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All articles

- Shucking the past: Can oysters thrive again?

- The other end of the weight spectrum: Very thin people

- Can a shift in strategy reduce intimate partner violence?

- Unsafe at home: The misery of intimate partner violence

- See something, say something? The science of speaking out

- Using pollen to make paper, sponges and more

- How a mysterious particle could explain the universe’s missing antimatter

- How the cavefish lost its eyes — again and again

- Civilizations of Africa through a new lens

- Uncovering the impact of artisanal fisheries

- Super-resolution microscopes showcase the inner lives of cells

- Mighty mitochondria: Cell powerhouses harnessed for healing

- Dogs and their people: Companions in cancer research

- Watching the world, one quintillionth of a second at a time

- How rogue jumping genes can spur Alzheimer’s, ALS

- HIV medications: Did fears about side effects come to pass?

- Worm-inspired treatments inch toward the clinic

- The history of the ocean, as told by tiny beautiful fossils

- How farmers can help rescue water-loving birds

- Viruses that roam the fungal kingdom

FOOD & ENVIRONMENT | VIEW ON WEBSITE

Shucking the past: Can oysters thrive again?

Dredging and pollution devastated the once-bountiful reefs. Careful science may help bring them back.

By Tim Vernimmen    09.10.2025

The Chesapeake Bay — the largest estuary in the continental United States — used to be packed with oysters, more than anyone today might imagine. Native Americans had been harvesting oysters there for more than 12,000 years before the arrival of Europeans, as evidenced by piles of discarded shells left behind in trash pits. In the late 1800s, annual harvests from the bay — by then dominated by people of European descent — peaked at an estimated 600 million to 1,200 million pounds.

In 2024, wild commercial harvests were less than 5 percent of that.

Overharvesting and pollution with sediments, sewage and fertilizer have mounted ever since the 1700s, a century after the first English settlement, Jamestown, was established on the James River that feeds into the bay. Today, global warming, sea level rise and acidification pose additional threats.

But the biggest destruction was from the method behind those record harvests: the practice of dredging, begun in the late 1800s, in which heavy metal rakes or toothed bars are dragged across the seafloor to scoop up loads of oysters at once. This obliterated most of the giant reefs formed by countless generations of oysters growing on top of each other.

Like coral reefs, these oyster reefs played crucial ecological roles, providing habitat and nurseries for many other species and filtering vast volumes of water. They offered essential services to people too, protecting coastlines and sustaining fisheries for thousands of years.

For decades, conservation organizations have been working to restore oyster populations in the bay, accruing data along the way to learn from successes and failures. Others have turned toward the distant past to understand what has been lost and assess what can be recovered.

Cliff digging

Some years back, conservation paleontologist Rowan Lockwood of William & Mary college in Williamsburg, Virginia, went to one of the few surviving fossil reefs, near Dutton, Virginia. She had long wanted to find out what the oyster reefs of the Chesapeake Bay used to be like before people started large-scale harvesting there.

When this reef was formed 245,000 to 195,000 years ago, the sea level was higher, so that today, the fossil reef sits well out of the water in the cliff face along the Piankatank River. “The oysters are all in life positions, still articulated,” says Lockwood. “They look like they died yesterday.” To interpret the fossils, she teamed up with marine biologist Roger Mann, also from William & Mary, who has been closely monitoring the Chesapeake oyster population for decades.

Though the number of oyster restoration projects is quickly increasing, they are largely concentrated in a few specific regions.

Based on the Dutton-area fossil reef as well as an extensive collection of shells in the Virginia Museum of Natural History taken from fossil reefs that no longer exist, Lockwood and Mann estimated that long ago, local oysters used to live four times as long (up to 21 years) and grow twice as big (up to 25 centimeters in diameter) at nearly 10 times the density of reefs in the area today.

This means that filter-feeding oysters would have been able to pass all of Chesapeake Bay’s water through their gills in one day, Mann and Lockwood calculated. Today, that might take close to a year.

If these giant reefs would magically reappear today, it might solve many of the bay’s problems. Nutrient-rich agricultural runoff and sewage cause huge algal blooms, and when these algae die and sink, bacteria bloom in turn, consuming so much oxygen that few other organisms survive at lower depths. “Lots of oysters could turn much of this stuff into oyster tissue and shell instead,” says Lockwood.

Dredging on

But how much recovery is realistic?

“It would be naive to think we can restore these systems to what they were like before we put 18 million people in the watershed of the Chesapeake Bay. That’s simply not going to happen,” Mann says. “What existed even a few hundred years ago will never, ever be recreated.”

And neither Mann nor Lockwood sees much value in the current, large-scale practice of releasing live larvae or young oysters into the bay. They say it is costly and that the large majority of released larvae are probably swiftly consumed by predators. “It’s like flushing them down the toilet,” says Lockwood.

Top, Tom Dobson sprays oyster shells covered in larvae off the side of a boat into the Tred Avon River, which ends in Chesapeake Bay. Bottom: Artificial structures called oyster castles placed near the mouth of Knitting Mill Creek on the Lafayette River in Virginia help to protect a shoreline from erosion. The artificial reefs provide a substrate that oysters can settle on.

CREDIT: PHOTO BY ETHAN WESTON (TOP), PHOTO BY WILL PARSON (BOTTOM) / CHESAPEAKE BAY PROGRAM

But, inspired by the astonishing size of many of the fossil shells, Lockwood argues that recovery could be significant if the practice of dredging was halted and restoration efforts were aimed at protecting large adult oysters, which filter more water, produce more offspring and help reefs grow tall.

This would require the introduction of large, solid structures that mimic the reefs that have been destroyed, she says. These would keep oysters from getting covered by the large amounts of sediment that wash into the Bay. They would also prevent dredging, which would be good for oysters — but not for fishers. “Watermen have been here for hundreds of years, and it’s a generational livelihood that we need to preserve,” she says. “So you’d have to be careful where you put these structures.”

Mann, who is working closely with the Virginia Marine Resources Commission on surveys to scientifically inform fisheries management, favors a less controversial approach: depositing empty oyster shells in select areas to entice naturally arriving oyster larvae to settle. The watermen are on board with this method, he says.

To date, this and other restoration efforts have helped to restore oyster reefs across nearly 1,800 acres in 10 different tributaries to the bay. Harvesting once every three years minimizes the impact on the early life stages, and oyster production has increased about eightfold, Mann says.

Restoration rising

Chesapeake Bay is far from the only place where people are trying to restore oyster populations. Marine ecologist Jessica Pruett of the University of Southern Mississippi and marine ecologist Rachel Smith of the University of California, Santa Barbara, coauthored a 2025 article in the Annual Review of Marine Science that found more than 2,000 restoration projects for the Eastern oyster (Crassostrea virginica) alone, and around 200 for other species, up from just a handful in the 1980s.

Restoration projects focusing on the Eastern oyster (Crassostrea virginica) are still the large majority, but other oyster species are receiving increasing attention, too.

Restoration success depends on local circumstances, says Smith. For example, just north of the mouth of the Chesapeake Bay, along the shores of Virginia, recovery has been rapid in a project that has been running for some 20 years. The site is “a different place than the bay, relatively pristine, with few water quality issues,” Smith says. “We’ve had a lot of success just by putting out oyster shells or artificial reefs made of concrete.” A study published in 2022 found that oyster density on reefs built from loose shells reached that of natural reefs in about six years, and that oyster-eating mud crabs quickly moved in. A 2021 study, meanwhile, found that oysters were larger and their densities were greater where artificial reefs made of concrete were built taller; taller reefs also more efficiently protected the shore against waves.

In some spots on Virginia’s Eastern Shore, though, oysters aren’t settling, despite the ostensibly favorable conditions.

Oyster behavior may play a role. Early on, the larvae are very tiny and at the mercy of sea currents, explains Pruett, who has studied them in the lab. But after a few weeks, they actively seek a place to settle. “They have an impressive ability to swim,” Pruett says. “When they find a place they like, they kind of ‘dive bomb’ down. And if it turns out not to be suitable, they can eject themselves back into the current.”

Considering what attracts oyster larvae may be an important focus for future research — there is some evidence to suggest, for example, that artificial reefs in lighter colors might reduce the warming influence of sunlight on oysters already stressed by climate change, which would be helpful in a warming world. But in at least one oyster species (the Pacific oyster, Crassostrea gigas) such reefs seem to attract fewer larvae; something about these reefs must be less appealing to them, or even putting them off.

There are many reasons to want to preserve or rebuild oyster reefs, researchers say. In addition to preserving natural ecosystems and the sustainable fisheries that depend on them, reefs may help to protect coastlines from storms and floods, which will become ever more urgent as climate change and rising sea levels give rise to more dangerous storms.

And because of all the organic material that accumulates in the reefs, oysters themselves might also help to absorb some of the carbon we emit into the atmosphere. Consumers can do their part by opting for oysters grown in cages, which are harvested without dredging and therefore without damaging reefs, Pruett says.

Oyster lovers might also ask staff in their favorite restaurant to make sure the empty shells don’t end up in dumpsites, she adds. “They can be recycled by restoration projects that return them back to the sea.” There, they can help to provide a substrate for oysters to settle on — so that perhaps, one day, our troubled world may once again become the oyster’s oyster.

10.1146/knowable-091025-1

Tim Vernimmen is a freelance science journalist based near Antwerp, Belgium. He has a long-standing interest in ecosystem restoration, but this is his very first oyster story.

HEALTH & DISEASE | VIEW ON WEBSITE

The other end of the weight spectrum: Very thin people

Researchers are exploring why some individuals are naturally super-lean and may struggle to gain weight. The causes of such constitutional thinness offer clues to the physiology of weight control.

By Ute Eberle    09.03.2025

Before weight coach Bella Barnes consults with new clients, she already knows what they’ll say. The women struggle with their weight, naturally. But they don’t want to lose pounds. They want to gain them.

Her clients find themselves too thin, and they’re suffering. “Last week, I signed up a client who wears leggings that have bum pads in them,” says Barnes, who lives in Great Britain. “I’ve had another client recently that, in summer, wears three pairs of leggings just to try and make herself look a bit bigger.”

These women belong to a demographic group that has been widely overlooked. As the world focuses on its billion-plus obese citizens, there remain people at the other end of the spectrum who are skinny, often painfully so, but don’t want to be. Researchers estimate that around 1.9 percent of the population are “constitutionally thin,” with 6.5 million of these people in the United States alone.

Constitutionally thin individuals often eat as much as their peers and don’t exercise hard. Yet their body mass index is below 18.5 — and sometimes as low as 14, which translates to 72 pounds on a five-foot frame — and they don’t easily gain weight. The condition is “a real enigma,” write the authors of a recent paper in the Annual Review of Nutrition. Constitutional thinness, they say, challenges “basic dogmatic knowledge about energy balance and metabolism.” It is also understudied: Fewer than 50 clinical studies have looked at constitutionally thin people, compared with thousands on unwanted weight gain.

Recently, researchers have started to investigate how naturally thin bodies are different. The scientists hope to unlock metabolic insights that will help constitutionally thin people gain weight. The work may also help overweight people lose pounds, since constitutional thinness appears to be “a mirror model” of obesity, says Mélina Bailly, a coauthor of the recent review and a physiological researcher at AME2P, a metabolism research lab at the University Clermont Auvergne in France.

Genetic and metabolic factors

Individuals who eat heartily but remain inexplicably skinny were first reported in the scientific literature in 1933. Decades later, a landmark 1990 experiment demonstrated how profoundly people differ in regulating their weight.

Twelve pairs of identical twins were fed 1,000 surplus calories for six days a week. After three months of such overfeeding — equivalent to an extra Big Mac and medium fries daily — the young men had gained an average of almost 18 pounds, mostly fat, but within a large range: One gained almost 30 pounds and another fewer than 10. The latter had somehow diffused around 60 percent of the extra energy.

The study also found that the variation of weight gain was three times greater between twin pairs than within them — indicating a genetic influence on the tendency to add pounds when overfed.

Other studies confirmed that constitutionally thin people largely “resist” weight gain, particularly when eating fatty foods. Whatever pounds they do gain through overfeeding rapidly vanish once they resume normal eating.

After bouts of overfeeding, bodies generally shed weight. But as this graph illustrates, there is variability in both responses to overfeeding and in the return to a body’s “normal” weight. (“Ad libitum” refers to a period in the experiment when participants eat what they want.)

This aligns with current thinking to some extent. Many researchers believe that our bodies have a preprogrammed weight “set point” or “set range” to which they try to return. That’s one reason few dieters manage to keep off lost weight long-term. Their metabolism slows down, burning fewer calories and making weight regain easier, particularly once the dieter stops restricting calories. (The system displays some flexibility, explaining why many of us put on inches around our midsections over the years.)

‘Skinny shaming’

As a group, lean individuals are probably as heterogeneous as overweight people. Some may stay thin because they have smaller appetites or feel full sooner. Others consume just as many calories as heavier individuals. One study found that constitutionally thin people eat 300-plus calories more per day than their metabolism needs. “They have a positive energy balance and they still resist weight gain,” says Bailly, a collaborator on NUTRILEAN, a project focused on constitutional thinness, at University Clermont Auvergne in France.

Like obese people, constitutionally thin people face their social stigma. Thin men may feel too scrawny to satisfy masculine ideals. Skinny women often lament lacking curves. People might suspect they are hiding eating disorders. They get “comments from random people on the street,” says Jens Lund, a postdoc in metabolic research at the Novo Nordisk Foundation Center for Basic Metabolic Research at the University of Copenhagen. “These people feel like they can’t go to toilet after a family dinner … because they are afraid that people would look at them as if they’re going out to puke, like having bulimia.”

Weight gain coach Barnes was never technically all the way in the constitutionally thin category, but she experienced plenty of such “skinny shaming” firsthand. Family members commented on her weight but dismissed her distress. “I felt like I could never speak about it,” she says. “People would be like, ‘That’s not a real problem,’ or ‘Just take some weight from me.’”

Where do the calories in constitutionally thin people go? Researchers have started eliminating possibilities.

Researchers are learning that there are large individual differences in how the body uses up calories. (Thermogenesis is the metabolic process in which calories are burned to generate heat.)

A 2021 meta-analysis offered some surprises. When Bailly and colleagues compiled data on thin people’s body composition, they discovered something unexpected: Constitutionally thin individuals carry nearly normal amounts of fat throughout their bodies. “It’s really unusual to have such low body weight combined with quite normal fat mass,” says Bailly.

What seems to be lacking is muscle mass. Constitutionally thin people have less of it — research has found that they have muscle fibers that are on average about 20 percent smaller than those of normal-weight people. Constitutionally thin people may also have reduced bone mass.

These facts suggest that there are health costs to leanness. Though studies are lacking, Bailly suspects that as they age, especially thin women might run a higher risk of osteoporosis, a dangerous weakening of the bones. The reduced muscle mass could also make everyday tasks, like opening jars or carrying groceries, more arduous.

And it could mean fewer protein reserves during illness, says Julien Verney, a physiological researcher at Clermont Auvergne’s metabolic lab and coauthor of the Annual Review of Nutrition paper.

In addition to body composition differences, researchers speculate that constitutionally thin bodies “waste” calories. For example, some studies suggest that while thin individuals exercise less, they fidget more.

They may also excrete more calories than others. While this hasn’t been explored specifically for lean people, it’s known that some people lose up to 10 percent of ingested calories through feces (and to a lesser extent, urine), compared to just 2 percent in others. In one study, a woman excreted 200 calories daily — equivalent to half a liter of soda.

Additional metabolic idiosyncrasies of constitutionally thin people may still await discovery. “We recently found some clues that may suggest more metabolic activity of their fat mass tissues,” says Bailly. “This is really surprising.” Other studies have already suggested that naturally thin people have more “brown fat” — a calorie-burning tissue that generates body heat.

To find more specific answers, Lund plans to launch an inpatient study at the University of Copenhagen. The study will use a metabolic chamber to track energy intake, expenditure and all routes of energy loss — including feces, urine and exhaled gases — in constitutionally thin people. Since 2020, Lund’s team has assembled a network of Danes who self-report as naturally lean, providing a unique pool for future research.

Constitutional thinness, as the 1990 twin study showed, has a strong genetic component: Research shows that 74 percent of very lean people have relatives with similar stature. As researchers identify gene variants, they realize that many of these — with names like FTO, MC4R and FAIM2 — are also involved in processes leading to obesity. Although they don't yet understand the specifics, scientists suspect that people with constitutional thinness may have unique activity patterns in genes related to energy production.

One such gene that has drawn researchers’ attention is ALK  (anaplastic lymphoma kinase). When scientists deleted this gene in mice, the animals became resistant to weight gain when fed high-fat diets — even in mouse strains genetically prone to obesity. The ALK gene seems to act in the brain, which then sends signals affecting the rate at which fat cells burn energy.

Genetics plays an important role in constitutional thinness, and researchers are starting to identify the genes involved. In mice, deleting one of them — a gene called Alk — made the animals resistant to weight gain when fed high-fat diets.

Understanding genetic mechanisms like these could lead to new treatments for both unhappily thin and unhappily obese people, says Lund. “If you can figure out what protects them from developing overweight, then whatever that mechanism is, you can then try to turn that into a drug,” he says. “There are so many signaling molecules in the body that we don’t even know exist.” The dream is to find a breakthrough as transformative as the latest obesity medications.

While researchers hunt for biological clues, Bella Barnes navigates the complexities of weight gain on her own. After years of trial and error, she gradually gained about 40 pounds by combining strength training with careful, intentional eating. At first, if she hadn’t reached her calories for the day, she’d just grab a packet of cookies — anything to get the numbers up. But she found more balance over time. “Not all calories are the same. You want to be eating whole foods,” she says. And a lot of them.

Today, Barnes has coached more than a hundred women on her weight gain techniques and has a strong TikTok following; she says that she’s proud of the strong body she’s built.

Maybe five more pounds, she adds, “would make me at my happiest.”

10.1146/knowable-090325-1

Ute Eberle is a science journalist in Baltimore. She has previously written stories for Knowable Magazine about bed bugs, cheese and the sounds of the soil.

THE MIND | VIEW ON WEBSITE

Can a shift in strategy reduce intimate partner violence?

New research, innovative programs and emboldened advocates are challenging decades-old conventions about how to respond to domestic abuse

By Katherine Ellison    08.28.2025

For decades, US states have fought male violence against spouses and partners on two fronts: with mandatory arrests and prosecutions, and through programs focused on reeducating men about their attitudes toward women.

Yet for nearly as long, researchers have gathered evidence that these strategies don’t work.

Instead, studies suggest that less punitive and more therapeutic tactics can better reduce repeated violence. In recent years, this has prompted some government agencies to change direction. Some leading domestic violence activists and researchers want to see that happen faster.

“We’ve simply got to have new approaches and new paradigms, because we haven’t done a very good job with all the stuff we’ve been doing,” says Jacquelyn Campbell, a professor of nursing at Johns Hopkins University and a national leader in research and advocacy related to domestic and intimate partner violence. “It’s 2025 — don’t we know more about human behavior and how brains work than we did in the 1990s?”

Perceived lenience toward men who have threatened or hurt women is understandably controversial. Yet momentum is growing for less frequent arrests — or at least more selective ones — and more attention to the emotional wounds and stress that can lead men to violence.

The feminist fight against male assaults

Today’s broad consensus about how to treat men charged with violence against wives and girlfriends began forming in the 1970s. In the decade prior, marital rape still wasn’t considered a crime and police often responded to panicked women’s calls with mild warnings to their spouses. Violence against women by spouses or boyfriends was still vastly underreported, even as the US Centers for Disease Control and Prevention would later report that about 41 percent of US women have experienced sexual or physical violence or stalking by an intimate partner during their lifetimes.

But then, half a century before #MeToo, second-wave feminists awakened Americans to the plight of women trapped in dangerous relationships. They dramatically improved women’s safety and welfare by empowering them financially — fighting for better access to jobs and reproductive health care — and pushing governments to confront violence against women that, as abundant research shows, is mostly and most lethally committed by men.

In the late 1980s and the 1990s, many state governments adopted versions of a comprehensive strategy to address intimate partner violence, known as the Duluth Model. Developed in the early 1980s by activists in Duluth, Minnesota, it favors ample victims’ services and robust law enforcement, including mandatory arrests when police have probable cause to suspect domestic violence. Duluth Model advocates have also supported pursuing prosecution regardless of the victim’s wishes.

These strategies are also reflected in the Violence Against Women Act, which Congress passed in 1994 and has reauthorized four times. The landmark legislation has distributed more than $11 billion, much of it for victims’ services such as shelters, counseling and a national hotline. Yet some researchers estimate that more than half of the funds have supported training of police and prosecutors to strengthen their response.

The Violence Against Women Act has helped to protect and support millions of survivors, while shining light on a crime once regarded as a private affair. From 1994 to 2010, as states adopted those get-tough policies, reports of intimate partner violence declined by 64 percent, according to the US Department of Justice.

Demonstrators take to London's streets in 2022 to protest violence against women in the annual Million Women Rise march.

CREDIT: GARRY KNIGHT / FLICKR

Yet the hard-hitting strategies have come under fire from scientists and advocates who charge that jailing abusers can exacerbate conditions that lead to violence, such as racism and poverty. “If we were willing to actually look at this as an economic problem, I truly believe we would make a greater dent in the rate of violence than with any other kind of intervention,” says legal scholar Leigh Goodmark of the University of Maryland Carey School of Law, author of a 2022 critique of the Violence Against Women Act in the Annual Review of Criminology.

Goodmark argues that the decline in reported intimate violence crime was part of an overall drop in crime since 1994. Other researchers attribute factors other than the Violence Against Women Act for that decline, including a steady drop in marriage rates starting in 1970, as well as improvements in women’s economic status and an older and presumably wiser population.

Indeed, a 2020 analysis of 11 published studies concluded that mandatory arrests have failed to stop most abusers from repeating their crimes. Aggressive prosecution may even increase the violence, according to Radha Iyengar Plumb, who in 2009, as a Harvard health policy researcher, reported an analysis of FBI data in the Journal of Public Economics. Plumb found that intimate partner homicides increased by about 60 percent in states with mandatory arrest laws, for reasons, she wrote, that could include victims’ reluctance to call police if it was likely to end in an arrest and batterers taking revenge if they did.

Such findings help to explain why 21 states now allow police more discretion.

Additionally, in recent decades several states and counties have retreated from the second front of America’s war on intimate partner violence: the confrontational programs abusers must attend in an attempt to get them to change their ways.

Power, control and pushback

Besides its support for robust police involvement, the Duluth Model includes a batterer-intervention curriculum, “Creating a Process of Change for Men Who Batter,” used today throughout the United States and in many other countries, often as a condition of parole. By the late 1990s, many states had begun combining the Duluth curriculum with cognitive behavioral therapy, or CBT, with the aim of helping abusers recognize and change unhelpful thinking patterns.

Inspired by now 40-year-old interviews with 200 women survivors of violence, the Duluth curriculum teaches participants that a patriarchal culture encourages men to use violence as a means of “power and control.” In weekly group classes, court-ordered participants study a “power and control wheel” that illustrates controlling tactics such as victim-blaming and using children as weapons.

This “power and control wheel” is included as part of the Duluth Model curriculum.

CREDIT: DOMESTIC ABUSE INTERVENTION PROJECT

Throughout the curriculum’s history, critics, including many scientists, have complained that it scolds and shames men. More important, they say, the Duluth program and others in more limited but also longtime use (including a precursor, Emerge, founded in 1977) have failed to stop abusers from committing new crimes.

Several state and local government agencies around the country have come to share that assessment. In 2014, the Washington State Institute for Public Policy determined that the Duluth curriculum failed to prevent repeated intimate partner violence. Subsequently, the state allowed alternative interventions to be used, according to Rebecca Goodvin, a senior research associate at the institute.

In Iowa and Nebraska, state prison administrators lost so much faith in existing programs like the Duluth curriculum that they ultimately turned to programs more focused on helping men manage their emotions. In California, which has long relied on Duluth-inspired curricula, a state law has allowed six counties to pilot alternative programs with “evidence-based practices.”

These public officials are responding to what researchers have called a tsunami of data challenging the effectiveness of the Duluth curricula. In one of the most frequently cited studies, clinical psychologist Julia Babcock of the University of Houston led a meta-analysis of research, published in 2004, examining commonly used batterer-intervention programs, including the Duluth-plus-CBT approach. She concluded that they had minimal impact on repeat crimes, based on police and partners’ reports.

CREDIT: ALI / ADOBE STOCK

Grim statistics

Violence against women – especially by intimate partners – is an urgent global public health issue, as described in the 2024 issue of the Annual Review of Public Health.

In the United States, roughly 41 percent of women and 26 percent of men have experienced sexual or physical violence or stalking by an intimate partner, according to the US Centers for Disease Control and Prevention. Throughout the world, some 51,000 girls and women were killed by a partner or family member in 2023, according to the United Nations Office on Drugs and Crime. The annual US cost for medical and mental health care services related to acute domestic violence has been estimated at more than $8 billion.

Nonfatal intimate partner violence has sharply declined since the early 1990s, together with most violent crimes. Yet some studies suggest that the severity of violence, including use of firearms, has increased, and that more women are being killed by men close to them. Between 2014 and 2023, murders of women by their intimate partners increased by 22 percent, according to an analysis of FBI data by Everytown Research.

— Katherine Ellison

Twenty years later, in a larger analysis, her conclusion was similarly discouraging.

“You can’t really make a great case for the Duluth Model,” she says.

Sympathy for the devils

Babcock’s news isn’t all bad. Her 2024 analysis includes studies comparing the Duluth-plus-CBT approach with newer alternatives, some of which achieved significantly better results. First in class was a program known as Achieving Change through Value-Based Behavior (ACTV), developed by clinical psychologist Amie Zarling at Iowa State University.

Zarling created ACTV by adapting a more mainstream approach, known as Acceptance and Commitment Therapy, which combines acceptance and mindfulness techniques. Using input from criminal justice experts and other sources, she incorporated tactics to better meet the needs of men accused of domestic violence. For example, ACTV emphasizes learning to be calm and deliberate, a skill Zarling says is often lacking in such men, likely because many have themselves been traumatized. The majority of those she studies, she says, have had four or more adverse childhood experiences such as physical or sexual abuse, neglect or witnessing violence at home.

Abundant research confirms this link. A 2009 study found that men who had suffered moderate to severe physical abuse in childhood were 3.9 to 4.5 times more likely to use violence against their partners as adults. “They never learned to regulate their emotions, and so many started using substances to deal with those trauma reactions, which just adds to the risk factors for domestic violence,” Zarling says.

As Zarling explains it, the main difference between Duluth-inspired approaches and ACTV, put simply, is that while the former tries to teach men to change their thoughts about their female partners, ACTV aims to help them choose behavior that matches their values, even in the presence of those thoughts. It’s a skill known as “psychological flexibility.”

In 2010, the Iowa Department of Corrections piloted ACTV with men required to complete an intervention program, after determining that the Duluth-inspired approach had failed to significantly reduce intimate partner violence.

This enabled Zarling and colleagues to conduct a large study comparing ACTV with Duluth-plus-CBT, using data from 3,474 men in Iowa who had been arrested for domestic assault and court-ordered to one or the other of the programs, each lasting 24 weeks. After one year, 3.6 percent of the men who had completed the ACTV program had been charged with a new episode of domestic violence, the 2017 study found, versus 7 percent of those who had completed the conventional treatment.

Four years later, researchers from Northwestern University published another study in the Journal of Consulting and Clinical Psychology comparing outcomes from ACTV with Duluth-plus-CBT. They looked at 725 men classified as medium or high risk for repeat offenses who were court-mandated to complete a batterer-intervention program with Ramsey County Community Corrections in Minnesota. After five years, 69.6 percent of those enrolled in the Duluth-inspired program had received a new conviction, compared to 34 percent of men in the ACTV program.

“We’ve simply got to have new approaches and new paradigms, because we haven’t done a very good job with all the stuff we’ve been doing.”

— JACQUELYN CAMPBELL

While Zarling continues her research, interest in her program is growing. Since 2024, several Nebraska prisons have been offering ACTV to incarcerated individuals, says criminologist Tara Richards of the University of Nebraska Omaha, who collaborates with public agencies to evaluate criminal justice programs.

In recent years, other jurisdictions, including in Vermont and Ramsey County, Minnesota, have also piloted or adopted ACTV for intimate partner offenders.

“They don’t want to be abusive”

Another emerging competitor to the Duluth curriculum is “Strength at Home,” which was adopted throughout the Veterans Administration in 2013. Intimate partner violence is unusually prevalent among military veterans who have experienced trauma, yet before that year few VA hospitals offered more than anger management classes.

Strength at Home is “trauma-informed,” says Casey Taft, who created the program as a staff psychologist at the National Center for PTSD in the VA Boston Healthcare System. It aims to help men understand the impact of their emotional wounds, whether stemming from childhood or combat, in a collaborative, empowering manner.

“Instead of trying to get really confrontational with our clients and force them to change, we treat them with respect and allow them to talk about their experiences in an open way, so that they take ownership over their actions,” says Taft. For the most part, he adds, “Our clients want to change. They don’t want to be abusive; they don’t want to have these problems with violence and anger.”

The US courts’ long reliance on the Duluth curriculum and other interventions that aren’t evidence-based is dangerous, says Taft. “You have violent folks who are hurting or killing their partners and we’re sending them to programs with no demonstrated effectiveness.”

Like most other batterer-intervention programs, Strength at Home requires men to meet weekly in groups in which members, guided by a facilitator, challenge and support each other. “We’d help each other; we’d give advice to each other, like, if that made you mad, how did you handle it? How could you have handled it better?” recalls Ran Stewart, a New York state construction worker who graduated a few years back from a Strength at Home program adapted for civilians. “We ended up being a brotherhood.”

Research support for Strength at Home includes a randomized controlled trial of 135 male veterans and 111 female partners, published in 2016. The veterans were assigned to either Strength at Home or treatment that offered support such as individual therapy, substance abuse programs and counseling for intimate partner violence. After researchers led by Taft interviewed clinicians, the veterans and their partners, the team concluded that Strength at Home was more effective than the enhanced program in reducing physical and psychological violence against partners. Three months after completion of the program, 26.7 percent of the treatment-as-usual participants committed new crimes, compared with 18.5 percent of those who completed Strength at Home.

In 2023, Taft published an additional study, this time including 1,754 participants at 73 VA clinics. It concluded that Strength at Home helped to reduce physical intimate partner violence by 17 percent and psychological intimate partner violence by 23 percent.

Since then, Taft has continued to test his approach on civilians, with support from a $2.8 million grant from the nonprofit Patient-Centered Outcomes Research Institute, created by the 2010 Patient Protection and Affordable Care Act. He expects to have results in 2030.

“I’m really looking forward to that data,” says Johns Hopkins researcher Campbell, who collaborated with Taft in a recent paper in the American Journal of Preventive Medicine, which called for more evidence-based programs for intimate partner violence offenders. “I would like to see Casey’s program in every community in the United States.”

Complexity after complexity

Scott Miller, executive director of Domestic Abuse Intervention Programs, which trains Duluth facilitators, says his nonprofit organization has never subjected the Duluth curriculum to a randomized controlled study. “We’re not scientists,” he says.

Indeed, studying behavior as complicated as intimate partner violence is a major challenge under any circumstances, but especially when done outside of controlled settings such as prisons or VA clinics. Convicted criminals may not show up. Partners may shade the truth for their own reasons. Studies are expensive and time-consuming, and researchers can’t offer no treatment as a comparison in controlled studies, since all participants must receive a program by law.

For the Duluth curriculum, the challenges are even more complex. The intervention was always intended to be part of a larger, coordinated community response, Miller says. “If you pluck our men’s group out of our system that we’ve designed and stick it as a standalone, it’s not going to operate the same way.”

Importantly, too, Duluth classes vary widely state to state and even group to group. Programs can last from 12 to 52 weeks. Group leaders range from experienced psychologists to people with no college experience, according to Miller. They receive three days of online training and a 324-page instruction manual and videos depicting vignettes of abuse, after which all are free to adapt the program.

“We didn’t want to be that prescriptive because we didn’t want to curtail creativity,” Miller says. “We wanted people to use it and figure out different ways of using it.”

“Instead of trying to get really confrontational with our clients and force them to change, we treat them with respect and allow them to talk about their experiences in an open way, so that they take ownership over their actions.”

— CASEY TAFT

Indeed, there’s nothing to stop group leaders from improvising beyond the instruction manual, notes Richards. “They all change it, supplement it, bring in different components, and are responsive to their groups. So it’s like comparing apples to oranges to bananas.” Other intervention programs are vulnerable to the same comparison challenges if facilitators implement them differently, she adds.

Amid all its challenges, the Duluth program has been evolving, says Miller. Over the summer of 2025, mindful of the new research and following a four-year review, Domestic Abuse Intervention Programs rolled out a fourth iteration of the curriculum that incorporated some elements of ACT.

As the field develops, experts say they would like to see more standardization of batterer programs, and more rigorous, independent evaluations of their impact.

Also important, according to Richards, is infusion of more resources so participants do not have to pay out-of-pocket for the programs. With fees of $25 to $75 per class, facilitators often struggle to retain participants who may be jobless or marginally employed. Batterer-intervention programs are, in fact, notorious for their dropout rates, with researchers reporting that up to 67 percent fail to complete them.

Zarling says she hopes that in coming years more researchers will join the field and help to develop new, empirically tested strategies to replace ineffective efforts.

“We are so programmed to hate these men, and there’s certainly some validity in that,” she says. “But what I think people tend to forget is that if we don’t help them, they’re just going to do it again and again.”

Editor’s note: This article was amended on September 3, 2025, to correct the name of the Patient-Centered Outcomes Research Institute. The word “Initiative” was incorrectly used instead of “Institute.”

10.1146/knowable-082825-1

Katherine Ellison is a Pulitzer Prize-winning journalist and author and coauthor of 12 nonfiction books, including Mothers & Murderers: A True Story of Love, Lies, Obsession … and Second Chances. Her articles have appeared in the New York Times, the Washington Post, the Atlantic and other publications.

HEALTH & DISEASE | VIEW ON WEBSITE

Q&A — Public health researchers Susan B. Sorenson and Heidi Stöckl

Unsafe at home: The misery of intimate partner violence

Public health researchers explain the levers that can reduce — or worsen — this global blight. A bright spot: There are more data than ever on strategies that can help.

By Katherine Ellison    08.27.2025

The statistics are staggering — and so is the toll on society. Throughout the world, roughly 27 percent of women ages 15 to 49 experience violence by intimate male partners at least once during their lifetimes. The scourge costs society trillions of dollars and seriously harms children’s mental health.

“Each case of violence in a woman’s life is a tragedy for herself and for those around her, affecting not only the woman and her health and well-being, but also her family and community,” write two public health researchers in the 2024 Annual Review of Public Health. In their article, Susan B. Sorenson of the University of Pennsylvania and Heidi Stöckl of the Ludwig Maximilian University of Munich detail the scope of this urgent public health issue and how it might be more vigorously addressed.

CREDIT: JAMES PROVOST (CC BY-ND)

Public health researcher Susan B. Sorenson

University of Pennsylvania

In 1986, Sorenson began teaching the first violence-prevention course in a US school of public health. She has authored more than 150 publications, many of them focused on the epidemiology and prevention of violence against women and, since retiring from her university position, has written a guide for parents of college students who have suffered a sexual assault.

Stöckl’s research focuses on the epidemiology of intimate partner violence and human trafficking, the global prevalence of intimate partner homicide and the perpetrators of child homicide, and trafficking for sexual exploitation and forced marriage. She conducted the first prevalence study on intimate partner violence during pregnancy in Germany and is currently investigating violence during pregnancy in Bangladesh.

CREDIT: JAMES PROVOST (CC BY-ND)

Public health researcher Heidi Stöckl

Ludwig Maximilian University of Munich

Knowable Magazine recently interviewed Sorenson and Stöckl. This conversation has been edited for length and clarity.

You have devoted much of your careers to studying violence against women. What led you to this topic?

Susan B. Sorenson: I grew up in a safe and loving environment, but at some point, I realized that wasn’t the case for everyone. At first, my focus was on individuals, but as I learned more, I came to recognize there is a bigger, more systemic picture that I wanted to explore.

Heidi Stöckl: I came to the topic from a human rights angle. I was always interested in human rights activism, and during an internship I had at Amnesty International, they launched the women's rights campaign — I guess I was sold by then. Women make up 50 percent of the population, but their issues do not get the same attention.

Intimate partner violence is an age-old problem. Why was it a timely topic for this recent review?

Stöckl: It may be age-old, but not much has been done to address it. In many places of the world, it’s always been considered an issue to be dealt with behind closed doors. But the availability of data today shows just how serious the issue is. The other point is that we now know what works to prevent it; we have interventions and programs that work.

Sorenson: Many global organizations and researchers around the world have collaborated to get us to a point where we have some very strong data. The Violence Prevention Information System at the World Health Organization has done an excellent job, compiling a database of nearly 2,000 studies. Their website identifies 12 prevention strategies, including school programs about dating violence, bystander intervention training, and microfinance — and nine “response strategies,” meaning programs for after violence occurs, such as shelters, home visiting and psychological therapy for survivors and children.

Additionally, the United Nations has a database of more than 10,000 measures that nearly 200 countries have taken to address violence against women.

The phrase “intimate partner violence” has come to replace terms such as wife-beating, spousal abuse and domestic violence. How should the problem best be defined?

Sorenson: “Intimate partner violence” is a way to be more specific about what we’re trying to measure. Domestic violence can have multiple meanings. Spouse abuse is another term that isn’t used much these days, given that such violence isn’t limited to marriages.

As we write in our review, intimate partner violence refers to “any behavior by a current or former male intimate partner, within the context of marriage, cohabitation, or any other formal or informal union, that causes physical, sexual, or psychological harm.” The World Health Organization says such behavior includes physical aggression, such as slapping, hitting, kicking and beating; sexual aggression, such as forced intercourse; and psychological abuse, such as intimidation, monitoring movements and other controlling behaviors.

Global estimates of physical and/or sexual violence by intimate partners against women who are, or have been, in an intimate relationship. Figures are from 2018.

I notice that in your definition of intimate partner violence, you specify violence by males. Yet one major US survey found that about two in five men have reported experiencing “contact sexual violence, physical violence, and/or stalking by an intimate partner in their lifetime.” Aren’t females also violent sometimes?

Sorenson: That’s correct: There can be female-on-female violence, as well as male-on-male and female-on-male violence, in an intimate relationship. But it’s a smaller part of the overall issue and, at this point, we have far less systematic data about it.

Why do you describe violence against women — and, more specifically, intimate partner violence — as a global public health issue?

Sorenson: Decades of research document a wide range of negative health outcomes. Being berated, threatened, assaulted or otherwise harmed is simply not health-enhancing. It’s a major cause of disability in and of itself while also contributing to conditions such as depression, HIV and traumatic brain injury.

There are huge financial costs, every year, which communities must pay. In 2012, in the US alone the costs of medical care, lost productivity, criminal justice and more due to intimate partner violence were estimated at $3.6 trillion over the victims’ lifetimes.

What does it mean to consider intimate partner violence as a global public health issue? How does that change the way it is treated?

Stöckl: It means it’s a problem that exists in every country, is highly prevalent and affects the lives of many women and children, with multiple other health consequences. Over the past two decades, we’ve shown the devastating effect it has on women’s mental and physical health and the impact it has on children. For instance, when women experience violence during pregnancy, their children can have long-term effects in terms of attention deficits and attachment issues.

Sorenson: Women are at risk of violence by a male intimate regardless of where they live in the world. In that way, intimate partner violence is like environmental concerns, infectious diseases and other problems that don’t stay within geographic or national boundaries. Acknowledging the reality that the risk goes beyond a specific locale can help lead to international collaboration to protect health through prevention and intervention.

Map showing lifetime estimates of physical and/or sexual intimate partner violence against women (aged 15 -49 years) who have ever had a partner. Estimates are from 2018.

Intimate partner violence is obviously a complex problem with a complex range of potential solutions. Which strategies have you found to be most effective?

Sorenson: There are so many ways you can intervene, with many of them backed up by credible studies. We describe some of these in the review.

Changing a woman’s financial situation can help quite a lot. We’ve long known that there are strong links between poverty and all kinds of violence. So, microfinance programs, in which low-income women can get access to small amounts of capital to start small businesses, have been very promising. For example, in the early 2000s, in villages in the rural Limpopo province of South Africa, researchers carried out a randomized controlled study, known as IMAGE (Intervention with Microfinance for AIDS and Gender Equity). They recruited 6,576 low-income women and men who were divided into three groups. One of the groups received microfinance loans and attended twice-a-month trainings that addressed gender roles, community mobilization and much more. In that group, intimate partner violence was reduced by 55 percent, according to a report in the Lancet in 2006.

Since then, many more well-designed studies have linked microfinance programs with less intimate partner violence. A 2023 review of 10 randomized clinical trials, with a total of 16,136 participants, published in JAMA Network Open, concluded that microfinance interventions can reduce psychological and emotional abuse as well as controlling behaviors.

In the United States, we’ve seen increasing evidence about the effectiveness of bystander intervention education for college and high school students. One popular evidence-based program known as “Green Dot” uses workshops and social marketing to train students in the skills they need to intervene when they see signs of violence.

Stöckl: The kinds of prevention efforts that work will obviously depend on where they take place. In low- and middle-income countries, where a lot of the work I’m doing takes place, I’d argue strongly in favor of couples’ interventions and tying empowerment programs like cash transfers to gender training to prevent violence from happening as a backlash.

What are really important are community interventions that tackle both women and men and norms in society, as a holistic approach. In the review, we write about the SASA! Study in eight communities in Kampala, Uganda. SASA means “now” in Kiswahili and is also an acronym for the phases of the approach: Start, Awareness, Support and Action. From 2007 to 2012, the program trained a cadre of activists who raised awareness among their friends, families and colleagues. This approach has helped reduce intimate violence and has since been replicated in 15 countries.

We definitely also need more investment in preventing violence by working with men, particularly with the most at-risk groups, such as men who abuse alcohol.

Let’s talk about a specific kind of intimate partner violence, namely homicide. The UN Office on Drugs and Crime reported that 51,000 women and girls were killed by an intimate partner or family member in 2023. But apparently, homicides connected with intimate partner violence have dropped a lot in the United States since the 1970s. What’s that about?

Stöckl: The drop in the US is really impressive and also very telling about the gendered patterns of intimate partner homicide. It’s driven mainly by fewer men being murdered by their partner. We’ve also seen a drop in homicides of women, but it’s, by far, not as steep. So what’s going on?

Criminologists have identified several key changes at the societal level that help explain this. Women mainly kill their partners while in a relationship with them, while men often do so during separation or afterwards. So that means a lot of the societal changes have been important. For example, marrying later in life reduces the risk of this type of homicide, which mainly occurs early in life. Other factors include women’s employment, less stigma about separation and, of course, the greater availability of domestic violence shelters, hotlines and other prevention measures. These have all worked in favor of men in terms of homicide risk, as marriages that weren’t working could be dissolved.

“We’ve made such important progress in defining and measuring the scope of intimate partner violence. And we know there are ways to prevent it.”

— SUSAN B. SORENSON

Sorenson: Although all that is true, it’s obvious that empowering women isn’t enough. We need to work more on interventions addressing men who kill their partners.

Can you think of some ways in which this problem could actually get worse?

Sorenson: Oh, yes, and I’ll tell you two ways this could happen. As global migration increases, women who are fleeing war and civil unrest, famine, and environmental disasters are at heightened risk. The community in which they were embedded has been torn apart and their previous support systems no longer exist.

Women are also at risk in refugee camps, where sexual coercion and assault can sometimes be the price for obtaining food and shelter.

Also, consider the increased use of electronic technology. Abusers can increasingly track movements and online activities, harass and shame their intimate partners on social media, and film sexual activity without consent and then post it online. With rare exceptions, tech companies and legislators have avoided regulating these activities.

What might be some of the biggest differences you see between how the US and Europe confront intimate partner violence?

Stöckl: A huge difference is the availability of guns in the US, which makes this violence so much more lethal. It’s just so much easier to kill someone, threaten to kill someone, and make the stakes of leaving an abusive relationship so much higher. Apart from that, I find it hard to make sweeping statements about the US, given how different many states are, both in their culture, their acceptance of violence, and the laws they have. Europe is similarly huge, with big differences between Nordic and southeastern European countries, which have many differences in culture and laws.

Last year, a particularly terrible case of intimate partner violence made the news, in which dozens of men were found guilty of raping Gisèle Pelicot, in assaults arranged by her husband while she was drugged and unconscious. The crimes prompted street demonstrations in France and outrage throughout the world. What did you make of it?

Sorenson: On the positive side, the trial raised a lot of awareness, including about changes we still need to see in laws and in cultural attitudes. Her husband admitted to the crimes, but then a lot of the men said, “I didn’t rape her because he had said it was OK” — as if he had authority over her body. I found it striking that this has happened against the backdrop of a rising manosphere where aggrieved men promote slogans like “Your body, my choice.”

We’ve made such important progress in defining and measuring the scope of intimate partner violence. And we know there are ways to prevent it. Yet this case illustrates how much still needs to be done. Governments really need to move faster to take some of the most promising programs to scale.

10.1146/knowable-082725-2

Katherine Ellison is a Pulitzer Prize-winning journalist and author and coauthor of 12 nonfiction books, including Mothers & Murderers: A True Story of Love, Lies, Obsession … and Second Chances. Her articles have appeared in the New York Times, the Washington Post, the Atlantic and other publications.

SOCIETY | VIEW ON WEBSITE

Q&A — Sociologist Patrick Bergemann

See something, say something? The science of speaking out

From tattling to whistleblowing, a sociologist explores what drives people to tell on one another

By Emily Laber-Warren    08.20.2025

Lea en español

Police rely on tips from ordinary people — witnesses, victims and whistleblowers — to investigate 95 percent of crimes. Sometimes, the decision to speak up is easily made, but in other cases, people elect to stay silent, leaving countless infractions unpunished. About half of violent crimes go unreported, according to estimates by the US Department of Justice.

And yet at certain historical moments, such as in the United States in the early 1950s, when fear of communism led to many false reports against individuals working in entertainment and public service, societies can become places where people readily denounce one another — often falsely, or for petty reasons.

CREDIT: JAMES PROVOST (CC BY-ND)

Sociologist Patrick Bergemann

Paul Merage School of Business at the University of California, Irvine

Tattling, whistleblowing, snitching, call it what you will: Patrick Bergemann has spent the past 15 years studying the many ways that people tell on one another, examining everything from Afghan villagers’ reports of illegal Taliban activity to informers’ charges of treason in 17th century Russia. In a recent article in the Annual Review of Sociology, he explores the social pressures that influence people’s decisions to expose, or conceal, wrongdoing.

The choice to report reflects not just the infraction but a person’s loyalties and whether they expect to receive rewards or retaliation from authorities and peers, says Bergemann, a sociologist at the Paul Merage School of Business at the University of California, Irvine, and author of Judge Thy Neighbor: Denunciations in the Spanish Inquisition, Romanov Russia and Nazi Germany.

Bergemann talked with Knowable Magazine about why and when people report crimes and bad behavior, and how, for repressive governments, encouraging people to rat on neighbors and coworkers can be a potent form of social control.

This conversation was edited for length and clarity.

The urge to tell on someone is so familiar. It goes back to childhood, when kids tattle on classmates or siblings.

It’s fascinating to see how fundamentally human this behavior is. There have been a few studies of young children showing that by the age of between 2 and 4, when children talk to adults, the primary thing they’re communicating about other children is the bad things they do. They’re not saying, “Oh I had so much fun playing with little Jimmy on the playground.” One study of preschoolers found that tattling represented more than 90 percent of communication about other children’s behavior.

Calling out others for wrongdoing (perceived or real) is a deeply human tendency that starts in early childhood.

CREDIT: ISTOCK.COM / FIGURE8PHOTOS

What first interested you, as a sociologist, in studying this phenomenon?

When I was looking for what to research for my dissertation, I stumbled onto the topic of reporting, and I realized a lot of the work that’s been done has been by psychologists and people thinking about the decision to report as a moral question. And it struck me that it’s also such a social decision. You’re potentially bringing harm to another person — I mean, they might deserve it completely, but still, it’s an act of potentially bringing someone to the attention of authorities that can investigate them. There are also broader relationships: How will people think about you and what you’ve done, and will they approve that you reported? So there are social consequences.

There are so many words for this kind of behavior. Why did you choose the term “reporting”?

Some people say whistleblowing. Some people say snitching. Snitching suggests you’re doing something wrong. You’re betraying people. Whistleblowing suggests a heroic act to help society. To me, “reporting” is the most value-neutral word I could come up with. It doesn’t suggest whether it’s right or wrong. It’s more descriptive of the act.

What are some of the main categories of reporting, as you see it?

Reporting can be categorized by the person reporting (for example, victim or bystander), the person reported on (acquaintance or stranger), the alleged behavior (violence, theft, fraud, etc.) and the authority reported to.

There’s crime reporting, when you’re alleging that someone broke a law. There’s also reporting on behavior that isn’t illegal but breaks policies within organizations. Some things are violations of both, and in those cases, individuals must decide whether to report internally, to organizational authorities, or externally, to government officials: The whole controversy in the Catholic Church about sexual abuse — a lot of that was actually reported internally but not to the police. And in my opinion, that’s part of the reason it was able to stay hidden for so long.

People have a strong interest in stopping bad behavior, but sometimes they don’t want to embarrass the organization within which it occurs. Reporting internally can potentially accomplish both goals, but only if organizational authorities take the reports seriously and seek to fix the problem.

Research has found that most people who report externally, such as to the police or the FBI, only do so after first reporting internally and not getting a positive response. I can't speak directly to the motivations of the parents of victims in the case of the Catholic Church, but I would imagine that people trusted the church to handle things, especially if they saw offending priests disappearing.

How do you find the data you use in your work?

A lot of times there aren’t a lot of records, or interest in sharing those records. For example, organizations don’t necessarily want to give me all the data about employees being reported for problems, because it might reflect poorly on them.

I would say I’m opportunistic. I try to find where information is actually available, and then go from there, which can be frustrating when you have situations you want to look into. It’s hard to study something you can’t gain access to.

Can you share a time when you serendipitously came across a treasure trove of data?

There are lots of records from the Spanish Inquisition, but most of them are summaries of trials, and that’s not reporting.

But I was digging through all my old notes and I realized there was this citation that I hadn’t followed up. This paper analyzed actual denunciations as reported to Inquisition officials. I got excited and I said, “Where did that come from?”

Turns out there was a book published in the 1980s by someone who actually went to the archives and transcribed this corpus of denunciations. I could order the book and see the literal texts, 400 and something of these, in the old 15th century Spanish, where the scribe was writing as the people came and reported — this person appeared on this day, from this village. It’s their summary of what the accusers were saying. That was an exciting one.

In your book, you explore how ordinary people turned each other in during the Spanish Inquisition, Nazi Germany and Romanov Russia — accusing colleagues, business owners, teachers and neighbors. What did you learn from that history?

I identified similar patterns in how denunciations change, depending on circumstances. At the start of the Inquisition, people were told that if they denounced the supposed heretics they knew, they would be protected from harm. But then that rule changed and reporting no longer offered personal protection.

The Russia case was a different historical period and context, of course, but I found a similar contrast between a set of people who had something to gain — they were in prison and thought they could help free themselves by denouncing others — versus a set of people who weren’t in prison and did not have that motivation.

In both cases you had the same three core actors: the denouncer, the person denounced and the authority. But people’s actions differed, depending on whether they felt that reporting would better their situation. In those cases, they tended to name people they thought would be most appealing to the authorities.

When they didn’t have those incentives, people instead tried to use reporting to harm their rivals — whether those were professional rivals, romantic rivals or political rivals.

In The Inquisition Tribunal (1812-19), Francisco Goya depicted one of the historical cases sociologist Patrick Bergemann studies to understand why people report on others.

CREDIT: FRANCISCO GOYA / PUBLIC DOMAIN

You’ve also studied more recent examples of people telling on each other, including whistleblowers in the federal government. What have you learned?

My colleague and I did a study using data from a US agency that administers surveys to tens of thousands of federal employees every three to four years. The 2010 version had a module asking about people’s experience observing wrongdoing in the workplace and how did they respond. Out of about 40,000 returned surveys, nearly 3,000 indicated knowledge of wrongdoing by a colleague.

What I was interested in was, how do social dynamics influence people’s willingness to report? The survey contained one item that spoke to this. People had to rate how much they agreed with the statement: “A spirit of cooperation and teamwork exists in my work unit.”

Our first finding was what most people would expect: The more cohesive your work group is, the less likely you are to report someone in your group. People feel loyal to their peers. They might tell the person to stop, but they don’t want to get them in trouble.

But what I think is particularly interesting is that if someone from outside the work group engages in wrongdoing, people on a cohesive team are more likely to report. It’s probably because you know your team members are going to support you and say, “You should listen to this person. You can’t retaliate against this person.”

Those dynamics speak to the complex social processes that go into whistleblowing decisions. It’s not that moral considerations don’t play a role, but they’re definitely not the whole story.

Edward Snowden, who leaked classified US National Security Administration documents in 2013, remains a polarizing symbol of whistleblowing in the digital era.

CREDIT: B. CHRISTOPHER / ALAMY STOCK PHOTO

How else can group dynamics influence decisions about reporting? For example, you’ve noted that when someone is offended by a sexist joke but no one else in the room reacts negatively, the offended person is less likely to view the behavior as sexual harassment and less likely to report it. Why is that?

Reporting is a two-stage process. The decision to report is the second stage. The first stage is simply realizing that something has happened that is worthy of being reported. We’re influenced by others at both stages.

You need to interpret something as misconduct or wrongdoing or illegal behavior in order to report it. There’s something called the bystander effect, where oftentimes we look around and see what other people are doing, even strangers. If they’re acting like nothing’s happening, then you might think, “Oh, I’m misinterpreting the situation.”

What factors enable false reporting to proliferate in a society?

A culture of false reporting is really only attainable if due process is not very strong. Because if the government is investigating everything very carefully, false reporting isn’t going to be very effective. I mean, there still might be some hardship on the person accused, but they’re going to find, “This was just spiteful, we’re not going to prosecute.”

When there’s strong due process, oftentimes you have penalties for false accusers as well. So I think a lot of the opportunities to falsely accuse emerge once the people accused start getting punished with little investigation, with little consideration of guilt or innocence.

Recently new laws and directives have emerged in the US that urge people to expose others, like the 2021 Texas law that offers a reward for turning in anyone who helped someone obtain an abortion, and a recent presidential directive requiring federal employees to expose colleagues who continue to promote diversity initiatives. Is this a new trend?

I would start by saying the government has a long history of trying to get people to report undesired behavior to the authorities. There are qui tam laws that allow people who report on others for cheating the government to get some of the money that’s recuperated. After 9/11, we had the “See something, say something” campaigns. And during the Covid-19 pandemic, New York City officials encouraged people to report when someone was not social distancing or wearing a face mask. According to a research paper I just finished, thousands of people reported their neighbors in a span of a couple of months.

Neighborhood Watch programs enlist residents to monitor and report on outsiders, reflecting the potentially volatile dynamics Patrick Bergemann studies.

CREDIT: ELLIN BELTZ / WIKIMEDIA COMMONS

Recently the Trump administration has encouraged people to call the ICE (Immigration and Customs Enforcement) tip line to report people for all sorts of things, including if you think they are undocumented. What is going on now is actually similar to the McCarthy era during the 1950s, when conservative members of the US government encouraged citizens to denounce each other for involvement in left-wing activities.

What are your thoughts on seeing this “turn in your neighbor” strategy expanding?

I think it serves a few purposes for government. One, it’s trying to recruit more people to your side, to make them participants in whatever it is you’re trying to do. It also helps to uncover what can be difficult to uncover through formal policing mechanisms. If it’s hard to identify who is undocumented or who is getting an abortion, then getting people to come forward with that makes sense.

And also, the more that people use reporting systems, the more it becomes normalized that these things should be dealt with by the authorities — not among neighbors, or ignored.

Encouraging reporting is also a way of inspiring more fear. If you start to worry that you’re going to get turned in and you don’t know who would do it, you start to trust your neighbors less.

There’s a really interesting paper that looked at social relationships in East Germany before and after the fall of communism. It found that in East Germany, people kept most of their social circle at arm’s length. They had a few very trusted contacts, oftentimes family members. This differed from the much broader social networks you’d see in West Germany, where people didn’t live under this regime of fear and denunciation.

Would you say that repressive governments are exploiting the natural human tendency to tattle for their own purposes?

I think that’s fair to say. Reporting really is a fundamental thing that we do from a very young age in many different types of forums and venues and across societies. Not that it’s always a resounding success when governments engage in these tactics.

In Nazi Germany, there was a lot of back and forth between government officials about what to do about all these petty reports they were getting. The authorities would have to deal with thousands and thousands of these, and they’d investigate them and realize it was something that, according to their rules, wasn’t worth dealing with. Hitler himself complained about this. I include a quote of his at the beginning of my book because it’s so surprising coming from someone who perpetrated so much cruelty. He said: “We are living at present in a sea of denunciations and human meanness.”

On the other hand, it was still worth their while. The Nazis didn’t change their system.

Are there historical examples where people refused to turn each other in?

During the Spanish Inquisition, inquisitors would come to villages and say, “Tell us about all the people who are committing heretical behavior against the church so we can punish them.” According to historian Henry Kamen, who wrote a book about the period, when ordinary people refused to cooperate, “the tribunal was impotent.” Without informers, the process can shut down. And when you have tight-knit groups where people are interconnected, you typically see more of this protective behavior.

Like … in the Mafia?

Oh absolutely. Within crime syndicates, anti-snitching norms are incredibly strong. But then you can imagine other settings where maybe we would think more positively about not reporting, where people are showing solidarity — standing up, in a sense, to a repressive government.

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Emily Laber-Warren heads the health and science reporting program at the Craig Newmark Graduate School of Journalism at the City University of New York.

TECHNOLOGY | VIEW ON WEBSITE

Using pollen to make paper, sponges and more

Reengineered, the powdery stuff could become a range of eco-friendly objects

By Sandy Ong    08.18.2025

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At first glance, Nam-Joon Cho’s lab at Singapore’s Nanyang Technological University looks like your typical research facility — scientists toiling away, crowded workbenches, a hum of machinery in the background. But the orange-yellow stains on the lab coats slung on hooks hint at a less-usual subject matter under study.

The powdery stain is pollen: microscopic grains containing male reproductive cells that trees, weeds and grasses release seasonally. But Cho isn’t studying irksome effects like hay fever, or what pollen means for the plants that make it. Instead, the material scientist has spent a decade pioneering and refining techniques to remodel pollen’s rigid outer shell — made of a polymer so tough it’s sometimes called “the diamond of the plant world” — transforming the grains to a jam-like consistency.

This microgel, Cho believes, could be a versatile building block for many eco-friendly materials, including paper, film and sponges.

A lot of people think of pollen, when it’s not fertilizing plants or feeding insects, as useless dust, but it has valuable applications if you know how to work with it, says Cho, who coauthored an overview of pollen’s prospective applications in the 2024 Annual Review of Chemical and Biomolecular Engineering. He’s not the only scientist to think so. Noemi Csaba, a nanotechnology and drug delivery researcher at the University of Santiago de Compostela in Spain, wants to develop hollowed-out pollen shells into protective vehicles to deliver drugs to the eyes, lungs and stomach.

Researchers studying pollen’s usefulness to people are a rare breed, Csaba says. “I find it a bit surprising,” she says. “Pollen is a very, very interesting biomaterial.”

Softening the shell

To begin working with pollen, scientists can remove the sticky coating around the grains in a process called defatting. Stripping away these lipids and allergenic proteins is the first step in creating the empty capsules for drug delivery that Csaba seeks. Beyond that, however, pollen’s seemingly impenetrable shell — made up of the biopolymer sporopollenin — had long stumped researchers and limited its use.

A breakthrough came in 2020, when Cho and his team reported that incubating pollen in an alkaline solution of potassium hydroxide at 80 degrees Celsius (176 degrees Fahrenheit) could significantly alter the surface chemistry of pollen grains, allowing them to readily absorb and retain water.

The resulting pollen is as pliable as Play-Doh, says Shahrudin Ibrahim, a research fellow in Cho’s lab who helped to develop the technique. Before the treatment, pollen grains are more like marbles: hard, inert and largely unreactive. After, the particles are so soft they stick together easily, allowing more complex structures to form. This opens up numerous applications, Ibrahim says, proudly holding up a vial of the yellow-brown slush in the lab.

When cast onto a flat mold and dried out, the microgel assembles into a paper or film, depending on the final thickness, that is strong yet flexible. It is also sensitive to external stimuli, including changes in pH and humidity. Exposure to the alkaline solution causes pollen’s constituent polymers to become more hydrophilic, or water-loving, so depending on the conditions, the gel will swell or shrink due to the absorption or expulsion of water, explains Ibrahim.

For technical applications, pollen grains are first stripped of their allergy-inducing sticky coating, in a process called defatting. Next, if treated with acid, they form hollow sporopollenin capsules that can be used to deliver drugs. If treated instead with an alkaline solution, the defatted pollen grains are transformed into a soft microgel that can be used to make thin films, paper and sponges.

This winning combination of properties, the Singaporean researchers believe, makes pollen-based film a prospect for many future applications: smart actuators that allow devices to detect and respond to changes in their surroundings, wearable health trackers to monitor heart signals, and more. And because pollen is naturally UV-protective, there’s the possibility it could substitute for certain photonically active substrates in perovskite solar cells and other optoelectronic devices.

Cho’s lab has also demonstrated that paper made from pollen can be printed on. It may be a sustainable alternative to traditional paper for writing, printing and packaging, according to Cho, who has patented the microgel’s production process. Producing traditional paper destroys trees and is resource-intensive, requiring up to 13 liters of water for every page made. Pollen is naturally released in bulk from seed-producing plants, and deriving paper from it requires only a few simple steps. Ink can be removed with a simple alkaline solution wash — a process that lets the paper be reused.

Additionally, freeze-dried pollen microgel forms porous sponges. These could be made into such things as scaffolds for tissue engineering, or used to stem bleeding or to absorb oil spills.

Cho’s team usually works with sunflower and camellia pollen that they purchase inexpensively as a bee pollen mixture, mainly from China. But they say their alkaline hydrolysis method would work well with a broad swath of plant species. Pollen is abundant, Cho adds — a single floret of the common sunflower, for instance, produces 25,000 to 67,000 grains every summer. Moreover, it’s easy to collect from bees in commercial hives.

Pollen-based products have some way to go before reaching the market, Ibrahim adds; the key right now is to predict challenges and devise sustainable solutions. With other biomaterials researchers are working on, such as chitosan and cellulose, a crustacean or a tree must be destroyed. Compared with that, pollen is considerably less resource-intensive: “We’re not destroying the plant,” he says. “We’re not even destroying the flowers.”

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Sandy Ong is a science writer based in Singapore. Find her on LinkedIn and X.

PHYSICAL WORLD | VIEW ON WEBSITE

How a mysterious particle could explain the universe’s missing antimatter

The Big Bang should have produced equal amounts of matter and antimatter, which would have annihilated each other in a spectacular burst of pure energy. But it didn’t. New experiments focused on understanding the enigmatic neutrino may offer insights.

By Dan Falk    08.13.2025

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Everything we see around us, from the ground beneath our feet to the most remote galaxies, is made of matter. For scientists, that has long posed a problem: According to physicists’ best current theories, matter and its counterpart, antimatter, ought to have been created in equal amounts at the time of the Big Bang. But antimatter is vanishingly rare in the universe. So what happened?

Physicists don’t know the answer to that question yet, but many think the solution must involve some subtle difference in the way that matter and antimatter behave. And right now, the most promising path into that unexplored territory centers on new experiments involving the mysterious subatomic particle known as the neutrino.

“It’s not to say that neutrinos are definitely the explanation of the matter-antimatter asymmetry, but a very large class of models that can explain this asymmetry are connected to neutrinos,” says Jessica Turner, a theoretical physicist at Durham University in the United Kingdom.

Let’s back up for a moment: When physicists talk about matter, that’s just the ordinary stuff that the universe is made of — mainly protons and neutrons (which make up the nuclei of atoms), along with lighter particles like electrons. Although the term “antimatter” has a sci-fi ring to it, antimatter is not all that different from ordinary matter. Typically, the only difference is electric charge: For example, the positron — the first antimatter particle to be discovered — matches an electron in its mass but carries a positive rather than a negative charge. (Things are a bit more complicated with electrically neutral particles. For example, a photon is considered to be its own antiparticle, but an antineutron is distinct from a neutron in that it’s made up of antiquarks rather than ordinary quarks.)

Various antimatter particles can exist in nature; they occur in cosmic rays and in thunderclouds, and are produced by certain kinds of radioactive decay. (Because people — and bananas — contain a small amount of radioactive potassium, they emit minuscule amounts of antimatter in the form of positrons.)

Small amounts of antimatter have also been created by scientists in particle accelerators and other experiments, at great effort and expense — putting a damper on science fiction dreams of rockets propelled by antimatter or planet-destroying weapons energized by it.

When matter and antimatter meet, they annihilate, releasing energy in the form of radiation. Such encounters are governed by Einstein’s famous equation, E=mc^2 — energy equals mass times the square of the speed of light — which says you can convert a little bit of matter into a lot of energy, or vice versa. (The positrons emitted by bananas and bodies have so little mass that we don’t notice the teeny amounts of energy released when they annihilate.) Because matter and antimatter annihilate so readily, it’s hard to make a chunk of antimatter much bigger than an atom, though in theory you could have everything from antimatter molecules to antimatter planets and stars.

But there’s a puzzle: If matter and antimatter were created in equal amounts at the time of the Big Bang, as theory suggests, shouldn’t they have annihilated, leaving a universe made up of pure energy? Why is there any matter left?

Excavation was completed in 2024 on the Long Baseline Neutrino Facility at the Sanford Underground Research Facility in Lead, South Dakota. The work was done in preparation for the Deep Underground Neutrino Experiment.

CREDIT: RYAN POSTEL / FERMI NATIONAL ACCELERATOR LABORATORY

Physicists’ best guess is that some process in the early universe favored the production of matter compared to the production of antimatter — but exactly what that process was is a mystery, and the question of why we live in a matter-dominated universe is one of the most vexing problems in all of physics.

Crucially, physicists haven’t been able to think of any such process that would mesh with today’s leading theory of matter and energy, known as the Standard Model of particle physics. That leaves theorists seeking new ideas, some as-yet-unknown physics that goes beyond the Standard Model. This is where neutrinos come in.

A neutral answer

Neutrinos are tiny particles without any electric charge. (The name translates as “little neutral one.”) According to the Standard Model, they ought to be massless, like photons, but experiments beginning in the 1990s showed that they do in fact have a tiny mass. (They’re at least a million times lighter than electrons, the extreme lightweights among normal matter.) Since physicists already know that neutrinos violate the Standard Model by having mass, their hope is that learning more about these diminutive particles might yield insights into whatever lies beyond.

Neutrinos have been slow to yield their secrets, however, because they barely interact with other particles. About 60 billion neutrinos from the Sun pass through every square centimeter of your skin each second. If those neutrinos interacted with the atoms in our bodies, they would probably destroy us. Instead, they pass right through. “You most likely will not interact with a single neutrino in your lifetime,” says Pedro Machado, a physicist at Fermilab near Chicago. “It’s just so unlikely.”

Experiments, however, have shown that neutrinos “oscillate” as they travel, switching among three different identities — physicists call them “flavors”: electron neutrino, muon neutrino and tau neutrino. Oscillation measurements have also revealed that different-flavored neutrinos have slightly different masses.

Neutrinos are known to oscillate, switching between three varieties or “flavors.” Exactly how they oscillate is governed by the laws of quantum mechanics, and the probability of finding that an electron neutrino has transformed into a muon neutrino, for example, varies as a function of the distance traveled. (The third flavor state, the tau neutrino, is very rare.)

Neutrino oscillation is weird, but it may be weird in a useful way, because it might allow physicists to probe certain fundamental symmetries in nature — and these in turn may illuminate the most troubling of asymmetries, namely the universe’s matter-antimatter imbalance.

For neutrino researchers, a key symmetry is called charge-parity or CP symmetry. It’s actually a combination of two distinct symmetries: Changing a particle’s charge flips matter into antimatter (or vice versa), while changing a particle’s parity flips a particle into its mirror image (like turning a right-handed glove into a left-handed glove). So the CP-opposite version of a particle of ordinary matter is a mirror image of the corresponding antiparticle. But does this opposite particle behave exactly the same as the original one? If not, physicists say that CP symmetry is violated — a fancy way of saying that matter and antimatter behave slightly differently from one another. So any examples of CP symmetry violation in nature could help to explain the matter-antimatter imbalance.

In fact, CP violation has already been observed in some mesons, a type of subatomic particle typically made up of one quark and one antiquark, a surprising result first found in the 1960s. But it’s an extremely small effect, and it falls far short of being able to account for the universe’s matter-antimatter asymmetry.

In July 2025, scientists working at the Large Hadron Collider at CERN near Geneva reported clear evidence for a similar violation by one type of particle from a different family of subatomic particles known as baryons — but this newly observed CP violation is similarly believed to be much too small to account for the matter-antimatter imbalance.

Charge-parity or CP symmetry is a combination of two distinct symmetries: Changing a particle’s charge from positive to negative, for example, flips matter into antimatter (or vice versa), while changing a particle’s parity flips a particle into its mirror image (like turning a right-handed glove into a left-handed glove). Consider an electron: Flip its charge and you end up with a positron; flip its “handedness” — in particle physics, this is actually a quantum-mechanical property known as spin — and you get an electron with opposite spin. Flip both properties, and you get a positron that’s like a mirror image of the original electron. Whether this CP-flipped particle behaves the same way as the original electron is a key question: If it doesn’t, physicists say that CP symmetry is “violated.” Any examples of CP symmetry violation in nature could help to explain the matter-antimatter imbalance observed in the universe today.

Experiments on the horizon

So what about neutrinos? Do they violate CP symmetry — and if so, do they do it in a big enough way to explain why we live in a matter-dominated universe? This is precisely the question being addressed by a new generation of particle physics experiments. Most ambitious among them is the Deep Underground Neutrino Experiment (DUNE), which is now under construction in the United States; data collection could begin as early as 2029.

DUNE will employ the world’s most intense neutrino beam, which will fire both neutrinos and antineutrinos from Fermilab to the Sanford Underground Research Facility, located 800 miles away in South Dakota. (There’s no tunnel; the neutrinos and antineutrinos simply zip through the earth, for the most part hardly noticing that it’s there.) Detectors at each end of the beam will reveal how the particles oscillate as they traverse the distance between the two labs — and whether the behavior of the neutrinos differs from that of the antineutrinos.

DUNE won’t pin down the precise amount of neutrinos’ CP symmetry violation (if there is any), but it will set an upper limit on it. The larger the possible effect, the greater the discrepancy in the behavior of neutrinos versus antineutrinos, and the greater the likelihood that neutrinos could be responsible for the matter-antimatter asymmetry in the early universe.

The Deep Underground Neutrino Experiment (DUNE), now under construction, will see both neutrinos and antineutrinos fired from below Fermilab near Chicago to the Sanford Underground Research Facility some 800 miles away in South Dakota. Neutrinos can pass through earth unaltered, with no need of a tunnel. The ambitious experiment may reveal how the behavior of neutrinos differs from that of their antimatter counterparts, antineutrinos.

For Shirley Li, a physicist at the University of California, Irvine, the issue of neutrino CP violation is an urgent question, one that could point the way to a major rethink of particle physics. “If I could have one question answered by the end of my lifetime, I would want to know what that’s about,” she says.

Aside from being a major discovery in its own right, CP symmetry violation in neutrinos could challenge the Standard Model by pointing the way to other novel physics. For example, theorists say it would mean there could be two kinds of neutrinos — left-handed ones (the normal lightweight ones observed to date) and much heavier right-handed neutrinos, which are so far just a theoretical possibility. (The particles’ “handedness” refers to their quantum properties.)

These right-handed neutrinos could be as much as 10^15 times heavier than protons, and they’d be unstable, decaying almost instantly after coming into existence. Although they’re not found in today’s universe, physicists suspect that right-handed neutrinos may have existed in the moments after the Big Bang — possibly decaying via a process that mimicked CP violation and favored the creation of matter over antimatter.

It’s even possible that neutrinos can act as their own antiparticles — that is, that neutrinos could turn into antineutrinos and vice versa. This scenario, which the discovery of right-handed neutrinos would support, would make neutrinos fundamentally different from more familiar particles like quarks and electrons. If antineutrinos can turn into neutrinos, that could help explain where the antimatter went during the universe’s earliest moments.

One way to test this idea is to look for an unusual type of radioactive decay — theorized but thus far never observed — known as “neutrinoless double-beta decay.” In regular double-beta decay, two neutrons in a nucleus simultaneously decay into protons, releasing two electrons and two antineutrinos in the process. But if neutrinos can act as their own antiparticles, then the two neutrinos could annihilate each other, leaving only the two electrons and a burst of energy.

A number of experiments are underway or planned to look for this decay process, including the KamLAND-Zen experiment, at the Kamioka neutrino detection facility in Japan; the nEXO experiment at the SNOLAB facility in Ontario, Canada; the NEXT experiment at the Canfranc Underground Laboratory in Spain; and the LEGEND experiment at the Gran Sasso laboratory in Italy. KamLAND-Zen, NEXT and LEGEND are already up and running.

While these experiments differ in the details, they all employ the same general strategy: They use a giant vat of dense, radioactive material with arrays of detectors that look for the emission of unusually energetic electrons. (The electrons’ expected neutrino companions would be missing, with the energy they would have had instead carried by the electrons.)

While the neutrino remains one of the most mysterious of the known particles, it is slowly but steadily giving up its secrets. As it does so, it may crack the puzzle of our matter-dominated universe — a universe that happens to allow inquisitive creatures like us to flourish. The neutrinos that zip silently through your body every second are gradually revealing the universe in a new light.

“I think we’re entering a very exciting era,” says Turner.

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Dan Falk (@danfalk.bsky.social) is a science journalist based in Toronto. His books include The Science of Shakespeare and In Search of Time.

LIVING WORLD | VIEW ON WEBSITE

How the cavefish lost its eyes — again and again

Mexican tetras that got swept into pitch-black caverns had no use for the energetically costly organs. They lost their eyes in multiple ways — and gained some nifty traits too.

By Tim Vernimmen    08.11.2025

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Mexican tetras are a most peculiar fish species. They occur in many rivers and lakes across Mexico and southern Texas, where they look perfectly ordinary. But unlike most other fishes, tetras also live in caves. And there, in the absence of light, they look dramatically different: They’re very pale and, remarkably, they lack eyes.

Time and again, whenever a population was swept into a cave and survived long enough for natural selection to have its way, the eyes disappeared. “But it’s not that everything has been lost in cavefish,” says geneticist Jaya Krishnan of the Oklahoma Medical Research Foundation. “Many enhancements have also happened.”

Though the demise of their eyes continues to fascinate biologists, in recent years attention has shifted to other intriguing aspects of cavefish biology. It has become increasingly clear that they haven’t just lost sight, but also gained many adaptations that help them to thrive in their cave environment, including some that may hold clues to treatments for obesity and diabetes in people.

Researchers look for cavefish in the Rio Subterráneo cave in Mexico.

CREDIT: COURTESY OF ANA SANTACRUZ

Casting off expensive eyes

It has long been debated why the eyes were lost. Some biologists used to argue that they just withered away over generations because cave-dwelling animals with faulty eyes experienced no disadvantage. But another explanation is now considered more likely, says evolutionary physiologist Nicolas Rohner of the University of Münster in Germany: “Eyes are very expensive in terms of resources and energy. Most people now agree that there must be some advantage to losing them, if you don’t need them.”

Scientists have observed that mutations in different genes involved in eye formation have led to eye loss. In other words, says Krishnan, “different cavefish populations have lost their eyes in different ways.”

Meanwhile, the fishes’ other senses tend to have been enhanced. Studies have found that cave-dwelling fish can detect lower levels of amino acids than surface fish can. They also have more tastebuds and a higher density of sensitive cells alongside their bodies that let them sense water pressure and flow.

Regions of the brain that process other senses are also expanded, says developmental biologist Misty Riddle of the University of Nevada, Reno, who coauthored a 2023 article on Mexican tetra research in the Annual Review of Cell and Developmental Biology. “I think what happened is that you have to, sort of, kill the eye program in order to expand the other areas.”

Killing the processes that support the formation of the eye is quite literally what happens. Just like non-cave-dwelling members of the species, all cavefish embryos start making eyes. But after a few hours, cells in the developing eye start dying, until the entire structure has disappeared. Riddle thinks this apparent inefficiency may be unavoidable. “The early development of the brain and the eye are completely intertwined — they happen together,” she says. That means the least disruptive way for eyelessness to evolve may be to start making an eye and then get rid of it.

Although eye development commences in cavefish embryos, the process ultimately stalls. Early on, there are clear differences in the activity patterns of genes (top image) involved in eye development. As a result, in cavefish embryos, the optic vesicle from which the eye develops is always smaller. Some 24 hours into development, the cells in the eye lens and the optic cup that usually becomes the rest of the eye start to die. After about five days, the light-sensing tissues at the back of the eye die too.

In what Krishnan and Rohner have called “one of the most striking experiments performed in the field of vertebrate evolution,” a study published in 2000 showed that the fate of the cavefish eye is heavily influenced by its lens. Scientists showed this by transplanting the lens of a surface fish embryo to a cavefish embryo, and vice versa. When they did this, the eye of the cavefish grew a retina, rod cells and other important parts, while the eye of the surface fish stayed small and underdeveloped.

Starving and binging

It’s easy to see why cavefish would be at a disadvantage if they were to maintain expensive tissues they aren’t using. Since relatively little lives or grows in their caves, the fish are likely surviving on a meager diet of mostly bat feces and organic waste that washes in during the rainy season. Researchers keeping cavefish in labs have discovered that, genetically, the creatures are exquisitely adapted to absorbing and storing nutrients. “They’re constantly hungry, eating as much as they can,” Krishnan says.

Intriguingly, the fish have at least two mutations that are associated with diabetes and obesity in humans. In the cavefish, though, they may be the basis of some traits that are very helpful to a fish that occasionally has a lot of food but often has none. When scientists compare cavefish and surface fish kept in the lab under the same conditions, cavefish fed regular amounts of standard fish food “get fat. They get high blood sugar,” Rohner says. “But remarkably, they do not develop obvious signs of disease.”

Fats can be toxic for tissues, Rohner explains, so they are stored in fat cells. “But when these cells get too big, they can burst, which is why we often see chronic inflammation in humans and other animals that have stored a lot of fat in their tissues.” Yet a 2020 study by Rohner, Krishnan and their colleagues revealed that even very well-fed cavefish had fewer signs of inflammation in their fat tissues than surface fish do.

Even in their sparse cave conditions, wild cavefish can sometimes get very fat, says Riddle. This is presumably because, whenever food ends up in the cave, the fish eat as much of it as possible, since there may be nothing else for a long time to come. Intriguingly, Riddle says, their fat is usually bright yellow, because of high levels of carotenoids, the substance in the carrots that your grandmother used to tell you were good for your … eyes.

“The first thing that came to our mind, of course, was that they were accumulating these because they don’t have eyes,” says Riddle. In this species, such ideas can be tested: Scientists can cross surface fish (with eyes) and cavefish (without eyes) and look at what their offspring are like. When that’s done, Riddle says, researchers see no link between eye presence or size and the accumulation of carotenoids. Some eyeless cavefish had fat that was practically white, indicating lower carotenoid levels.

Instead, Riddle thinks these carotenoids may be another adaptation to suppress inflammation, which might be important in the wild, as cavefish are likely overeating whenever food arrives.

Studies by Krishnan, Rohner and colleagues published in 2020 and 2022 have found other adaptations that seem to help tamp down inflammation. Cavefish cells produce lower levels of certain molecules called cytokines that promote inflammation, as well as lower levels of reactive oxygen species — tissue-damaging byproducts of the body’s metabolism that are often elevated in people with obesity or diabetes.

Krishnan is investigating this further, hoping to understand how the well-fed cavefish remain healthy. Rohner, meanwhile, is increasingly interested in how cavefish survive not just overeating, but long periods of starvation, too.

No waste

On a more fundamental level, researchers still hope to figure out why the Mexican tetra evolved into cave forms while any number of other Mexican river fish that also regularly end up in caves did not. (Globally, there are more than 200 cave-adapted fish species, but species that also still have populations on the surface are quite rare.) “Presumably, there is something about the tetras’ genetic makeup that makes it easier for them to adapt,” says Riddle.

Though cavefish are now well-established lab animals used in research and are easy to purchase for that purpose, preserving them in the wild will be important to safeguard the lessons they still hold for us. “There are hundreds of millions of the surface fish,” says Rohner, but cavefish populations are smaller and more vulnerable to pressures like pollution and people drawing water from caves during droughts.

One of Riddle’s students, David Perez Guerra, is now involved in a committee to support cavefish conservation. And researchers themselves are increasingly careful, too. “The tissues of the fish collected during our lab’s last field trip benefited nine different labs,” Riddle says. “We wasted nothing.”

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Tim Vernimmen is a freelance science journalist based near Antwerp, Belgium. He’d become a bit of a cavefish last winter but thankfully returned to surface-fish mode in spring.

SOCIETY | VIEW ON WEBSITE

Q&A — Archaeologist Chapurukha M. Kusimba

Civilizations of Africa through a new lens

Small settlements and the scourge of slavery left gaps in Africa’s archaeological record. Yet sites and artifacts are revealing clues to the continent’s more recent history. An archaeologist explains the findings and threats to this heritage.

By Amber Dance    08.07.2025

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The continent of Africa is recognized as the place where humankind originated and evolved over millennia. From famous ancestors like Lucy, the Australopithecus afarensis remains unearthed in Ethiopia in 1974, to the Turkana Boy, a Homo erectus fossil found in Kenya in 1984, archaeological evidence has shown time and again that Africa is the ultimate homeland of not just early hominins, but also modern Homo sapiens, who arose about 300,000 years ago and departed in successive waves to populate much of Earth.

Of course, the story of humans in Africa doesn’t end with their migration away from the mother continent. After all, many stayed put. But there’s a big information gap. Although researchers have plumbed much of humankind’s deep past, far less is known about what was happening across much of Africa at the time when permanent settlements were emerging elsewhere starting some 6,000 years ago: in places like Mesopotamia, for example, and later in China and India, as well as Egypt in Africa’s northeastern tip.

CREDIT: JAMES PROVOST (CC BY-ND)

Archaeologist Chapurukha M. Kusimba

University of South Florida

In part, that’s because African individuals did not cram together as closely as they did in more well-known cradles of civilization. So it’s less likely that modern archaeologists will discover major towns or cities. Another factor is the slave trade that slashed a 400-year wound through African history and led many communities to be abandoned. Longstanding biases about the continent, too, have left the full story of Africa’s cultures, trade and urbanism out of many history lessons.

That’s starting to change. Recent advances in East African archaeology reveal advanced civilizations that established international trade relationships and developed powerful and practical technologies during the most recent 11,700 years — the Holocene Epoch — as Chapurukha M. Kusimba, an archaeologist at the University of South Florida in Tampa, describes in the 2024 Annual Review of Anthropology.

Kusimba, who grew up in Kenya and has regularly returned there for research, says East African archaeology is evolving as more Africans and women join the field. Knowable Magazine spoke with Kusimba about African civilization and the practice of archaeology there today, as well as threats new and old that the research must contend with — from ongoing demolition of ancient sites to make way for growing populations to recent funding cuts by US institutions that long supported such studies.

This conversation has been edited for length and clarity.

I’d like to start with a question you raised in your review: Whose past is East African archaeology about?

East Africa is homeland to all of us. I’ve sometimes joked with Kenyan politicians that any human being entering Kenya should not have to present a passport, because they’re actually coming home.

I think when many of us think about East Africa, we think about the seminal work of anthropologists Louis and Mary Leakey on human origins, and the discovery of the hominin Lucy. But what do we know about the rise of civilization among modern humans, Homo sapiens, in Africa?

The human origins question has been settled, but we know precious little about the emergence of civilization in Africa.

Most Holocene archaeologists define civilization, in part, in terms of settling down in one place, which happened elsewhere starting around 6,000 years ago. But I think in Africa, that model creates a major problem because Africa is so huge, and population numbers remained low, so it was very difficult to have a critical mass of people to congregate together. So you can’t find many places in Africa that you can compare with, for example, the Near East.

That doesn’t necessarily mean settlements didn’t exist. But the jury’s still out, because we don’t have the kind of intensified site research that’s been carried out in other places. And it’s very difficult to conduct surveys, say, under the dunes of the Sahara Desert. That desert would have been much more habitable during the humid “Green Savannah” period 14,500 to 5,000 years ago, but it’s just impossible to find sites under those massive sand dunes.

We do know of some sites. For example, people were settling together as early as 3000 BCE in the site of Kadero along the Nile. There is evidence of houses, stone tools, pottery and jewelry, as well as bones of people and domesticated animals.

Still, Africanists can’t compete with Mesopotamia, with Egypt, with Mesoamerica. The result is that when you pull out any book that teaches civilization, there is only a very small section devoted to sub-Saharan civilizations.

East Africa is home to many important archeological sites that were settled in the Holocene Era, a handful of which are shown in the above map. The landmass known in the post-colonial period as Madagascar is labeled to orient the viewer; the site of the discovery of the hominin Lucy in present-day Ethiopia is also shown.

So what was going on in Africa as Mesopotamia and other regions were tending farms and building cities?

The African communities appear to have been mobile much longer. We think this is true because there are few sites of long-term settlement. The sites that are well preserved tend to be rock-shelter sites that were probably temporarily inhabited.

Nonetheless, these people were highly advanced; they ate well and lived healthy lives. For example, the Sangoan peoples of eastern and central Africa had advanced stone tool technologies and bone fishhooks. And there were people making carbon steel 2,000 years ago.

There is often a tendency to think of the European Stone Age as the first, the original, the most sophisticated phase of stone working. But you have stone tool technologies in modern-day Ethiopia and Kenya starting 2.8 to 3 million years ago, earlier than it began in Europe.

Of course, the European Paleolithic tools were incredibly sophisticated, but the core stone was relatively easy to work; in contrast, African stone is much harder to work than European stone. If you give any modern flintknapper African rock, they immediately recognize how difficult it is. But Africans were using these very tough materials to make extremely sophisticated tools.

And what happened when Africans finally started to settle down?

In most cases, permanent settlements appear in Africa 3,000 or 4,000 years after they did in places like the Near East. About 8,000 years ago, we begin to see more extensive evidence of settled life in modern-day western Kenya, eastern Uganda and the African Great Lakes region — and I think climate change might have been a reason behind that societal change. Suddenly, around 7,000 to 8,000 years ago you have a dry spell that lasts for about 700 years, and that’s when you see the introduction of pastured livestock.

So Africans did get there eventually, but we don’t see the real emergence of highly complex chiefdoms and societies, with more division of wealth, in much of Africa until about 2,500 years ago. That division of wealth is apparent in differences between households. Some have exotic items from distant places and most others didn’t. Just like today, there are things that only elites can acquire. Most likely, they were gifts, given to grease the wheels of business for trade of desirable items.

For example, the port town of Mtwapa, near modern-day Mombasa, Kenya, was inhabited from about 1100 to 1750 CE. Wealthy inhabitants possessed multiroom homes with coral door frames and roof tiles, indoor plumbing and wells; poorer denizens lived in single-room homes of mud and wood, with grass or coconut thatch roofs. Wealthy citizens also reserved the right to the most sacred burial places, near a key religious site.

From about 2,000 years ago, there were towns all over sub-Saharan Africa, including inland and along the coasts. But many African settlements were smaller in size compared to similar communities elsewhere. For example, the medieval site of Gedi, in modern-day Kenya, was massive by African standards, but at about 48 acres of built-up areas, it was much smaller than contemporary sites in India, China or the Near East. But we believe these sites were built and inhabited by Africans, not immigrants from other civilizations, because 96 percent of artifacts such as pottery, metals and beads found in those cities are of local origin.

Gedi is another precolonial African site that was occupied from about 1000 to 1500 CE. The courthouse from the site is shown.

CREDIT: CHAPURUKHA M. KUSIMBA

A perfect example of an advanced community, located inland, would be the region of Great Zimbabwe, which was inhabited from about the 11th to 15th centuries CE. It covered about 50,000 square kilometers, including early village settlements and a stone city built later. Great Zimbabwe is an amazing place, but the residential quarters were built out of mud, stone and thatch so they didn’t preserve well archaeologically.

How did these societies interact with the rest of the world?

My work and the work of others shows that before the African slave trade, which reached the continent’s interior with slave caravans starting in the 17th century, Africans were trading with other cultures. We’ve found glass and carnelian beads of Indian origin in every archaeology site in sub-Saharan Africa. Chinese and Indian historians also describe the presence of African mariners in their own towns, so the trade was bidirectional: Africans traded ivory and gold for products such as Chinese porcelain and Indian cloth.

Crops were also exchanged. For example, sorghum is a traditional African crop. It’s hard to date its origins, but it was being cultivated in Africa from at least the fourth millennium BCE. And it arrives in places like India later. Meanwhile, the banana, first domesticated in southeast Asia, arrived in central Africa more than a thousand years ago.

And Africans were trading as equals. Here’s one reason I think so: From at least 800 CE, there is clear evidence that people were engaging in the ivory trade, but they traded in mostly cut ivory. This allowed them to weigh it, grade it, and assign value consistent with quality. Cut ivory was also easier to transport from inland to trade partners on the coast. Before the slave trade Africans financed and were in charge of the ivory and other industries.

Later, around the 1500s when smaller-scale slave trading began in some regions, that evidence disappears and you begin to see transportation and sale of whole, unprocessed ivory tusks. Similarly, around that time, the evidence of industries such as iron smelting and weaving disappears. The emergence of slavery led to loss of control of their own industries. Work is outsourced, and materials such as cloth are imported. So as people lose skills and become more dependent on external trade, you begin to see a real decline in the political economy of these places.

Research suggests that many of the glass beads found in African archaeological sites were made locally, but others came from overseas via established trade relationships.

CREDIT: LAURE DUSSUBIEUX / THE FIELD MUSEUM

How else did the slave trade impact African civilizations?

The 400 years of slavery had a huge, huge effect on this continent. Africans were being invaded both from the Islamic world and, of course, the Western world.

Up to that point, communities had settled in comfortable places, such as plains and valleys. There are numerous abandoned settlements with single-household villages, but also remnants of crops such as mangoes, oranges and rice in what is now the Tsavo National Park. These communities provided food to more urban cities along the coasts.

But then, suddenly, they all disappeared. From around the 1450s up to the time of the colonial period beginning in the 1870s, we have found little evidence of new, permanent buildings in the interior of Africa — why is nothing being constructed there? In Tsavo, for example, people migrated to uninhabitable but defensible lands, such as hillsides and mountains, for safety. They could not go back to the plains because they were not safe.

As these events were happening inland, we also begin to see the abandonment of the coastal towns. They lost their inland food supply. Prior to the slave trade, there were 250 thriving towns in Kenya and Somalia alone. By the time the 400 years of slavery are over, there were, perhaps, less than 10 of those towns still being sustainably inhabited.

Slavery and the slave trade led to a loss of knowledge, of power, of memory. This violent gap that history created would open Africa for others to exploit while also conveniently blaming Africans for not being innovative, for not having industries, for not contributing much to global history, even though they did have advanced societies and technologies.

Yet despite this, I think we must credit Africans for their resilience. Despite the genocide that they experienced, they’re still standing.

How has East African archaeology changed over your career?

I’m now in my 60s. In my time, there were a handful of African-born archaeologists, probably fewer than five. But today the number of African-born archaeologists, most of whom are our students, has grown. It’s rare to see a major paper on East Africa that does not include African authors — though, unfortunately perhaps, the names of those in leadership positions, such as museum directors and department chairs, are often on these publications, which creates the impression that young scientists who do most of the research are not being fully acknowledged.

On the other hand, in Europe and the United States, there has been a huge increase in the number of women archaeologists. Obviously, during the colonial period, most of the archaeologists were men, and perhaps they were not much interested in questions of gender dynamics in prehistoric societies. Today most active North American archaeologists working in East Africa are women.

This presents a lot of opportunities: For the first time, we have a moment in which women can have a real footprint in the kinds of topics they want to pursue — for example, what role did prehistoric African women play in shaping these societies?

But there are also challenges for these scholars, because there are parts of East Africa and elsewhere where it might be much harder for women leading an expedition to get the kind of respect they richly deserve and have earned.

African bioarchaeologist Sewasew Hailesellasie Assefa analyzes remains from Gedi. More women and Africans are joining the field.

CREDIT: CHAPURUKHA M. KUSIMBA

What would you like to see archaeologists in East Africa pursue in the future?

We are in the news all the time with major discoveries — but most of the time, it’s new information about large sites that are already well known, and that have been studied since the colonial period. A lot of studies are being done on museum collections in Europe and North America, too. Many of these artifacts were collected during the colonial period and are often criticized today because some of them were looted from their original locations, and many people think these artifacts should be returned to their original countries. We are not seeing surveys and descriptions of new sites, and that concerns me.

I think that East African archaeology is very much tied to global climate change, and this is something that is really important to us today. If you look at the history of people living in East Africa for 4 million years: What did they do to survive? How did they cope with climate change? We could learn a lot from that research.

Many sites that have been all but forgotten, but deserve attention, are Homo erectus sites. Homo erectus is, anatomically, our direct ancestor. They lived from about 1.9 million to 110,000 years ago. Homo erectus is credited with learning to manage fire, which may have enabled their kind to leave Africa and inhabit other parts of the world. We’ve seen so many advances in biochemistry and in the study of ancient DNA, and I hope these techniques could be applied to Homo erectus sites to reveal more than we know now. But their rapid destruction in Kenya is alarming.

What other sites have been lost, or are at risk?

The Leakeys did a great job in sensitizing East Africans to their long past and their responsibility to care for that history. You can go to any part of Tanzania, Kenya or Ethiopia and find people who are proud of that past, who welcome archaeologists to do all kinds of research.

But we are also dealing with population growth. When I was young, Kenya’s population was about 8 million, then 15 million, and now it is more than 55 million. There’s been similar population explosions in Tanzania, in Uganda, in Rwanda, in Burundi, in Ethiopia. And these people must live somewhere. As in the past many people have migrated. And they move into new areas where they are less emotionally engaged in local histories; they destroy archaeological sites that hold the histories and sacred knowledge of earlier residents.

So we have lost a lot of urban sites along the east coast of Africa. I think we archaeologists need to communicate their importance better, and these nations need to manage the heritage sites better. If we can conserve some of these sites, we can make our case for their future study. If we don’t, we will fail future generations of young men and women who want to be archaeologists.

Will East African archaeology be able to continue in the face of such threats, including the loss of those sites and funding woes?

Most African governments, with the exception of South Africa and Egypt, do not have dedicated funds for this kind of research. The bulk of funding for archaeology has always come from the United States and Europe. For example, the US National Science Foundation has been one of the engines that funded a lot of archaeology research around the world, but US funding of research has been slashed recently.

I think that those moments of change are very important, not only for people in East Africa, but for the rest of us. These funding cuts are very tragic, but this research is very important, and despite threats to supporting research on our origins, I remain optimistic that we’ll find a way to continue research of the deep history of humankind in East Africa.

Editor’s note: This article was updated on August 19, 2025, to correct the date, location and type of iron production. People were producing carbon steel at least 2,000 years ago in part of East Africa, not high-carbon steel 2,900 years ago in modern Uganda.

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Amber Dance is a freelance science journalist in the Los Angeles area and a special contributor for Knowable Magazine.

SOCIETY | VIEW ON WEBSITE

Q&A — Self-governance and marine sustainability scientist Xavier Basurto

Uncovering the impact of artisanal fisheries

Small-scale fishing has long been ignored by public policy, scientific research and global economics, but its potential to help end hunger and poverty is huge. New work is bringing it out of the shadows.

By Iván Carrillo    07.31.2025

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When Xavier Basurto first arrived on the island of Newfoundland, he realized that the surrounding seas did more than define the horizon — they defined the very lives of its inhabitants. A Mexican self-governance and marine sustainability scientist, Basurto had come to this spot on the eastern tip of Canada in 1997 as part of a student exchange program. At that time, the region was suffering from the collapse of one of its most valuable resources: the Atlantic cod (Gadus morhua). An indefinite fishing moratorium was affecting the livelihoods of 40,000 small-scale and industrial-scale fishermen and workers at fish processing plants.

At Newfoundland’s Memorial University, the young student found that some fishermen had decided to reinvent themselves by returning to the classroom. One day, one of them confronted a professor describing aquaculture techniques, pivoting the discussion instead to social issues. “That made a big impression on me,” Basurto says. After all, human and cultural issues were what largely determined whether these technical aspects of fishing “were implemented or not, whether they worked or not, or whether they were adopted or not.”

It was a thought that has shaped the approach from which Basurto — now at Stanford University — has sought to understand the complexity of what is termed artisanal fishing — small-scale fishing that is a way of life, more than a job or trade. Basurto wants to understand the practice not only as an activity of food production and commerce, traditionally measured in millions of tons of catch and in monetary value, but as a social, ecological and cultural practice of people in coastal communities.

CREDIT: JAMES PROVOST (CC BY-ND)

Self-governance and marine sustainability scientist Xavier Basurto

Stanford University

It is an activity often overlooked by governments, scientists, nongovernmental organizations and the private sector, yet its scale is huge. In a recent analysis in Nature, Basurto and his coauthors estimate that artisanal fishing accounts for at least 40 percent of global fish catches. In addition, small-scale catches are made by 90 percent of the world’s fishing population and generate 44 percent of the total economic value of fish that is taken from the sea and landed in ports for sale.

But perhaps most revealing is the practice’s social and nutritional importance: One in 12 people in the world depends, partially or completely, on artisanal fishing for their livelihood. In addition, artisanal fishing has the potential to provide essential micronutrients — vitamins and minerals that the body requires in small amounts to function properly — to one in four people on the planet.

Small-scale fishing is also wrapped up in marine conservation, as it takes place in highly productive and biodiverse ecosystems.

Basurto talked with Knowable Magazine about artisanal fishing and why, given its crucial role in food security and marine conservation, it doesn’t have a more central place in political and scientific decision-making. This conversation has been edited for length and clarity.

How do you define artisanal fishing? What is its main difference from industrial fishing?

Artisanal fishing differs from industrial fishing in that the latter takes place in more oceanic waters, with the use of much more technology, capital and automation, and less labor.

The definition of artisanal fishing is controversial because it is very difficult to arrive at a definition that encompasses the full diversity of practices it includes. In some places, artisanal fishing is done on foot, without boats. In others, it is done in wooden canoes, fiberglass boats or even more sophisticated vessels. But in general terms, it includes pre-catch, catch and post-catch activities in coastal areas, carried out with simple technologies, little investment and high labor intensity.

To arrive at more concrete definitions, we would need to identify as many forms of artisanal fishing around the world as possible, and create categories that capture them in a reliable, consistent and practical way. For example, we have identified a category that we call “small-scale fishing as a nutritional and income safety net,” characterized by the use of little technology and little capital in shallow coastal and estuarine waters in the Global South. The catch is usually for personal consumption or is exchanged or sold in local markets, and the owners of the equipment or boats generally work individually or in family cooperatives, without a paid crew. Other examples include women that gather clams and oysters in estuaries in the Philippines or Thailand, or free divers harvesting chocolate clams in the state of Baja California Sur to sell in local restaurants.

Gloria Temporada, 59, shows her catch of mussels in Tangub, Philippines, harvested from shallow, coastal banks that emerge with the tide. Such banks are just one of many diverse environments where small-scale fishing takes place.

CREDIT: © FAO / DAVID HOGSHOLT

There is another category that we call “small-scale fisheries as economic engines.” These are characterized by greater capital, investment and technology, which makes them more formalized and integrated into national economies. Motorized vessels with better storage and refrigeration capacity mean less dependence on coastal waters and local markets, sometimes sustaining trade between distant locations.

Considering both artisanal and industrial fishing, what is the current state of fishing globally?

The status is very diverse. On the one hand, in rich countries, you have very well-managed industrial fisheries. Fishing that could be described as sustainable because a lot of information is available, and that information is used.

On the other hand, in developing countries, you have many industrial fisheries that are overexploited and where information is available but little is done in terms of management.

Artisanal fishing is also very diverse and exists in both developing and developed countries. I believe it has the same characteristics: There are very well-managed artisanal fisheries in the United States, Canada, Iceland, Japan and Norway, which have a very good level of information, and not so much in developing countries, where there is almost no management and a lot of overfishing.

What is the role of artisanal fishing in global food security and nutrition?

Globally, artisanal fishing is much more important than industrial fishing as a source of food.

Although industrial fishing dominates global catches in terms of volume, it is artisanal fishing that plays a decisive role as a source of nutrition and livelihood for millions of people. It accounts for at least 40 percent of the world’s fish catch — some 37.3 million tons per year — but the true value of artisanal fishing lies not only in quantity, but in who it feeds. Potentially, up to 2.3 billion people could obtain 20 percent of their essential micronutrient intake through it. Many of these people belong to highly marginalized populations, as is the case in Africa and Oceania.

Likewise, our research showed that, in the countries analyzed, an average of 79 percent of small-scale fisheries catch is destined for domestic use, confirming that its main use is to meet local nutritional needs. In industrial fishing, only 62 percent of the catch is destined for direct human consumption, while the remaining 38 percent is used for nonfood purposes, such as the production of fish meal used in cosmetics or pet food.

Artisanal fishing is especially important for food in regions where access to food with high nutritional value is limited, whether for economic reasons related to the high cost of transportation to marginalized areas, or geographical reasons — extremely hot or desert regions, high latitudes with very short growing seasons, or areas subject to seasonal flooding, such as the Amazon or the Sundarbans delta in the Bay of Bengal.

In regions where artisanal fishing is key to food security, high levels of malnutrition and hunger persist. According to data from 2023, 384.5 million people in Asia and 298.4 million in Africa suffer from hunger. How can this situation be explained?

In some of these places, the supply of nutrients from artisanal fishing exceeds the consumption of these nutrients. In other words, people prefer to eat other foods with lower nutritional value, even though they have access to fish with high nutritional quality.

In other cases, poor handling of fish once it has been caught causes it to lose its nutritional value. For example, not putting it on ice immediately, either because of ignorance or lack of resources to buy ice. In other cases, the food culture does not make appropriate use of all the nutrients available: Eating only the fillet has less nutritional value than eating the head as well, which contains many more micronutrients than the fillet.

In your study published in Nature, you highlight the contribution of essential micronutrients that artisanal fisheries can provide to billions of people. How did you calculate this potential contribution?

“The most important thing is to understand that artisanal fishing is not a job, but a way of life. It is not an occupation. It is an identity.”

— XAVIER BASURTO

First, fish catch data were collected from 58 countries and extrapolated to cover a total of 186 countries. The objective was to quantify how much artisanal fisheries could contribute to local nutrition.

Recognized databases (such as FishBase and INFOODS) were then used to obtain information on six key nutrients found in aquatic products: calcium, iron, selenium, zinc, vitamin A and omega-3 fatty acids. Although the latter is not a micronutrient in the strict sense, it was included because of its relevance to human health.

With this information, the average concentration of nutrients per group of fish species was estimated, weighted according to catch volume. This concentration was then multiplied by the annual amount of fish caught, and by the edible portion.

To understand how much this represents per person, the total daily nutrients were divided by the population living within 20 kilometers of the sea or freshwater bodies, and the per capita contribution was estimated.

Finally, this nutritional contribution was compared with the total micronutrient consumption of each country, using global dietary data.

According to the research, artisanal catches have the potential to contribute on average 20 percent of the dietary intake of six key micronutrients: up to 50 percent of omega-3 fatty acids, 28 percent of selenium, more than 10 percent of calcium and zinc, 9 percent of iron, and 3 percent of vitamin A.

In the Infiernillo Channel, Sonora, Mexico, divers like the one in the photo enter the sea to catch callos de hacha (Atrina maura), mollusks highly prized for ceviche. Diving is a form of artisanal fishing.

CREDIT: XAVIER BASURTO

Despite its great economic and social importance, artisanal fishing has historically been invisible. Why is there this lack of recognition?

To understand the causes, we must understand the history of Western fisheries science, which was developed by scientists from rich countries to solve industrial fisheries management problems. As a result, economic resources, accounting strategies, data collection and official management were concentrated on industrial fishing.

In the 20th century, as fishing technology advanced, so did the knowledge of how to fish in large quantities and to understand how many fish there are. As industrial fishing became more organized, more information was demanded. Industrial fishing is organized into trade associations and, therefore, has historically developed a constant dialogue and reciprocal political-economic relationships with decision-makers at the government level.

Governments respond by producing science at universities in the United States, Canada, Japan, Norway and Iceland, among others. But this is science about industrial fishing, not science designed for artisanal fishing. It is not science created by developing countries. All these factors have resulted in a dominance of attention from decision-makers toward industrial fishing.

So, there is no interest in looking at artisanal fishers?

Exactly. That is one of the factors. In many cases, artisanal fishers are not organized into associations. The other factor is that, even if the government had an interest without artisanal fishers asking for it, it is difficult to collect data from fishers who are widely dispersed along the coast, in isolated places where the government has little access or influence. And the third factor is that states may say, “Well, what’s the point if the income they generate is not enough to justify government spending?”

A fisherman uses a cast net — a type of circular fishing net with small weights distributed around its edge — to catch shrimp in the Mar Muerto Lagoon in Chiapas, Mexico. The fisherman throws the net into the lagoon so that it spreads out in the air before sinking into the water, and the shrimp are caught when the net is pulled in. This is a traditional practice long used to catch crustaceans, mollusks and small fish.

CREDIT: XAVIER BASURTO

Is this from the perspective of developed countries?

From the perspective of the first world but, more importantly, from the perspective that the only thing you get from fishing is money. It is a perspective where the only thing that comes out of the water is volume of fish and money.

Why is it important to go beyond fish volume?

It is very important to go beyond the catch to change the perception that only money comes out of the water. And to value artisanal fishing in a different way. The activity can also promote gender equality in rural populations; a culture of involvement in fisheries management by fishermen, through giving them more management rights; essential micronutrients for food security; employment and work dignity. By quantifying all these contributions, it is easier to see them and make it tangible that fish is not just catch volume. It is much more than that.

What role do women play?

Four out of 10 fishermen are women. They may be part of the family business — wives, mothers, daughters — or simply women from the community hired to do the work. In this calculation, we take into account pre-catch, catch and post-catch activities. It is in the latter where women’s participation is much more prominent. Their activities include cleaning, processing, packaging, marketing and selling the fish. Their work remains invisible because, in many cases, fishing is only understood as the process of catching fish.

A woman spreads out sprats in the sun on the shores of Lake Tanganyika, Tanzania. Her work reflects the essential role of women in the post-harvest chain of artisanal fishing.

CREDIT: © FAO / LUIS TATO

Because of that, rights to participate in decision-making or be counted in censuses that determine who is eligible for social security funds or unemployment benefits, among other things, are only granted to the individual on the boat. It is that individual who is considered and labeled a “fisher.” The rest of the population working in pre- and post-catch activities does not exist in the statistics or social security programs such as health insurance and access to retirement, sickness or disability pensions.

Not only does this make the role of women invisible, but it also makes them very vulnerable to machismo and sexism, as in the case of Lake Victoria in Kenya, where it has reached the extreme that women can only sell fish if they perform sexual favors for men, as demonstrated by Kathryn Fiorella, an environmental scientist and epidemiologist at Cornell, in her study.

What public policies should be established to strengthen artisanal fishing?

I’ll tell you something very specific: preferential access areas. This is a policy that exists in many countries but is rarely used, whereby artisanal fishers have preferential rights to use a strip of coastline. We don’t have data to know what percentage of artisanal fishing benefits from this, but we do know that at least 44 coastal countries have them in their regulations and that the impact could be very positive for artisanal fishing if they were monitored and respected. They can be scaled up by designating more preferential access areas in places where they don’t exist and implementing them through monitoring.

What is life like for a family that lives and works in artisanal fishing?

Well, I think the most important thing is to understand that artisanal fishing is not a job, but a way of life. That it is not an occupation — it is not that I am a fisherman during the day and someone else the rest of the time. It is an identity.

What does that mean? It means that part of your culture, part of what makes you who you are, is completely interwoven with the activity of fishing.

Can artisanal fishing contribute to the sustainability of the seas?

Of course, because the activity takes place in the most productive areas, where there is greater biodiversity. Fishermen are the users of these ecosystems.

So we have to work with those users. We may say, “No, they don’t know how to do it,” and we may think that a new user will be able to do it better. But most likely they will not, because they have even less knowledge, since their culture does not depend on that ecosystem.

Artisanal fishermen are essential because, in many cases, generations have been rooted in these places. They have an interest in being able to continue living there in the future. And therefore, it is more likely that fishermen will be willing to tackle problems that require effective collective action to find solutions to the most important challenges facing the sustainability of our seas — such as overfishing, pollution, mass tourism, irresponsible aquaculture, and oil, gas and mineral exploitation.

Fishermen will not always be able to find solutions on their own. Achieving long-term sustainable solutions will require the involvement of other sectors of society. We must not forget that although they are the ones who depend most on the solutions, they are also the ones with the fewest resources to achieve them.

Article translated by Debbie Ponchner

10.1146/knowable-073125-1

Iván Carrillo is a science journalist and documentary filmmaker based in Spain covering topics such as climate change, pollution and biodiversity conservation. He is currently an explorer for the National Geographic Society and a Pulitzer Center fellow. He is the founder and editor of Historias Sin Fronteras and Celsius Media.

TECHNOLOGY | VIEW ON WEBSITE

Super-resolution microscopes showcase the inner lives of cells

Advanced light microscopy techniques have come into their own — and are giving scientists a new understanding of human biology and what goes wrong in disease

By Katarina Zimmer    07.15.2025

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Using a tiny, spherical glass lens sandwiched between two brass plates, the 17th century Dutch microscopist Antonie van Leeuwenhoek was the first to officially describe red blood cells and sperm cells in human tissues, and observe “animalcules” — bacteria and protists — in the water of a lake.

Increasingly powerful light microscopes followed, revealing cell organelles like the nucleus and energy-producing mitochondria. But by 1873, scientists realized there was a limit to the level of detail. When light passes through a lens, the light gets spread out through diffraction. This means that two objects can’t be distinguished if they’re less than roughly 250 nanometers (250 billionths of a meter) apart — instead, they’ll appear as a blur. That put the inner workings of cell structures off limits.

Electron microscopy, which uses electron beams instead of light, offers higher resolution. But the resulting black-and-white images make it hard tell proteins apart, and the method only works on dead cells.

Now, however, optics engineers and physicists have developed sophisticated tricks to overcome the diffraction limit of light microscopes, opening up a new world of detail. These “super-resolution” light microscopy techniques can distinguish objects down to 100 nanometers and sometimes even less than 10 nanometers. Scientists attach tiny, colored fluorescent tags to individual proteins or bits of DNA, often in living cells where they can watch them in action. As a result, they are now filling in key knowledge gaps about how cells work and what goes wrong in neurological diseases and cancers, or during viral infections.

“We can really see new biology — things that we were hoping to see but hadn’t seen before,” says molecular cell biologist Lothar Schermelleh, who directs an imaging center at the University of Oxford in the United Kingdom. Here’s some of what scientists are learning in this new age of light microscopy.

Overcoming the diffraction limit

Super-resolution microscopy uses a variety of techniques to detect detail that would normally be hidden by the diffraction limit, Schermelleh explains. Single-molecule localization microscopy, for instance, takes advantage of the fact that spots on an image are easier to localize with precision when they appear in isolation rather than clustered together. Scientists label the molecules of interest with fluorescent tags designed to spontaneously emit light. As the probes twinkle on and off, computational models estimate exactly where each molecule is located — and reconstruct a high-resolution image of the sample.

Another technique, stimulated emission depletion, scans the samples with lasers that are surrounded by a second, donut-shaped ring of lasers that cancel out the fluorescent light around the area of interest, sharpening the microscope’s resolution. A third method, called structured illumination microscopy, illuminates samples with a striped pattern of light. These stripes interfere with the light emanating from the sample in ways that allow scientists to infer additional detail about the image.

The fundamentals of these techniques were developed in the early 2000s, but they’ve only recently become widespread and accessible enough for biologists to use routinely, Schermelleh says. “We now have really lots of projects that use super-resolution microscopy as a genuine tool for biological discovery,” he says, “not just for making nice images.”

Revising biology textbooks

These techniques have already revealed new cell structures. Scientists have discovered that neurons have a unique kind of scaffold, called the membrane-associated periodic skeleton, or MPS, which provides rigidity and form and helps to regulate the signals that pass from one neuron to the next and to maintain the cells’ overall function. “The MPS is involved in almost all the neuronal functions,” says Columbia University neurobiologist Victor Macarrón-Palacios, who recently reported with colleagues that a particular protein, paralemmin-1, is responsible for organizing the intricate structure of the MPS.

Specialized microscopy techniques have revealed that nerve cells have a special type of internal skeleton called the membrane-associated periodic skeleton. The well-ordered nanoarchitecture of this skeleton is regulated by a protein called paralemmin-1 (fluorescently labeled in this image).

CREDIT: VICTOR MACARRÓN-PALACIOS / MAX PLANCK INSTITUTE FOR MEDICAL RESEARCH

Other cell structures, too, turn out to be more complex than they seemed. Earlier in 2025, biophysicist Melike Lakadamyali of the University of Pennsylvania and colleagues discovered that organelles called lysosomes, whose textbook role is to break down waste material in cells, can have different combinations of proteins on their surfaces. This likely relates to additional functions that specific lysosomes have, such as sensing nutrients and repairing broken membranes.

Scientists also have been studying how organelles interact with one another. Cell biologist Jennifer Lippincott-Schwartz of the Howard Hughes Medical Institute’s Janelia Research Campus in Virginia, for instance, is scrutinizing the structures that mitochondria use to dock onto the protein-making endoplasmic reticulum, which supplies calcium and fats to mitochondria.

Such studies might help reveal the causes of disease. Last year, Lippincott-Schwartz learned that mutations in the VAPB gene, which is believed to contribute to the nerve-killing disease amyotrophic lateral sclerosis (ALS), may interfere with the ability of the endoplasmic reticulum to connect to mitochondria, she says. This could alter the function of these powerhouses and help explain how ALS arises. “We’re just learning what these various genetic mutations that underlie some of these diseases are actually doing at the cell biological level.”

Gazing into human DNA

Scientists have also been peering into the nucleus and studying the DNA inside it. Human DNA, if removed from a single cell and stretched out, would span about two yards. To squeeze inside the nucleus, it wraps itself around proteins called histones, creating a string-of-beads combo known as chromatin. The chromatin further loops and twists, to form our chromosomes.

Chromatin loops and bunches, or domains, can only be studied in detail with super-resolution microscopy, for instance by tagging segments of DNA with fluorescent probes, says Schermelleh, who has been studying how the material arranges itself in 3D in mammalian cells. “The size scale is just below the diffraction limit, so it couldn’t be assessed before.”

Within a fibroblast cell nucleus, the DNA-binding histone protein called H2B is fluorescently labeled in yellow. The top half was imaged with conventional wide-field fluorescence microscopy; the bottom half was imaged with super-resolution microscopy.

CREDIT: M.A. RICCI ET AL / CELL 2015

Research by Lakadamyali has revealed, for instance, that the DNA-histone strings of beads organize into much more variable structures than scientists had assumed, with some regions of DNA more tightly packed than others.

This packaging determines how accessible a given region of DNA is. And that’s important, because different cells in the body, say heart cells or neurons, use only a specific subset of their genes. The ones they use are left in a looser, more accessible state, while the silenced ones are packed tight.

In 2015, Lakadamyali found that embryonic stem cells, which can develop into any cell type, have a very loose chromatin structure compared to more specialized cells, which have silenced the genes they don’t need. “We can actually determine whether a cell is a stem cell or a differentiated cell based on the spatial organization of chromatin,” says Lakadamyali, who coauthored a 2023 overview of super-resolution techniques in the Annual Review of Biophysics.

Improving cancer therapies

Scientists are also examining cells affected by disease. For example, biophysicist Markus Sauer of the University of Würzburg in Germany is studying certain receptor proteins on the surfaces of cancer cells that are used as targets in cancer-killing therapies. For blood cancers, for instance, scientists have genetically engineered immune cells to find and kill cancer cells that have specific surface proteins.

But the techniques commonly used to analyze the proteins on patients’ cancer cells and match patients with effective therapies don’t give a full picture, Sauer says. That was illustrated back in 2015, when physicians discovered they could successfully treat patients with the blood cancer multiple myeloma with therapies that target a receptor called CD19 — even though CD19 hadn’t been spotted on multiple myeloma cancer cells with standard methods.

Sauer and colleagues found in 2019 that the CD19 proteins were clearly visible with super-resolution microscopy. They learned that to do their killing job, the immune therapies require as few as 10 CD19 proteins among hundreds or thousands of other proteins on a cancer cell surface.

A new microscopy technique can light up the protein CD19 on the surface of cancer cells. Detecting the protein, shown here on a cell from a patient with multiple myeloma, helps determine which patients could benefit from CD19-targeting therapies.

CREDIT: MARKUS SAUER

These microscopy techniques can be used to better match patients to effective therapies, Sauer says. His more recent research has identified a new receptor protein for therapies to target, and helped elucidate the exact process of tumor killing — knowledge that could help improve the potency of immune therapies. “You have to visualize those processes at molecular level,” he says.

Filming viral invasions

The wily tricks viruses use to infect human cells and reproduce are also under investigation. Understanding such dynamics could help scientists develop new antiviral medicines, says virologist Christian Sieben of the Helmholtz Centre for Infection Research in Germany.

Earlier in 2025, for example, Sieben reported how the influenza A virus infects human cells. By tagging viral and human proteins, he and colleagues watched the virus first latch onto single receptor proteins on the cell surface. The virus then waited until other receptor proteins, moving around in the fluid cell membrane, accumulated nearby. Only when the virus attached to multiple receptors could it enter the cell, Sieben and his colleagues learned.

And in 2024, a team of scientists at Stanford University examined how the Covid-19 virus replicates inside human cells. Using fluorescent tags to label the virus’s genetic material, biophysicist Leonid Andronov and colleagues found that SARS-CoV-2 makes a bubble with a double membrane in which it copies its genetic material. This probably prevents destruction by the cell, Andronov says.

When the Covid-19 virus is being copied in human cells, it hides from the cell’s immune system by wrapping itself inside double-membrane bubbles, seen as clumpy aggregates of the virus’s fluorescently labeled genetic material. The cell’s nucleus appears as a dark circle in the middle.

CREDIT: L. ANDRONOV ET AL / NATURE COMMUNICATIONS 2024

As more and more scientists use super-resolution microscopy to illuminate the goings-on inside cells, how much more detail can they expect to see? Refinements like creating smaller fluorescent probes — so that one can label multiple sites along a single protein — could push the resolution further, Lakadamyali says.

Perhaps one day super-resolution advances might rival those of electron microscopy. After all, just two decades ago, “we didn’t know that we could break the diffraction limit,” she says. “We’ve made so much progress in a 20-year period. I think it’s possible.”

Editor’s note: This article was updated on July 17, 2025, to correct the hyperlinked article on the phrase “have different combinations of proteins.”

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Katarina Zimmer is a science and environment journalist based in Berlin and a special contributor to Knowable Magazine. Her work has also appeared in the Atlantic, National Geographic, Scientific American, Mongabay, BBC Future and elsewhere. Check out more of her work at www.katarinazimmer.com.

TECHNOLOGY | VIEW ON WEBSITE

Mighty mitochondria: Cell powerhouses harnessed for healing

Infusion of the tiny, sausage-shaped structures helps to rejuvenate tissues deprived of blood. Researchers hope the technique can treat a variety of damaged organs.

By Jackie Rocheleau    07.08.2025

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James McCully was in the lab extracting tiny structures called mitochondria from cells when researchers on his team rushed in. They’d been operating on a pig heart and couldn’t get it pumping normally again.

McCully studies heart damage prevention at Boston Children’s Hospital and Harvard Medical School and was keenly interested in mitochondria. These power-producing organelles are particularly important for organs like the heart that have high energy needs. McCully had been wondering whether transplanting healthy mitochondria into injured hearts might help restore their function.

The pig’s heart was graying rapidly, so McCully decided to try it. He loaded a syringe with the extracted mitochondria and injected them directly into the heart. Before his eyes, it began beating normally, returning to its rosy hue.

Since that day almost 20 years ago, McCully and other researchers have replicated that success in pigs and other animals. Human transplantations followed, in babies who suffered complications from heart surgery — sparking a new field of research using mitochondria transplantation to treat damaged organs and disease. In the last five years, a widening array of scientists have begun exploring mitochondria transplantation for heart damage after cardiac arrest, brain damage following stroke and damage to organs destined for transplantation.

This graphic depicts the basic steps and results of mitochondrial transplantation. Scientists think that donor mitochondria fuse with the recipient cells’ mitochondrial networks. Then they work to shrink the size of the infarct (the area of tissue dying from lack of blood and oxygen), among other effects. Scientists have studied such transplants in kidneys, livers, muscle, brains, hearts and lungs.

Mitochondria are best known for producing usable energy for cells. But they also send molecular signals that help to keep the body in equilibrium and manage its immune and stress responses. Some types of cells may naturally donate healthy mitochondria to other cells in need, such as brain cells after a stroke, in a process called mitochondria transfer. So the idea that clinicians could boost this process by transplanting mitochondria to reinvigorate injured tissue made sense to some scientists.

From studies in rabbits and rat heart cells, McCully’s group has reported that the plasma membranes of cells engulf the mitochondria and shuttle them inside, where they fuse with the cell’s internal mitochondria. There, they seem to cause molecular changes that help recover heart function: When comparing blood- and oxygen-deprived pig hearts treated with mitochondria to ones receiving placebos, McCully’s group saw differences in gene activity and proteins that indicated less cell death and less inflammation.

About 10 years ago, Sitaram Emani, a cardiac surgeon at Boston Children's Hospital, reached out to McCully about his work with animal hearts. Emani had seen how some babies with heart defects couldn’t fully recover after heart surgery complications and wondered whether McCully’s mitochondria transplantation method could help them.

During surgery to repair heart defects, surgeons use a drug to stop the heart so they can operate. But if the heart is deprived of blood and oxygen for too long, mitochondria start to fail and cells start to die, in a condition called ischemia. When blood begins flowing again, instead of returning the heart to its normal state, it can damage and kill more cells, resulting in ischemia-reperfusion injury.

Since McCully’s eight years of studies in rabbits and pigs hadn’t revealed safety concerns with mitochondria transplantation, McCully and Emani thought it would be worth trying the procedure in babies unlikely to regain enough heart function to come off heart-lung support.

The left image shows rat heart cells that did not receive a transplant. The three other images show (left to right): donated mitochondria (yellow-green) outside of rat heart cells two hours after transplantation; donor mitochondria inside cells eight hours later; and donor mitochondria inside and outside of cells 24 hours later.

CREDIT: A. MASUZAWA ET AL / AMERICAN JOURNAL OF PHYSIOLOGY–HEART AND CIRCULATORY PHYSIOLOGY 2013

Parents of 10 patients agreed to the experimental procedure, which was approved by the institute’s review board. In a pilot that ran from 2015 to 2018, McCully extracted pencil-eraser-sized muscle samples from the incisions made for the heart surgery, used a filtration technique to isolate mitochondria and checked that they were functional. Then the team injected the organelles into the baby’s heart.

Eight of those 10 babies regained enough heart function to come off life support, compared to just four out of 14 similar cases from 2002 to 2018 that were used for historical comparison, the team reported in 2021. The treatment also shortened recovery time, which averaged two days in the mitochondrial transplant group compared with nine days in the historical control group. Two patients did not survive — in one case, the intervention came after the rest of the baby’s organs began failing, and in another, a lung issue developed four months later. The group has now performed this procedure on 17 babies.

The transplant procedure remains experimental and is not yet practical for wider clinical use, but McCully hopes that it can one day be used to treat kidney, lung, liver and limb injuries from interrupted blood flow.

The results have inspired other clinicians whose patients suffer from similar ischemia-reperfusion injuries. One is ischemic stroke, in which clots prevent blood from reaching the brain. Doctors can dissolve or physically remove the clots, but they lack a way to protect the brain from reperfusion damage. “You see patients that lose their ability to walk or talk,” says Melanie Walker, an endovascular neurosurgeon at the University of Washington School of Medicine in Seattle. “You just want to do better and there’s just nothing out there.”

Walker came across McCully’s mitochondrial transplant studies 12 years ago and, in reading further, was especially struck by a report on mice from researchers at Massachusetts General Hospital and Harvard Medical School that showed the brain’s support and protection cells — the astrocytes — may transfer some of their mitochondria to stroke-damaged neurons to help them recover. Perhaps, she thought, mitochondria transplantation could help in human stroke cases too.

She spent years working with animal researchers to figure out how to safely deliver mitochondria to the brain. She tested the procedure’s safety in a clinical trial with just four people with ischemic stroke, using a catheter fed through an artery in the neck to manually remove the blockage causing the stroke, then pushing the catheter further along and releasing the mitochondria, which would travel up blood vessels to the brain.

A colored transmission electron micrograph of a mitochondrion (green) and some other cellular structures. In addition to being the “powerhouses of the cell,” mitochondria are involved in regulating other processes such as programmed cell death, cell differentiation and aspects of immune function.

CREDIT: KEITH R. PORTER / SCIENCE SOURCE

The findings, published in 2024 in the Journal of Cerebral Blood Flow & Metabolism, show that the infused patients suffered no harm; the trial was not designed to test effectiveness. Walker’s group is now recruiting participants to further assess the intervention’s safety. The next step will be to determine whether the mitochondria are getting where they need to be, and functioning. “Until we can show that, I do not believe that we will be able to say that there’s a therapeutic benefit,” Walker says.

Researchers hope that organ donation might also gain from mitochondria transplants. Donor organs like kidneys suffer damage when they lack blood supply for too long, and transplant surgeons may reject kidneys with a higher risk of these injuries.

To test whether mitochondrial transplants can reinvigorate them, transplant surgeon-scientist Giuseppe Orlando of Wake Forest University School of Medicine in Winston-Salem and his colleagues injected mitochondria into four pig kidneys, and a control substance into three pig kidneys. In 2023 in the Annals of Surgery, they reported fewer dying cells in the mitochondria-treated kidneys, and far less damage. Molecular analyses also showed a boost in energy production.

It’s still early days, Orlando says, but he’s confident that mitochondria transplantation could become a valuable tool in rescuing suboptimal organs for donation.

The studies have garnered both excitement and skepticism. “It’s certainly a very interesting area,” says Koning Shen, a postdoctoral mitochondrial biologist at the University of California, Berkeley, and coauthor of an overview of the signaling roles of mitochondria in the 2022 Annual Review of Cell and Developmental Biology. She adds that scaling up extraction of mitochondria and learning how to store and preserve the isolated organelles are major technical hurdles to making such treatments a larger reality. “That would be amazing if people are getting to that stage,” she says.

“I think there are a lot of thoughtful people looking at this carefully, but I think the big question is, what’s the mechanism?” says Navdeep Chandel, a mitochondria researcher at Northwestern University in Chicago. He doubts that donor mitochondria fix or replace dysfunctional native organelles, but says it’s possible that mitochondria donation triggers stress and immune signals that indirectly benefit damaged tissue.

Whatever the mechanism, some animal studies do suggest that the mitochondria must be functional to impart their benefits. Lance Becker, chair of emergency medicine at Northwell Health in New York who studies the role of mitochondria in cardiac arrest, conducted a study comparing fresh mitochondria, mitochondria that had been frozen then thawed, and a placebo to treat rats following cardiac arrest. The 11 rats receiving fresh, functioning mitochondria had better brain function and a higher rate of survival three days later than the 11 rats receiving a placebo; the non-functional frozen-thawed mitochondria did not impart these benefits.

It will take more research into the mechanisms of mitochondrial therapy, improved mitochondria delivery techniques, larger trials and a body of reported successes before mitochondrial transplants can be FDA-approved and broadly used to treat ischemia-reperfusion injuries, researchers say. The ultimate goal would be to create a universal supply of stored mitochondria — a mitochondria bank, of sorts — that can be tapped for transplantation by a wide variety of health care providers.

“We’re so much at the beginning — we don’t know how it works,” says Becker. “But we know it’s doing something that is mighty darn interesting.”

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Jackie Rocheleau is an independent science journalist covering the life sciences and medicine with a particular focus on the brain. Follow her on Bluesky @JackieRocheleau.bsky.social.

HEALTH & DISEASE | VIEW ON WEBSITE

Dogs and their people: Companions in cancer research

Canine and human cancers bear many similarities — studies in dogs are helping to develop treatments for both species

By Bob Holmes    07.01.2025

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After a train carrying chemicals derailed and caught fire in East Palestine, Ohio, in 2023, residents were exposed to carcinogens such as vinyl chloride, acrolein and dioxin. Since tumors are typically slow to develop, it could take decades to know what that did to the locals’ cancer risk, but there may be a quicker route to an answer: The residents’ dogs were also exposed, and dogs develop cancer more quickly.

Studying dogs and their cancers turns out to be an excellent way to learn more about cancer in people. And it’s not just that dogs and owners share exposures to many of the same environmental carcinogens. Researchers are also learning that cancers develop along remarkably similar pathways in the two species.

The faster pace at which canine cancers progress also means that researchers testing new therapies can get quicker results than they can in human clinical trials. This benefits scientists, dogs and their owners, proponents say.

“Man’s best friend is man’s best biomedical friend,” says Matthew Breen, a geneticist at North Carolina State University. “It’s like having a mobile biosentinel organism that can help inform us about our own medical prospects over the next 25 years.”

Dogs in the vanguard

The biomedical bond between people and dogs is not new; veterinarians have long treated their canine patients with drugs developed for use in people, and doctors have relied on dogs to test therapies and procedures before deploying them in the clinic. Techniques to treat the bone cancer osteosarcoma without amputating the patient’s limb, for example, were first developed in dogs.

Yet today this cross-fertilization is no longer an occasional, sporadic benefit. Researchers are realizing that canine tumors parallel those in people so closely that dogs may be the best reference point for understanding many of our own cancers.

One of the most important similarities between canine and human cancers is that they arise spontaneously, as the end result of a protracted struggle at the cellular level: Over the course of years, cells accumulate genetic damage that disables normal controls on cell division, and emerging tumors evolve ways to evade the immune system. That complexity means there can be many different pathways to cancer that differ from tumor to tumor — and, it turns out, even from cell to cell within a single tumor.

The cancers indicated here show underlying similarities between dogs and people. Some, such as blood, lung, breast and bladder cancers, may have shared environmental risk factors.

Traditional lab-mouse approaches to studying cancer miss much of that heterogeneity, because the system is more artificial: Researchers typically have to implant tumors into inbred strains of mice whose immune systems have been suppressed.

New genetic research underscores how similar the accumulating damage is in dogs and people. In a yet-to-be-published study, Elinor Karlsson, a genomicist at the UMass Chan Medical School, and her colleagues looked at gene sequences from more than 15,000 human tumors of 32 different types and more than 400 canine tumors of seven different types.

The aim was to identify genetic mutations that were present in the cancers but not in normal cells of the same individual. Such mutations were presumably not inherited but instead were likely to represent genetic damage accumulated over a lifetime, some of which can result in cancer.

That damage looked remarkably similar in the two species, says Karlsson. “Genetically, in terms of what’s driving cancers, it’s basically the same genes in dogs and humans.” Many of the dog tumors, for example, had mutations in genes already known to drive human cancers, such as the tumor suppressor gene PTEN (often mutated in breast and prostate cancers, among others) and the cell-division regulator NRAS (involved in melanoma and other cancers). Notably, mutations often occurred in or near the same locations in the genes in both species, suggesting that they may cause similar dysfunctions.

A similar recent finding came from researchers at FidoCure, a California-based company working on canine cancer. Scientists there are investigating how tumors with specific genetic mutations respond to human therapies. The team reviewed records of 1,108 dogs with cancer, finding that dogs whose tumors carried particular mutations had higher survival rates if they were treated with a human drug specific to that mutation. This implies that the underlying biology of the cancers may be similar in the two species, and if so, researchers ought to be able to work in the other direction, too — using dogs as a test bed to develop new therapies for people.

That has already paid off in a few cancer therapies first developed in dogs that are now in clinical trials or approved for use for people, says Amy LeBlanc, a veterinary oncologist and director of the comparative oncology program at the National Cancer Institute. Examples include immunotherapies for brain cancers; viral therapy that targets lymphoma; and drug therapies against multiple myeloma, lymphoma and brain tumors. Results like FidoCure’s suggest that these therapies could be just the vanguard of many more such drugs.

Veterinary oncologist Amy LeBlanc of the National Cancer Institute sits with Roxy, a cancer patient enrolled in a clinical trial. Dog cancers are so much like our own that researchers can investigate therapies in dogs before they proceed to human trials.

CREDIT: COURTESY OF AMY LEBLANC

A faster path to answers

Cancers progress faster in dogs, which means that clinical trials yield results more quickly. For example, tumors often produce an unusual abundance of malformed RNA molecules. Researchers have shown, in mice, that targeting these molecules with a vaccine can delay or prevent the onset of cancers. But testing a preventive vaccine in people wouldn’t yield results for many years, even decades — and funding agencies aren’t likely to support such a long and expensive study based solely on data from mice.

CREDIT: PIXABAY

Breed-specific cancers

Many dog breeds are particularly susceptible to certain cancers, the result of centuries of inbreeding for appearance and behavioral traits that inadvertently selected for undesirable traits as well.

Golden retrievers and Labradors tend to get cancers of the blood vessel lining, for example, while rottweilers, Irish wolfhounds and racing greyhounds get a lot of bone cancers, and boxers and Scottish terriers are prone to lymphoma. These breed differences can help researchers to spot the gene mutations that increase the risk of particular cancer types.

Knowing the genetics of cancer susceptibility can also help dog breeders avoid risky gene variants and, eventually, produce less cancer-prone breeds. That can save — or at least postpone — a lot of heartache from the early loss of a beloved pet. But it also can make a big difference for providers of service dogs, where premature death can cut short the working lives of expensively trained animals.

Veterinary scientist Frances Chen of the UMass Chan Medical School and her colleagues have begun mapping the genomes of golden retrievers and Labrador retrievers to identify gene variants associated with cancer risk. “We’re not at the point where we can say, ‘Here are the genes we’ve discovered,’” says Chen. However, they have narrowed the search to particular regions of the genome.

Ultimately, Chen says, researchers should be able to build genetic risk scores for individual animals that breeders can use in their breeding programs.

— Bob Holmes

“It would be an enormous leap to go from the mouse studies to some kind of gigantic, 15- or 20-year human cancer prevention study,” says Douglas Thamm, a veterinary oncologist at Colorado State University.

Instead, Thamm and his colleagues tested the vaccine in dogs, which shrinks the timeline to just five years. All the data — from 804 dogs — have now been collected, and the researchers are analyzing them, with an answer on the vaccine’s effectiveness expected by the end of 2025.

Cancer detection techniques, too, can benefit from testing in dogs. Many golden retrievers, for example, will eventually develop a cancer of the blood vessels called hemangiosarcoma (see box). Drugs can usually forestall the cancer’s progression, but many dogs will eventually relapse. Karlsson and her colleagues are studying whether they can detect that relapse in blood samples drawn from affected dogs, a technique known as liquid biopsy.

The technique is still under development, but the hope is that spotting early signs of relapse will allow veterinarians to abandon failing therapies and try something else more quickly, says project coleader Cheryl London, a veterinary medical oncologist and immunologist at Tufts University, who coauthored a 2016 overview of the similarities between dog and human cancers. In contrast, she notes, doctors can’t ethically try experimental treatments on people until standard treatments have clearly failed.

Eventually, liquid biopsy might be used to screen for previously undetected cancers in both dogs and people, Karlsson says. Here, too, golden retrievers are likely to prove invaluable: Because so many of the dogs will eventually develop cancer, researchers don’t need to screen many animals to find enough tumors to study.

Environmental watchdogs

There’s another important way that dogs can benefit the study of cancer — as environmental sentinels. “Dogs live in our environment,” says Breen. “They breathe the same air, they drink the same water. The dog runs across the same herbicide-treated grass that our grandkids run over.” If those exposures increase the risk of cancer in dogs, they’re likely to do so in people, too, since the genomic pathways leading to cancer are so similar.

In people, exposures to various environmental carcinogens might take 25 years to produce full-blown cancers, Breen says. “But the accelerated lifespan of a dog means they may only need to be exposed to it for two or three years.” That makes dogs a quicker way to spot the chemicals that potentially pose the greatest danger to people.

Dogs live with us, so they are exposed to many of the same cancer-causing chemicals in the environment, including cigarette smoke. Because cancers usually progress more quickly in dogs, researchers can watch the animals for clues to environmental cancer risks in people.

CREDIT: LORRAINE POOLE / SHUTTERSTOCK

Breen and his colleagues recently put this sentinel idea to the test. They were interested in environmental toxins that might contribute to bladder cancer. The team knew that in dogs, genetic damage that accumulates in cells of the bladder wall often includes a specific mutation called BRAF V595E that is an early marker for bladder cancer. Earlier research had suggested environmental chemicals were linked to the cancer — but which ones?

To find out, the team identified 25 dogs with the BRAF V595E mutation using urine samples. Then they sent out specially designed silicone tags for the dogs. They also sent tags to 76 dogs (matched for breed, sex and age) that lacked the mutation. Each wore the silicone for five days, during which time it absorbed chemicals from the home environment. The owners then returned the tags to the researchers, who extracted and analyzed the chemicals.

The analysis identified 25 chemicals that were more abundant in the dogs with the mutation, and therefore carcinogen candidates. These included flame retardants, plasticizers and combustion byproducts from smoking, fires and vehicle emissions. “They’re the classic kinds of chemicals that are in everybody’s house,” says Breen. An earlier study by Breen and his team noted similar exposure patterns recorded by silicone tags on dogs and silicone wristbands worn by their owners.

A similar approach may help to measure the cancer risk from other environmental exposures, such as the train derailment in East Palestine. To that end, Karlsson and her colleagues recently mailed silicone tags to about 75 dog owners who live near the site. The researchers are now measuring chemicals in the tags and screening blood samples from the dogs to detect genetic changes linked to cancer.

If dogs exposed to chemicals in that train derailment are showing a higher rate of these mutations in their blood, says Karlsson, they and their owners might need to be monitored for an increased risk of cancer.

As researchers continue to study the links between cancers of dogs and people, they often reiterate the benefits that accrue not just to science, but to dog owners and their sick pets. The pets receive highly sophisticated cancer care that their owners might not have access to otherwise, and the owners may get a little more time with their companions. “We’re not experimenting on these animals to their detriment,” says Thamm. “We’re trying to help those individuals.” That, he and others say, is a source of great satisfaction.

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Bob Holmes is a science writer and poodle owner based in Edmonton, Canada. He is a special contributor to Knowable Magazine.

PHYSICAL WORLD | VIEW ON WEBSITE

Watching the world, one quintillionth of a second at a time

An attosecond is no time at all for a person. Not so for electrons, atoms and molecules. Laser-wielding scientists are revealing the action.

By Ivan Amato    06.24.2025

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Just about anybody who played hide-and-seek as a kid remembers counting, with eyes (presumably) covered, in units of one-one-thousand. “One-one-thousand. Two-one-thousand. Three-one-thousand.” It’s one way to develop a feel for the duration of a second. If you live to be 80 years old, you will experience 2,522,880,000 seconds, not any one of which feels like a long time. When you think about time, it’s usually in many-second durations, like minutes, days and years. Unless you become a world-class athlete where differences measured in tenths, hundredths and maybe even thousandths of seconds can mean winning or losing Olympic gold, you might not think intervals shorter than a second are worth a second thought.

But what if you allow yourself to imagine what happens in the world at ever shorter time intervals? What if you had a temporal microscope for zooming in on time the way optical, electron and scanning tunneling microscopes let you zero in on ever finer spatial dimensions, even down to the atomic scale?

Welcome to the world of a cadre of scientists, some of them Nobel Prize winners, who live in the fastest science lane possible right now — the realm of attoseconds. By leveraging the evolution of laser science and technology, they have trained their attention on molecular, atomic and electronic behavior of ever finer temporal durations — from millionths (micro) to billionths (nano) to trillionths (pico) to quadrillionths (femto) to quintillionths (atto) of seconds.

It’s in the attosecond-by-attosecond time frame that lots of the sausage of physics and chemistry is made and can be probed. It is where light and electrons do much of the blindingly fast negotiation by which the energy they have to give and take redistributes as they interact. These are temporal realms that set the stage for many chemistry antics: things like electrons shifting between excited higher-energy states and lower-energy states and molecules morphing from reactants into products. In these instants, a chemical ring might open, an electron might fly away leaving a positively charged ion behind, or a photon might beam outward carrying spectroscopic intel that helps scientists figure out what just happened. These are the hidden micromatters that contribute to everything from photosynthesis in leaves to the photophysical basis of vision and the bond-making-and-breaking that underlies the multi-trillion-dollar chemical industry.

To those who wield state-of-the-art laser systems and light detectors to capture glimpses of the exquisitely fast happenings in these tiny contexts, even a microsecond or nanosecond can seem like an awfully long time. When you can watch molecules and reactions in attosecond time frames, “there’s this vast other space that is open to you,” says Stephen Leone, a physical chemist at the University of California, Berkeley, who recently chronicled his lifelong research adventure as an “attosecond chemist” in an autobiographical essay in the Annual Review of Physical Chemistry. With short-enough pulses, he says, you can begin to observe the very movements of electrons that underlie the breaking or making of a chemical bond.

Here is what one attosecond looks like when you write it out: 0.000000000000000001 s. That’s a billionth of a billionth of a second. An oh-wow factoid that attosecond aficionados sometimes roll out is that there are as many attoseconds in one second as there have been seconds ticking since the Big Bang. One tick on your kitchen clock amounts to an eternity of attoseconds. Here’s another head-shaking attosecond fact: In one attosecond, light — which moves at the incomprehensible sprint of 186,000 miles per second — travels the span of a single atom.

The universe is a billion billion heartbeats old and there have been a billion billion attoseconds in each of those heartbeats.

Attoseconds are a natural time frame for atoms and their electrons, says John Gillaspy, a research physicist at the National Institute of Standards and Technology and former program director of atomic, molecular and optical experimental physics at the National Science Foundation. “When you think about an electron orbiting a nucleus like a little planet moving around the Sun,” he says, “the time scale for the orbit is about 1 to 1,000 attoseconds.” (He concedes that he often defers to this early 20th century metaphor for atoms because, he says in a spirit of commiseration, “if you try to envision them quantum mechanically, you’re liable to get quite confused and disturbed.”)

To do attosecond science, you might start with a top-line femtosecond laser that produces millionths-of-billionths-of-a-second infrared pulses. Then, to produce even shorter-wavelength attosecond laser pulses, you likely will need a pulse-shortening technique, called high harmonic generation (HHG), which won some of its developers the 2023 Nobel Prize in physics.

Leone has put such tools and techniques to use in what are called pump-probe studies. These have two main parts. First, he and his team might vent a gas of, say, krypton atoms or methane molecules into the pathway of laser pulses. These pulses carry the photons that will interact with electrons in the sample particles. Then the scientists direct attosecond laser pulses at the sample at different delay times after the initial pulse, taking pains to measure the electromagnetic signals or electrons that emerge. The attosecond-precise monitoring of these signals can amount to a stop-motion movie of electrons, atoms or molecules.

There are as many attoseconds in one second as there have been seconds ticking since the Big Bang.

In deep chemistry speak, Leone lists some of the attosecond- and femtosecond-fast shifts in electronic energy states and behavior that such techniques have opened to observations in unprecedented detail: chemical bond breaking, yes, but also more subtle yet influential energetic happenings that can thwart reactions or nudge molecules to change shape. These are phenomena in which theory has long outpaced experimental data. These subtler actions include “curve crossings” and “conical intersections,” which are terms reflective of the mathematical and geometric depictions of the energy-constrained behavioral “choices” electrons have to make in atoms and molecules. Does this or that electron hold on to enough energy to cause a bond to break? Or does it vent that energy within the molecule or material more gently to elicit, say, a vibration between bonded atoms, or morph the molecule’s shape from one isomer to another?

These secret, on-the-fly choices made by electrons leave their traces all over in our biology and could have practical applications — such as repairing broken chromosomes, detecting diseases from chemical hints in the molecular brew of our blood, or engineering laser pulses to produce never-before-seen molecules. “We didn’t understand any of this detail previously and now, I think, it has come into much greater clarity,” Leone says. It suggests ways to elicit specific electronic motions that one needs to break this or that bond or to cause a desired reaction, he adds.

The hushed, darkened labs of these laser-wielding experimentalists have an otherworldly feel. A typical centerpiece is a vibration-suppression table with surfaces as still as any place on Earth. Painstakingly aligned there are miniature Stonehenges of lenses and crystal elements that shift, split and recombine laser beams, compress or expand light pulses, and impart tiny delays into when pulses reach samples and detectors. Feeding into these optical pathways are the ultrashort laser pulses and, downstream, the sample atoms and molecules (supplied from nozzles attached to gas tanks or from heated crystals). Much of these setups must reside in steampunk-esque vacuum chambers so that air molecules don’t sop up the precious data-bearing light or electron signals before they can make it to detectors and spectrometers.

As this snapshot of Stephen Leone’s lab suggests, doing attosecond science is better suited for the technophilic among us.

CREDIT: COURTESY OF STEPHEN LEONE

“It’s all a very complicated camera to produce some of the shortest events in time that humans can produce,” says theoretical chemist Daniel Keefer of the Max Planck Institute for Polymer Research in Mainz, Germany, coauthor of a 2023 article in the Annual Review of Physical Chemistry on the applications of ultrafast X-ray and HHG for probing molecules.

Keefer’s primary tasks include calculating for experimentalists the laser-pulse energies and other conditions most suitable for the studies they plan to do, or helping them infer the electronic behavior in molecules hidden in the spectroscopic data they collect in the lab. But as elementary as these studies can be, some of the phenomena he has studied are as relevant to everyone as keeping their genes intact and functioning.

“It’s all a very complicated camera to produce some of the shortest events in time that humans can produce.”

— DANIEL KEEFER

Consider that the combination of ultrafast laser pulses and spectroscopic observation empowered him and colleagues to better understand how some of the celebrity molecules of biology, RNA and DNA, manage to quickly dissipate enough of the energy of incoming ultraviolet photons to prevent that energy from wreaking gene-wrecking, photochemical damage. It comes down to the way electrons within the molecules can benignly vent the UV energy by going back to their lowest-energy orbitals.

“This is one mechanism by which potential photodamage is prevented in living organisms exposed to sunlight,” Keefer says. These genetic molecules “absorb UV light all the time and we’re not having a lot of photodamage because they can just get rid of the energy almost instantaneously, and that greatly reduces the risk of your DNA breaking.”

Accelerating into the fastest lane

To generate attosecond laser pulses, scientists first ping a gas of atoms with an infrared laser. The laser beam gives a kick to every atom it passes, shaking the electrons back and forth in lockstep with its infrared light waves. This forces the electrons to emit new light waves. But they do so with overtones, the way a guitar string vibrates at not only a fundamental frequency but also a range of higher-frequency harmonic vibrations, or acoustic overtones. In the case of infrared laser light, the overtones are at much higher frequencies in the attosecond range, which correspond to ultraviolet or even X-ray wavelengths.

That’s a huge bonus for attosecond scientists. When packed into supershort pulses, light of these wavelengths can carry sufficient energy to cause electrons to migrate within a molecule’s framework. That influences how the molecule will react. Or the laser pulses can coerce electrons to leave the scene entirely, which is one of the ways atoms and molecules become ionized.

It takes today’s shortest possible laser pulses to observe electronic behavior inside atoms and molecules. Three scientists who devised the technology allowing attosecond light pulses to be generated received the 2023 Nobel Prize in Physics.

CREDIT: © JOHAN JARNESTAD / THE ROYAL SWEDISH ACADEMY OF SCIENCES

Gillaspy says that when he thinks of attosecond pulses of light, and yet-shorter pulses in the future (which would be measured in zeptoseconds), his science dreams diverge from spying on the private lives of electrons and toward what becomes possible by packing more energy into ever shorter pulses. Do this, Gillaspy says, and the power confined in the pulse can amplify, albeit ever so briefly, to astronomical levels. It’s akin to the way a magnifying glass can concentrate a dull, palm-sized patch of sunlight into a pinpoint of brilliant sunlight that can ignite a piece of paper.

Concentrate enough laser power into a short-enough pulse, Gillaspy says, and you might gain access to the quantum vacuum, by which he means the lowest possible energy state that space can have. The quantum vacuum has only been indirectly measured and it sports a generous share of weirdness. Presumably, for example, the “nothingness” of that vacuum actually seethes with “virtual” matter-antimatter particle pairs that poof into and out of existence by the bazillions, in slices of time even faster than attoseconds.

“If you could get the laser intensity strong enough you might rip apart the virtual particles from each other in the quantum vacuum and make them real” — which is to say, observable, says Gillaspy. In other words, it could become possible to separate, detect and measure the members of those transient pairs of virtual particles before they annihilate each other and disappear back into the vacuum. “This is where we could be ripe for fundamental discoveries,” Gillaspy says — although for now, he notes, the capability to produce the required laser intensities remains far off.

Jun Ye, a physicist at JILA, a joint research center of the University of Colorado and the National Institute of Standards and Technology, is deploying attosecond physics in pursuit of another believe-it-or-not goal. He intends to tap HHG to detect that mysterious cosmic stuff known as dark matter.

Despite never having directly detected dark matter in everyday life or in a laboratory, scientists presume its existence to make sense of the distribution and motions of matter on galactic scales. Without the presence of dark matter — in far more abundance than ordinary matter — and its cosmic-scale gravitational influences, the universe would literally look and behave differently. If the theory is true, a tantalizing consequence is that dark matter — whatever it is — should be abundantly present all around us here on Earth and so should be, in principle, detectable in a lab.

Ye is hoping to exploit HHG physics to develop a type of energy-measuring technique, called nuclear spectroscopy, that is especially suited to discern subtle energy shifts in the nuclei of atoms. In this context, it’s the multitude of wavelengths of light that HHG naturally produces that make this spectroscopic technique so revealing. This, Ye says, could enable him to monitor minute variations in regular-matter atoms that might be caused by previously unknown interactions with dark matter.

At the heart of his plan is a new type of clock, a nuclear clock, that he and colleagues at JILA and elsewhere have been developing. The ticks of these clocks are based on nuclear oscillations (in the bundle of neutrons and protons in thorium-229 nuclei) rather than the electronic oscillations atomic clocks have been based on.

“If the dark matter out there interacts with regular matter, then potentially it will interact with neutrons and protons in atomic nuclei differently than with electrons,” Ye says. And if that is so, comparisons of spectroscopy data from the two types of clocks stand a chance of finally unveiling a dark matter influence on normal matter that has been in operation all along.

“This is how a lot of things start,” says Gillaspy. “Breakthroughs can start with physicists and chemists just getting fascinated by some new thing, like attosecond phenomena, and then . . . you never know. You don’t even imagine what kind of capabilities are going to arise from that.”

Editor’s note: This article was corrected on June 24, 2025, to clarify that John Gillaspy is former program director, not current program director, of atomic, molecular and optical experimental physics at the National Science Foundation.

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Ivan Amato, a longtime science writer, book author, podcaster and science café host, has covered topics ranging from venomous caterpillars to secret Cold War technologies. He recently has embraced the sci-art practice of crystal photomicrography to uncover beauty hidden in tiny places (IG: ivanamato61; ivanamato.com).

HEALTH & DISEASE | VIEW ON WEBSITE

How rogue jumping genes can spur Alzheimer’s, ALS

Our genomes are peppered with DNA segments called retrotransposons that can move from place to place. When unleashed, some can kill nerves and promote inflammation — a discovery that may inspire treatments for neurodegeneration.

By Amber Dance    06.17.2025

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Back in 2008, neurovirologist Renée Douville observed something weird in the brains of people who’d died of the movement disorder ALS: virus proteins.

But these people hadn’t caught any known virus.

Instead, ancient genes originally from viruses, and still lurking within these patients’ chromosomes, had awakened and started churning out viral proteins.

Our genomes are littered with scraps of long-lost viruses, the descendants of viral infections often from millions of years ago. Most of these once-foreign DNA bits are a type called retrotransposons; they make up more than 40 percent of the human genome.

Our genomes are riddled with DNA from ancient viral infections known as jumping genes. The majority of these are retrotransposons, which copy themselves via RNA intermediates; a smaller portion are cut-and-paste DNA transposons.

Many retrotransposons seem to be harmless, most of the time. But Douville and others are pursuing the possibility that some reawakened retrotransposons may do serious damage: They can degrade nerve cells and fire up inflammation and may underlie some instances of Alzheimer’s disease and ALS (amyotrophic lateral sclerosis, or Lou Gehrig’s disease).

The theory linking retrotransposons to neurodegenerative diseases — conditions in which nerve cells decline or die — is still developing; even its proponents, while optimistic, are cautious. “It’s not yet the consensus view,” says Josh Dubnau, a neurobiologist at the Renaissance School of Medicine at Stony Brook University in New York. And retrotransposons can’t explain all cases of neurodegeneration.

Yet evidence is building that they may underlie some cases. Now, after more than a decade of studying this possibility in human brain tissue, fruit flies and mice, researchers are putting their ideas to the ultimate test: clinical trials in people with ALS, Alzheimer’s and related conditions. These trials, which borrow antiretroviral medications from the HIV pharmacopeia, have yielded preliminary but promising results.

Meanwhile, scientists are still exploring how a viral reawakening becomes full-blown disease, a process that may be marked by what Dubnau and others call a “retrotransposon storm.”

Genes that jump

A retrotransposon is a kind of “jumping gene.” These pieces of DNA can (or once could) move around in the genome by either copying or removing themselves from one spot and then pasting themselves into a new spot. Retrotransposons are copy-and-pasters.

Many retrotransposons are old companions: Some predate the evolution of Homo sapiens or even the split between plants and animals, Dubnau says. Their predecessors may have alternated between riding along stitched into a host chromosome and existing outside of it, he suggests.

Some retrotransposons, after all that time, retain their ability to hop around human DNA. To do so, they copy themselves with the enzyme reverse transcriptase, which is also used by some viruses like HIV to copy RNA sequences into DNA. Once they’re copied, the remnant viruses can pop into new locations on chromosomes.

Jumping genes use different mechanisms to move around in the genome.

If it’s terrifying to think of a genome littered with retroviral genes, some capable of bouncing around the genome, don’t fret, says Douville, now at the University of Manitoba in Winnipeg. Remarkably, some retrotransposons have taken on helpful jobs, assisting the body with tasks like maintaining stem cells and development of the embryo and nervous system.

And many retrotransposons are dormant or broken, and the cell has means to keep them (mostly) quiet. One technique is to stash them in DNA regions that are wound up so tight that the molecular machines needed to copy genes can’t get near them.

In essence, the cell shoves them into a closet and slams the door shut.

But evidence is building that as people age, that closet door can creak open, letting retrotransposons spill out. Exactly what they do then isn’t certain. Some scientists think it’s not so much that they are jumping around and mutating DNA, but that their viralesque RNAs and proteins can screw up normal cellular activities.

“I think what’s actually driving toxicity when transposons are activated is they’re making all these factors that look like a virus to the cell,” says Bess Frost, a neurobiologist at Brown University in Providence, Rhode Island. The cell reacts, quite reasonably, with defensive inflammation, which is commonly associated with neurodegeneration.

Retrotransposons also seem to team up with rogue proteins classically linked to neurodegeneration, damaging or killing nerve cells, and perhaps even setting off the disease in the first place.

Making the ALS connection

Scientists long suspected a link between viruses and ALS, which causes degeneration of the motor neurons that control movement. But the connection, when it was finally found, wasn’t quite what anyone predicted.

In the early 2000s, scientists reported that some people with ALS had the viral enzyme reverse transcriptase in their blood and, more rarely, spinal fluid. Some had as much reverse transcriptase as a person with an HIV infection.

But at the time, says Dubnau, “Nobody could find a virus.”

Finally, Douville and colleagues discovered evidence for one of those leftover viruses, a kind of retrotransposon called HERV-K, in the brains of some people who had died of ALS. From there, scientists began to build a case linking jumping genes to ALS in people, lab animals and cells in dishes. A team reported in 2017 that numerous jumping genes had been activated in the brains of certain people with ALS.

In one of the first studies to link retroviruses and neurodegeneration, researchers hunted for evidence that genes from the retrovirus known as HERV-K had been turned on in the brain tissue of people who died of ALS, compared to those who died from other causes. The activity of a HERV-K gene called pol, which is involved in copying the retroviral genome, was revved up in many ALS samples.

Douville’s colleagues also documented damage inflicted by HERV-K: When they put a gene from the retrotransposon into mice, the animals’ nerve cell projections shriveled and they exhibited ALS-like symptoms.

As the scientists zeroed in on what might be waking up HERV-K, a familiar protein turned up. Called TDP-43, it had already been linked to ALS. But even before that, it was found to be involved in cells’ responses to the retrovirus HIV.

Scientists discovered in the 1990s that TDP-43 works in the cell’s nucleus, where it hinders activation of HIV genes. It also regulates human genes there. But in the neurons of people with ALS or a related condition, frontotemporal dementia (FTD), TDP-43 departs the nucleus and goes on to form abnormal clumps in the cytoplasm. The globs have been associated with a number of neurodegenerative conditions and can spread from cell to cell. And when TDP-43 vacates the nucleus, it also creates a gap in gene regulation, throwing off the activity levels of many genes.

TDP-43 gone bad is sufficient to cause neurodegeneration, but studies indicate its desertion of its nuclear role can also wake up retrotransposons. When TDP-43 leaves the nucleus, tightly coiled DNA next to certain retrotransposons starts to loosen up and unravel, a study of cells from the brains of people who died of ALS or FTD revealed. And researchers saw that in cultured cells, this loss of TDP-43 freed certain retrotransposons from their restraints. The closet door was now ajar, in other words, allowing the retrotransposons to jump out and around.

Meanwhile, Dubnau and collaborators, were looking at data on TDP-43 and the genes it controls in rats, mice and people. They found that TDP-43 can naturally stick to the RNAs of a variety of jumping genes, suggesting a way that normal TPD-43 might continue to corral them, even if they’ve managed to get copied into RNA. That interaction was altered in people with FTD and in rodents with abnormally high or low amounts of TDP-43 — very much as if TDP-43 was unable to control the jumping genes anymore.

The Dubnau group also turned to fruit flies. Both old age and the human TDP-43 gene caused retrotransposons in the fly brain to sneak out of the chromosomal closet, inducing brain cells to kill their neighbors and prompting neurodegeneration, the group reported in a series of papers from 2013 to 2023. Moreover, activation of certain retrotransposons also caused TDP-43 to clump together outside of the nucleus, creating a vicious cycle whereby TDP-43 and the retrotransposons reinforce each other’s abnormal behaviors. Past a certain point, says Dubnau, “It just takes off.”

Based on the sum of all these findings, Dubnau suggests a possible way that ALS could develop: Normally, TDP-43 in the nucleus helps to repress retrotransposons. But if aging or some other disturbance causes TDP-43 to decamp, those once-silenced retrotransposons spring to life, producing virus-like RNAs and proteins. While the retrotransposons might induce disease on their own, by jumping into new DNA locations or spurring inflammation, they also act on TDP-43. They force more TDP-43 to leave the nucleus and clump in the cytoplasm, causing further neurodegeneration that spreads to neighboring cells.

This isn’t the cause of all kinds of ALS, which is a complex disorder with many possible triggers. But in a 2019 study of postmortem brain samples, Dubnau and colleagues found that about one in five people with ALS had high levels of retrotransposon activation and TDP-43 dysfunction.

A link to tau and Alzheimer’s

As that ALS story was developing, other scientists were pursuing a connection between retrotransposons and another toxic protein in neurodegeneration: the tau protein, which twists into unruly tangles in the brain cells of people with Alzheimer’s disease. It affects retrotransposons because it, like TDP-43, plays a role in keeping retrotransposons quiet, says Frost.

That maintenance is a downstream effect of tau’s association with the cell’s interior skeleton. That skeleton is physically linked to the nucleus’s skeletal structure, which in turn anchors the tightly wound-up DNA that silences retrotransposons. When tau goes bad, it changes the structure of the cell’s main skeleton, making it more rigid. Frost and colleagues found that this structural defect propagates all the way to the nuclear skeleton and the chromosomes, just like tightening the strands on one side of a net could change the shape of the other side.

This structural effect can unlock the tightly wound bits of chromosome in fruit flies, which damages their neurons, Frost reported in 2014. By 2018, she’d shown that tau problems unleashed jumping genes in the flies.

“They were legitimately jumping,” she says, going from their original chromosomal locations to other ones in the fly’s brain cells. And the jumping genes contributed to the death of nerve cells.

Frost and colleagues also studied mammals — mice — and in 2022 they reported that retrotransposons were also activated in mice with dysfunctional tau.

Meanwhile, Frost and others examined brain cells from people who’d died of tau-related diseases such as Alzheimer’s, which also revealed activated retrotransposons.

“They were legitimately jumping.”

— BESS FROST

This awakening of retrotransposons appears to happen early in the disease, according to the work of another team published in 2022. In blood samples from people on their way to developing Alzheimer’s disease, the copying of retrotransposon genes into RNAs spiked, creating a “retrotransposon storm,” just before their symptoms got bad enough to be labeled Alzheimer’s.

A tactic from HIV treatment

This growing body of evidence suggests that reactivating once-quiet retrotransposons, whether via dysfunctional tau or TDP-43, can create havoc. A potential treatment quickly comes to mind: Since these retrotransposons are a lot like viruses, scientists reason that antiviral drugs could help.

Handily, doctors already have medications that stymie retroviruses: Millions of people take antiretroviral drugs to keep HIV in check or prevent it from gaining a foothold in their cells.

Indeed, multiple studies over several years have investigated drugs from the HIV treatment playbook that block the enzyme reverse transcriptase. And in cells, flies and mice the drugs have dialed down retrotransposon activity and neurodegeneration.

These medications are well understood and generally safe, and are already in trials for neurodegenerative disease. For example, researchers have tested the safety of a 24-week antiretroviral course in 40 people with ALS. Not only did most people safely complete the trial, but the levels of HERV-K in their blood went down, and they seemed to have a delay in progression of their ALS symptoms, the researchers reported in 2019.

Frost recently published results from a small trial in which 12 people with early Alzheimer’s disease took a reverse transcriptase inhibitor for 24 weeks. Her main goal was to determine if the treatment was safe, and it was — but the researchers also observed a drop in signs of inflammation in the participants’ spinal fluid.

Both Dubnau and Frost serve on the scientific advisory board for Transposon Therapeutics, which tested its own reverse transcriptase inhibitor in 42 people with ALS and/or FTD. The company says the drug was tolerable and yielded signs of less neurodegeneration and inflammation, plus a delay in the inevitable worsening of symptoms. The company is planning a larger trial; it also plans to test its drug in people with ALS, Alzheimer’s and a related tau-based disease, progressive supranuclear palsy.

Neither Frost nor Dubnau, who together recently summarized the field for the Annual Review of Neuroscience, believes that antiretroviral drugs alone are the solution to transposon-fueled Alzheimer’s or ALS. As Douville notes, the drugs were designed to act only on specific target enzymes — they won’t do anything to other retrotransposon genes, RNAs or proteins, which could also spur nerve-damaging inflammation.

Meanwhile, scientists are looking beyond ALS and Alzheimer’s as evidence accumulates that retrotransposons may contribute to other neurodegenerative and inflammatory conditions, such as Parkinson’s disease and multiple sclerosis.

“It’s really picking up speed,” Frost says.

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Knowable Magazine contributor Amber Dance, a freelance science writer in the Los Angeles area, covered ALS research for several years at Alzforum.

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HIV medications: Did fears about side effects come to pass?

The emergence of antiretroviral drugs saved millions of lives — but some worried about long-term health problems. Here’s how that turned out.

By Tammy Worth    06.10.2025

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Miguel, a 63-year-old Los Angeles teacher, recently marked the 38th anniversary of his diagnosis with HIV. The doctor had told him he would be dead in a couple of years. He lived fearful that each passing one might be his last.

Miguel started to take AZT (azidothymidine), the first antiretroviral drug used to treat HIV and AIDS, and then moved to a succession of other drugs. While he was on one called Crixivan, he experienced hollowed cheeks and increased fat in his chin, characteristic of early HIV medications. He escaped other early effects: severe headaches, muscle pain, insomnia, anemia and other blood disorders. “Gay men were talking about it being very harmful to the body,” says Miguel (not his real name, for privacy reasons). “But it was a crapshoot; if you take this terrible thing, at least you have a fighting chance.”

The drugs saved many millions of lives, but some doctors wondered about long-term effects of the early medications. They saw lipid disturbances and severe neuropathy: numbness, tingling and pain in the limbs. Some predicted a future of early heart disease and heart attacks among gay men and others infected by HIV.

Today it’s known that people with HIV receiving antiviral treatments do tend to have higher rates of certain chronic health conditions. But researchers still aren’t fully sure what causes what. Research has shown that some HIV drugs, particularly the early ones, increase certain risks, but so, too, does low-level persistence of the virus in the body. Sorting out the causes is important to monitoring and treating this group of patients, who now can expect to live a close-to-normal lifespan.

More than 50 antiretroviral medicines, which keep HIV from replicating and spreading, are approved by the US Food and Drug Administration. They are generally taken as a regimen, combining two or three medications from different drug classes.

People taking AZT, the first drug to be approved, often found themselves with a condition known as wasting, or involuntary weight loss of 10 percent or more. In contrast, some of today’s drugs appear to cause weight gain, says Kristine Erlandson, an infectious disease specialist at UCHealth University of Colorado Hospital. In a 2024 report of 2,624 HIV-positive people, published in Clinical Infectious Diseases, she found that the mean weight gain was almost eight pounds in the first year of antiretroviral therapy.

During roughly nine years of follow-up, about 5 percent of participants were diagnosed with diabetes and 14 percent with metabolic syndrome (a group of conditions including obesity, low levels of “good,” or HDL, cholesterol and high blood sugar), and 16 participants had a stroke. While some people have pronounced weight gain on the new HIV drugs, “there are many people on these medications that have a totally normal weight,” Erlandson says. “We don’t know who it will be that gains, or why.”

More generally, researchers have linked HIV-positive people with a slate of conditions normally associated with advancing years: cardiovascular disease, cognitive impairment, diabetes and frailty. “In the early days of the epidemic, people were starting to scream that people with HIV were having premature aging,” says Peter Reiss, a former internal medicine doctor and infectious disease specialist at the Amsterdam University Medical Center. “But there was really no data to back that statement up.”

To get answers, in 2010 Reiss and colleagues began a study called AGEhIV that followed 1,146 people in Amsterdam over about six years. Just over half were HIV-positive, and a similar group without HIV made up the rest.

The scientists found that people with HIV were indeed more likely to have hypertension, heart attacks, osteoporosis, kidney disease and peripheral artery disease (where arteries in the legs and abdomen narrow, slowing blood flow). Nearly all of the HIV-positive participants were taking HIV medications, with near-undetectable levels of the virus, Reiss says, “so you’re really talking about what is happening in effectively treated HIV.”

This graphic was adapted from the AGEhIV cohort study, agehiv.nl/en/, which tracked more than 1,100 people, more than half of whom were HIV-positive, for about six years. The aim was to figure out whether people who were HIV-positive developed a greater number of age-related health conditions — even when being effectively treated — than those who were HIV-negative.

Reiss and colleagues also found a link to cancers not traditionally associated with infection by HIV, such as ones of the stomach, lungs and blood. Of 38 people who died during the years of the study, 16 succumbed to such cancers, and all but one were in the HIV-positive group.

Many other population studies have been conducted through the years, and findings generally align: People with HIV appear to have an increased risk of various chronic diseases, as well as an average life expectancy five to 10 years shorter than people who are HIV-negative.

For example, a 2022 review of 47 reports on antiretroviral therapy reported that having HIV doubled the risk of cardiovascular disease and increased the risk of bone and muscle conditions like sarcopenia (a gradual loss of muscle mass and strength), depression and cancer. And a large US study published in 2020 found that in 2016, people without HIV could expect to live nine more years on average than people with HIV. They also averaged more than 16 years free of other health conditions than the HIV group.

In good news, the life expectancy gap was down dramatically, from a 22-year difference in the early 2000s, largely because of modern antiretrovirals and early treatment commencement, scientists think.

“In the early days of the epidemic, people were starting to scream that people with HIV were having premature aging. But there was really no data to back that statement up.”

— PETER REISS

What causes these differences? It’s important to know, because these disproportionate rates of chronic illness harm people’s lives and are costly, noted Anthony Fauci, former director of the National Institute of Allergy and Infectious Diseases, and colleagues in a 2019 opinion article in the journal JAMA. Monthly costs for treating someone with HIV plus cardiovascular disease or chronic kidney disease were $1,400 to $5,000 more per month than for someone with HIV alone, they wrote.

Lifestyle is one contributing factor. People with HIV tend to have higher rates of smoking, alcohol use, depression and anxiety, says Reiss. But, he adds, this can’t account for all the increase in early onset of age-related conditions.

Medication connections, meanwhile, continue to emerge. Abacavir, to name one example, has recently been linked to cardiovascular disease, says Priscilla Hsue, chief of cardiology at UCLA Health. At the 2024 AIDS Conference, researchers reported that people who had taken the drug had a 50 percent greater risk of major cardiovascular problems such as heart attack and stroke, and those currently taking it had a 42 percent higher risk, compared to people on other antiretroviral treatments.

Another possible contributor to chronic diseases is the effects of HIV on the body, even when the infection is well controlled. The virus is still there, activating the immune system and inducing low-level inflammation.

Knowing that antiretrovirals or HIV-induced inflammation may hasten the onset of conditions like cancer and cardiovascular disease could be a reason to change clinical screening and detection practices of such conditions for people with HIV, Reiss says. He has evidence from the AGEhIV study that much damage is done to the body in the early stages of infection, perhaps before treatment commences. That argues for better screening of people at high risk of having HIV and for early treatment commencement to help mitigate health issues later, he says.

One encouraging report from a large clinical trial known as REPRIEVE, involving more than 7,500 participants, was that taking a statin medication reduced rates of heart attacks, strokes and other cardiac problems among people with HIV by 35 percent. The five-year trial’s findings, published in 2023, have been incorporated into clinical guidelines for treating people with HIV.

Miguel, the longtime patient who started with AZT, says the standard message from doctors for people with HIV is to live as healthily as possible to avoid premature aging and related conditions. Today, he is being treated for diabetes and is in remission for anal cancer. He can’t know if HIV or the drugs that sustain him, or neither, caused the conditions, but he does not give it much thought.

“I have a great marriage, a lovely home, I have dogs and a job that I love,” he says. “The amazing thing is I am still here.”

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Tammy Worth is an award-winning health-care reporter and editor based in Kansas City, Missouri. Her work can be found at www.tammyworth.net.

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Worm-inspired treatments inch toward the clinic

Infection by certain wrigglers may reduce inflammation and fight obesity and diabetes. Scientists are at work to turn the findings into therapies.

By Amber Dance    06.03.2025

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The experiment was a striking attempt to investigate weight control. For six weeks, a group of mice gorged on lard-enriched mouse chow, then scientists infected the mice with worms. The worms wriggled beneath the animals’ skin, migrated to blood vessels that surround the intestines, and started laying eggs.

Bruno Guigas, a molecular biologist at the Leiden University Center for Infectious Diseases in the Netherlands, led this study some years back and the results, he says, were “quite spectacular.” The mice lost fat and gained less weight overall than mice not exposed to worms. Within a month or so, he recalls, the scientists barely needed their scale to see that the worm-infested mice were leaner than their worm-free counterparts. Infection with worms, it seems, reversed obesity, the researchers reported in 2015.

While it’s true that worms gobble up food their hosts might otherwise digest, that doesn’t seem to be the only mechanism at work here. There’s also some intricate biology within the emerging scientific field of immunometabolism.

Over the past couple of decades, researchers have recognized that the immune system doesn’t just fight infection. It’s also intertwined with organs like the liver, the pancreas and fat tissue, and implicated in the progression of obesity and type 2 diabetes. These and other metabolic disorders generate a troublesome immune response — inflammation — that worsens metabolism still further. Metabolic disease, in other words, is inflammatory disease.

Scientists have also observed a metabolic influence of worms in people who became naturally infected with the parasites or were purposely seeded with worms in clinical trials. While the physiology isn’t fully understood, the worms seem to dampen inflammation, as discussed in the 2024 Annual Review of Nutrition.

“We’re never going to cure or treat metabolic disease with worm infections,” says Guigas. They cause unpleasant side effects like nausea, and it would be impractical to dose millions of people with parasites. But worms can be valuable tools for scientists to understand the feedback between inflammation and metabolism. The findings could inspire more traditional, less ick-inducing treatments.

The worms’ good turns

The worms we’re talking about are helminths such as flukes and roundworms. While they’ve largely been eliminated from developed nations, an estimated 1.5 billion people worldwide carry them. They can be dangerous in high numbers, and cause symptoms such as diarrhea and malnutrition in those at high risk, including children and immunocompromised individuals, and during pregnancy.

Hookworms are one of the groups being studied for potential impact on metabolism. Natural infection happens when the worms are excreted by an infectious host and penetrate the skin of a new host.

But for most people, infection with a few worms is pretty benign. “Throughout human evolution, I think, there’s been this nice sort of truce,” says Paul Giacomin, an immunologist at James Cook University in Cairns, Australia. As part of that detente, he says, helminths evolved molecules that tell the human immune system, “I’m not here, don’t worry about me.” In turn, people might have evolved to depend a bit on worms to temper inflammation.

Today, metabolic disease is a massive global problem, with obesity affecting an estimated 890 million people. Some 580 million have type 2 diabetes, which arises when the hormone insulin, which controls blood sugar levels, is in short supply or the body’s cells become insensitive to it.

Links between metabolic disease and worm infection emerged from research on human populations. Studies in Australia, Turkey, Brazil, China, India and Indonesia showed that people with metabolic conditions such as diabetes were less likely to have helminth infections, and vice versa. “This observation is quite strong,” says Ari Molofsky, an immunologist at the University of California, San Francisco.

Going a step further, scientists observed what happened when they provided deworming treatments. “The overwhelming majority of the studies showed that deworming worsens your metabolic health,” says Giacomin.

Scientists looked to lab mice for additional clues. Molofsky and colleagues, in 2011, reported that when they infected mice on high-fat food with the gut worm Nippostrongylus brasiliensis, the infection improved blood sugar control. Similarly, in Guigas’ study, published in 2015, the worms — blood flukes called Schistosoma mansoni — improved not just weight, but also blood sugar processing. And the worms needn’t be alive: Even molecules collected from crushed worm eggs improved metabolism.

Blood flukes like Schistosoma mansoni are another type of worm being investigated for their metabolism-regulating properties. In this magnified image, a male and female are shown together.

CREDIT: EYE OF SCIENCE / SCIENCE SOURCE

The going hypothesis is that metabolic problems kick off a vicious immunometabolic cycle. First, Guigas says, damaged cells in metabolic organs cry for help, releasing molecular signals that call in immune cells. When the immune cells arrive, they morph into forms that promote a type of inflammation called Th1. Th1 responses are good at combating viruses, but they’re the wrong choice here. Th1 can aggravate metabolic problems by impairing insulin manufacture, altering insulin signaling and amplifying insulin resistance.

Thus, instead of helping, the immune cells cause further stress in the metabolic tissues. So the tissues call in more immune cells — and the cycle repeats.

Worms seem to break the cycle. In great part, that’s probably because their “I’m not here” message causes a different kind of immune response, Th2, that dampens the Th1 reaction and re-normalizes the system. Other mechanisms might also be at work: Worms might reduce appetite; it’s known they can alter gut microbes; and Guigas suspects they can also manipulate creatures’ metabolisms via non-immune pathways.

“The parasitic worms are real masters at controlling inflammation,” says Giacomin, who coauthored an article on helminths and immunity in the 2021 Annual Review of Immunology. Thus, scientists interested in controlling immunometabolic disease might take cues from these wriggly little metabolic masterminds. In fact, researchers have already tested helminths to control inflammation in autoimmune conditions such as inflammatory bowel disease.

Worms can enter through the mouth or skin. They can indirectly influence the immune state of a variety of tissues, even ones they don’t inhabit. This, in turn, influences metabolism.

The accumulating evidence linking worms to metabolic benefits in animals and people inspired Giacomin and colleagues to conduct a trial of their own. Commencing in 2018, they decided to try the hookworm Necator americanus in 27 obese people who had insulin resistance, putting them at risk for type 2 diabetes. The researchers applied worm larvae in patches on the subjects’ arms; after passing through the skin, the worms would travel through the blood stream, to the lungs and then to the small intestine. An additional 13 participants were assigned to placebo patches with Tabasco sauce to mimic the itch of entering worms.

N. americanus is a common cause of hookworm infections across much of the world. While most cases are asymptomatic, the time when the worms are attaching to the intestinal wall can cause symptoms like nausea and low iron levels, especially if there are a lot of worms. So the main goal was to determine if the treatment was safe, trying doses of 20 or 40 worms. Many subjects suffered short-term unpleasantness such as bloating or diarrhea as they adjusted to their new intestinal tagalongs, but overall, most did fine.

After 12 months, the people who got hookworms had lower insulin resistance and reduced fasting blood sugar levels. After two years, those who received 20 worms had lost an average of 11 pounds — though not all individuals lost weight, and some gained.

“It was quite convincing that the worms were having some sort of beneficial effect,” says Giacomin. The subjects were convinced too: When the study was over, the researchers offered deworming, but most participants elected to keep their worms.

Giacomin and Guigas hope to identify worm components or invent worm-inspired molecules to produce similar effects without whole parasites. Giacomin cofounded a company, Macrobiome Therapeutics in Cairns, to develop hookworm molecules into treatments. Such medications might be based on the wriggly parasites, but they’d be an easier pill to swallow.

Editor’s note: This article was corrected on July 7, 2025. It earlier said that obesity affects an estimated 890 million people and that another 580 million have type 2 diabetes. In fact, the populations with obesity and the populations with type 2 diabetes are overlapping — so the word “another” has been removed.

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Amber Dance is a freelance science journalist in the Los Angeles area and a special contributor for Knowable Magazine.

LIVING WORLD | VIEW ON WEBSITE

The history of the ocean, as told by tiny beautiful fossils

Bountiful remains of foraminifera reveal how organisms responded to climate disturbances of the past. They can help predict the future, too.

By Tim Vernimmen    05.28.2025

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Climate change and declining biodiversity are the two biggest environmental crises facing humankind today, but predicting how they’ll play out together is tricky. Ideally, scientists would study how life on Earth responded to previous periods of drastic climate change, but the fossil record for most species is spotty.

The fossils of foraminifera are an exception, however: They’re everywhere.

These unicellular marine organisms are encased in shells often built from calcium carbonate, the main ingredient of chalk (which derives from shells of foraminifera and other creatures that rain down on the seafloor when they die). Their name, derived from Latin, refers to the holes connecting the different chambers inside their often-beautiful shells. A fringe of extensions protruding around the shell allows them to find and collect food.

“When you look at a living foram, it’s like a little grain of sand with a big sunburst of snotty tentacles around it,” says paleoceanographer Chris Lowery of the University of Texas at Austin.

This picture shows a living foraminiferan, on the right, of the species Globigerinella calida, fished out of the southwestern Indian Ocean with a plankton net in 2009. The tentacles it uses to feed and move are clearly visible, extending a significant distance from the shell.

CREDIT: TRACY AZE / UNIVERSITY OF PLYMOUTH

Most foraminiferan species reside on the seafloor, but paleontologists are particularly interested in planktonic species, which live suspended in open water. Because of their astonishing numbers and short lives, their fossils are found globally across the ocean floor.

This has allowed researchers to reconstruct in detail which species flourished and which suffered when climate changed in the past, all by studying the shells and the chemical clues they contain. “If you do a little bit of chemistry on a foram shell, you can reconstruct things like the water temperature when it was growing,” says micropaleontologist Andy Fraass of the University of Victoria in Canada. “So they can tell us a lot about oceanic conditions.”

Researchers study the fossils by drilling into ocean sediment to reveal layer upon layer of the calcareous shells. The deeper they go, the further they look back in time. “You can pull up a tube of mud from the ocean floor, and take samples along its length, and they’ll each contain thousands of forams: a detailed record of their local history,” Lowery says.

Researchers on board a research vessel in 2022 in the western South Atlantic take samples along the length of sediment cores in search of marine fossils. The sediment being examined dates from the Paleocene-Eocene Thermal Maximum — a warming event from 56 million years ago.

CREDIT: CHRIS LOWERY & IODP

Mass extinction

This kind of work has helped to reveal that planktonic foraminifera first showed up in the Jurassic period about 180 million years ago and experienced a major crisis when an asteroid hit the Earth some 66 million years ago. “Everyone talks about the dinosaurs going extinct at that time,” says micropaleontologist Paul Pearson of University College London, “but we know the details of what happened from foram fossils. First, there are many, then a distinct layer formed right after the impact, and [then there are] very few after.”

The impact vaporized rocks, releasing large quantities of sulfur and dust into the air. “That, and smoke from the many fires, blocked out sunlight for years,” says Lowery, who was part of an ocean-drilling expedition in 2016 investigating the crater left by the asteroid. “This prevented the algae at the base of the marine food chain from doing photosynthesis and caused many ecosystems to collapse.” Deep-seafloor-dwelling foraminifera, which were far away from the surface and were able to keep feeding on the remains of dead organisms, were mostly fine, but nine out of 10 planktonic species went extinct.

After this mass extinction, it took about 10 million years for foraminiferan species diversity to recover, Fraass and Lowery reported in 2019. “When species go extinct, it’s as if a big branch of their family tree breaks off,” says Fraass. “And it takes a lot of time to re-evolve enough diversity to regrow a branch.”

Foraminiferan fossils allow researchers to plot foraminifera diversity through time. The catastrophic events marking the Cretaceous-Paleogene and Eocene-Oligocene boundaries caused dramatic drops in the number of species observed in the fossil record.

Yet for those that survived the carnage, this created opportunities. “With so many species gone, there is less competition for previously rare resources, and even unusual individuals may have a shot, and perhaps be surprisingly successful,” says marine ecologist Tracy Aze of the University of Plymouth in the United Kingdom.

Soon after the impact, a new type of foraminiferan appeared, says Pearson, “studded with spines that may have helped them to float as well as capture more food.”

Hot and cold

While the asteroid’s sun-blocking fallout caused a period of severe cooling, the next big crisis sounds eerily more familiar: About 56 million years ago, the average temperature on the planet increased by up to 5 degrees Celsius, possibly due to greenhouse gas emissions from volcanic activity.

Seafloor foraminifera in deep waters were badly hit, likely because high levels of CO_2 entering the ocean caused acidification that damaged their calcareous shells — such effects are the greatest at large depths. But this time, few plankton species went extinct, in part because foraminifera escaped the warmth by moving to colder areas.

“In the tropics, it may have become too hot for them to survive, with water temperatures up to 40 degrees C,” Aze says. “But we see many tropical species show up in more temperate areas — while temperate species shifted polewards, as they are again doing today.” Many foraminifera found refuge in or near the Southern Ocean around Antarctica.

Another mass extinction started around 33.9 million years ago, caused by a big dip in temperatures in a period called the Eocene-Oligocene transition. This foreshadowed a gradual cooling that would culminate in the most recent ice age. “We jokingly refer to the Oligocene as the Uglyocene,” says Aze. All the weird and wonderful planktonic foraminifera disappeared, and only some small unornamented ones remained. “We’re not sure why.”

As before, that big crisis created big opportunities, and new species evolved with new habits and habitats. Currents originating at the poles caused increasing temperature differences between ocean layers that peaked near the equator. This created a wider range of conditions that supported a rich variety of species.

In a 2023 study, Aze and others showed that around 15 million years ago, the global spread of foraminiferan diversity became roughly what it is now — greatest near the equator and gradually decreasing toward the poles.

Uncertain future

What do these past events tell us about what we might expect for foraminiferan diversity — and that of other species — on a planet we are rapidly warming up today?

In a 2023 study, Pearson and colleagues used foraminifera fossil data to predict the fate of the ocean’s twilight zone, a region 200 to 1,000 meters below the surface. They estimated that the food supply reaching the middle of this zone will decline more than 20 percent in a mild warming scenario in which the average global surface temperature rise stays below 2 degrees Celsius, and decline up to 70 percent in the unlikely event that temperatures rise 6 degrees by 2100. That’s because warming increases the rate of decay of falling organic debris, so that less of it reaches the twilight zone.

This would likely wreak havoc in this vast but understudied part of the world that provides crucial habitat to many marine animals that dive for prey as well as to unique species like lanternfish that descend there during the day.

Already, says Aze, organisms are shifting their ranges poleward in response to global warming and, in step, scientists have noted a dip in diversity of foraminifera around the equator. “That will likely expand,” she says.

Though some species may find temporary refuge by moving toward the poles, the pace of climate change may be too rapid for many. A 2024 study of foraminifera trends found that foraminiferan abundance has declined almost 25 percent over the past 80 years.

That might be a bad sign for biodiversity in other groups of creatures, which often follow foraminiferan trends. Since foraminifera as a group bounced back from several mass extinctions, they are very unlikely to disappear, says Fraass. But recovery may take a long time, and humanity’s involvement makes predicting the near future especially difficult. Or as Lowery put it: “Ask me again in a couple thousand years.”

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Tim Vernimmen is a freelance science journalist based near Antwerp, Belgium. He considered writing this story in chalk, but then you probably wouldn’t read it.

FOOD & ENVIRONMENT | VIEW ON WEBSITE

How farmers can help rescue water-loving birds

Cranes, sandpipers, ducks, geese and many other waterbirds have lost essential rest stops along their seasonal migration routes. Bird-friendly agriculture can assist in filling the gaps.

By Lela Nargi    05.20.2025

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James Gentz has seen birds aplenty on his East Texas rice-and-crawfish farm: snow geese and pintails, spoonbills and teal. The whooping crane couple, though, he found “magnificent.” These endangered, long-necked behemoths arrived in 2021 and set to building a nest amid his flooded fields. “I just loved to see them,” Gentz says.

Not every farmer is thrilled to host birds. Some worry about the spread of avian flu, others are concerned that the birds will eat too much of their valuable crops. But as an unstable climate delivers too little water, careening temperatures and chaotic storms, the fates of human food production and birds are ever more linked — with the same climate anomalies that harm birds hurting agriculture too.

In some places, farmer cooperation is critical to the continued existence of whooping cranes and other wetland-dependent waterbird species, close to one-third of which are experiencing declines. Numbers of waterfowl (think ducks and geese) have crashed by 20 percent since 2014, and long-legged wading shorebirds like sandpipers have suffered steep population losses. Conservation-minded biologists, nonprofits, government agencies and farmers themselves are amping up efforts to ensure that each species survives and thrives. With federal support in the crosshairs of the Trump administration, their work is more important (and threatened) than ever.

Their collaborations, be they domestic or international, are highly specific, because different regions support different kinds of agriculture — grasslands, or deep or shallow wetlands, for example, favored by different kinds of birds. Key to the efforts is making it financially worthwhile for farmers to keep — or tweak — practices to meet bird forage and habitat needs.

Traditional crawfish-and-rice farms in Louisiana, as well as in Gentz’s corner of Texas, mimic natural freshwater wetlands that are being lost to saltwater intrusion from sea level rise. Rice grows in fields that are flooded to keep weeds down; fields are drained for harvest by fall. They are then re-flooded to cover crawfish burrowed in the mud; these are harvested in early spring — and the cycle begins again.

A pair of whooping cranes. Sightings of charismatic birds like these on their land can hook farmers on conservation.

CREDIT: SARA ZIMORSKI / LOUISIANA DEPARTMENT OF WILDLIFE AND FISHERIES

That second flooding coincides with fall migration — a genetic and learned behavior that determines where birds fly and when — and it lures massive numbers of egrets, herons, bitterns and storks that dine on the crustaceans as well as on tadpoles, fish and insects in the water.

On a biodiverse crawfish-and-rice farm, “you can see 30, 40, 50 species of birds, amphibians, reptiles, everything,” says Elijah Wojohn, a shorebird conservation biologist at nonprofit Manomet Conservation Sciences in Massachusetts. In contrast, if farmers switch to less water-intensive corn and soybean production in response to climate pressures, “you’ll see raccoons, deer, crows, that’s about it.” Wojohn often relies on word-of-mouth to hook farmers on conservation; one learned to spot whimbrel, with their large, curved bills, got “fired up” about them and told all his farmer friends. Such farmer-to-farmer dialogue is how you change things among this sometimes change-averse group, Wojohn says.

In the Mississippi Delta and in California, where rice is generally grown without crustaceans, conservation organizations like Ducks Unlimited have long boosted farmers’ income and staying power by helping them get paid to flood fields in winter for hunters. This attracts overwintering ducks and geese — considered an extra “crop” — that gobble leftover rice and pond plants; the birds also help to decompose rice stalks so farmers don’t have to remove them. Ducks Unlimited’s goal is simple, says director of conservation innovation Scott Manley: Keep rice farmers farming rice. This is especially important as a changing climate makes that harder. 2024 saw a huge push, with the organization conserving 1 million acres for waterfowl.

A Louisiana farmer harvests crawfish before draining fields to plant rice. Rice-crawfish farms are becoming crucial for waterbirds as natural wetlands disappear.

CREDIT: RICHARD ELLIS / ALAMY STOCK PHOTO

Some strategies can backfire. In Central New York, where dwindling winter ice has seen waterfowl lingering past their habitual migration times, wildlife managers and land trusts are buying less productive farmland to plant with native grasses; these give migratory fuel to ducks when not much else is growing. But there’s potential for this to produce too many birds for the land available back in their breeding areas, says Andrew Dixon, director of science and conservation at the Mohamed Bin Zayed Raptor Conservation Fund in Abu Dhabi, and coauthor of an article about the genetics of bird migration in the 2024 Annual Review of Animal Biosciences. This can damage ecosystems meant to serve them.

Recently, conservation efforts spanning continents and thousands of miles have sprung up. One seeks to protect buff-breasted sandpipers. As they migrate 18,000 miles to and from the High Arctic where they nest, the birds experience extreme hunger — hyperphagia — that compels them to voraciously devour insects in short grasses where the bugs proliferate. But many stops along the birds’ round-trip route are threatened. There are water shortages affecting agriculture in Texas, where the birds forage at turf grass farms; grassland loss and degradation in Paraguay; and in Colombia, conversion of forage lands to exotic grasses and rice paddies these birds cannot use.

Conservationists say it’s critical to protect habitat for “buffies” all along their route, and to ensure that the winters these small shorebirds spend around Uruguay’s coastal lagoons are a food fiesta. To that end, Manomet conservation specialist Joaquín Aldabe, in partnership with Uruguay’s agriculture ministry, has so far taught 40 local ranchers how to improve their cattle grazing practices. Rotationally moving the animals from pasture to pasture means grasses stay the right length for insects to flourish.

Buff-breasted sandpipers like the one depicted here feast on insects that thrive in grasses grazed short by cattle. A Uruguay project encourages farmers to adjust their grazing practices so that insect supplies remain plentiful.

CREDIT: TOM WILBERDING / FLICKR

There are no easy fixes in the North American northwest, where bird conservation is in crisis. Extreme drought is causing breeding grounds, molting spots and migration stopover sites to vanish. It is also endangering the livelihoods of farmers, who feel the push to sell land to developers. From Southern Oregon to Central California, conservation allies have provided monetary incentives for water-strapped grain farmers to leave behind harvest debris to improve survivability for the 1 billion birds that pass through every year, and for ranchers to flood-irrigate unused pastures.

One treacherous leg of the northwest migration route is the parched Klamath Basin of Oregon and California. For three recent years, “we saw no migrating birds. I mean, the peak count was zero,” says John Vradenburg, supervisory biologist of the Klamath Basin National Wildlife Refuge Complex. He and myriad private, public and Indigenous partners are working to conjure more water for the basin’s human and avian denizens, as perennial wetlands become seasonal wetlands, seasonal wetlands transition to temporary wetlands, and temporary wetlands turn to arid lands.

Taking down four power dams and one levee has stretched the Klamath River’s water across the landscape, creating new streams and connecting farm fields to long-separated wetlands. But making the most of this requires expansive thinking. Wetland restoration — now endangered by loss of funding from the current administration — would help drought-afflicted farmers by keeping water tables high. But what if farmers could also receive extra money for their businesses via eco-credits, akin to carbon credits, for the work those wetlands do to filter-clean farm runoff? And what if wetlands could function as aquaculture incubators for juvenile fish, before stocking rivers? Klamath tribes are invested in restoring endangered c’waam and koptu sucker fish, and this could help them achieve that goal.

As birds’ traditional resting and nesting spots become inhospitable, a more sobering question is whether improvements can happen rapidly enough. The blistering pace of climate change gives little chance for species to genetically adapt, although some are changing their behaviors. That means that the work of conservationists to find and secure adequate, supportive farmland and rangeland as the birds seek out new routes has become a sprint against time.

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Lela Nargi is a journalist covering the links between food and agriculture systems, climate science and social justice issues. Find her at lelanargi.com.

LIVING WORLD | VIEW ON WEBSITE

Viruses that roam the fungal kingdom

Mushrooms and other fungi can harbor hidden companions — and some of these may fight pesky or dangerous molds

By Amber Dance    05.14.2025

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Did you know that mushrooms can get sick?

It was in 1948, in a Pennsylvania mushroom farm operated by the La France brothers, that scientists first observed a mushroom malady featuring puny caps and crooked stems. But only in 1962 did researchers finally realize viruses were behind La France disease, as it came to be called, and that viruses caused other fungal afflictions as well — thus launching a whole new field of study.

Today, scientists researching fungal viruses are enjoying a “golden age of discovery,” says Matt Kasson, a mycologist (aka fungus researcher) at West Virginia University in Morgantown. Researchers are finding all sorts of weird and wonderful interactions between fungi and their viruses and even between fungal viruses and plants or animals. Most fungal viruses don’t seem to do much of anything to their hosts, but others definitely do: Sometimes they cause sickness, sure, but sometimes they offer surprising benefits.

Even today, most fungi remain undescribed, and analyses of their viruses are scarcer still. So there’s plenty more to learn. These days, scientists can use DNA and RNA sequencing to detect signs of viruses inside fungi even if there are no other indications that a virus is there. Scientists are particularly interested in fungal viruses that cause disease in fungi that are themselves pathogens to plants, animals or even people — making the viruses potential allies against fungal infection and pests.

Here, Knowable Magazine  shares some fun facts about viruses and the fungi they infect.

Viruses show up in all kinds of fungi, in all kinds of forms.

This computer-generated image depicts the structure of a partitivirus that infects a type of Penicillium mold.

CREDIT: SCIENCE PICTURE CO. / SCIENCE SOURCE

“Almost all fungi have viruses — they’re extremely common,” says Marilyn Roossinck, a virus ecologist retired from Penn State University in University Park. She adds: “They’re so cool.”

Many plant and animal viruses enclose their genes within a protein coat or even a membranous bubble, creating a particle that can flit from host to host. But “fungal viruses are very exceptional,” says Nobuhiro Suzuki, a virologist at Okayama University in Kurashiki, Japan.

Some have no coat at all, notes Suzuki, who coauthored an article about fungal virus diversity and evolution for the Annual Review of Phytopathology. They never seem to leave their host’s comfortable embrace. And in one interesting case, Suzuki and colleagues came across a virus that has no coat of its own but borrows the coat of another virus. They named the borrower yado-kari, the Japanese term for hermit crab, which translates to “borrowing a room to stay.” They called the other virus yado-nushi, for “landlord.”

Whether or not they sport outerwear, most fungal viruses don’t find new homes by going outside the host like, say, a flu virus does. They’re typically transmitted when two fungal strands meet in the soil. Strands from related fungi can fuse, sharing insides — and their viruses.

Fungal viruses also vary greatly in their genomes: Some get by with one or a handful of genes; others are genomic giants, with more than 300 genes.

Fungal viruses are so common that some fungi are homes to multiple types — in one study, a fungus was found to contain 17 different viruses, and others have more than 20, says Jiatao Xie, a fungal virologist at the Huazhong Agricultural University in Wuhan, China, who coauthored a discussion of fungal virus diversity and evolution in the Annual Review of Microbiology. And they show up in a diverse array of hosts, such as fungi that live in marine environments, including in sea grass and sea cucumbers, or fungi that have emerged from thawing permafrost.

Viruses can give fungi properties they didn’t have before.

The panic grass Dichanthelium lanuginosum that grows in the geothermally heated soils of Yellowstone National Park can only thrive if it contains the fungus Curvularia protuberata as well as a virus of the fungus.

Back in the early 2000s, colleagues of Roossinck found an interesting fungus-plant pairing in Yellowstone National Park, where soils can reach temperatures of 50 degrees Celsius or higher. When the grass was alone, growing at 50 degrees caused it to shrivel and lose its green hue. If occasionally exposed to 65 degrees, it died. But if the grass hosted the fungus Curvularia protuberata, the pair could withstand 50 degrees and intermittent 65-degree spikes.

Roossinck, curious, investigated further, and found that the heat tolerance happened only when the fungus contained a virus that the team named Curvularia thermal tolerance virus.

In other words, the heat-tolerant pair was really a trio. “The virus has to be there,” says Roossinck. “They have to have all three.”

Scientists used viruses to track white-nose syndrome in bats.

The US spread of the white nose fungus in bats appears to be facilitated by a fungal virus that enhances spore formation.

CREDIT: RYAN VON LINDEN, NEW YORK DEPARTMENT OF ENVIRONMENTAL CONSERVATION / FLICKR

The white-nose syndrome that has killed more than 6 million bats in North America since 2006 is caused by a fungus, Pseudogymnoascus destructans, that grows on the creatures’ snouts, ears and wings. Roossinck was not surprised to discover that this fungus harbors a virus. It’s a member of the Partitiviridae family, which have two or three genes and form polyhedral particles.

It’s been hard to map the spread of white-nose syndrome because bats travel so far. The virus provided a solution: Roossinck and colleagues traced the fungus by tracking mutations in the quickly evolving gene responsible for the virus’s coat. Changes in that gene over time revealed how the fungus-virus pair moved from Connecticut to other parts of the Eastern United States, and even to Washington state.

The virus is unique to North American P. destructans and it is, Roossinck thinks, what makes the fungus so destructive: Only fungi containing the virus can make plentiful viable spores, helping it spread from bat to bat.

Some viruses shuttle between fungi and plants.

Certain viruses can be shared by fungi and plants, fungi and animals, or plants and animals, allowing cross-kingdom transmission that influences crops, their fungal pathogens and the insects that transmit viruses.

Many plants and fungi are tightly linked — so much so that viruses can cross between them. In China’s Inner Mongolia province, researchers found a root-rot fungus, Rhizoctonia solani, in a potato plant. That fungus had a hanger-on: the cucumber mosaic virus, which usually infects (you guessed it) cucumbers, among many other fruits, vegetables, herbs and weeds. In the lab, the virus could be passed from plants to fungi. Once inside fungi, it could spread to other plants.

So, cucumber mosaic virus is a plant-focused virus that also has a taste for fungi. The same research team next tested whether a fungus-focused virus could also be passed into plants. They found that the coatless Cryphonectria hypovirus 1, which typically infects fungi, could indeed infect tobacco plants. Alone, it could get into the leaves it was placed on but it couldn’t spread to other plant parts. But if another virus, like the tobacco mosaic virus, was also present, both viruses could travel around the plant. That’s because the tobacco plant virus contributed a “movement protein” that helped both viruses travel. The researchers think this ability to cross host kingdoms may be an important factor in viral spread and evolution.

Fungal viruses can protect plants — and maybe even animals — from fungal infections.

Scientists have developed a treatment for crops that uses a fungus that is infected with a virus. The treatment, which works like a vaccine against plant-harming fungi, resulted in noticeably greater rice yield (rightmost sheaves) than in untreated crops (leftmost sheaves).

CREDIT: COURTESY OF JIATAO XIE

If fungi are the enemy of farmers growing plants, then viruses of fungi could be the farmers’ best friends.

Indeed, this has been shown before. In the mid-1900s, European scientists battling a fungus of chestnut trees discovered that the Cryphonectria hypovirus 1 slows the infection, giving the trees time to mount an immune response. “It worked pretty well,” says Kasson; the virus became a flagship example of viral biocontrol. Unfortunately, the same virus largely failed to protect American chestnuts; most of the American fungi were of genetic types unable to accept transfer of the virus from the donor fungi.

But the idea stands. Xie and his Huazhong colleague Daohong Jiang are developing a virus to help crops like rapeseed and soybean. It fights the fungus pest Sclerotinia sclerotiorum, which causes white mold in more than 700 plant species, Xie says. The virus, SsHADV-1, weakens the fungus’s ability to cause disease — but there’s more to it than that. Unlike most fungal viruses, it can leave the fungus and spread as free particles, or be transmitted by a fungus-eating gnat. Moreover, in a fungal Jekyll-and-Hyde switcheroo, the virus turns the fungus from something that harms plants to something that benefits them.

That’s because the virus-weakened fungus acts kind of like a vaccine. Exposure to the infected fungus triggers plant defenses, making the plants better able to fight off other kinds of disease, not just white mold. The virus-fungus combo also alters the plants’ hormone signaling and circadian rhythms in ways that boost growth.

Xie and colleagues developed a way to spray virus-infected fungal fragments over crops as a natural fungicide. The sprayed bits act as vaccine by outcompeting, or infecting, any plant-harming Hyde fungi until all that’s left is vaccinesque Jekyll. Indeed, Xie says, field trials showed that the treatment boosted yield of rapeseed, rice and wheat.

The potential to transmit the virus by spray (or insect) makes it “a really big deal,” says Timothy James, a mycologist at the University of Michigan in Ann Arbor. Though the viral treatment hasn’t yet hit the market, patents are approved in China, Canada and the United States, Xie says. If successful, it would join the virus that weakens chestnut-blight fungus as another example of viral biocontrol.

And scientists speculate they might be able to protect animals from fungi, too, with the right viruses. James, for example, is trying protect amphibians from a deadly chytrid fungus, using what he’s learned from a virus that infects it. And Roossinck has experimented with viruses that infect Aspergillus mold, which can cause allergic reactions, often in people with asthma or cystic fibrosis, and fatal lung infections in immunocompromised people.

Those other treatments haven’t happened yet, says Xie. For now, it’s “just a thought.”

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Knowable contributor Amber Dance, a science writer in the Los Angeles area, wishes the fungi that keep growing on her raspberries would pick up a virus.

Table of Contents

Knowable Magazine: 2025 Sep 14

All articles

Shucking the past: Can oysters thrive again?

The other end of the weight spectrum: Very thin people

Can a shift in strategy reduce intimate partner violence?

Unsafe at home: The misery of intimate partner violence

See something, say something? The science of speaking out

Using pollen to make paper, sponges and more

How a mysterious particle could explain the universe’s missing antimatter

How the cavefish lost its eyes — again and again

Civilizations of Africa through a new lens

Uncovering the impact of artisanal fisheries

Super-resolution microscopes showcase the inner lives of cells

Mighty mitochondria: Cell powerhouses harnessed for healing

Dogs and their people: Companions in cancer research

Watching the world, one quintillionth of a second at a time

How rogue jumping genes can spur Alzheimer’s, ALS

HIV medications: Did fears about side effects come to pass?

Worm-inspired treatments inch toward the clinic

The history of the ocean, as told by tiny beautiful fossils

How farmers can help rescue water-loving birds

Viruses that roam the fungal kingdom