well below the 95 percent needed to maintain herd immunity.

Now, in the face of a new increase in measles deaths, Kennedy appears more interested in scoring political points than boosting national vaccination rates. He has accused Pennsylvania’s governor, Josh Shapiro, of “the weaponization of infectious disease fears for political gain”; Shapiro, in turn, charged Kennedy with “playing games with public health” after the CDC declined to update its measles statistics to include the deaths in his state. Kennedy’s stated reason for the omission is that the agency is “applying a consistent national standard.” But the delay marks a shift in policy: Last year, the CDC counted both Texas girls’ deaths and the death of the adult in New Mexico after the states announced them. (In a post on X, Kennedy wrote that the National Center for Health Statistics will determine if measles is the true cause of the deaths in Pennsylvania after examining death records; a spokesperson for the Department of Health and Human Services did not respond to questions about that investigation. In a statement, Pennsylvania’s health department said that its investigation had determined that all four deaths met the criteria for measles-associated fatalities.)

Tomorrow, Kennedy is scheduled to be the keynote speaker at the annual conference for Children’s Health Defense, the anti-vaccine organization that he founded before becoming health secretary. Children’s Health Defense has a long history of ginning up fears about the vaccine for measles, mumps, and rubella while downplaying the seriousness of the diseases. Kennedy does, too. In July 2021, Kennedy told attendees at an Amish country fair in Pennsylvania, “The cure for measles is chicken soup and vitamin A.” In fact, no known cure for measles exists; vitamin A has shown some promise in people with severe vitamin A deficiency, which is exceedingly rare in the United States. Since becoming health secretary, he has stated publicly that vaccination is “the most effective way to prevent measles infection,” but as I’ve reported, he also undercut that message by telling the father of a girl who died in West Texas that “you don’t know what’s in the vaccine anymore.” Kennedy has been a stronger advocate for measles itself, which he’s falsely credited with boosting resistance to cancer and cardiac disease, than he has for the vaccine that prevents it.

[Read: What RFK Jr. told grieving Texas families about the measles vaccine]

As cases and deaths rise, the reality becomes harder to ignore: Measles, a disease the country seemingly overcame 30 years ago, is once again killing Americans.

The AI Pandemic Isn’t On Its Way

2026-09-11T13:12:58-04:00

Last month, a team of scientists published a high-profile paper describing how they’d taught an AI model to help produce brand-new, deadly viruses. The AI—a “genome-language model” trained on DNA sequences—had designed multiple new genomes that scientists then synthesized into functional viruses. And some of those viruses were capable of killing bacteria in a dish.

News of AI-made viruses went over poorly. The loudest reaction to the study (which had been released as a preprint about a year ago) was fear. Now that AI can design viruses that go after bacteria, perhaps someone could use the technology to manufacture pathogens that harm people—sparking a major outbreak, even a devastating pandemic. This potential threat evoked some of the same concerns that politicians, researchers, and tech leaders (including Bill Gates) have raised. And these fears are only gaining traction: On Thursday, Anthropic released a report that sparked a round of doom-laden headlines, detailing several instances in which the company banned accounts that were using its LLM, Claude, for what could have been reputable research efforts—or efforts to develop biological weapons.

AI, which has repeatedly proved itself capable of exceeding user expectations and bypassing guardrails, is a formidable force; many fears about its potential biological threat stem from its relentless pace of development and the possibility that it could make independent breakthroughs, exceeding researchers’ own understanding, especially if AIs eventually achieve recursive self-improvement—that is, models designing newer and smarter models. Kevin Esvelt, a biologist at MIT and a co-founder of Secure Bio, a biosecurity nonprofit, told me that although he thinks the probability of an AI-driven pandemic remains quite low, the consequences of such a catastrophe would be so large that “it’s very important that we drive that probability down as low as we can.”

But many other biologists, especially infectious-disease experts and virologists, told me that the threat of a pandemic need not loom particularly large on the list of AI-made threats. To the scientists most familiar with the minutiae of growing, modifying, and testing viruses in a lab, and the havoc they can wreak in the real world, the viruses that have already arisen through evolution, or will soon enough, still present much more immediate perils. In other words, humans should be investing aggressively in pandemic preparation, but not because of AI.

To be clear, viruses made with the help of AI could pose some threat. The experts I spoke with agreed that, in the wrong hands, AI could be used to speed infectious destruction, to a degree. To create the bacterium-killing virus, scientists led by a group at Stanford University and the Arc Institute fed the AI model, called Evo, only viral genomes that attack bacteria. Those genomes are much simpler and smaller than ones coding for viruses that go after humans. In theory, though, with a similar technique, researchers could train AI on the genomes of viruses that infect humans, with the aim of manufacturing novel pathogens. Or perhaps—as some people worry is likelier, easier, and more dangerous—users could ask AI to adjust specific traits of viruses known to cause disease, until those pathogens can skirt available vaccines.

Scientists have long been able to manipulate viral genetics without AI. This kind of “gain of function” research has stirred its own political and scientific controversy—especially in discussions about the origins of COVID-19—and the Trump administration has restricted federal funding for it. But current AI models have the capacity to “put a supreme battery in the back of the things that people were already doing,” Brandon Ogbunu, an evolutionary biologist and infectious-diseases modeler at Yale University, told me. Tom Inglesby, the director of the Johns Hopkins Center for Health Security, worries about bad actors using AI to surmount some of the limits of their own technical expertise. Ideally, models powerful enough to suggest new viral genomes should be subject to strict, formal review, Inglesby said; perhaps they could even be limited to training on only certain types of benign data. (For instance, the team that built Evo trained it only on viruses that kill bacteria, and withheld any data about viruses that can harm more complex life forms, including humans.) Esvelt advocates for restricting access to certain models entirely.

Other researchers, however, including the virologists I spoke with, pointed out that another set of safeguards is already in place: how little we humans—the creators and users of AI—understand about pathogenic viruses. For AI to map out more effective pathogens, people must be able to feed it data on what makes viruses highly transmissible, dangerous, and able to circumvent immune safeguards.

But these concepts are complex and murky enough that the chasm AI would need to cross is wide; researchers lack much of the basic knowledge they’d need to train an AI properly on such topics. “Right now, the data is junk going in,” Seema Lakdawala, a virologist at Emory University, told me. Generations of virologists have not come up with firm answers to key questions about what makes certain viruses better at causing diseases than others, or why some people are more susceptible to particular infections than others. Even expert virologists may struggle to ask AI the best prompts to guide it in useful directions.

In her own research on viral transmission, Lakdawala hasn’t found LLMs such as Claude and ChatGPT particularly helpful or correct, she told me, even when she’s asked them questions far simpler than “How do I make a pandemic virus?” (for example, basic questions about the flu-virus genome). Brian Hie, the lead researcher on the team that designed Evo, told me he’s also unconvinced “that AI would even be the method of choice for someone trying to make a dangerous pathogen.” It does not know enough about pathogens, because we don’t know enough about pathogens.

Esvelt, at MIT, argues that AI might not need to understand viruses perfectly, or even that well, to stumble across a dangerous iteration of one. AIs might also improve rapidly enough to make more sense of the existing data than human researchers ever have. But no matter how good AIs get, they so far have no way to build and test new pathogens, Gigi Gronvall, a health-security expert at the Johns Hopkins Bloomberg School of Public Health, told me. Even a very motivated human—whether they wanted to spark a pandemic for a government or terrorist organization, or for their own ends—would still have to pick through AI-generated possibilities, successfully synthesize them, assess them for enhanced (or at least sufficient) transmissibility and virulence, produce a sufficient quantity to do serious damage, and then release that payload of new virus into the world. All of that requires substantial skill in the lab, as well as expensive equipment and lab animals. It’s not impossible, but it certainly isn’t easy, either.

The practice of building new viruses in a laboratory is fickle: “Even if I give two experienced scientists the same protocol, they’re going to do it differently, and the results could come out differently,” Linsey Marr, a viral-transmission researcher at Virginia Tech, told me. Tinkering with viruses the old-fashioned way has also taught researchers that many hypotheses about what should make a virus more contagious or dangerous don’t pan out. Researchers cannot simply tune up a virus’s transmissibility or virulence like a dial; such changes can come with serious costs, including rendering the entire pathogen nonfunctional—incapable of infecting or hurting a person at all.

Evolution is already a master at tinkering with life forms and building upon their most successful—or dangerous—traits. Viruses are constantly trying out new versions of themselves and aren’t limited by human expectations about what “dangerous” agents of disease look like. Evolving pathogens also need no assistance from malevolent actors to start epidemics; in nature, where species constantly mingle, new outbreaks begin all the time. And nature has an elegant way of dealing with mistakes: Unviable iterations of life simply never come to exist at all. As good as AI is getting, “I can’t look anyone in the eye and say that process is any more harmful than what nature is already operating,” Ogbunu, the Yale evolutionary biologist, said.

The virologists I spoke with did agree that AI models should be monitored and regulated, but were wary of limitations that would hinder AI’s ability to speed the development of new vaccines, shore up viral surveillance, boost epidemiological modeling, or otherwise benefit public-health and infectious-disease research. (Even the types of bacterium-killing viruses that caused such an uproar could be deployed against antibiotic-resistant infections.)

Worries about killer viruses are already interfering with such lines of research. Among the examples of potential threats in Anthropic’s report were gain-of-function work on chikungunya virus and research about how flu viruses adapt to mammals—projects that could have been malicious or, in theory, could improve therapeutics or outbreak detection, respectively. (The company said in the report that it couldn’t confirm whether the queries represented the pursuit of knowledge for the public good or attempts at bioterrorism, and had erred on the side of caution.) Lakdawala and Marr told me that, recently, when they have asked Claude or ChatGPT about, say, genetic quirks in the flu-virus genome or using UV light to inactivate viruses, the AI flagged or halted their conversations. “It happens to me almost daily,” Marr said. (An OpenAI spokesperson wrote over email that “today’s models are specifically trained to withhold biological information that could enable harm” and that researchers “pursuing legitimate biological and life sciences work” can apply to its Trusted Access programs, which require proof of identification. Anthropic did not respond to a request for comment.)

Lakdawala and Marr are now trying to develop their own framework to help AI models distinguish legitimate scientific pursuits from nefarious ones. Both say that it’s difficult: What would the criteria be? Who would be the final arbiters of those criteria and of ambiguous cases? And none of those guardrails would address the most extreme concerns about viruses created by AI—that a self-improving intelligence might eventually be able to deliberately design, manufacture, and release a pathogen. For now, though, AI is still a tool. We’re still in charge of the questions we ask it, the data we feed it, and the fate of any virus that it might suggest we create.

The Los Angeles Rams Are Trying to Defeat Time

2026-09-10T15:27:07-04:00

Usually, when the San Francisco 49ers and the Los Angeles Rams play, it’s a relatively short commute. But this evening, the teams will kick off the NFL’s first-ever regular-season game in Australia.

The two teams have taken diametrically opposite approaches to preventing the 8,000-mile journey from disorienting their stars. The 49ers boarded their 16-hour flight to Melbourne nine days ago and have spent the intervening time training, watching Aussie rules football, and winning the majority of local support. The Rams landed yesterday, just 24 hours before the game. They’re betting on being in Australia so briefly that players’ brains and bodies won’t notice the difference. That makes the game the most high-profile test of jet-lag-evasion techniques in American sports history.

Anyone who has hurled across several time zones in one go knows how wide-awake and helplessly sleepy you can feel at inappropriate hours upon landing—a major inconvenience for professional football players, whose career depends on how they perform during one very specific period. Circadian rhythms can also affect performance in less obvious ways. Compounds that encourage inflammation, for instance, spike at night, when the body is doing less and can direct more energy toward fighting infection. A new time zone throws that optimal function off tilt and can cause stomach issues, cognitive impairment, headaches, and mood changes.

Teams at a circadian disadvantage tend to play worse. One study that analyzed every NFL game from 1970 to 2011 with a kickoff after 8 p.m. ET found that West Coast teams did better than oddsmakers expected in two out of every three games, regardless of whether they were home or away. Head coaches are also more likely to make the risky call to attempt an offensive play on a fourth down during evening games when they travel west compared with any other direction.

Because the consequences of jet lag are well established, the real question is how to avoid them. In 2021, 26 sleep researchers and clinicians articulated their best answer in the journal Sports Medicine. Among other recommendations, they noted that fully recovering from jet lag takes one day for each time zone crossed. The 49ers seem to have followed that model by leaving more than a week ahead of the game. (Melbourne is 17 hours ahead of California, but for body-clock purposes, that’s the same as being seven hours behind.) Kyle Shanahan, the 49ers’ head coach, told reporters last month that he would have loved to have just shown up in Australia the day before but that the experts he’d spoken with had all recommended arriving earlier. “I was a little bit on the fence,” he said. “Science wasn’t.”

The Rams, by contrast, are attempting to not switch their body clock at all. They have spent the past few weeks practicing in the late afternoon, which aligns with Friday’s mid-morning kickoff in Melbourne. Their head coach, Sean McVay, said at a Sunday press conference that the team will “have kind of a rhythm” when they land. “We’ve tested it out with some guys, and we feel like it’s been positive,” he added. The strategy is not without precedent: In 1994, Allen Johnson, an American hurdler, decided to live as if he were on East Coast time when competing in European tournaments. His coaching team strongly disagreed, but he won four world championships and Olympic gold. Last year, the Rams arrived in London the day before a game against a strong Jacksonville Jaguars team and won.

Jamie Zeitzer, a circadian physiologist and a co-director of Stanford’s Center for Sleep and Circadian Sciences, described the Rams’ strategy to me as “high risk, high reward.” If the Rams really feel as though they’re playing in the afternoon, they might have a slight advantage over opponents who feel as though they’re playing in the morning. During the late afternoon, circadian rhythms prompt optimal muscle strength and coordination, and core body temperature peaks, increasing alertness with it. Plus, a week might not be long enough for the 49ers to stop suffering the effects of their travel. Some people just take longer to recover, and a long-haul flight, jet lag, hotel life, and unfamiliar foods can lead to days of poor sleep, Zeitzer said. The 49ers have spent their September experiencing time as a pliable, erratic force. Shanahan told reporters that he was “a little confused” in a recent press conference, during which he also struggled to identify the day of the week. (It was Monday.)

Still, Zeitzer thinks the Rams have chosen the worse jet-lag strategy. If the players are to get any rest at all, their 24-hour stretch in Melbourne before game time needs to be carefully managed. From his experience consulting with professional teams, adults are hard to control. Meeta Singh, a doctor who has served as a sleep consultant for multiple NFL teams, thinks that players simply won’t be able to sleep. Singh is one of the co-authors of the Sports Medicine recommendations, which suggest that athletes maintain a “reduced exercise schedule” and do hand-eye-coordination drills in the 72 hours after a long-haul flight. The Rams won’t even be in Australia for 72 hours.

Sleep became a major metric for all sorts of professional sports teams after the NBA distributed more than 2,000 Oura rings to its players during the depths of the coronavirus pandemic. “Once you can show a coach numbers, sleep stops being a soft topic and becomes something they can manage, like training load or nutrition,” Singh told me. Many NFL teams now have a sleep specialist and a performance-science team working on circumventing jet lag. To prep players for time shifts before they depart, 14 NFL teams, including the 49ers, have installed in their training facilities lighting systems designed to mold circadian rhythms. The system, called BrainLit, mimics daylight according to a “recipe” that each team specifies, Kyle Harris, the CEO of the company, told me. On the 49ers’ flight to Melbourne—on the world’s largest and most expensive passenger airliner, with lie-flat seats that extend to seven feet—each player received his own sleep guidelines. Tom Clark, a sports scientist who advises NFL teams with international games, told me that many teams establish each player’s chronotype, or natural preference to sleep and wake at certain hours, and use that information to prescribe optimal sleep habits.

Roger Goodell, the commissioner of the NFL, eventually wants 16 international games to take place each season. By the time Super Bowl LXI rolls around this February, teams will have played in Rio de Janeiro, London, Paris, Madrid, Munich, and Mexico City. For future seasons, the league is considering adding games in the United Arab Emirates and Japan; Goodell insists that an NFL team will be based outside the U.S. in his lifetime.

Perhaps such a punishing schedule will settle debates once and for all about how to handle jet lag. Whatever the marginal impact of sleep strategy, though (and some games are decided on the margins), usually “the better team will win even if they’re playing on the moon,” Clark said. And the Rams are this year’s Super Bowl favorites.

Medicine Needs to Get Serious About AI

2026-09-08T12:54:01-04:00

For as long as ChatGPT has existed, Americans have been asking it, “Could that funny little spot on my toe be cancer?” And as AI has advanced over the past few years, doctors have begun to use specialized models to ask much the same questions in clinics. In the face of these developments, professional medical societies have presented a unified front: Doctors must always have the final say in clinical care.

We disagree. As the medical societies allow, physicians’ enhancing their work with AI tools may be a perfectly good way to deliver medicine. (One of us—Khosla—has in fact invested in a primary-care start-up, co-founded by his son, in which doctors supervise AI assistants.) But for Americans to get the best health care possible, we need to be willing to experiment with models that put AI in control.

This notion has caused a stir in the medical community. When we published a commentary in the Journal of the American Medical Association last month arguing that AI-only care could soon become superior to care provided by human physicians, the CEO of the American Medical Association denounced us as undermining the patient-doctor relationship. The organization’s position was unchanged: AI should be relegated to a supporting role in clinical care. It’s an argument that ignores the available evidence and could hold untold numbers of Americans back from better health.

Much of modern medicine—including managing hypertension, determining the right treatment for many cancers, and addressing chemotherapy side effects—is largely algorithmic. A physician needs to ask a patient targeted questions, determine possible diagnoses, order tests to identify the correct one, offer a treatment plan, and adjust it depending on how the patient responds. That series of actions is steered by detailed guidelines from professional societies.

Yet doctors—despite the best of intentions—make plenty of mistakes when following those steps. Studies indicate that up to 15 percent of American patients are misdiagnosed each year, leading to tens of thousands of preventable deaths. That’s why health-care providers have software that notifies them if they, say, prescribe a deadly dose of a drug. Any software that could practice medicine autonomously would be similarly specialized: not generic ChatGPT, but a model trained in medical knowledge with the appropriate guardrails to minimize risks and mistakes. Such a model could check for drug interactions more consistently and comprehensively than physicians. And it would be able to check in with patients much more frequently than human health-care providers do.

Some AI models have already proved adept at such tasks. In one study published last year, expert physicians judged Google’s Articulate Medical Intelligence Explorer—a highly trained AI model for medical diagnosis and reasoning—as significantly better than human doctors at getting actors playing patients to open up. The “patients” revealed more about their complaints, along with their medical, family, and medication history, all of which can be crucial for an accurate diagnosis. In a 2023 study, patients with type 2 diabetes were randomized to have their insulin dose adjusted by physicians or autonomous AI. The machines got patients to a stable dose faster than human physicians, and their patients took their insulin more reliably and had less distress related to their diabetes.

What about the physician-AI hybrids that medical associations are backing? Research on them is sparse, and more is needed. A 2025 review of 52 studies concluded that, on balance, such hybrids “neither outperformed medical AI alone nor surpassed the best of clinicians.” In at least a few of those studies, human-AI hybrids outperformed AI alone. But in those hybrid teams, the AI controlled the final clinical decision—the opposite of what the AMA and others have in mind.

Medical organizations are not entirely closed-minded to the possibility of change. For example, last week the American College of Physicians published a position paper that allowed that “fully autonomous AI is possible,” but cautioned that its use should be infrequent and “limited to low-risk, low-complexity decisions, and always allow for bringing a clinician into the loop.” John Whyte, the CEO of the AMA, told The Atlantic that he was “disappointed” in the quality of the analysis in our JAMA commentary last month. He questioned the design of the studies we reviewed, many of which involved simulated situations with actors or a retrospective review of existing cases rather than real clinical outcomes, and did not follow patients for years or decades. We agree that longer-term, real-world studies are necessary; hopefully, once advanced AI medical tools have existed for more than a handful of years, results will begin to arrive. Whyte was enthusiastic about further study of physicians controlling AI tools, but only cautiously open to further exploration of autonomous AI in medicine, arguing that the latter would need to be highly regulated.

Reasons exist, of course, to be skeptical of AI-driven medical care. In nine of the 51 studies we reviewed, human physicians outperformed the machines. But some of these tested older AI models or general-use AI models that weren’t trained on medical information and specific guardrails for patient care. Prominent physicians have also argued that real-life doctors are harried by 15-minute appointments and administrative burdens such as prior authorization. That is certainly true, but it is also irrelevant to many of the experiments we reviewed, which examined relatively hassle-free simulations of medical appointments.

One of the most common objections to an AI-doctor future is that robots lack the human connection that patients need to build trust. The American College of Physicians’ recent position paper, for example, cited AI’s inability to make eye contact. But consider that doctors, too, can be robotic. In a Gallup survey conducted late last year, 21 percent of respondents said they had turned to AI because they had previously felt dismissed by a health-care provider. In the 2025 study of Google’s AMIE, patient actors reported that the AI was more emotionally supportive than the physicians were. In a systematic review of 15 studies comparing AI chatbots with physicians, 13 found that AI had significantly higher perceived empathy.

Like human physicians, AI is not and never will be perfect. But isn’t the possibility of reducing fatalities caused by physician error—even by just a little—worth exploring? Instead of writing off a possible source of progress, the medical community should help answer the key questions raised by AI: How should researchers devise ethical, real-world situations to test autonomous AI models? How should governments and professional organizations regulate them? And how should medical education be reformed so that human doctors can continue to do what they uniquely can?

Hundreds of years ago, doctors believed that disease was caused by an imbalance of “humors” in the body. Even after Louis Pasteur proved that bacteria caused infection and Joseph Lister introduced sterile surgical techniques, physicians cut patients to have them bleed out what ailed them, not bothering to clean the knife or their hands. But medicine progresses. Humans have learned from our past mistakes and created new drugs, procedures, and treatments to massively lengthen lifespan and improve quality of life.

Today need not be any different. Doctors have been presented with a powerful tool that has the potential to improve care for millions of people. It’s their duty not to stand in the way.

Cereal Has Strayed Too Far

2026-09-08T12:44:15-04:00

Breakfast-cereal boxes are a window into both the politics of food and American culture. As a particularly timely example, since Robert F. Kennedy Jr. took office last year as secretary of health and human services, he has called for the removal of artificial dyes from breakfast cereals. On Fox News in 2024, he lamented that the bright colors in Froot Loops are “literally poisoning our kids.” (How exactly these dyes interact with human health is complicated.)

Cereal companies responded right away. General Mills announced last month that it had transitioned its entire U.S. portfolio of cereals—including Trix and Lucky Charms—to all-natural dyes made from fruits, veggies, and spices. Kellogg had previously announced plans to do the same by the end of 2027. Target stopped selling any cereals with artificial colors earlier this year.

For the Make America Healthy Again movement, the removal of artificial dyes is a big win. But cereal still comes with a major concern for many consumers. Nearly all ready-to-eat breakfast cereals sold in the United States—and especially those marketed to children—are presweetened.

The initial loading of breakfast cereals with sugar has been attributed to a single person: Jim Rex, a heating-equipment salesman who lived in Pennsylvania in the early 20th century. As the story goes, Rex was appalled by the spoonfuls of sugar his kids added to their breakfast cereals and set out to create a version that would not induce such behavior. His brilliant contribution: a glossy honey coating on puffed wheat, a cereal he named Ranger Joe Wheat Honnies in 1939.

It didn’t take long for Rex’s strategy to backfire. By 1949, Post had launched Sugar Crisp. Kellogg introduced Sugar Pops in 1951, Sugar Frosted Flakes in 1952, and Froot Loops in 1963, each among the company’s all-time best sellers. General Mills launched Sugar Smiles in 1953. The next year, the company added sugar and artificial colors to its Kix cereal, thus creating Trix.

In 1950, such presweetened cereals represented just 5 percent of all cereals sold, but by the mid-1970s, kids accounted for almost 40 percent of all cereal consumption. In 2014, the Environmental Working Group estimated that kids could ingest about nine pounds of sugar a year just by eating a serving of cereal every day.

Advocates for children’s health have long complained about the high sugar content of breakfast cereals. In the early 1970s, Congress held hearings to highlight cereal’s inadequate nutritional quality. Cereal companies objected, arguing, correctly, that grains are nutritious. But they also responded by trying to make their products appear less sugary.

They began by removing the S-word from cereal names, and some substituted honey for sugar on the theory that people perceive honey as more wholesome and nutritious. In the 1990s, companies hit on another clever strategy: If they used multiple sugar types, they could list grains first on a product’s ingredients but sprinkle sugars throughout the list. Cereals looked healthier, but when Consumer Reports compared the sugars in 27 breakfast cereals in 2008, it found that many were still 50 percent sugar by weight. Rumors circulated that federal agencies were working to set nutrition standards for foods advertised on television programs aimed at children younger than 12, which would likely spell trouble for sugary cereals.

In 2009, General Mills pledged to reduce sugar in its most popular kids’ cereals—most of which had at least 12 grams a serving—to single digits. Its pledge would apply to 10 cereals, including some of its most popular, such as Lucky Charms and Cocoa Puffs. The results were mixed. By 2012, General Mills had reached the single-digit goal for Cinnamon Toast Crunch, Cookie Crisp, and more. Some of this success was due to decreased serving size. And the best General Mills could do for Lucky Charms was 10 grams of sugar in a three-quarters-cup serving—which the company found to be the minimum sweet spot for kids’ acceptance. The project had encountered a harsh reality: Kids like sugar, and companies remove it at their peril.

Sugary cereal is not just a consumer concern; it is also a matter of government nutrition policy. Since 1980, the federal Special Supplemental Nutrition Program for Women, Infants, and Children (WIC) has limited the sugars in cereals it will cover to six grams an ounce, about half of the amount in typical cereals aimed at kids. WIC can be a lucrative business for cereals that qualify, so the limit has induced companies to take two actions. The first is to formulate new cereals with less sugar specifically for the WIC market. In 2006, for example, General Mills introduced a new kid-targeted cereal, Dora the Explorer, “lightly sweetened cinnamon corn puffs,” with six grams of sugar in a 27-gram serving—an amount that meets the WIC standards.

The second is to petition to change how sugar in cereals is counted. When the six-gram rule went into effect, in the early 1980s, Kellogg immediately objected. Its Bran Flakes met the WIC standards, but Raisin Bran did not; it contained 12 grams of sugar an ounce, seven from the raisins. Kellogg argued that raisins are healthy and pointed out that WIC was encouraging women to add raisins to their diet to increase their iron intake. For decades, despite Kellogg’s persistent efforts, the U.S. Department of Agriculture did not budge. But times change. In 2024, USDA issued its third comprehensive update to the WIC food package since 1975. The agency retained the six-gram limit but specified that it applied only to added, not total, sugars. It said the policy change was justified to align with listing “added sugars” on food labels and with the government publication Dietary Guidelines for Americans, and to create a “more permissive standard for products containing naturally occurring sugars.”

The distinction between natural and added sugars has continued under Kennedy. The new dietary guidelines, released in January, declare that no amount of added sugar is recommended for healthy eating. At a press conference announcing the new guidelines, Kennedy told reporters, “Today, our government declares war on added sugar.”

Current breakfast cereals have less sugar than they did years ago, but it’s hard to remove completely. Some amount of sugar is still needed to mask the bitter taste of added vitamins. Sugar also helps cereal flakes, puffs, and Os hold their shape in milk. Less sugar is better for kids’ health, but more is better for structural integrity—and taste.

For a truly healthy cereal, look to a time before Jim Rex. The most nutritious option will have one ingredient: wheat or oats. Even if you add your own teaspoon of sugar, it will be only four grams.

This article has been adapted from Marion Nestle and Lisa Sutherland’s new book, Sugar Coated.

The Dark Side of Mindfulness

2026-09-04T09:00:00-04:00

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In 2004, Willoughby Britton, then a doctoral candidate in clinical psychology at the University of Arizona, began recruiting participants for a study that, she felt sure, would show meditation improves sleep.

Britton, a meditation teacher, was so devoted to the practice that she saw herself as a “double agent,” someone who uses science to promote meditation. Although she had grown up in a nonpracticing Episcopalian home, she’d become deeply invested in Buddhist teachings. She read meditation books in her spare time and at one point considered becoming a Buddhist nun. She was confident that meditation improved most things, including sleep; it had already improved much about her own life.

For her study, Britton split 26 participants into two groups: one that would go through an eight-week-long meditation class, and one that would serve as a control group. She brought them all into a lab to sleep overnight while sensors measured their brain waves, muscle activity, and eye movements.

But when she reviewed the results, she was dismayed to find they were the opposite of what she had predicted. The participants in the meditation group slept more fitfully, with more frequent awakenings, than those who didn’t meditate. They spent more time in “Stage 1,” the lightest sleep phase, from which people are easily roused. “Graph after graph after graph, no matter how you looked at it—number of awakenings, number of micro arousals, number of Stage 1 minutes,” Britton told me, the amount of meditation that the subjects practiced was directly correlated with worse sleep quality.

Britton wasn’t sure what had happened. Had she done something wrong? Designed the study poorly? Was the result a fluke, a random finding that didn’t mean much? Or perhaps meditators just need less sleep. At the time, promoting meditation was more important to her than scientific ethics, and she worried that publishing the results would mean “harming the dharma”—criticizing the teachings of the Buddha. So she didn’t.

On a meditation retreat not long after this, she was chatting about her study with a meditation teacher when the teacher said, “I don’t know why all you psychologists try to make meditation into a relaxation technique. Everyone knows if you meditate enough, you stop sleeping.”

On some level, Britton must have known this. At that point, she had spent years both meditating and studying the brain. Because most kinds of meditation aim to enhance concentration, the practice can act like a stimulant. And just as chemical stimulants such as caffeine and Adderall can interfere with sleep, so, too, can excessive meditation.

What else, she wondered, did meditation teachers know that they weren’t telling people? Gradually, starting with that sleep study, the tiers of thought propping up Britton’s worldview—that Buddhism is a cure-all, and that meditation was always beneficial, and could never cause harm—would collapse. Over time, she would find that meditation, a multibillion-dollar industry that is promoted as a treatment for anxiety, chronic pain, alcohol abuse, addiction, and many other ailments, can sometimes, for some people, cause severe and lasting side effects: depression, anxiety, even acute psychosis. Losing the belief system that had been foundational to her life would lead her to produce a trailblazing body of research about the adverse effects of meditation, and then to found a clinical practice geared toward helping the people—a lot of them, as it turns out—who believe that meditation has harmed them.

Britton has straight blond hair, blue eyes, and a muted affect. When you say something to her, she pauses, as if considering whether or not to smile. A colleague once suggested to her that she might be autistic. “And I’m like, ‘Okay,’” she told me one day recently.

She grew up on a farm in Massachusetts with parents who believed that a person should find a problem that isn’t being solved and embrace it as their niche. Her father’s niche was fermenting waste from local businesses and selling it as compost.

Britton was, by her own description, a weird kid who spent a lot of time by herself. She was always asking strange questions like “What is looking out of my eyes?”

One day during the summer break after her junior year at Colgate University, where she was majoring in neuroscience, Britton went over to the house of her best friend, Sarah, a champion athlete at Dartmouth, and discovered her lying lifeless on the bed, a hunting rifle on the floor and a splatter of blood on the wall. Overwhelmed by the pressure of competitive sports, Sarah had taken her own life.

After Sarah’s death, Britton developed symptoms of PTSD. She grew afraid of crossing the street and of driving. She didn’t like opening doors, because she feared she might find a dead body behind them. At one point, while killing rats at her bench in the National Institutes of Health lab where she worked between college and graduate school, she watched the blood drain from their eyes and wondered aloud to a colleague, “Where does it go?” “In the freezer,” the colleague responded. But Britton wasn’t asking about the rat’s body, but its life force. Where did that go?

She was reluctant to take medication, so her father sent her the book A Path With Heart, by the famous meditation teacher Jack Kornfield. She appreciated Kornfield’s explanation for why humans are so prone to rumination—“over and over we feel the familiar tug of thoughts and reactions that take us away from the present moment,” he writes—and that he offered a way out via meditation. She began meditating for half an hour to an hour each day.

In graduate school, Britton initially focused her research on the neuroscience of near-death experiences, but for her dissertation she pivoted to studying meditation, which had been so steadying for her personally.

Meditation was, even then, having a moment. In 2005, the filmmaker David Lynch established a foundation that aimed to promote Transcendental Meditation in colleges and schools. Soon, tech CEOs were flocking to mindfulness summits to learn about “wisdom in the workplace” or “conscious leadership,” and a mindfulness class for Google employees regularly had a long waiting list. High-powered celebs including Oprah and Arianna Huffington credited meditation for centering them amid their empire building. LeBron James partnered with Calm, a multibillion-dollar meditation-and-sleep app. Today, according to one study, about half of all Americans have tried meditation, and about a fifth meditate regularly.

Meditation’s popularity is well-founded. Although the practice has long been supported by the more woo-woo corners of the wellness industry, as well as by Eastern philosophy, an accumulating body of scientific research has suggested that it has all kinds of measurable benefits. Major studies show that meditation can alleviate anxiety and depression—at least about as well as the antidepressant Lexapro can, but without the cost and with fewer side effects. Even short periods of meditation have shown notable effects on the brain: Several studies have found that eight weeks of meditation training can reduce reactivity in the amygdala, the emotion center of the brain, and another showed that meditation could help activate brain regions involved in attention, memory, and perspective-taking in people with social-anxiety disorder. Other reputable studies have linked meditation to positive mood; improved immune function; reduced chronic inflammation; less back pain; lower blood pressure; enhanced self-awareness; better attention spans; greater compassion; and even reduced feelings of loneliness in older adults.

Beyond the scientific evidence, Britton believes that meditation became popular because it’s a health hack that people can do independently, without relying on expensive medical care. The practice suggests that “underneath all of your thinking is some beautiful, basic state” just waiting to be discovered, she said. It probably helps, she added, that meditation is “this ancient thing from Asia and therefore seems more legit or real or something.”

In graduate school, Britton became a serious meditator in the Western insight tradition, which includes sitting and focusing on an “anchor,” such as one’s breath, sometimes for hours at a time. Britton describes it as an austere practice intended to “train the mind.” She molded her life around ancient Buddhist principles. When colleagues remarked on her plain appearance, she said, “Why would I adorn myself?”

Soon, Britton immersed herself in Tibetan studies. Instead of reading novels at night, she’d read dharma books. Her belief at this time, she said, was that “getting enlightened is the most helpful thing you could do for the world.” She considered dropping out of academia to move to a monastery in Asia, which would have meant renouncing her former life, taking a vow of celibacy, and living under a new name.

But she stayed in the United States and continued her academic work, while also training to teach mindfulness-based stress reduction (MBSR), a secular meditation program developed in the ’70s by a molecular biologist named Jon Kabat-Zinn, and a related course called mindfulness-based cognitive therapy. These classes promise to help everyday people with their stress, low moods, and chronic pain; alongside daily meditation practice, they typically include some non-Buddhist teachings from psychology and literature.

Britton moved to Rhode Island to begin her clinical residency at Brown University’s Warren Alpert Medical School. She didn’t know anyone, and, working 12-hour days, she felt intimidated by the cutthroat Ivy League academic life. To fill the time she had to herself, she started meditating for three hours a day.

One night, after meditating on her balcony for an hour, she went back inside and noticed that her house felt like someone else’s home. A picture of her with two friends looked like a picture of three people she happened to know.

Britton decided to take a walk, and as she strolled the streets of Providence, she felt like a bird sitting on her own shoulder, watching herself. She walked into a creperie where she noticed two people arguing. When they both turned and glared at her, she thought, Oh my God, I forgot that I am a person.

What Britton was experiencing is called dissociation, a state that can occasionally be evolutionarily useful—it can help people push through a task when faced with overwhelming terrors. But according to Britton and other researchers, it can happen to extreme meditators too. Britton told me that extensive meditation can prompt the prefrontal cortex to essentially shut off the brain’s emotional centers, causing feelings to seem blunted. And without the typical emotions that we project onto objects, familiar things—our hands, our homes—can start to look foreign. Heleen Slagter, a cognitive neuroscientist at the Vrije Universiteit Amsterdam who studies meditation, says that part of the way the brain gives rise to our sense of self is by predicting how we will interact with the world in the future. If you spend enough time zeroing in on the present moment, as one aims to do during meditation, Slagter says, your sense of the future can start to recede—and with it your sense of self. This can produce dissociation.

Britton began dissociating a few times a week. She had trouble driving because she couldn’t sense where her body began and ended. She’d watch a sappy commercial and suddenly notice her face was wet, not realizing she had shed tears. She felt porous, like other people’s states of mind were her own, a fact that became especially disturbing when she was treating suicidal patients. The dissociation continued for six or seven years, sometimes happening during meditation, but other times at random.

When she told meditation teachers about the dissociation, she said they told her she had entered a new stage of enlightenment—that she was “riding the ox backward.” She had “seen the truth of no-self,” they said, and this was a good thing. They told her to keep meditating, which made the dissociation worse. Somehow, Britton got through her postdoc, but she wasn’t entirely functional. She didn’t date anyone for a decade.

Lauren Lancaster for The Atlantic

Willoughby Britton at home in Vermont. Now retired from Brown University, she runs an organization that counsels people who have had distressing experiences during or after meditation, such as insomnia, anxiety, depression—even psychosis.

Even before she started dissociating, another layer of Britton’s worldview began to crumble after she moved to Rhode Island and was working at an inpatient psychiatric hospital as part of her residency. One day, someone came in from a meditation-retreat center in a state of florid psychosis. Three months later, another psychotic meditator came in, from the same retreat center. That’s weird, Britton thought. Do they know each other? They did not.

It’s well known that psychedelics such as LSD can spark psychotic breaks, but meditation can produce altered states of consciousness almost as powerful as those induced by psychedelics. The brain likes and expects a certain amount of input; go long enough without doing anything and the neurons might start to fire spontaneously, producing, say, flashes of light or made-up memories. Inuit people in the Arctic Circle have been known to experience a type of hysteria known as piblokto, which might be brought on by the sensory deprivation of long winters. No one seems to know why, exactly, psychedelics and meditation can both occasionally prompt psychosis, but it might have to do with the fact that both can have the effect of “rewiring your brain,” which can be a positive thing but can also mean your brain just doesn’t work the way it used to. It might become more easily influenced, for example, or impart grave significance on unimportant events.

At this point in her research, Britton’s studies were still mostly focused on the benefits of meditation, such as on how it can be helpful for depressed people and substance-abusing teens. But now, when she spoke about her studies at conferences, she’d sometimes briefly mention some of the potential adverse effects of meditation. Afterward, people would corner her in the halls or in the bathroom and tell her they’d had negative experiences with meditation—everything from increased depression to psychotic breaks.

She started to wonder whether the unintended effects of meditation might extend beyond a few anecdotes and her own experience with dissociation. Centuries ago, meditation was practiced mostly by monks and other spiritual seekers in East Asia and India; it wasn’t something ordinary people did, Pierce Salguero, a historian of Buddhism and medicine at Penn State Abington and the editor of the book Meditation Sickness, told me. The point of meditation was never merely to relax or just “clear your mind” but to wholly rearrange one’s relationship to one’s thoughts. This might make sense for a Buddhist monk pursuing the great unbinding, but not for a random Brooklynite who just wants to be more productive at work. The “no-self” teachings of Buddhism can be at odds with the goals of Westerners, who are generally aiming to be their best selves, not to disconnect from themselves.

Britton began to perceive that the research on mindfulness contained a giant lacuna: its potential risks. Meditation researchers, she felt, tended not to find adverse effects among their study participants because they didn’t ask their participants about them. What’s more, many meditation studies are funded by pro-meditation organizations, and some study participants might feel pressured to say that their mental health improved after meditating. There’s no such thing as a placebo for meditation, which complicates studying its effects. When Britton looked for past studies on the risks of meditation, she found mostly isolated case reports and small studies—one of which found that two of 27 long-term meditators had had “profound adverse effects,” including confusion, depression, and severe shaking.

Britton still believed in many of the potential benefits of meditation, but she began to rethink her role as a booster for it. “It just seemed like the world does not need another meditation researcher who’s going to promote meditation,” Britton told me. “We’re like Starbucks—there’s one on every corner.” Assessing the extent and severity of possible negative effects of meditation, she decided, would be her version of a problem to solve—her niche. In 2007, she began interviewing meditators for what would become the first comprehensive study of meditation’s adverse effects.

In 2010, Britton met a religious-studies scholar named Jared Lindahl at a conference. At that point, Britton had been meditating so much that she saw stars even with her eyes open—usually either one blue star or one white star—a phenomenon that Buddhists call nimitta. Lindahl had written his dissertation on visual light experiences of this sort. Meeting him, Britton said, “was having somebody understand a part of my experience that no one else had understood.” They wrote a paper about meditation-induced light experiences together, began meditating together, and, eventually, fell in love. The year she met Lindahl, she also finally published the sleep study she’d conducted in Arizona—the one showing that too much meditation can keep people awake.

Lindahl joined her on the meditation-challenges project, for which they conducted interviews about various types of adverse effects experienced and witnessed by 60 meditators and 32 meditation teachers—a smallish sample that is nevertheless rather large for qualitative studies such as this one. They finally published their first study, called “The Varieties of Contemplative Experience,” in 2017, nearly 10 years after they started it.

The most common adverse effects, reported by 82 percent of the meditators (which, importantly, included only people who had experienced an adverse effect of any kind), were “fear, anxiety, panic, or paranoia.” Second-most common were “changes in motivation or goal,” experienced by 78 percent. (Britton later talked with one meditator who sat on her couch for two years, unable to do much of anything, though most of the motivational effects reported were less dramatic.) Smaller numbers reported experiencing delusions, hallucinations, physical pain, rage, and suicidality. The effects lasted for a median duration of one to three years, and the majority of the sample indicated “moderate to severe” impairment in at least one area.

Although the study suggests that what’s most likely to cause problems is intensive meditation—sitting in silence in a retreat hall for hours or days on end—28 percent of the meditators had issues arise from their everyday non-retreat practice, and 25 percent of those in the study were meditating less than an hour each day.

Being an experienced or even expert meditator didn’t necessarily protect people. “I was like, ‘You’ve written a bunch of dharma books. How come you never mentioned this?’” she told me she asked one of the teachers. “And he’s like, ‘Well, it’s not good advertising.’” Notably, much of Britton’s sample of people harmed by meditation had graduate degrees; Britton believes that this is because high achievers tend to try to “ace” meditation, by, say, ignoring any internal sense that something might be wrong. (This struck me as similar to the endurance it takes to earn a Ph.D.: Power through years of pain and tedium for the promise of a big payoff at the end.)

As a study, “The Varieties of Contemplative Experience” had some inherent limitations. Because it recruited people who had had negative experiences, the study could conclude nothing about their prevalence. The study also couldn’t definitively prove causality—for instance, it’s possible that the meditators’ symptoms happened after meditation, but for unrelated reasons. Some Buddhists would also say that experiencing negative emotions or other bad effects is supposed to be part of the practice. But by and large, the study was well received and widely cited in the field. It acknowledged its own limitations and, if anything, respect has grown for it over time.

In part that’s because subsequent studies, some of which Britton was involved with and some not—and some of which were conducted in part by the most well-known academic boosters of meditation—have provided sturdy evidence that some percentage of meditators do experience negative effects from it, ranging from mild to severe. The frequency of bad effects found varies, but most studies, and most experts I talked with, estimate that about 10 percent of all meditators experience them, with the prevalence being considerably higher in certain situations. Richard Sears, a clinical psychologist and Zen master who’s been practicing meditation for some 40 years, has said that he thinks Britton’s research is important. “Something is happening” to these meditators who have bad experiences, “and we should be aware of it. This is opening up a conversation.”

Britton and Lindahl went on to publish many other studies on meditation’s dark aspects, including delusion-like ideation and feeling bolts of electricity traveling through the body. One study subject grew paranoid at a meditation retreat, left, and on the way home believed that street signs were delivering secret messages just to her; another became convinced that she needed to save the world from a “black Tantric plot” contrived by retreat-center staffers, threw water in her meditation teacher’s face and slapped the center’s director; a third began experiencing “messianic visions” about the “need to sacrifice myself in some way for the benefit of saving mankind” and was convinced that meditation teachers were communicating with him in secret code; a fourth reported that meditation awakened an “energy” inside him with “a will of its own” that once almost compelled him to jump from a balcony because it “wanted to lift up and fly.” None of these people had previously experienced any psychosis or been treated for mental illness.

Different types of meditation seem to have different adverse effects on the people who experience them. In one of Britton’s studies, a “noting” practice—labeling thoughts or body sensations—was more likely to trigger anxiety, whereas focusing on an anchor such as one’s breath was more likely to prompt a depressive episode. Overall, Britton has found that about one in 10 people who have meditated, even once, had an adverse effect that lasted more than a month—a rate that, were meditation a drug, would qualify as “very common” under the standard classification used for adverse drug reactions. More frequent meditation tends to increase negative effects, Britton said.

The body of evidence that Britton and Lindahl have amassed showing that meditation can sometimes cause harm is now bolstered by others’ research. A Clemson University study found that mindfulness can paradoxically increase distress. (Cultivating a hopeful outlook was more effective than mindfulness at shoring up workers’ resilience and well-being.) A 2020 study found that 3 to 7 percent of schoolteachers and university students in the U.K. who took a mindfulness class reported “unpleasant experiences”—including anxiety, distressing memories, obsessive thoughts, and physical pain; another study found that a quarter of meditators experienced “unwanted effects” such as panic attacks, nausea, headaches, dizziness, insomnia, and dissociation, though most of these effects were transitory. A German research group studying more than 1,300 regular meditators around the world found that 13 percent experienced adverse effects, including a small number who experienced “very severe effects with lasting consequences” or “extremely severe effects” that were life-threatening or required hospitalization. Yet another large survey found that a quarter of meditators, and a higher percentage of nonreligious meditators, had a “particularly unpleasant meditation-related experience.”

To some extent, this is to be expected. It would be odd if a single treatment, billed as the solution for dozens of mental and physical problems, alleviated all of these ailments without any side effects. In medicine, “if it’s not doing any harm, then it’s probably also not helping,” Nicholas Van Dam, a psychologist at the University of Melbourne who has co-authored papers with Britton, told me. Along with a team of researchers in Australia, Van Dam found that about 9 percent of meditators in their survey reported a functional impairment arising from a meditation-related problem, including sleep changes and a sense of disconnection from others. Van Dam’s team suggested that people should be warned that meditation is contraindicated for certain groups, just as certain medications should not be given to some people. Miguel Farias, an experimental psychologist at Coventry and Oxford Universities who specializes in the science of meditation, told me that the early literature on cognitive behavioral therapy, from the ’70s and ’80s, recommended against meditating during a depressive episode. “Physical activity is a wonderful antidote to depression,” Farias said. But “meditation makes you physically be more passive.” In a systematic review, Farias and his co-authors found that adverse events among all meditators were “not uncommon,” appearing in 65 percent of the studies reviewed; the most prevalent symptoms were anxiety and depression.

Some of the side effects these researchers are finding may be attributable to the fact that, in the years since Eastern traditions of meditation were introduced to the West in the 19th century, this once primarily religious ritual has expanded far beyond its original intent; its more sweeping remit may have consequences that the practice’s original Buddhist context might have prevented. But as Salguero and others pointed out, early Buddhist texts cautioned that “meditation sickness” plagued even the devout contemplatives of earlier eras: In one eighth-century Chinese writing, the Buddha warns of 50 “demonic states” in which meditators could become trapped, including hallucinations, sorrow, anxiety, suicidal thoughts, and possession by ghosts.

While working on my most recent book, about personality change, I wanted desperately to change one thing about myself in particular: to bring down my stratospheric level of neuroticism, the personality trait associated with anxiety and depression. When I Googled how to reduce depression and anxiety, the first drug-free thing that came up was meditation.

So I signed up for an online mindfulness-based-stress-reduction class—the kind of meditation that Britton also once taught, and which now has hundreds of classes and instructors to choose from around the country.

I found some of the class’s Buddhist teachings, though watered down for newbies, very helpful, and by the end of the eight-week class, a test revealed that my neuroticism score had, indeed, ticked down. This surprised me because I’m bad at meditating, so I would spend entire 45-minute sessions reviewing my to-do list, my worries, and other earthly matters.

What annoyed me the most, though, was the way the meditation teachers talked, which tended toward New Age–isms in passive voice. “There’s a subtle striving in what you shared,” one of the teachers responded when I asked a question about how to make “mindful walking” more restorative. “Maybe you want for it to be relaxing and not challenging. But that’s not the reason we practice. We practice for the sake of practicing and to meet with whatever is arising.”

This is what Britton calls a “thought-terminating cliché”: a profound-seeming phrase deployed by people in power to quash debate—or, as Britton put it, a way for teachers to politely convey “Shut the fuck up and do what I say.”

But many Buddhists and meditation teachers would agree with my instructor: Feeling, and observing, discomfort is part of the point. In keeping with this, a good number of the meditators whom Britton has interviewed told her that when they had brought up their symptoms with meditation teachers, the teachers dismissed them, saying things like “It gets worse before it gets better” and “What you resist persists.”Their teachers would suggest that all negative experiences are inherently growth opportunities, or that perhaps the person was meditating incorrectly. The mentality seemed to be “Try our product and if you don’t like it, then you did it wrong,” Britton said.

This attitude tracks with what I heard from a few experienced meditators who suffered acute distress while meditating. One man told me that after a long retreat, when he began experiencing spasms that would seize up half his face, his meditation teacher just told him to relax more. Two other experienced meditators I talked with, Terran Palmer-Angell and Carmen Maria Alvarez, also told me that some fellow meditators at a long retreat they attended, organized by the Center for Contemplative Research, had experienced psychotic breaks or developed tics, including one man who would rotate his head around compulsively. The teacher and one of the center’s co-founders, B. Alan Wallace, they said, told them that it was just “an involuntary movement” and nothing to be concerned about.

Palmer-Angell and Alvarez emphasized that their experiences reflected this specific retreat, and not meditation in general. Eva Natanya, the center’s other co-founder, told me that “no one has been diagnosed with a psychotic break by a psychiatrist” at the retreat since its founding, in 2020. However, she said that some “individuals develop physical tics” because of a “burst of energy” while meditating. She said these tics are sometimes referred to as “involuntary movements,” and that initially, meditators might be encouraged to “let it go and go back to meditating because that energy will work itself out by itself.” She added that she herself worked with the person with the compulsive head rotations by “asking questions and listening.” She said the center has multiple forms of support available, including meetings with herself and Wallace, psychological counseling, appointments with doctors, and physiotherapy.

Britton remembers peddling a version of this logic as an MBSR teacher herself. “I was trying to tell people ‘Nothing is good or bad, but thinking makes it so,’” channeling Hamlet and Stoic philosophy. For a while, this idea seemed radical, and constructively life-changing: The secret to a good life is to just be okay with whatever! But then her own meditation practice started to make her think “like, Okay, but wait; I don’t feel like I exist now.”That didn’t seem like a good thing, no matter how you thought about it.

Lauren Lancaster for The Atlantic

Having moved away from Buddhism, Britton now finds her own kind of tranquility in the natural world, taking care of her plants and chopping wood.

After Britton and Lindahl published the “Varieties” study, the phone in their lab started ringing. People experiencing psychosis, dissociation, tics, and other problems after meditating were asking for help. The meditators felt confused and ashamed, like they had damaged themselves. Traditional psychotherapists, they said, didn’t understand what they were going through—and neither did anyone else. How can you hurt yourself meditating?

The surge in outreach prompted Britton to open what she called Cheetah House—a play on citta, the Sanskrit word for “consciousness”—and develop it into a full-fledged nonprofit aimed at helping people who have had difficult meditation experiences. Based at first out of her house in Providence, it now serves 200 people a month, entirely over Zoom.

The Cheetah House program consists mostly of talks with experts, sessions with a “care team” member, and support groups with other meditators who have had distressing experiences. The program is priced on a sliding scale; most people pay $50 a session with a care-team member, and $100 or more for a session with Britton herself.

Many of Cheetah House’s clients have (relatively) manageable problems such as anxiety and insomnia, but Britton told me that, once or twice a month, she gets a call from someone whose family member has had a psychotic break triggered by meditation. Far more rarely, people have killed themselves after intensive meditation retreats. “When people say that I’m fearmongering,” Britton told me, “my response is, ‘We haven’t even gotten into the suicides yet.’” She recently decided to start a support group for the parents of meditators who experienced severe psychiatric symptoms after 13 families, four of whose children had already died, expressed interest.

Between half and three-quarters of Cheetah House’s clientele began having symptoms after a meditation retreat, Britton told me. People often go on retreats to try to deepen their practice or to “relax”—but these are generally not relaxing affairs. Many retreats involve waking up at dawn, eating very little, and sitting perfectly still while focusing on one’s breath for hours on end. Several days of this, Britton said, can cause neurons to become more sensitive, such that minor stimuli, like the ticking of a clock or the sound of another person’s breath, can start to feel overwhelming—as can emotions such as rage and grief. Kieran Fox, a psychiatrist at UC San Francisco and an experienced meditator, told me that retreats are “some of the hardest things I’ve ever done in my entire life. And that’s including med school.”

Among the Cheetah House clients I interviewed, retreats were a common trigger for adverse effects. One meditator, Dan Millstein, told me that after a 10-day retreat, he spent years feeling emotionally shut down and disconnected, like he was “living behind a glass wall or a veil.” Another man, Billy, who asked that I not use his last name, had been meditating regularly for a decade when a seven-day silent retreat ratcheted up his physical and mental anxiety: Shivering relentlessly, he started feeling better when he stopped meditating.

About 15 years ago, a woman who asked to remain anonymous was on her second 10-day silent retreat when she began feeling a twitch in her face that developed into an urge to roll her head around. She felt like electricity was shooting through her body. She would shake uncontrollably and at times writhe on the floor. Eventually, she was hospitalized for psychosis. She was later diagnosed with complex PTSD, and although she’s learned how to manage those symptoms, she told me that she still experiences involuntary muscle movements today. Another woman, Rebecca Fischer, told me that, more than 12 years after a retreat she attended, she still has chronic pain in her legs and back.

A good number of Cheetah House’s clients do suffer ill effects outside of retreats. In the days after meditating at home with an app, a client named Susan Small told me she was driving when “my whole sense of myself disappeared,” and she went on to experience “waves of terror” for months. A man named Eoin told me that after eight days of doing 30-minute audio meditations on his own every morning, he started feeling like a “nervous wreck,” on the edge of psychosis, and like he didn’t really know who he was, a phenomenon called depersonalization.

These people and other clients said they appreciated hearing from fellow meditators with similar experiences, and that Cheetah House helped them feel less like a “misfit toy,” as Millstein put it. They’d had a hard time finding support elsewhere, in part because one of the most common recommendations for emotional distress is to try meditating. Many of her clients, Britton said, seem relieved when she tells them it’s okay if they want to stop.

One recent New Year’s Eve, Britton hosted what she jokingly called a “parallel play” party—a kind of get-together for introverts where everyone works on a craft so they don’t have to talk much. She made margaritas, and friends and colleagues brought over magazines to cut up for collages. A few hours in, someone held up an article from the magazine Psychotherapy Networker and said, “Hey, is this about you?”

The story was, indeed, about Cheetah House, and Britton waited until everyone left to read it. One quote in particular stopped her cold:

“There should be a trigger warning for the Cheetah House website,” says renowned Buddhist teacher and clinical psychologist Jack Kornfield. “Too much of it is misleading information and over-the-top fearmongering.”

This was the Jack Kornfield, the mindfulness guru who wrote A Path With Heart, the book that had launched Britton’s journey into Buddhism. He was like a father figure and a mentor to her. Jack Kornfield thought she was fearmongering. Now all she could think was “Thanks, Dad.” She spent a week in bed after that. (Kornfield declined to comment.)

As she continued with her research, Britton gradually started to feel iced out of the Buddhist circles that had once comprised her entire personal and professional networks. She said a Buddhist organization sent her a threatening letter after she interviewed members of their community. One time, after she gave a talk about adverse effects at a conference, Britton said a prominent meditation researcher cornered her outside and yelled, “I don’t believe you!” (The researcher denies saying this.)

Invitations to conferences started to dry up—and when she did receive them, she said, it would turn out to be an invite to debate whether meditation-related challenges even existed—“just an insult to everyone that I’ve interviewed,” she said.

“If you want to build a bridge, you can’t just be like, A bridge is gonna be so cool. You have to think about where could it possibly fail,” Britton told me. “And it’s so unpopular to be that person.” Her former postdoc, Roman Palitsky, told me that Britton suffered for pointing out the problems with the bridge. “Nobody was doing meditation difficulties before her, not seriously anyway,” he said. “And I think large parts of the meditation world kind of turned on her.”

Some of this criticism can be chalked up to differing interpretations of the science, and of how best to treat stubborn afflictions such as anxiety and depression when all of the remedies have potential downsides. “Is it better for an anxious person to be meditating or on Lexapro?” is not an easily answerable question. Fox, the UCSF psychiatrist, told me that some of the neuroscientific effects that Britton attributes to meditation, such as increased activity in the insula, can also be interpreted as a sign of better “autonomic awareness”—basically, being more attuned to the inner workings of your body—rather than a sign of trauma or panic.

But some of the criticism seems to emanate from a reflexive defensiveness on the part of meditation’s promoters, who—perhaps understandably, given the abundant benefits that have shown to be associated with the practice—don’t want to tarnish the reputation of a good thing.

I’ve noticed that people are apt to defend meditation with a zeal I haven’t witnessed since evangelical youth group in my teens. You don’t enjoy meditation? Good, you’re not supposed to enjoy it. You say it doesn’t work for you? Well, you’re just not doing it right. The answer to every problem with meditation seems to be more meditation.

This touchiness can extend to meditation researchers, most of whom are meditators themselves; academic meetings Britton attended would sometimes kick off with a meditation. Nicholas Van Dam, the University of Melbourne psychologist, told me that meditation communities tend to carry a sense that “if you say anything bad, you’re negating the good.” Farias mentioned that after he included a chapter about meditation’s risks in his book The Buddha Pill, some of his friends “were very, very annoyed,” and a couple of them told him that “we could not be publicly seen as associates.”

Some pro-meditation researchers are more evenhanded—recognizing the value of Britton’s findings even if they quibble with aspects of them. Eric Loucks, the director of the Mindfulness Center at Brown, pointed out that a person can have a challenging experience during meditation and still find their overall meditation practice to be beneficial. He also noted that several studies have found mindfulness-based interventions to have fewer side effects than pharmacological treatments, including Lexapro. Still, he called Britton “innovative” and “courageous,” and said her work influenced not only his own views and scholarship—including updates to the standard MBSR curriculum, which the Mindfulness Center now maintains—but also mindfulness research as a whole. “Just looking for the good stuff,” he said, is not his goal. “We really want to know the truth.”

But several meditation teachers I interviewed did seem protective of the practice. Carol Greco, a psychologist at the University of Pittsburgh and an MBSR teacher, once co-authored a paper that aimed to “dispel the notion” that anxiety, pain, and psychosis “are adverse events due to mindfulness meditation.” She seemed chagrined that I was working on this story, writing in an email, “I would rather talk with you about how meditation can be helpful.” When Britton’s studies began coming out, she said, it “brought a heightened awareness of the potential of trauma in a person’s background and how we can create a safe environment.” But her “heart hurt” because “it felt like it was making mindfulness and meditation seem like it’s really dangerous and really bad.” She told me that in her two decades as a meditation teacher she’s never seen a serious adverse event like psychosis or dissociation.

A few of the scholars I interviewed who defended meditation acknowledged some of Britton’s findings, at least implicitly. Richard Davidson, a University of Wisconsin at Madison professor of psychiatry and psychology who is a well-known mindfulness researcher, told me that, as far as relaxation techniques go, meditation is fairly benign. He believes that for most people there’s a greater risk of harm from not meditating than there is from meditating, because the physical and emotional benefits of the practice are so robust, and he’s co-authored studies supporting that claim. But, he added, people with serious psychiatric disorders should meditate only under the guidance of a mental-health professional who also happens to be a meditator—advice that would probably come as news to the many thousands of people who meditate by using apps at home.

The Buddhist scholar and teacher Gil Fronsdal told me that although he doesn’t think meditation causes adverse effects, retreats may exacerbate preexisting psychological problems. (Britton said adverse effects can crop up even for people without prior mental-health conditions.) Fronsdal recalled one meditator who gradually lost touch with reality after a monthlong retreat: She stalked Fronsdal’s wife, became homeless, and spent hours in a medical-law library researching how it was that Fronsdal had managed to exchange his wife’s spine for hers. Having schizophrenic people on meditation retreats has been “one of my most challenging situations as a teacher,” he told me. He said that people with psychosis shouldn’t go on meditation retreats, and neither should people who are “hyper-anxious”—a quality that described me when I sat for a daylong MBSR retreat for my book.

The substantial and sometimes hostile pushback against her work has made Britton hypervigilant. Maybe excessively so: To my eye, she sometimes detects criticism where there isn’t any. When I asked her to describe what it was like working at Brown’s largely pro-meditation research group while publishing study after study finding that meditation can be risky, she wouldn’t say much more than that the situation could be “tense.” (Loucks, the Mindfulness Center’s director, denied that there was tension.) “When it comes to somebody choosing their religion or your friendship,” she told me at one point, “they will choose their religion every time.”

Starting in the early 2020s, Britton and Lindahl struggled to find funding to continue studying the downsides of meditation; they said an organization once rejected their proposal for a grant on “transformative experiences” for being too critical of religion. She says that when they submitted papers to academic journals, the peer-review comments for the papers focusing on the risks of meditation were “six times longer” than for those focusing on the benefits.

Equanimity is a cornerstone of Buddhist thought; Britton herself had repeated the words to rooms full of meditation students many times: “Nothing is good or bad, but thinking makes it so.” But she was starting to think that, actually, some things are good and other things are bad. Sure, you can just accept everything, but sometimes you shouldn’t. She had made a big contribution to the field; it seemed to me like she was feeling done with Brown, with academia, with living in Rhode Island, with all of it.

When Britton first met Lindahl, he persuaded her to start taking one day off a week, something she had not done in two decades. Then it was two days. Then she stopped teaching in the summers. Soon, they were scouting for a plot of land in Vermont they could move to. They now live in an off-the-grid cabin in the woods, where a botanical drawing greets visitors on a wall by the entryway. What is the human soul, the caption reads, but a claw pointing back to the forest?

Britton is consulting on a research project with her former postdoc, Palitsky, who is now at Emory University and running a much larger, longitudinal study of meditation-related challenges. This summer, both she and Lindahl officially left Brown. They’re enjoying exploring “other sections of the bookstore,” as she put it. Running Cheetah House takes up the bulk of her time now.

Britton stopped meditating in 2017, around the time she published the “Varieties” study, and she “began to have a less romantic and more nuanced view of Buddhism.” Now she finds her own kind of tranquility in the natural world, taking care of her plants and chopping wood.

It’s important to emphasize that neither Britton’s research nor her work with Cheetah House clients has turned her against meditation per se; it’s just attuned her to the importance of doing it safely. Meditating for longer than about 30 minutes a day tends to be associated with more negative side effects, she said, and certain types of meditation can be a poor fit for certain people. (For instance, some anxious people shouldn’t do a “body scan” type of meditation, because they are already too focused on their body.) People considering extended meditation retreats should try meditating for a few hours at home first, to be sure they can tolerate long stretches. And those who experience challenges with their meditation practice should consider changing the kind of meditation they’re doing, modifying their practice, or just not meditating. “Treat meditation like any other relationship,” she said. “If you feel like shit with that person, maybe it’s time to break up.”

Spending so much time with Britton made me want to revisit my own adventures in Buddhism and what I had found valuable about it. Mostly, I found old notes about how much I hated meditating: “This is the part of the book where I’m not having a lot of fun”; “I would literally rather give birth than do nothing for 45 minutes”; “I’m just an anxious immigrant who fears you can mindful yourself onto a park bench.”

But I also came across some teachings that I did appreciate, and which I’m going to oversimplify here because I’m not a Buddhist. Among them: The Buddha taught that people should pursue a “middle way” between decadent indulgence and rigid austerity—to not live mindlessly, but to not be so ascetic as to immiserate yourself. “Avoiding these two extremes,” one sutta reads, “the Realized One understood the middle way of practice.” Maybe he was onto something.

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How ‘Somatics’ Became the Solution to Modern Life

2026-09-03T07:00:00-04:00

When clients go to Sybil Ottenstein for therapy, they tend to arrive with answers. Many of them have seen shrinks before. They can tell her which events from their past were formative, and point to the ripple effects in their current life. They’re like detectives, she told me, with all the dots connected on their corkboard of evidence. Intellectually, they’ve cracked the case. The problem is that they don’t feel any better.

That’s why they’re seeking something different from Ottenstein: somatic psychotherapy. Traditional talk therapy could be seen as a top-down approach. You identify problems in your thinking, your habits, or your life, and hope that by working through them, you can resolve physical manifestations of emotional issues—the chest palpitations of anxiety, the stomachache of stress. Somatic therapy, by contrast, works from the bottom up. Ottenstein typically starts her sessions by asking clients to slow down and pay attention to corporeal sensations: “What does it feel like in your chest? In your throat?” As they talk, she encourages them to stay in their body, to let themselves feel whatever is coming up. People cry. They yawn. They scream. They stretch. They dance.

The word somatic, according to Merriam-Webster, merely means “of, relating to, or affecting the body.” But recently, it’s been popping up everywhere, appended to a variety of practices that involve tuning in to physical symptoms in order to ameliorate psychological ones. Somatic therapists like Ottenstein have noticed a significant bump in interest; one of the major somatic-therapy training programs reported that its applicants more than doubled from 2020 to 2023. Other practitioners offer somatic dance, somatic yoga, somatic workouts. (The terms seem a touch redundant.)

[Read: How did healing ourselves get so exhausting?]

On Instagram, hundreds of thousands of posts appear with the hashtag #somatic. A “somatic exercise” trainer who goes by the “Workout Witch” (nearly 2 million followers) teaches small, repetitive movements meant to discharge negative feelings—curl your head down for “sorrow/despair,” pull your right ear for “overwhelm”—and promises that “trauma can be released from your hips.” All over my feed, fit young women are humming, hitting their sternum, pinching their nose bridge, and bouncing their knees all the way to inner peace.

[Read: These Millennials can’t get out of their head]

Much of the time, as with many other wellness ventures, someone stands to make money. At one somatic-workout class I attended, where a staffer told me that the goal was to “move stagnant energy out,” the lobby featured a gift-shop corner with jewelry, T-shirts, and $65 “body gloss” from a brand called Oui the People. But clearly, plenty of Americans are willing to pay for the promise of a psychic cleanse. Practitioners refer to “stuck energy,” to “trapped emotions,” to “resetting” a nervous system caught in fight-or-flight mode. “We have all these ways of just storing that gunk inside,” Ottenstein told me. I pictured, uncomfortably, a thick, black goo running through my veins.

Somatics—the whole roomy umbrella of practices—might seem like an odd fit for the information age, when people are more accustomed to finding answers on the internet than within themselves. But that could be precisely the draw for thinkers and analyzers who are tired of ruminating in anxious circles, who spend their days in front of a laptop and nights scrolling an iPhone. For millennia, people have yearned to break out of the confines of their bodies; they’ve searched—through religion, spirituality, drugs—for transcendence. Now, for some, the existential quest is inverted: Instead of seeking to escape their prison of flesh and bones, they want to reinhabit it.

The origin of somatics is difficult to pinpoint, though it’s certainly not recent. Some credit Wilhelm Reich, a student of Freud’s, who theorized in the early 1900s that patients held tension in their bodies—“muscular armor”—as a subconscious defense against trauma, leading to aches, pains, and inflammation. But it wasn’t until the 1970s that the field began to formalize, developed in part by the American philosophy professor Thomas Hanna, who defined somatics as the study of “the body as perceived from within.” That same decade, a UC Berkeley biophysics doctoral student, Peter Levine, developed “somatic experiencing”: a therapeutic method based on the idea that people, like other animals, react to trauma with a flight, fight, or freeze response, powered by a burst of adrenaline. After the source of danger is gone, Levine argued, they have pent-up “survival energy” to unleash: They need to physically shake it off. He pointed to videos of impalas, quaking and buckling after surviving a cheetah attack. When humans go through something upsetting, Ottenstein told me, “we go to work the next day.”

This idea—that trauma is held in the body, and thus must be physically remedied—was once fairly niche. In recent years, though, it has been jolted into prominence. The psychiatrist Bessel van der Kolk’s book The Body Keeps the Score, which argues for somatic treatments of PTSD, was first released in 2014 and was not an immediate hit. In 2021, it reached the No. 1 spot on the New York Times best-seller list for paperback nonfiction. And although it has been accused of resting on shaky science, it has continued to dominate the charts for years.

Van der Kolk wrote about violent assaults, wartime atrocities, severe childhood abuse—circumstances that many readers hadn’t directly experienced. Yet The Body Keeps the Score seemed to resonate anyway. When it gained momentum, lots of Americans had spent the previous year safe in their homes, baking bread and taking Zoom calls. (“When people say the pandemic has been a collective trauma,” van der Kolk told The Atlantic that year, “I say, absolutely not.”) Most had also, however, been detached from the rich sensory experience of interacting with the external world. Now here was a book about people who’d felt estranged from their own body—and then, through simple movement, play, and touch, found their way back to their surroundings, and to themselves.

[Read: The self-help that no one needs right now]

In the years since, most people have emerged from pandemic isolation. Yet the share of Americans who say they frequently experience stress, which has been rising for decades, has continued its upward trend. Talk therapy remains popular, but it’s not always affordable or accessible—and much of the time, it doesn’t take physical symptoms into account. Meanwhile, many medical doctors don’t consider psychological causes of physical ailments. Stress in particular is “like this mythical creature,” Aditi Nerurkar, a physician at Harvard Medical School, told me. “And we don’t have a lot of time. We have to focus on your hemoglobin. Did you get a mammogram? Did you get a pap smear? What is your cholesterol?”

No wonder, then, that somatics is a flourishing industry. Many Americans already distrust medical institutions; maybe they want to bypass the dismissive doctor, or the therapist who wants to rehash every daddy issue but can’t seem to fix anything. So they turn to this strange constellation of New Age–y courses, TikTok sages, and licensed counselors. Some offerings target people with capital-T Trauma; others claim to be for just about anyone. Many present themselves as alternatives to more traditional paths to mental well-being. The question is whether they can really help the frazzled masses.

Somatics does get a lot of things right. Plenty of bodily sensations are, at root, psychological. Some communication does need to happen between the brain and the rest of the body. That’s how you know to respond to danger: The amygdala triggers the nervous system to increase your heart rate, deliver more blood to muscles, and release a flood of adrenaline. When I spoke with Nerurkar, she rattled off an incomplete list of physical symptoms that might result from stress: headaches, dizziness, nausea, vision changes. When she was in residency training, she said, she experienced what felt like a “stampede of wild horses” across her chest and was convinced that she had a heart problem—until her doctors, having conducted a battery of tests, recommended that she seriously consider chilling out.

And many components of somatic practice have evidence to back them up. Interoception, or awareness of one’s own physical signals, really can be important for well-being—perhaps because it increases people’s sense of attunement with their body, connection with the present moment, or agency over otherwise vague and inscrutable sensations. Mindfulness meditation, which involves interoception, has been shown to decrease stress and anxiety and even reduce physical pain. Yoga and breathing exercises can decrease amygdala activation and lead to better concentration, memory, and executive function.

But the somatics packaging of these techniques is alluring partly because of the emotional liberation it promises. Somaticists tend to describe a clear path: identify a physical signal, connect it to its psychic cause, then let it go. If the nervous system overactivates, surely you can just reset it. If the body holds trauma, surely the body can relinquish it.

These were always just metaphors, though, and imperfect ones. The amygdala doesn’t have a reboot button. There is no viscous gunk of emotional pain to flush out. The Body Keeps the Score has been somewhat debunked; critics have argued that van der Kolk incorrectly described certain studies, and that he seems to have made up others entirely. (Responding to the writer Emi Nietfeld’s critique in Mother Jones, van der Kolk said that at times he drew on unpublished data.) Trauma experts have pushed back on his wholesale condemnation of talk therapy, which can be, according to a mountain of evidence, very helpful for treating PTSD. There’s also something ironic in how certain somaticists—ostensibly advocates for the mind-body connection—talk as if the two are separated by a nearly unbridgeable gap: the physical burden of trauma unreachable through thinking or conversation, and perhaps not even accessible to conscious awareness.

[Read: Why we’re still talking about the ‘trauma plot’]

So somatics isn’t a miracle cure. And it’s probably right to be skeptical of influencers who seek to collect on people’s need to feel at home in their body. But that doesn’t mean somatics can’t be helpful. Much of it, after all, turns out to be pretty straightforward. Movement is good, generally. Breathing is good. Stepping away from your screen—stretching your limbs, remembering you are real and tangible and mortal—is good.

When I signed up for that somatic-exercise class, I expected that I might leave rolling my eyes, but I secretly hoped I’d walk out lighter, more alive and connected to myself and the world. What I found was something in between. The actual workout couldn’t have been more basic: It consisted largely of squats, jumping jacks, crunches, some yoga—downward dog, child’s pose. Occasionally the instructor would remind us to check in with our bodies: “What are you being invited into? And I don’t mean the burpee.” Or: “Let the chin enter the conversation.” Otherwise it hardly seemed uniquely somatic, or uniquely anything.

Then again, I had the post-workout endorphin glow. I’d left my apartment and shut my phone in a locker. An hour later, I exited the studio somewhat baffled. But walking out onto a busy Manhattan street, I felt a little more conscious of the sun on my cheek, the solidness of the ground pushing against my feet. This was silly, I thought. And also: Maybe I’ll come back.

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The Truth About American Food Safety

2026-09-02T10:27:57-04:00

The phrase When it rains, it pours isn’t one you like to see applied to outbreaks of foodborne illness, yet here we are. The summer started with a diarrhea-causing parasite called Cyclospora cayetanensis, which infested iceberg lettuce. Then came news of Shiga toxin–producing bacteria in organic frozen berries, and a Salmonella outbreak linked to Whole Foods guacamole that eventually got traced to tainted jalapeños. (Pico de gallo, salsa fresca, and a variety of spicy dips have also been implicated.) Ricotta-style cheese was recalled for Listeria. Both Salmonella and E. coli were found in products from the aptly named Everything Sprouts. And 10,000 cases of lightly fried tofu were flagged for potential contamination with printing ink.

This flood of food-contamination events comes at just the time when our systems to prevent such outbreaks may be hobbled. Since last year, three cyclospora-research projects at the Department of Agriculture have lost either their funding or staffing, the CDC team that tracks the parasite’s genetics has nearly disappeared, and experienced government employees responsible for food safety have left their job or been fired.

The bureaucracy is crumbling, and the produce aisle is a mess. But let’s be fair: The status quo on foodborne illness was never very good. According to 2019 estimates from the CDC, Americans suffer (sometimes unaware) through at least 9.9 million bouts of foodborne illness each year; more than 50,000 people end up in the hospital, and about 1,000 die. Depending on how you measure outbreak numbers—whether by FDA investigations into foodborne illnesses, for instance, or by the number of food-product recalls—the 2026 statistics have been pretty much in line with recent history. How quickly we forget the Salmonella-dusted cucumbers of summer 2024 that sickened more than 500 souls. Or the cantaloupes that killed half a dozen people in 2023. Occasional salad-based catastrophes have been the norm for many years. Food-safety experts say that something on the order of 150 million meals of leafy greens are served in this country every day. Now as always, a very small proportion of them will make you ill.

But one of this summer’s outbreaks does suggest that our “very small proportion” might be growing into a slightly larger very small proportion. Although the jalapeño and berry outbreaks have had many doleful precedents of their size and scope, the cyclospora summer stands alone. Annual cases of its associated diarrheal disease, called cyclosporiasis, have been slowly increasing over time, from hundreds in the 2010s to a few thousand in the early 2020s. (This is, in part, due to faster diagnosis: One used to have to find the parasite’s oocysts under a microscope; now the fragments of its DNA can be identified in a rapid-PCR screening test.) This year, though, the CDC has confirmed 17,180 cases of the illness, and many thousands more suspected cases still need to be examined. State-level agencies have tallied more than 30,000 infections. “It’s just absolutely crazy,” Kalmia Kniel, an expert in microbial food safety at the University of Delaware and a former president of the International Association for Food Protection, told me. “It is completely overwhelming and insane that this happened.” I suppose it’s nice to know the sense of overwhelm afflicts experts too.

No one seems to know exactly how or why this year’s cyclosporiasis caseload got so big. The largest group of cases, which has been centered in the upper Midwest, has been linked to iceberg lettuce grown in Mexico. Kniel suspects that in Michigan, the parasite may have worked its way from the feces of the first infected people into the local water supply, spawning a secondary, local outbreak. Michael Osterholm, who runs the University of Minnesota’s Center for Infectious Disease Research and Policy and previously spent 15 years as the state’s head epidemiologist, told me that he’s seen no evidence to support the secondary-outbreak theory. Either way, some mystery remains as to how the parasite got into the food supply in Mexico. Taylor Farms, which recalled its iceberg lettuce in July, is “one of the leading produce companies in terms of food safety,” Kniel said. And yet here we are.

Perhaps the government could be doing more to resolve some of this uncertainty. On this point, though, expert opinions vary widely. Kniel said that, at least at first, the FDA and the CDC appeared to be posting information about the cyclospora situation more slowly than they had in past years. Steven Mandernach, the executive director of the Association of Food and Drug Officials and a former food-safety official in Iowa, told me that as far as he can tell, information has been coming out just as efficiently as ever. Osterholm believes that the sky is falling. “We have hit an all-time low, in my 50 years in public health, in our capacity to identify and respond to foodborne outbreaks,” he said, adding that the government’s slow response time on the cyclospora outbreak was nothing less than “public-health malpractice.” In an emailed statement, Grace Davis Jamison, a Department of Health and Human Services spokesperson, wrote, “Claims that HHS has lacked transparency overlook the extensive information FDA and CDC have shared as investigations progress including timely updates that help the public understand potential risks and make informed decisions.” She also said that no FDA investigators had been lost to staffing changes, and that the CDC laboratory that supports foodborne-outbreak investigations was likewise “unaffected.”

Perhaps this disagreement can be squared by acknowledging the failings of the past. The system has long been underfunded while needed changes were delayed, Barbara Kowalcyk, the director of George Washington University’s Institute for Food Safety and Nutrition Security, told me. The recent departures of experienced personnel, to retirements and layoffs, have made things only worse. “We had one hand tied behind our back before this administration happened, and now we have both hands tied,” she said. (How exactly this might translate into disease outbreaks in years ahead remains unclear.)

History suggests that few new investments in food safety come before a tragic outbreak of disease. “It was the 1993 Jack in the Box outbreak that really changed things at USDA,” Kowalcyk said, referring to the undercooked, contaminated hamburgers that killed four children who had eaten at the fast-food chain. A 2006 outbreak of E. coli in bagged spinach, which caused hundreds of illnesses and $200 million in lost spinach sales, helped inspire the passage of the Food Safety Modernization Act. Now we have the cyclospora summer. “I think that this is going to drive another paradigm shift,” Kowalcyk said.

Cyclosporiasis is, by the grace of God, a relatively gentle and self-limiting disease. Many people recover on their own within a few weeks. And for all of the tens of thousands of cases that have been registered in recent months (and the many more infections that were never diagnosed), just two deaths have been reported. Their loss is a tragedy; the economic devastation caused by falling lettuce prices, and the fact that many consumers have spent months in fear of eating leafy greens, is a shame. But given that this summer’s cyclospora plague stands among the largest foodborne-illness outbreaks in the nation’s history, these outcomes seem modest.

Consider this a solace and a warning: Our summer of contamination could have been much worse.