Medical News

Recently, a balmy spring day left me feeling parched. I needed a beverage—stat!—and had forgotten my water bottle at home. I ducked into a nearby CVS to pick up a drink.

The choices were so overwhelming, I nearly forgot my thirst. The drink aisle included a bevy of the usual thirst-quenching options—and some that looked like they belonged in an apothecary rather than next to the LaCroix. Row upon row of multicolored cans and bottles held drinks with purposes beyond mere hydration and flavor. Some promised to improve my energy, immunity, or gut health. Others claimed to stimulate mind states such as clarity, balance, or calm. Fizzy or flat, juice or tea, high in protein or in probiotics?

Drinks with a purpose, known as “functional beverages,” have become unavoidable in many supermarkets, drugstores, and gas stations across the country. On top of Vitamin Water and traditional energy drinks like Red Bull and Monster, you can find options such as BRĒZ, a supposedly mood-shifting elixir infused with mushrooms and cannabis and SkinTē, a “collagen sparkling tea.” Kin Euphorics, a line of drinks launched by the supermodel Bella Hadid that’s available at Target, sells one meant to boost energy, level up immunity, and make your skin glow. Simply picking out a drink has never been harder.

Drinks have always been about more than taste and hydration—think of coffee, alcohol, and soda. Energy drinks first appeared in stores in the 1960s, before exploding in popularity in the 2000s. Yet the expansion of a drink’s promised effects beyond inebriation or energy is “a little bit newer,” Ernest Baskin, a food-marketing professor at Saint Joseph’s University, told me.

Some of the products I spotted at the pharmacy included an caffeinated shot called Tru Energy and its extra-strength sibling, Tru Power; pastel-colored cans of Recess, a seltzer with magnesium and adaptogens to promote calmness; and Poppi, a soda for gut health. Even the energy drinks are no longer just a few hyper-sweet, hyper-caffeinated options: Newer brands tout health benefits, such as added vitamins, and come in a wider variety of formulations, including seltzers, coffees, and teas.

These functional beverages are booming. By one estimate, the industry is expected to be worth $54 billion in North America alone this year. Grocers report that functional beverages are vying for prime shelf space traditionally occupied by sodas, bottled water, and even alcohol. Encountering the staggering range of supplements, nutrients, and other additives now present in the drink aisle can make choosing a drink feel deeply stressful, more like picking up medication than grabbing a bottle on the go.

Part of the reason functional drinks have exploded is the same reason that there are lots of protein bars and low-sugar snacks: If it sounds healthy, more people will buy it. Americans are “increasingly interested in health,” Baskin said. That’s how you end up with something like Bai—a line of “water beverages” infused with antioxidants and electrolytes—and prebiotic sodas that contain ingredients including live bacteria and fiber. Even Nestlé’s Nesquik, a chocolate drink I enjoyed as a child, comes in a “protein power” version. The fact that these drinks can be sold at a premium has endeared them to stores, Baskin said. A single can of Celsius energy drink or Olipop prebiotic soda costs $3 at Target.

Of course, as in all things wellness, whether any of these products actually does what it says to do is far from guaranteed. Certainly, a drink stuffed with huge amounts of caffeine will be energizing. Others are more suspect. A sparkling water brand called Good Idea goes so far as to claim to balance blood sugar. Safety Shot, packaged in cans labeled with a blue medical cross, is sold as a hangover cure, promising to rapidly lower blood-alcohol levels. (Products marketed as supplements, as opposed to beverages, are less rigorously regulated by the FDA.)

Drink makers have swooped in to capitalize on the ongoing cultural obsession with hydration—one in which Stanley Cups are a must-have item and influencers suggest that clear skin is just a bottle of water away. That has created an opening for more fantastical functional beverages that promise to be a quick fix for all kinds of health concerns—stress, anxiety, insomnia, and unhappiness.

Read: It’s just a water bottle

Recess, one of the drinks I saw at CVS, is positioned as an antidote to a hectic world, helping sippers feel “calm cool collected.” Among the ingredients it highlights are hemp and adaptogens, a category loosely defined as substances that help the body deal with stress. Some drinks claim to promote a shift in mood, equating health with happiness; others, to induce sleep. An energy shot called Magic Mind, touting buzzy ingredients such as nootropics, lion’s-mane mushrooms, and the calming plant ashwagandha, is marketed as a path to a clear mind.

Maybe it’s not surprising that people crave products claiming to bottle some form of respite. Younger adults, to whom most of these drinks are targeted, are drinking less booze but also using more marijuana: They want altered states, if just not in alcohol form. In lieu of happy-hour drinks at a bar, some functional beverages are positioned as something to gather around. One called hiyo describes itself as a “mindful social tonic”; another, called Three Spirit, is meant to “make moods and enhance connections.”

Yet as I stood in the drink aisle, with its shelves of mood elixirs and wellness tonics, these products strangely made me feel worse. Passing on these drinks can seem like a missed opportunity; after all, who doesn’t need some kind of boost these days? Perhaps the appeal of these beverages is less about their actual effect and more about the feeling they sell—that you can take a step toward self-optimization one sip at a time.

I had walked into the CVS just wanting a drink, but being confronted with all those options made me anxious that I didn’t want enough—as if my current state was unacceptable. After spotting a bottle of Kin Euphorics, I pulled up its website and filled out an online quiz: “How do you want to feel?” it asked. Energized, rejuvenated, balanced, or calm? All I wanted to feel was hydrated.

I first met Daniel Kahneman about 25 years ago. I’d applied to graduate school in neuroscience at Princeton University, where he was on the faculty, and I was sitting in his office for an interview. Kahneman, who died today at the age of 90, must not have thought too highly of the occasion. “Conducting an interview is likely to diminish the accuracy of a selection procedure,” he’d later note in his best-selling book, Thinking, Fast and Slow. That had been the first finding in his long career as a psychologist: As a young recruit in the Israel Defense Forces, he’d assessed and overhauled the pointless 15-to-20-minute chats that were being used for sorting soldiers into different units. And yet there he and I were, sitting down for a 15-to-20-minute chat of our own.

I remember he was sweet, smart, and very strange. I knew him as a founder of behavioral economics, and I had a bare familiarity with the work on cognitive biases and judgment heuristics for which he was soon to win a Nobel Prize. I did not know that he’d lately switched the focus of his research to the science of well-being and how to measure it objectively. When I said during the interview that I’d been working in a brain-imaging lab, he began to talk about a plan he had to measure people’s level of delight directly from their brain. If neural happiness could be assessed, he said, then it could be maximized. I had little expertise—I’d only been a lab assistant—but the notion seemed far-fetched: You can’t just sum up a person’s happiness by counting voxels on a brain scan. I was chatting with a genius, yet somehow on this point he seemed … misguided?

I still believe that he was wrong, on this and many other things. He believed so, too. Daniel Kahneman was the world’s greatest scholar of how people get things wrong. And he was a great observer of his own mistakes. He declared his wrongness many times, on matters large and small, in public and in private. He was wrong, he said, about the work that had won the Nobel Prize. He wallowed in the state of having been mistaken; it became a topic for his lectures, a pedagogical ideal. Science has its vaunted self-corrective impulse, but even so, few working scientists—and fewer still of those who gain significant renown—will ever really cop to their mistakes. Kahneman never stopped admitting fault. He did it almost to a fault.

Whether this instinct to self-debunk was a product of his intellectual humility, the politesse one learns from growing up in Paris, or some compulsion born of melancholia, I’m not qualified to say. What, exactly, was going on inside his brilliant mind is a matter for his friends, family, and biographers. Seen from the outside, though, his habit of reversal was an extraordinary gift. Kahneman’s careful, doubting mode of doing science was heroic. He got everything wrong, and yet somehow he was always right.

In 2011, he compiled his life’s work to that point into Thinking, Fast and Slow. Truly, the book is as strange as he was. While it might be found in airport bookstores next to business how-to and science-based self-help guides, its genre is unique. Across its 400-plus pages Kahleman lays out an extravagant taxonomy of human biases, fallacies, heuristics, and neglects, in the hope of making us aware of our mistakes, so that we might call out the mistakes that other people make. That’s all we can aspire to, he repeatedly reminds us, because mere recognition of an error doesn’t typically make it go away. “We would all like to have a warning bell that rings loudly whenever we are about to make a serious error, but no such bell is available, and cognitive illusions are generally more difficult to recognize than perceptual illusions,” he writes in the book’s conclusion. “The voice of reason may be much fainter than the loud and clear voice of an erroneous intuition.” That’s the struggle: We may not hear that voice, but we must attempt to listen.

Kahneman lived with one ear cocked; he made errors just the same. The book itself was a terrific struggle, as he said in interviews. He was miserable while writing it, and so plagued by doubts that he paid some colleagues to review the manuscript and then tell him, anonymously, whether he should throw it in the garbage to preserve his reputation. They said otherwise, and others deemed the finished book a masterpiece. Yet the timing of its publication turned out to be unfortunate. In its pages, Kahneman marveled at great length over the findings of a subfield of psychology known as social priming. But that work—not his own—quickly fell into disrepute, and a larger crisis over irreproducible results began to spread. Many of the studies that Kahneman had touted in his book—he called one an “instant classic” and said of others, “Disbelief is not an option”—turned out to be unsound. Their sample sizes were far too small, and their statistics could not be trusted. To say the book was riddled with scientific errors would not be entirely unfair.

If anyone should have caught those errors, it was Kahneman. Forty years earlier, in the very first paper that he wrote with his close friend and colleague Amos Tversky, he had shown that even trained psychologists—even people like himself—are subject to a “consistent misperception of the world” that leads them to make poor judgments about sample sizes, and to draw the wrong conclusions from their data. In that sense, Kahneman had personally discovered and named the very cognitive bias that would eventually corrupt the academic literature that he cited in his book.

In 2012, as the extent of that corruption became apparent, Kahneman intervened. While some of those whose work was now in question grew defensive, he put out an open letter calling for more scrutiny. In private email chains, he reportedly goaded colleagues to engage with critics and to participate in rigorous efforts to replicate their work. In the end, Kahneman admitted in a public forum that he’d been far too trusting of some suspect data. “I knew all I needed to know to moderate my enthusiasm for the surprising and elegant findings that I cited, but I did not think it through,” he wrote. He acknowledged the “special irony” of his mistake.

Kahneman once said that being wrong feels good, that it gives the pleasure of a sense of motion: “I used to think something and now I think something else.” He was always wrong, always learning, always going somewhere new. In the 2010s, he abandoned the work on happiness that we’d discussed during my grad-school interview, because he realized—to his surprise—that no one really wanted to be happy in the first place. People are more interested in being satisfied, which is something different. “I was very interested in maximizing experience, but this doesn’t seem to be what people want to do,” he told Tyler Cowen in an interview in 2018. “Happiness feels good in the moment. But it’s in the moment. What you’re left with are your memories. And that’s a very striking thing—that memories stay with you, and the reality of life is gone in an instant.”

The memories remain.

“In my lifetime, I never dreamed that we would be talking about medicines that are providing hope for people like me,” Oprah Winfrey says at the top of her recent prime-time special on obesity. The program, called Shame, Blame and the Weight Loss Revolution, is very clear on which medicines she means. At one point, Oprah stares into the camera and carefully pronounces their brand names for the audience: “Ozempic and Wegovy,” she says. “Mounjaro and Zepbound.” The class of drugs to which these four belong, called GLP-1 receptor agonists, is the reason for the special.

For a brief and telling moment, though, Oprah’s story of the revolution falters. It happens midway through the program, when she’s just brought on two obesity doctors, W. Scott Butsch and Amanda Velazquez, to talk about the GLP-1 wonder drugs. “Were you all surprised in your practices when people started losing weight?” she asks. Butsch gets a little tongue-tied: “Yeah, I mean, I think we have—we’ve already been using other medications for the last 10, 20 years,” he says. “But these were just a little bit more effective.”

Oprah is nonplussed. She didn’t know about these other drugs, before Ozempic, that were already helping people with obesity. “Where was I?” she cries. “Where was the announcement?” Velazquez milks the moment for a laugh—“We didn’t have TikTok; that was our problem,” she says—and the show moves on. Whatever the identity of these medicines that came before, these almost-as-effective ones, they will not receive another mention. The show proceeds as if they don’t exist.

And yet: They do. Amid the hype around the GLP-1s, with their multibillion-dollar sales and corresponding reputation as a modern miracle of medicine, a sort of pharmaco-amnesia has taken hold across America. Patients and physicians alike have forgotten, if indeed they ever knew, that the agents of the “weight-loss revolution”—Ozempic and Wegovy, Mounjaro and Zepbound—are just the latest medications for obesity. And that older drugs—among them Qsymia, Orlistat, and Contrave—are still available. Indeed, the best of these latter treatments might produce, on average, one-half the benefit you’d get from using GLP-1s in terms of weight loss, at less than one-30th the price.

That result should not be ignored. Given the lack of widespread insurance coverage for the newer drugs, as well as marked lapses in supplies, many people have been left out of Oprah’s revolution. For last week’s special, she interviewed a mother and her daughter who say, to pursed-lipped expressions of concern, that they’d love to be on a drug like Wegovy or Zepbound, but “cannot access it financially.” Although the Centers for Medicare and Medicaid Services has just announced that GLP-1 drugs for obesity may now be covered for seniors who also have cardiovascular disease, insurers have been pulling back. Next week, the North Carolina state workers’ health plan will cut off GLP-1 coverage for close to 25,000 people. Other, older drugs could help curb this crisis.

[Read: Older Americans are about to lose a lot of weight]

The newer drugs are much more potent. Semaglutide, the active ingredient in Ozempic and Wegovy, produced an additional 12 percent loss of body weight, on average, compared with placebos in clinical trials; the equivalent result for the highest dose of tirzepatide, which is in Mounjaro and Zepbound, was 18 percent. Meanwhile, the most popular of the older drugs for treating obesity, an amphetamine derivative called phentermine, has been shown to produce, on average, a 3 or 4 percent loss of total body weight. When phentermine is prescribed along with another older drug called topiramate—they’re sold in combination as Qsymia—the effect is stronger: more than 9 percent additional weight loss as compared with placebo, according to one trial.

The newer drugs have also been investigated in very large numbers of patients and been shown to measurably reduce obesity-related complications such as strokes, heart attacks, and death. “We have all this data showing that GLP-1 drugs are reducing cardiovascular events and having other benefits,” Eduardo Grunvald, the medical director of the weight-management program at UC San Diego Health, told me, “and we have no data on the other drugs on those issues.” (Like many prominent obesity doctors, including Butsch and Velazquez, Grunvald has received thousands of dollars in consulting fees and honoraria from the maker of Wegovy. He has also received payments from the company behind Contrave.) All else being equal, the GLP-1s are the better option.

But all else is rarely equal. For one thing, the average weight-loss effects reported in the literature can’t tell you how each specific patient will respond to treatment. When people take Wegovy or Zepbound, more than half of them are strong responders, according to the published research, with weight loss that amounts to more than 15 percent. At the same time, roughly one in seven people gets no clear benefit at all. The older drugs also have a diversity of outcomes. Qsymia doesn’t seem to work for about one-third of those who take it, but another third finds Ozempesque success, losing at least 15 percent of body weight. “I’ve had patients who have lost as much or more weight with Qsymia as they do with GLP-1s,” Grunvald said. “It’s about finding that lock and key for a particular individual.”

[Read: Ozempic can turn into No-zempic]

Depending on that fit, a patient may end up saving quite a bit of money. Since 2016, Sarah Ro, a primary-care physician based in Hillsborough, North Carolina, has run a weight-management program that serves rural communities. She’s been treating patients with the older drugs, she told me, and getting good results: “I regularly have people losing 50 pounds on phentermine alone, or phentermine-topiramate.” These drugs are generally covered by insurance, but Ro prescribes them as generics that are cheap enough to pay for out of pocket either way. “It’s like 10 to 11 bucks for phentermine, and 12 bucks for topiramate,” she said. A similar month’s supply of Wegovy or Zepbound injections is listed at more than $1,000.

“I have to be honest with you, the whole craze and wave of uptake of the GLP-1 medications was a little bit of a surprise to me,” Grunvald said. “We had this decade of drugs that were actually effective, but people really didn’t latch onto them.” Again, he emphasized the obvious fact that the GLP-1 medications work much better, overall, than the old ones. But he and other experts with whom I spoke suggested that the higher potency alone cannot explain an utter turnabout in patient demand, from nearly zero to almost unmanageable.

Several noted that the older drugs are “stigmatized,” as Grunvald put it. In particular, a lot of people are wary of phentermine, on account of its status as an amphetamine derivative, and also its connection to the “fen-phen” scandal of the 1990s, when it was sold as part of an enormously popular (and effective) drug combination that turned out to have dangerous effects on people’s hearts. But as David Saxon of the University of Colorado’s Anschutz Medical Campus explained to me, the problems with fen-phen derived from the “fen” and not the “phen”—which is to say, a different drug called fenfluramine. “Phen,” for its part, has been prescribed as a weight-loss drug for more than half a century—far longer than any GLP-1 agonist has been on the market—and has shown no clear signs of causing serious problems. Its known side effects are similar to those of Adderall, a drug that is now used by more than 40 million Americans.

Topiramate brings other risks, including birth defects, tingling sensations, and changes in mood. Especially at higher doses, it can lead to brain fog. But again, the specifics here will vary from one patient to the next. And GLP-1s have their own side effects, most notably gastrointestinal distress that can be quite unpleasant. About one-sixth of people taking semaglutide are forced to stop; a guest on Oprah’s special said she had to quit after ending up in the emergency room, vomiting blood. Some of these patients may do just fine on phentermine or topiramate. “Honestly, I see more side effects with the GLP-1 drugs than with the other drugs,” Grunvald told me. “I get more messages and phone calls about side effects than I used to.”

Some of the older drugs’ peculiar side effects can even wind up being useful, Ro suggested. Many of her patients with obesity are fond of Mountain Dew, she told me; some are drinking two liters every day. She counsels cutting back on sugary beverages, but topiramate can really help, because it can distort the taste of carbonation. In the clinical literature, this dysgeusia is deemed unwanted—it’s called a “taste perversion.” For Ro, it can be a tool for weaning off unhealthy habits. “We have such a wonderful response to using topiramate,” she said.

Now she’s girding for the change in North Carolina’s health-insurance coverage for state workers. She tells her patients not to panic; if they can’t afford to pay for Wegovy or Zepbound out of pocket, she can switch them to different agents. “Everybody’s talking about GLP-1s, and it’s like, ‘GLP-1s or bust,’” she said. “And I’m going, ‘Hello! You know, my patients never had that much access to GLP-1s anyway.’” Those patients may not end up getting the best possible treatments for obesity—add this to the running list of health disparities—but they can have a drug that works. For anyone who is living with meaningful complications of obesity, having some weight loss will likely be better than having none at all.

If Oprah never got the memo, the problem may have less to do with medicine than with expectation. The older drugs can work, but their average effects on body weight are in the range of 5 to 10 percent, which is about what some people can expect to achieve through major changes to their lifestyle. “Remember, you’re fighting against the cultural current that says, ‘What, you’re taking one of those medicines? That’s awful! You ought to be able to do that yourself,’” Ted Kyle, a pharmacist and an obesity-policy consultant, told me. “The efficacy is not enough to get you over that hump of cultural resistance, and of the stigma attached to taking medicines for obesity.” And then, when a patient on an older drug has reached their new plateau for body weight, which could be just 10 pounds less than where they were before, they may not be so inclined to keep up with their prescription. Are they really going to stay on a medication for the rest of their life, if its effects are not utterly transformative?

Again, it all depends on who you are. Just like the drugs, lifestyle interventions must be used indefinitely, and just like the drugs, they may work out great for certain patients and be of little help to others. “There are some people who get a response to a diet that is comparable to bariatric surgery,” Kyle told me. “It’s just not many of them. And it takes a really smart provider of obesity care to say, ‘You know what, I’m going to work with you to get you to your best possible outcomes.’” (Many primary-care doctors simply aren’t trained in how to use the older drugs, Ro said.) If we aren’t ready to give up on recommending healthy diets and more exercise, then let’s not forget the other options. These drugs work. The weight-loss revolution didn’t start in 2021.

America is in a funk, and no one seems to know why. Unemployment rates are lower than they’ve been in half a century and the stock market is sky-high, but poll after poll shows that voters are disgruntled. President Joe Biden’s approval rating has been hovering in the high 30s. Americans’ satisfaction with their personal lives—a measure that usually dips in times of economic uncertainty—is at a near-record low, according to Gallup polling. And nearly half of Americans surveyed in January said they were worse off than three years prior.

Experts have struggled to find a convincing explanation for this era of bad feelings. Maybe it’s the spate of inflation over the past couple of years, the immigration crisis at the border, or the brutal wars in Ukraine and Gaza. But even the people who claim to make sense of the political world acknowledge that these rational factors can’t fully account for America’s national malaise. We believe that’s because they’re overlooking a crucial factor.

Four years ago, the country was brought to its knees by a world-historic disaster. COVID-19 hospitalized nearly 7 million Americans and killed more than a million; it’s still killing hundreds each week. It shut down schools and forced people into social isolation. Almost overnight, most of the country was thrown into a state of high anxiety—then, soon enough, grief and mourning. But the country has not come together to sufficiently acknowledge the tragedy it endured. As clinical psychiatrists, we see the effects of such emotional turmoil every day, and we know that when it’s not properly processed, it can result in a general sense of unhappiness and anger—exactly the negative emotional state that might lead a nation to misperceive its fortunes.

The pressure to simply move on from the horrors of 2020 is strong. Who wouldn’t love to awaken from that nightmare and pretend it never happened? Besides, humans have a knack for sanitizing our most painful memories. In a 2009 study, participants did a remarkably poor job of remembering how they felt in the days after the 9/11 attacks, likely because those memories were filtered through their current emotional state. Likewise, a study published in Nature last year found that people’s recall of the severity of the 2020 COVID threat was biased by their attitudes toward vaccines months or years later.

[From the May 2021 issue: You won’t remember the pandemic the way you think you will]

When faced with an overwhelming and painful reality like COVID, forgetting can be useful—even, to a degree, healthy. It allows people to temporarily put aside their fear and distress, and focus on the pleasures and demands of everyday life, which restores a sense of control. That way, their losses do not define them, but instead become manageable.

But consigning painful memories to the River Lethe also has clear drawbacks, especially as the months and years go by. Ignoring such experiences robs one of the opportunity to learn from them. In addition, negating painful memories and trying to proceed as if everything is normal contorts one’s emotional life and results in untoward effects. Researchers and clinicians working with combat veterans have shown how avoiding thinking or talking about an overwhelming and painful event can lead to free-floating sadness and anger, all of which can become attached to present circumstances. For example, if you met your old friend, a war veteran, at a café and accidentally knocked his coffee over, then he turned red and screamed at you, you’d understand that the mishap alone couldn’t be the reason for his outburst. No one could be that upset about spilled coffee—the real root of such rage must lie elsewhere. In this case, it might be untreated PTSD, which is characterized by a strong startle response and heightened emotional reactivity.

We are not suggesting that the entire country has PTSD from COVID. In fact, the majority of people who are exposed to trauma do not go on to exhibit the symptoms of PTSD. But that doesn’t mean they aren’t deeply affected. In our lifetime, COVID posed an unprecedented threat in both its overwhelming scope and severity; it left most Americans unable to protect themselves and, at times, at a loss to comprehend what was happening. That meets the clinical definition of trauma: an overwhelming experience in which you are threatened with serious physical or psychological harm.

[Read: Why are people nostalgic for early-pandemic life?]

Traumatic memories are notable for how they alter the ways people recall the past and consider the future. A recent brain-imaging study showed that when people with a history of trauma were prompted to return to those horrific events, a part of the brain was activated that is normally employed when one thinks about oneself in the present. In other words, the study suggests that the traumatic memory, when retrieved, came forth as if it were being relived during the study. Traumatic memory doesn’t feel like a historical event, but returns in an eternal present, disconnected from its origin, leaving its bearer searching for an explanation. And right on cue, everyday life offers plenty of unpleasant things to blame for those feelings—errant friends, the price of groceries, or the leadership of the country.

To come to terms with a traumatic experience, as clinicians know, you need to do more than ignore or simply recall it. Rather, you must rework the disconnected memory into a context, and thereby move it firmly into the past. It helps to have a narrative that makes sense of when, how, and why something transpired. For example, if you were mugged on a dark street and became fearful of the night, your therapist might suggest that you connect your general dread with the specifics of your assault. Then your terror would make sense and be restricted to that limited situation. Afterward, the more you ventured out in the dark, perhaps avoiding the dangerous block where you were jumped, the more you would form new, safe memories that would then serve to mitigate your anxiety.

Many people don’t regularly recall the details of the early pandemic—how walking down a crowded street inspired terror, how sirens wailed like clockwork in cities, or how one had to worry about inadvertently killing grandparents when visiting them. But the feelings that that experience ignited are still very much alive. This can make it difficult to rationally assess the state of our lives and our country.

One remedy is for leaders to encourage remembrance while providing accurate and trustworthy information about both the past and the present. In the early days of the pandemic, President Donald Trump mishandled the crisis and peddled misinformation about COVID. But with 2020 a traumatic blur, Trump seems to have become the beneficiary of our collective amnesia, and Biden the repository for lingering emotional discontent. Some of that misattribution could be addressed by returning to the shattering events of the past four years and remembering what Americans went through. This process of recall is emotionally cathartic, and if it’s done right, it can even help to replace distorted memories with more accurate ones.

President Biden invited the nation to grieve together in 2021, when American death counts reached 500,000, and again in 2022, when they surpassed 1 million. In his 2022 State of the Union address, he rightly acknowledged that “we meet tonight in an America that has lived through two of the hardest years this nation has ever faced,” before urging Americans to “move forward safely.” But in the past two years, he, like almost everyone else, has largely tried to proceed as if everyone is back to normal. Meanwhile, American minds and hearts simply aren’t ready—whether we realize it or not.

[Read: The Biden administration killed America’s collective pandemic approach]

Perhaps Biden and his advisers fear that reminding voters of such a dark time would create more trouble for his presidency. And yet, our work leads us to believe that the effect would be exactly the opposite. Rituals of mourning and remembrance help people come together and share in their grief so that they can return more clear-eyed to face daily life. By prompting Americans to remember what we endured together, paradoxically, Biden could help free all of us to more fully experience the present.

On Sunday evening, I fed a bowl of salmon, broccoli, and rice to my eight-month-old son. Or rather, I attempted to. The fish went flying; greens and grains splattered across the walls. Half an hour later, bedtime drew near, and he hadn’t eaten a thing. Exasperated, I handed him a baby-food pouch—and he inhaled every last drop of apple-raspberry-squash-carrot mush.

For harried parents like myself, baby pouches are a lifeline. These disposable plastic packets are sort of like Capri-Suns filled with blends of pureed fruits and vegetables: A screw-top cap makes for easy slurping, potentially even making supervision unnecessary. The sheer ease of baby pouches has made them hyper-popular—and not just for parents with infants who can’t yet eat table food. They are commonly fed to toddlers; even adults sometimes eat baby pouches.

But after my son slurped up all the goo and quickly went to sleep, I felt more guilty than relieved. Giving him a pouch felt like giving up, or taking a shortcut. No parent has the time or energy to make healthy, homemade food all the time, but that doesn’t stop Americans from still thinking “they need to try harder,” Susan Persky, a behavioral scientist at the NIH who has studied parental guilt, told me. That can leave parents stuck between a pouch and a hard place.

Baby pouches have practically become their own food group. These shelf-stable time-savers debuted in 2008, and now come in a staggering range of blends: Gerber sells a carrot, apple, and coriander version; another, from Sprout Organics, contains sweet potato, white bean, and cinnamon. Containing basically just fruits and veggies, pouches are generally seen as a “healthy” option for kids. A 2019 report found that the product accounts for roughly a quarter of baby-food sales. Around the same time, a report on children attending day care showed that pouches are included in more than a quarter of lunch boxes, and some kids get more than half their lunchtime nutrition from them.

But pouches should be just a “sometimes food,” Courtney Byrd-Williams, a professor at the University of Texas’s Houston School of Public Health, told me. When you stack up their drawbacks, relying on them can really start to feel dispiriting. Although pouches are generally produce-based, they tend to have less iron than fortified cereal does and more added sugars than jarred baby food. Excess sweetness may encourage kids to eat more than necessary and could promote a sweet tooth that could later contribute to diet-related chronic disease.

If consumed in excess, pouches may also get in the way of kids learning how to eat real food. Unlike jarred baby food, which tends to contain a single vegetable or several, pouches usually include fruit to mask the bitter with the sweet. “If we’re only giving them pouches,” Byrd-Williams said, “are they learning to like the vegetable taste?” And because the purees are slurped, they don’t give infants the opportunity to practice chewing, potentially delaying development. In 2019, the German Society for Pediatrics and Adolescent Medicine went so far as to issue a statement against baby pouches, warning that eating them may delay eating with a spoon or fingers.

And then, the scariest scenario: Earlier this month, the CDC reported that hundreds of kids may have lead poisoning from pouches containing contaminated applesauce. Perhaps more troubling, a recent analysis by Consumer Reports found that even certain pouches on the market that weren’t implicated in the contamination scandal also contain unusually high levels of lead.

Naturally, these concerns can make parents anxious. Online, caregivers fret that their reliance on the products might leave their child malnourished. Some worry that their kid will never learn how to eat solid food or figure out how to chew. Pouches, to be clear, are hardly a terrible thing to feed your kid. They can be a reliable way to get fruits and vegetables into picky kids, offering a convenience that is unrivaled.

But pouch guilt doesn’t stem entirely from health concerns. By making parenting easier, they also are a reminder of what expectations parents aren’t meeting. I wanted to be the kind of mom who would consistently make my son home-cooked food and persevere through a tough meal, but on Sunday, I was just too exhausted. Guilt is a fact of life for many parents. Virtually anything can trigger it: going to work, staying at home, spending too much time on your phone, not buying supersoft bamboo baby clothes. If parents can have unrealistic standards about it, it’s fair game. “There’s just a lot of guilt about what parents should be doing,” Byrd-Williams said.

But feeding children is especially fraught. Parents are often told what they should feed their children—breast milk, fresh produce—but never how to do so; they’re left to figure that out on their own. About 80 percent of mothers and fathers experience guilt around feeding, Persky told me—about giving their kids sugary or ultra-processed foods or caving to requests for junk. Guilt might be an impetus for better food choices, but Persky said she has found the opposite: Parents who are made to feel guilty about the way they feed their kids end up choosing less healthy foods. “It’s hard to parent when you’re struggling with self-worth,” she said.

Pouch guilt has less to do with the products themselves and more to do with what they represent: convenience, ease, a moment of respite. Asking for a break conflicts with the core expectations of American parenthood, particularly motherhood. At every turn, parents are pressured to do more for their kids; on social media, momfluencers tout home-cooked baby food and meticulously styled birthday parties. The American mentality is that the “moral and correct way to do things is to have infinite willpower,” Persky said, and in this worldview, “shortcuts seem like an inherently bad thing.” Raising children is supposed to be about hard work and self-sacrifice—about pureeing carrots at home instead of buying them in a plastic packet. But when parents are constantly short on time, sometimes the best they can do is scrape together as much as they can, one squeeze pouch after another.

At six months pregnant, Sonja Lee Finnegan flew from Switzerland to France to buy $20,000 worth of drugs from a person she had never met. The drug she was after, Trikafta, is legal in Switzerland and approved for cystic fibrosis, a rare genetic disease that fills the lungs with thick mucus. Finnegan could not get it from a doctor, because she herself does not have cystic fibrosis. But the baby she was carrying inside her does, and she wanted to start him on the Trikafta as early as possible—before he was even born.

She felt so strongly because Trikafta is, without exaggeration, a miracle drug. As I wrote in the latest issue of this magazine, the daily pills have in the past five years transformed cystic fibrosis from a fatal disease into one where most patients can live an essentially normal life. Trikafta, a combination of three drugs, is not a cure, and it does not entirely reverse organ damage already caused by CF, but patients who grew up believing they would die young are instead saving for retirement. And children born with CF today can expect to live to a ripe old age, as long as they start the drugs early.

How early is best? The drugs are officially approved for CF patients as young as 2, but a handful of enterprising mothers in the United States have gotten it prescribed off-label, to treat children diagnosed in the womb. Where doctors are more cautious, mothers are still pushing the limits of when to start the drugs. A mom in Canada sent her husband across the border to get Trikafta from someone in the United States. And Finnegan flew to France to meet a patient willing to sell their excess supply.

Getting hold of Trikafta is in fact the hardest part. Parents told me of both insurance plans and obstetricians skeptical of a powerful new medication never tested in pregnant women—and not without reason. Trikafta has side effects, and it is new enough that not all of its ramifications are fully understood. But Finnegan pored over all the research she could find and decided that Trikafta was worth it. For $20,000, she bought a five-months supply—a relative bargain compared with Trikafta’s list price of $300,000-plus a year in the United States.

To her, it was worth $20,000 for her son to avoid CF complications that can require major surgery at birth. It was worth $20,000 to prevent permanent damage to his organs that begins even in utero. She felt lucky she could afford it at all. Trikafta in pregnancy is not currently standard practice, but a miracle drug was out there. For her son, she would figure out a way to get it.

The very first expecting moms on Trikafta were women with CF taking the drugs for themselves. Not long after the medication became available, in the fall of 2019, doctors noticed a baby boom in the CF community. Trikafta, it turns out, affects more than the lungs; it can also reverse the infertility common in women with CF, thought to be caused by unusually thick cervical mucus. (Most men with CF are born infertile, because the vas deferens, which carries sperm, never develops.)

Experts worried at first about what Trikafta could do to developing fetuses. “People were like, ‘Don’t do this. We don’t know if it’s a teratogen’”—a substance that causes birth defects, says Ted Liou, the director of the adult-CF center at the University of Utah. (The CF doctors quoted in this article have all conducted clinical trials for or received speaking or consulting fees from Vertex, the manufacturer of Trikafta and several other drugs for CF.) That fear turned out to be unfounded: Hundreds of babies later, there has been, at least anecdotally, no uptick in severe birth defects.

[Read: The cystic-fibrosis breakthrough that changed everything]

Doctors started to see hints that Trikafta in utero could help babies with CF too. Of the hundreds of children born to mothers on Trikafta, only a few of the babies had CF themselves. This is because cystic fibrosis is a recessive disorder, meaning a mother with CF could have a child with CF only if the father also passed on a CF mutation. But the first documented case came to the attention of Christopher Fortner, the director of the CF center and pediatric-CF program at SUNY Upstate, who published a case report in 2021. Trikafta, he told me, made a clear difference for this baby girl.

Cystic fibrosis is caused by an imbalance of salt and water in the body, and this affects developing organs even before birth. One in five infants with CF are born with an intestinal blockage caused by meconium—the normally sticky black stool of newborns—that has turned too thick and hard to pass. This is called meconium ileus, and in the worst cases, the intestines can rupture. Emergency surgery is necessary. Elsewhere in the body, the pancreas never forms properly with CF. “By the time they’re born, their pancreas is really not a functional organ,” Fortner said. Adults on Trikafta still have to take pancreatic enzymes with every meal, but there is some evidence that young children can gain pancreatic function if they begin the CF drugs early enough.

When this baby girl was born, though, her meconium and her pancreas levels were normal from the very start; the standard newborn screening for CF would have never caught her. Fortner started her on enzymes as a precaution, but he stopped them after a week. She is 3 years old now and in preschool. Unlike generations of CF kids before her, she will never have to see the school nurse for enzymes every time she wants to eat. And she may never suffer the recurring lung infections that once made CF ultimately fatal. “The life she’s living,” Fortner said, “that was a whole lot like a cure to me.”

Moms who do not have CF themselves have a much harder time getting their unborn children on Trikafta. In 2021, Yolanda Huffhines’s second child was diagnosed with CF prenatally, after a genetic test was recommended because Huffhines’s first child had cystic fibrosis. The diagnosis did not come as a shock this time, but she began to worry when the baby showed signs of meconium ileus while still in utero.

After coming across a study in ferrets, Huffhines brought the idea of Trikafta to her doctors, who were not all enthused. Her obstetrician in particular was against it. But she found that CF doctors were more willing to weigh the well-known risks of cystic fibrosis—especially meconium ileus—against the less well-known risks of Trikafta. She asked Patrick Flume, who directs the adult-CF center at the Medical University of South Carolina, what he would do if it were his wife and child. He told her he would get Trikafta, and he agreed to help.

Even with a sympathetic doctor, getting Trikafta wasn’t easy. First, Flume tried giving her a stash from a patient who no longer needed it, which was vetoed because his hospital couldn’t ensure that it had been properly stored. Then he asked the manufacturer, Vertex, which also said no. (The company told me it couldn’t provide Trikafta to anyone outside the drug’s official indications.) Finally, Flume told me, he decided to write a prescription as if the mother were his patient. When the insurance company asked if she had at least one copy of a specific CF mutation that Trikafta was developed for, he answered yes, truthfully. Because Huffhines is a carrier, she does have one copy. She started Trikafta at 32 weeks, and by the time her daughter was born, the meconium ileus had disappeared.

Huffhines’s experience on Trikafta was not entirely smooth, though. The drugs come with some well-documented side effects, such as cataracts and liver damage, that have to be monitored, Flume told me, as with any new drug. Although Trikafta during pregnancy went fine for Huffhines, she started to experience unusual symptoms when she continued the medication so her daughter could get it through breast milk. Her usual migraines started going “through the roof,” and her scheduled blood work revealed that her liver enzymes had gone haywire—a sign of liver damage. She had to stop.  

Quitting Trikafta cold turkey could be harmful for newborns, though, which Huffines knew from studying the ferret research. (Suddenly withdrawing, Fortner told me, may cause pancreatitis.) She wondered: Was it possible to give a baby Trikafta directly? The pills would be too big, obviously, but her husband had scales for gunpowder that could weigh down to the milligram. She got a new one overnighted, and she began crushing the pills to give to her daughter—a technique that has since been taught to other moms. Her daughter did well. Huffhines’s doctors ended up publishing a case report in 2022—the first documenting a carrier of CF taking Trikafta.  

The long-term impacts of being on Trikafta in utero still need to be studied. The oldest child is still only 3. In adults, a small minority who have started Trikafta have reported sudden and severe anxiety, insomnia, depression, or other neuropsychiatric symptoms. The link is not fully proven or understood in adults, and it’s completely unexplored for fetal brain development. Elena Schneider-Futschik, a pharmacologist at the University of Melbourne, told me she is collaborating with researchers in the United Kingdom to get long-term developmental data on children exposed to Trikafta before birth. For now, she said, “we don’t know.”

Fortner, who has heard from several pregnant mothers since his first case report, said he does not deter parents already set on getting Trikafta, but he does not, in all cases, push them toward it, either. Given the unknowns, he’s not sure that the benefits outweigh the risks. The clearest exceptions are cases of meconium ileus, in which doing nothing comes with its own costs. Flume told me about a recent patient whose baby was showing signs of an intestinal blockage and whose insurance initially denied Trikafta. The medication was eventually approved—but the mom went into labor the day she was due to start. Her baby needed emergency surgery. “This is something that did not need to happen,” he said.

By the time Finnegan, in Switzerland, went looking for Trikafta last year, she had the earlier cases as models. Her baby wasn’t showing signs of meconium ileus, but she didn’t want to wait until he did, if he was going to end up down that path. Although her doctors were supportive, they could not get her Trikafta. That’s why she had to take unorthodox measures.

She took her first pill in August, and her son was born in October with a working pancreas and no intestinal blockage. He is far too young for this to matter, but she hopes that the Trikafta allowed his vas deferens to develop normally too. Someday, he might want children of his own, and the impacts of getting Trikafta in utero might carry over into the next generation.

Finnegan has been documenting her experience on social media, where she says her posts have inspired other pregnants moms to get on Trikafta for their unborn children. She knows of about 20 now, and after she got in touch with Schneider-Futschik, the researcher decided to survey these moms too. Meanwhile, Finnegan is sharing the stories of other moms as well, making note of details such as how long the mom was on Trikafta, what side effects she experienced, whether meconium ileus was resolved, and if insurance covered the drugs—a case series, of sorts, presented on Instagram. They are still few enough that every case is notable. In the future, though, all of this might become the utterly unremarkable standard of care.

When Steve Edsel was a boy, his adoptive parents kept a scrapbook of newspaper clippings in their bedroom closet. He would ask for it sometimes, poring over the headlines about his birth. Headlines like this: “Mother Deserts Son, Flees From Hospital,” Winston-Salem Journal, December 30, 1973.

The mother in question was 14 years old, “5 feet 6 with reddish brown hair,” and she had come to the hospital early one morning with her own parents. They gave names that all turned out to be fake. And by 8 o’clock that evening, just hours after she gave birth, they were gone. In a black-and-white drawing of the mother, based on nurses’ recollections, she has round glasses and sideswept bangs. Her mouth is grimly set.

The abandoned boy was placed in foster care with a local couple, the Edsels, who later adopted him. Steve knew all of this growing up. His parents never tried to hide his origins, and they always gave him the scrapbook when he asked. It wasn’t until he turned 14, though, that he really began to wonder about his birth mom. “I’m 14,” he thought at the time. “This is how old she was when she had me.”

Steve began looking for her in earnest in his 20s, but the paper trail quickly ran cold. When he turned 40, he told his wife, Michelle, that he wanted to give the search one last go. This was in 2013. AncestryDNA had started selling mail-in test kits the previous year, so he bought one. His matches at first seemed unpromising—some distant relatives—but when he began posting in a Facebook group for people seeking out biological family, he got connected to a genetic genealogist named CeCe Moore. Moore specializes in finding people via distant DNA matches, a technique made famous in 2018 when it led to the capture of the Golden State Killer. But back then, genetic genealogy was still new, and Moore was one of its pioneers. She volunteered to help Steve.

Within just a couple of weeks, she had narrowed down the search to two women, cousins of the same age. On Facebook, Steve could see that one cousin had four kids, and she regularly posted photos of them, beautiful and smiling. They looked well-off, their lives picture-perfect— “like a storybook,” Steve says. The other woman was unmarried; she didn’t have kids. She was not friends with her immediate family on Facebook, and she had moved halfway across the country from them. One evening—a Saturday, Steve clearly remembers—Moore asked to speak with him by phone.

She confirmed what he had already suspected: His birth mom was the second woman. But Moore had another piece of news too. She had unexpectedly figured out something about his biological father as well. It looks like your parents are related. Steve didn’t know what to say. Do you understand what I mean? He said he thought so. Either your mom’s father or your mom’s brother is your father. A sea of emotions rose to a boil inside him: anger, hurt, worthlessness, disgust, shame, and devastation all at once. In his years of wondering about his birth, he had never, ever considered the possibility of incest. Why would he? What were the chances?

In 1975, around the time of Steve’s birth, a psychiatric textbook put the frequency of incest at one in a million.

But this number is almost certainly a dramatic underestimate. The stigma around openly discussing incest, which often involves child sexual abuse, has long made the subject difficult to study. In the 1980s, feminist scholars argued, based on the testimonies of victims, that incest was far more common than recognized, and in recent years, DNA has offered a new kind of biological proof. Widespread genetic testing is uncovering case after secret case of children born to close biological relatives—providing an unprecedented accounting of incest in modern society.

The geneticist Jim Wilson, at the University of Edinburgh, was shocked by the frequency he found in the U.K. Biobank, an anonymized research database: One in 7,000 people, according to his unpublished analysis, was born to parents who were first-degree relatives—a brother and a sister or a parent and a child. “That’s way, way more than I think many people would ever imagine,” he told me. And this number is just a floor: It reflects only the cases that resulted in pregnancy, that did not end in miscarriage or abortion, and that led to the birth of a child who grew into an adult who volunteered for a research study.

Most of the people affected may never know about their parentage, but these days, many are stumbling into the truth after AncestryDNA and 23andMe tests. Steve’s case was one of the first Moore worked on involving closely related parents. She now knows of well over 1,000 additional cases of people born from incest, the significant majority between first-degree relatives, with the rest between second-degree relatives (half-siblings, uncle-niece, aunt-nephew, grandparent-grandchild). The cases show up in every part of society, every strata of income, she told me.

[Read: When a DNA Test Shatters Your Identity]

Neither AncestryDNA nor 23andMe informs customers about incest directly, so the thousand-plus cases Moore knows of all come from the tiny proportion of testers who investigated further. This meant, for example, uploading their DNA profiles to a third-party genealogy site to analyze what are known as “runs of homozygosity,” or ROH: long stretches where the DNA inherited from one’s mother and father are identical. For a while, one popular genealogy site instructed anyone who found high ROH to contact Moore. She would call them, one by one, to explain the jargon’s explosive meaning. Unwittingly, she became the keeper of what might be the world’s largest database of people born out of incest.

In the overwhelming majority of cases, Moore told me, the parents are a father and a daughter or an older brother and a younger sister, meaning a child’s existence was likely evidence of sexual abuse. She had no obvious place to send people reeling from such revelations, and she was not herself a trained therapist. After seeing many of these cases, though, she wanted people to know they were not alone. Moore ended up creating a private and invite-only support group on Facebook in 2016, and she tapped Steve and later his wife, Michelle, to become admins, too. The three of them had become close in the months and years after the search for his birth mom, as they navigated the emotional fallout together.

One day this past January, Michelle, who also works as Moore’s part-time assistant, told me she had spoken with four new people that week, all of them with ROH high enough to have parents who were first-degree relatives. She used to dread these calls. “I would stumble over my words,” she told me. But not anymore. She tells the shaken person on the line that they can join a support group full of people who are living the same reality. She tells them they can talk to her husband, Steve.

When Steve first discovered the truth about his biological parents, a decade ago, he had no support group to turn to, and he did not know what to do with the strange mix of emotions. He was genuinely happy to have found his birth mom. He had never looked like his adoptive parents, but in photos of her and her family, he could see his eyes, his chin, and even the smirky half-grin that his face naturally settles into.

But he radiated with newfound anger, too, on her behalf. He could not know the exact circumstances of his conception, and his DNA test alone could not determine whether her older brother or her father was responsible. But Steve could not imagine a consensual scenario, given her age. The bespectacled 14-year-old girl who disappeared from the hospital had remained frozen in time in his mind, even as he himself grew older, got married, became a stepdad. He felt protective of that young girl.  

As badly as he wanted to know his birth mom, he worried she would not want to know him. Would his sudden reappearance dredge up traumatic memories—memories she had perhaps been trying to outrun her whole adult life, given how far she had moved and how little she seemed connected to her family? A religious man, Steve prayed over it and settled on handwriting a letter. He included a couple of paragraphs about his life, some photos, and a message that he loved her. He left out what he knew about his paternity. And he took care to send the letter by certified mail, so that he could confirm its receipt and so that it would not accidentally fall into anyone else’s hands.

She never responded. But Steve knew that she had received it: The post office sent him the green slip that she had signed upon delivery, and he scrutinized her signature—her actual name, written by her actual hand. At 40 years old, he touched for the first time something his mother had just touched, held something she had just held. He put the slip inside the pages of his Bible.

Steve had never faulted his mother for leaving him at the hospital, and finding out about his paternity made him even more understanding. But the revelation also made him struggle with who he was. Did it mean that something was wrong with him, written into his DNA from the moment of his conception? On a podcast later, he admitted to feeling like trash, “like something that somebody had just thrown away.” Those first six months after his discovery were the hardest six months of his life.

Across human cultures, incest between close family members is one of the most universal and most deeply held taboos. A common explanation is biological: Children born from related parents are more likely to develop health complications, because their parents are more likely to be carriers of the same recessive mutations. From the 1960s to the ’80s, a handful of studies following a few dozen children born of incest documented high rates of infant mortality and congenital conditions.

But in the past, healthy children born from incestuous unions would have never come to the attention of doctors. As widespread DNA testing has uncovered orders of magnitude more people whose parents are brother and sister or parent and child, it’s also shown that plenty of those people are perfectly healthy. “There is a large element of chance in whether incest has a poor outcome,” according to Wilson, the geneticist. It depends on whether those runs of homozygosity contain recessive disease-causing mutations. All of us have some of these runs in our DNA—usually less than 1 percent of the genome in Western populations, higher in cultures where cousin marriage is common. But that number is about 25 percent, Wilson said, in people born from first-degree relatives. While the odds of a genetic disease are much higher, the outcome is far from predetermined.

Still, these numbers make people wonder. Steve was born with a heart murmur, which required open-heart surgery at ages 13 and 18, though he does not know for sure the cause; heart defects are among the more common birth defects in the general population. He and Michelle were also never able to have children together. Others in the Facebook group have shared their struggles with autoimmune diseases, fibromyalgia, eye problems, and so on—though these are often hard to definitively link to incest. Health problems arising from incest might manifest in any number of ways, depending on exactly which mutations are inherited. “When I go to the doctor and they ask me my family history, I wonder: How much do I need to go into it?” says Mandy, another member of the group. (I am identifying some people by first name only, so they can speak freely about their family and medical histories.) How much experience would a typical doctor have with incest, anyway?

After Mandy first learned that her father was her mother’s uncle, she went looking for stories about other people like her. All she could find were “gross fantasies” online and medical-journal articles about health problems. She felt very lonely. “I don’t have anybody I can talk to about this,” she remembers thinking. “Nobody knows what to say.” When she found the Facebook group, she could see that she was far from the only one like her. She watched the others cycle, too, through the stages of denial, anger, bargaining, depression, and acceptance.

She does not know exactly what happened between her biological parents, but her mother was 17, and her mother’s uncle was in his 30s. The discovery, for all the hurt that it surfaced, has helped Mandy reconcile some of her childhood experiences. Unlike Steve, she was raised by her biological mother, and she believed her mother’s husband to be her biological father. He mostly ignored her, but her mother was cruel. She treated Mandy differently than she did her younger brothers. “At least now I have more of an answer as to why,” Mandy told me. “I wasn’t a bad kid and unlovable.”

Kathy was also raised by her mother, though she had an early inkling that her dad was not her biological dad. Their blood types were incompatible, and she heard rumors about her mother and grandfather. Although her mother’s family was violent and chaotic, she was close to her dad’s family, especially her granny on that side. “They’ve been my rock,” she told me. By the time Kathy took a DNA test confirming that her dad was not her biological dad, she had spent a lifetime distancing herself from her biological family and embracing one with whom she shared no DNA.

Hers was, in some ways, the opposite journey of adoptees such as Steve, who wanted so badly to know his biological family. But the two of them have become close. Kathy remembers how angry he used to be on his mother’s behalf. She told him that she used to be angry too, but she had to leave it behind. “It’s not going to bring me any peace. It’s not going to bring my mother any peace,” she recalled saying. And it wouldn’t undo what had been done to his mother by her father or her brother so many years ago.

In the end, Steve was able to identify his biological father, though not through any particular feat of genetic sleuthing. One day, two and a half years after his DNA test, he logged in to AncestryDNA and saw a parent match. It was his mother’s older brother. From the site, he could see that his father-uncle had logged in once, presumably seen that Steve was his son, and—even after Steve sent him a message—never logged back on again.

By then, his initial anger had started to dissipate. He still felt deeply for his birth mom. Michelle says that her husband has always been a sensitive guy—she makes fun of him for crying at movies—but he’s become even more empathetic. The feelings of worthlessness he initially struggled with has given way to a sense of purpose; he and Michelle now spend hours on the phone talking with others in the support group.

Steve has still never spoken to his birth mother. He tried writing to her a second time, sending a journal about his life—but she returned it unopened. He messages her occasionally on Facebook, sending photos of grandkids and puppies he’s raised. Every year, he wishes her a happy birthday. She has not replied, but she has also not blocked him.

When the journal came back unopened, Steve decided to try messaging his mother’s cousin—the other woman he’d initially thought could be his birth mom. He yearned for some kind of connection with someone in his biological family. He wrote to the cousin about his mom—but not his dad—and she  actually replied. She told him that she and his mom had been close as children, Steve recounted, but she did not know about a pregnancy. To her, it had seemed like her cousin one day “fell off the face of the Earth,” he says. She agreed to read his journal, and the two of them soon began speaking on the phone about their families.

Months later, Steve felt like he could finally share the truth about his biological father, and the cousin again accepted him for who he was. They met for the first time in 2017 when she was visiting a nearby town, and she later invited Steve and Michelle to Thanksgiving. Last year, she extended another invitation to a large family gathering. Steve’s immediate biological family was not there, but hers was, and they all knew about him and his mom and his dad. They greeted him with hugs, and they took photos together as a family. “It felt like a relief,” he told me, like a burden had been lifted from him. In this family, he was not a secret.  

Measles seems poised to make a comeback in America. Two adults and two children staying at a migrant shelter in Chicago have gotten sick with the disease. A sick kid in Sacramento, California, may have exposed hundreds of people to the virus at the hospital. Three other people were diagnosed in Michigan, along with seven from the same elementary school in Florida. As of Thursday, 17 states have reported cases to the CDC since the start of the year. (For comparison, that total was 19, plus the District of Columbia, for all of 2023, and just 6 for 2022.) “We’ve got this pile of firewood,” Matthew Ferrari, the director of the Center for Infectious Disease Dynamics at Penn State, told me, “and the more outbreaks that keep happening, the more matches we’re throwing at it.”

Who’s holding the matchbook? There’s an easy answer to who’s at fault. One of the nation’s political parties, and not the other, turned against vaccines to some extent during the pandemic, leading to voter disparities in death rates. One party, and not the other, has a presumptive presidential candidate who threatens to punish any school that infringes on parental rights by requiring immunizations. And one party, but not the other, appointed a vaccine-skeptical surgeon general in Florida who recently sidestepped standard public-health advice in the middle of an outbreak. The message from Republicans, as The Washington Post’s Alexandra Petri joked in a recent column, can sound like this: “We want measles in the schools and books out of them!”

But the politics of vaccination, however grotesque it may be in 2024, obscures what’s really going on. It’s true that vaccine attitudes have become more polarized. Conservative parents in particular may be opting out of school vaccine requirements in higher numbers than they were before. In the blood-red state of Idaho, for example, more than 12 percent of kindergartners received exemptions from the rules for the 2022–23 school year, a staggering rate of refusal that is up by half from where it was just a few years ago. Politicized recalcitrance is unfortunate, to say the least, and it can be deadly. Even so, America’s political divides are simply not the cause of any recent measles outbreak. The virus has returned amid a swirl of global health inequities. Any foothold that it finds in the U.S. will be where hyperlocal social norms, not culture-war debates, are causing gaps in vaccine access and acceptance. The more this fact is overlooked, the more we’re all at risk.

Consider where the latest measles cases have been sprouting up: By and large, the recent outbreaks have been a blue-state phenomenon. (Idaho has so far been untouched; the same is true for Utah, with the nation’s third-highest school-vaccine-exemption rate.) Zoom into the county level, and you’ll find that the pattern is repeated: Measles isn’t picking on Republican communities; if anything, it seems to be avoiding them. The recent outbreak in Florida unfolded not in a conservative area such as Sarasota, where vaccination coverage has been lagging, but rather in Biden-friendly Broward County, at a school where 97 percent of the students have received at least one MMR shot. Similarly, the recent cases in Michigan turned up not in any of the state’s MAGA-voting, vaccine-forgoing areas but among the diverse and relatively left-wing populations in and around Ann Arbor and Detroit.

Stepping back to look at the country as a whole, one can’t even find a strong connection—or, really, any consistent link at all—between U.S. measles outbreaks, year to year, and U.S. children’s vaccination rates. Sure, the past three years for which we have student-immunization data might seem to show a pattern: Starting in the fall of 2020, the average rate of MMR coverage for incoming kindergarteners did drop, if only by a little bit, from 93.9 to 93.1 percent; at the same time, the annual number of reported measles cases went up almost tenfold, from 13 to 121. But stretch that window back one more year, and the relationship appears to be reversed. In 2019, America was doing great in terms of measles vaccination—across the country, 95.2 percent of kindergartners were getting immunized, according to the CDC—and yet, in spite of this fantastic progress, measles cases were exploding. More than 1,200 Americans got sick with the disease that year, as measles took its greatest toll in a generation.

It’s not that our high measles-vaccination coverage didn’t matter then or that our slightly lower coverage doesn’t matter now. Vaccination rates should be higher; this is always true. In the face of such a contagious disease, 95 percent would be good; 99 percent much better. When fewer people are protected, more people can get sick. In Matthew Ferrari’s terms, a dropping immunization rate means the piles of firewood are getting bigger. If and when the flames do ignite, they could end up reaching farther, and burning longer, than they would have just a year or two ago. In the midst of any outbreak large enough, where thousands are affected, children will die.

[Read: The good news about vaccine hesitancy]

Despite America’s fevered national conversation about vaccines, however, rates of uptake simply haven’t changed that much. Even with the recent divot in our national vaccine rates, the country remains in broad agreement on the value of immunity: 93 percent of America’s kindergartners are getting measles shots, a rate that has barely budged for decades. The sheer resilience of this norm should not be downplayed or ignored or, even worse, reimagined as a state of grace from which we’ve fallen. Our protection remains strong. In Florida, the surgeon general’s lackadaisical response to the crisis at the Broward County elementary school did not produce a single extra case of the disease, in spite of grim predictions to the contrary, almost certainly thanks to how many kids are already vaccinated.

At the same time, however, measles has been thriving overseas. Its reemergence in America is not a function of the nation’s political divides, but of the disease’s global prevalence. Europe had almost 60,000 cases last year, up from about 900 in 2022. The World Health Organization reports that the number of reported cases around the world surged to 306,000, after having dropped to a record low of 123,000 in 2021. As the pandemic has made apparent, our world is connected via pathogens: Large outbreaks in other countries, where vaccination coverage may be low, have a tendency to seed tiny outbreaks in the U.S., where coverage has been pretty high, but narrow and persistent cracks in our defenses still remain. (In 2022, more than half of the world’s unvaccinated infants were concentrated in just 10 countries; some of these are measles hotspots at this moment.) This also helps explain why so many Americans got measles in 2019. That was a catastrophic year for measles around the world, with 873,000 reported cases in total, the most since 1994. We had pretty good protection then, but the virus was everywhere—and so, the virus was here.

[Read: Florida’s experiment with measles]

In high-income countries such as the U.S., Ferrari told me, “clustering of risk” tends to be the source of measles outbreaks more than minor changes in vaccine coverage overall. Even in 2019, when more than 95 percent of American kindergarteners were getting immunized, we still had pockets of exposure where protection happened to be weakest. By far the biggest outbreak from that year occurred among Hasidic Jewish populations in New York State. Measles was imported via Israel from the hot spot of Ukraine, and took off within a group whose vaccination rates were much, much lower than their neighbors’. In the end, more than 1,100 people were infected during that outbreak, which began in October 2018 and lasted for nearly a year. “A national vaccination rate has one kind of meaning, but all outbreaks are local outbreaks,” Noel Brewer, a professor at the University of North Carolina at Chapel Hill and a member of the federal Advisory Committee on Immunization Practices, told me. “They happen on a specific street in a specific group of houses, where a group of people live and interact with each other. And those rates of vaccination in that specific place can drop well below the rate of coverage that will forestall an outbreak.”

We’ve seen this time and time again over the past decade. When bigger outbreaks do occur in the U.S., they tend to happen in tight-knit communities, where immunization norms are radically out of sync with those of the rest of American society, politics aside. In 2014, when an outbreak of nearly 400 cases took hold in Ohio, almost entirely within the Amish community, the local vaccination rate was estimated to be about 14 percent. (The statewide number for young children at that time was more than 95 percent.) In 2011 and 2017, measles broke out among the large Somali American community in Minnesota, where anti-vaccine messaging has been intense, and where immunization rates for 2-year-olds dropped from 92 percent 20 years ago to 35 percent in 2021. An outbreak from the end of 2022, affecting 85 people in and around Columbus, Ohio, may well be linked to the nation’s second-biggest community of Somalis.

Care must be taken in how these outbreaks are discussed. In Minnesota, for example, state health officials have avoided calling out the Somali community, for fear of stigmatizing. But another sort of trouble may arise when Americans overlook exactly who’s at risk, and exactly why. Experts broadly agree that the most effective way to deal with local outbreaks is with local interventions. Brewer pointed out that during the 2019 outbreak in New York, for example, nurses who belonged to local Jewish congregations took on the role of vaccine advocates. In Minnesota, the Department of Health has brought on more Somali staff, who coordinate with local Somali radio and TV stations to share its message. Yet these efforts can be obscured by news coverage of the crisis that points to a growing anti-science movement and parents giving up on vaccination all across the land. When measles spread among New York’s orthodox Jews, The New York Times reported on “an anti-vaccine fervor on the left that is increasingly worrying health authorities.” When the virus hit Columbus, NBC News noted that it was “happening as resistance to school vaccination requirements is spreading across the country.”

Two different public-health responses can be undertaken in concert, the experts told me: You treat the problem at its source, and you also take the chance to highlight broader trends. A spate of measles cases in one community becomes an opportunity for pushing vaccination everywhere. “That’s always an important thing for us to do,” Ferrari said. Even so, the impulse to nationalize the problem will have its own, infelicitous effects. First, it’s meaningfully misleading. By catastrophizing subtle shifts in vaccination rates, we frighten many parents for no reason. By insisting that every tiny outbreak is a product of our national politics, we distract attention from the smaller measures that can and should be taken—well ahead of any upsurge of disease—to address hyperlocal vaccination crises. And by exaggerating the scale of our divisions—by asserting that we’ve seen a dangerous shift on a massive scale, or an anti-vaccine takeover of the Republican Party—we may end up worsening the very problem that worries us the most.

We are a highly vaccinated nation, our politics notwithstanding. Telling people otherwise only fosters more division; it feeds the feeling that taking or refusing measles shots is an important mode of self-expression. It further polarizes health behavior, which can only widen the cracks in our defenses. “We have become quite militant and moralistic about vaccination,” Brewer told me, “and we probably would do well to be less absolute.” Measles outbreaks overseas are growing; measles outbreaks here will follow. Their specific causes ought not be ignored.

The irony undergirding the new wave of obesity drugs is that they initially weren’t created for obesity at all. The weight loss spurred by Ozempic, a diabetes drug in the class of so-called GLP-1 agonists, gave way to Wegovy—the same drug, repackaged for obesity. Zepbound, another medication, soon followed. Now these drugs have a new purpose: heart health.

On Friday, the FDA approved the use of Wegovy for reducing the risk of heart attack, stroke, and death in adults who are overweight and have cardiovascular disease. The move had been anticipated since the publication of a landmark trial in the fall, which showed the drug’s profound effects on cardiovascular  health. The decision could usher in a new era where GLP-1 drugs become mainstream, opening up access to millions of Americans who previously didn’t qualify for Wegovy.

Some of the obstacles stopping people from getting the drug may also begin to crumble. Insurance companies commonly deny coverage of Wegovy because obesity is seen as a cosmetic concern rather than a medical one, but that argument may not hold up for cardiovascular disease. “This new FDA indication is HUGE,” Katherine Saunders, an obesity-medicine physician at Weill Cornell Medicine, told me in an email. Wegovy may soon be within reach for many more Americans—that is, if they can find it.

In practice, Wegovy is maddeningly hard to get hold of. Shortages of injectable semaglutide, the active ingredient in Wegovy and Ozempic, have been ongoing since March 2022; currently, most doses of Wegovy are in limited supply. As the popularity of semaglutide has skyrocketed, demand has completely outstripped the capacity of its manufacturer, Novo Nordisk. The drug comes in injection pens containing a glass vial; “these are not easy products to make,” Lars Fruergaard Jørgensen, the CEO of Novo Nordisk, said in August. In response to the shortages, the company withheld its supply of lower Wegovy doses last year. Because treatment on the medication must begin in low doses, this meant that new patients who wanted to start on Wegovy functionally couldn’t. In January, the company began “more than doubling the amount of the lower-dose strengths” of the drug, a Novo Nordisk spokesperson told me, and it plans to gradually increase overall supply throughout the rest of the year.

The ongoing shortages have left providers and patients feeling stuck. “It is devastating to prescribe a lifesaving medication for a patient and then find out it’s not covered or we can’t locate supply,” Saunders said. Doctors are scrambling to make do with what’s available. Ivania Rizo, an endocrinologist at Boston Medical Center, told me she has had to turn to older GLP-1 drugs such as Saxenda to “bridge” patients to higher doses of Wegovy, although now that is in shortage too. Patients can spend each day calling pharmacy after pharmacy in search of one with Wegovy in stock, Rizo said. In desperation, some have turned to versions of the drug that are custom-made by compounding pharmacies with little oversight, despite the FDA expressing concerns about them. The shots are supposed to be taken weekly, but others have attempted to stretch their doses beyond that.

That the new FDA approval could very mainstream obesity drugs may create long-needed pressure to help resolve these shortages. It makes clear that Wegovy is a lifesaving medication not only for people with obesity but also for those with cardiovascular disease—the leading cause of death in the U.S.—putting the impetus on Novo Nordisk to ramp up production. But in the short term, the access issues may persist. “The new approval is very likely to worsen shortages, because the demand for Wegovy will continue to climb—now at an even faster pace,” Saunders said.

If patients think they’re stuck now, they’re about to feel entrenched. Wegovy is the only obesity drug that has been approved to reduce the risk of heart attacks, but none of its competitors is easily available either. Supplies of certain dosages of Eli Lilly’s Mounjaro, a diabetes drug whose active ingredient is sold for obesity as Zepbound, are limited, and shortages are expected later this year. “We need supply to increase dramatically,” Saunders said. Both Novo Nordisk and Eli Lilly have invested heavily in expanding production capacity, but some of the new plants won’t open until 2029.

For all of its advantages, the FDA approval has a sobering effect on the unrelenting hype around GLP-1s. So much of the excitement around obesity drugs has focused on the future, as dozens of pharmaceutical companies develop more powerful drugs, and commentators imagine a world without obesity. In the process, the issues of the present have gone overlooked. More drugs won’t make much of a difference if the drugs themselves are out of reach.

Recently, a photo of rice left me confused. The rice itself looked tasty enough—fluffy, well formed—but its oddly fleshy hue gave me the creeps. According to the scientists who’d developed it, each pink-tinged grain was seeded with muscle and fat cells from a cow, imparting a nutty, umami flavor.

In one sense, this “beef rice” was just another example of lab-grown meat, touted as a way to eat animals without the ethical and environmental impacts. Though not yet commercially available, the rice was developed by researchers in Korea as a nutrition-dense food that can be produced sustainably, at least more so than beef itself. Although it has a more brittle texture than normal rice, it can be cooked and served in the same way. Yet in another sense, this rice was entirely different. Lab-grown meat aims to replicate conventional meat in every dimension, including taste, nutrition, and appearance. Beef rice doesn’t even try.

Maybe that’s a good thing. Lab-grown meat, also widely known as cultivated meat, has long been heralded as the future of food. But so far, the goal of perfectly replicating meat as we know it—toothy, sinewy, and sometimes bloody—has proved impractical and expensive. Once-abundant funding has dried up, and this week, Florida moved toward becoming the first state to ban sales of cultivated meat. It seems unlikely that whole cuts of cultivated meat will be showing up on people’s plates anytime soon—but maybe something like beef rice could. The most promising future of lab-grown meat may not look like meat at all, at least as we’ve always known it.

The promise of cultivated meat is that you can have your steak and eat it too. Unlike the meatless offerings at your grocery store, cultivated meat is meat—just created without killing any animals. But the science just isn’t there yet. Companies have more or less figured out the first step, taking a sample of cells from a live animal or egg and propagating them in a tank filled with a nutrient-rich broth. Though not cheaply: By one estimate, creating a slurry of cultivated cells costs $17 a pound or more to produce.

The next step has proved prohibitively challenging: coaxing that sludge of cells to mature into different types—fat, muscle, connective tissue—and arranging them in a structure resembling a solid cut of meat. Usually, the cells need a three-dimensional platform to guide their growth, known as a scaffold. “It’s something that is very easy to get wrong and hard to get right,” Claire Bomkamp, a senior scientist at the Good Food Institute, a nonprofit supporting meat alternatives, told me. So far, a few companies have served up proofs of concept: In June, the United States approved the sale of cultivated chicken from Upside Foods and Good Meat. However it is virtually impossible to come by now.

The basic science of lab-grown meat can be used for more than just succulent chicken breasts and medium-rare steaks. Cells grown in a tank function essentially like ground meat, imparting a meaty flavor and mouthfeel to whatever they are added to, behaving more like an ingredient or a seasoning than a food product. Hybrid meat products, made by mixing a small amount of cultivated-meat cells with other ingredients, are promising because they would be more cost-effective than entire lab-grown steaks or chicken breasts but meatier than purely plant-based meat.

Already, the start-up SciFi Foods is producing what has been described as a “fatty meat paste” that is intended to be mixed with plant-based ingredients to make burgers. Only small amounts are needed to make the burgers beefy; each costs less than $10 to make, according to the company—still considerably more than a normal beef patty, but the prices should come down over time. Maybe it sounds weird, but that’s not so different from imitation crab—which doesn’t contain much or any crab at all. A similar premise underlies the plant-based bacon laced with cultivated pork fat that I tried last year. Was it meat? I’m not sure. Did it taste like it? Absolutely.

Meat can be so much more than what we’ve always known. “We don’t have to make meat the same way that it’s always come out of an animal,” Bomkamp said. “We can be a little bit more expansive in what our definition of meat is.” Beef rice, which essentially uses rice as a miniature scaffold to grow cow cells, falls into this category. It isn’t particularly meaty—only 0.5 percent of each grain is cow—but the scientists who developed it say the proportion could change in future iterations. It’s framed as a way to feed people in “underdeveloped countries, during war, and in space.”

Eventually, cultivated meat could impart a whiff of meatiness to blander foods, creating new, meat-ish products in the process that are more sustainable than regular meat and more nutritious than plants. Beef rice is one option; meat grown on mushroom roots is in development. Even stranger foods are possible. Bomkamp envisions using the technology to make thin sheets of seafood—combining elements of salmon, tuna, and shrimp—to wrap around a rainbow roll of sushi. In this scenario, cultivated meat probably won’t save the planet from climate change and animal suffering. “It wouldn’t serve its original function of being a direct replacement for commercial meat,” Daniel Rosenfeld, who studies perceptions of cultivated meat at UCLA, told me. But at the very least, it could provide another dinner option.

Of course, it’s in the interest of the cultivated-meat industry to suggest that cultivated meat isn’t just outright doomed. No doubt some vegetarians would cringe at the thought, as would some dedicated carnivores. But considering how much meat Americans eat, it’s not hard to imagine a future in which cultivated cells satisfy people searching for a new kind of meat product. Imagine the salad you could make with chicken cells grown inside arugula, or bread baked with bacon-infused wheat. But should those prove too difficult to produce, I’d happily take a bowl of beef rice, in all its flesh-tinged glory.