You wake up with a stuffy nose, so you head to the pharmacy, where a plethora of options awaits in the cold-and-flu aisle. Ah, how lucky you are to live in 21st-century America. There’s Sudafed PE, which promises “maximum-strength sinus pressure and nasal congestion relief.” Sounds great. Or why not grab DayQuil in case other symptoms show up, or Tylenol Cold + Flu Severe should whatever it is get really bad? Could you have allergies instead? Good thing you can get Benadryl Allergy Plus Congestion, too.
Unfortunately for you and me and everyone else in this country, the decongestant in all of these pills and syrups is entirely ineffective. The brand names might be different, but the active ingredient aimed at congestion is the same: phenylephrine. Roughly two decades ago, oral phenylephrine began proliferating on pharmacy shelves despite mounting—and now damning—evidence that the drug simply does not work.
“It has been an open secret among pharmacists,” says Randy Hatton, a pharmacy professor at the University of Florida, who filed a citizen petition in 2007 and again in 2015 asking the FDA to reevaluate phenylephrine. This week, an advisory panel to the FDA voted 16–0 that the drug is ineffective orally, which could pave the way for the agency to finally pull the drug.
If so, the impact would be huge. Phenylephrine is combined with fever reducers, cough suppressants, or antihistamines in many popular multidrug products such as the aforementioned DayQuil. Americans collectively shell out $1.763 billion a year for cold and allergy meds with phenylephrine, according to the FDA, which also calls the number a likely underestimate. That’s a lot of money for a decongestant that, again, does not work.
Over-the-counter oral decongestants weren’t always this bad. But in the early 2000s, states began restricting access to pseudoephedrine—a different drug that actually is effective against congestion—because it could be used to make meth; the Combat Methamphetamine Epidemic Act, signed in 2006, took the restrictions national. You can still buy real-deal Sudafed containing pseudoephedrine, but you have to show an ID and sign a logbook. Meanwhile, manufacturers filled over-the-counter shelves with phenylephrine replacements such as Sudafed PE. The PE is for phenylephrine, but you would be forgiven for not noticing the different name.
“Thet switch from pseudoephedrine to phenylephrine was a big mistake,” says Ronald Eccles, who ran the Common Cold Unit at Cardiff University until his retirement. Eccles was critical of the switch back in 2006. The evidence, he wrote at the time, was already pointing to phenylephrine as a lousy oral drug.
Problems started showing up quickly. Hatton, who was then a co-director of the University of Florida Drug Information Center, started getting a flurry of questions about phenylephrine: Does it work? What’s the right dose? Because my patients are complaining that it’s not doing anything. He decided to investigate, and he went deep. Hatton filed a Freedom of Information Act request for the data behind FDA’s initial evaluation of the drug in 1976. He soon found himself searching through a banker’s box of records, looking for studies whose raw data he and a postdoctoral resident typed up by hand to reanalyze. The 14 studies the FDA had considered at the time had mixed results. Five of the positive ones were all conducted at the same research center, whose results looked better than everyone else’s. Hutton’s team thought that was suspicious. If you excluded those studies, the drug no longer looked effective at its usual dose.
All told, the case for phenylephrine was not great, but the case against was no slam dunk either. When Hatton and colleagues at the University of Florida, including Leslie Hendeles, filed a citizen petition, they asked the agency to increase the maximum dose to something that could be more effective. They did not ask to pull the drug entirely.
There was more damning evidence to come, though. The petition led to a first FDA advisory committee meeting, in 2007, where scientists from a pharmaceutical company named Schering-Plough, which later became Merck, presented brand-new data. The company had begun studying the drug, Hatton and Hendeles recalled, because it was interested in replacing the pseudoepinephrine in its allergy drug Claritin-D. But these industry scientists did not come to defend phenylephrine. Instead, they dismantled the very foundation of the drug’s supposed efficacy.
They showed that almost no phenylephrine reaches the nasal passages, where it theoretically could reduce congestion and swelling by causing blood vessels to constrict. When taken orally, most of it gets destroyed in the gut; only 1 percent is active in the bloodstream. This seemed to be borne out by what people experienced when they took the drug—which was nothing. The scientists presented two morestudies that found phenylephrine to be no better than placebo in people congested because of pollen allergies.
These studies, the FDA later wrote, were “remarkable,” changing the way the agency thought about how oral phenylephrine works in the body. But experts still weren’t ready to write the drug off entirely. The 2007 meeting ended with the advisory committee asking for data from higher doses.
The story for phenylephrine only got worse from there. In hopes of making an effective product, Merck went to study higher doses in two randomized clinical trials published in 2015 and 2016. “We went double, triple, quadruple—showed no benefit,” Eli Meltzer, an allergist who helped conduct the trials for Merck, said at the FDA-advisory-panel meeting this week. In other words, not only is phenylephrine ineffective at the labeled dosage of 10 milligrams every four hours, it is not even effective at four times that dose. These data prompted Hatton and Hendeles to file a second citizen petition and helped prompt this week’s advisory meeting. This time, the panel didn’t need any more data. “We’re kind of beating a dead horse … This is a done deal as far as I’m concerned. It doesn’t work,” one committee member, Paul Pisarik, said at the meeting. The advisory’s 16–0 vote is not binding, though, so it’s still up to the FDA to decide what to do about phenylephrine.
In any case, phenylephrine is not the only cold-and-flu drug with questionable effectiveness in its approved form. The common cough drugs guaifenesin and dextromethorphan have both come under fire. But we lack the robust clinical-trial data to draw a definitive conclusion on those one way or the other. “What really helped our case is the fact that Merck funded those studies,” Hatton says. And that Merck let its scientists publish them. Failed studies from drug companies usually don’t see the light of day because they present few incentives for publication. Changing the consensus on phenylephrine took an extraordinary set of circumstances.
It also required two dogged guys who have now been at this work for nearly two decades. “We’re just a couple of older professors from the University of Florida trying to do what’s best for society,” Hatton told me. When I asked whether they would be tackling other cold medications, he demurred: “I don’t know if either one of us has another 20 years in us.” He would instead like to see public funding for trials like Merck’s to reevaluate other over-the-counter drugs.
There are other effective decongestants on pharmacy shelves. Even though phenylephrine does not work in pill form, “phenylephrine is very effective if you spray it into the nose,” Hendeles says. Neo-Synephrine is one such phenylephrine spray. Other nasal sprays containing other decongestants, such as Afrin, are also effective. But the only other common oral decongestant is pseudoephedrine, which requires that extra step of asking the pharmacist. Restricting pseudoephedrine has not curbed the meth epidemic, either. Meth-related overdoses are skyrocketing, after Mexican drug rings perfected a newer, cheap way to make methamphetamine without using pseudoephedrine at all. This actually effective drug still remains behind the counter, while ineffective ones fill the shelves.
Over the past eight months, I’ve spent a mind-boggling amount of time and money trying to keep an invisible poison at bay. It started at my daughter’s 12-month checkup, when her pediatrician told me she had a concerning amount of lead in her blood. The pediatrician explained that, at high levels, lead can irreversibly damage children’s nervous system, brain, and other organs, and that, at lower levels, it’s associated with learning disabilities, behavior problems, and other developmental delays. On the drive home, I looked at my baby in her car seat and cried.
The pediatrician told me that we needed to get my daughter’s lead level down. But when I began to try to find out where it was coming from, I learned that lead can be found in any number of places: baby food, house paint, breast milk, toys, cumin powder. And it’s potent. A small amount of lead dust—equal to one sweetener packet—would make an entire football field “hazardous” by the EPA’s standards.
My husband and I spent nearly $12,000 removing highly contaminated soil from our backyard, replacing old windows, and sealing an old claw-foot bathtub. We mopped the floors at night, obsessively washed our daughter’s hands, and made sure to feed her plenty of iron, calcium, and vitamin C, which are thought to help limit the body’s absorption of lead. Four months later, when we went back to the pediatrician, her lead levels had sunk from 3.9 micrograms per deciliter of blood to 2.2 mcg/dL. That was better, but still far from zero. And according to the CDC, the World Health Organization, and the Mayo Clinic, zero is the only safe amount of lead.
We’re one of thousands of families who have gone through that ordeal this year. At least 300,000 American children have blood lead levels above 3.5 mcg/dL, the CDC’s so-called reference value. But parents are largely left on their own to get lead out of their kids’ lives. Families who can afford an abundance of caution can sink tens of thousands of dollars into the project. And they still might never hit zero.
When Suz Garrett learned that her 1-year-old son, Orrin, had four micrograms of lead in every deciliter of his blood, she and her husband waited for guidance from their doctor or the county health department, but none came. So they sent Orrin to stay with family while they repainted their 19th-century Richmond, Virginia, house and covered the open soil with mulch. Band-Aids like these are cost-effective, but every time you pry open an old window, or your dog tracks in dirt from the neighbors’ yard, invisible specks of lead dust can build up again.
For nearly a year, the Garretts cleaned religiously. Orrin’s blood levels are still detectable—currently, he’s at 2.1 mcg/dL. Garrett and her husband are fed up. In a few months they’re moving to a new house, one they took out a $200,000 construction loan to renovate. “We ended up gutting it so we would know there’s no lead paint,” Garrett said.
A few years ago, children like Orrin Garrett and my daughter wouldn’t have been a cause for concern. Until 2012, children were identified as having a blood lead “level of concern” at 10 mcg/dL or more. But for the past decade, the CDC has used a reference value to identify children who have more lead in their blood than most others. The reference number is based on statistics, not health outcomes. When most children tested below 5 mcg/dL, the reference level was five. Today, it is 3.5.
The reference level has trended down along with lead exposure, which has dropped by 95 percent since the 1970s thanks to policies that removed lead from gasoline, paint, plumbing, and food. But confusion and concern about what classifies as lead poisoning has risen.
Scientists and public-health officials still can’t say exactly how low lead exposure needs to be to prevent damage for any individual child. When Kim Dietrich, an epidemiologist and a developmental neuropsychologist, started his career in the ’70s, the general consensus was that levels above 40 to 60 micrograms took a significant toll on the developing brain. But work by Dietrich and others showed that harm can be caused at much lower levels. In the early 2000s, pooled data from seven large studies from around the world, including one Dietrich conducted in Cincinnati, showed that an increase in children’s blood-lead concentration from 2.4 to just 10 mcg/dL corresponded with a four-point drop in their IQ. That’s a scary prospect. But, Dietrich told me, “it’s very important not to confuse findings from these large population-level studies with individual impacts.”
Discerning the effect of low lead levels—below about 10 mcg/dL—on cognitive health is an extremely complicated issue. “If you’ve got a blood alcohol content of 0.2, you’re likely to be horribly dangerous behind the wheel no matter who you are. Lead is a little bit different. Your child’s two might be worse than my child’s 10,” Gabriel Filippelli, a biogeochemist who studies lead exposure in urban environments, told me. Part of the variation in outcomes could be the result of factors we still don’t understand, like a child’sgenetic makeup.
Policing low levels of lead exposure in children costs parents both financially and emotionally. Mary Jean Brown, the former chief of the CDC’s Healthy Homes and Lead Poisoning Prevention Program, told me that concerned parents should be careful not to create a self-fulfilling prophecy. “Most children will not exhibit any symptoms when they have blood levels of 5 or 10 micrograms per deciliter,” she told me. But “if the mother or someone else says, ‘Johnny’s not like everybody else,’ pretty soon, Johnny isn’t like everybody else.”
This type of anxiety is familiar to Tanisha Bowman, a health-care worker in Pittsburgh who has spent nearly three years trying to lower her daughter’s blood lead levels. They initially peaked at 20 mcg/dL, and have ranged from two to six over the past year. “There was never anything wrong with her. She was always measuring four to six months ahead,” Bowman said. But it was impossible not to read scary headlines about lead and assume they applied to her daughter. When she had tantrums around the age of 2, Bowman started wondering if she had ADHD, which is sometimes associated with lead exposure. “I will never know what impact, if any, this had on her. And nobody will ever be able to tell me,” she said. (Bowman’s daughter has had no diagnosis related to lead.)
In the absence of a specific, outcome-based number to help parents decide when to worry, a mantra has emerged among doctors, reporters, and health institutions: There is no safe level of lead. Filippelli said that he’s used the catchphrase, but it’s a bit misleading. “There is no valid research source to support the ‘No amount of lead exposure is safe’ idea, beyond that fact that to avoid the potential of harm, you should avoid exposure,” he explained in an email.
As well intentioned as the guidance might be, avoiding all exposure is an impossible quest. Tricia Gasek, a mother of three who lives in New Jersey, tried desperately to locate the source of lead in her children’s blood. She spent $1,000 hiring a “lead detective” to test her home with an XRF device and getting consultations with experts, plus another $600 replacing leaded lights on the front door. Ultimately, she learned that she also had elevated levels and concluded that the lead in her son’s blood was coming from her breast milk—possibly, her doctors thought, from exposure she had as a child. The process was exhausting. “It’s just crazy. Why am I the one figuring all this out?” she says.
Parents simply can’t get to zero without help. Lead is invisible and pervasive. Although the Flint, Michigan, water crisis and recent product recalls have raised awareness about lead leaching from corroding pipes and hiding inside baby food, the biggest sources of exposure for children are the spaces where they live and play: inside houses and apartments with old, degrading paint and yards with contaminated soil. For many, there is no easy escape. Lead contamination is most common in low-income neighborhoods, which means Black and Hispanic kids are disproportionately affected.
Many local health departments, including the one where I live, offer home visits to help identify sources of lead, but in many cases only when levels are above 10 mcg/dL. So the majority of children with elevated lead levels receive little or no assistance at all, and families have to play detective, social worker, and home remodeler all at once.
This is paradoxical, because the problem of low-level lead exposure cannot be solved by focusing on one child or one home at a time. My family’s efforts helped lower our daughter’s lead levels slightly, but they did nothing to address the more widespread problem of lead in our neighborhood, to which she and all the other children nearby are still exposed. Instead of having every lead-exposed family play whack-a-mole in their own home, Filippelli says that if he were appointed czar of lead, he would do a national analysis of high-risk neighborhoods and households, perform targeted testing to confirm hazards, and remediate at scale. There would have to be coordination between the Department of Housing and Urban Development and the Environmental Protection Agency, and such programs could cost up to $1 trillion and take a decade. But, he says, we could significantly reduce lead exposure across the board. The trickle-down effects of half a million children becoming smarter, healthier adults would reach everyone, even if we can’t say exactly how much smarter or healthier they’d be.
For now, my family is still navigating this maze on our own. I’m trying to think of low-level lead exposure as a risk factor—like air pollution and forever chemicals—instead of a diagnosis. Meanwhile, my daughter is doing just fine. As a family, we’ll continue to avoid what lead we can; we’ve decided to spend a whopping $25,000 to repaint the chipping exterior of our house. But we’re still going to let our kid play at the park and climb the walls. After all, there’s no stopping her.
Fine, I’ll admit it! I am exhausted from watching heavy plots about murder mysteries and docudramas detailing scandals. I’ve had enough of watching all the bad in the world. And after a long day of work I’m in no mood to follow a plot-heavy show.
What I really want is to kick back, relax, and watch mindless entertainment. Thanks to the resurgence of Y2K fashion this year, I’ve been yearning to go back to my roots…I’m talking about the kind of trashy reality television that only the early 2000s could manifest.
There’s nothing more satisfying and utterly delicious than watching a group of people act like heathens in front of a camera just for the sake of good TV. In the early 2000s, if there was a camera, anyone would do anything to become famous.
They’d say anything, do anything, and manufacture dramatized situations simply for the sake of viewership. And we ate it up. And let’s be frank: they just don’t make them like they used to.
Compared to what we grew up with, the current slate of reality TV is lame. These days, people try their hand at earning fame through Instagram and TikTok. But in the heyday of reality TV, you had to get off your ass and work. Read: be on TV.
There was a plethora of shows to choose from. It wasn’t just The Kardashians and a smattering of overproduced beachside dating shows. There was Say Yes To The Dress, The Hills, My Super Sweet 16, Four Weddings, and more!
And yes, I’m a fan ofLove Island and Love is Blind, but they’re not the same. I miss following a bunch of rabid 20-somethings around who didn’t care how the public perceived them. Most reality TV contestants nowadays use their shows as a stepping stone into the Influencer World — boring. I miss when there were zero stakes.
The cast of Jersey Shore got into multiple fistfights every season. The children on My Super Sweet 16 were openly entitled and outwardly rude. Everyone in every show would say the most outrageous statements that you wouldn’t dare whisper on national television.
These days, it’s all about image. The Kardashians use their Hulu show to give you a look into their lives. But much of this promotes their brands and addresses scandals we’ve known about for months. And Love Island members were all fighting for a Princess Polly endorsement from day one.
Bring me back to the “anything goes” mentality of the early 2000s. I miss watching out-of-touch heiresses like Paris Hilton and Nicole Richie try out mundane, “poor” tasks like going to a grocery store or working in a restaurant. Take me back to the simpler times of The Simple Life.
My recent aching for this niche genre of reality cinema started when I stumbled across seasons 4 and 6 of My Super Sweet 16 on Hulu and was hooked. Then I turned to old episodes of Jersey Shore. Who knows what mind-numbing show is next?
And while I get my Sweet Sixteen fix on Paramount Plus, I am openly encouraging TLC and MTV to go back to producing raw reality television. I want the cast to not have any hopes or dreams for their careers and put their all into these shows.
There’s never a bad time to recap my favorite moments from the most iconic reality TV shows. So here we go:
Jersey Shore
Can we all just take a moment to remember the time Sam got mad at Ronnie for making fun of her Fred Flintstone big toe pic.twitter.com/5i1OB5PllS — realitytvshow (@bgcslave) August 20, 2018
When Ron and Sam got into a fight because Ron made fun of Sam’s big toe. Iconic, ridiculous, and just amazing.
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A decade into her optometry career, Marina Su began noticing something unusual about the kids in her New York City practice. More of them were requiring glasses, and at younger and younger ages. Many of these kids had parents who had perfect vision and who were baffled by the decline in their children’s eyesight. Frankly, Su couldn’t explain it either.
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In optometry school, she had been taught—as American textbooks had been teaching for decades—that nearsightedness, or myopia, is a genetic condition. Having one parent with myopia doubles the odds that a kid will need glasses. Having two parents with myopia quintuples them. Over the years, she did indeed diagnose lots of nearsighted kids with nearsighted parents. These parents, she told me, would sigh in recognition: Oh no, not them too. But something was changing. A generation of children was suddenly seeing worse than their parents. Su remembers asking herself, as she saw more and more young patients with bad eyesight that seemed to have come out of nowhere: “If it’s only genetics, then why are these kids also getting myopic?”
What she noticed in her New York office a few years ago has in fact been happening around the world. In East and Southeast Asia, where this shift is most dramatic, the proportion of teenagers and young adults with myopia has jumped from roughly a quarter to more than 80 percent in just over half a century. In China, myopia is so prevalent that it has become a national-security concern: The military is worried about recruiting enough sharp-eyed pilots from among the country’s 1.4 billion people. Recent pandemic lockdowns seem to have made eyesight among Chinese children even worse.
For years, many experts dismissed the rising myopia rates in Asia as an aberration. They argued that Asians are genetically predisposed to myopia and nitpicked the methodology of studies conducted there. But eventually the scope of the problem and the speed of change became impossible to deny.
In the U.S., 42 percent of 12-to-54-year-olds were nearsighted in the early 2000s—the last time a national survey of myopia was conducted—up from a quarter in the 1970s. Though more recent large-scale surveys are not available, when I asked eye doctors around the U.S. if they were seeing more nearsighted kids, the answers were: “Absolutely.” “Yes.” “No question about it.”
In Europe as well, young adults are more likely to need glasses for distance vision than their parents or grandparents are now. Some of the lowest rates of myopia are in developing countries in Africa and South America. But where Asia was once seen as an outlier, it’s now considered a harbinger. If current trends continue, one study estimates, half of the world’s population will be myopic by 2050.
The consequences of this trend are more dire than a surge in bespectacled kids. Nearsighted eyes become prone to serious problems like glaucoma and retinal detachment in middle age, conditions that can in turn cause permanent blindness. The risks start small but rise exponentially with higher prescriptions. The younger myopia starts, the worse the outlook. In 2019, the American Academy of Ophthalmology convened a task force to recognize myopia as an urgent global-health problem. As Michael Repka, an ophthalmology professor at Johns Hopkins University and the AAO’s medical director for government affairs, told me, “You’re trying to head off an epidemic of blindness that’s decades down the road.”
The cause of this remarkable deterioration in our vision may seem obvious: You need only look around to see countless kids absorbed in phones and tablets and laptops. And you wouldn’t be the first to conclude that staring at something inches from your face is bad for distance vision. Four centuries ago, the German astronomer Johannes Kepler blamed his own poor eyesight, in part, on all the hours he spent studying. Historically, British doctors have found myopia to be much more common among Oxford students than among military recruits, and in “more rigorous” town schools than in rural ones. A late-19th-century ophthalmology handbook even suggested treating myopia with a change of air and avoidance of all work with the eyes—“a sea voyage if possible.”
By the early 20th century, experts were coalescing around the idea that myopia was caused by “near work,” which might include reading and writing—or, these days, watching TV and scrolling through Instagram. In China, officials have become so alarmed that they’ve proposed large-scale social changes to curb myopia in children. Written exams are now limited before third grade, and video games are restricted. One elementary school reportedly installed metal bars on its desks to prevent kids from leaning in too close to their schoolwork.
Spend too much time scrutinizing text or images right in front of you, the logic goes, and your eyes become nearsighted. “Long ago, humans were hunters and gatherers,” says Liandra Jung, an optometrist in the Bay Area. We relied on our sharp distance vision to track prey and find ripe fruit. Now our modern lives are close-up and indoors. “To get food, we forage by getting Uber Eats.”
This is a pleasingly intuitive explanation, but it has been surprisingly difficult to prove. “For every study that shows an effect of near work on myopia, there’s another study that doesn’t,” says Thomas Aller, an optometrist in San Bruno, California. Adding up the number of hours spent in front of a book or screen does not seem to explain the onset or progression of nearsightedness.
A number of theories have rushed to fill this confusing vacuum. Maybe the data in the studies are wrong—participants didn’t record their hours of near work accurately. Maybe the total duration of near work is less important than whether it’s interrupted by short breaks. Maybe it’s not near work itself that ruins eyes but the fact that it deprives kids of time outdoors. Scientists who argue for the importance of the outdoors are further subdivided into two camps: those who believe that bright sunlight promotes proper eye growth versus those who believe that wide-open spaces do.
Something about modern life is destroying our ability to see far away, but what?
Asking this question will plunge you into a thicket of scientific rivalries—which is what happened when I asked Christine Wildsoet, an optometry professor at UC Berkeley, about the biological plausibility of these myopia theories. Over the course of two hours, she paused repeatedly to note that the next part was contentious. “I’m not sure which controversy we’re up to,” she said at one point. (It was No. 4, and there were still three more to come.) But, she also noted, these theories are essentially two sides of the same coin: Anyone who does too much near work is also not spending much time outside. Whichever theory is true, you can draw the same practical conclusion about what’s best for kids’ vision: less time hunched over screens, more time on outdoor activities.
By now, scientists have moved past the faulty assumption that myopia is purely genetic. That idea took hold in the ’60s, when studies of twins showed that identical twins had more similar patterns of myopia than fraternal ones, and persisted in the academic world for decades. DNA does indeed play a role in myopia, but the tricky factor here is that identical twins don’t just share the same genes; they’re exposed to many of the same environmental stimuli, too.
Glasses, contacts, and laser surgery all help nearsighted people see better. But none of these fixes corrects the underlying anatomical problem of myopia. Whereas a healthy eye is shaped almost like an orb, a nearsighted one is more like an olive. To slow the progression of myopia, we would have to stop the elongation of the eyeball.
Which we already know how to do. Treatments to slow the progression of myopia—called “myopia control” or “myopia management”—exist. They’re just not widely known in America.
Over the past two decades, eye doctors—mostly in Asia—have discovered that special lenses and eye drops can slow the progression of nearsightedness in children. Maria Liu, a myopia researcher who grew up in Beijing, told me that she first became interested in nearsightedness as a teenager, when she began watching classmates at her school for gifted children get glasses one by one. In this intensely competitive academic environment, she remembers spending the hours of 6:30 a.m. to 10 p.m. on schoolwork, virtually all indoors. By the time she finished university, nearly all of her fellow students needed glasses, and she did too.
Years later, when she started an ophthalmology residency in China, she met many young patients who wore orthokeratology lenses—also known as OrthoK—a type of overnight contact lens that temporarily alters the way light enters the eye by reshaping the clear front layer of the eyeball, thus improving vision during the day. Liu noticed, anecdotally, that those who wore OrthoK seemed to have better vision down the line than those who wore glasses. Could long-term use of the lenses somehow prevent elongation of the eye, thus impeding myopia’s progression? It turns out that other scientists and doctors across Asia were noticing the same trend. In 2004, a randomized controlled study in Hong Kong of OrthoK confirmed Liu’s hunch.
By then, Liu had moved to the U.S., and she soon began a doctoral program in vision science at Berkeley to study myopia. Her classmates, she recalls, were tackling exotic-sounding topics such as gene therapy and retinal transplants and wondered why she was studying “something that’s so boring.” She ended up working in Wildsoet’s lab, researching the development of myopia in young chick eyes.
In humans, the majority of babies are born farsighted. Our eyes start slightly too short, and they grow in childhood to the right length, then stop. This process has been finely calibrated over millions of years of evolution. But when the environmental signals don’t match what the eye has evolved to expect—whether that’s due to too much near work, not enough outdoor time, some combination of the two, or another factor—the eye just keeps growing. This process is irreversible. “You can’t make a longer eyeball shorter,” Liu said. But you can interrupt growth by counteracting these faulty signals, which is what myopia control is designed to do.
When Liu became a professor at Berkeley after receiving her Ph.D., she started envisioning a myopia-control clinic—the first of its kind in the U.S.—that could bridge the gap between research and practice. By then, she knew that many doctors in China were already successfully using OrthoK for myopia control.
Photo-illustration by Vanessa Saba. Sources: Nick Dolding / Getty; Tina Caunt / EyeEm / Getty.
The school administration was skeptical. Liu says that the clinical director didn’t see how the clinic would benefit optometry students, or how it could attract enough patients to be worthwhile financially. But in 2013, Liu started it anyway, as a one-woman operation. She began seeing patients on Sundays in borrowed exam rooms with no extra pay and without relinquishing any of her teaching or clinical duties. Within months, her schedule was full. The Berkeley Myopia Control Clinic now runs four days a week and has 1,000 active patients—some of whom drive hours through Bay Area traffic to get there. Liu was one of the only people at the school who anticipated the clinic’s massive success. Jung, who is also an assistant clinical professor at Berkeley, told me that Liu’s knowledge of the latest myopia-control treatments made it feel like she came “from the future.”
When I arrived at the clinic at 8 a.m. on a Saturday morning this past spring—an hour at which the rest of the campus was still quiet—it was already filling up with optometry students and residents who work there as part of their training. Liu, who is petite with neat, wavy hair, moved through the clinic with frightful efficiency. One moment she was examining eyes, the next talking down a parent whose son’s contact-lens shipment had gone missing, the next warning staffers about a malfunctioning printer.
The clinic offers three different treatments: OrthoK, multifocal soft contact lenses, and atropine eye drops. The first two both work by tweaking how light enters the eye, producing a signal for the eyeball to stop lengthening. Atropine, in contrast, is a drug that seems to chemically alter the growth pathway of the eye when used at low doses. (It also dilates the pupil; Cleopatra reportedly used it to make her eyes more beautiful.) These treatments slow myopia progression on average by about 50 percent. The original clinical trials validating them were mostly conducted in Asia starting in the mid-2000s. And the American Optometric Association’s evidence-based committee published a report advising its members on how to use myopia control last year. Until quite recently, though, none of these treatments had been approved by the FDA for myopia control. Any optometrists who wanted to offer them had to go off label. And any patient who wanted to use them had to find the right doctor.
It’s not a coincidence that Liu’s clinic found early success in the Bay Area, which has a large Asian population. Eye doctors I spoke with in multiple cities across the U.S. said it was usually Asian parents who came in asking for myopia control. The parents I met at the clinic skewed Asian and, on that Saturday, particularly Chinese—first-generation immigrants who speak Mandarin seek Liu out on the days she is personally in the clinic. Many of them heard about myopia control from fellow immigrants or friends in Asia. George Tsai, whose 8-year-old son was at the clinic for an OrthoK appointment, told me that his wife, who grew up in China, had learned of myopia control through WeChat, the messaging app popular in the country and among the Chinese diaspora.
Liu has a second phone, which she uses to manage three WeChat groups full of parents with kids in myopia control across North America. The questions flood in day and night. “First thing in the morning, I look at this WeChat group. Who has lost a lens? Who has red eyes? Who has other problems?” she said. “And again, before I go to bed.” She started the first group with a parent of one of her patients. When it hit the maximum number of members allowed on WeChat, they created a second, and then a third. The groups now contain a total of 1,500 parents.
In general, Liu told me, Asian parents tend to be a lot more motivated because myopia “is much better perceived or accepted as a disease in Asian culture.” I know this firsthand, as the child of Chinese immigrants. Distressed about my worsening vision in elementary school, my mother would regularly admonish me, standing my pencil case upright to measure the distance between my head and my desk. She also made me do eye exercises developed in China, which I was vindicated to finally learn, in the course of reporting this story, do not work. This was the late ’90s, when there really was nothing to be done about myopia progression. But in the parents I met at the Berkeley clinic, I saw the same determination I once saw in my own. They had uprooted their lives and come to a foreign country and now here they were, hoping to bestow upon their kids any advantage, any edge that modern science could give.
There is another reason that the Bay Area, with its high median income, has been fertile ground for myopia control: The treatments are expensive. Many of the parents I met at the clinic were engineers or doctors. At Berkeley, OrthoK costs more than $450 for one pair of lenses, plus $1,600 for the initial fitting, not including the fees for several follow-up appointments a year. Soft contact lenses can run from several hundred to more than $1,000 a year. And a year’s supply of atropine eye drops costs hundreds of dollars. Kids are typically in myopia control until their mid-teens to early 20s. Vision insurance does not cover any of these treatments.
Multinational eye-care companies now see myopia control as a hot potential market. They’re vying for FDA approval of new lenses and improved formulations of atropine, which can be patented rather than sold as a cheaper generic. The business case is obvious: If half of the world is myopic by 2050, that’s a huge pool of would-be customers. “How often do you have an opportunity to have an impact on a condition that will affect one out of two people? There’s nothing else on the planet that I’m aware of,” says Joe Rappon, the former chief medical officer of SightGlass Vision, a small California company whose myopia-control technology was jointly acquired by the eye-care giants CooperVision and Essilor.
In November 2019, the FDA green-lighted the first—and currently only—treatment specifically designed to slow the progression of myopia in the U.S., a soft contact lens from CooperVision called MiSight. Many more treatments, though, are in trials in the U.S., including several types of spectacles that tweak the way light enters the eye in order to slow its growth. Some are already on the market in Europe and Canada.
Once those glasses get approved in the U.S., “that’s going to open the floodgates of myopia management,” Barry Eiden, an optometrist in Deerfield, Illinois, told me. The earlier you can start slowing myopia progression in kids, the better the outcome, he explained, but parents sometimes balk at the idea of putting drugs or contacts into the eyes of their young children. They don’t have the same problem with glasses.
In the future, Liu told me, she hopes FDA approvals will spur vision insurance to cover myopia control at least partially, making the treatments affordable to more parents. Meanwhile, CooperVision has already revved up its MiSight marketing machine. It’s targeting exactly the parents you would expect: In my own Brooklyn neighborhood of Park Slope, where you regularly see toddlers in $1,000-plus Uppababy strollers, an optometry shop recently hung a big banner advertising MiSight with two smiling kids. An optometrist in downtown San Francisco told me that parents who have seen MiSight’s ads are now coming into her office asking for it by name. The word-of-mouth era of myopia control is ending; the mass-advertising era is beginning.
Within the optometry business, myopia control often gets compared to braces—another treatment for which middle- and upper-class parents who want the best for their kids will dutifully shell out thousands of dollars. This comparison feels apt in a different way, too. Braces are also a modern solution to a relatively modern affliction. The teeth of cavemen, anthropologists have marveled, were incredibly straight. Crooked teeth appear in the archaeological record only when our ancestors transitioned from chewing raw meat and vegetables to eating cooked and processed grains. Our jaws are now smaller and weaker from disuse, our teeth more crowded and crooked. Today, braces are the way we retrofit our ill-adapted bodies for contemporary life.
We may not know exactly how ogling screens all day and spending so much time indoors are affecting us, or which is doing more damage, but we do know that myopia is a clear consequence of living at odds with our biology. The optometrists I spoke with all said they try to push better vision habits, such as limiting screen time and playing outside. But this only goes so far. Today, taking a phone away from a teenager may be no more practical than feeding a toddler a raw hunter-gatherer diet.
So this is where we’ve ended up, for those of us who can even afford it: adding chemicals and putting pieces of plastic in our eyes every day, in hopes of tricking them back to their natural state.
This article appears in the October 2022 print edition with the headline “The Myopia Generation.”
