There are few news subjects more reliably depressing than nutritional science. 

A glance at the headlines will tell you that sugar is bad for you, red meat is bad for you, and alcohol is really, really bad for you. The message seems to be that if a food or drink gives you even an iota of pleasure, it’s almost certain that your body will pay for it, sooner or later.

But there is one exception, a glorious concoction that was first consumed in ninth-century Ethiopia, that fueled the Age of Enlightenment, that has kept our troops going from the Revolutionary War to today. It is one of the first globally traded commodities, connecting producers in Africa, South America, and Southeast Asia to consumers around the world in a $245 billion market. It can be had flat or steamed, long or short, hot or iced, black or with milk, and in any number of combinations that end in the letters “-cino.” 

However you take it, the equivalent of more than 2 billion cups of it are consumed every day. Unlike so many other products we experience in our daily lives, it’s actually been getting better and better. And medical science is increasingly finding that all those cups are actually good for us.

I’m referring, of course, to the daily miracle that is coffee. Our grandparents were told to cut back on this dirty-tasting beverage but today, it has become one of the most studied and virtuous and quietly luxurious parts of the human diet. All in all, coffee — yes, coffee — is one of the best reasons to be alive in the year 2026.

Coffee and cigarettes

A generation ago, coffee was supposed to be something you quit, like cigarettes or that second martini. Doctors would warn pregnant women against drinking it; cardiologists would tell their middle-aged patients to give it up. The World Health Organization’s International Research Agency for Cancer kept it on its “possibly carcinogenic” list for 25 years, only downgrading it in 2016 after a review of the evidence found no clear link. 

Why exactly was something as seemingly innocuous as coffee considered a real health threat for so long? Coffee contains caffeine (yes, even decaf in small amounts), caffeine is a stimulant, and stimulants can have an impact on heart health. There were 20th-century studies that linked coffee consumption to pancreatic cancer, bladder cancer, and even birth defects. None of those studies have held up to scrutiny, however, and the reason why is a classic bugaboo of medical research: confounding factors. 

For much of the 20th century, coffee went with cigarettes like peanut butter goes with jelly — except, in this case, peanut butter is largely innocuous, while jelly is actively trying to murder you. Based on data collected between 1976 and 1980, heavy coffee drinkers in the US were six to seven times more likely to be smokers than non-coffee drinkers. All that smoking among coffee drinkers in the past meant they were more likely to suffer heart disease or cancer or any other health threat that cigarettes are connected to, and that showed up in the studies. But it wasn’t the cup of coffee that was doing the damage. It was the cigarette they were smoking alongside it. 

As smoking collapsed, a new generation of better-designed studies took a clearer view of coffee’s health effects. Major prospective cohort studies followed enormous populations for decades, with smoking properly accounted for, and looked at coffee consumption against outcomes ranging from dementia to liver cancer to all-cause mortality. The results were almost embarrassingly consistent in coffee’s favor. The recently released USDA Dietary Guidelines officially classify unsweetened coffee as “healthy,” and consumption of up to roughly four cups a day is considered safe for most adults. Even pregnant women can enjoy a cup or two a day.

So that’s the baseline: Coffee will not kill you. But more recent research suggests coffee is more than simply benign. It’s something that can actively benefit your health in numerous ways.

It’s good for you. Really.

The study arrived in JAMA in March, and I read it with a cup of joe close by. Researchers at Mass General Brigham, Harvard, and the Broad Institute had been following 131,821 American doctors and nurses for 43 years (possibly the longest single piece of evidence we will ever get on a daily dietary habit and a chronic disease), and by the end of the study, 11,033 had developed dementia. But the participants who drank two to three cups of caffeinated coffee a day were 18 percent less likely to be among them. A separate Cleveland Clinic analysis tied the effect specifically to caffeinated coffee. Nature described the relationship in coffee drinkers as “slower brain aging.”

That study didn’t appear out of nowhere. It joins a five-year run in which essentially every major endpoint in coffee research has come back in favor of the bean.

A 2019 meta-analysis in the European Journal of Epidemiology covering 40 cohort studies and millions of participants found the lowest all-cause mortality risk at intakes of about 3.5 cups a day, and a 2025 analysis confirmed it in US adults. A meta-analysis of 30 prospective studies covering 1.18 million participants found a 29 percent reduction in diabetes risk at the highest intake category, with risk dropping by 6 percent with each additional daily cup. Both caffeinated and decaffeinated coffee delivered protection, which points to chlorogenic acid and other polyphenols, rather than caffeine, as the active mechanism. Just keep it black — add sugar or artificial sweeteners and the benefit largely disappears.

The liver may be the single organ that benefits most. A PLOS One meta-analysis found 39 percent lower odds of cirrhosis among coffee drinkers; a Wiley analysis found a 44 percent reduction in liver-cancer risk for those drinking two or more cups daily. The protective effect extends to fatty liver disease and viral hepatitis. Coffee is, plausibly, doing something for liver health that no medication does at population scale.

So what’s actually happening at the biological level? Coffee is the largest single source of polyphenols and antioxidants in the average Western diet, and its main bioactive compound, chlorogenic acid, suppresses several pro-inflammatory pathways while raising the body’s antioxidant defenses. While caffeine may be the reason most of us turn to coffee in the bleary morning hours, it’s the biochemistry running alongside it that is doing most of the medical work. The coffee mug is, in plain pharmacological terms, a delivery system for some of the most well-studied anti-inflammatory compounds humans have ever measured. 

Plus, it’s really good. 

How coffee got better

It wasn’t always, though. For most of the 20th century, Americans subsisted on canned, pre-ground, vacuum-packed grocery-store coffee like Folgers or Maxwell House. Worse, by the 1970s, almost a third of all coffee imported into the US was being turned — nay, perverted — into instant, like Sanka or Folgers Crystals. 

Perhaps not surprisingly, per-capita coffee consumption in the US fell almost continuously from a 1946 peak through the early 1990s. It wasn’t until the coming of Starbucks — now reviled as a harbinger of gentrification — that Americans showed that they would pay more for coffee that didn’t taste as if it had been strained through a gym sock. 

Then in the 2000s came specialty roasters such as Blue Bottle, Stumptown, Intelligentsia, Counter Culture, and Verve, which treated coffee the way good wineries treat wine — single origin, single farm, traceable lots, careful roast profiles, brewing methods tuned to the specific bean. The Specialty Coffee Association developed the cupping protocol and the 100-point scoring system that gave coffees an objective quality scale. 

And guess what? As the coffee got better, we drank more of it. In 2024 the National Coffee Association reported that 45 percent of US adults had drunk speciality coffee in the past day, up around 80 percent since 2011 and surpassing conventional coffee consumption for the first time. Globally, the speciality coffee market hit $111.5 billion in 2025, while the number of specialty coffee shops in the US grew 21 percent between 2017 and 2022. Which means that one, a cafe probably opened up down the street from you while you were reading this, and two, there’s no excuse now for bad coffee.

A cup of progress

Coffee isn’t a cure-all, even if it can sometimes feel that way at 7 am on a Monday. Caffeine has a half-life of five to six hours in most adults, so drinking after 2 pm can mess with your sleep, which in turn can negate many of the health benefits of consumption. That’s one reason why a 2025 analysis found that while morning-only coffee drinkers were 16 percent less likely to die of any cause than non-drinkers, that benefit largely disappeared for all-day drinkers. For much the same reason, overconsumption — more than four cups or so in a day — can lead to anxiety, headaches, and worse heart health. Regularly adding sugar or milk will dilute or eliminate those benefits as well. 

There’s also reason to fear for the future of coffee. Coffee beans are sensitive souls, and climate change risks upsetting the very specific environments needed to make a decent cup. A 2026 review by the agricultural lender Rabobank projected that 20 percent of currently cultivated land for arabica beans may become unsuitable by 2050, while devastating coffee leaf rust outbreaks in Central America are projected to worsen as temperature ranges expand the fungus’s range upward. Some regions like Ethiopia may actually become more hospitable with warming, but if saving the world isn’t a good enough reason to support climate action, maybe saving your cuppa will be.

The more we learn about the things we eat and drink, it seems the more we have to worry about. But coffee is the exception. Its nutritional profile has improved under rigorous examination, just as its taste profile has improved under ever greater specialization and globalization. You’re not just drinking coffee every morning. You’re drinking a cup of progress.

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In a lab room, a toddler, deaf from birth, sits while a tone plays. There’s no reaction. His face does not change. 

Six weeks later, after a single injection of an experimental gene therapy, the same toddler is back in the same room. The tone plays. The toddler’s head turns toward the sound. And somewhere just off screen, the child’s grandfather says his name. The boy turns and looks. He can hear.

“When the parents realized their child had a response to sound they cried,” says Dr. Yilai Shu of the Eye & ENT Hospital of Fudan University, who co-led the trial, in a video that showed the results. “The whole family cried.” The video cuts to another child, thirteen weeks post-treatment, dancing to music.

This is what gene therapy can do in 2026. The clip comes from the international clinical trial of an OTOF gene therapy run by Mass Eye and Ear and China’s Fudan University that provided the underlying science behind a drug the Food and Drug Administration (FDA) approved last week.

On April 23, the FDA granted accelerated approval to Otarmeni, a gene therapy from the pharma company Regeneron for severe-to-profound hearing loss caused by mutations in a gene called OTOF. In a pivotal trial, 80 percent of treated patients gained measurable hearing, and 42 percent reached the level needed to pick up whispers. Two and a half years after treatment, 90 percent of patients in the underlying multi-center trial were still hearing.

It’s a drug that certainly feels like a miracle to those in the trials, taking patients from silence to sound. But what can feel almost as miraculous is how far the broader field of gene therapies like Otarmeni — which deliver a working copy of a broken gene directly into a patient’s cells — have come.

In 1999, the nascent field of gene therapy all but collapsed when a teenager named Jesse Gelsinger died four days after being injected with an experimental gene therapy at the University of Pennsylvania, the first publicly identified death in a gene therapy clinical trial. In the years that followed, funding evaporated, careers ended, and “gene therapy” became a cautionary tale.

It took years and major changes in how gene therapies are delivered for the field to recover. And now, 27 years after Gelsinger’s tragic death, we have a gene therapy that can effectively reverse some kinds of congenital hearing loss. The next decade is no longer about whether gene therapy can deliver clinical results. It’s about whether it can deliver results to enough patients, at prices people can actually pay, for diseases that affect more than a few hundred kids a year. 

Get those answers right, and what feels like a miracle to some in 2026 could become ordinary medicine.

Back from the brink

After Gelsinger died, the FDA halted gene therapy trials in the US, the National Institutes of Health tightened oversight, and the principal investigator of the Penn study — James Wilson — was barred from clinical trials for five years and stripped of his administrative titles. In the lean years that followed, two things happened.

The first was a change in delivery. Gene therapies use engineered viruses to deliver restorative genes to a patient’s cells. The therapy used on Gelsinger was carried by an adenovirus, which are highly immunogenic, meaning the human immune system recognizes them and reacts violently. It was that immune reaction that killed Gelsinger. 

In the aftermath, the field increasingly turned to adeno-associated viruses (AAV), which are smaller, more tolerable, and capable of slipping a payload into the right cells without setting off a five-alarm immune reaction. AAV vectors are now the workhorse of in vivo gene therapy, including in Otarmeni.

The second thing that happened was CRISPR. Adapted in 2012 by Jennifer Doudna and Emmanuelle Charpentier into a precision gene-editing tool, CRISPR could do something AAV could not: find a specific spot in the patient’s own DNA and rewrite the letters there, correcting the broken gene in place. CRISPR also earned gene therapy a cultural moment it hadn’t had since before Gelsinger. Money and talent flooded back into the field — including into the AAV programs that produced Otarmeni.

Disease by disease

The clearest sign something has shifted in the field is the lengthening list of therapy approvals. In December 2017, the FDA cleared Luxturna for hereditary blindness from RPE65 mutations — the first gene therapy in the US for an inherited disease. Two years later, Zolgensma was approved for spinal muscular atrophy, a wasting disease that kills children before age two in its severe form. In 2022, Hemgenix made hemophilia B the first bleeding disorder with a one-shot fix. In 2023, Casgevy and Lyfgenia did the same for sickle cell, with Casegevy becoming the first FDA-approved CRISPR therapy.

The sickle cell approvals matter most because they are the first for a patient population that is large; 100,000 Americans suffer from it — mostly Black, and historically underserved. The gene therapies are also proof of concept that the underlying CRISPR mechanism can be redirected at multiple different targets. Verve Therapeutics is using base editing to permanently disable PCSK9, a gene that controls how much LDL cholesterol stays in the bloodstream, with the promise of one-time treatment instead of daily statins for patients at high cardiovascular risk. Early trial data showed a 53 percent average drop in LDL cholesterol. Trials are open for additional hereditary-blindness genes, Pompe disease, and a long list of single-gene conditions. 

The cost of magic

The science is working, but paying for it is another matter.

These are the list prices for the recent approvals: Luxturna at $850,000 per patient, Zolgensma at $2.13 million, Casgevy at $2.2 million, Lyfgenia at $3.1 million, Hemgenix at $3.5 million. Two-thirds of US sickle cell patients are on Medicaid, and only 16,000 are eligible for Casgevy under the current label. Regeneron has pledged to provide Otarmeni for free in the US, but that works only because the OTOF patient pool is small — an estimated 50 babies a year. That math won’t work for more common disorders.

While cost may not be a problem for the families that could qualify for Otarmeni, it’s not the only concern. Cochlear implants, the standard treatment for OTOF patients for decades, have been contested within Deaf culture since the 1980s, with many arguing that deafness should be seen as identity rather than deficit. Gene therapy applied to infants makes that question all the more fraught, since the children treated with gene therapy cannot consent to the change. And not everyone would make that choice.

Beyond economic and cultural questions, we lack gene therapy for Alzheimer’s, schizophrenia, or any of the polygenic — meaning, caused by multiple genes — conditions that cause massive amounts of suffering. The cochlear is a good gene-therapy target because it is small and accessible, and OTOF is a single-gene disorder. The brain and Alzheimer’s are neither of those things. The platform that is working in one child’s inner ear in 2026 is not about to deliver universal cures by 2030, or well beyond.

What gene therapies will do, however, is keep filling in the list. The next time a parent gets a rare-disease diagnosis for their child, the question will increasingly be not whether someone is working on a gene therapy, but how soon it will be ready.

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Devon Fritz had his midlife crisis a little early. 

He spent his 20s writing tax software, staying on track to hit all the life targets he’d set for himself: house, kids, financial security. And then, one day, he did the math and projected forward what the next 20 years of his life would look like. But instead of relief, “I had this weird feeling that I’d totally missed the target,” he told me recently. 

“I looked around at my colleagues, who kind of felt stuck in this place,” he said. “They had gotten to this cushy job where things were good, pay was good, benefits were good, but nobody seemed happy.”

This might sound familiar. Who among us hasn’t had the occasional crisis of meaning, perhaps mentally scored to the Talking Heads’ “Once in a Lifetime”? (The last part might just be me.) But most of us shake off those existential doubts and press on, for better or for worse. 

Devon Fritz, however, is not like you or me. Searching for a more meaningful life and career, he tried volunteering with refugee-aid groups in Germany during the 2015 migrant crisis — only to be discouraged by how slow, unresponsive, and ineffective he found the nonprofit world. 

Eventually, at a conference in Oxford, England, he discovered effective altruism, or EA. EA is built on the idea that we should use rigorous evidence and cost-benefit analysis to do the most good possible, very much including how we donate to charity. A dollar to one organization might save a life; a dollar to another might buy a commemorative tote bag. EA takes that gap in impact seriously and follows the math wherever it leads, always searching for the donation or the act that can create the most measurable positive impact, especially in terms of lives saved. 

The idea clicked with Fritz, and over the next several years, he rebuilt his career around a single, very EA-inflected question: How can you build a career that really matters? The result is his book The High-Impact Professional’s Playbook, the manual Fritz says he wished he’d had during his early existential crisis. The book lays out concrete paths through which a person with a regular job can actually create outsized positive impact on the world. 

What follows are five of the most useful ideas from it. And while Fritz’s framework comes out of effective altruism — which, with all its hyper-rationality, can sometimes seem cold or weird to outsiders — he argues that the lessons have value for everyone.

“Being impactful — in its best form — doesn’t tell you what to do,” he told me. “It just says do stuff. Figure out what’s good, and do something that’s really good.” 

Next best may be better than best

The intellectual spine of Fritz’s book is a concept called “counterfactuality,” which, I’ll admit, may make you want to stop reading now. But while it’s a 22-point word in Scrabble, counterfactuality is actually pretty simple. For any action meant to do good, ask yourself: What would have happened if I hadn’t done it? If the honest answer is “basically the same thing,” your actual impact is smaller than you think.

Haindavi Kandarpa, one of the case studies in Fritz’s book, was at Boston Consulting Group working on public health and education projects in India and Bangladesh. That sounds both important and good, but when Kandarpa asked the counterfactual question about her own role, the answer was devastating: Nothing would really change. If she wasn’t doing it, someone equally competent would have taken her slot and done roughly the same work. That realization led her to leave for a charity startup incubator.

A lot of the standard advice about doing good falters when faced with the counterfactual. If 500 people apply for a job at an elite nonprofit and one gets it, the actual impact of the hire is the often-small gap between them and the closet runner-up. Fritz’s paradoxical conclusion is that you can have more counterfactual impact in obscure places nobody is looking — like the charity ranked fifth on the effectiveness list, not first. That can be hard to hear, especially for high performers used to competing for every top prize, but the status hit is worth it for the sake of actually making a difference.

It’s not just what you do — it’s what you do with your money

Unless you’re a full-time volunteer or are extremely bad at salary negotiation, you get money for your work. And what you do with that money can be just as impactful as what you did to get it.

According to a 2024 GiveWell analysis cited in his book, you can statistically save one human life if you give just $3,000 — provided it’s to the most effective charity. Switching just 10 percent of your charitable giving from a typical charity to an evidence-backed one can help up to 100 times more people or animals, all for the same cost. That is a life-saving impact.

This is the move with the lowest barrier to entry in the entire book, and the one most influenced by effective altruism. You don’t have to quit your job, move countries, or learn a new skillset. You keep doing what you’re doing but write the check — or, better, set up a recurring transfer — to an organization on a credible evaluator’s list. (GiveWell is a great place to begin.) You can start at 1 percent of income and see how it feels.

Your workplace is a lever

Most people don’t think of their workplace as something they can change. But if you have any influence over procurement, hiring, 401(k) match programs, charitable giving policies, or the company’s public positions, you have access to budgets and decisions that could dwarf what you can do on your own. 

A mid-level manager who convinces their company to enroll in a workplace-giving program that defaults to effective charities can route more money in a single policy change than they could personally donate over a decade.

Nonprofits desperately need people who know how things work

The most consistently surprising path in Fritz’s book is trusteeship and advisory work. Charities and NGOs are often filled with well-meaning people who desperately want to do good, Fritz told me, but “they don’t have anybody even thinking” about quotidian details like finance. Luciana Vilar, another case study in the book, spent years in corporate finance before joining two nonprofit boards and was routinely the only person in the room who knew how to build a real budget.

If you are a competent finance person, lawyer, HR professional, or operations manager — which includes basically anyone who has worked inside a functioning company — you probably have skills that even well-funded nonprofits are desperate for. Giving few hours of your week to board or advisory time can unlock capacity an organization can’t buy, and it doesn’t require a career switch.

Your network has more leverage than you think

Fritz’s most striking claim is that the most time-efficient path to making a difference isn’t your career or your donations; it’s the people you already know. 

If an effective but under-resourced charity is trying to fill a role, and you spend an hour emailing the five people in your network who’d be a good fit, and one gets hired, the counterfactual math of what you’ve done is absurdly high. And it didn’t require you to change jobs or write a check. All you had to do was send some emails. 

It’s the path Fritz himself has taken, starting High Impact Professionals, which has placed dozens of mid-career people into higher-impact roles, all while rigorously measuring its own counterfactual impact. (When a candidate in the network takes a job, they ask the employer how good the next-best candidate was. When it’s very close, they count less impact.)

The same network effects can work with donations. Fritz describes people raising $1,000 or more by posting on social media a few weeks before their birthday, asking friends to donate to an effective charity instead of sending a gift. A lot of “how can I make a difference” agonizing is really about not wanting to look at the lever that’s already in your hand.

I’ve talked to enough people lately, including myself in the mirror, to know that low-grade despair is becoming our default setting. The problems of the world feel too large, individual action feels too small, and it can feel like the honest move is to just tend your garden. But when I pushed Fritz on this, he gave me an answer I keep coming back to. “There are big problems,” he acknowledged. “But that means it’s a great time to jump in and try to solve them.” 

That can sound naive — but it’s also right. A world without problems wouldn’t need any of us. The world we actually have needs all the help it can get, and the bar for being useful in it is lower than we think.

This story was originally published in The Highlight, Vox’s member-exclusive magazine. To get access to member-exclusive stories every month, become a Vox Member today.

When the Swedish botanist Carl Linnaeus published Systema Naturae in 1735, he set out to classify every living thing on Earth — inventing the naming system we still use today and personally describing more than 10,000 species of plants and animals. 

Nearly three centuries later, with satellites mapping every continent and AI models that can identify a bird by its song, you might assume we’d pretty much finished the job Linnaeus started. We’ve been to the bottom of the ocean. We’ve sequenced the human genome. Surely we’ve cataloged our roommates on this planet.

We have not. Not even close. Scientists estimate we’ve identified somewhere around one-tenth of all species on Earth — meaning for every species with a name, roughly nine more are waiting in an unsampled river or an unexplored cave.

Or even a museum drawer where they’ve been gathering dust for decades. Hundreds of thousands of unnamed species are already sitting in museum and herbarium collections right now. A quarter of new species descriptions involve specimens more than 50 years old. As the University of Arizona ecologist John Wiens put it: “It’s a poorly known planet that we live on.”

And now many of that planet’s residents are in trouble. The Intergovernmental Science-Policy Platform on Biodiversity and Ecosystem Services (IPBES) estimates that around 1 million animal and plant species are threatened with extinction, and that extinction rates are at least tens to hundreds of times higher than the background norm. The current extinction rate is somewhere between 100 and 1,000 times the “natural” rate, and the species vanishing fastest are disproportionately the ones we haven’t catalogued yet: small invertebrates, tropical fungi, deep-sea organisms in habitats we’ve barely surveyed. The race to describe what’s out there has real stakes. You can’t protect what you haven’t found.

So here’s the good news: When it comes to the species on Earth, we’re not actually falling behind. We’re speeding up.

A study published in December in Science Advances by Wiens and colleagues analyzed 1.9 million species from the Catalogue of Life and found that between 2015 and 2020, scientists described more than 16,000 new species per year — the highest rate in the 270-year history of modern taxonomy. Wiens argues that 15 percent of every species known to science has been discovered in just the past two decades.

This was supposed to be going the other direction. Earlier research had suggested that the rate of species description peaked around 1900, back when naturalists in pith helmets were tramping through the tropics and shipping specimens back to European museums in wooden crates. The assumption was that the easy discoveries had been made, and we were in the long tail of diminishing returns. 

Wiens’s data says otherwise. “Some scientists have suggested that the pace of new species descriptions has slowed down and that this indicates we are running out of new species to discover,” he told ScienceDaily. “But our results show the opposite.”

How we got faster

The biggest driver is the DNA revolution. Genome sequencing costs have plummeted from $95 million per human genome in 2001 to hundreds of dollars by the early 2020s — dropping faster than Moore’s Law for long stretches of time. That cost drop has made DNA barcoding cheap enough for widespread use, allowing researchers to distinguish species that look identical to the naked eye but are genetically distinct.

A technique called environmental DNA (eDNA) now lets scientists detect species from trace genetic material — a bit of shed skin in a river, cellular fragments in a soil sample. A single water sample can reveal dozens of species, including rare ones that traditional surveys would miss entirely. In 2025, researchers analyzing archived aerosol filters reconstructed biodiversity data for more than 2,700 genera from airborne eDNA collected over 34 years.

Then there’s the citizen science explosion. iNaturalist, founded in 2008, has passed 200 million verifiable observations — doubling from 100 million in about two years. Over 4 million people around the world are now photographing and uploading every spider, mushroom, and wildflower they encounter, and AI-assisted identification helps sort the results. 

In 2023, two Australian citizen scientists helped discover Inimia nat, an entirely new genus of mantis — the first of its subfamily named since before the moon landing. (The “I. nat” is a nod to the platform.) In Brisbane, a group of young students discovered a fly species previously undetected in Australia and won a Eureka Prize for it. 

And finally, we started looking where we’d never looked. The Ocean Census, a 10-year initiative launched in 2023, has identified 866 likely new marine species across 10 expeditions. A single month-long Schmidt Ocean Institute expedition off the coast of Chile may have turned up more than 100 new species: corals, glass sponges, squat lobsters. (Some estimates find only about 10 percent of marine species have been described, which makes the ocean less a frontier than an entire undiscovered country.) 

In Laos, a zipline tour guide spotted what turned out to be a new dragon lizard genus. In Japan, an undergraduate named Yoshiki Ochiai found a new man-o’-war species on Gamo Beach — a popular surf spot in Sendai — and brought the creature to the lab in a plastic bag. 

And sometimes, we can even find species we’d thought had already gone extinct Attenborough’s long-beaked echidna, one of only five living egg-laying mammals, was rediscovered in 2023 after not being seen since 1961 — captured on the last day of an Oxford expedition into the Cyclops Mountains of Indonesia.

The race against disappearance

But discovery is not protection — and the gap between naming a species and saving it is widening.

A study from Wiens’s own lab found that the proportion of threatened species among newly described ones has risen from 11.9 percent (for species described in the 18th century) to 30 percent today, and is projected to reach 47 percent by 2050. The pattern has become grimly routine: a species gets a name and a Red List designation almost simultaneously. 

The Tapanuli orangutan, described in 2017, was listed critically endangered immediately with fewer than 800 individuals. Every new bird species described in Brazil’s Atlantic Forest between 1980 and 2010 was already threatened. According to Kew Gardens, three in four undescribed plant species are estimated to be threatened with extinction before anyone even names them.

There’s also a whole category that scientists call “dark extinction”: species that vanish before anyone knows they existed. One study estimated that dark extinctions could substantially increase known bird extinction numbers. The IPBES estimates more than 500,000 species have too little habitat left for long-term survival, making them effectively dead species walking (or crawling, or flying). Even as scientists describe new species at record rates, the tropical habitats where most undiscovered species live are being destroyed fastest.

So the race is real. But what the Wiens study shows is that it is still a race — and for the first time in the history of biology, we have the tools to run it faster. The golden age of species discovery isn’t a nostalgic label for the era of Darwin and Wallace. It’s happening now, in sequencing labs and on surf beaches and through the cameras of millions of ordinary people. Linnaeus described 10,000 species in a lifetime of work. We’re now finding that many every seven months. The question is whether we can keep accelerating before the things we haven’t yet found disappear for good.

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