Medical News

Every night before bedtime, my daughter tilts back her head so that a pair of metal plates inside her mouth can be cranked apart another quarter of a millimeter. We turn a jackscrew with a wire tip; it spreads the bones within her upper jaw. At times she groans or even cries: she says that she can feel the pressure up into her nose.

This is normal. My daughter is 9 years old. She has a palate expander.

So does her best friend, and, by her count, so does nearly one in four of the kids in her fourth-grade class. On Reddit’s r/braces forum, a practitioner based in Frisco, Texas, said he was surprised by “how many parents ask me, ‘Hey, does my child need an expander? Everyone else seems to have one.’” His colleagues seemed to notice something similar. “Everybody’s being told they have a narrow jaw, and everyone’s being given an expander,” Neal Kravitz, the editor in chief of the Journal of Clinical Orthodontics, told me.

A generation ago, getting braces was a rite of passage into seventh grade. Today, the reshaping of a child’s smile may commence a few years earlier, at 7, 8, or 9 years old. At that point, the two sides of the upper jawbone haven’t yet joined together, a fact that is propitious for a different orthodontic process: instead of straightening, expansion. During this phase of life, when kids still have some baby teeth, a tiny dungeon rack may be wedged between a child’s upper teeth, then used to spread her upper jaw and—proponents say—introduce essential room for sprouting teeth.

The expander is an old device; debates about its use are hardly any younger. What seems to have been the first expander was described in 1860, in the journal The Dental Cosmos, by a San Francisco dentist named Emerson Angell. He wrote of “an apparatus, simple and efficient,” that he’d placed into the mouth of a young patient. Then he’d told her to expand it, day by day, by advancing a central screw—just as my daughter does today. But the journal’s editors were skeptical of Angell’s work. We “must beg leave to differ with the writer in the conclusion arrived at,” they announced in a prefatory note, foreshadowing a long disagreement within the field.

This concerned the merits of expansion versus those of extraction—whether a child’s jaw should be broadened to accommodate her teeth, or whether certain teeth should be pulled to accommodate her jaw. Around the turn of the 20th century, the influential orthodontist Edward Angle favored jaw broadening; he believed that all children should have their teeth intact, nestled in a capacious jaw, as exemplified by a human skull that had been ransacked from an Indian burial mound not far from where he practiced, which he called “Old Glory.” A few decades later, though, orthodontic research found that expanded jaws might still “relapse” into a narrow shape. By the 1970s, pulling teeth became the rule, Daniel Rinchuse, a Seton Hill University professor of orthodontics, told me.

This consensus was itself short-lived, he said—not because the field had come across some new and better mouth-expanding tech but because of fears about the supposed ill effects of doing too many extractions. Some dentists claimed that what was then the standard approach in orthodontics could even lead to painful disorders of the temporomandibular joint, or TMJ. In the face of these concerns, expanders made a comeback.

Eventually, some orthodontists started claiming that expanders had another major benefit—that prying open a child’s palate could improve her breathing and prevent sleep apnea. Some now recommend this airway-focused intervention not just for kids my daughter’s age but for toddlers too.

The basis for the trend was never really scientific, though. “Do expanders prevent obstructive sleep apnea? In capital letters: NO WAY,” Kravitz said. “There are endless research papers on this stuff.” The problem isn’t that expanders have no value, he continued; it’s that they’re clearly overused. According to Rinchuse, who co-edited the book Evidence-Based Clinical Orthodontics, the idea that extracting teeth will lead to joint disorders has never been proved. Indeed, no “high-quality evidence” supports expansion of the upper jaw for any reason, he said, except in cases where a child has been diagnosed with posterior “crossbite.” He said that, overall, orthodontic practice is less constrained by evidence than other fields of health care are, because the ill effects of bad decisions will be slight. As he put it, “In orthodontics, no one dies.”

Steven Siegel, the current president of the American Association of Orthodontists, acknowledged that some practitioners may be inclined to put a rack on every child’s palate: “There are some abuses,” he told me. But he also argued that the recent increase in expander use hasn’t really been dramatic, and that for the most part, the devices are used to positive effect. For people with a narrow jaw and crowded teeth, he said, expanders can prevent the need for extractions down the road; some kids, at least, could see improvements in their breathing. When I noted that I’d heard the opposite on both counts from Kravitz and Rinchuse, he responded that they simply disagreed. “I have great respect for both of them,” he said. “I would say that there is a controversy.”

For the record, my daughter is delighted by the treatment she’s received: In a recent family interview, conducted over breakfast, she described her course of orthodontics as “cool and fun.” Her orthodontist (who happens to be a former high-school classmate) has been thoughtful and communicative, and I’ve recommended her to several other families. Still, despite the fact that no one dies from orthodontics, one might also choose to avoid a treatment that costs several thousand dollars, has disputed benefits, and may cause modest pain—not to mention any moral injury that may accrue from tilting back your daughter’s head and cranking open metal plates to wrench her face apart.

And despite whatever caused expander mania, its existence can be jarring for a parent who grew up in the prior era of orthodontics. Indeed, the period during which this trend developed—from, say, the late 1980s until the early 2020s—happens to coincide with the stretch that intervened between my own entry into middle school and my daughter’s. For my fellow members of this cohort, expansion of the fourth-grade palate appears to be a strange and sudden social norm. During one visit to the orthodontist, my daughter and I found a handful of children about her age seated in a line of dental chairs, with technicians leaning over each of them to turn the screw of their expander. It was like we’d all gathered there for some initiation rite for children of the tribe that dwells on Cobble Hill in Brooklyn—a ritual of widening.

Not long after that, I called up Luke Glowacki, an anthropologist at Boston University who co-directs a research project in Ethiopia’s Omo Valley, where body modifications—and dental modifications in particular—are not uncommon. He told me about social groups there and elsewhere in which a child’s teeth might be filed down to points or a person’s lower lip stretched out with a plate.

Is orthodontics any different? It presents itself as curative and scientific, but many orthodontists’ websites are replete with beauty claims as well: An expander may “protect your child’s facial appearance” or provide “enhancement to the facial profile.” Siegel said that a broadened palate gives “a more aesthetic width of the smile.” Kravitz said that it could help shrink the unattractive gaps inside a person’s cheeks—“dark buccal corridors,” in the language of the field.

In East Africa, dental and other body modifications carry similar ambiguities of purpose. Filing down a person’s teeth, for instance, or removing them altogether “may also be done for ostensible health reasons,” Glowacki said. Some body-modification rituals could be understood to ward off harmful spirits, for example. In other words, they’re prophylactic. Glowacki also told me about a Nyangatom woman he knows who has scars carved into both her shoulder and forehead. The former are purely decorative, but she’d received the latter on account of being sick.

Glowacki is a parent, too, and I asked him whether his training as an anthropologist affected how he thought about expanders or other anatomical procedures, such as ear piercing, that are carried out on children in the United States at industrial scale. “You’re not gonna find any society in the world that doesn’t modify their body in some way in accordance with their ideas of beauty or of health,” he said. “We’re doing what societies all over the world do.” If now I’ve paid an orthodontist to reshape my daughter’s mouth, maybe that’s just human nature.

On a recent Tuesday morning, I was blessed with a miracle in a mini-mart. I had set out to find the protein bar I kept hearing about, only to find a row of empty boxes. But then I spotted the shimmer. Pushed to the back of one carton, gleaming in its gold wrapper, was a single Salted Peanut Butter David Protein Bar. It was mine.

David bars are putty-like rectangles of pure nutritional efficiency: 28 grams of protein stuffed into 150 calories, or roughly the equivalent of eight egg whites cooked without oil. They are booming right now. After all, in this era of protein mania, one must always be optimizing. A Quest bar might get you 20 grams of protein for just under 200 calories, but David—named after Michelangelo’s masterpiece—does more for less. “Humans aren’t perfect,” promises one David tagline, “but David is.” Why, given the possibility of perfection, would you accept eight grams less?

If a food with more protein is better, then it follows that a food with less is worse. After eating my David bar, I couldn’t help but feel a little bit bad about my dinner of brown rice and spicy chickpeas. A cup of Eden Foods organic chickpeas (240 calories) gets you a measly 12 grams. Now that I was living in the world of David, I was newly ambivalent about eating anything that wasn’t chunks of unadulterated protein. I am fueling, I thought, shoving cubes of baked tofu into my mouth. Did you know that green peas have an unusual amount of protein for a vegetable? With unsettling frequency, I began to add frozen peas to my dinners. (They’re not great on cacio e pepe, it turns out.)

I have become quietly obsessed with this one single macronutrient. How could I not be? Everything is protein now: There are protein chips and protein ice creams and cinnamon protein Cheerios. Lemonade is protein, and so is water. Last month, Chipotle introduced a “high protein cup” consisting of four ounces of cubed chicken. Melanie Masarin, the founder and CEO of Ghia, a nonalcoholic-drink brand, recently told me that an investor asked her whether Ghia has plans for a high-protein aperitif. No, but the investor’s logic was obvious: Healthy people, the kind who tend to watch their drinking, only want one thing. This week, the federal government released its latest set of dietary guidelines—including a newly inverted food pyramid. At the top is protein.

[Read: Protein madness has gone too far]

In some ways, protein is just the latest all-consuming nutritional fixation. For decades, the goal was to avoid fat, which meant that pretzels were good and peanut butter was bad and fat-free Snackwell’s devil’s-food cookie cakes were a cultural phenomenon. Then Americans rediscovered fat and villainized carbs. But protein is different. Whatever your dreams are, protein seems to be the answer. It supports muscle gain, for those trying to bulk up, but it’s also satiating, which means people trying to lose weight are also advised to eat more protein. It has the power to make you bigger and more jacked, but also smaller and more delicate. People on GLP-1s are supposed to be especially mindful of their protein intake, to prevent muscle loss on extremely low-calorie diets, but so are weight lifters.

It is a nutritional philosophy that encourages not restriction but abundance: as much protein as possible, all the time. You can have your cake and eat it too (as long as it is made with “protein flour”). In a world where the very act of eating feels fraught, layered with a lifetime of rules and fads and judgments about what food is and is not “good,” protein offers absolution: You don’t have to feel bad about this. It has so many grams! What a beautifully straightforward recommendation: Eat more of this one thing that happens to be everywhere, and that frequently tastes good.

The low rattle of protein mania—the protein matchas and protein Pop-Tarts and protein seasonings to sprinkle on your protein chicken cubes—can be as maddening as it is inescapable. Everybody knows that you are supposed to eat a varied diet with many different types of foods that provide many different nutrients. But only protein is endowed with a special kind of redemptive power. Nobody is pretending that tortilla chips are a cornerstone of a balanced diet, but if they’re protein tortilla chips (7 grams), well, then maybe they’re at least fine. This is fantastic news if your goal is to enjoy tortilla chips, but it does have a tendency to recast all food that has not been protein-ified—either by nature or by the addition of whey-protein isolate—as a minor failure. It is depressing to look at a pile of roasted vegetables, arranged elegantly over couscous, and think: I will try harder tomorrow. I know, because I do it.

Protein is supposed to allow people to realize their untapped potential—to make us stronger and sharper. I suspect, though, that I would be stronger and sharper if I could stop ambiently thinking about my protein intake. That the world is now covered in a protein-infused haze provides constant reminders that I am falling short. Lots of protein evangelists will tell you that this is how cavemen ate, and therefore it is good. I think the best part of being a caveman would be not worrying about protein.

As nutritional trends go, there are worse obsessions than protein. Even if there is still significant debate about how much protein one needs, you are unlikely to send yourself into kidney failure because you protein-maxxed too hard. But the fanatical focus on protein as the true answer, the universal key to transforming the body you have into the one you want—7 grams, 28 grams, 11 grams, a chicken smoothie—feels eerily familiar. We counted calories, grams of fat, carbohydrates, trying to distill the messy science of nutrition into one single quantitative metric. Protein, for all its many virtues, is just another thing to count.

On a recent Tuesday morning, I was blessed with a miracle in a mini-mart. I had set out to find the protein bar I kept hearing about, only to find a row of empty boxes. But then I spotted the shimmer. Pushed to the back of one carton, gleaming in its gold wrapper, was a single Salted Peanut Butter David Protein Bar. It was mine.

David bars are putty-like rectangles of pure nutritional efficiency: 28 grams of protein stuffed into 150 calories, or roughly the equivalent of eight egg whites cooked without oil. They are booming right now. After all, in this era of protein mania, one must always be optimizing. A Quest bar might get you 20 grams of protein for just under 200 calories, but David—named after Michelangelo’s masterpiece—does more for less. “Humans aren’t perfect,” promises one David tagline, “but David is.” Why, given the possibility of perfection, would you accept eight grams less?

If a food with more protein is better, then it follows that a food with less is worse. After eating my David bar, I couldn’t help but feel a little bit bad about my dinner of brown rice and spicy chickpeas. A cup of Eden Foods organic chickpeas (240 calories) gets you a measly 12 grams. Now that I was living in the world of David, I was newly ambivalent about eating anything that wasn’t chunks of unadulterated protein. I am fueling, I thought, shoving cubes of baked tofu into my mouth. Did you know that green peas have an unusual amount of protein for a vegetable? With unsettling frequency, I began to add frozen peas to my dinners. (They’re not great on cacio e pepe, it turns out.)

I have become quietly obsessed with this one single macronutrient. How could I not be? Everything is protein now: There are protein chips and protein ice creams and cinnamon protein Cheerios. Lemonade is protein, and so is water. Last month, Chipotle introduced a “high protein cup” consisting of four ounces of cubed chicken. Melanie Masarin, the founder and CEO of Ghia, a nonalcoholic-drink brand, recently told me that an investor asked her whether Ghia has plans for a high-protein aperitif. No, but the investor’s logic was obvious: Healthy people, the kind who tend to watch their drinking, only want one thing. This week, the federal government released its latest set of dietary guidelines—including a newly inverted food pyramid. At the top is protein.

[Read: Protein madness has gone too far]

In some ways, protein is just the latest all-consuming nutritional fixation. For decades, the goal was to avoid fat, which meant that pretzels were good and peanut butter was bad and fat-free Snackwell’s devil’s-food cookie cakes were a cultural phenomenon. Then Americans rediscovered fat and villainized carbs. But protein is different. Whatever your dreams are, protein seems to be the answer. It supports muscle gain, for those trying to bulk up, but it’s also satiating, which means people trying to lose weight are also advised to eat more protein. It has the power to make you bigger and more jacked, but also smaller and more delicate. People on GLP-1s are supposed to be especially mindful of their protein intake, to prevent muscle loss on extremely low-calorie diets, but so are weight lifters.

It is a nutritional philosophy that encourages not restriction but abundance: as much protein as possible, all the time. You can have your cake and eat it too (as long as it is made with “protein flour”). In a world where the very act of eating feels fraught, layered with a lifetime of rules and fads and judgments about what food is and is not “good,” protein offers absolution: You don’t have to feel bad about this. It has so many grams! What a beautifully straightforward recommendation: Eat more of this one thing that happens to be everywhere, and that frequently tastes good.

The low rattle of protein mania—the protein matchas and protein Pop-Tarts and protein seasonings to sprinkle on your protein chicken cubes—can be as maddening as it is inescapable. Everybody knows that you are supposed to eat a varied diet with many different types of foods that provide many different nutrients. But only protein is endowed with a special kind of redemptive power. Nobody is pretending that tortilla chips are a cornerstone of a balanced diet, but if they’re protein tortilla chips (7 grams), well, then maybe they’re at least fine. This is fantastic news if your goal is to enjoy tortilla chips, but it does have a tendency to recast all food that has not been protein-ified—either by nature or by the addition of whey-protein isolate—as a minor failure. It is depressing to look at a pile of roasted vegetables, arranged elegantly over couscous, and think: I will try harder tomorrow. I know, because I do it.

Protein is supposed to allow people to realize their untapped potential—to make us stronger and sharper. I suspect, though, that I would be stronger and sharper if I could stop ambiently thinking about my protein intake. That the world is now covered in a protein-infused haze provides constant reminders that I am falling short. Lots of protein evangelists will tell you that this is how cavemen ate, and therefore it is good. I think the best part of being a caveman would be not worrying about protein.

As nutritional trends go, there are worse obsessions than protein. Even if there is still significant debate about how much protein one needs, you are unlikely to send yourself into kidney failure because you protein-maxxed too hard. But the fanatical focus on protein as the true answer, the universal key to transforming the body you have into the one you want—7 grams, 28 grams, 11 grams, a chicken smoothie—feels eerily familiar. We counted calories, grams of fat, carbohydrates, trying to distill the messy science of nutrition into one single quantitative metric. Protein, for all its many virtues, is just another thing to count.

The flu situation in the United States right now is, in a word, bad. Infections have skyrocketed in recent weeks, filling hospitals nearly to capacity; viral levels are “high” or “very high” in most of the country. In late December, New York reported the most flu cases the state had ever recorded in a single week. My own 18-month-old brought home influenza six days before Christmas: He spiked a fever above 103 degrees for days, refusing foods and most fluids; I spent the holiday syringing electrolyte water into his mouth, while battling my own fever and chills. This year’s serving of flu already seems set to be more severe than average, Seema Lakdawala, a flu virologist at Emory University, told me. This season could be a reprise of last winter’s, the most severe on record since the start of the coronavirus pandemic—or, perhaps, worse.

At the same time, what the U.S. is experiencing right now “fits within the general spectrum of what we would expect,” Taison Bell, an infectious-disease and critical-care physician at the University of Virginia Health System, told me. This is simply how the flu behaves: The virus is responsible for one of the roughest respiratory illnesses that Americans regularly suffer, routinely causing hundreds of thousands of people to be hospitalized annually in the U.S., tens of thousands of whom die. (So far this season, the flu has killed more than 5,000 people, including at least nine children.) Influenza is capable of even worse—sparking global pandemics, for instance, including some of the deadliest in history. These current tolls, however, are well within the bounds of just how awful the “seasonal” flu can be. “It’s another flu year, and it sucks,” Bell said.

Although flu is a ubiquitous winter illness, it is also one of the least understood. Scientists have been puzzling over the virus for decades, but many aspects of its rapid evolution and transmission patterns, as well as the ways in which our bodies defend against it, remain frustratingly mysterious. Flu seasons, as a rule, differ drastically from one another, and “we don’t have a great understanding of why one ends up being more severe than another,” Samuel Scarpino, an infectious-disease-modeling researcher at Northeastern University, told me. Experts’ flu-dar has also been especially out of whack in recent years, since the arrival of COVID-19 disrupted typical flu-transmission patterns. (An entire lineage of flu, for instance, may have been driven to extinction by pandemic-mitigation measures.) The virus is still finding its new norm.

Even so, a few things about this season’s ongoing torment are clear. Much of the blame rests on the season’s dominant flu variant—subclade K, which belongs to the H3N2 group of influenza. As flus go, H3N2s tend to be more likely to hospitalize and kill people; most of the worst flu seasons of the past decade in the U.S. have been driven by H3N2 surges. Subclade K doesn’t seem to be an unusually virulent variant, which is to say it’s probably no more likely to cause severe disease than a typical version of H3N2. But it does seem to be better at dodging our immune defenses, making the net effect similar, because it can lead to more people getting sicker than they otherwise would. That’s not a trivial effect for a disease that, even in mild cases, can cause days of high fevers and chills, followed by potentially weeks of that delightful run-over-by-a-truck feeling.

At UVA Health, Bell has seen a major uptick in people testing positive for the virus in recent weeks. Like others, his hospital is close to full, straining its capacity to treat other illnesses, he said. In Michigan, too, where Molly O’Shea cares for children at multiple pediatric practices, “we are seeing a ton of influenza, just a ton,” she told me. “Our schedule is overflowing.” Several of her school-age patients have wound up in the hospital, despite being previously healthy; a few have ended up with serious complications such as pneumonia and brain inflammation. The worst cases, she said, have been among the children who didn’t get their annual flu shot.

Flu vaccines are not among the most impressive immunizations in our roster. Although they’re generally pretty effective at protecting against severe disease, hospitalization, and death, they don’t reliably stave off infection or transmission. And they’re frequently bamboozled by the virus itself, which shape-shifts so frequently throughout the year, as it ping-pongs from hemisphere to hemisphere, that by the time flu vaccines roll out to the public, they’re often at least a little out of sync with what’s currently circulating.

That’s another aggravating factor this year. Researchers first detected subclade K in June, months after experts selected the strains that would go into the fall flu-vaccine formulation. Recent data suggest that vaccination may still elicit some immune defenses that recognize subclade K, and preliminary estimates from the United Kingdom suggest that this year’s formulations may be especially effective at preventing severe disease in children, who, along with the elderly, are highly vulnerable to the flu. (For all the misery my family endured, none of us ended up in the hospital—which suggests that our vaccinations did their job.)

Children also tend to be the biggest drivers of flu’s spread. “They are the source, many times, of explosions of transmission,” Lakdawala told me. In the U.K., for instance, which experienced an unusually early start to the flu season, school-age kids appear to have driven much of the epidemic, Scarpino pointed out. In the U.S., too, case rates among children have been particularly high. Although the vaccine primarily limits severe disease, it can also affect how quickly the virus travels through a community. And yet only about half of American kids get the vaccine each year, despite long-standing universal recommendations for annual immunization. “It’s a vaccine that parents have never really treated as a vaccine that every child should get,” O’Shea said.

Those choices might be influenced by the ways many people underestimate the flu—a term often used to describe any cold-weather ailment that comes with a runny nose, cough, or even gastrointestinal upset. In reality, flu has long ranked as one of the U.S.’s top 10 or top 15 causes of death—a scourge that, through its impact on the health-care system, the workforce, and the economy at large, costs the country billions of dollars each year. Against such a substantial threat, we should be using “everything in our toolbox to protect ourselves,” Lakdawala said.

Yet the Trump administration is actively impeding the process of flu vaccination. Health and Human Services Secretary Robert F. Kennedy Jr. has also said that it may be “a better thing” if fewer people are immunized against the flu—and insisted, incorrectly, that “there is no scientific evidence that the flu vaccine prevents serious illness, hospitalizations, or death in children.” The federal government recommended annual flu vaccines for all children until earlier this month, when HHS pushed through changes that demoted multiple immunizations from its recommended schedule. HHS now says that families should consult with their health-care provider before taking the shot. Such a recommendation suggests that the vaccines’ overall benefits are ambiguous enough to require discussion—and puts an additional burden on both patients and health-care providers, who can administer what was once a routine vaccine only after a conversation that must then be documented.

The nation’s leaders have also compromised one of the country’s best chances to develop more effective, better-matched flu vaccines in the future, by defunding research into mRNA vaccines. The current flu-vaccine manufacturing process takes so long that the included strains for the Northern Hemisphere must be selected by February or so—which provides plenty of time for the virus to evolve before the autumn rollout begins, as happened this year. “We pretty regularly have a bad match for the flu,” Scarpino said. mRNA vaccines promised the possibility of faster development, allowing researchers to stay more closely on the flu’s heels and switch out viral ingredients in as little as two or three months. That degree of flexibility also would have sped the response to the next flu pandemic.

In an email, Andrew Nixon, HHS’s deputy assistant secretary for media relations, disputed the characterization that the department’s new policies impede flu vaccination, writing, “Providers continue to offer flu vaccines, and insurance coverage remains unchanged. The recommendation supports shared clinical decision-making between patients and clinicians and does not prevent timely vaccination. People can continue to receive flu vaccines if they choose to do so.”

For the current season, much of the U.S.’s fate may already be sealed: Fewer than half of Americans have gotten a flu vaccine this season, while the virus continues to spread. “If you find yourself in a place where there are people sick with flu, you’re probably gonna get sick,” Scarpino said. That logic likely holds true for his own family, in Massachusetts, where flu activity has been high for weeks. They’ve so far made it through unscathed, but Scarpino said, “I feel like it’s a matter of time.”

The flu situation in the United States right now is, in a word, bad. Infections have skyrocketed in recent weeks, filling hospitals nearly to capacity; viral levels are “high” or “very high” in most of the country. In late December, New York reported the most flu cases the state had ever recorded in a single week. My own 18-month-old brought home influenza six days before Christmas: He spiked a fever above 103 degrees for days, refusing foods and most fluids; I spent the holiday syringing electrolyte water into his mouth, while battling my own fever and chills. This year’s serving of flu already seems set to be more severe than average, Seema Lakdawala, a flu virologist at Emory University, told me. This season could be a reprise of last winter’s, the most severe on record since the start of the coronavirus pandemic—or, perhaps, worse.

At the same time, what the U.S. is experiencing right now “fits within the general spectrum of what we would expect,” Taison Bell, an infectious-disease and critical-care physician at the University of Virginia Health System, told me. This is simply how the flu behaves: The virus is responsible for one of the roughest respiratory illnesses that Americans regularly suffer, routinely causing hundreds of thousands of people to be hospitalized annually in the U.S., tens of thousands of whom die. (So far this season, the flu has killed more than 5,000 people, including at least nine children.) Influenza is capable of even worse—sparking global pandemics, for instance, including some of the deadliest in history. These current tolls, however, are well within the bounds of just how awful the “seasonal” flu can be. “It’s another flu year, and it sucks,” Bell said.

Although flu is a ubiquitous winter illness, it is also one of the least understood. Scientists have been puzzling over the virus for decades, but many aspects of its rapid evolution and transmission patterns, as well as the ways in which our bodies defend against it, remain frustratingly mysterious. Flu seasons, as a rule, differ drastically from one another, and “we don’t have a great understanding of why one ends up being more severe than another,” Samuel Scarpino, an infectious-disease-modeling researcher at Northeastern University, told me. Experts’ flu-dar has also been especially out of whack in recent years, since the arrival of COVID-19 disrupted typical flu-transmission patterns. (An entire lineage of flu, for instance, may have been driven to extinction by pandemic-mitigation measures.) The virus is still finding its new norm.

Even so, a few things about this season’s ongoing torment are clear. Much of the blame rests on the season’s dominant flu variant—subclade K, which belongs to the H3N2 group of influenza. As flus go, H3N2s tend to be more likely to hospitalize and kill people; most of the worst flu seasons of the past decade in the U.S. have been driven by H3N2 surges. Subclade K doesn’t seem to be an unusually virulent variant, which is to say it’s probably no more likely to cause severe disease than a typical version of H3N2. But it does seem to be better at dodging our immune defenses, making the net effect similar, because it can lead to more people getting sicker than they otherwise would. That’s not a trivial effect for a disease that, even in mild cases, can cause days of high fevers and chills, followed by potentially weeks of that delightful run-over-by-a-truck feeling.

At UVA Health, Bell has seen a major uptick in people testing positive for the virus in recent weeks. Like others, his hospital is close to full, straining its capacity to treat other illnesses, he said. In Michigan, too, where Molly O’Shea cares for children at multiple pediatric practices, “we are seeing a ton of influenza, just a ton,” she told me. “Our schedule is overflowing.” Several of her school-age patients have wound up in the hospital, despite being previously healthy; a few have ended up with serious complications such as pneumonia and brain inflammation. The worst cases, she said, have been among the children who didn’t get their annual flu shot.

Flu vaccines are not among the most impressive immunizations in our roster. Although they’re generally pretty effective at protecting against severe disease, hospitalization, and death, they don’t reliably stave off infection or transmission. And they’re frequently bamboozled by the virus itself, which shape-shifts so frequently throughout the year, as it ping-pongs from hemisphere to hemisphere, that by the time flu vaccines roll out to the public, they’re often at least a little out of sync with what’s currently circulating.

That’s another aggravating factor this year. Researchers first detected subclade K in June, months after experts selected the strains that would go into the fall flu-vaccine formulation. Recent data suggest that vaccination may still elicit some immune defenses that recognize subclade K, and preliminary estimates from the United Kingdom suggest that this year’s formulations may be especially effective at preventing severe disease in children, who, along with the elderly, are highly vulnerable to the flu. (For all the misery my family endured, none of us ended up in the hospital—which suggests that our vaccinations did their job.)

Children also tend to be the biggest drivers of flu’s spread. “They are the source, many times, of explosions of transmission,” Lakdawala told me. In the U.K., for instance, which experienced an unusually early start to the flu season, school-age kids appear to have driven much of the epidemic, Scarpino pointed out. In the U.S., too, case rates among children have been particularly high. Although the vaccine primarily limits severe disease, it can also affect how quickly the virus travels through a community. And yet only about half of American kids get the vaccine each year, despite long-standing universal recommendations for annual immunization. “It’s a vaccine that parents have never really treated as a vaccine that every child should get,” O’Shea said.

Those choices might be influenced by the ways many people underestimate the flu—a term often used to describe any cold-weather ailment that comes with a runny nose, cough, or even gastrointestinal upset. In reality, flu has long ranked as one of the U.S.’s top 10 or top 15 causes of death—a scourge that, through its impact on the health-care system, the workforce, and the economy at large, costs the country billions of dollars each year. Against such a substantial threat, we should be using “everything in our toolbox to protect ourselves,” Lakdawala said.

Yet the Trump administration is actively impeding the process of flu vaccination. Health and Human Services Secretary Robert F. Kennedy Jr. has also said that it may be “a better thing” if fewer people are immunized against the flu—and insisted, incorrectly, that “there is no scientific evidence that the flu vaccine prevents serious illness, hospitalizations, or death in children.” The federal government recommended annual flu vaccines for all children until earlier this month, when HHS pushed through changes that demoted multiple immunizations from its recommended schedule. HHS now says that families should consult with their health-care provider before taking the shot. Such a recommendation suggests that the vaccines’ overall benefits are ambiguous enough to require discussion—and puts an additional burden on both patients and health-care providers, who can administer what was once a routine vaccine only after a conversation that must then be documented.

The nation’s leaders have also compromised one of the country’s best chances to develop more effective, better-matched flu vaccines in the future, by defunding research into mRNA vaccines. The current flu-vaccine manufacturing process takes so long that the included strains for the Northern Hemisphere must be selected by February or so—which provides plenty of time for the virus to evolve before the autumn rollout begins, as happened this year. “We pretty regularly have a bad match for the flu,” Scarpino said. mRNA vaccines promised the possibility of faster development, allowing researchers to stay more closely on the flu’s heels and switch out viral ingredients in as little as two or three months. That degree of flexibility also would have sped the response to the next flu pandemic.

In an email, Andrew Nixon, HHS’s deputy assistant secretary for media relations, disputed the characterization that the department’s new policies impede flu vaccination, writing, “Providers continue to offer flu vaccines, and insurance coverage remains unchanged. The recommendation supports shared clinical decision-making between patients and clinicians and does not prevent timely vaccination. People can continue to receive flu vaccines if they choose to do so.”

For the current season, much of the U.S.’s fate may already be sealed: Fewer than half of Americans have gotten a flu vaccine this season, while the virus continues to spread. “If you find yourself in a place where there are people sick with flu, you’re probably gonna get sick,” Scarpino said. That logic likely holds true for his own family, in Massachusetts, where flu activity has been high for weeks. They’ve so far made it through unscathed, but Scarpino said, “I feel like it’s a matter of time.”

Updated at 6:00 PM ET on January 12, 2026

Antiviral drugs for influenza, the best known of which is Tamiflu, are—let’s be honest—not exactly miracle cures. They marginally shorten the course of illness, especially if taken within the first 48 hours. But amid possibly the worst flu season in 25 years, driven by a variant imperfectly matched to the vaccine, these underused drugs can make a bout of flu a little less miserable. So consider an antiviral. And specifically, consider Xofluza, a lesser-known drug that is in fact better than Tamiflu.

The culprit behind this awful flu season is subclade K, a variant of H3N2 discovered too late to be incorporated into this year’s flu vaccine. Early data suggest the shot likely does confer at least some protection against this variant, but the jury is still out on whether that protection is much eroded from usual. What is undeniable, though, is a recent explosion of influenza cases. In New York, which was hit early and hard, the number of people hospitalized for flu broke records. Across the rest of the country, cases have been going up a “straight line,” nearly everywhere all at once, which is highly unusual, Arnold Monto, an epidemiologist at the University of Michigan who has been studying influenza for some 60 years, told me last week. Cases seem to be finally leveling off now, but much misery still lies ahead.

For flu, antivirals are a second but oft-overlooked line of defense after vaccines. “We are dramatically and drastically underutilizing influenza antivirals,” Janet Englund, a pediatric-infectious-disease specialist at the University of Washington, told me. Even the older, more commonly prescribed drug Tamiflu reaches only a tiny percentage of flu patients every year. Actual numbers are hard to come by, but compare the estimated 1.2 million prescriptions for Tamiflu and its generic form in 2023 with the some 40 million people who likely got the flu in the winter of 2023–24. Xofluza is even less popular, and exact prescription numbers even harder to find. But they are possibly somewhere from just 1 to 10 percent that of Tamiflu.

The two antivirals are equally effective at allaying symptoms, both shortening the duration of flu by about a day. But Xofluza, which was approved in 2018, offers some tangible benefits over Tamiflu.

First, Xofluza is simply more convenient, a single dose compared with Tamiflu’s 10, which are taken over five days, twice a day. It also causes fewer of the gastrointestinal side effects, such as vomiting and nausea, that patients on Tamiflu will sometimes experience. All in all, a course of Xofluza might be easier for you—or your kid already queasy from the flu itself—to get down and keep down. (That is, if they are old enough to take it: Xofluza is approved for kids ages 5 and up in the United States, but ages 1 and up in Europe; only Tamiflu is recommended for kids down to newborn age as well as for women who are pregnant or breastfeeding.)

Second, Xofluza makes you less contagious to the rest of your family. It drives down the amount of virus spewed by sick patients more quickly than Tamiflu, possibly because of differences in how the two drugs work. Whereas Xofluza stops the virus from replicating, Tamiflu can only prevent already replicated viruses from exiting infected cells to infect others. In a study that Monto led last year, Xofluza cut household transmission by almost one-third compared with a placebo. Tamiflu might reduce transmission too, according to other studies, but probably to a lesser degree than Xofluza.

Third, Xofluza is better at heading off serious post-flu complications such as pneumonia or myocarditis. Patients on Xofluza needed fewer ER visits and hospitalizations than did those on Tamiflu, according to studies of large real-world data sets from insurance claims and medical records. This means that Xofluza should be the antiviral of choice for high-risk patients, including those over 65, who are most prone to these complications, Frederick Hayden, a flu expert at the University of Virginia who led one of the original Xofluza trials, told me. (Hayden has consulted on an unpaid basis, aside from travel expenses, for the companies behind Xofluza.)

The fourth advantage is less relevant to this season because the dominant subclade belongs to the influenza A family. But Xofluza is noticeably more effective against influenza B than Tamiflu, which tends to falter against this family of viruses.

Despite these benefits, awareness of Xofluza remains low. “It hasn’t been used as much as it should be,” Monto said, for reasons of cost and accessibility. Tamiflu, first approved in 1999, is available as a generic for less than $30 even without insurance. Xofluza is still patented and runs $150 to $200 a person. Because it’s less popular, pharmacies are less likely to stock it, making doctors less eager to prescribe it, and so on. In October, though, the company that markets Xofluza in the U.S. launched a direct-to-customer program that sells the drug for the comparably bargain price of $50 without insurance, along with same-day delivery in some areas. Even the flu-drug experts I spoke with, though, were not all aware of this new, more accessible route. The CDC still lists Tamiflu first and foremost in its recommendations, too.

For flu antivirals to be more widely used would also require better testing. Both Xofluza and Tamiflu are most effective within the first 48 hours of symptoms, and the earlier the better. Traditionally, a sick person would have to get to a doctor, get a flu test, get a prescription, and finally get to a pharmacy—which can easily put them past the first 48 hours. But COVID popularized at-home rapid testing, and combination COVID-flu tests have landed on pharmacies shelves recently. With telehealth and home delivery, you can get an antiviral without ever leaving the house.  

Still, the at-home tests are expensive, Englund pointed out, about $20 a pop here, compared with just a couple of bucks in Europe. The expense can add up for a whole family. In Japan, where antivirals are widely used, nearly everyone with a flu-like illness gets a routine rapid test and, if necessary, antivirals, both largely covered by the public health-care system. (Xofluza was developed by the Japanese company Shionogi, which also makes Xocova, a promising COVID antiviral my colleague Rachel Gutman-Wei has written about that is not available in the U.S.)

If the U.S. were better at using antivirals, especially in the high-risk patients, the number of Americans dying of flu—roughly 38,000 last year—would likely drop, Cameron Wolfe, an infectious-diseases expert at Duke, told me. Doctors recommend that people at high risk for flu take antivirals prophylactically, upon exposure to anyone with flu, before symptoms appear. Both Xofluza and Tamiflu as prophylaxis can cut the chances of getting sick by upwards of 80 percent.

For healthy people who fall ill, antivirals can ease the burden of flu, which is nasty even when it is not deadly. “I don’t want you to be out of work longer than you need to be. I don’t want you to not be a caregiver for your kids,” Wolfe said. “Maybe you have business travel coming up, and I don’t want you to be sick still on that plane.” With challenges around access to antivirals, he said that “the best drug is the one you can get.” Both Tamiflu and Xofluza can make this historically bad flu season a little more bearable.

This story originally stated that Xocova, not Xofluza, when given as a prophylaxis for flu, cut the chance of illness by 80 percent. Xocova is a COVID antiviral.

Updated at 6:00 PM ET on January 12, 2026

Antiviral drugs for influenza, the best known of which is Tamiflu, are—let’s be honest—not exactly miracle cures. They marginally shorten the course of illness, especially if taken within the first 48 hours. But amid possibly the worst flu season in 25 years, driven by a variant imperfectly matched to the vaccine, these underused drugs can make a bout of flu a little less miserable. So consider an antiviral. And specifically, consider Xofluza, a lesser-known drug that is in fact better than Tamiflu.

The culprit behind this awful flu season is subclade K, a variant of H3N2 discovered too late to be incorporated into this year’s flu vaccine. Early data suggest the shot likely does confer at least some protection against this variant, but the jury is still out on whether that protection is much eroded from usual. What is undeniable, though, is a recent explosion of influenza cases. In New York, which was hit early and hard, the number of people hospitalized for flu broke records. Across the rest of the country, cases have been going up a “straight line,” nearly everywhere all at once, which is highly unusual, Arnold Monto, an epidemiologist at the University of Michigan who has been studying influenza for some 60 years, told me last week. Cases seem to be finally leveling off now, but much misery still lies ahead.

For flu, antivirals are a second but oft-overlooked line of defense after vaccines. “We are dramatically and drastically underutilizing influenza antivirals,” Janet Englund, a pediatric-infectious-disease specialist at the University of Washington, told me. Even the older, more commonly prescribed drug Tamiflu reaches only a tiny percentage of flu patients every year. Actual numbers are hard to come by, but compare the estimated 1.2 million prescriptions for Tamiflu and its generic form in 2023 with the some 40 million people who likely got the flu in the winter of 2023–24. Xofluza is even less popular, and exact prescription numbers even harder to find. But they are possibly somewhere from just 1 to 10 percent that of Tamiflu.

The two antivirals are equally effective at allaying symptoms, both shortening the duration of flu by about a day. But Xofluza, which was approved in 2018, offers some tangible benefits over Tamiflu.

First, Xofluza is simply more convenient, a single dose compared with Tamiflu’s 10, which are taken over five days, twice a day. It also causes fewer of the gastrointestinal side effects, such as vomiting and nausea, that patients on Tamiflu will sometimes experience. All in all, a course of Xofluza might be easier for you—or your kid already queasy from the flu itself—to get down and keep down. (That is, if they are old enough to take it: Xofluza is approved for kids ages 5 and up in the United States, but ages 1 and up in Europe; only Tamiflu is recommended for kids down to newborn age as well as for women who are pregnant or breastfeeding.)

Second, Xofluza makes you less contagious to the rest of your family. It drives down the amount of virus spewed by sick patients more quickly than Tamiflu, possibly because of differences in how the two drugs work. Whereas Xofluza stops the virus from replicating, Tamiflu can only prevent already replicated viruses from exiting infected cells to infect others. In a study that Monto led last year, Xofluza cut household transmission by almost one-third compared with a placebo. Tamiflu might reduce transmission too, according to other studies, but probably to a lesser degree than Xofluza.

Third, Xofluza is better at heading off serious post-flu complications such as pneumonia or myocarditis. Patients on Xofluza needed fewer ER visits and hospitalizations than did those on Tamiflu, according to studies of large real-world data sets from insurance claims and medical records. This means that Xofluza should be the antiviral of choice for high-risk patients, including those over 65, who are most prone to these complications, Frederick Hayden, a flu expert at the University of Virginia who led one of the original Xofluza trials, told me. (Hayden has consulted on an unpaid basis, aside from travel expenses, for the companies behind Xofluza.)

The fourth advantage is less relevant to this season because the dominant subclade belongs to the influenza A family. But Xofluza is noticeably more effective against influenza B than Tamiflu, which tends to falter against this family of viruses.

Despite these benefits, awareness of Xofluza remains low. “It hasn’t been used as much as it should be,” Monto said, for reasons of cost and accessibility. Tamiflu, first approved in 1999, is available as a generic for less than $30 even without insurance. Xofluza is still patented and runs $150 to $200 a person. Because it’s less popular, pharmacies are less likely to stock it, making doctors less eager to prescribe it, and so on. In October, though, the company that markets Xofluza in the U.S. launched a direct-to-customer program that sells the drug for the comparably bargain price of $50 without insurance, along with same-day delivery in some areas. Even the flu-drug experts I spoke with, though, were not all aware of this new, more accessible route. The CDC still lists Tamiflu first and foremost in its recommendations, too.

For flu antivirals to be more widely used would also require better testing. Both Xofluza and Tamiflu are most effective within the first 48 hours of symptoms, and the earlier the better. Traditionally, a sick person would have to get to a doctor, get a flu test, get a prescription, and finally get to a pharmacy—which can easily put them past the first 48 hours. But COVID popularized at-home rapid testing, and combination COVID-flu tests have landed on pharmacies shelves recently. With telehealth and home delivery, you can get an antiviral without ever leaving the house.  

Still, the at-home tests are expensive, Englund pointed out, about $20 a pop here, compared with just a couple of bucks in Europe. The expense can add up for a whole family. In Japan, where antivirals are widely used, nearly everyone with a flu-like illness gets a routine rapid test and, if necessary, antivirals, both largely covered by the public health-care system. (Xofluza was developed by the Japanese company Shionogi, which also makes Xocova, a promising COVID antiviral my colleague Rachel Gutman-Wei has written about that is not available in the U.S.)

If the U.S. were better at using antivirals, especially in the high-risk patients, the number of Americans dying of flu—roughly 38,000 last year—would likely drop, Cameron Wolfe, an infectious-diseases expert at Duke, told me. Doctors recommend that people at high risk for flu take antivirals prophylactically, upon exposure to anyone with flu, before symptoms appear. Both Xofluza and Tamiflu as prophylaxis can cut the chances of getting sick by upwards of 80 percent.

For healthy people who fall ill, antivirals can ease the burden of flu, which is nasty even when it is not deadly. “I don’t want you to be out of work longer than you need to be. I don’t want you to not be a caregiver for your kids,” Wolfe said. “Maybe you have business travel coming up, and I don’t want you to be sick still on that plane.” With challenges around access to antivirals, he said that “the best drug is the one you can get.” Both Tamiflu and Xofluza can make this historically bad flu season a little more bearable.

This story originally stated that Xocova, not Xofluza, when given as a prophylaxis for flu, cut the chance of illness by 80 percent. Xocova is a COVID antiviral.

Before Adam Sharples became a molecular physiologist studying muscle memory, he played professional rugby. Over his years as an athlete, he noticed that he and his teammates seemed to return to form after the offseason, or even from an injury, faster than expected. Rebuilding muscle mass and strength came easy: It was as if their muscles remembered what to do.

In 2018, Sharples and his research lab, now at the Norwegian School of Sport Sciences in Oslo, were the first to show that exercise could change how our muscle-building genes work over the long term. The genes themselves don’t change, but repeated periods of exertion turns certain genes on, spurring cells to build muscle mass more quickly than before. These epigenetic changes have a lasting effect: Your muscles remember these periods of strength and respond favorably in the future.

Intuitively, this makes sense. Past exercise primes your muscles to respond more robustly to more exercise. Over the past few years, Sharples’s lab has found that muscles have additional molecular mechanisms for remembering exercise; he and other scientists have been building on this research, too, confirming epigenetic muscle memory in young and aged human muscle, after different modes of training, as well as in mice. Now 40 years old, Sharples is still thinking about how our muscles remember but has lately been investigating the inverse trajectory: Do muscles have a similar memory for weakness?

The answer appears to be yes. “Our new data shows that muscle does not just remember growth—it also remembers wasting,” Sharples told me, of a study published in preprint on bioRxiv and currently in peer review for Advanced Science. “The more encounters you have with injury and illness, the more susceptible your muscle is to further atrophy. And, well—that’s what aging is, isn’t it?”

The Norwegian government’s research council has been funding Sharples’s research and has a vested interest in the lab’s discoveries. In the next decade, Norway is expected to become a “super-aged society,” in which more than one in five people are age 65 or older. Japan and Germany have already crossed this threshold, and the United States is expected to reach it by 2030. Age-related muscle weakness is a major factor in falling risk; falling is a leading cause worldwide of injury and death in people 65 and older. Better understanding how muscles remember and react to their weakest moments is a crucial step toward knowing what to do about it.

As part of the new study, Sharples’s team studied repeated periods of atrophy in young human muscle, using a knee brace and crutches to immobilize participants’ legs for two weeks at a time. This level of disuse, Sharples said, is comparable to real-world situations in which muscle rapidly loses size and function—limb immobilization after fractures or other injuries, periods of hospitalization or bed rest, reduced weight-bearing during recovery. A couple of years ago, I went to observe this research for my book On Muscle; one study participant, an avid skier and cyclist, told me he was shocked by how significantly the muscles in his leg deteriorated after just a couple of weeks of immobilization. The team also ran a concurrent study in aged rat muscle, in collaboration with Liverpool John Moores University; in both studies, repeated periods of disuse led to epigenetic changes—shifts in the way genes were expressed.

These changes affected the core functions of muscle cells, hampering the genes in mitochondria—the powerhouses of the cell, which generate the energy required to contract and relax muscle fibers. Letting muscles weaken suppressed genes involved in mitochondrial function and energy production in particular, including genes that are essential for muscle endurance and recovery. The researchers also found that a key marker of mitochondrial abundance dropped more drastically after repeated atrophy than after the first episode, indicating that repeated disuse makes muscle more vulnerable. In other words, the evidence suggests that every time you fall down the hole, it becomes more difficult to climb back out.  

Similar changes occurred in both the young human muscle and the aged rat muscle. But the young muscle could adapt and recover. After repeated atrophy, it showed a less exaggerated gene-expression response than the aged muscle did. “There seems to be some resilience and protection with young muscle the second time around,” Sharples said. He likened this to an immune-system response: Young muscle responds better to atrophy the second time because it has encountered it before and knows how to bounce back. By contrast, aged muscle becomes more sensitive after repeated atrophy, showing a worsened response with the second episode.

How long our muscles hold on to any of these memories is still up for debate. “Because of our study periods, we do know with some certainty that epigenetic memories can last at least three to four months, and that protein changes can also be retained,” Sharples said. “How long after that is difficult to say. But we know from our studies of cancer patients that epigenetic changes in muscle were retained even 10 years out from cancer survival.”

This was startling to hear. If an adverse health event is dramatic enough, like cancer, our muscles can carry the effects of that for a decade or more. More typically, though, inactivity, aging, and repeated episodes of disuse may gradually shift the system toward a state in which weakness becomes more entrenched and recovery slower.

Understanding what drives muscle to remember being in stress situations—either beneficial, like exercise, or damaging, like illness—could help us better judge what to do about this, says Kevin Murach, an associate professor at the University of Arkansas who studies aging and skeletal muscle and who was not involved in the new study. Knowing the mechanisms that drive beneficial changes at the molecular level could help develop drugs with similar effects. On the other end of the spectrum, if illness and immobilization have long-term negative effects, Murach told me, the next question to answer is: “Can we use exercise to offset that?”

Both Murach and Sharples said the data are getting only more robust that strength training, paired with endurance or high-intensity interval training, is the best therapy to protect against age-related loss of muscle and function. “Perhaps the key takeaway is that at any point along this continuum, new exercise or loading stimuli can still shift the balance back towards growth and health,” Sharples said. “I don’t think there is a point at which muscle can’t respond at all—it simply becomes less efficient when repeatedly weakened or when older.”

Identifying genes associated with muscle growth, as well as pharmaceutical targets, could mean that drugs or gene therapy may eventually be able to assist with boosting muscle response for people who cannot exercise. Murach and Sharples cautioned, though, that stimulating muscle-cell growth can have unintended consequences, in part because growth pathways are common across cell types—including cancer cells.

What the new work does show is that our muscle mass is not a blank slate. “What we’re finding suggests that our muscles may carry a history of both strength and weakness,” Sharples said. It’s shaped by factors including age, baseline muscle health, previous atrophy events, and previous exercise training. “And that history shapes how our muscles respond in the future.” I came away from our conversation thinking about the battle between positive muscle memory for strength and negative muscle memory for atrophy as a kind of tug-of-war: The two are constantly in tension, but the more experiences you have of one or the other, the more it pulls you into its embrace.

Before Adam Sharples became a molecular physiologist studying muscle memory, he played professional rugby. Over his years as an athlete, he noticed that he and his teammates seemed to return to form after the offseason, or even from an injury, faster than expected. Rebuilding muscle mass and strength came easy: It was as if their muscles remembered what to do.

In 2018, Sharples and his research lab, now at the Norwegian School of Sport Sciences in Oslo, were the first to show that exercise could change how our muscle-building genes work over the long term. The genes themselves don’t change, but repeated periods of exertion turns certain genes on, spurring cells to build muscle mass more quickly than before. These epigenetic changes have a lasting effect: Your muscles remember these periods of strength and respond favorably in the future.

Intuitively, this makes sense. Past exercise primes your muscles to respond more robustly to more exercise. Over the past few years, Sharples’s lab has found that muscles have additional molecular mechanisms for remembering exercise; he and other scientists have been building on this research, too, confirming epigenetic muscle memory in young and aged human muscle, after different modes of training, as well as in mice. Now 40 years old, Sharples is still thinking about how our muscles remember but has lately been investigating the inverse trajectory: Do muscles have a similar memory for weakness?

The answer appears to be yes. “Our new data shows that muscle does not just remember growth—it also remembers wasting,” Sharples told me, of a study published in preprint on bioRxiv and currently in peer review for Advanced Science. “The more encounters you have with injury and illness, the more susceptible your muscle is to further atrophy. And, well—that’s what aging is, isn’t it?”

The Norwegian government’s research council has been funding Sharples’s research and has a vested interest in the lab’s discoveries. In the next decade, Norway is expected to become a “super-aged society,” in which more than one in five people are age 65 or older. Japan and Germany have already crossed this threshold, and the United States is expected to reach it by 2030. Age-related muscle weakness is a major factor in falling risk; falling is a leading cause worldwide of injury and death in people 65 and older. Better understanding how muscles remember and react to their weakest moments is a crucial step toward knowing what to do about it.

As part of the new study, Sharples’s team studied repeated periods of atrophy in young human muscle, using a knee brace and crutches to immobilize participants’ legs for two weeks at a time. This level of disuse, Sharples said, is comparable to real-world situations in which muscle rapidly loses size and function—limb immobilization after fractures or other injuries, periods of hospitalization or bed rest, reduced weight-bearing during recovery. A couple of years ago, I went to observe this research for my book On Muscle; one study participant, an avid skier and cyclist, told me he was shocked by how significantly the muscles in his leg deteriorated after just a couple of weeks of immobilization. The team also ran a concurrent study in aged rat muscle, in collaboration with Liverpool John Moores University; in both studies, repeated periods of disuse led to epigenetic changes—shifts in the way genes were expressed.

These changes affected the core functions of muscle cells, hampering the genes in mitochondria—the powerhouses of the cell, which generate the energy required to contract and relax muscle fibers. Letting muscles weaken suppressed genes involved in mitochondrial function and energy production in particular, including genes that are essential for muscle endurance and recovery. The researchers also found that a key marker of mitochondrial abundance dropped more drastically after repeated atrophy than after the first episode, indicating that repeated disuse makes muscle more vulnerable. In other words, the evidence suggests that every time you fall down the hole, it becomes more difficult to climb back out.  

Similar changes occurred in both the young human muscle and the aged rat muscle. But the young muscle could adapt and recover. After repeated atrophy, it showed a less exaggerated gene-expression response than the aged muscle did. “There seems to be some resilience and protection with young muscle the second time around,” Sharples said. He likened this to an immune-system response: Young muscle responds better to atrophy the second time because it has encountered it before and knows how to bounce back. By contrast, aged muscle becomes more sensitive after repeated atrophy, showing a worsened response with the second episode.

How long our muscles hold on to any of these memories is still up for debate. “Because of our study periods, we do know with some certainty that epigenetic memories can last at least three to four months, and that protein changes can also be retained,” Sharples said. “How long after that is difficult to say. But we know from our studies of cancer patients that epigenetic changes in muscle were retained even 10 years out from cancer survival.”

This was startling to hear. If an adverse health event is dramatic enough, like cancer, our muscles can carry the effects of that for a decade or more. More typically, though, inactivity, aging, and repeated episodes of disuse may gradually shift the system toward a state in which weakness becomes more entrenched and recovery slower.

Understanding what drives muscle to remember being in stress situations—either beneficial, like exercise, or damaging, like illness—could help us better judge what to do about this, says Kevin Murach, an associate professor at the University of Arkansas who studies aging and skeletal muscle and who was not involved in the new study. Knowing the mechanisms that drive beneficial changes at the molecular level could help develop drugs with similar effects. On the other end of the spectrum, if illness and immobilization have long-term negative effects, Murach told me, the next question to answer is: “Can we use exercise to offset that?”

Both Murach and Sharples said the data are getting only more robust that strength training, paired with endurance or high-intensity interval training, is the best therapy to protect against age-related loss of muscle and function. “Perhaps the key takeaway is that at any point along this continuum, new exercise or loading stimuli can still shift the balance back towards growth and health,” Sharples said. “I don’t think there is a point at which muscle can’t respond at all—it simply becomes less efficient when repeatedly weakened or when older.”

Identifying genes associated with muscle growth, as well as pharmaceutical targets, could mean that drugs or gene therapy may eventually be able to assist with boosting muscle response for people who cannot exercise. Murach and Sharples cautioned, though, that stimulating muscle-cell growth can have unintended consequences, in part because growth pathways are common across cell types—including cancer cells.

What the new work does show is that our muscle mass is not a blank slate. “What we’re finding suggests that our muscles may carry a history of both strength and weakness,” Sharples said. It’s shaped by factors including age, baseline muscle health, previous atrophy events, and previous exercise training. “And that history shapes how our muscles respond in the future.” I came away from our conversation thinking about the battle between positive muscle memory for strength and negative muscle memory for atrophy as a kind of tug-of-war: The two are constantly in tension, but the more experiences you have of one or the other, the more it pulls you into its embrace.