Medical News

For more than 50 years, America’s official position on marijuana has been seen as nonsensical. By classifying pot as a Schedule I drug, the federal government has lumped it with heroin and LSD as substances with “no currently accepted medical use and a high potential for abuse.” In 1972, two years after marijuana was relegated to the most restrictive category of drugs in America, a government report found that weed’s “actual impact on society does not justify a social policy designed to seek out and firmly punish those who use it.”

Even with the federal classification, states have been experimenting with marijuana legalization for nearly three decades. These laws have led to fewer marijuana-related arrests without dramatic increases in crime, and they haven’t substantially spiked the rate of illicit adolescent cannabis use. Although fully legalizing recreational marijuana remains controversial, it’s clear that smoking a joint from your local dispensary is not the same as using heroin.

Now America’s marijuana policies are getting a bit more in line with the actual science. Today, Donald Trump signed an executive order directing the government to move the drug to Schedule III, a classification for substances with “moderate to low potential for physical and psychological dependence.” As the president emphasized in the Oval Office, the action “doesn’t legalize marijuana in any way, shape, or form.” Selling marijuana without a prescription will still be a federal crime, just as trafficking anabolic steroids (also a Schedule III drug) is illegal.

The biggest impact from today’s action will likely be on medical research. Marijuana studies have been stymied because researchers who want to experiment with Schedule I drugs need to be closely vetted by the federal government. During the signing ceremony for the executive order, Health and Human Services Secretary Robert F. Kennedy Jr. argued that the new classification will let scientists better understand the drug. That’s the hope of Ryan Vandrey, a cannabis researcher at Johns Hopkins University. Vandrey’s lab was cleared to do cannabis research while marijuana was still in Schedule I, but he hopes that this loosening of restrictions will open up “a huge number of possibilities for us to get at both the health benefits and health risks of cannabis as a whole,” he told me.

[Read: The new war on weed]

At the same time, by rescheduling the drug, the government runs the risk of signaling that marijuana is no big deal. “We need to be very clear in our messaging—especially to young people—that rescheduling does not mean cannabis is harmless,” Scott Hadland, a professor at Harvard Medical School and a pediatrician who treats adolescent addiction, told me. The government needs to figure out a way to tell Americans that even though marijuana is not as dangerous as heroin, it’s still an addictive drug. That’s not an easy message to communicate. Prior to signing the executive order today, the president touted the purported benefits of marijuana for certain medical conditions, but he also echoed the “Just Say No” drug campaign of decades past. “Unless a drug is recommended by a doctor for medical reasons, just don’t do it,” he said. (The White House did not respond to a request for comment.)

When talking about the risks of marijuana, you can easily to come off as a scold. Roughly 50 percent of Americans have tried the drug, and according to a 2024 study, the number of people using cannabis daily or near daily now eclipses the number who drink alcohol at a similar frequency. (Trump emphasized today that weed rescheduling polls well.) Even so, the risks of marijuana are real. The CDC estimates that three in 10 cannabis users exhibit some signs of dependency.

It doesn’t help that marijuana isn’t the same as when it was first scheduled, back in 1970. The drug has become significantly stronger over the past several decades. The average joint in the ’70s contained about 2 percent THC, the main psychoactive component of marijuana. In 2025, dispensaries regularly stock joints that have more than 35 percent THC. Studies have shown that use of higher-concentration marijuana is associated with serious mental-health outcomes, such as psychosis. In 2017, there were more than 100,000 hospitalizations for pot-linked psychosis, one study found. Vandrey said that he hopes rescheduling will help researchers better interrogate the “very strong correlation” between heavy marijuana use and psychosis.

None of this is to say that marijuana should stay a Schedule I drug, as it has for decades. In spite of this classification, millions of Americans have continued to use it. The government is now finally backing away from a misguided position about the risks of pot. But it still has to contend with the drug’s complications.

Updated at 12:29 p.m. on December 17, 2025

When Donald Trump nominated Jay Bhattacharya to be the director of the National Institutes of Health, a shake-up seemed inevitable. Typically, the agency—a $48 billion grant-making institution and the world’s largest public funder of biomedical research—has been led by a medical researcher with extensive administrative experience. Bhattacharya was a health economist without specialized training in infectious disease, who’d come to prominence for his heterodox views on COVID policies and who has criticized the NIH for stifling dissent.

The NIH has been transformed this year. And most of the layoffs, policy changes, and politically motivated funding cuts—notably, to infectious-disease research—have happened under Bhattacharya’s watch. But inside the agency, officials describe Bhattacharya as a largely ineffectual figurehead, often absent from leadership meetings, unresponsive to colleagues, and fixated more on cultivating his media image than on engaging with the turmoil at his own agency. “We don’t really hear from or about Jay very much,” one official told me. (Most of the current and former NIH officials who spoke with me for this article requested anonymity out of fear of retaliation.) Many officials call Bhattacharya “Podcast Jay” because of the amount of time that he has spent in his office recording himself talking. “Bhattacharya is too busy podcasting to do anything,” one official told me.

Instead, Matthew Memoli, the agency’s principal deputy director, “is the one wielding the axe,”the official said. This time last year, Memoli was a relatively low-ranking flu researcher at the NIH’s National Institute of Allergy and Infectious Diseases (NIAID). Then, in January, the Trump administration appointed him to be the agency’s acting director. At the time, other NIH officials considered Memoli to be a placeholder, temporarily empowered to carry out the administration’s orders. But “there’s been no change since Jay got put in,” one NIH official told me. To the agency officials I spoke with, Memoli, now second in command, still looks to be very much in charge.

Neither Bhattacharya nor Memoli agreed to an interview; the Trump administration responded to my request for comment after this story was published. This account did “not reflect Dr. Bhattacharya’s leadership approach or the way decisions are made at NIH,” Andrew Nixon, a spokesperson for the Department of Health and Human Services, said in an email. “Dr. Bhattacharya has deep respect for the agency, its staff, and its scientific mission, which is rooted in gold-standard science and in the interests of public health.”

To better understand Bhattacharya and Memoli’s leadership, I spoke with 18 current and former NIH officials, whose positions at the agency have spanned a breadth of specialties and administrative roles, and reached out to several of Bhattacharya’s former colleagues. The officials’ first impressions of Bhattacharya—who has argued that the NIH could do more “to promote innovative science”—were of an outsider and a radical, whose ideas could have changed the agency for better or worse. In recent months, NIH officials have come to see him as so disengaged that they hardly worry about his impact. Memoli, by contrast, knows just enough about the agency—and, in particular, its approach to infectious disease—to help destroy it.

Memoli’s appointment to acting director in January floored his colleagues—many of whom had never heard his name before. Like Bhattacharya, Memoli had no previous track record of executive leadership or in overseeing the awarding of federal grants. But officials quickly deduced what about Memoli might have appealed to the administration: In 2021, he described COVID-vaccine mandates as “extraordinarily problematic” in an email to Anthony Fauci, then the director of NIAID, whom the Trump administration has repeatedly tried to discredit. Then, last year, when asked to submit a routine statement about diversity, equity, and inclusion, Memoli sent in one that called the term DEI “offensive and demeaning.” By September, the NIH, under Bhattacharya’s leadership, had done away with DEI statements for its scientists, describing them as “loyalty oaths” that Memoli had “courageously stood against.”

In his two months as acting director, Memoli enacted the Trump administration’s agenda with aplomb, pushing through the mass cancellation of grants focused on topics such as DEI, transgender health, and COVID-19; multiple NIH leaders were ousted while he was acting director, including Jeanne Marrazzo, who served as the director of NIAID until early April. “His major function was to do the administration’s bidding,” Michael Lauer, who led the NIH’s grant-making division before he departed the agency in February, told me.

That same month, while Memoli was still acting director, he began to call Health Secretary Robert F. Kennedy Jr.’s attention to the flu-vaccine research he’d done with his mentor, Jeffery Taubenberger, another NIAID scientist. By early May—after Memoli had been installed as Bhattacharya’s deputy, and Taubenberger as the acting director of NIAID—HHS had redirected about half a billion dollars, once set aside to develop new COVID-19 vaccines and drugs, to their vaccine work. (Outside researchers criticized the grant as an unjustifiably enormous sum; in an email to me in May, Memoli insisted that the grant would support “more than one project,” but did not answer follow-up questions about how much of that sum would furnish his research specifically.)

Part of a deputy’s job is to take some load off the director. But under normal circumstances, people “wouldn’t really notice who the deputy director is,” one official told me; the director is expected to set policy and lead. Although Bhattacharya has continued to reiterate his own goals for the NIH—including advancing more innovative research—his recent visions for the agency have largely followed administration talking points such as diverting resources toward chronic disease and clamping down on “dangerous” virological research. Yet the director seems out of touch with the reality of that agenda: In his public appearances, internal meetings, and on social media, Bhattacharya has delivered conflicting and sometimes erroneous accounts of the NIH’s grant-making policies. Both publicly and internally, he has fixated more on defending himself against criticism he received for his COVID-policy views from 2020 than on the NIH’s current state of affairs, several officials said.

Bhattacharya, in his own way, still seems to be serving the administration by championing its talking points. But Memoli is the one most visibly throttling the NIH’s capacity to fund research and pushing out some of the agency’s most experienced and internally respected leaders. To officials at the agency, his actions look like those of a leader who has been given broad discretion to shrink down the agency’s infectious-disease work—an area where he may have a few personal grievances. “People are afraid of him,” one official said, pausing. “I’m afraid of him.”

Memoli’s history at the NIH appears to have given him a particular zeal for dismantling it. In his two decades at the agency, Memoli has developed a reputation as a self-aggrandizing co-worker, eager to champion himself and dismissive of people he hasn’t felt he could benefit professionally from, three officials who worked with him prior to 2025 told me. At various points, scientists at the agency lodged complaints about his unprofessional behavior toward colleagues, two NIH officials told me. Memoli, meanwhile, complained that “he wasn’t being given enough,” one of them said. Some of his scientific work was solid, but peers inside and outside the agency criticized some as unremarkable, leaving Memoli with a chip on his shoulder, the two officials said.

Of the NIH’s 27 institutes and centers, NIAID, where Memoli once worked, has been among the hardest hit this year, losing most of its senior leadership and a large number of its infectious-disease-focused grants. Since January, multiple officials who denounced the administration’s stance on infectious diseases and vaccines have had Memoli brush aside their concerns in meetings, then been ousted from their roles, three officials told me.

Given the Trump administration’s desire to pare down infectious-disease research, NIAID and prominent officials such as Marrazzo, who succeeded Fauci as director, were always clear targets for cuts. (Yesterday, Marrazzo filed a lawsuit that named Memoli and Bhattacharya and that alleged that she was illegally fired after she had filed a whistleblower complaint about actions of NIH leadership that endangered public health; HHS declined to comment on the lawsuit.) But in some cases, three officials told me, Memoli appears to have pushed lesser-known officials out of their roles after more personal clashes, including Sarah Read, who was NIAID’s principal deputy director and who repeatedly questioned the circumstances of Memoli and Taubenberger’s sizable vaccine grant. (Read has since left the agency.) Memoli also recently detailed Carl Dieffenbach, the director of NIAID’s Division of AIDS, to another branch of NIH after the two clashed over the administration’s approach to HIV research. Days later, he gave Dieffenbach a scoring of one out of five on a performance review—potential grounds for termination—before human-resources personnel forced him to revise that rating, because he lacked evidence for them, two officials told me. (Read and Dieffenbach declined to comment.)

Memoli has also argued that funding for HIV-vaccine research—which Dieffenbach oversaw—is wasteful and should be cut. The NIH is expected to soon divert up to a third of its AIDS budget toward improving the delivery of existing HIV tools, such as the new drug lenacapavir. At least some of that push has come from Bhattacharya, who has publicly advocated (including on his own The Director’s Desk podcast) for reallocating HIV funds on the grounds that established interventions could resolve the AIDS crisis on their own. But whereas Bhattacharya has waffled when asked how such an investment would affect other research, two officials told me, Memoli has insisted in internal meetings that it should come at the expense of research into HIV vaccines, which is widely considered to be essential to ending the HIV pandemic. Despite being a vaccine researcher himself, he’s “gleefully making these cuts,” one official told me. “Because it means he did something.”

Allowing Memoli to be the executor of the Trump administration’s cuts could serve the independent-thinker persona that Bhattacharya has tried to cultivate. But the NIH officials I spoke with, and one scientist who knew Bhattacharya prior to his appointment at the agency, doubted that his distance was so calculated. Trying to discredit the scientific establishment from the sidelines is far easier than trying to enact reform from its center. At the NIH, the embittered insider may leave the more memorable legacy.

This story was updated to include a comment from the Department of Health and Human Services.

Without fail, any corporation accused of conspiring against public health will be compared to Big Tobacco. When oil companies downplayed the threat of climate change, they were allegedly following in the footsteps of cigarette manufacturers. The NFL’s strategy for disputing the link between football and concussions has similarly been likened to the tobacco industry’s actions. The online-gambling industry has supposedly acted like Big Tobacco, as have the tech industry and the plastic industry.

Earlier this month, one such comparison ended up in a lawsuit. In the first such case of its kind, San Francisco sued several of the nation’s largest food companies—including Kraft Heinz, Nestle USA, and PepsiCo—alleging that they had copied the tobacco industry’s playbook by deliberately engineering processed food to be irresistible and then concealing the risks. “They used Big Tobacco tactics to research, design, and sell addictive products,” David Chiu, the city attorney, said at a press conference.

What is this comparison really saying? An executive focused on selling more Oreos or cans of Mountain Dew might have an interest in encouraging unhealthy dietary habits, but that is not self-evidently the same as the misdeeds of the tobacco industry, which for decades covered up the evidence that cigarettes cause cancer while continuing to sell what’s been called the most dangerous consumer product ever.

I ran the analogy by several nutrition experts. “Of course, food is more complicated than tobacco,” Marion Nestle, an emeritus professor at New York University, told me. The risks of cigarettes are well established, but researchers still struggle to define what even counts as an ultra-processed food, let alone pinpoint the exact reason these foods prompt people to overeat. However, there are notable similarities between the two industries and the products they sell, she said. Researchers do know that ultra-processed foods such as Coca-Cola and Pringles are among the biggest contributors to obesity and other diet-related diseases, which are linked to an estimated 1 million deaths in the United States each year.

[Read: Coke, Twinkies, Skittles, and … whole-grain bread?]

The two industries also use similar strategies to cast doubt on the dangers of their products. Junk-food companies “know the harm they’re doing, and they do it anyway,” Robert Lustig, an emeritus professor of pediatrics at UC San Francisco, told me. Consider Coca-Cola: Roughly a decade ago, the food giant funded a think tank that reportedly attempted to shift the focus of obesity away from poor diets and instead highlight the role that exercise can play in weight management. Like Big Tobacco, food companies have also attempted to convince consumers that some of their unhealthy products might actually be good for them. In 2016, Coca-Cola settled a lawsuit filed by consumer advocates alleging that the company falsely advertised Vitaminwater as containing just vitamins and water; as part of the settlement, the company agreed to change its marketing and note on its bottles that the drink contains sweeteners.

For decades, Big Tobacco and Big Food were in many cases one and the same. In 1985, the tobacco giant R. J. Reynolds bought Nabisco; three years later, Philip Morris, the company responsible for the Marlboro Man, acquired Kraft Foods. Philip Morris later purchased Nabisco and absorbed it into Kraft, before relinquishing control of the company in 2007. It was during this time period that junk food became so irresistible. A recent study found that from 1988 to 2001, foods developed by tobacco-owned companies versus other companies were far more likely to be “hyperpalatable,” meaning they contained large quantities of carbs, fat, and salt.

Food companies deny comparisons to Big Tobacco. A spokesperson for the Consumer Brands Association, a lobbying group that represents packaged-food companies, told me that “attempting to classify foods as unhealthy simply because they are processed, or demonizing food by ignoring its full nutrient content, misleads consumers and exacerbates health disparities.” I reached out to the 11 food companies named in the San Francisco lawsuit and heard back from only Coca-Cola. A company spokesperson told me in an email that comparisons between Big Food and Big Tobacco are flawed, and pointed out that Coca-Cola also sells a variety of “low‑ and no‑sugar options.” In response to the claims that Coca-Cola has downplayed the effects of its products on obesity, the spokesperson said that the company has since strengthened its “transparency standards” and allows the researchers it funds to “control the design, data and publication to ensure objectivity.”

Comparing Big Food and Big Tobacco is certainly an evocative rhetorical device. It underscores the severity of America’s obesity problem, and it points out that the way food is manufactured can itself be part of the problem. Villainizing food companies has become a popular message—one that has galvanized Health and Human Services Secretary Robert F. Kennedy Jr. and his “Make America Healthy Again” movement. Food giants “are literally poisoning our children systematically for profit,” Kennedy said last year. As HHS secretary, Kennedy has cracked down on ultra-processed food, pushing states to ban the purchase of soda with food stamps and pressuring companies to phase out synthetic food dyes.

[Read: Republicans are right about soda]

And yet, Americans still love Big Food. Hershey’s, Heinz Ketchup, and M&M’s are among America’s most trusted brands, according to a recent Morning Consult report. As a result, drastic measures that would improve diet-related disease in this country—the kinds that were used against the tobacco industry—are still quite unpopular. Cigarette taxes have proved to reduce smoking rates, but attempts to levy even a small tax on soda have failed in cities across the country. Other ideas, such as creating a minimum age to buy junk food, aren’t even discussed by lawmakers. I asked Chiu, the San Francisco city attorney, if he would support such a policy, and he punted. “My office is employing our tools as we can to address this crisis in front of us,” he told me, “but we welcome other actors and stakeholders to be involved.”

In some ways, comparing Big Food to Big Tobacco undersells just how difficult it will be to remedy the problems with the American diet. To push Americans away from cigarettes, public-health advocates had a simple message: Don’t smoke. There is no equivalent slogan for food. Although roughly 40 percent of American adults smoked in the 1960s, when cigarettes were at their most popular, ultra-processed foods are everywhere in 2025. They make up more than 50 percent of what adults eat at home. They’re not just Kit Kat bars and Twinkies but also Campbell’s soup, Wonder Bread, and Hot Pockets. The world can live without cigarettes, but the same cannot be said of food.

On the Friday after Thanksgiving, Vinay Prasad, the FDA’s top vaccine regulator, made a claim that shocked the public-health establishment. “For the first time,” he wrote in a leaked email to his staff, “the US FDA will acknowledge that COVID-19 vaccines have killed American children.” The agency had supposedly identified at least 10 children who died from getting COVID shots.

To say the email was poorly received by vaccine experts and physicians would be an understatement. Prasad’s claim provoked a rapid series of rebuttals. A response from 12 former FDA commissioners, published in The New England Journal of Medicine on Wednesday, called Prasad’s memo “a threat to evidence-based vaccine policy and public health security.” All of the potential vaccine-related deaths reported to the government, presumably including those to which Prasad referred, had already been reviewed by the agency’s staff, the former commissioners wrote, and “different conclusions” had been reached. Elsewhere, doctors and scientists declared that absolutely no evidence links COVID-19 vaccines to death in children; and that in order to suggest otherwise, Prasad and his colleagues had engaged in an “evidence-manufacturing mission,” a “dumpster dive” for shoddy data, or—worse—a campaign of lying.

Prasad is among the public-health officials who, under the leadership of Robert F. Kennedy Jr., have been systematically undermining the nation’s confidence in immunizations. Prasad has not yet offered up any documentation to support his assertion, and his count of vaccine-related deaths may well turn out to be inflated. The memo’s overheated rhetoric and lengthy recitation of political grievances also raise some doubts about his claims.

Yet there’s something troubling—and telling—in the fact that his memo has provoked people to deny even the possibility of COVID-vaccine-related deaths. The idea that mRNA-based shots have, tragically, killed a very small number of children is not far-fetched. It also doesn’t imply a catastrophic threat to public health, given that tens of millions of doses of these vaccines have safely been given out to young people. From the start of the coronavirus pandemic, lack of nuance has been a problem with public-health messaging—one that anti-vaccine advocates have made use of to great effect. Now, in a moment when public health in America is under existential threat, this insistence that no evidence exists for vaccine-related deaths risks adding to the crisis.

No public-health authorities deny that COVID shots can have some ill effects. Adverse reactions are possible with all medical interventions. The mRNA-based vaccines produced by Pfizer and Moderna, in particular, are known to cause myocarditis—inflammation of the heart—on rare occasions, especially in teenage boys and young men. The form of myocarditis that occurs after vaccination is typically far less severe than the one caused by viruses; for unclear reasons, mRNA-related cases have largely disappeared in recent years. But this condition can be deadly, and considering the hundreds of millions of mRNA doses that have been administered to Americans, even extraordinarily unlikely outcomes may well be inevitable.

[Read: ‘It feels like the CDC is over’]

In August 2021, U.S. physicians published details of a 42-year-old man’s post-vaccination death from myocarditis in The New England Journal of Medicine. Similar cases trickled in from other countries too. South Korean researchers and public-health officials, who tracked postimmunization fatalities very closely, identified a total of 21 deaths from vaccine-induced myocarditis—all in adults—during their country’s initial COVID-inoculation campaign, which reached more than 44 million people. And in 2022, one of my former instructors, the forensic pathologist James Gill, Connecticut’s chief medical examiner, found that children could also be at risk of death. Writing in a peer-reviewed journal, he and his colleagues described the cases of two teenage boys who died of heart damage after receiving their second Pfizer dose.

So why is Prasad’s allegation that a very small number of kids have died from COVID shots being treated as some unholy aberration? I reached out to Paul Offit, a former member of the CDC’s immunization advisory committee who had described the memo’s assertions as being “fairly fantastic.” He told me that although Prasad’s claim may ultimately pan out, he does not consider the published case reports definitive, nor does he believe that the shots have led to any deaths. “It’s not terribly convincing that this vaccine killed anybody,” he said.

Michael Osterholm, the director of the Center for Infectious Disease Research and Policy at the University of Minnesota, gave the same response: He doesn’t think that the COVID shots have yet been linked to any deaths, and he trusts the judgment of the officials who had first reviewed these cases. (Like Offit, he allowed for the possibility that such cases might be identified in the future.)

When I reached out to Krutika Kuppalli, an infectious-disease physician who works on vaccine safety, she told me that high-quality studies from around the world have clearly demonstrated that there isn’t any wave of mRNA-related deaths. Population-level data show no increase in mortality from the Pfizer or Moderna COVID shots. This means that if the immunizations do cause death, it happens so infrequently as to be statistically undetectable. (Abundant evidence shows that the vaccines reduce mortality from SARS-CoV-2. That statistical signal is clear as day.)

[Read: Revenge of the COVID contrarians]

But there’s a disconnect among the sort of studies cited by Kuppalli and doctors’ observations on the ground. The latter may get written up in case reports of vaccine-related deaths, and although any single finding from this literature can be debatable, that doesn’t mean it ought to be ignored. Cause-of-death determinations happen every day in medicine, based on the most likely explanation of the facts. Yet when vaccines might be involved, that standard seems to change: Suddenly, authorities demand an impossibly high level of evidence.

Experts told me that any of the published cases of death from an mRNA vaccine could have resulted from some alternative cause, such as a preexisting condition or hidden infection. True enough, but these cases were thoroughly investigated. Many of the diagnoses were confirmed by autopsy, which is considered the gold-standard diagnostic approach. The 21 Korean deaths, in particular, were verified by a panel of specialists in cardiology, infectious disease, and epidemiology. Surely these, at least, should meet the bar for establishing a person’s cause of death—but the doctors and public-health professionals I spoke with for this story insisted that such reports don’t amount to slam-dunk proof. “These are important for hypothesis generation and mechanistic understanding,” Kuppalli said, “but they do not establish causality for death.”

Many mainstream experts have been drawing from the same playbook that COVID skeptics used at the height of the pandemic. Five years ago, they and others asked: Were thousands of American children truly getting hospitalized for COVID, or did they get hospitalized for some other reason and just happened to have COVID? Now we get a similar question: Did the teenagers who died after getting their Pfizer shots die from COVID vaccination, or did they just happen to die from something else after having been vaccinated?

The CDC itself has at times adopted this turbocharged incredulity. After Gill’s team published about the two teens, who died after receiving mRNA vaccines in the spring or summer of 2021, Tom Shimabukuro, then a high-level official in the CDC’s Immunization Safety Office, and several other agency staffers wrote a scathing letter to the journal, claiming that important facts had been omitted. They said the agency had found laboratory evidence of infection—a virus in one case and a bacterium in the other—and that at least the latter “suggested an alternate cause of death” that should have been mentioned in the paper.

[Read: Mortality numbers may have more to do with politics than science]

The CDC’s critique, however, was premised on errors so rudimentary that any trained pathologist should be able to spot them: The PCR test used to detect the virus in one case is known to be unreliable for determining a true infection, for example; the bacteria implicated in the other typically grow only after a patient is deceased. Given the flimsy reasoning behind the CDC’s rebuttal, Gill’s cases could easily be among the 10 deaths that the FDA is now touting. Yet according to a June 2025 presentation by the director of the CDC’s Immunization Safety Office, “no known deaths or cardiac transplants” were seen in individuals ages 12 to 29 with post-vaccine myocarditis from January to November 2021. Another slide said there was “no increased risk of death following mRNA COVID-19 vaccines.” (Neither the Department of Health and Human Services nor Shimabukuro responded to questions about this story.)

Some defensiveness about the data on vaccine-related harms is understandable. Anti-vaccine activists, the HHS secretary among them, have spent years stoking unfounded fears about mRNA vaccines; doing so has almost certainly resulted in otherwise preventable deaths among those who refused to get vaccinated. And it may well be that this administration’s claims about the harms from COVID shots are unfounded, and that no persuasive evidence will ever be provided. (The FDA has indicated that supporting data will be released later this month.) But given what is already known, the public-health establishment should be prepared for the alternative. Accepting and acknowledging reasonable proof of that reality would be an important part of effectively combating the government’s current vaccine skepticism. How can medical professionals discuss the favorable risk-benefit profile of these shots if they aren’t willing to acknowledge their worst risk? Denial also creates opportunities for those who want to break the system to rebuild it. In his memo, Prasad presents a very small number of allegedly catastrophic events as a revelation of such grave importance that “swift action” must be taken in regard to the COVID vaccines and the immunization approval process overall.

The possibility—perhaps the likelihood—that a handful of vaccine-related deaths occurred and were downplayed by medical authorities does not undermine the fact that COVID vaccination, on the whole, has prevented death on a massive scale. Nor does it justify sweeping changes to vaccine regulations. Rather, it suggests the need for some targeted reforms, such as improvements to the country’s vaccine-adverse-event reporting system—and also tells us that a strategy of minimizing tragic outcomes, however rare, may not be the best way to protect a vital instrument of public health.

Updated at 11:35 a.m. ET on December 8, 2025

For a decade after its discovery, CRISPR gene editing was stuck on the cusp of transforming medicine. Then, in 2023, scientists started using it on sickle-cell disease, and Victoria Gray, a  patient who lived with constant pain—like lightning inside her body, she has said—got the first-ever FDA-approved CRISPR gene-editing treatment. Her symptoms vanished; so did virtually everyone else’s in the clinical trial she was a part of.

This year, the technology has started to press beyond its next barrier. Most of the 8 million people globally who have sickle-cell disease share the same genetic mutation; treating rare disorders will require dealing with many different mutations, even within the same disease. And although rare diseases affect 30 million Americans in total, relatively few people are diagnosed with each one. Fyodor Urnov, a scientific director of UC Berkeley’s Innovative Genomics Institute (IGI), showed me a list of rare diseases and pointed to one carried by only 50 people. “Who’s going to work on a disease with 50 patients?” he asked. And even within one disorder, each person might need their own customized CRISPR treatment. Drug developers have little financial incentive to spend years and millions of dollars designing therapies that may need to be tailored to literally one person.

The technology is ready to treat at least some of these diseases, though. “There’s a whole toolbox now that can target arguably any part of the genome pretty precisely,” Krishanu Saha, a gene-editing researcher at the University of Wisconsin at Madison, told me. If researchers could build one CRISPR platform for a single disease, or even several similar ones, and tweak that template to suit each patient, they could target extremely rare disorders more quickly and economically. Maybe the first patient’s treatment for a disease takes $2 million and a year of development; by the third patient, the cost should be down to, say, $100,000 and a month of development, Urnov said, because you’ve already proved that the reused components are safe.

“We have been moving in the direction of thinking about CRISPR as a platform for some years,” Jennifer Doudna, the IGI’s founder, who shares the Nobel Prize for discovering CRISPR gene editing, told me. But, in her mind, 2025 was the first time many people understood its potential. A baby named KJ Muldoon is a big reason why.

In February, Muldoon became the first child to receive one of these customized CRISPR gene-editing treatments, tailored to fix his specific mutation. People born with his rare genetic disease, a type of urea-cycle disorder, have about a 50 percent chance of living past infancy. If they do, they live with extreme developmental delays and usually require a liver transplant. But when he was six months old, Muldoon got his bespoke treatment, and now he’s a healthy 1-year-old. His therapy was proof that custom gene-editing treatments can work and that they can be spun up relatively quickly, yet safely.

His treatment also gives scientists a chance to try the platform approach. The next child treated for a urea-cycle disorder should now be able to receive a CRISPR treatment from Muldoon’s template, tweaked to their unique DNA. CRISPR technology uses guide RNA, a molecular GPS of sorts, to send an editor protein to a particular address in someone’s DNA. Targeting a different mutation just means changing the address. Muldoon’s case put more momentum, too, behind personalized gene editing in general. The federal government recently announced two major  programs that offer funding to scientists working on personalized treatments for rare diseases. The focus now, Doudna said, is figuring out how to make customized CRISPR “available to anyone who needs it.”

For years, one of the main roadblocks has been the U.S. drug-regulatory system. Its approval processes were designed for traditional drugs that help many people, not a bespoke treatment that helps one child in Philadelphia. The FDA has considered each treatment, even for the same disease, as a different drug. Biochemically, two therapies might be the equivalent of a pizza with pepperoni and another with artichokes. But under the FDA approval process, “you go back to square one. You recertify the oven. You recertify the person who throws the disk of dough. You confirm the cheese is still safe to eat,” Urnov, who was also part of the team that designed Muldoon’s treatment, said. The FDA has been trying to change that process over the past few years, and last month, two of its top officials, Marty Makary and Vinay Prasad, announced a new drug pathway that could speed up approvals for personalized rare-disease treatments. The framework was inspired in large part by the success of Muldoon’s therapy. (The FDA did not respond to a request for comment.)

The new pathway opens the door to the platform approach that scientists have hoped to take. If researchers could prove they’d successfully treated a small number of patients for one rare genetic disease, they could continue customizing treatments for other mutations, and potentially also for similar conditions. That streamlined process could finally attract for-profit players—the best shot at actually getting these customized therapies to patients en masse, Doudna said. “If we’re able to bundle trials together so that we’re able to treat multiple related diseases without starting from scratch, that could completely change the economics of treating rare disease,” she said.

The first clinical trials in this model will begin soon. Urnov and his colleagues plan to investigate a platform for rare immune disorders; Rebecca Ahrens-Nicklas and Kiran Musunuru, the geneticists who treated Muldoon at the Children’s Hospital of Philadelphia, told me they are planning to start one this winter for children with various types of urea-cycle disorder. If all goes according to plan, another child should receive a treatment based on Muldoon’s in the near future.

Working this way does put more responsibility on scientists to test their therapies thoroughly, Ahrens-Nicklas said. Gene editing can go wrong: A treatment may accidentally alter the wrong part of a patient’s DNA, or the delivery mechanism could trigger a deadly immune reaction in their body. “If you have to treat fewer subjects in order to get that approval, you want to make sure that you’re really robustly measuring the safety on those few subjects” and communicating any risks to the wider gene-editing community, she said. But done well, these trials are a major step toward getting more custom treatments out to more people.

All of the researchers I spoke with emphasized that these are early days. Because of how the current gene-editing delivery mechanisms work, scientists are mostly limited to treating disorders in the blood and liver. And researchers are focused on single diseases, or groups of similar ones, for now. Their dream would be to have a CRISPR platform that could address many disparate disorders, but the current reality is that many, many families will still go without bespoke therapies. Muldoon’s treatment “took a team of people at both nonprofits and for-profit companies in multiple countries working at a scale I have never seen before,” Doudna said. And they changed his life. His parents weren’t sure if he’d ever be able to sit upright on his own, but recently, Muldoon took his first steps. The press has dubbed him a “miracle baby.” Now miracles like his need to become commonplace.

This article originally misstated the full name of the Children’s Hospital of Philadelphia.

Updated at 4:33 p.m. ET on December 5, 2025

In case there was any doubt before, it’s now undeniable that Robert F. Kennedy Jr.’s allies are in charge of the country’s vaccine policy. The latest evidence: His handpicked vaccine advisory committee voted today to scrap the decades-old guidance that all babies receive the hepatitis-B vaccine shortly after birth. Now the panel recommends that only children born to mothers who test positive for the infection or have unknown status automatically receive a shot at birth. Everyone else has the option of a shot at birth or—as the committee recommends—waiting until at least two months after birth.

Those who favor the change argue that other countries, such as Denmark and Finland, vaccinate only newborns of mothers who test positive, and that rates of infection are relatively low in the United States. All of this is true. But in the U.S., many expectant mothers don’t get tested for hepatitis B, and even if they do, those tests sometimes fail to pick up the virus. The rationale for giving the vaccine right away is to wipe out an infection that will afflict the majority of people who contract it as babies for the rest of their life (and, for as many as a quarter of those chronically infected, result in their death from cirrhosis or liver cancer). The World Health Organization and the American Academy of Pediatrics both endorse the universal birth dose. “When you remove that foundation, you essentially cause the whole prevention process to collapse,” Noele Nelson, a former CDC researcher who has published multiple papers on hepatitis B, told me.

The meeting, which began yesterday, was also proof that Kennedy, and those he’s empowered, no longer feel bound by previous norms. In June, Kennedy fired every outside adviser on the committee, alleging unspecified conflicts of interests (even though members are required to disclose those conflicts and recuse themselves when necessary). He has since stacked the board with members who share his doubts about vaccine safety. During the previous meeting, in September, those new members seemed at times unaware of basic facts about vaccines and often unsure about what they were voting on. In the end, their recommendations were fairly modest, advising that children younger than 4 receive two separate shots for MMR and chickenpox.

This week’s meeting was, if anything, more chaotic. Days before it started, Martin Kulldorff, a former Harvard Medical School professor who had been chair of the advisory board, left the committee for a position at the Department of Health and Human Services. The new chair is Kirk Milhoan, a pediatric cardiologist who is a member of the Independent Medical Alliance, a group that has promoted the use of ivermectin to treat COVID-19 despite clinical trials showing that the drug isn’t effective against the virus. But Milhoan didn’t show up in person for the meeting, leaving the moderating duties to Vice Chair Robert Malone, the author of the conspiracy-theory-driven book PsyWar and a hero to people who oppose COVID vaccination; Malone has called Anthony Fauci “an accomplice to mass murder.” (HHS did not respond to a request for comment, nor did Malone or Milhoan.) In the days leading up to the decision on the hepatitis-B shot, committee members received four different versions of the question they’d be voting on, and the final language is still difficult to decipher.

[Read: The most extreme voice on RFK Jr.’s new vaccine committee]

The meeting was dominated by presentations not from career CDC staff, as it was even in September, but from fringe figures who are closely aligned with Kennedy. Mark Blaxill—a longtime Kennedy ally in the anti-vaccine cause who now works for the CDC—gave a presentation about hepatitis-B-vaccine safety. He noted that he’d been “a critic of the CDC for many years, so it’s been an honor and a privilege to work on the inside and to address some of these issues.” Another presenter, Cynthia Nevison, is a research associate at the University of Colorado at Boulder’s Institute of Arctic and Alpine Research. She is also one of Blaxill’s co-authors on a 2021 paper on rising autism rates that was retracted after the journal’s editors and publisher concluded that they had made a host of errors, including misrepresenting data. (Blaxill told me that the paper was later published with “modest additions” in another journal.)

Just as the meeting was more chaotic than earlier iterations, the pushback was even sharper. Cody Meissner, a pediatrician and committee member who’d also served on the board during the Obama administration, noted, accurately, that rates of hepatitis B have declined in the United States “thanks to the effectiveness of our current immunization program.” Malone interjected—as he did at several points in the meeting—that this was merely Meissner’s opinion. “These are facts, Robert,” Meissner responded. Joseph Hibbeln, a fellow committee member, shouted that there hadn’t been “any information or science presented” about whether delaying the hepatitis-B dose by two months made sense. Amy Middleman, a pediatrician and representative of the Society for Adolescent Health and Medicine, urged the committee “to go back to our true experts” at the CDC. Adam Langer, a longtime CDC expert who is the acting principal deputy director of the center that oversees hepatitis prevention, at one point cautioned the committee not to use countries such as Denmark, which has a much smaller population and more comprehensive prenatal care, as a basis for comparison. Most panelists seem not to have cared.

In the end, the concerns of the committee’s few dissenters—along with the chorus of objections from representatives of medical organizations—were disregarded. The committee voted overwhelmingly (8–3) to change the recommendation. “This has a great potential to cause harm, and I simply hope that the committee will accept its responsibility when this harm is caused,” Hibbeln said afterward. The board also voted that parents should have the option of testing their children’s antibody titers against hepatitis B before they receive subsequent doses of the vaccine—a move for which, several meeting participants pointed out, there is little scientific support. A senior CDC scientist wrote to me that it was the “least science-based, most illogical public health recommendation in U.S. history.” The committee’s decisions are not final yet: The CDC director still needs to sign off on them. Because Kennedy pushed out Susan Monarez less than a month after she was confirmed as director, the decision will rest with the acting director, Jim O’Neill, whom Kennedy selected as deputy HHS secretary and who has no background in medicine.

[Read: ‘It feels like the CDC is over’]

The new normal for the vaccine advisory committee appears to be the appearance of vigorous scientific debate in which the experts are either not consulted or simply disregarded. That doesn’t bode well, because the committee apparently plans to reconsider the rest of the childhood-immunization schedule—something Kennedy promised Senator Bill Cassidy, who chairs the Senate health committee, that he would not do. Earlier today, the committee heard a presentation from Aaron Siri, a lawyer who worked for Kennedy’s presidential campaign and has represented clients who believe that their children were injured by vaccines. He used his time to spell out his doubts about the childhood-vaccine schedule.

According to Malone, the committee had asked Paul Offit and Peter Hotez, both widely respected vaccine experts, to appear as well. In an email, Hotez told me he declined because the board “appears to have shifted away from science and evidence-based medicine.” Offit told me in an email that he didn’t remember being asked to attend but that he would have declined because the committee “is now an illegitimate process run by anti-vaccine activists.” Even Cassidy, who has mostly stopped short of directly criticizing Kennedy’s actions in office, slammed Siri’s appearance in front of the committee, posting on X earlier this week that the committee was now “totally discredited.” (When I asked Siri for comment, he pointed me to an X post in which he’d challenged Cassidy to a public debate on vaccines. A spokesperson for Cassidy’s office did not respond to a request for comment.)

At the end of today’s meeting, the board gave a preview of its next target: aluminum salts, which are used in a number of childhood inoculations to boost immune response. (A presentation on the topic by Kulldorff was originally scheduled for today, but was removed from the agenda last night.) A recent study of more than 1 million Danish children found no evidence that aluminum salts are associated with neurodevelopmental disorders such as autism. Yet Milhoan, the new chair, said concerns had “reached a threshold where it needs to be considered.” Another member, Retsef Levi, speculated about how new safety trials might be conducted. If the committee decides at its next meeting, in February, that a common ingredient, used in vaccines for decades, is unsafe, it could upend childhood immunization in the United States. Which is, of course, exactly what many of Kennedy’s longtime allies have wanted all along.

Throughout the 2000s, the music charts were rife with references to Rogaine. Jay-Z invoked the hair-restoration drug as a synonym for staying power. Weezer described it, begrudgingly, as a means of rejuvenation. Ingrid Michaelson, in a song about accepting one’s flaws, pledged to buy the drug for her partner when he inevitably lost his hair.

Now, as the Millennials who grew up on this music are fast approaching their Rogaine era, the hair-loss industry is eager to receive them—particularly the many women coming around to the idea that they might want to buy Rogaine for themselves too. Over roughly the past decade, hair-loss treatments aimed at women have broken into mainstream consumer culture, alerting women simultaneously to the possibility of balding and the potential to fix it.

Women have always been the target audience for shampoos, hair masks, hot-oil treatments, and so on. But those products aim to improve the appearance of existing hair, not grow more of it. Products specifically for hair loss have historically targeted male users. When Rogaine launched in 1988, it was available only for men. (The women’s version came three years later.)

Advertising for hair loss has, accordingly, mostly focused on men. Throughout the big-hair craze of the 1980s and ’90s, infomercials for men’s spray-on hair were all over TV. In a Rogaine ad from 2001, a narrator asks: “Will she feel the same way if you lose your hair?” (The answer: “Sure, she’ll just feel it about somebody else.”) Hair-growth treatments are an easy sell for men because many will go bald in midlife. Yet 40 percent of women experience some amount of hair loss by the time they turn 50. They just haven’t been as comfortable talking about it as men, Rachael Gibson, a hair-culture expert known online as the Hair Historian, told me.

Now brands and their ambassadors have taken the microphone. Nutrafol, a women-focused hair-supplement company that launched in 2016, has started selling its products at Sephora and Ulta. My Instagram feed is full of female influencers holding up fistfuls of loose hair and presenting sparsely populated scalps—then hawking serums, supplements, and shampoos that supposedly restored their voluminous mane. (Before watching these videos, I had no suspicions that my hair was falling out; afterward, I was convinced that with the right products, I could look absolutely equine.) When Hers launched in 2018, it offered topical minoxidil, the generic form of Rogaine. Over the past three years or so, many providers (including Hers) have started prescribing oral minoxidil, a hypertension drug, off-label to treat hair loss, which can be a welcome alternative to sticky topical versions. Hers and its men’s counterpart, Hims, also sell some of their hair-loss products at Walmart.

The proliferation of women’s hair-restoration products is impossible to separate from the booming menopause market. As pop-culture depictions of menopause have become more prominent over the past few years, numerous drugs, supplements, and telehealth platforms have sprung up to address it. Shoshana Marmon, a dermatology professor at New York Medical College, told me that she has observed a growing number of influencers targeting women in midlife, when hair usually starts to thin. Midi Health, a menopause-focused telehealth platform, started offering oral and topical minoxidil in 2023, and it screens patients for common issues, such as iron deficiency and thyroid problems, that can drive hair loss, Kathleen Jordan, Midi Health’s chief medical officer, told me. And because fluctuating hormones during menopause are a major driver of hair loss in women, hormone-replacement therapy can sometimes help.

Of course, hair-loss companies are ready to sell these products to anyone, not just aging women. In beauty chains and drugstores, numerous oral hair-loss supplements containing ingredients such as biotin and vitamin A are displayed alongside shampoos and conditioners. Last year, products for thinning hair and scalp health were among the fastest-growing categories in the roughly $450 billion prestige-hair-product market, according to the market-research firm Circana. Widespread hair loss during the coronavirus pandemic may have juiced demand for hair-loss products, and the rise of direct-to-consumer telehealth companies likely accelerated the trend: Hair-loss treatment is popular at Hims and Hers, a company spokesperson told me, because many people find hair loss embarrassing and telehealth allows them to seek help discreetly.

[Read: The year America’s hair fell out]

The most commonly prescribed hair-loss drugs are well established and generally trustworthy. Minoxidil is the “gold standard” of active ingredients for hair loss, Paradi Mirmirani, a dermatologist with Kaiser Permanente, told me. In both topical and oral forms, it works by slowing or reversing hair-follicle shrinkage, which tends to happen as hormones fluctuate. A drug called finasteride is sometimes used to reduce shedding; Midi Health combines it with minoxidil and two less-used hair-loss drugs in a “Regrowth Serum.” But finasteride is most commonly prescribed to men; it isn’t FDA-approved for women for hair loss, because it can be dangerous to pregnant women and their fetuses. (It has also been linked to panic attacks and suicidal thoughts in some men.)

Meanwhile, hair-loss supplements, like all supplements, are somewhat of a tangle. The highest-quality evidence available offers some support for swallowing ingredients such as zinc, pumpkin-seed oil, and omega-3 and omega-6 fatty acids, Elizabeth Houshmand, a fellow with the American Academy of Dermatology, told me. But purity, dosing, and consistency vary widely among products, and their safety and effectiveness aren’t regulated by the FDA. Herbal supplements that lower DHT, a hormone that shrinks the hair follicle, can sometimes be beneficial, but medications are “the only thing that really does work,” Spencer Kobren, the founder of the American Hair Loss Association, a consumer-advocacy group, told me.

The predominantly male focus of the hair-loss industry, combined with women’s reticence about thinning hair, has left many women clueless about the possibility that they, too, may lose their hair. “We hear all the time from our consumers that ‘I didn’t know,’” Cindy Gustafson, the CEO of Nutrafol, told me. Some are too embarrassed to bring it up with their provider, fearing that their concern will be criticized as vain or, worse, dismissed as just a part of life, Jordan said. Unlike men, who are generally more aware of hair-loss drugs and use them as a first line of treatment, women tend to rely on trusted friends and hairstylists for advice, Kobren said, noting that they usually try four to six non-pharmaceutical hair-loss products before consulting a doctor. Unfortunately, he added, women also tend to spend the most on hair-regrowth snake oil.

[Read: Soon there will be unlimited hair]

Women today are in an unprecedented position: They’re receiving more messages than ever about the possibility of balding, even as they’re bombarded with products to fix it. Perhaps this shift will make women more comfortable taking their hair concerns to their doctor, rather than to friends and influencers. But it seems equally likely to change nothing. Like smooth skin and mental clarity, perfect hair suddenly seems within reach at any age—as long as you’re willing to pay.

“Ozempic is about to be old news,” my colleague Yasmin Tayag wrote in 2023, just before an even more powerful obesity drug, tirzepatide, then best known as Mounjaro, was approved. Well, two years later, Mounjaro is becoming old news, too. A whole slew of next-generation obesity drugs are on the horizon, some already advanced enough in clinical trials to be looking as good as—if not better than—those already on the market. The novel medications continue to push the upward limits of weight loss, now to almost 25 percent of body weight on average, but they also differ in their modes of action. They target different cells and different parts of cells in the brain and body.

Obesity, after all, is not monolithic. “We don’t have a disease of obesity. We have a disease of obesities,” Angela Fitch, chief medical officer at Knownwell, a national obesity-care clinic, and a former president of the Obesity Medicine Association, told me. With the coming explosion of obesity drugs, doctors could soon match each patient’s condition to their optimal medication: A 25-year-old with fatty-liver disease may need a different drug than a 75-year-old with low muscle mass. About 100 million adults live with obesity in just the U.S., a market massive enough for multiple mediations to find a niche. “One size will not fit all, and one size will not be best for all,” Richard DiMarchi, a chemist at Indiana University who has worked on obesity drugs at both Eli Lilly and Novo Nordisk, told me.

The most obvious way obesity drugs are not one-size-fits-all is that those on the market do not actually work for all. Although patients on semaglutide, the drug in Ozempic and Wegovy, lost on average 10 percent of their body weight, a third lost less than 5 percent in one clinical trial. Some even gain weight taking the drug. And others suffer such terrible side effects, including constant nausea and vomiting, that they cannot take it at all.

Ozempic functions by mimicking a single hormone called GLP-1; the drug’s mode of action is relatively simple but limited. To improve upon Ozempic, drugmakers have started targeting GLP-1 in combination with other hormones linked to hunger and satiety. The second drug currently on the market, the tirzepatide found in Mounjaro and Zepbound, resembles GLP-1 in addition to another hormone called GIP, hitting receptors for both in the brain. The GIP component may serve a double function, promoting additional satiety while suppressing some of the nausea caused by GLP-1. However tirzepatide truly works—and experts caution that no one knows—it prompts, on average, about 20 percent weight loss. It’s only the first of the “GLP-1 plus” drugs to market.

Other GLP-1-plus drugs in development include GLP-1 plus amylin, GLP-1 plus glucagon, and GLP-1 plus anti-GIP, which surprisingly could work as well as Mounjaro’s combination of GLP-1 plus GIP. (“If you aren’t confused,” Randy Seeley, an obesity researcher at the University of Michigan, told me, “you aren’t paying attention.”) In fact, all of these combinations seem to work—at least based on preliminary data from clinical trials—even as a precise understanding of the science lags. Some of the hormone mimics, such as for amylin, might also work alone. And others could be remixed into combinations of more than two. The drug retatrutide, which is in trials, is a triple hitter that targets GLP-1 plus glucagon plus GIP receptors, all at once. In an early Phase 2 trial, patients lost on average 24 percent of their weight, the highest of any obesity drug so far. The best responders lost upwards of 40 percent.

Even more intriguing than the top-line weight-loss numbers are metabolic changes unique to particular drugs. Glucagon, for example, ramps up liver metabolism; drugs based on this hormone could help break down fat accumulated in the livers of patients who also have fatty-liver disease. (The FDA is expediting review of one such drug, survodutide, for liver-disease patients.) Meanwhile, GLP-1-based drugs appear to protect against cardiovascular disease, even independent of weight loss. Patients prone to heart disease might fare best on medication that includes a GLP-1 component. When it comes to obesity, Seeley said, “your flavor of metabolic disease will be different than the next person’s.” Obesity drugs of the future may finally reflect that diversity, too.

An extensive menu of obesity drugs that work via distinct biological mechanisms means that patients will have more options to try. If they aren’t losing weight on drug A, they can move on to drug B or C. Experts don’t yet understand why the drugs work differently in different people, but hormone receptors in our brains likely vary in subtle yet important ways. The new drugs not only hit distinct combinations of hormone receptors; they also each tickle those receptors in a unique way.

In the near future, doctors and patients will probably have to trial-and-error their way to what works best. Further down the line, experts tell me, they hope to have a test, such as a blood test, that can forecast how patients will fare. Doctors could tell patients that they’ve got five different drugs at the ready, “and if I do this one test on you, I do this one test on you, I can predict which one of these drugs is the best for you,” Jonathan Campbell, an obesity researcher at Duke University, told me.

Maximum weight loss might not always be the goal for everyone though. The 40 percent that some people lose on retatrutide would be far too much for a patient barely over the BMI cutoff for obesity. Patients who don’t need to optimize weight loss may choose to prioritize convenience instead, which drugmakers are also happy to oblige. Most obesity drugs on the market are formulated as weekly injections. But Eli Lilly is developing a daily pill called orforglipron, and Amgen is testing a monthly injection called MariTide. And some patients, especially those who are elderly with already low muscle mass, might need extra help preserving their strength. The powerful appetite suppression that induces fat loss can induce muscle loss too. A number of drugmakers are now trialing obesity drugs in combination with various muscle-preserving drugs.

A mere decade ago, obesity drugs powerful enough for people to routinely drop double-digit percentages of their body weight were unheard-of. Today, there are two, and they feel ubiquitous. In yet another 10 years, this toolbox of just two obesity drugs will likely appear tiny and outdated. The next phase of the obesity-drug revolution is coming, with more drugs to choose from.

There’s a fairy tale about Thanksgiving that gets refuted every fall. Does eating turkey really make you fall asleep? When science writers check in with the experts, they always get the same response: No, no, no, and no. Also no and no.

These holiday debunkers tell you what the science says: Turkey meat is not a sedative. They tell you what the studies show: Drumsticks don’t produce fatigue. And then they take another step, however ill-advised: They lay out different reasons Thanksgiving dinner might be sleep inducing. Even as these stories bust the turkey-coma myth, they end up replacing it with other fables.

The trouble began nearly half a century ago. It started with warm milk—a sleep aid that was the subject of its own lightly flavored brand of science journalism. Was it true that a mug of milk could help you go to sleep? Yes, the experts said, because milk has tryptophan! This one amino acid worked something like a natural “sleeping pill,” a psychiatry professor told The New York Times in 1983. “Once again,” the Times said, “an old wives’ tale, the one about warm milk before bedtime, has received scientific support.”

Indeed, a tryptophanic fever was about to spread across America. By the end of the decade, tryptophan was being widely sold in supplements as a treatment for insomnia; an aid for beating jet leg; and also a fix for depression, PMS, and drug dependence. (Tryptophan was even talked about as a suicide preventive.) To explain its wondrous potency, scientists noted that when tryptophan made its way into the brain, it could be converted into the neurotransmitter serotonin. According to the thinking of the time, serotonin was the molecule of relaxation and well-being. Early studies seemed to show that it led to sleep.

Turkey, too, contains some tryptophan. Thus the sleepy-turkey myth was born. But even from the start, experts knew the theory had some complications. In the first place—as every Thanksgiving-myth-debunking article notes—turkey doesn’t have a lot of tryptophan. In fact, almost every other kind of meat has more. One serving of turkey breast contains 244 milligrams of tryptophan; one serving of clams contains 243. You’ll get less tryptophan from turkey, ounce for ounce, than you will from octopus or cheddar cheese. And in the second place, even taking high-dose tryptophan supplements doesn’t seem to do so much for sleep. (In 2017, the American Academy of Sleep Medicine recommended against the use of tryptophan as a treatment for insomnia on account of its “absence of demonstrated efficacy.”)

If only that could be the end of it. The early experts on the topic had laid out some other dietary theories of ensleepification. Tryptophan was soporific, the MIT neuroendocrinologist Richard Wurtman and his colleagues said, but its effects were limited by the degree to which it crossed the blood-brain barrier. Other nutrients from foods could get in its way. But Wurtman, who died in 2022, found that when you ingest a bunch of carbohydrates, the resulting spike of insulin can shunt away the amino acids that normally compete with tryptophan. As he saw it, carbs have a “sedating effect” in the human diet, by helping tryptophan to make its way from the gut into the brain. If it seemed as though a mug of warm, protein-rich milk was helping people get to sleep, that’s because they must also have been eating cake.

Wurtman was already floating this idea—let’s call it the sleepy-carbs hypothesis—in the early 1980s, and it has been repeated in the press ever since. Almost all articles about the turkey-coma myth now point at carbohydrate-heavy side dishes, the sweet potatoes and the pie, and claim that these Thanksgiving foods, not the turkey, really knock you out.

This merely swaps one highly suspect notion for another. Studies find that meals with lots of carbohydrates don’t really make you sleepy. (They may have some small effects on how you sleep, such as an increase in the time you spend in REM, the dreaming phase.) More to the point, the old idea that serotonin is a simple, sleep-promoting signal in the brain is fully out of fashion; later research found that serotonin may also be a potent source of wakefulness, and that its function in the sleep-wake cycle is both complicated and diverse.

Nutritionists may now be more inclined to look at melatonin, a hormone that is synthesized (like serotonin) from dietary tryptophan. One line of research looks at whether sour cherries or beefsteak tomatoes might be useful as a sleep aid, because these foods are known to be rich in naturally occurring melatonin. When taken as a supplement, melatonin seems to have a small effect on sleep onset and sleep quality; when taken as a tomato, it may also have some benefits. That said, the American Academy of Sleep Medicine recommends against the use of melatonin as a treatment for insomnia for a similar reason that it recommends against tryptophan: insufficient evidence of clinically meaningful results.

In short, all the science here is pretty weak. Yet the turkey-myth debunkers pile on the speculations. The sleepy-carbs hypothesis is just the start. What accounts for post-Thanksgiving lethargy? Many experts blame the fact that we’re consuming so much food, and overeating makes you tired on its own. (Some even cite the old-fashioned and unlikely notion that heavy digestion deprives your brain of oxygen.) But the evidence that people are more inclined to fall asleep, for any reason, after pigging out—that they experience what’s known among the cognoscenti as “postprandial somnolence”—is equivocal, at best.

This is science—and this is science journalism—of the sort that only makes you dumber the more of it you read. Here are some other reasons you might feel tired after eating dinner on Thanksgiving: You have consumed some alcoholic beverages; you have traveled a long distance; you have gotten trapped in some exhausting conversation with your cousin’s wife. Also maybe this: Dinner time is over, and the sky is dark, and a lot of time has passed since the last time you were sleeping.

And allow me to lay out one final possibility: What if Thanksgiving dinner doesn’t even make you sleepy in the first place? Could the very basis for the turkey-coma myth, and for all of its debunkings, be a sham? I could find no data to suggest that the Thanksgiving-meal effect is real. “Nobody’s tested this,” Faris Zuraikat, a nutrition and sleep scientist at Columbia University, told me when I called him for this story. So here we are today, dressing up a folk belief about the holiday with pseudoscientific rationales. It’s a pointless and exhausting project. We should be thankful if it ends.